Researchers are suggesting that there is a link between the number of friends you have and the size of the region of the brain -- known as the orbital prefrontal cortex -- that is found just above the eyes. A new study shows that this brain region is bigger in people who have a larger number of friendships.
Their study is published on 1 February 2012 in the journal, Proceedings of the Royal Society B.
The research was carried out as part of the British Academy Centenary 'Lucy to Language' project, led by Professor Robin Dunbar of the University of Oxford in a collaboration with Dr Joanne Powell and Dr Marta Garcia-Finana at Liverpool University, Dr Penny Lewis at Manchester University and Professor Neil Roberts at Edinburgh University.
The study suggests that we need to employ a set of cognitive skills to maintain a number of friends (and the keyword is 'friends' as opposed to just the total number of people we know). These skills are described by social scientists as 'mentalising' or 'mind-reading'- a capacity to understand what another person is thinking, which is crucial to our ability to handle our complex social world, including the ability to hold conversations with one another. This study, for the first time, suggests that our competency in these skills is determined by the size of key regions of our brains (in particular, the frontal lobe).
Professor Dunbar, from the Institute of Cognitive and Evolutionary Anthropology, explained: '"Mentalising" is where one individual is able to follow a natural hierarchy involving other individuals' mind states. For example, in the play 'Othello', Shakespeare manages to keep track of five separate mental states: he intended that his audience believes that Iago wants Othello to suppose that Desdemona loves Cassio [the italics signify the different mind states]. Being able to maintain five separate individuals' mental states is the natural upper limit for most adults.'
The researchers took anatomical MR images of the brains of 40 volunteers at the Magnetic Resonance and Image Analysis Research Centre at the University of Liverpool to measure the size of the prefrontal cortex, the part of the brain used in high-level thinking. Participants were asked to make a list of everyone they had had social, as opposed to professional, contact with over the previous seven days. They also took a test to determine their competency in mentalising.
Professor Robin Dunbar, said: 'We found that individuals who had more friends did better on mentalising tasks and had more neural volume in the orbital frontal cortex, the part of the forebrain immediately above the eyes. Understanding this link between an individual's brain size and the number of friends they have helps us understand the mechanisms that have led to humans developing bigger brains than other primate species. The frontal lobes of the brain, in particular, have enlarged dramatically in humans over the last half million years.'
Dr Joanne Powell, from the Department of Psychology, University of Liverpool, said: 'Perhaps the most important finding of our study is that we have been able to show that the relationship between brain size and social network size is mediated by mentalising skills. What this tells us is that the size of your brain determines your social skills, and it is these that allow you have many friends.'
Professor Dunbar said: 'All the volunteers in this sample were postgraduate students of broadly similar ages with potentially similar opportunities for social activities. Of course, the amount of spare time for socialising, geography, personality and gender all influence friendship size, but we also know that at least some of these factors, notably gender, also correlate with mentalising skills. Our study finds there is a link between the ability to read how other people think and social network size.'
Professor Dunbar's research was funded by the British Academy Centenary Research Project and by the British Academy Research Professorship. His research has already examined the different brain sizes of different species, but this study looks at the differences within species. Professor Dunbar published a paper last year, which found that people living near to the Poles needed larger brains for visual processing because of the dimmer light conditions.
Super-human brain technology sparks ethics debate
A British ethics group has launched a debate on the ethical dilemmas posed by new technologies that tap into the brain and could bring super-human strength, highly enhanced concentration or thought-controlled weaponry.
With the prospect of future conflicts between armies controlling weapons with their minds, the Nuffield Council on Bioethics launched a consultation on Thursday to consider the risks of blurring the lines between humans and machines.
"Intervening in the brain has always raised both hopes and fears in equal measure. Hopes of curing terrible diseases, and fears about the consequences of trying to enhance human capability beyond what is normally possible," said Thomas Baldwin, a professor of philosophy at Britain's York University who is leading the study.
"These challenge us to think carefully about fundamental questions to do with the brain: What makes us human? What makes us an individual? And how and why do we think and behave in the way we do?."
The Council, an independent body which looks at ethical issues raised by new developments in biology and medicine, wants to focus on three main areas of neurotechnologies that change the brain: brain-computer interfaces (BCIs), neurostimulation techniques such as deep brain stimulation (DBS) or transcranial magnetic stimulation (TMS), and neural stem cell therapy.
These technologies are already at various stages of development for use in the treatment of medical conditions including Parkinson's disease, depression and stroke, and experts think they could bring significant benefits, especially for patients with severe brain disease or damage.
GROWING FAST
But they also have huge potential outside the health context. In military applications, BCIs are being used to develop weapons or vehicles controlled remotely by brain signals, and there is big commercial scope in the gaming industry with the development of computer games controlled by people's thoughts.
Speaking at a briefing to launch the consultation, Baldwin said the estimated total global market for all neurotechnologies - including pharmaceuticals for the treatment of brain disorders - is around $150 billion.
"Setting pharmaceuticals aside, the value of the market for the devices and technologies we are dealing with is something in the region of $8 billion, and growing fast," he said.
Kevin Warwick, a professor of Cybernetics at the University of Reading and a supporter of more neurotechnology research, said some experimental brain technologies had great potential in medicine.
"From the brain signals, a brain computer interface could translate a person's desire to move ... and then use those signals to operate a wheelchair or other piece of technology," he said. "For someone who has locked-in syndrome, for example, and cannot communicate, a BCI could be life-changing."
But he and Baldwin also stressed there are concerns about safety of some experimental techniques that involve implants in the brain, and about the ethics of using such technology in other medicine and other fields.
"If brain-computer interfaces are used to control military aircraft or weapons from far away, who takes ultimate responsibility for the actions? Could this be blurring the line between man and machine?" Baldwin said.
The ethics council's consultation is at www.nuffieldbioethics.org/neurotechnology. The deadline for responses is April 23 and it expects to publish a report with recommendations in 2013.
With the prospect of future conflicts between armies controlling weapons with their minds, the Nuffield Council on Bioethics launched a consultation on Thursday to consider the risks of blurring the lines between humans and machines.
"Intervening in the brain has always raised both hopes and fears in equal measure. Hopes of curing terrible diseases, and fears about the consequences of trying to enhance human capability beyond what is normally possible," said Thomas Baldwin, a professor of philosophy at Britain's York University who is leading the study.
"These challenge us to think carefully about fundamental questions to do with the brain: What makes us human? What makes us an individual? And how and why do we think and behave in the way we do?."
The Council, an independent body which looks at ethical issues raised by new developments in biology and medicine, wants to focus on three main areas of neurotechnologies that change the brain: brain-computer interfaces (BCIs), neurostimulation techniques such as deep brain stimulation (DBS) or transcranial magnetic stimulation (TMS), and neural stem cell therapy.
These technologies are already at various stages of development for use in the treatment of medical conditions including Parkinson's disease, depression and stroke, and experts think they could bring significant benefits, especially for patients with severe brain disease or damage.
GROWING FAST
But they also have huge potential outside the health context. In military applications, BCIs are being used to develop weapons or vehicles controlled remotely by brain signals, and there is big commercial scope in the gaming industry with the development of computer games controlled by people's thoughts.
Speaking at a briefing to launch the consultation, Baldwin said the estimated total global market for all neurotechnologies - including pharmaceuticals for the treatment of brain disorders - is around $150 billion.
"Setting pharmaceuticals aside, the value of the market for the devices and technologies we are dealing with is something in the region of $8 billion, and growing fast," he said.
Kevin Warwick, a professor of Cybernetics at the University of Reading and a supporter of more neurotechnology research, said some experimental brain technologies had great potential in medicine.
"From the brain signals, a brain computer interface could translate a person's desire to move ... and then use those signals to operate a wheelchair or other piece of technology," he said. "For someone who has locked-in syndrome, for example, and cannot communicate, a BCI could be life-changing."
But he and Baldwin also stressed there are concerns about safety of some experimental techniques that involve implants in the brain, and about the ethics of using such technology in other medicine and other fields.
"If brain-computer interfaces are used to control military aircraft or weapons from far away, who takes ultimate responsibility for the actions? Could this be blurring the line between man and machine?" Baldwin said.
The ethics council's consultation is at www.nuffieldbioethics.org/neurotechnology. The deadline for responses is April 23 and it expects to publish a report with recommendations in 2013.
High Blood Sugar Lowers Chances of Surviving a Heart Attack
Patients with high blood sugar run an increased risk of dying if they have a heart attack, and diabetics are less likely to survive in-hospital cardiac arrest than non-diabetics, reveals research at the Sahlgrenska Academy, at the University of Gothenburg, Sweden.
Diabetes is common among patients with coronary artery disease, and this is a potentially lethal combination: a thesis from the University of Gothenburg's Sahlgrenska Academy reveals that diabetes in coronary artery disease patients brings a significantly increased risk of premature death.
Smaller chance of surviving
Doctoral student and researcher Petur Petursson investigated the connection between blood sugar disorders and survival following heart attacks and cardiac arrest. His thesis shows that patients with diabetes have a smaller chance of surviving in-hospital cardiac arrest. Diabetes and pre-diabetes are also associated with a less favourable prognosis following coronary artery surgery.
"Type 2 diabetics with suspected coronary artery disease who are on insulin therapy have lower survival," he explains. "We've not been able to demonstrate the exact cause, but much of it may be because those on insulin therapy have more severe disease."
Need for careful management
Petur Petursson says that the results underline the need for careful management of patients with coronary artery disease and the importance of accurately diagnosing and managing blood sugar disorders.
"Medical personnel can pretty much assume that coronary artery disease patients will have some kind of blood sugar disorder, so there must be established strategies for managing these disorders at every heart clinic in the country."
The thesis Aspects of Abnormal Glucose Regulation in Various Manifestations of Coronary Artery Disease was defended on 23 February.
Diabetes is common among patients with coronary artery disease, and this is a potentially lethal combination: a thesis from the University of Gothenburg's Sahlgrenska Academy reveals that diabetes in coronary artery disease patients brings a significantly increased risk of premature death.
Smaller chance of surviving
Doctoral student and researcher Petur Petursson investigated the connection between blood sugar disorders and survival following heart attacks and cardiac arrest. His thesis shows that patients with diabetes have a smaller chance of surviving in-hospital cardiac arrest. Diabetes and pre-diabetes are also associated with a less favourable prognosis following coronary artery surgery.
"Type 2 diabetics with suspected coronary artery disease who are on insulin therapy have lower survival," he explains. "We've not been able to demonstrate the exact cause, but much of it may be because those on insulin therapy have more severe disease."
Need for careful management
Petur Petursson says that the results underline the need for careful management of patients with coronary artery disease and the importance of accurately diagnosing and managing blood sugar disorders.
"Medical personnel can pretty much assume that coronary artery disease patients will have some kind of blood sugar disorder, so there must be established strategies for managing these disorders at every heart clinic in the country."
The thesis Aspects of Abnormal Glucose Regulation in Various Manifestations of Coronary Artery Disease was defended on 23 February.
Paul Allen gives $300 million to expand brain research
Microsoft Corp co-founder Paul Allen has donated an additional $300 million to a foundation aimed at expanding research into how the brain works and how best to treat brain-related disorders.
The Allen Institute for Brain Science, based in Seattle, was established with a 2003 contribution of $100 million from the former Microsoft executive, who then donated another $100 million.
The latest contribution of $300 million will support the first four years of a 10-year plan to address critical questions about how the brain works.
Allen Jones, the institute's chief executive officer, said the questions had to be answered if "we are to understand and treat autism, Alzheimer's disease, depression, traumatic brain injury and the myriad other brain-related diseases and disorders that affect all of us either directly or indirectly."
The Allen Institute for Brain Science, based in Seattle, was established with a 2003 contribution of $100 million from the former Microsoft executive, who then donated another $100 million.
The latest contribution of $300 million will support the first four years of a 10-year plan to address critical questions about how the brain works.
Allen Jones, the institute's chief executive officer, said the questions had to be answered if "we are to understand and treat autism, Alzheimer's disease, depression, traumatic brain injury and the myriad other brain-related diseases and disorders that affect all of us either directly or indirectly."
Obesity Raises Death Risk Tied to Sleeping Pills
Obesity appears to significantly increase the risk of death tied to sleeping pills, nearly doubling the rate of mortality even among those prescribed 18 or fewer pills in a year, researchers have reported.
"Obesity emerged as a marker of increased vulnerability," said Robert Langer, M.D., M.P.H., at the annual American Heart Association's Epidemiology and Prevention | Nutrition, Physical Activity and Metabolism 2012 Scientific Sessions in San Diego.
"The associations between sleeping pills and increased mortality were present, and relatively stronger, even in people aged 18 to 54," said Dr. Langer, a family physician and epidemiologist with the Jackson Hole Center for Preventive Medicine in Jackson, Wyo.
"Obese patients appear particularly vulnerable, perhaps through interaction with sleep apnea," said study co-author Daniel Kripke, a psychiatrist with Scripps Clinic's Viterbi Family Sleep Center in San Diego.
He noted that sleeping pills were previously associated with more and longer pauses in breathing in people with sleep apnea.
Among obese patients, use of sleeping pills was associated with about one extra death per year for every 100 people who were prescribed the medications, Dr. Langer said.
Higher risk for men
Additionally, men who took sleeping pills were about twice as likely to die as women who received the medications, after accounting for other factors, he said.
These new findings were the latest to emerge from a Scripps Clinic-led study of almost 40,000 patients, which was initially published in late February in the open-access online journal BMJ Open.
The research was the first to show that eight of the most commonly used hypnotic drugs were associated with increased hazards of mortality and cancer, including the popularly prescribed medications zolpidem (known by the brand name Ambien) and temazepam (also known as Restoril), Dr. Kripke said.
Those drugs had been thought to be safer than older hypnotics because of their shorter duration of action but were found to have associations with excess deaths no different from the older drugs they have largely replaced.
In order to eliminate the possibility that other factors led to the results, study participants who were prescribed sleeping pills were matched with control patients of similar ages, gender and health who did not receive hypnotics.
The newest findings were delivered by Dr. Langer during an oral session at the American Heart Association conference that focused on drug safety.
For obese patients in the study who had an average body mass index of 38.8, the risk of death was 8.1 times higher on average among those who were prescribed the smallest number of pills (18 or fewer annually) when compared with similar study participants who did not take the medications. The mortality rate was 9.3 times higher on average among obese patients receiving the largest number of pills (132 or more annually).
Death was 4.6 times more likely on average among all patients who received any amount of sleeping pills.
The study cast a shadow over a growing segment of the pharmaceutical industry that expanded by 23 percent in the United States from 2006 to 2010 and generated about $2 billion in annual sales.
Using data stored in an electronic medical record that has been in place for more than a decade, the researchers obtained information on almost 40,000 patients cared for by a large integrated health system in the northeastern United States.
The research included 10,531 sleeping pill users who were prescribed the medications for an average of 2.5 years and 23,674 control participants who were not prescribed the drugs. Information came from outpatient clinic visits conducted between Jan. 1, 2002, and Sept. 30, 2006.
"It is important to note that our results are based on observational data, so even though we did everything we could to ensure their validity, it's still possible that other factors explain the associations," said co-author Lawrence Kline, D.O., who is medical director of the Viterbi Family Sleep Center. "We hope our work will spur additional research in this area using information from other populations."
Funding for the study came from the Scripps Health Foundation and other philanthropic sources.
Alternatives to medications
The research should prompt physicians to consider alternatives to hypnotic medications, Dr. Kline said.
Clinicians at the Viterbi Family Sleep Center focus on cognitive therapy that teaches patients to better understand the nature of sleep. For example, some people suffering from insomnia might require less than the eight hours of sleep commonly recommended for each night.
Patients also can benefit from practicing good sleeping habits and relaxation, as well as taking advantage of the body's natural clock, which is driven by the rising and setting of the sun, Dr. Kline said. "Understanding how to use the circadian rhythm is a very powerful tool that doesn't require a prescription," he said.
When insomnia results from emotional problems such as depression, doctors should treat the psychological disorder rather than prescribe sleeping pills that could prove to be harmful, Dr. Kripke said.
"Obesity emerged as a marker of increased vulnerability," said Robert Langer, M.D., M.P.H., at the annual American Heart Association's Epidemiology and Prevention | Nutrition, Physical Activity and Metabolism 2012 Scientific Sessions in San Diego.
"The associations between sleeping pills and increased mortality were present, and relatively stronger, even in people aged 18 to 54," said Dr. Langer, a family physician and epidemiologist with the Jackson Hole Center for Preventive Medicine in Jackson, Wyo.
"Obese patients appear particularly vulnerable, perhaps through interaction with sleep apnea," said study co-author Daniel Kripke, a psychiatrist with Scripps Clinic's Viterbi Family Sleep Center in San Diego.
He noted that sleeping pills were previously associated with more and longer pauses in breathing in people with sleep apnea.
Among obese patients, use of sleeping pills was associated with about one extra death per year for every 100 people who were prescribed the medications, Dr. Langer said.
Higher risk for men
Additionally, men who took sleeping pills were about twice as likely to die as women who received the medications, after accounting for other factors, he said.
These new findings were the latest to emerge from a Scripps Clinic-led study of almost 40,000 patients, which was initially published in late February in the open-access online journal BMJ Open.
The research was the first to show that eight of the most commonly used hypnotic drugs were associated with increased hazards of mortality and cancer, including the popularly prescribed medications zolpidem (known by the brand name Ambien) and temazepam (also known as Restoril), Dr. Kripke said.
