О некоторых особенностях амбидекстров

Интересные новости на http://www.scienceblog.com/cms/mixed-handed-children-more-likely-have-mental-health-language-and-scholastic-problems.html. Вообще-то странно. Мне всегда казалось, что люди с в равной степени развитыми полушариями мозга, должны быть более успешны... А оказывается, не всегда:
Children who are mixed-handed, or ambidextrous, are more likely to have mental health, language and scholastic problems in childhood than right- or left-handed children, according to a new study published today in the journal Pediatrics.
The researchers behind the study, from Imperial College London and other European institutions, suggest that their findings may help teachers and health professionals to identify children who are particularly at risk of developing certain problems.
Around one in every 100 people is mixed-handed. The study looked at nearly 8,000 children, 87 of whom were mixed-handed, and found that mixed-handed 7 and 8-year old children were twice as likely as their right-handed peers to have difficulties with language and to perform poorly in school.
When they reached 15 or 16, mixed-handed adolescents were also at twice the risk of having symptoms of attention deficit/hyperactivity disorder (ADHD). They were also likely to have more severe symptoms of ADHD than their right-handed counterparts. It is estimated that ADHD affects between 3 to 9 percent of school-aged children and young people.
The adolescents also reported having greater difficulties with language than those who were left- or right-handed. This is in line with earlier studies that have linked mixed-handedness with dyslexia.
Little is known about what makes people mixed-handed but it is known that handedness is linked to the hemispheres in the brain. Previous research has shown that where a person's natural preference is for using their right hand, the left hemisphere of their brain is more dominant.
Some researchers have suggested that mixed-handedness indicates that the pattern of dominance is not that which is typically seen in most people, i.e. it is less clear that one hemisphere is dominant over the other. One study has suggested that ADHD is linked to having a weaker function in the right hemisphere of the brain, which could help explain why some of the mixed-handed students in today's study had symptoms of ADHD.
Dr Alina Rodriguez, the lead researcher on the study from the School of Public Health at Imperial College London, said: "Mixed-handedness is intriguing -- we don't know why some people prefer to make use of both hands when most people use only one. Our study is interesting because it suggests that some children who are mixed handed experience greater difficulties in school than their left- and right-handed friends. We think that there are differences in the brain that might explain these difficulties, but there needs to be more research.
"Because mixed-handedness is such a rare condition, the number of mixed-handed children we were able to study was relatively small, but our results are statistically and clinically significant. That said, our results should not be taken to mean that all children who are mixed-handed will have problems at school or develop ADHD. We found that mixed-handed children and adolescents were at a higher risk of having certain problems, but we'd like to stress that most of the mixed-handed children we followed didn't have any of these difficulties," added Dr Rodriguez.
To study the effects of mixed-handedness, Dr Rodriguez and her colleagues looked at prospective data from a cohort of 7,871 children from Northern Finland. Using questionnaires, the researchers assessed the children when they reached 7 to 8 years of age and again at 15 to 16 years of age.
When the children were aged 8, the researchers asked parents and teachers to assess their linguistic abilities, scholastic performance and behaviour. The teachers reported whether children had difficulties in reading, writing or mathematics and rated the children's academic performance as below average, average or above average.
The adolescents' parents and the adolescents themselves completed follow-up questionnaires when they were 15-16 years of age, with the children evaluating their school performance in relation to their peers and the parents assessing their children's behaviour, on a questionnaire that is widely used to identify ADHD symptoms.
The research was funded by the Academy of Finland; Sigrid Juselius Foundation, Finland; Thule Institute, University of Oulu, Finland; and the National Institute of Mental Health. Dr Rodriguez received support from VINNMER.