Those drugs had been thought to be safer than older hypnotics because of their shorter duration of action but were found to have associations with excess deaths no different from the older drugs they have largely replaced.
In order to eliminate the possibility that other factors led to the results, study participants who were prescribed sleeping pills were matched with control patients of similar ages, gender and health who did not receive hypnotics.
The newest findings were delivered by Dr. Langer during an oral session at the American Heart Association conference that focused on drug safety.
For obese patients in the study who had an average body mass index of 38.8, the risk of death was 8.1 times higher on average among those who were prescribed the smallest number of pills (18 or fewer annually) when compared with similar study participants who did not take the medications. The mortality rate was 9.3 times higher on average among obese patients receiving the largest number of pills (132 or more annually).
Death was 4.6 times more likely on average among all patients who received any amount of sleeping pills.
The study cast a shadow over a growing segment of the pharmaceutical industry that expanded by 23 percent in the United States from 2006 to 2010 and generated about $2 billion in annual sales.
Using data stored in an electronic medical record that has been in place for more than a decade, the researchers obtained information on almost 40,000 patients cared for by a large integrated health system in the northeastern United States.
The research included 10,531 sleeping pill users who were prescribed the medications for an average of 2.5 years and 23,674 control participants who were not prescribed the drugs. Information came from outpatient clinic visits conducted between Jan. 1, 2002, and Sept. 30, 2006.
"It is important to note that our results are based on observational data, so even though we did everything we could to ensure their validity, it's still possible that other factors explain the associations," said co-author Lawrence Kline, D.O., who is medical director of the Viterbi Family Sleep Center. "We hope our work will spur additional research in this area using information from other populations."
Funding for the study came from the Scripps Health Foundation and other philanthropic sources.
Alternatives to medications
The research should prompt physicians to consider alternatives to hypnotic medications, Dr. Kline said.
Clinicians at the Viterbi Family Sleep Center focus on cognitive therapy that teaches patients to better understand the nature of sleep. For example, some people suffering from insomnia might require less than the eight hours of sleep commonly recommended for each night.
Patients also can benefit from practicing good sleeping habits and relaxation, as well as taking advantage of the body's natural clock, which is driven by the rising and setting of the sun, Dr. Kline said. "Understanding how to use the circadian rhythm is a very powerful tool that doesn't require a prescription," he said.
When insomnia results from emotional problems such as depression, doctors should treat the psychological disorder rather than prescribe sleeping pills that could prove to be harmful, Dr. Kripke said.
Leukemia gene mutations linked to survival odds
Advances in genetic profiling are paving the way for more precise, and effective, treatment of the aggressive bone marrow cancer known as acute mylogenous leukemia, or AML, according to new research.
Two studies, published in the latest edition of the New England Journal of Medicine, show that genetic testing can guide doctors in how best to use current therapies as well as identify new drug targets.
"As lots of studies identify new alterations in genes in leukemia and other cancers, we need to begin to understand how these alterations in DNA can predict outcomes and determine differences in treatment," said Dr. Ross Levine of Memorial Sloan-Kettering Cancer Center in New York, the lead author of one of the studies.
Such personalized therapy is considered the new frontier for medical practice, and hopes for its success underpin a $5.7 billion hostile bid by drugmaker Roche Holding for gene sequencing company Illumina.
The second study, from Washington University in St. Louis, found that 85 percent of bone marrow cells in patients with myelodysplastic syndrome, a blood-related disorder that can precede AML, were linked to mutations in progressive cancer.
The Sloan-Kettering study analyzed bone marrow samples from 502 AML patients for mutations in 18 genes associated with the disease. The researchers were able to categorize two-thirds of the patients into groups clearly defined by their survival chances.
The study found that high-dose chemotherapy improved the rate of survival for patients with three specific genetic mutations, compared with standard-dose chemo.
It also showed that genetic profiling makes it possible to more precisely determine which patients are most likely to have their leukemia return after treatment.
AML is typically cured in about 40 percent of adults between the ages of 18 and 60, according to Levine.
"We were able to identify a very large subset of patients who need new therapies," he said. "Another set was found to do incredibly well with existing therapies, and that is very informative."
The American Cancer Society estimates that AML will be diagnosed in nearly 14,000 Americans this year and that more than 10,000 people will die from the disease.
Gene profiling for AML, and most other cancers, is not currently part of standard clinical practice.
"There are aspects of this that are ready to be adopted," Levine said, adding that the immediate hurdles are the cost of genetic testing and intellectual property rights pertaining to genes that have been patented.
And questions remain about the number of genetic mutations that AML patients should be screened for.
"It is exciting to think that the goal of personalized medicine is quickly approaching," Dr. Lucy Godley said in a NEJM editorial. "But it will require careful thought to implement genomic-based clinical evaluation in a way that is meaningful for patients."
Two studies, published in the latest edition of the New England Journal of Medicine, show that genetic testing can guide doctors in how best to use current therapies as well as identify new drug targets.
"As lots of studies identify new alterations in genes in leukemia and other cancers, we need to begin to understand how these alterations in DNA can predict outcomes and determine differences in treatment," said Dr. Ross Levine of Memorial Sloan-Kettering Cancer Center in New York, the lead author of one of the studies.
Such personalized therapy is considered the new frontier for medical practice, and hopes for its success underpin a $5.7 billion hostile bid by drugmaker Roche Holding for gene sequencing company Illumina.
The second study, from Washington University in St. Louis, found that 85 percent of bone marrow cells in patients with myelodysplastic syndrome, a blood-related disorder that can precede AML, were linked to mutations in progressive cancer.
The Sloan-Kettering study analyzed bone marrow samples from 502 AML patients for mutations in 18 genes associated with the disease. The researchers were able to categorize two-thirds of the patients into groups clearly defined by their survival chances.
The study found that high-dose chemotherapy improved the rate of survival for patients with three specific genetic mutations, compared with standard-dose chemo.
It also showed that genetic profiling makes it possible to more precisely determine which patients are most likely to have their leukemia return after treatment.
AML is typically cured in about 40 percent of adults between the ages of 18 and 60, according to Levine.
"We were able to identify a very large subset of patients who need new therapies," he said. "Another set was found to do incredibly well with existing therapies, and that is very informative."
The American Cancer Society estimates that AML will be diagnosed in nearly 14,000 Americans this year and that more than 10,000 people will die from the disease.
Gene profiling for AML, and most other cancers, is not currently part of standard clinical practice.
"There are aspects of this that are ready to be adopted," Levine said, adding that the immediate hurdles are the cost of genetic testing and intellectual property rights pertaining to genes that have been patented.
And questions remain about the number of genetic mutations that AML patients should be screened for.
"It is exciting to think that the goal of personalized medicine is quickly approaching," Dr. Lucy Godley said in a NEJM editorial. "But it will require careful thought to implement genomic-based clinical evaluation in a way that is meaningful for patients."
Magnitude 7.2 quake hits central Chile
A magnitude 7.2 earthquake hit central Chile on Sunday, shaking buildings in the capital of Santiago and the government emergency agency, ONEMI, said it was preventively evacuating some areas of the coast.
The quake struck 64 miles west north west of the town of Talca at a depth of 6.2 miles, the U.S. Geological Survey said.
Magnitude 7.0 quakes or greater are capable of causing widespread, heavy damage.
ONEMI said, however, that the quake was not expected to generate a tsunami off the coast.
The latest earthquake hit near the same central region that struck by a massive 8.8 magnitude earthquake in 2010 and ensued tsunamis in 2010 that killed about 500 people.
The central area is home to some important copper mines, but the bulk of output in the world's top copper exporting nation is concentrated in the far northern region.
The quake struck 64 miles west north west of the town of Talca at a depth of 6.2 miles, the U.S. Geological Survey said.
Magnitude 7.0 quakes or greater are capable of causing widespread, heavy damage.
ONEMI said, however, that the quake was not expected to generate a tsunami off the coast.
The latest earthquake hit near the same central region that struck by a massive 8.8 magnitude earthquake in 2010 and ensued tsunamis in 2010 that killed about 500 people.
The central area is home to some important copper mines, but the bulk of output in the world's top copper exporting nation is concentrated in the far northern region.
Forming Social Memories
Does a specific memory exist for events involving humans? French researchers from the Vulnerability, Adaptation and Psychopathology Laboratory (CNRS/Université Paris VI) and Canadian researchers from Douglas Hospital, McGill University (Montreal) have identified the internal part of the prefrontal cortex as the key structure for the memory formation of social information.
Social events like a party with friends, a work meeting or a row with a spouse are an integral part of daily life. Our ability to remember these events, and more particularly to remember the people and the relationship we have with them, is absolutely vital if we are to be well adapted to our social life. Different parts of the brain, particularly the hippocampus, are directly involved in learning and memory. Some of these regions are specialized in learning certain types of information, such as the amygdala, which is specialized in the memory of emotions.
The French team (led by Philippe Fossati ) and Canadian team have just identified a specific region of the frontal cortex which, they claim, is specialized in recording and learning social information. They used functional magnetic resonance imaging to measure the brain activity of 17 volunteers as they performed memory tasks involving pictures of social scenes (people and interactions) and nonsocial scenes (landscapes with no humans). This enabled them to identify the internal part of the prefrontal cortex, called the medial prefrontal cortex, as the key structure for encoding the social information in an image.
Previous studies carried out by the same researchers had associated this prefrontal region to processes of thinking about oneself and others. Their work suggests that, over and above emotions, the analysis of specifically human information could facilitate learning and remembering, by using brain structures specialized in the analysis of mental states and empathy. This opens up important perspectives for understanding the mechanisms of human expressions and mental disorders (e.g. schizophrenic disorders and autism), which affect social and relational skills.
Reference: Modulation of memory formation by stimulus content: specific role of the medial prefrontal cortex in the successful encoding of social pictures, Harvey, P.O., Fossati, P., Lepage, M. Journal of Cognitive Neuroscience, February 2007.
Social events like a party with friends, a work meeting or a row with a spouse are an integral part of daily life. Our ability to remember these events, and more particularly to remember the people and the relationship we have with them, is absolutely vital if we are to be well adapted to our social life. Different parts of the brain, particularly the hippocampus, are directly involved in learning and memory. Some of these regions are specialized in learning certain types of information, such as the amygdala, which is specialized in the memory of emotions.
The French team (led by Philippe Fossati ) and Canadian team have just identified a specific region of the frontal cortex which, they claim, is specialized in recording and learning social information. They used functional magnetic resonance imaging to measure the brain activity of 17 volunteers as they performed memory tasks involving pictures of social scenes (people and interactions) and nonsocial scenes (landscapes with no humans). This enabled them to identify the internal part of the prefrontal cortex, called the medial prefrontal cortex, as the key structure for encoding the social information in an image.
Previous studies carried out by the same researchers had associated this prefrontal region to processes of thinking about oneself and others. Their work suggests that, over and above emotions, the analysis of specifically human information could facilitate learning and remembering, by using brain structures specialized in the analysis of mental states and empathy. This opens up important perspectives for understanding the mechanisms of human expressions and mental disorders (e.g. schizophrenic disorders and autism), which affect social and relational skills.
Reference: Modulation of memory formation by stimulus content: specific role of the medial prefrontal cortex in the successful encoding of social pictures, Harvey, P.O., Fossati, P., Lepage, M. Journal of Cognitive Neuroscience, February 2007.
Study finds electrotherapy dampens brain connections
Scientists have discovered how electroconvulsive or electric shock therapy - a controversial but effective treatment - acts on the brains of severely depressed people and say the finding could help improve diagnosis and treatment of mental illness.
Electroconvulsive therapy (ECT) involves first anaesthetizing the patient and then electrically inducing a seizure.
It has a controversial reputation - gained in part because of its role in the 1975 film "One Flew Over The Cuckoo's Nest" starring Jack Nicholson - but is a potent and effective treatment for patients with mood disorders like severe depression.
Yet despite it being used successfully in clinical practice around the world for more than 70 years, scientists have until now not been entirely clear how or why it works.
Now a team from Aberdeen University in Scotland has shown for the first time that ECT affects the way different parts of the brain involved in depression communicate with each other.
In a study published in the Proceedings of the National Academy of Sciences (PNAS) journal they found ECT appears to turn down overactive connections between parts of the brain that control mood and parts that control thinking and concentrating.
This stops the overwhelming impact that depression has on patients' ability to enjoy life and carry out day-to-day activities, they said.
"We've solved a 70-year-old therapeutic riddle," said Ian Reid, a professor of psychiatry at the University of Aberdeen who led the study.
"Our key finding is that if you compare the connections in the brain before and after ECT, ECT reduces the connection strength," he said in a statement.
"For the first time we can point to something that ECT does in the brain that makes sense in the context of what we think is wrong in people who are depressed."
In recent years, experts have developed a new theory on how depression affects the brain that suggests there is a "hyperconnection" between the areas of the brain involved in emotional processing and mood change and the parts of the brain involved in thinking and concentrating.
David Nutt, a professor of neuropsychopharmacology at Imperial College London who was not involved in the ECT study, said its findings "make a lot of sense.
"The disabling of connections between different areas of the brain is what I would have predicted from the depression literature," he said in an emailed comment.
He said the results also chime with a study Nutt published in January which found that psilocybin, the active ingredient in the psychedelic drug known as magic mushrooms, also disrupts this network of connections and may also be effective in treating severe depression.
The electrotherapy study involved using functional magnetic resonance imaging (fMRI) to scan the brains of nine severely depressed patients before and after ECT and then applying complex mathematical analysis to investigate brain connectivity.
Aberdeen University's chair of neuroimaging Christian Schwarzbauer, who devised the new method for analyzing the connectivity data, said it enabled the team to see to what extent more than 25,000 different brain areas communicated with each other.
He said the new method could also be applied to a wide range of other brain disorders such as schizophrenia, autism, or dementia, and "may lead to a better understanding of the underlying disease mechanisms and the development of new diagnostic tools."
The researchers said they now hope to continue monitoring the patients to see if the depression and hyperconnectivity returns. They also want to compare their ECT findings with the effects of other therapies used to treat depression such as psychotherapy and anti-depressants.
Electroconvulsive therapy (ECT) involves first anaesthetizing the patient and then electrically inducing a seizure.
It has a controversial reputation - gained in part because of its role in the 1975 film "One Flew Over The Cuckoo's Nest" starring Jack Nicholson - but is a potent and effective treatment for patients with mood disorders like severe depression.
Yet despite it being used successfully in clinical practice around the world for more than 70 years, scientists have until now not been entirely clear how or why it works.
Now a team from Aberdeen University in Scotland has shown for the first time that ECT affects the way different parts of the brain involved in depression communicate with each other.
In a study published in the Proceedings of the National Academy of Sciences (PNAS) journal they found ECT appears to turn down overactive connections between parts of the brain that control mood and parts that control thinking and concentrating.
This stops the overwhelming impact that depression has on patients' ability to enjoy life and carry out day-to-day activities, they said.
"We've solved a 70-year-old therapeutic riddle," said Ian Reid, a professor of psychiatry at the University of Aberdeen who led the study.
"Our key finding is that if you compare the connections in the brain before and after ECT, ECT reduces the connection strength," he said in a statement.
"For the first time we can point to something that ECT does in the brain that makes sense in the context of what we think is wrong in people who are depressed."
In recent years, experts have developed a new theory on how depression affects the brain that suggests there is a "hyperconnection" between the areas of the brain involved in emotional processing and mood change and the parts of the brain involved in thinking and concentrating.
David Nutt, a professor of neuropsychopharmacology at Imperial College London who was not involved in the ECT study, said its findings "make a lot of sense.
"The disabling of connections between different areas of the brain is what I would have predicted from the depression literature," he said in an emailed comment.
He said the results also chime with a study Nutt published in January which found that psilocybin, the active ingredient in the psychedelic drug known as magic mushrooms, also disrupts this network of connections and may also be effective in treating severe depression.
The electrotherapy study involved using functional magnetic resonance imaging (fMRI) to scan the brains of nine severely depressed patients before and after ECT and then applying complex mathematical analysis to investigate brain connectivity.
Aberdeen University's chair of neuroimaging Christian Schwarzbauer, who devised the new method for analyzing the connectivity data, said it enabled the team to see to what extent more than 25,000 different brain areas communicated with each other.
He said the new method could also be applied to a wide range of other brain disorders such as schizophrenia, autism, or dementia, and "may lead to a better understanding of the underlying disease mechanisms and the development of new diagnostic tools."
The researchers said they now hope to continue monitoring the patients to see if the depression and hyperconnectivity returns. They also want to compare their ECT findings with the effects of other therapies used to treat depression such as psychotherapy and anti-depressants.
Windows Phone struggles to break catch-22 as app makers hold off
Apps, apps, apps! That is the main challenge that Microsoftand Nokia, who are trying to claw back market share from Apple Inc's iPhone and Google's Android in the red hot smartphone market, face now.
And so far the going does not look too good for the challengers and their warhorse Windows Phone platform.
Apps, short for applications, are small pieces of software that do useful or fun things on cellphones. The huge number and variety of apps in Apple and Google stores are a key factor that has helped the companies emerge as dominant players in the lucrative smartphone market.
On Monday, Microsoft and Nokia said they would invest a total of 18 million euros ($23.9 million) into a new mobile application development program, AppCampus, at Helsinki's Aalto University during the next three years.
The move underscores the seriousness with which the two companies view the problem.
Most popular global apps such as Facebook, Twitter, Foursquare and Evernote are available on the Windows Phone platform, but makers of many niche or local apps have shied away.
The number of apps available in the Windows Phone Marketplace now exceeds 65,000, surpassing those at another rival Research in Motion's BlackBerry store. But that is still far short of around half a million apps available on the Apple App Store and Google Play, according to app researcher Distimo.
Worse still, only 37 percent of developers are keen to make apps for Windows Phone, showed the latest IDC/Appcelerator survey. That number, slightly down from the previous survey, compared with the 89 percent interested in iPhone and 79 percent in Android phones.
"Mobile developers' interest for the Windows platform has been for the least very lukewarm over the last two years, with no sign of improvement," Sanford C. Bernstein analyst Pierre Ferragu said.
Microsoft launched its latest Windows Phone 7.5 operating system, Mango, last year to good reviews. And Nokia, struggling to reclaim smartphone handset marketshare from nimbler rivals such as Apple and Samsung Electronics, launched its Lumia line of phones running on Mango late last year.
Lumia phones look sleek and spiffy, with live, tiled icons that automatically update news, weather, pictures and social feeds. But the fewer number of apps and their quality are hobbling the phones' appeal to customers.
Finn Christian Lindholm, a Helsinki-based partner at digital design agency Fjord, believes the latest Windows Phones are interesting enough to challenge the iPhone.
The key to both companies' strategy to gain in the smartphone market would be how they break out of the vicious cycle -- the low sales of the Windows phones holding back app makers, and consumers shunning the phones for lack of the apps they are accustomed to.
"They need to break the Catch-22 before there is enough volume and natural pull," Lindholm said.
SHRINKING MARKETSHARE
Monday's announcement by Microsoft and Nokia is an attempt to find new solutions to the problem, in addition to paying third-party developers for the apps.
They hope the program, which will provide support, coaching and also funding for app makers, will boost the number of unique and outstanding apps on Windows Phone.
It's an uphill road for a new platform. Microsoft's share of the smartphone market fell to just 2 percent last quarter, from 3 percent a year ago and 13 percent four years earlier, according to Strategy Analytics.
Last month, Windows Phone lost also its highly respected chief of developer relations, Brandon Watson, who left for Amazon.com Inc, which is taking on established players in the mobile devices market with its Kindle e-readers.
Apart from Nokia, which has a lot riding on the platform, Microsoft has little support from other handset makers, such as Samsung, which are clearly focused on their Android offerings.
That is not surprising as the other handset makers are struggling to sell their Windows Phone models. They, unlike Nokia, can only dream of payments from Microsoft for promoting and supporting its software. Last quarter, Microsoft paid $250 million to Nokia on this account.
NO TALKING TOM CAT
On Friday, Rovio, the maker of the wildly popular Angry Birds game, created a scare when media reports said the latest version of the game -- Angry Birds Space -- will skip the Windows platform.
Rovio Chief Executive Mikael Hed later told Reuters that the company is working toward getting the game to Windows Phone but did not specify when it will be available.
Showing how difficult a task that Microsoft and Nokia face, many small app developers, such as Outfit7 -- maker of the popular Talking Tom Cat app -- and Joby -- which makes a camera app -- said they have no plans to be on Windows Phone either.
Pioneers in augmented reality -- a technology that combines the digital and real worlds, and is one of the hottest areas of wireless -- are also holding back.
"We have enough work in keeping Android and iPhone apps up to date, as well as in enhancing our augmented reality capabilities on them," said Maarten Lens-Fitzgerald, co-founder of Dutch-based augmented reality firm Layar.
Jeff Janer, co-founder and CEO of Springpad, which makes the namesake app that allows users to store, organize and share content, raised the main concern of the app makers: Will the hard work to move to a new platform pay off?
"When considering a new platform, we look to balance cost of development and support against potential return in terms of market opportunity and the ability to cost-effectively reach the market," said Janer, who currently has no plans to develop an app for Windows Phone.
For many small developers, it is a question of cost and how fast they can recoup the investment.
It would probably take six man-months to build an app for Windows phone and if that was contract work it would be $60,000 or more, said Adam Saltsman, co-founder of Semi Secret Software, which makes the Wurdle word game.
The small customer base for Windows Phone is forcing developers to charge more for the apps, turning off customers further. Most apps that are available for 99 cents on Google Play cost $2.99 on the Windows Phone Marketplace.
Andreas Bernstrom, CEO of Rebtel, one of the most popular Internet-based calling applications on iPhone and Android, said the company has Windows Phone on its development roadmap for later this year but has not yet started work.
"I don't know what the market will be like in six months, maybe we need to focus on tablets or something else," he said.
Jeffrey Glueck, chief executive of Skyfire Labs Inc, which makes the eponymous mobile Web browser, said the main driver for developing on Windows Phone will be carrier requests. "So far, we're only getting requests around Android and iPhone."
That is one more challenge for Microsoft and Nokia.
And so far the going does not look too good for the challengers and their warhorse Windows Phone platform.
Apps, short for applications, are small pieces of software that do useful or fun things on cellphones. The huge number and variety of apps in Apple and Google stores are a key factor that has helped the companies emerge as dominant players in the lucrative smartphone market.
On Monday, Microsoft and Nokia said they would invest a total of 18 million euros ($23.9 million) into a new mobile application development program, AppCampus, at Helsinki's Aalto University during the next three years.
The move underscores the seriousness with which the two companies view the problem.
Most popular global apps such as Facebook, Twitter, Foursquare and Evernote are available on the Windows Phone platform, but makers of many niche or local apps have shied away.
The number of apps available in the Windows Phone Marketplace now exceeds 65,000, surpassing those at another rival Research in Motion's BlackBerry store. But that is still far short of around half a million apps available on the Apple App Store and Google Play, according to app researcher Distimo.
Worse still, only 37 percent of developers are keen to make apps for Windows Phone, showed the latest IDC/Appcelerator survey. That number, slightly down from the previous survey, compared with the 89 percent interested in iPhone and 79 percent in Android phones.
"Mobile developers' interest for the Windows platform has been for the least very lukewarm over the last two years, with no sign of improvement," Sanford C. Bernstein analyst Pierre Ferragu said.
Microsoft launched its latest Windows Phone 7.5 operating system, Mango, last year to good reviews. And Nokia, struggling to reclaim smartphone handset marketshare from nimbler rivals such as Apple and Samsung Electronics, launched its Lumia line of phones running on Mango late last year.
Lumia phones look sleek and spiffy, with live, tiled icons that automatically update news, weather, pictures and social feeds. But the fewer number of apps and their quality are hobbling the phones' appeal to customers.
Finn Christian Lindholm, a Helsinki-based partner at digital design agency Fjord, believes the latest Windows Phones are interesting enough to challenge the iPhone.
The key to both companies' strategy to gain in the smartphone market would be how they break out of the vicious cycle -- the low sales of the Windows phones holding back app makers, and consumers shunning the phones for lack of the apps they are accustomed to.
"They need to break the Catch-22 before there is enough volume and natural pull," Lindholm said.
SHRINKING MARKETSHARE
Monday's announcement by Microsoft and Nokia is an attempt to find new solutions to the problem, in addition to paying third-party developers for the apps.
They hope the program, which will provide support, coaching and also funding for app makers, will boost the number of unique and outstanding apps on Windows Phone.
It's an uphill road for a new platform. Microsoft's share of the smartphone market fell to just 2 percent last quarter, from 3 percent a year ago and 13 percent four years earlier, according to Strategy Analytics.
Last month, Windows Phone lost also its highly respected chief of developer relations, Brandon Watson, who left for Amazon.com Inc, which is taking on established players in the mobile devices market with its Kindle e-readers.
Apart from Nokia, which has a lot riding on the platform, Microsoft has little support from other handset makers, such as Samsung, which are clearly focused on their Android offerings.
That is not surprising as the other handset makers are struggling to sell their Windows Phone models. They, unlike Nokia, can only dream of payments from Microsoft for promoting and supporting its software. Last quarter, Microsoft paid $250 million to Nokia on this account.
NO TALKING TOM CAT
On Friday, Rovio, the maker of the wildly popular Angry Birds game, created a scare when media reports said the latest version of the game -- Angry Birds Space -- will skip the Windows platform.
Rovio Chief Executive Mikael Hed later told Reuters that the company is working toward getting the game to Windows Phone but did not specify when it will be available.
Showing how difficult a task that Microsoft and Nokia face, many small app developers, such as Outfit7 -- maker of the popular Talking Tom Cat app -- and Joby -- which makes a camera app -- said they have no plans to be on Windows Phone either.
Pioneers in augmented reality -- a technology that combines the digital and real worlds, and is one of the hottest areas of wireless -- are also holding back.
"We have enough work in keeping Android and iPhone apps up to date, as well as in enhancing our augmented reality capabilities on them," said Maarten Lens-Fitzgerald, co-founder of Dutch-based augmented reality firm Layar.
Jeff Janer, co-founder and CEO of Springpad, which makes the namesake app that allows users to store, organize and share content, raised the main concern of the app makers: Will the hard work to move to a new platform pay off?
"When considering a new platform, we look to balance cost of development and support against potential return in terms of market opportunity and the ability to cost-effectively reach the market," said Janer, who currently has no plans to develop an app for Windows Phone.
For many small developers, it is a question of cost and how fast they can recoup the investment.
It would probably take six man-months to build an app for Windows phone and if that was contract work it would be $60,000 or more, said Adam Saltsman, co-founder of Semi Secret Software, which makes the Wurdle word game.
The small customer base for Windows Phone is forcing developers to charge more for the apps, turning off customers further. Most apps that are available for 99 cents on Google Play cost $2.99 on the Windows Phone Marketplace.
Andreas Bernstrom, CEO of Rebtel, one of the most popular Internet-based calling applications on iPhone and Android, said the company has Windows Phone on its development roadmap for later this year but has not yet started work.
"I don't know what the market will be like in six months, maybe we need to focus on tablets or something else," he said.
Jeffrey Glueck, chief executive of Skyfire Labs Inc, which makes the eponymous mobile Web browser, said the main driver for developing on Windows Phone will be carrier requests. "So far, we're only getting requests around Android and iPhone."
That is one more challenge for Microsoft and Nokia.
Leukemia Stem Cells Identified
Stem cell researchers at UCLA have identified a type of leukemia stem cell and uncovered the molecular and genetic mechanisms that cause a normal blood stem cells to become cancerous.
The discovery may lead to new therapies that target these leukemia stem cells, attacking the disease at its very root and killing the early cells that give rise to the mature cancer cells. The study appears in the May 22, 2008 issue of the journal Nature.
Scientists now believe stem cells are responsible for the origin of many cancers and their ability to become drug resistant and spread throughout the body. Current cancer therapies don't target cancer stem cells, only the cancer cells that are generated by them. Scientists theorize that the cancer stem cells -- a very small population when compared with mature cancer cells - lay dormant while the cancer cells are killed. Later, sometimes years later, the cancer stem cells begin to self-renew and differentiate into malignant cells, causing a recurrence of the disease.
If scientists could understand the biology of cancer stem cells and find a way to kill them, it might provide what the oncology research community never talks about -- a potential cure for certain cancers. If the cancer stem cells could be sought out and eliminated from the body, the cancer could not re-grow.
Led by Dr. Hong Wu, a professor of medical and molecular pharmacology and a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, the UCLA team has for the first time identified and isolated the stem cells responsible for a type of leukemia known as T-cell or acute T-lymphoblastic leukemia, an aggressive and deadly cancer that , can occur in both children and adults. The team also discovered the mechanisms by which blood stem cells -- the cells that become the various cells in the blood supply -- are converted to malignant leukemia stem cells, providing potential targets for therapies to home in on and attack those stem cells.
"One of the main challenges in cancer biology is to identify cancer stem cells and define the molecular and genetic events required for transforming normal cells into cancer stem cells," said Wu, who also is a researcher at UCLA's Jonsson Comprehensive Cancer Center and senior author of the Nature study. "With this study, we've been able to do that in one type of leukemia."
In mouse models that developed T-cell leukemia, the team studied the cancerous cells and, using a sorting method that sought out certain cell surface markers, was able to identify the leukemia stem cells. Those cells were isolated and then transplanted into other mouse models to see if they developed T-cell leukemia, a sign that the team had been successful in finding the leukemia stem cells.
The team also wanted to know how blood stem cells become cancerous and studied the cells at the molecular and genetic level to uncover those mechanisms.
"We thought that multiple genetic or molecular alterations would have to occur for cancer to develop," said Wei Guo, a postdoctoral student in Wu's lab and the first author of the study. "In this case, we were able to find those alterations."
The alterations found that collaboratively contribute to leukemia stem cell formation were the deletion of the PTEN tumor suppressor gene, a chromosomal translocation involving c-myc, a gene known to result in cancer that is usually regulated and kept in line, and the activation of a cell signaling pathway called beta catenin.
Wu and her team currently are testing therapies that target the alterations they discovered, hoping to interrupt the process that causes the blood stem cells to become leukemia stem cells, thereby preventing the cancer. They're also looking for other alterations that might be at play in transforming the normal stem cells into cancerous stem cells.
The discovery may lead to new therapies that target these leukemia stem cells, attacking the disease at its very root and killing the early cells that give rise to the mature cancer cells. The study appears in the May 22, 2008 issue of the journal Nature.
Scientists now believe stem cells are responsible for the origin of many cancers and their ability to become drug resistant and spread throughout the body. Current cancer therapies don't target cancer stem cells, only the cancer cells that are generated by them. Scientists theorize that the cancer stem cells -- a very small population when compared with mature cancer cells - lay dormant while the cancer cells are killed. Later, sometimes years later, the cancer stem cells begin to self-renew and differentiate into malignant cells, causing a recurrence of the disease.
If scientists could understand the biology of cancer stem cells and find a way to kill them, it might provide what the oncology research community never talks about -- a potential cure for certain cancers. If the cancer stem cells could be sought out and eliminated from the body, the cancer could not re-grow.
Led by Dr. Hong Wu, a professor of medical and molecular pharmacology and a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, the UCLA team has for the first time identified and isolated the stem cells responsible for a type of leukemia known as T-cell or acute T-lymphoblastic leukemia, an aggressive and deadly cancer that , can occur in both children and adults. The team also discovered the mechanisms by which blood stem cells -- the cells that become the various cells in the blood supply -- are converted to malignant leukemia stem cells, providing potential targets for therapies to home in on and attack those stem cells.
"One of the main challenges in cancer biology is to identify cancer stem cells and define the molecular and genetic events required for transforming normal cells into cancer stem cells," said Wu, who also is a researcher at UCLA's Jonsson Comprehensive Cancer Center and senior author of the Nature study. "With this study, we've been able to do that in one type of leukemia."
In mouse models that developed T-cell leukemia, the team studied the cancerous cells and, using a sorting method that sought out certain cell surface markers, was able to identify the leukemia stem cells. Those cells were isolated and then transplanted into other mouse models to see if they developed T-cell leukemia, a sign that the team had been successful in finding the leukemia stem cells.
The team also wanted to know how blood stem cells become cancerous and studied the cells at the molecular and genetic level to uncover those mechanisms.
"We thought that multiple genetic or molecular alterations would have to occur for cancer to develop," said Wei Guo, a postdoctoral student in Wu's lab and the first author of the study. "In this case, we were able to find those alterations."
The alterations found that collaboratively contribute to leukemia stem cell formation were the deletion of the PTEN tumor suppressor gene, a chromosomal translocation involving c-myc, a gene known to result in cancer that is usually regulated and kept in line, and the activation of a cell signaling pathway called beta catenin.
Wu and her team currently are testing therapies that target the alterations they discovered, hoping to interrupt the process that causes the blood stem cells to become leukemia stem cells, thereby preventing the cancer. They're also looking for other alterations that might be at play in transforming the normal stem cells into cancerous stem cells.
Knocking Out Survival Protein Could Aid Leukemia Treatment
An effective way to fight leukemia might be to knock out a specific protein that protects cancer cells from dying, a new study shows. The findings suggest that a drug that can block this “survival protein” might on its own be an effective therapy.
Health & Medicine
Leukemia
Lymphoma
Cancer
Lung Cancer
Brain Tumor
Skin Cancer
Reference
Leukemia
Lymphoma
Tumor suppressor gene
BRCA1
But such a drug used in combination with several existing drugs might also offer an effective one-two punch against drug-resistant forms of chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL). The two forms of cancer kill about 20,500 Americans yearly.
The survival protein is called Mcl1. It usually helps keep normal cells healthy and is involved in the development of the components of the immune system, but it can also help prolong survival of cancer cells.
Cells with an overabundance of the protein are also more resistant to anticancer drugs such as rituximab, which has revolutionized the treatment of certain chronic and acute leukemias.
“Our findings demonstrate that Mcl1 may be an effective target for drugs directed against CLL and ALL,” says principal investigator John C. Byrd, professor of internal medicine and director of the hematologic malignancies program at Ohio State's James Cancer Hospital and Solove Research Institute.
“These results give us a rationale for lowering the amount of this protein in CLL cells and suggest that this should enhance the action of rituximab and perhaps other agents as well.”
Rituximab is an antibody-based drug that targets CLL and ALL cells and causes the cells to self-destruct. “We've shown that knocking down Mcl1 can, by itself, cause CLL cells to die, and that this effect might enhance the activity of rituximab,” says first author Rehan Hussain, a postdoctoral fellow with Ohio State's Comprehensive Cancer Center.
Byrd, Hussain and their collaborators conducted this research using cancer cells from 17 CLL patients and ALL cell lines grown in the laboratory.
The investigators placed molecules called small interfering RNA (siRNA) inside the cells and found that the tiny molecules greatly reduced the amount of the survival protein, causing many of the cells to die. The effect was the same even in cells that came from patients with advanced cancer or from patients with tumors that resisted conventional treatment.
When the researchers treated cells with both siRNA and the drug rituximab, the combination killed significantly more leukemia cells than the drug alone. Overall, says Byrd, “Our data indicate that specifically targeting Mcl1 might be effective in the treatment of CLL, particularly when combined with rituximab.”
Funding from the National Cancer Institute, the Leukemia & Lymphoma Society and the D. Warren Brown Foundation supported this research. Byrd is the D. Warren Brown Professor of Leukemia Research and a Clinical Scholar of the Leukemia & Lymphoma Society. The study by researchers at the Ohio State University Comprehensive Cancer Center is published online in the journal Clinical Cancer Research.
Health & Medicine
Leukemia
Lymphoma
Cancer
Lung Cancer
Brain Tumor
Skin Cancer
Reference
Leukemia
Lymphoma
Tumor suppressor gene
BRCA1
But such a drug used in combination with several existing drugs might also offer an effective one-two punch against drug-resistant forms of chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL). The two forms of cancer kill about 20,500 Americans yearly.
The survival protein is called Mcl1. It usually helps keep normal cells healthy and is involved in the development of the components of the immune system, but it can also help prolong survival of cancer cells.
Cells with an overabundance of the protein are also more resistant to anticancer drugs such as rituximab, which has revolutionized the treatment of certain chronic and acute leukemias.
“Our findings demonstrate that Mcl1 may be an effective target for drugs directed against CLL and ALL,” says principal investigator John C. Byrd, professor of internal medicine and director of the hematologic malignancies program at Ohio State's James Cancer Hospital and Solove Research Institute.
“These results give us a rationale for lowering the amount of this protein in CLL cells and suggest that this should enhance the action of rituximab and perhaps other agents as well.”
Rituximab is an antibody-based drug that targets CLL and ALL cells and causes the cells to self-destruct. “We've shown that knocking down Mcl1 can, by itself, cause CLL cells to die, and that this effect might enhance the activity of rituximab,” says first author Rehan Hussain, a postdoctoral fellow with Ohio State's Comprehensive Cancer Center.
Byrd, Hussain and their collaborators conducted this research using cancer cells from 17 CLL patients and ALL cell lines grown in the laboratory.
The investigators placed molecules called small interfering RNA (siRNA) inside the cells and found that the tiny molecules greatly reduced the amount of the survival protein, causing many of the cells to die. The effect was the same even in cells that came from patients with advanced cancer or from patients with tumors that resisted conventional treatment.
When the researchers treated cells with both siRNA and the drug rituximab, the combination killed significantly more leukemia cells than the drug alone. Overall, says Byrd, “Our data indicate that specifically targeting Mcl1 might be effective in the treatment of CLL, particularly when combined with rituximab.”
Funding from the National Cancer Institute, the Leukemia & Lymphoma Society and the D. Warren Brown Foundation supported this research. Byrd is the D. Warren Brown Professor of Leukemia Research and a Clinical Scholar of the Leukemia & Lymphoma Society. The study by researchers at the Ohio State University Comprehensive Cancer Center is published online in the journal Clinical Cancer Research.
Potential New Way To Make A Good Anti-Leukemia Drug Even Better
A recently identified cancer-causing protein makes the anti-leukemia drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture.
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. Imatinib slows down the spread of cancer by blocking the enzyme's activity. But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib.
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. Imatinib slows down the spread of cancer by blocking the enzyme's activity. But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib.
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.
Stop Signal for Leukemia Stem Cells
There are numerous specialized growth factors that are responsible for cells of different tissues of our body to divide and differentiate when needed. These hormone-like factors bind to matching receptors on the surface of their target cells and thus give order for the cell to divide. However, a single genetic alteration can be sufficient for the whole system to get out of control. If, for example, the gene for such a growth factor or for the matching receptor is hyperactive, then the cell permanently receives signals to divide -- and this can result in cancer.
Such defective growth signals play a role in many cancers. Thus, breast cancer cells in about 20 percent of affected women form too many receptors for the Her2/neu growth factor; in bowel cancer doctors frequently find an overproduction of the EGF growth factor.
Jointly with colleagues from France, Canada and the U.S., scientists headed by Professor Dr. Andreas Trumpp of the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have now discovered that in T-cell acute lymphoblastic leukemia (T-ALL), too, malignant growth is driven by a particular growth factor. In this case, it is the insulin-like growth factor 1 (IGF1) which plays the key role.
The investigators found out that there is an oversupply of IGF1 receptors in T-ALL. The leukemia cells therefore become particularly sensitive to IGF1 signals. When the researchers blocked the IGF1 receptors using specific inhibitors or turned off the gene coding for the receptor, the blood cancer cells ceased to grow. This worked both in murine cancer cells and in human leukemia cells.
However, blockage of the IGF1 signal not only stopped cancer cell growth. Moreover, the dangerous cancer stem cells lost their capability of self-renewal. This was shown by the investigators in a classic experiment called serial transplantation. They transplanted T-ALL cells that formed only small amounts of IGF1 receptors on their surface into mice. Although T-ALL cells normally always cause leukemia in recipient animals, only very few mice developed leukemia after injection of the modified T-ALL. For the team this was the most important clue that leukemia stem cells were either absent or no longer active, because they are the only ones that can initiate leukemia.
"We only need to reduce the level of IGF1 receptors slightly in order to deprive cancer stem cells of their self-renewal capacity. Apparently, leukemia stem cells are particularly dependent on strong IGF1 signals," explained Dr. Hind Medyouf, first author of the article.
Acute lymphoblastic leukemias are the most frequent malignancies in children; however, elderly adults may be affected, too. The group's results open up new prospects for treatment, because substances inhibiting the IGF1 receptor are already available and are currently being tested for other types of cancers such as breast cancer in clinical trials. Andreas Trumpp, a stem cell specialist, explains: „Elderly T-ALL patients have a particularly high recurrence rate after seemingly successful chemotherapy. Inhibition of the IGF1 signaling pathway would target the leukemia stem cells in particular and might therefore prevent recurrence of the cancer."
Such defective growth signals play a role in many cancers. Thus, breast cancer cells in about 20 percent of affected women form too many receptors for the Her2/neu growth factor; in bowel cancer doctors frequently find an overproduction of the EGF growth factor.
Jointly with colleagues from France, Canada and the U.S., scientists headed by Professor Dr. Andreas Trumpp of the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ) have now discovered that in T-cell acute lymphoblastic leukemia (T-ALL), too, malignant growth is driven by a particular growth factor. In this case, it is the insulin-like growth factor 1 (IGF1) which plays the key role.
The investigators found out that there is an oversupply of IGF1 receptors in T-ALL. The leukemia cells therefore become particularly sensitive to IGF1 signals. When the researchers blocked the IGF1 receptors using specific inhibitors or turned off the gene coding for the receptor, the blood cancer cells ceased to grow. This worked both in murine cancer cells and in human leukemia cells.
However, blockage of the IGF1 signal not only stopped cancer cell growth. Moreover, the dangerous cancer stem cells lost their capability of self-renewal. This was shown by the investigators in a classic experiment called serial transplantation. They transplanted T-ALL cells that formed only small amounts of IGF1 receptors on their surface into mice. Although T-ALL cells normally always cause leukemia in recipient animals, only very few mice developed leukemia after injection of the modified T-ALL. For the team this was the most important clue that leukemia stem cells were either absent or no longer active, because they are the only ones that can initiate leukemia.
"We only need to reduce the level of IGF1 receptors slightly in order to deprive cancer stem cells of their self-renewal capacity. Apparently, leukemia stem cells are particularly dependent on strong IGF1 signals," explained Dr. Hind Medyouf, first author of the article.
Acute lymphoblastic leukemias are the most frequent malignancies in children; however, elderly adults may be affected, too. The group's results open up new prospects for treatment, because substances inhibiting the IGF1 receptor are already available and are currently being tested for other types of cancers such as breast cancer in clinical trials. Andreas Trumpp, a stem cell specialist, explains: „Elderly T-ALL patients have a particularly high recurrence rate after seemingly successful chemotherapy. Inhibition of the IGF1 signaling pathway would target the leukemia stem cells in particular and might therefore prevent recurrence of the cancer."
How To Design A Cancer-Killing Virus
One new way to treat individuals with cancer that is being developed is the use of viruses that infect and kill cancer cells while leaving normal cells unharmed. These viruses are known as virotherapeutics.
In a new study, David Kirn and colleagues at Jennerex Biotherapeutics, San Francisco, have described the development of a new virotherapuetic with antitumor effects in both mice and rabbits.
After selecting a highly potent strain of poxvirus that was able to traffic to tumors when administered intravenously to mice the authors engineered the virus such that it would target only specific cancer cells -- those with increased expression of a protein known as E2F and/or activation of signaling downstream of a protein known as EGFR.
Further engineering to enable the virus to produce the soluble factor GM-CSF was designed to enhance the induction of anti-tumor immune responses. In addition to its antitumor effects in mice and rabbits, the virotherapeutic showed high selectivity for cancer cells in tumor-bearing rabbits and in human tissue samples, leading the authors to suggest that this virotherapeutic should be tested in clinical trials for the treatment of cancer.
Article: Rational strain selection and engineering creates a broad-spectrum, systemically effective oncolytic poxvirus, JX-963, Journal of Clinical Investigation, October 25, 2007.
In a new study, David Kirn and colleagues at Jennerex Biotherapeutics, San Francisco, have described the development of a new virotherapuetic with antitumor effects in both mice and rabbits.
After selecting a highly potent strain of poxvirus that was able to traffic to tumors when administered intravenously to mice the authors engineered the virus such that it would target only specific cancer cells -- those with increased expression of a protein known as E2F and/or activation of signaling downstream of a protein known as EGFR.
Further engineering to enable the virus to produce the soluble factor GM-CSF was designed to enhance the induction of anti-tumor immune responses. In addition to its antitumor effects in mice and rabbits, the virotherapeutic showed high selectivity for cancer cells in tumor-bearing rabbits and in human tissue samples, leading the authors to suggest that this virotherapeutic should be tested in clinical trials for the treatment of cancer.
Article: Rational strain selection and engineering creates a broad-spectrum, systemically effective oncolytic poxvirus, JX-963, Journal of Clinical Investigation, October 25, 2007.
Combinatorial Therapy Allows Viruses to Destroy Tumors
For several years, researchers have been developing a new approach to treating cancer that uses viruses to infect and kill cancer cells while leaving normal cells unharmed. Recent data have indicated that this approach, which is known as oncolytic virotherapy, has potential.
Now, Richard Vile and colleagues, at the Mayo Clinic, Rochester, have found that this approach can be combined with a standard clinical therapy to provide substantial regression and cure of tumors in mice, leading them to suggest that this combinatorial approach could be of tremendous benefit in the clinic.
Tumors that grow to a certain size need to form new blood vessels if they are to continuing growing and spread to other sites. One of the molecules that controls this new blood vessel growth, VEGF, is the target of drugs used to treat several forms of cancer. In this study, the authors found that modulating VEGF signaling, for example by transiently stopping anti-VEGF therapy in mice harboring cancer cells expressing high levels of VEGF, allowed the cells that line tumor blood vessels to be targeted and killed by viruses.
Importantly, as this approach targets the cells lining tumor blood vessels, rather than specific types of tumor cells, the authors suggest that this combinatorial approach to therapy could be used to treat a wide range of cancers.
The research appears in the Journal of Clinical Investigation.
Now, Richard Vile and colleagues, at the Mayo Clinic, Rochester, have found that this approach can be combined with a standard clinical therapy to provide substantial regression and cure of tumors in mice, leading them to suggest that this combinatorial approach could be of tremendous benefit in the clinic.
Tumors that grow to a certain size need to form new blood vessels if they are to continuing growing and spread to other sites. One of the molecules that controls this new blood vessel growth, VEGF, is the target of drugs used to treat several forms of cancer. In this study, the authors found that modulating VEGF signaling, for example by transiently stopping anti-VEGF therapy in mice harboring cancer cells expressing high levels of VEGF, allowed the cells that line tumor blood vessels to be targeted and killed by viruses.
Importantly, as this approach targets the cells lining tumor blood vessels, rather than specific types of tumor cells, the authors suggest that this combinatorial approach to therapy could be used to treat a wide range of cancers.
The research appears in the Journal of Clinical Investigation.
Unlocking The Body's Defenses Against Cancer
Scientists have discovered a way of allowing healthy cells to take charge of cancerous cells and stop them developing into tumours in what could provide a new approach to treating early-stage cancers.
University of Manchester researchers found that a special type of the chemicals known as 'kinase inhibitors' opened up communication channels on the surface of cells that enabled healthy cells to 'talk' to the cancer cells.
"When we added the chemicals to a mixture of healthy and cancerous cells in a flask the diseased cells stopped multiplying and began acting like normal cells again," said Dr Ian Hampson, who carried out the research with wife Dr Lynne Hampson.
"Further tests revealed that the chemicals helped the cancer cells form connections with surrounding healthy cells that allowed these normal cells to take charge of the mechanism by which cancer cells divide and grow out of control."
Cell division occurs naturally and continuously in human organs and tissue as part of the body's normal repair processes to combat wear and tear but in cancer the cells divide in an uncontrolled way.
Dr Hampson says the findings, published in the British Journal of Cancer, are all the more exciting because the chemicals, which were developed with colleagues at the University of Salford, appear to be relatively non-toxic and the positive effect on the cancer cells persists even when the chemicals are withdrawn.
"When the chemicals were added to a culture containing just cancer cells they had little effect," said Dr Hampson, who is based in Manchester's School of Cancer and Imaging Sciences. "It was only when we added the chemicals to a mixture of cancer cells and normal cells – similar to how you would find them in the body – that growth was suppressed.
"Intriguingly, the connections that allowed the healthy cells to communicate with the cancer cells stayed open even when the kinase inhibitors were removed indicating that a potential drug based on these chemicals could be given as a short course of treatment.
"Furthermore, the chemicals are non-poisonous and do not actually kill cells like conventional cancer therapies, such as chemotherapy and radiotherapy, so if we were able to develop a drug it is likely to have far fewer side-effects."
The team say the next stage of their research will be to find out exactly how the chemicals are able to increase the number of connections between cancer and normal cells. Once this is known, it should be possible to produce a drug based on these chemicals that could hopefully be used in humans.
Dr Lynne Hampson added: "We are currently applying for funding to carry out further research into the biochemistry of how these chemicals cause the effect we have observed. We also intend to investigate the use of different types of cell cultures to assess the potency and range of activity of these agents."
The research was funded by the Association for International Cancer Research, The Humane Research Trust, The Caring Cancer Research Trust, Kidscan and the Cancer Prevention Research Trust.
University of Manchester researchers found that a special type of the chemicals known as 'kinase inhibitors' opened up communication channels on the surface of cells that enabled healthy cells to 'talk' to the cancer cells.
"When we added the chemicals to a mixture of healthy and cancerous cells in a flask the diseased cells stopped multiplying and began acting like normal cells again," said Dr Ian Hampson, who carried out the research with wife Dr Lynne Hampson.
"Further tests revealed that the chemicals helped the cancer cells form connections with surrounding healthy cells that allowed these normal cells to take charge of the mechanism by which cancer cells divide and grow out of control."
Cell division occurs naturally and continuously in human organs and tissue as part of the body's normal repair processes to combat wear and tear but in cancer the cells divide in an uncontrolled way.
Dr Hampson says the findings, published in the British Journal of Cancer, are all the more exciting because the chemicals, which were developed with colleagues at the University of Salford, appear to be relatively non-toxic and the positive effect on the cancer cells persists even when the chemicals are withdrawn.
"When the chemicals were added to a culture containing just cancer cells they had little effect," said Dr Hampson, who is based in Manchester's School of Cancer and Imaging Sciences. "It was only when we added the chemicals to a mixture of cancer cells and normal cells – similar to how you would find them in the body – that growth was suppressed.
"Intriguingly, the connections that allowed the healthy cells to communicate with the cancer cells stayed open even when the kinase inhibitors were removed indicating that a potential drug based on these chemicals could be given as a short course of treatment.
"Furthermore, the chemicals are non-poisonous and do not actually kill cells like conventional cancer therapies, such as chemotherapy and radiotherapy, so if we were able to develop a drug it is likely to have far fewer side-effects."
The team say the next stage of their research will be to find out exactly how the chemicals are able to increase the number of connections between cancer and normal cells. Once this is known, it should be possible to produce a drug based on these chemicals that could hopefully be used in humans.
Dr Lynne Hampson added: "We are currently applying for funding to carry out further research into the biochemistry of how these chemicals cause the effect we have observed. We also intend to investigate the use of different types of cell cultures to assess the potency and range of activity of these agents."
The research was funded by the Association for International Cancer Research, The Humane Research Trust, The Caring Cancer Research Trust, Kidscan and the Cancer Prevention Research Trust.
Aspirin May Lower the Risk of Pancreatic Cancer
The use of aspirin at least once per month is associated with a significant decrease in pancreatic cancer risk, according to results of a large case-control study presented at the AACR 102nd Annual Meeting 2011, held in Orlando, Florida, April 2-6.
Xiang-Lin Tan, Ph.D., M.D., a research fellow at Mayo Clinic in Rochester, Minn., said the findings from this large collaborative study are preliminary and do not encourage widespread use of aspirin for this purpose.
"The results are not meant to suggest everyone should start taking aspirin once monthly to reduce their risk of pancreatic cancer," said Tan. "Individuals should discuss use of aspirin with their physicians because the drug carries some side effects."
For the current study, Tan and colleagues enrolled 904 patients who had documented pancreatic cancer and compared them with 1,224 healthy patients. All patients were at least 55 years old and reported their use of aspirin, NSAIDs and acetaminophen by questionnaire.
Results showed that people who took aspirin at least one day during a month had a 26 percent decreased risk of pancreatic cancer compared to those who did not take aspirin regularly. The effect was also found for those who took low-dose aspirin for heart disease prevention at 35 percent lower risk, according to Tan.
The researchers did not see a benefit from non-aspirin NSAIDs or acetaminophen. "This provides additional evidence that aspirin may have chemoprevention activity against pancreatic cancer," said Tan. He added that more data must be gathered before we can prove a real benefit.
Xiang-Lin Tan, Ph.D., M.D., a research fellow at Mayo Clinic in Rochester, Minn., said the findings from this large collaborative study are preliminary and do not encourage widespread use of aspirin for this purpose.
"The results are not meant to suggest everyone should start taking aspirin once monthly to reduce their risk of pancreatic cancer," said Tan. "Individuals should discuss use of aspirin with their physicians because the drug carries some side effects."
For the current study, Tan and colleagues enrolled 904 patients who had documented pancreatic cancer and compared them with 1,224 healthy patients. All patients were at least 55 years old and reported their use of aspirin, NSAIDs and acetaminophen by questionnaire.
Results showed that people who took aspirin at least one day during a month had a 26 percent decreased risk of pancreatic cancer compared to those who did not take aspirin regularly. The effect was also found for those who took low-dose aspirin for heart disease prevention at 35 percent lower risk, according to Tan.
The researchers did not see a benefit from non-aspirin NSAIDs or acetaminophen. "This provides additional evidence that aspirin may have chemoprevention activity against pancreatic cancer," said Tan. He added that more data must be gathered before we can prove a real benefit.
Regular Aspirin Intake Halves Cancer Risk, Study Finds
Scientists including those from Queen's University have discovered that taking regular aspirin halves the risk of developing hereditary cancers.
Hereditary cancers are those which develop as a result of a gene fault inherited from a parent. Bowel and womb cancers are the most common forms of hereditary cancers. Fifty thousand people in the UK are diagnosed with bowel and womb cancers every year; 10 per cent of these cancers are thought to be hereditary.
The decade-long study, which involved scientists and clinicians from 43 centres in 16 countries and was funded by Cancer Research UK, followed nearly 1,000 patients, in some cases for over 10 years. The study found that those who had been taking a regular dose of aspirin had 50 per cent fewer incidents of hereditary cancer compared with those who were not taking aspirin.
The research focused on people with Lynch syndrome which is an inherited genetic disorder that causes cancer by affecting genes responsible for detecting and repairing damage in the DNA. Around 50 per cent of those with Lynch syndrome develop cancer, mainly in the bowel and womb. The study looked at all cancers related to the syndrome, and found that almost 30 per cent of the patients not taking aspirin had developed a cancer compared to around 15 per cent of those taking the aspirin.
Those who had taken aspirin still developed the same number of polyps, which are thought to be precursors of cancer, as those who did not take aspirin but they did not go on to develop cancer. It suggests that aspirin could possibly be causing these cells to destruct before they turn cancerous.
Over 1,000 people were diagnosed with bowel cancer in Northern Ireland last year; 400 of these died from the disease. Ten per cent of bowel cancer cases are hereditary and by taking aspirin regularly the number of those dying from the hereditary form of the disease could be halved.
Professor Patrick Morrison from Queen's University in Belfast, who led the Northern Ireland part of the study, said: "The results of this study, which has been ongoing for over a decade, proves that the regular intake of aspirin over a prolonged period halves the risk of developing hereditary cancers. The effects of aspirin in the first five years of the study were not clear but in those who took aspirin for between five and ten years the results were very clear."
"This is a huge breakthrough in terms of cancer prevention. For those who have a history of hereditary cancers in their family, like bowel and womb cancers, this will be welcome news. Not only does it show we can reduce cancer rates and ultimately deaths, it opens up other avenues for further cancer prevention research. We aim now to go forward with another trial to assess the most effective dosage of aspirin for hereditary cancer prevention and to look at the use of aspirin in the general population as a way of reducing the risk of bowel cancer.
"For anyone considering taking aspirin I would recommend discussing this with your GP first as aspirin is known to bring with it a risk of stomach complaints, including ulcers."
The research was published online Oct. 28 in The Lancet.
Hereditary cancers are those which develop as a result of a gene fault inherited from a parent. Bowel and womb cancers are the most common forms of hereditary cancers. Fifty thousand people in the UK are diagnosed with bowel and womb cancers every year; 10 per cent of these cancers are thought to be hereditary.
The decade-long study, which involved scientists and clinicians from 43 centres in 16 countries and was funded by Cancer Research UK, followed nearly 1,000 patients, in some cases for over 10 years. The study found that those who had been taking a regular dose of aspirin had 50 per cent fewer incidents of hereditary cancer compared with those who were not taking aspirin.
The research focused on people with Lynch syndrome which is an inherited genetic disorder that causes cancer by affecting genes responsible for detecting and repairing damage in the DNA. Around 50 per cent of those with Lynch syndrome develop cancer, mainly in the bowel and womb. The study looked at all cancers related to the syndrome, and found that almost 30 per cent of the patients not taking aspirin had developed a cancer compared to around 15 per cent of those taking the aspirin.
Those who had taken aspirin still developed the same number of polyps, which are thought to be precursors of cancer, as those who did not take aspirin but they did not go on to develop cancer. It suggests that aspirin could possibly be causing these cells to destruct before they turn cancerous.
Over 1,000 people were diagnosed with bowel cancer in Northern Ireland last year; 400 of these died from the disease. Ten per cent of bowel cancer cases are hereditary and by taking aspirin regularly the number of those dying from the hereditary form of the disease could be halved.
Professor Patrick Morrison from Queen's University in Belfast, who led the Northern Ireland part of the study, said: "The results of this study, which has been ongoing for over a decade, proves that the regular intake of aspirin over a prolonged period halves the risk of developing hereditary cancers. The effects of aspirin in the first five years of the study were not clear but in those who took aspirin for between five and ten years the results were very clear."
"This is a huge breakthrough in terms of cancer prevention. For those who have a history of hereditary cancers in their family, like bowel and womb cancers, this will be welcome news. Not only does it show we can reduce cancer rates and ultimately deaths, it opens up other avenues for further cancer prevention research. We aim now to go forward with another trial to assess the most effective dosage of aspirin for hereditary cancer prevention and to look at the use of aspirin in the general population as a way of reducing the risk of bowel cancer.
"For anyone considering taking aspirin I would recommend discussing this with your GP first as aspirin is known to bring with it a risk of stomach complaints, including ulcers."
The research was published online Oct. 28 in The Lancet.
Attacking Bowel Cancer On Two Fronts
Stem cells in the intestine, which when they mutate can lead to bowel cancers, might also be grown into transplant tissues to combat the effects of those same cancers, the UK National Stem Cell Network (UKNSCN) annual science meeting heard March 31.
Professor Nick Barker of the Institute of Medical Biology in Singapore will explain how he and his team identified that the stem cells which are crucial to maintaining a healthy intestine are also the site at which bowel cancers first begin, and how he also hopes to use healthy stem cells to regenerate tissues to help patients with Crohn's disease and some cancers.
Having discovered a gene that is only turned on in these particular stem cells Professor Barker and his team have been able to isolate the cells in mice and grow small pieces of intestine in the lab. The researchers hope that if they are able to grow larger pieces, they will be able to produce transplant tissues to replace damaged intestines.
Professor Barker explains: "Processing our dinner every day is a tough job so the lining of our intestines quickly get worn out. To keep the intestine working stem cells in little pockets along the surface replace the lining, cell by cell, about once a week.
"We already knew these stem cells existed for a while we didn't know much about them because it was difficult to distinguish them from all of the other types of cells in our intestines. Our team was able to single them out and study them because we discovered a gene that is only turned on in these particular stem cells."
Once the researchers had found this gene they were able to track where the stem cells occur throughout the body finding that, as well as the intestine, the stomach lining and in hair follicles, the cells were also present in bowel tumours.
Professor Barker continues: "We hope that studying these stem cells will be doubly useful: One day we hope to grow large enough pieces in the lab to form replacement tissues for transplant; and by studying the cells we will be able to find new ways to prevent them from mutating and hence leading to cancer.
"Bowel cancer is the third most common type of cancer in England and an estimated 38,000 new cases are diagnosed each year. We know these stem cells are both implicated in causing the cancer but that they also could be useful for treating disease so we hope that studying them will help us to understand how to attack the disease on two fronts.
Professor Nick Barker of the Institute of Medical Biology in Singapore will explain how he and his team identified that the stem cells which are crucial to maintaining a healthy intestine are also the site at which bowel cancers first begin, and how he also hopes to use healthy stem cells to regenerate tissues to help patients with Crohn's disease and some cancers.
Having discovered a gene that is only turned on in these particular stem cells Professor Barker and his team have been able to isolate the cells in mice and grow small pieces of intestine in the lab. The researchers hope that if they are able to grow larger pieces, they will be able to produce transplant tissues to replace damaged intestines.
Professor Barker explains: "Processing our dinner every day is a tough job so the lining of our intestines quickly get worn out. To keep the intestine working stem cells in little pockets along the surface replace the lining, cell by cell, about once a week.
"We already knew these stem cells existed for a while we didn't know much about them because it was difficult to distinguish them from all of the other types of cells in our intestines. Our team was able to single them out and study them because we discovered a gene that is only turned on in these particular stem cells."
Once the researchers had found this gene they were able to track where the stem cells occur throughout the body finding that, as well as the intestine, the stomach lining and in hair follicles, the cells were also present in bowel tumours.
Professor Barker continues: "We hope that studying these stem cells will be doubly useful: One day we hope to grow large enough pieces in the lab to form replacement tissues for transplant; and by studying the cells we will be able to find new ways to prevent them from mutating and hence leading to cancer.
"Bowel cancer is the third most common type of cancer in England and an estimated 38,000 new cases are diagnosed each year. We know these stem cells are both implicated in causing the cancer but that they also could be useful for treating disease so we hope that studying them will help us to understand how to attack the disease on two fronts.
How Music Helps Prevent Organ Rejection
Music has a fundamental affect on humans. It can reduce stress, enhance relaxation, provide a distraction from pain, and improve the results of clinical therapy. New research published in BioMed Central's open access journal Journal of Cardiothoracic Surgery demonstrates that music can reduce rejection of heart transplants in mice by influencing the immune system.
The link between the immune system and brain function is not clearly understood, nevertheless music is used clinically to reduce anxiety after heart attack, or to reduce pain and nausea during bone marrow transplantation. There is some evidence that music may act via the parasympathetic nervous system, which regulates the bodily functions that we have no conscious control over, including digestion.
Researchers from Japan investigated if music could influence the survival of heart transplants in mice. They found that opera and classical music both increased the time before the transplanted organs failed, but single frequency monotones and new age music did not.
The team led by Dr Masanori Niimi pinpointed the source of this protection to the spleen. Dr Uchiyama and Jin revealed, "Opera exposed mice had lower levels of interleukin-2 (IL-2) and interferon gamma (IFN-γ). They also had increased levels of anti-inflammatory IL-4 and IL-10. Significantly these mice had increased numbers of CD4+CD25+ cells, which regulate the peripheral immune response."
It seems that music really does influence the immune system -- although the mechanism behind this still is not clear. Additionally, this study only looked at a limited selection of composers, so the effect of music on reducing organ rejection may not be limited to opera.
The link between the immune system and brain function is not clearly understood, nevertheless music is used clinically to reduce anxiety after heart attack, or to reduce pain and nausea during bone marrow transplantation. There is some evidence that music may act via the parasympathetic nervous system, which regulates the bodily functions that we have no conscious control over, including digestion.
Researchers from Japan investigated if music could influence the survival of heart transplants in mice. They found that opera and classical music both increased the time before the transplanted organs failed, but single frequency monotones and new age music did not.
The team led by Dr Masanori Niimi pinpointed the source of this protection to the spleen. Dr Uchiyama and Jin revealed, "Opera exposed mice had lower levels of interleukin-2 (IL-2) and interferon gamma (IFN-γ). They also had increased levels of anti-inflammatory IL-4 and IL-10. Significantly these mice had increased numbers of CD4+CD25+ cells, which regulate the peripheral immune response."
It seems that music really does influence the immune system -- although the mechanism behind this still is not clear. Additionally, this study only looked at a limited selection of composers, so the effect of music on reducing organ rejection may not be limited to opera.
Daytime Nap Can Benefit A Person's Memory Performance
A brief bout of non-REM sleep (45 minutes) obtained during a daytime nap clearly benefits a person's declarative memory performance, according to a new study.
The study, authored by Matthew A. Tucker, PhD, of the Center for Sleep and Cognition and the department of psychiatry at Harvard Medical School, focused on 33 subjects (11 males, 22 females) with an average age of 23.3 years. The participants arrived at the sleep lab at 11:30 a.m., were trained on each of the declarative memory tasks at 12:15 p.m., and at 1 p.m., 16 subjects took a nap while 17 remained awake in the lab. After the nap period, all subjects remained in the lab until the retest at 4 p.m.
It was discovered that, across three very different declarative memory tasks, a nap benefited performance compared to comparable periods of wakefulness, but only for those subjects that strongly acquired the tasks during the training session.
"These results suggest that there is a threshold acquisition level that has to be obtained for sleep to optimally process the memory," said Dr. Tucker. "The importance of this finding is that sleep may not indiscriminately process all information we acquire during wakefulness, only the information we learn well."
It is recommended that adults get between seven and eight hours of nightly sleep.
The article "Enhancement of Declarative Memory Performance Following a Daytime Nap is Contingent on Strength of Initial Task Acquisition" was published in the February 1 issue of the journal Sleep.
The study, authored by Matthew A. Tucker, PhD, of the Center for Sleep and Cognition and the department of psychiatry at Harvard Medical School, focused on 33 subjects (11 males, 22 females) with an average age of 23.3 years. The participants arrived at the sleep lab at 11:30 a.m., were trained on each of the declarative memory tasks at 12:15 p.m., and at 1 p.m., 16 subjects took a nap while 17 remained awake in the lab. After the nap period, all subjects remained in the lab until the retest at 4 p.m.
It was discovered that, across three very different declarative memory tasks, a nap benefited performance compared to comparable periods of wakefulness, but only for those subjects that strongly acquired the tasks during the training session.
"These results suggest that there is a threshold acquisition level that has to be obtained for sleep to optimally process the memory," said Dr. Tucker. "The importance of this finding is that sleep may not indiscriminately process all information we acquire during wakefulness, only the information we learn well."
It is recommended that adults get between seven and eight hours of nightly sleep.
The article "Enhancement of Declarative Memory Performance Following a Daytime Nap is Contingent on Strength of Initial Task Acquisition" was published in the February 1 issue of the journal Sleep.
Scientists Reprogram Cancer Cells With Low Doses of Epigenetic Drugs
Experimenting with cells in culture, researchers at the Johns Hopkins Kimmel Cancer Center have breathed possible new life into two drugs once considered too toxic for human cancer treatment. The drugs, azacitidine (AZA) and decitabine (DAC), are epigenetic-targeted drugs and work to correct cancer-causing alterations that modify DNA.
The researchers said the drugs also were found to take aim at a small but dangerous subpopulation of self-renewing cells, sometimes referred to as cancer stem cells, which evade most cancer drugs and cause recurrence and spread.
In a report published in the March 20, 2012, issue of Cancer Cell, the Johns Hopkins team said their study provides evidence that low doses of the drugs tested on cell cultures cause antitumor responses in breast, lung, and colon cancers.
Conventional chemotherapy agents work by indiscriminately poisoning and killing rapidly-dividing cells, including cancer cells, by damaging cellular machinery and DNA. "In contrast, low doses of AZA and DAC may re-activate genes that stop cancer growth without causing immediate cell-killing or DNA damage," says Stephen Baylin, M.D., Ludwig Professor of Oncology and deputy director of the Johns Hopkins Kimmel Cancer Center.
Many cancer experts had abandoned AZA and DAC for the treatment of common cancers, according to the researchers, because they are toxic to normal cells at standard high doses, and there was little research showing how they might work for cancer in general. Baylin and his colleague Cynthia Zahnow, Ph.D., decided to take another look at the drugs after low doses of the drugs showed a benefit in patients with a pre-leukemic disorder called myelodysplastic syndrome (MDS). Johns Hopkins investigators also showed benefit of low doses of the drugs in tests with a small number of advanced lung cancer patients. "This is contrary to the way we usually do things in cancer research," says Baylin, noting that "typically, we start in the laboratory and progress to clinical trials. In this case, we saw results in clinical trials that made us go back to the laboratory to figure out how to move the therapy forward."
For the research, Baylin and Zahnow's team worked with leukemia, breast, and other cancer cell lines and human tumor samples using the lowest possible doses that were effective against the cancers. In all, the investigators studied six leukemia cell lines, seven leukemia patient samples, three breast cancer cell lines, seven breast tumor samples (including four samples of tumors that had spread to the lung), one lung cancer tumor sample, and one colon cancer tumor sample. The team treated cell lines and tumor cells with low-dose AZA and DAC in culture for three days and allowed the drug-treated cells to rest for a week. Treated cells and tumor samples were then transplanted into mice where the researchers observed continued antitumor responses for up to 20 weeks. This extended response was in line with observations in some MDS patients who continued to have anticancer effects long after stopping the drug.
The low-dose therapy reversed cancer cell gene pathways, including those controlling cell cycle, cell repair, cell maturation, cell differentiation, immune cell interaction, and cell death. Effects varied among individual tumor cells, but the scientists generally saw that cancer cells reverted to a more normal state and eventually died. These results were caused, in part, by alteration of the epigenetic, or chemical environment, of DNA. Epigenetic activities turn on certain genes and block others, says Zahnow, assistant professor of oncology and the Evelyn Grolman Glick Scholar at Johns Hopkins.
The research team also tested AZA and DAC's effect on a type of metastatic breast cancer cell thought to drive cancer growth and resist standard therapies. Metastatic cells are difficult to study in standard laboratory tumor models, because they tend to break away from the original tumor and float around in blood and lymph fluids. The Johns Hopkins team re-created the metastatic stem cells' environment, allowing them to grow as floating spheres. "These cells were growing well as spheres in suspension, but when we treated the cells with AZA, both the size and number of spheres were dramatically reduced," says Zahnow.
The precise mechanism of how the drugs work is the focus of ongoing studies by Baylin and his team. "Our findings match evidence from recent clinical trials suggesting that the drugs shrink tumors more slowly over time as they repair altered mechanisms in cells and genes return to normal function and the cells may eventually die," says Baylin.
The results of clinical trials in lung cancer, led by Johns Hopkins' Charles Rudin, M.D., and published late last year in Cancer Discovery, also indicate that the drugs make tumors more responsive to standard anticancer drug treatment. This means, they say, that the drugs could become part of a combined treatment approach rather than a stand-alone therapy and as part of personalized approaches in patients whose cancers fit specific epigenetic and genetic profiles.
Low doses of both drugs are approved by the U.S. Food and Drug Administration for the treatment of MDS and chronic myelomonocytic leukemia (CMML). Clinical trials in breast and lung cancer have begun in patients with advanced disease, and trials in colon cancer are planned.
In addition to Baylin and Zahnow, other investigators participating in this study include Hsing-Chen Tsai, Huili Li, Leander Van Neste, Yi Cai, Carine Robert, Feyruz V. Rassool, James J. Shin, Kirsten M. Harbom, Robert Beaty, Emmanouil Pappou, James Harris, Ray-Whay Chiu Yen, Nita Ahuja, Malcolm V. Brock, Vered Stearns, David Feller-Kopman, Lonny B. Yarmus, Yi-Chun Lin, Alana L. Welm, Jean-Pierre Issa, Il Minn, William Matsui, Yoon-Young Jang, and Saul J. Sharkis.
The researchers said the drugs also were found to take aim at a small but dangerous subpopulation of self-renewing cells, sometimes referred to as cancer stem cells, which evade most cancer drugs and cause recurrence and spread.
In a report published in the March 20, 2012, issue of Cancer Cell, the Johns Hopkins team said their study provides evidence that low doses of the drugs tested on cell cultures cause antitumor responses in breast, lung, and colon cancers.
Conventional chemotherapy agents work by indiscriminately poisoning and killing rapidly-dividing cells, including cancer cells, by damaging cellular machinery and DNA. "In contrast, low doses of AZA and DAC may re-activate genes that stop cancer growth without causing immediate cell-killing or DNA damage," says Stephen Baylin, M.D., Ludwig Professor of Oncology and deputy director of the Johns Hopkins Kimmel Cancer Center.
Many cancer experts had abandoned AZA and DAC for the treatment of common cancers, according to the researchers, because they are toxic to normal cells at standard high doses, and there was little research showing how they might work for cancer in general. Baylin and his colleague Cynthia Zahnow, Ph.D., decided to take another look at the drugs after low doses of the drugs showed a benefit in patients with a pre-leukemic disorder called myelodysplastic syndrome (MDS). Johns Hopkins investigators also showed benefit of low doses of the drugs in tests with a small number of advanced lung cancer patients. "This is contrary to the way we usually do things in cancer research," says Baylin, noting that "typically, we start in the laboratory and progress to clinical trials. In this case, we saw results in clinical trials that made us go back to the laboratory to figure out how to move the therapy forward."
For the research, Baylin and Zahnow's team worked with leukemia, breast, and other cancer cell lines and human tumor samples using the lowest possible doses that were effective against the cancers. In all, the investigators studied six leukemia cell lines, seven leukemia patient samples, three breast cancer cell lines, seven breast tumor samples (including four samples of tumors that had spread to the lung), one lung cancer tumor sample, and one colon cancer tumor sample. The team treated cell lines and tumor cells with low-dose AZA and DAC in culture for three days and allowed the drug-treated cells to rest for a week. Treated cells and tumor samples were then transplanted into mice where the researchers observed continued antitumor responses for up to 20 weeks. This extended response was in line with observations in some MDS patients who continued to have anticancer effects long after stopping the drug.
The low-dose therapy reversed cancer cell gene pathways, including those controlling cell cycle, cell repair, cell maturation, cell differentiation, immune cell interaction, and cell death. Effects varied among individual tumor cells, but the scientists generally saw that cancer cells reverted to a more normal state and eventually died. These results were caused, in part, by alteration of the epigenetic, or chemical environment, of DNA. Epigenetic activities turn on certain genes and block others, says Zahnow, assistant professor of oncology and the Evelyn Grolman Glick Scholar at Johns Hopkins.
The research team also tested AZA and DAC's effect on a type of metastatic breast cancer cell thought to drive cancer growth and resist standard therapies. Metastatic cells are difficult to study in standard laboratory tumor models, because they tend to break away from the original tumor and float around in blood and lymph fluids. The Johns Hopkins team re-created the metastatic stem cells' environment, allowing them to grow as floating spheres. "These cells were growing well as spheres in suspension, but when we treated the cells with AZA, both the size and number of spheres were dramatically reduced," says Zahnow.
The precise mechanism of how the drugs work is the focus of ongoing studies by Baylin and his team. "Our findings match evidence from recent clinical trials suggesting that the drugs shrink tumors more slowly over time as they repair altered mechanisms in cells and genes return to normal function and the cells may eventually die," says Baylin.
The results of clinical trials in lung cancer, led by Johns Hopkins' Charles Rudin, M.D., and published late last year in Cancer Discovery, also indicate that the drugs make tumors more responsive to standard anticancer drug treatment. This means, they say, that the drugs could become part of a combined treatment approach rather than a stand-alone therapy and as part of personalized approaches in patients whose cancers fit specific epigenetic and genetic profiles.
Low doses of both drugs are approved by the U.S. Food and Drug Administration for the treatment of MDS and chronic myelomonocytic leukemia (CMML). Clinical trials in breast and lung cancer have begun in patients with advanced disease, and trials in colon cancer are planned.
In addition to Baylin and Zahnow, other investigators participating in this study include Hsing-Chen Tsai, Huili Li, Leander Van Neste, Yi Cai, Carine Robert, Feyruz V. Rassool, James J. Shin, Kirsten M. Harbom, Robert Beaty, Emmanouil Pappou, James Harris, Ray-Whay Chiu Yen, Nita Ahuja, Malcolm V. Brock, Vered Stearns, David Feller-Kopman, Lonny B. Yarmus, Yi-Chun Lin, Alana L. Welm, Jean-Pierre Issa, Il Minn, William Matsui, Yoon-Young Jang, and Saul J. Sharkis.
Sleep Helps Reduce Errors In Memory, Research Suggests
Sleep may reduce mistakes in memory, according to a first-of-its-kind study led by a cognitive neuroscientist at Michigan State University.
See Also:
Health & Medicine
Sleep Disorder Research
Insomnia Research
Alzheimer's Research
Mind & Brain
Memory
Sleep Disorders
Insomnia
Reference
Memory bias
Sleep deprivation
Circadian rhythm sleep disorder
Rapid eye movement
The findings, which appear in the September issue of the journal Learning & Memory, have practical implications for everyone from students flubbing multiple choice tests to senior citizens confusing their medications, said Kimberly Fenn, principal investigator and MSU assistant professor of psychology.
“It’s easy to muddle things in your mind,” Fenn said. “This research suggests that after sleep you’re better able to tease apart the incorrect aspect of that memory.”
Fenn and colleagues from the University of Chicago and Washington University in St. Louis studied the presence of false memory in groups of college students. While previous research has shown that sleep improves memory, this study is the first to address errors in memory, she said.
Study participants were exposed to lists of words and then, 12 hours later, exposed to individual words and asked to identify which words they had seen or heard in the earlier session. One group of students was trained in the morning (10 a.m.) and tested after the course of a normal sleepless day (10 p.m.), while another group was trained at night and tested 12 hours later in the morning, after at least six hours of sleep.
Three experiments were conducted, using different stimuli. In each, the students who had slept had fewer problems with false memory – choosing fewer incorrect words.
How does sleep help? The answer isn’t known, Fenn said, but she suspects it may be due to sleep strengthening the source of the memory. The source, or context in which the information is acquired, is a vital element of the memory process.
Or perhaps the people who didn’t sleep during the study were simply bombarded with information over the course of the day, affecting their memory ability, Fenn said.
Further research is warranted, she said, adding that she plans to study different population groups, particularly the elderly.
“We know older individuals generally have worse memory performance than younger individuals. We also know from other research that elderly individuals tend to be more prone to false memories,” Fenn said. “Given the work we’ve done it’s possible that sleep may actually help them to reject this false information. And potentially this could help to improve their quality of life in some way.”
See Also:
Health & Medicine
Sleep Disorder Research
Insomnia Research
Alzheimer's Research
Mind & Brain
Memory
Sleep Disorders
Insomnia
Reference
Memory bias
Sleep deprivation
Circadian rhythm sleep disorder
Rapid eye movement
The findings, which appear in the September issue of the journal Learning & Memory, have practical implications for everyone from students flubbing multiple choice tests to senior citizens confusing their medications, said Kimberly Fenn, principal investigator and MSU assistant professor of psychology.
“It’s easy to muddle things in your mind,” Fenn said. “This research suggests that after sleep you’re better able to tease apart the incorrect aspect of that memory.”
Fenn and colleagues from the University of Chicago and Washington University in St. Louis studied the presence of false memory in groups of college students. While previous research has shown that sleep improves memory, this study is the first to address errors in memory, she said.
Study participants were exposed to lists of words and then, 12 hours later, exposed to individual words and asked to identify which words they had seen or heard in the earlier session. One group of students was trained in the morning (10 a.m.) and tested after the course of a normal sleepless day (10 p.m.), while another group was trained at night and tested 12 hours later in the morning, after at least six hours of sleep.
Three experiments were conducted, using different stimuli. In each, the students who had slept had fewer problems with false memory – choosing fewer incorrect words.
How does sleep help? The answer isn’t known, Fenn said, but she suspects it may be due to sleep strengthening the source of the memory. The source, or context in which the information is acquired, is a vital element of the memory process.
Or perhaps the people who didn’t sleep during the study were simply bombarded with information over the course of the day, affecting their memory ability, Fenn said.
Further research is warranted, she said, adding that she plans to study different population groups, particularly the elderly.
“We know older individuals generally have worse memory performance than younger individuals. We also know from other research that elderly individuals tend to be more prone to false memories,” Fenn said. “Given the work we’ve done it’s possible that sleep may actually help them to reject this false information. And potentially this could help to improve their quality of life in some way.”
Meditation Can Lower Blood Pressure, Study Shows
Transcendental Meditation is an effective treatment for controlling high blood pressure with the added benefit of bypassing possible side effects and hazards of anti-hypertension drugs, according to a new meta-analysis conducted at the University of Kentucky.
The meta-analysis evaluated nine randomized, controlled trials using Transcendental Meditation as a primary intervention for hypertensive patients. The practice of Transcendental Meditation was associated with approximate reductions of 4.7 mm systolic blood pressure and 3.2 mm diastolic blood pressure.
The study's lead author, Dr. James W. Anderson, professor of medicine at the University of Kentucky College of Medicine, said that blood pressure reductions of this magnitude would be expected to be accompanied by significant reductions in risk for atherosclerotic cardiovascular disease—without drug side effects. Anderson's most recent findings reinforce an earlier study that found Transcendental Meditation produces a statistically significant reduction in high blood pressure that was not found with other forms of relaxation, meditation, biofeedback or stress management.
"Adding Transcendental Medication is about equivalent to adding a second antihypertension agent to one's current regimen only safer and less troublesome," Anderson said.
The Centers for Disease Control and Prevention (CDC) estimates that 1 out of 3 American adults have high blood pressure. Having high blood pressure increases one's chances of developing heart disease, stroke, congestive heart failure and kidney disease.
The study appears in the March issue of the American Journal of Hypertension.
The meta-analysis evaluated nine randomized, controlled trials using Transcendental Meditation as a primary intervention for hypertensive patients. The practice of Transcendental Meditation was associated with approximate reductions of 4.7 mm systolic blood pressure and 3.2 mm diastolic blood pressure.
The study's lead author, Dr. James W. Anderson, professor of medicine at the University of Kentucky College of Medicine, said that blood pressure reductions of this magnitude would be expected to be accompanied by significant reductions in risk for atherosclerotic cardiovascular disease—without drug side effects. Anderson's most recent findings reinforce an earlier study that found Transcendental Meditation produces a statistically significant reduction in high blood pressure that was not found with other forms of relaxation, meditation, biofeedback or stress management.
"Adding Transcendental Medication is about equivalent to adding a second antihypertension agent to one's current regimen only safer and less troublesome," Anderson said.
The Centers for Disease Control and Prevention (CDC) estimates that 1 out of 3 American adults have high blood pressure. Having high blood pressure increases one's chances of developing heart disease, stroke, congestive heart failure and kidney disease.
The study appears in the March issue of the American Journal of Hypertension.
Memory Links to 40 Winks
When it comes to executing items on tomorrow's to-do list, it's best to think it over, then "sleep on it," say psychologists at Washington University in St. Louis.
People who sleep after processing and storing a memory carry out their intentions much better than people who try to execute their plan before getting to sleep. The researchers have shown that sleep enhances our ability to remember to do something in the future, a skill known as prospective memory.
Moreover, researchers studying the relationship between memory and sleep say that our ability to carry out our intentions is not so much a function of how firmly that intention has been embedded in our memories. Rather, the trigger that helps carry out our intentions is usually a place, situation or circumstance -- some context encountered the next day -- that sparks the recall of an intended action.
These are the key findings from a study published online this month in Psychological Science of the relationship between memory and sleep. Researchers Michael Scullin, doctoral candidate in psychology, and his adviser, Mark McDaniel, PhD, professor of psychology in Arts & Sciences, are focusing on "prospective memory" -- things we intend to do -- as opposed to "retrospective memory" -- things that have happened in the past.
Prospective memory includes such things as remembering to take a medication, buying a Mother's Day card or bringing home the ice cream for a birthday party. While the vast majority of sleep literature in psychology is devoted to retrospective memory, this study is the first foray into the relationship between sleep and prospective memory, the kind of memory we put to work every day. The findings, researchers say, offer important contributions to the understanding of the role sleep plays in cognition as well as memory.
Let's say that you intend to give a colleague a message tomorrow, McDaniel explains. Seeing the colleague the next day will be a strong cue for remembering to give the message. But, during the time your brain encoded the intention, you're also vaguely thinking of a meeting the two of you will attend the next afternoon. The context of the conference room is weakly associated with your intention to give the message even though you haven't really thought explicitly about associating the room with the message.
The Scullin/McDaniel study shows that sleep strengthens the weak association between the conference room (the context) and the delivery of the message (the intention). But sleep does little or nothing with the stronger association between the person and the message.
"We found that sleep benefits prospective memory by strengthening the weak associations in the brain, and that hasn't been shown before," Scullin says.
"One of the more provocative findings we have is that sleep didn't strengthen the link between the explicit cue, which is the person, and the intention, rather it strengthened the weak association and the intention," McDaniel says.
Here's how they showed it:
The researchers tested four different groups each of 24 Washington University students. Two were control groups -- one tested in the morning, the other in the evening -- to eliminate the notion that the biological clock might play any role in memory function. Another group was prepped for tests in the morning then tested twelve hours later in the evening before getting to sleep. The fourth group learned the test routine in the evening, went home and slept, then were tested 12 hours later in the morning.
Participants were given instructions for three tests in this order and the tests later were given in blocks of 150 items in the same order: a living/non-living test, in which they decided if a word (cat, for instance, or skate) indicated a living or non-living entity; a lexical decision test, in which participants decided if a string of letters was a word or nonsense; and a semantic category test, in which a word was classified by participants into a category, baseball, for instance, in the category of sport.
After learning the last test, participants were told that in the midst of these ongoing tests -- given to represent such everyday activities as driving, watching TV, listening to a teacher -- the words table or horse would pop up on a screen, and when they saw them, they were to press the "Q" button. This represented the prospective memory intention.
The researchers found that participants who tested in the morning following sleep overwhelmingly performed the prospective memory task better in the semantic category test, or context, than in the other two, and they found no such correlation in the group who tested sleepless.
The crux of the finding rests on the fact that the prospective memory instruction was given right after the semantic category practice. In this context, those who slept remembered the prospective memory intention better than in the other categories.
"Sleep promoted the remembering to do the prospective memory task when that one context was present, but not when some other context was present," McDaniel says. "That's because of temporal contiguity -- the fact that the participants were told to hit that 'Q' button right after they were exposed to the semantic category context.
"The idea is that the semantic category test is weakly associated with the prospective memory intention -- it's weakly floating around in the mind and becomes weakly associated with the prospective memory test," McDaniel says.
To return to the colleague and message analogy, because before sleeping you remembered you had a message to deliver to your colleague and you would see him in the conference room tomorrow, sleep enhances the likelihood that you will tell him in the conference room, but not in some other context, the office, elevator, the mail room, for example.
The researchers believe that the prospective memory process occurs during slow wave sleep -- an early pattern in the sleep cycle -- involving communication between the hippocampus and cortical regions. The hippocampus is very important in memory formation and reactivation and the cortical regions are keys to storing memories.
"We think that during slow wave sleep the hippocampus is reactivating these recently learned memories, taking them up and placing them in long-term storage regions in the brain," Scullin says. "The physiology of slow wave sleep seems very conducive to this kind of memory strengthening."
People who sleep after processing and storing a memory carry out their intentions much better than people who try to execute their plan before getting to sleep. The researchers have shown that sleep enhances our ability to remember to do something in the future, a skill known as prospective memory.
Moreover, researchers studying the relationship between memory and sleep say that our ability to carry out our intentions is not so much a function of how firmly that intention has been embedded in our memories. Rather, the trigger that helps carry out our intentions is usually a place, situation or circumstance -- some context encountered the next day -- that sparks the recall of an intended action.
These are the key findings from a study published online this month in Psychological Science of the relationship between memory and sleep. Researchers Michael Scullin, doctoral candidate in psychology, and his adviser, Mark McDaniel, PhD, professor of psychology in Arts & Sciences, are focusing on "prospective memory" -- things we intend to do -- as opposed to "retrospective memory" -- things that have happened in the past.
Prospective memory includes such things as remembering to take a medication, buying a Mother's Day card or bringing home the ice cream for a birthday party. While the vast majority of sleep literature in psychology is devoted to retrospective memory, this study is the first foray into the relationship between sleep and prospective memory, the kind of memory we put to work every day. The findings, researchers say, offer important contributions to the understanding of the role sleep plays in cognition as well as memory.
Let's say that you intend to give a colleague a message tomorrow, McDaniel explains. Seeing the colleague the next day will be a strong cue for remembering to give the message. But, during the time your brain encoded the intention, you're also vaguely thinking of a meeting the two of you will attend the next afternoon. The context of the conference room is weakly associated with your intention to give the message even though you haven't really thought explicitly about associating the room with the message.
The Scullin/McDaniel study shows that sleep strengthens the weak association between the conference room (the context) and the delivery of the message (the intention). But sleep does little or nothing with the stronger association between the person and the message.
"We found that sleep benefits prospective memory by strengthening the weak associations in the brain, and that hasn't been shown before," Scullin says.
"One of the more provocative findings we have is that sleep didn't strengthen the link between the explicit cue, which is the person, and the intention, rather it strengthened the weak association and the intention," McDaniel says.
Here's how they showed it:
The researchers tested four different groups each of 24 Washington University students. Two were control groups -- one tested in the morning, the other in the evening -- to eliminate the notion that the biological clock might play any role in memory function. Another group was prepped for tests in the morning then tested twelve hours later in the evening before getting to sleep. The fourth group learned the test routine in the evening, went home and slept, then were tested 12 hours later in the morning.
Participants were given instructions for three tests in this order and the tests later were given in blocks of 150 items in the same order: a living/non-living test, in which they decided if a word (cat, for instance, or skate) indicated a living or non-living entity; a lexical decision test, in which participants decided if a string of letters was a word or nonsense; and a semantic category test, in which a word was classified by participants into a category, baseball, for instance, in the category of sport.
After learning the last test, participants were told that in the midst of these ongoing tests -- given to represent such everyday activities as driving, watching TV, listening to a teacher -- the words table or horse would pop up on a screen, and when they saw them, they were to press the "Q" button. This represented the prospective memory intention.
The researchers found that participants who tested in the morning following sleep overwhelmingly performed the prospective memory task better in the semantic category test, or context, than in the other two, and they found no such correlation in the group who tested sleepless.
The crux of the finding rests on the fact that the prospective memory instruction was given right after the semantic category practice. In this context, those who slept remembered the prospective memory intention better than in the other categories.
"Sleep promoted the remembering to do the prospective memory task when that one context was present, but not when some other context was present," McDaniel says. "That's because of temporal contiguity -- the fact that the participants were told to hit that 'Q' button right after they were exposed to the semantic category context.
"The idea is that the semantic category test is weakly associated with the prospective memory intention -- it's weakly floating around in the mind and becomes weakly associated with the prospective memory test," McDaniel says.
To return to the colleague and message analogy, because before sleeping you remembered you had a message to deliver to your colleague and you would see him in the conference room tomorrow, sleep enhances the likelihood that you will tell him in the conference room, but not in some other context, the office, elevator, the mail room, for example.
The researchers believe that the prospective memory process occurs during slow wave sleep -- an early pattern in the sleep cycle -- involving communication between the hippocampus and cortical regions. The hippocampus is very important in memory formation and reactivation and the cortical regions are keys to storing memories.
"We think that during slow wave sleep the hippocampus is reactivating these recently learned memories, taking them up and placing them in long-term storage regions in the brain," Scullin says. "The physiology of slow wave sleep seems very conducive to this kind of memory strengthening."
Sleep Apnea Patients Have Greatly Increased Risk Of Severe Car Crashes
People with obstructive sleep apnea have a markedly increased risk of severe motor vehicle crashes involving personal injury, according to a new study.
The study of 800 people with sleep apnea and 800 without the nighttime breathing disorder found that patients with sleep apnea were twice as likely as people without sleep apnea to have a car crash, and three to five times as likely to have a serious crash involving personal injury. Overall, the sleep apnea group had a total of 250 crashes over three years, compared with 123 crashes in the group without sleep apnea.
While many previous studies have shown that sleep apnea patients are at increased risk of car crashes, this study is the first to look at the severity of those crashes. "We were surprised not only about how many of the sleep apnea patients' crashes involved personal injury, but that some patients had fairly mild sleep apnea and were still having serious crashes," says Alan Mulgrew, M.D., of the UBC Sleep Disorders Program in Vancouver, British Columbia.
Patients' self-reported feeling of sleepiness was not found to be linked with an increased risk of car crashes, suggesting that patients are unaware of their driving hazard, Dr. Mulgrew says. Even patients with fairly mild sleep apnea were at increased risk of car crashes. "Based on these findings, I now consider driving risk when deciding on treatment for patients with mild sleep apnea," he says.
The study is the biggest one to combine validated sleep apnea diagnosis through an overnight sleep study called polysomnography, with data from insurance records to verify motor vehicle crashes and their severity.
In obstructive sleep apnea, the upper airway narrows, or collapses, during sleep. Periods of apnea end with a brief partial arousal that may disrupt sleep hundreds of times a night. Obesity is a major risk factor for sleep apnea.
The study found that while in the general population men have more vehicle crashes than women, among sleep apnea patients, men and women crash at a similar rate.
Although the issue of treatment is not addressed by this study, Dr. Mulgrew notes that data from other groups suggests that crashes related to sleep apnea are preventable.
This research was presented at the American Thoracic Society 2007 International Conference, on Sunday, May 20. "Severity of Motor Vehicle Crashes in Obstructive Sleep Apnea Patients"
The study of 800 people with sleep apnea and 800 without the nighttime breathing disorder found that patients with sleep apnea were twice as likely as people without sleep apnea to have a car crash, and three to five times as likely to have a serious crash involving personal injury. Overall, the sleep apnea group had a total of 250 crashes over three years, compared with 123 crashes in the group without sleep apnea.
While many previous studies have shown that sleep apnea patients are at increased risk of car crashes, this study is the first to look at the severity of those crashes. "We were surprised not only about how many of the sleep apnea patients' crashes involved personal injury, but that some patients had fairly mild sleep apnea and were still having serious crashes," says Alan Mulgrew, M.D., of the UBC Sleep Disorders Program in Vancouver, British Columbia.
Patients' self-reported feeling of sleepiness was not found to be linked with an increased risk of car crashes, suggesting that patients are unaware of their driving hazard, Dr. Mulgrew says. Even patients with fairly mild sleep apnea were at increased risk of car crashes. "Based on these findings, I now consider driving risk when deciding on treatment for patients with mild sleep apnea," he says.
The study is the biggest one to combine validated sleep apnea diagnosis through an overnight sleep study called polysomnography, with data from insurance records to verify motor vehicle crashes and their severity.
In obstructive sleep apnea, the upper airway narrows, or collapses, during sleep. Periods of apnea end with a brief partial arousal that may disrupt sleep hundreds of times a night. Obesity is a major risk factor for sleep apnea.
The study found that while in the general population men have more vehicle crashes than women, among sleep apnea patients, men and women crash at a similar rate.
Although the issue of treatment is not addressed by this study, Dr. Mulgrew notes that data from other groups suggests that crashes related to sleep apnea are preventable.
This research was presented at the American Thoracic Society 2007 International Conference, on Sunday, May 20. "Severity of Motor Vehicle Crashes in Obstructive Sleep Apnea Patients"
Sleep Makes Your Memories Stronger, and Helps With Creativity
As humans, we spend about a third of our lives asleep. So there must be a point to it, right? Scientists have found that sleep helps consolidate memories, fixing them in the brain so we can retrieve them later. Now, new research is showing that sleep also seems to reorganize memories, picking out the emotional details and reconfiguring the memories to help you produce new and creative ideas, according to the authors of an article in Current Directions in Psychological Science.
"Sleep is making memories stronger," says Jessica D. Payne of the University of Notre Dame, who co-wrote the review with Elizabeth A. Kensinger of Boston College. "It also seems to be doing something which I think is so much more interesting, and that is reorganizing and restructuring memories."
Payne and Kensinger study what happens to memories during sleep, and they have found that a person tends to hang on to the most emotional part of a memory. For example, if someone is shown a scene with an emotional object, such as a wrecked car, in the foreground, they're more likely to remember the emotional object than, say, the palm trees in the background -- particularly if they're tested after a night of sleep. They have also measured brain activity during sleep and found that regions of the brain involved with emotion and memory consolidation are active.
"In our fast-paced society, one of the first things to go is our sleep," Payne says. "I think that's based on a profound misunderstanding that the sleeping brain isn't doing anything." The brain is busy. It's not just consolidating memories, it's organizing them and picking out the most salient information. She thinks this is what makes it possible for people to come up with creative, new ideas.
Payne has taken the research to heart. "I give myself an eight-hour sleep opportunity every night. I never used to do that -- until I started seeing my data," she says. People who say they'll sleep when they're dead are sacrificing their ability to have good thoughts now, she says. "We can get away with less sleep, but it has a profound effect on our cognitive abilities."
"Sleep is making memories stronger," says Jessica D. Payne of the University of Notre Dame, who co-wrote the review with Elizabeth A. Kensinger of Boston College. "It also seems to be doing something which I think is so much more interesting, and that is reorganizing and restructuring memories."
Payne and Kensinger study what happens to memories during sleep, and they have found that a person tends to hang on to the most emotional part of a memory. For example, if someone is shown a scene with an emotional object, such as a wrecked car, in the foreground, they're more likely to remember the emotional object than, say, the palm trees in the background -- particularly if they're tested after a night of sleep. They have also measured brain activity during sleep and found that regions of the brain involved with emotion and memory consolidation are active.
"In our fast-paced society, one of the first things to go is our sleep," Payne says. "I think that's based on a profound misunderstanding that the sleeping brain isn't doing anything." The brain is busy. It's not just consolidating memories, it's organizing them and picking out the most salient information. She thinks this is what makes it possible for people to come up with creative, new ideas.
Payne has taken the research to heart. "I give myself an eight-hour sleep opportunity every night. I never used to do that -- until I started seeing my data," she says. People who say they'll sleep when they're dead are sacrificing their ability to have good thoughts now, she says. "We can get away with less sleep, but it has a profound effect on our cognitive abilities."
Meditation May Be An Effective Treatment For Insomnia
Meditation may be an effective behavioral intervention in the treatment of insomnia, according to a research abstract that will be presented on June 9, at Sleep 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies.
Results indicate that patients saw improvements in subjective sleep quality and sleep diary parameters while practicing meditation. Sleep latency, total sleep time, total wake time, wake after sleep onset, sleep efficiency, sleep quality and depression improved in patients who used meditation.
According to principal investigator Ramadevi Gourineni, MD, director of the insomnia program at Northwestern Memorial Hospital in Evanston, Ill., insomnia is believed to be a 24-hour problem of hyperarousal, and elevated measures of arousals are seen throughout the day.
"Results of the study show that teaching deep relaxation techniques during the daytime can help improve sleep at night," said Gourineni.
The study gathered data from 11 healthy subjects between the ages of 25 and 45 years with chronic primary insomnia. Participants were divided into two intervention groups for two months: Kriya Yoga (a form of meditation that is used to focus internalized attention and has been shown to reduce measures of arousal) and health education. Subjective measures of sleep and depression were collected at baseline and after the two-month period.
Both groups received sleep hygiene education; members of the health education group also received information about health-related topics and how to improve health through exercise, nutrition, weight loss and stress management.
Abstract Title: Effects of Meditation on Sleep in Individuals with Chronic Insomnia
Results indicate that patients saw improvements in subjective sleep quality and sleep diary parameters while practicing meditation. Sleep latency, total sleep time, total wake time, wake after sleep onset, sleep efficiency, sleep quality and depression improved in patients who used meditation.
According to principal investigator Ramadevi Gourineni, MD, director of the insomnia program at Northwestern Memorial Hospital in Evanston, Ill., insomnia is believed to be a 24-hour problem of hyperarousal, and elevated measures of arousals are seen throughout the day.
"Results of the study show that teaching deep relaxation techniques during the daytime can help improve sleep at night," said Gourineni.
The study gathered data from 11 healthy subjects between the ages of 25 and 45 years with chronic primary insomnia. Participants were divided into two intervention groups for two months: Kriya Yoga (a form of meditation that is used to focus internalized attention and has been shown to reduce measures of arousal) and health education. Subjective measures of sleep and depression were collected at baseline and after the two-month period.
Both groups received sleep hygiene education; members of the health education group also received information about health-related topics and how to improve health through exercise, nutrition, weight loss and stress management.
Abstract Title: Effects of Meditation on Sleep in Individuals with Chronic Insomnia
Sleep Enforces The Temporal Sequence In Memory
We have usually quite strong memories of past events like an exciting holiday or a jolly birthday party. However it is not clear how the brain keeps track of the temporal sequence in such memories: did Paul spill a glass of wine before or after Mary left the party?
Previous findings from a research group headed by Jan Born at the University of Lübeck have confirmed the widely held view that long-term memories are formed particularly during sleep, and that this process relies on the brain replaying recently encoded experiences during the night. The same research group now provides evidence that sleep not only strengthens the content of a memory but also the particular order in which they were experienced, probably by a replay of the experiences in "forward" direction.
Students were asked to learn triplets of words presented one after the other. Afterwards they slept, whereas in a control condition no sleep was allowed. Later, recall was tested by presenting one word and asking which one came before and which one came after during learning. Sleep was found to enhance word recall, but only when the students were asked to reproduce the learned words in forward direction.
This finding shows that sleep associated consolidation of memories enforces the temporal structure of the memorized episode that otherwise might be blurred to a timeless puzzle of experiences.
Previous findings from a research group headed by Jan Born at the University of Lübeck have confirmed the widely held view that long-term memories are formed particularly during sleep, and that this process relies on the brain replaying recently encoded experiences during the night. The same research group now provides evidence that sleep not only strengthens the content of a memory but also the particular order in which they were experienced, probably by a replay of the experiences in "forward" direction.
Students were asked to learn triplets of words presented one after the other. Afterwards they slept, whereas in a control condition no sleep was allowed. Later, recall was tested by presenting one word and asking which one came before and which one came after during learning. Sleep was found to enhance word recall, but only when the students were asked to reproduce the learned words in forward direction.
This finding shows that sleep associated consolidation of memories enforces the temporal structure of the memorized episode that otherwise might be blurred to a timeless puzzle of experiences.
Internet-Based Intervention May Improve Insomnia
An online insomnia intervention based on established face-to-face cognitive behavioral therapy techniques appears to improve patients' sleep, according to a new report.
About one-third of adults report symptoms of insomnia and approximately 10 percent meet diagnostic criteria for an insomnia disorder, according to background information in the article. The condition decreases quality of life, impairs daytime functioning, has personal and public health consequences and results in an estimated $41 billion in reduced productivity every year.
Cognitive behavioral therapy—a psychological treatment focusing on the behaviors and dysfunctional thoughts that contribute to sleep problems—is one of the most effective treatments for insomnia. "Unfortunately, availability of cognitive behavioral therapy is severely limited for many reasons, including lack of trained clinicians, poor geographical distribution of knowledgeable professionals, expense and inaccessibility to treatment and clinicians," the authors write.
Lee M. Ritterband, Ph.D., of the University of Virginia Health System, Charlottesville, and colleagues evaluated the effectiveness of an Internet intervention based on cognitive behavioral therapy techniques among 44 adults (average age 44.9) who had a history of sleep difficulties lasting longer than 10 years on average. A total of 22 participants were randomly assigned to a control group and 22 received the Internet intervention, SHUTi. The highly interactive nine-week program uses text, graphics, animations, vignettes, quizzes and games to present behavioral, educational and cognitive techniques for improving sleep. For instance, patients were advised to avoid reading and watching television in the bedroom, stop daytime napping and change unhelpful beliefs and thoughts (including worries about the consequences of insomnia) that may exacerbate sleep difficulties.
Participants completed daily sleep diaries before and after the intervention and also rated their symptoms on the seven-item Insomnia Severity Index, which produces a score from zero (no symptoms) to 28 (severe insomnia). Among individuals who received the intervention, scores on the index improved from 15.73 to 6.59, whereas scores did not change for the control group. These gains were maintained at a six-month follow-up assessment.
"An Internet intervention has the potential of meeting the large unmet treatment need of the population with insomnia by providing effective treatment through the Web," they continue. "An effective and inexpensive Internet intervention would expand treatment options for large numbers of adults with insomnia, especially those whose geographical location prohibits access to relevant care, and could be a substantive first-line treatment choice."
This study was supported by a grant from the National Institute of Mental Health, National Institutes of Health.
About one-third of adults report symptoms of insomnia and approximately 10 percent meet diagnostic criteria for an insomnia disorder, according to background information in the article. The condition decreases quality of life, impairs daytime functioning, has personal and public health consequences and results in an estimated $41 billion in reduced productivity every year.
Cognitive behavioral therapy—a psychological treatment focusing on the behaviors and dysfunctional thoughts that contribute to sleep problems—is one of the most effective treatments for insomnia. "Unfortunately, availability of cognitive behavioral therapy is severely limited for many reasons, including lack of trained clinicians, poor geographical distribution of knowledgeable professionals, expense and inaccessibility to treatment and clinicians," the authors write.
Lee M. Ritterband, Ph.D., of the University of Virginia Health System, Charlottesville, and colleagues evaluated the effectiveness of an Internet intervention based on cognitive behavioral therapy techniques among 44 adults (average age 44.9) who had a history of sleep difficulties lasting longer than 10 years on average. A total of 22 participants were randomly assigned to a control group and 22 received the Internet intervention, SHUTi. The highly interactive nine-week program uses text, graphics, animations, vignettes, quizzes and games to present behavioral, educational and cognitive techniques for improving sleep. For instance, patients were advised to avoid reading and watching television in the bedroom, stop daytime napping and change unhelpful beliefs and thoughts (including worries about the consequences of insomnia) that may exacerbate sleep difficulties.
Participants completed daily sleep diaries before and after the intervention and also rated their symptoms on the seven-item Insomnia Severity Index, which produces a score from zero (no symptoms) to 28 (severe insomnia). Among individuals who received the intervention, scores on the index improved from 15.73 to 6.59, whereas scores did not change for the control group. These gains were maintained at a six-month follow-up assessment.
"An Internet intervention has the potential of meeting the large unmet treatment need of the population with insomnia by providing effective treatment through the Web," they continue. "An effective and inexpensive Internet intervention would expand treatment options for large numbers of adults with insomnia, especially those whose geographical location prohibits access to relevant care, and could be a substantive first-line treatment choice."
This study was supported by a grant from the National Institute of Mental Health, National Institutes of Health.
Sleep Strengthens Your Memory
Sleep not only protects memories from outside interferences, but also helps strengthen them, according to research presented at the American Academy of Neurology's 59th Annual Meeting in Boston.
The study looked at memory recall with and without interference (competing information). Forty-eight people between the ages of 18 and 30 took part in the study. All had normal, healthy sleep routines and were not taking any medications. Participants were divided evenly into four groups--a wake group without interference, a wake group with interference, a sleep group without interference and a sleep group with interference. All groups were taught the same 20 pairs of words in the initial training session.
The wake groups were taught the word pairings at 9 a.m. and then tested on them at 9 p.m. after 12 hours awake. The sleep groups were taught the word pairs at 9 p.m. and tested on them at 9 a.m. after a night of sleep. Just prior to testing, the interference groups were given a second list of word pairs to remember. The first word in each pair was the same on both lists, but the second word was different, testing the brain's ability to handle competing information, known as interference. The interference groups were then tested on both lists.
The study found that people who slept after learning the information performed best, successfully recalling more words. Those in the sleep group without interference were able to recall 12 percent more word pairings from the first list than the wake group without interference. With interference, the recall rate was 44 percent higher for the sleep group.
"This is the first study to show that sleep protects memories from interference," said study author Jeffrey Ellenbogen, MD, with Harvard Medical School in Boston, MA, and Fellow of the American Academy of Neurology. "These results provide important insights into how the sleeping brain interacts with memories: it appears to strengthen them. Perhaps, then, sleep disorders might worsen memory problems seen in dementia."
The study looked at memory recall with and without interference (competing information). Forty-eight people between the ages of 18 and 30 took part in the study. All had normal, healthy sleep routines and were not taking any medications. Participants were divided evenly into four groups--a wake group without interference, a wake group with interference, a sleep group without interference and a sleep group with interference. All groups were taught the same 20 pairs of words in the initial training session.
The wake groups were taught the word pairings at 9 a.m. and then tested on them at 9 p.m. after 12 hours awake. The sleep groups were taught the word pairs at 9 p.m. and tested on them at 9 a.m. after a night of sleep. Just prior to testing, the interference groups were given a second list of word pairs to remember. The first word in each pair was the same on both lists, but the second word was different, testing the brain's ability to handle competing information, known as interference. The interference groups were then tested on both lists.
The study found that people who slept after learning the information performed best, successfully recalling more words. Those in the sleep group without interference were able to recall 12 percent more word pairings from the first list than the wake group without interference. With interference, the recall rate was 44 percent higher for the sleep group.
"This is the first study to show that sleep protects memories from interference," said study author Jeffrey Ellenbogen, MD, with Harvard Medical School in Boston, MA, and Fellow of the American Academy of Neurology. "These results provide important insights into how the sleeping brain interacts with memories: it appears to strengthen them. Perhaps, then, sleep disorders might worsen memory problems seen in dementia."
Mild Head Injuries Increase Risk Of Sleep Disorders
A mild head injury can increase your chance of developing a sleep disorder, according to a study published in the April 3, 2007, issue of Neurology®, the scientific journal of the American Academy of Neurology. Researchers say these findings highlight the need for improved diagnosis and treatment of sleep disorders in mild traumatic brain injury patients who complain of insomnia.
"As many as 40 to 65 percent of people with mild traumatic brain injury complain of insomnia," said study author Liat Ayalon, PhD, with the University of California, San Diego. "This is concerning since sleeping problems may exacerbate other brain injury symptoms such as headache, emotional distress, and cognitive impairment, making the rehabilitation process much harder."
For the study, researchers assessed 42 people who reported to the Sheba Medical Center in Israel with complaints of insomnia after mild traumatic brain injury. Those suspected of having a circadian rhythm sleep disorder (CRSD) (i.e. problems with the timing of sleep) underwent scans, sleep studies, and had their oral temperature and saliva melatonin measured.
The study found 15 of the 42 patients, or 36 percent, had a CRSD. Of those, eight people had a delayed sleep phase syndrome with problems falling asleep and waking up, and seven people had irregular sleep-wake patterns.
"The frequency of sleep disorders in this study is considerably higher than the rate of these disorders among people attending sleep clinics for insomnia, which is seven to 10 percent," said Ayalon.
Ayalon said these findings suggest that sleep disorders that involve changes in the timing of sleep may be relatively frequent among brain injury patients and should be considered when these patients report sleeping problems to avoid misdiagnosis. "Misdiagnosis of these patients as insomniac may lead to prescription of medications, which help people fall asleep but don't help normalize the sleep-wake cycle," said Ayalon.
In addition, Ayalon said since circadian rhythm sleep disorders are often associated with cognitive and psychological problems, treatment might ultimately lead to improvement in other brain injury related symptoms. Ayalon said further studies are needed to explain the mechanism behind CRSDs in people with brain injury.
"As many as 40 to 65 percent of people with mild traumatic brain injury complain of insomnia," said study author Liat Ayalon, PhD, with the University of California, San Diego. "This is concerning since sleeping problems may exacerbate other brain injury symptoms such as headache, emotional distress, and cognitive impairment, making the rehabilitation process much harder."
For the study, researchers assessed 42 people who reported to the Sheba Medical Center in Israel with complaints of insomnia after mild traumatic brain injury. Those suspected of having a circadian rhythm sleep disorder (CRSD) (i.e. problems with the timing of sleep) underwent scans, sleep studies, and had their oral temperature and saliva melatonin measured.
The study found 15 of the 42 patients, or 36 percent, had a CRSD. Of those, eight people had a delayed sleep phase syndrome with problems falling asleep and waking up, and seven people had irregular sleep-wake patterns.
"The frequency of sleep disorders in this study is considerably higher than the rate of these disorders among people attending sleep clinics for insomnia, which is seven to 10 percent," said Ayalon.
Ayalon said these findings suggest that sleep disorders that involve changes in the timing of sleep may be relatively frequent among brain injury patients and should be considered when these patients report sleeping problems to avoid misdiagnosis. "Misdiagnosis of these patients as insomniac may lead to prescription of medications, which help people fall asleep but don't help normalize the sleep-wake cycle," said Ayalon.
In addition, Ayalon said since circadian rhythm sleep disorders are often associated with cognitive and psychological problems, treatment might ultimately lead to improvement in other brain injury related symptoms. Ayalon said further studies are needed to explain the mechanism behind CRSDs in people with brain injury.
People Learn While They Sleep, Study Suggests
People may be learning while they're sleeping -- an unconscious form of memory that is still not well understood, according to a study by Michigan State University researchers.
The findings are highlighted in the Journal of Experimental Psychology: General.
"We speculate that we may be investigating a separate form of memory, distinct from traditional memory systems," said Kimberly Fenn, assistant professor of psychology and lead researcher on the project. "There is substantial evidence that during sleep, your brain is processing information without your awareness and this ability may contribute to memory in a waking state."
In the study of more than 250 people, Fenn and Zach Hambrick, associate professor of psychology, suggest people derive vastly different effects from this "sleep memory" ability, with some memories improving dramatically and others not at all. This ability is a new, previously undefined form of memory.
"You and I could go to bed at the same time and get the same amount of sleep," Fenn said, "but while your memory may increase substantially, there may be no change in mine." She added that most people showed improvement.
Fenn said she believes this potential separate memory ability is not being captured by traditional intelligence tests and aptitude tests such as the SAT and ACT.
"This is the first step to investigate whether or not this potential new memory construct is related to outcomes such as classroom learning," she said.
It also reinforces the need for a good night's sleep. According to the National Sleep Foundation, people are sleeping less every year, with 63 percent of Americans saying their sleep needs are not being met during the week.
"Simply improving your sleep could potentially improve your performance in the classroom," Fenn said.
The findings are highlighted in the Journal of Experimental Psychology: General.
"We speculate that we may be investigating a separate form of memory, distinct from traditional memory systems," said Kimberly Fenn, assistant professor of psychology and lead researcher on the project. "There is substantial evidence that during sleep, your brain is processing information without your awareness and this ability may contribute to memory in a waking state."
In the study of more than 250 people, Fenn and Zach Hambrick, associate professor of psychology, suggest people derive vastly different effects from this "sleep memory" ability, with some memories improving dramatically and others not at all. This ability is a new, previously undefined form of memory.
"You and I could go to bed at the same time and get the same amount of sleep," Fenn said, "but while your memory may increase substantially, there may be no change in mine." She added that most people showed improvement.
Fenn said she believes this potential separate memory ability is not being captured by traditional intelligence tests and aptitude tests such as the SAT and ACT.
"This is the first step to investigate whether or not this potential new memory construct is related to outcomes such as classroom learning," she said.
It also reinforces the need for a good night's sleep. According to the National Sleep Foundation, people are sleeping less every year, with 63 percent of Americans saying their sleep needs are not being met during the week.
"Simply improving your sleep could potentially improve your performance in the classroom," Fenn said.
Naps Help Your Memory, New Study Suggests
A ninety minute daytime nap helps speed up the process of long term memory consolidation, a recent study conducted by Prof. Avi Karni and Dr. Maria Korman of the Center for Brain and Behavior Research at the University of Haifa found. "We still don't know the exact mechanism of the memory process that occurs during sleep, but the results of this research suggest the possibility that it is possible to speed up memory consolidation, and in the future, we may be able to do it artificially," said Prof. Karni.
Long term memory is defined as a permanent memory that doesn't disappear or that disappears after many years. This part of our memory is divided into two types -- memories of "what" (for example: what happened yesterday or what one remembers from an article one read yesterday) and memories of "how to" (for example: how to read Hebrew, how to drive, play basketball or play the piano).
In this new research, which was conducted by researchers at the University of Haifa in cooperation with the Sleep Laboratory at the Sheba Medical Center and researchers from the Department of Psychology at the University of Montreal, it was revealed that a daytime nap changes the course of consolidation in the brain. Two groups of participants in the study practiced a repeated motor activity which consisted of bringing the thumb and a finger together at a specific sequence. The research examined the "how" aspect of memory in the participants' ability to perform the task quickly and in the correct sequence. One of the groups was allowed to nap for an hour and a half after learning the task while the other group stayed awake.
The group that slept in the afternoon showed a distinct improvement in their task performance by that evening, as opposed to the group that stayed awake, which did not exhibit any improvement. Following an entire night's sleep, both groups exhibited the same skill level. "This part of the research showed that a daytime nap speeds up performance improvement in the brain. After a night's sleep the two groups were at the same level, but the group that slept in the afternoon improved much faster than the group that stayed awake," stressed Prof. Karni.
A second experiment showed that another aspect of memory consolidation is accelerated by sleep. It was previously shown that during the 6-8 hours after completing an effective practice session, the neural process of "how" memory consolidation is susceptible to interference, such that if, for example, one learns or performs a second, different task, one's brain will not be able to successfully remember the first trained task.
A third group of participants in the University of Haifa study learned a different thumb-to-finger movement sequence two hours after practicing the first task. As the second task was introduced at the beginning of the 6-8 hour period during which the brain consolidates memories, the second task disturbed the memory consolidation process and this group did not show any improvement in their ability to perform the task, neither in the evening of that day nor on the following morning. However, when a fourth group of participants was allowed a 90 minute nap between learning the first set of movements and the second, they did not show much improvement in the evening, but on the following morning these participants showed a marked improvement of their performance, as if there had been no interference at all.
"This part of the study demonstrated, for the first time, that daytime sleep can shorten the time "how to" memory becomes immune to interference and forgetting. Instead of 6-8 hours, the brain consolidated the memory during the 90 minute nap," explains Prof. Karni who added that while this study demonstrates that the process of memory consolidation is accelerated during daytime sleep, it is still not clear which mechanisms sleep accelerates in the process.
The elucidation of these mechanisms, say the researchers, could enable the development of methods to accelerate memory consolidation in adults and to create stable memories in a short time. Until then, if you need to memorize something quickly or if your schedule is filled with different activities which require learning "how" to do things, it is worth finding the time for an afternoon nap.
The research was published in the scientific journal Nature Neuroscience.
Long term memory is defined as a permanent memory that doesn't disappear or that disappears after many years. This part of our memory is divided into two types -- memories of "what" (for example: what happened yesterday or what one remembers from an article one read yesterday) and memories of "how to" (for example: how to read Hebrew, how to drive, play basketball or play the piano).
In this new research, which was conducted by researchers at the University of Haifa in cooperation with the Sleep Laboratory at the Sheba Medical Center and researchers from the Department of Psychology at the University of Montreal, it was revealed that a daytime nap changes the course of consolidation in the brain. Two groups of participants in the study practiced a repeated motor activity which consisted of bringing the thumb and a finger together at a specific sequence. The research examined the "how" aspect of memory in the participants' ability to perform the task quickly and in the correct sequence. One of the groups was allowed to nap for an hour and a half after learning the task while the other group stayed awake.
The group that slept in the afternoon showed a distinct improvement in their task performance by that evening, as opposed to the group that stayed awake, which did not exhibit any improvement. Following an entire night's sleep, both groups exhibited the same skill level. "This part of the research showed that a daytime nap speeds up performance improvement in the brain. After a night's sleep the two groups were at the same level, but the group that slept in the afternoon improved much faster than the group that stayed awake," stressed Prof. Karni.
A second experiment showed that another aspect of memory consolidation is accelerated by sleep. It was previously shown that during the 6-8 hours after completing an effective practice session, the neural process of "how" memory consolidation is susceptible to interference, such that if, for example, one learns or performs a second, different task, one's brain will not be able to successfully remember the first trained task.
A third group of participants in the University of Haifa study learned a different thumb-to-finger movement sequence two hours after practicing the first task. As the second task was introduced at the beginning of the 6-8 hour period during which the brain consolidates memories, the second task disturbed the memory consolidation process and this group did not show any improvement in their ability to perform the task, neither in the evening of that day nor on the following morning. However, when a fourth group of participants was allowed a 90 minute nap between learning the first set of movements and the second, they did not show much improvement in the evening, but on the following morning these participants showed a marked improvement of their performance, as if there had been no interference at all.
"This part of the study demonstrated, for the first time, that daytime sleep can shorten the time "how to" memory becomes immune to interference and forgetting. Instead of 6-8 hours, the brain consolidated the memory during the 90 minute nap," explains Prof. Karni who added that while this study demonstrates that the process of memory consolidation is accelerated during daytime sleep, it is still not clear which mechanisms sleep accelerates in the process.
The elucidation of these mechanisms, say the researchers, could enable the development of methods to accelerate memory consolidation in adults and to create stable memories in a short time. Until then, if you need to memorize something quickly or if your schedule is filled with different activities which require learning "how" to do things, it is worth finding the time for an afternoon nap.
The research was published in the scientific journal Nature Neuroscience.
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