Роль поврежлений ДНК в атаксии Фридриха

Очередные открытия связанные с изучением моих любимейших повреждений ДНК описаны на http://www.scienceblog.com/cms/excess-dna-damage-found-cells-patients-friedreichs-ataxia-29177.htm:
PITTSBURGH, Jan. 14 -- Elevated levels of DNA damage have for the first time been found in the cellular mitochondria and nuclei of patients with the inherited, progressive nervous system disease called Friedreich's ataxia (FRDA), says a multicenter research team led by an expert from the University of Pittsburgh Cancer Institute (UPCI). The findings, described today in PLoS Genetics, shed light on the molecular abnormalities that lead to the disease, as well as point the way to new therapeutic approaches and the development of biomarker blood tests to track its progression.
"In FRDA, mutations in the gene frataxin reduce production of a protein that plays a role in keeping iron levels in balance within mitochondria," explained Bennett Van Houten, Ph.D., Richard M. Cyert Professor of Molecular Oncology and leader of the molecular and cellular cancer biology program at UPCI, and professor, Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine. "Frataxin binds iron and helps build iron-sulfur clusters, which are important constituents of cellular proteins.
"While iron is what allows blood cells to carry oxygen, too much iron is toxic to the body," said Astrid C. Haugen, lead author and program analyst at the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health (NIH). "Friedreich's ataxia leads to iron overload, setting the stage for cumulative DNA damage that eventually affects patients' nerve and muscle cells."
According to the National Institute of Neurological Disorders and Stroke (NINDS), about 1 out of 50,000 Americans has Friedreich's ataxia. Symptoms appear from 5 to 15 years of age and include ataxia, or gait disturbance, that results from degeneration of nerves in the spinal cord and muscle; muscle wasting; and speech problems. Heart enlargement, arrhythmias, and heart failure are common and often the cause of early death in the most severely affected. Patients typically require wheelchairs within 10 to 20 years after symptoms begin.
For the study, the researchers profiled gene activity in blood samples from FRDA children to search for biomarkers of the disease, as compared to young healthy donors. Those data were compared to blood tests from FRDA adults, and the latter compared to a second group of healthy individuals.
"We saw gene activity patterns that are associated with responses to DNA damage, and our comparisons and follow-up tests showed us that FRDA patients have far more damage than seen in healthy people," said Dr. Van Houten, who noted that everyone has some DNA damage, at various stages of repair, in their cells. "We found gene expression signatures that correlated with frataxin levels, age of disease onset and a standardized measure of patient disability."
"If further testing validates the set of genes and activity profiles as predictive biomarkers, they could be useful in assessing the current status of a patient's illness as well as the response to experimental therapies in clinical trials," he said. "Also, new drug targets might be found in the DNA repair and iron-processing pathways affected by the lack of frataxin, generating much-needed treatment breakthroughs."
The study team includes researchers from NIEHS; NINDS; Durham, N.C.-based Expression Analysis Inc.; Duke University; Université Pierre et Marie Curie, Paris; and Hôpital Pitié-Salpêtrière, Paris.
This work was supported by the NIH Intramural Program and a Bench-to-Bedside award.
About UPCI
As the only NCI-designated comprehensive cancer center in western Pennsylvania, UPCI is a recognized leader in providing innovative cancer prevention, detection, diagnosis, and treatment; bio-medical research; compassionate patient care and support; and community-based outreach services. UPCI investigators are world-renowned for their work in clinical and basic cancer research.
About the University of Pittsburgh School of Medicine
As one of the nation's leading academic centers for biomedical research, the University of Pittsburgh School of Medicine integrates advanced technology with basic science across a broad range of disciplines in a continuous quest to harness the power of new knowledge and improve the human condition. Its Department of Pharmacology & Chemical Biology fosters an intellectual and physical environment in which basic chemical principles are applied to the understanding of cell signaling events with the goal of creating new therapeutic strategies. Driven mainly by the School of Medicine and its affiliates, Pitt has ranked among the top 10 recipients of funding from the National Institutes of Health since 1997 and now ranks fifth in the nation, according to preliminary data for fiscal year 2008. Likewise, the School of Medicine is equally committed to advancing the quality and strength of its medical and graduate education programs, for which it is recognized as an innovative leader, and to training highly skilled, compassionate clinicians and creative scientists well-equipped to engage in world-class research. The School of Medicine is the academic partner of UPMC, which has collaborated with the University to raise the standard of medical excellence in Pittsburgh and to position health care as a driving force behind the region's economy. For more information about the School of Medicine, see www.medschool.pitt.edu.



Средство борьбы с кокаином!

Интересные новости. Новый способ борьбы с кокаиновой зависимостью описан на http://www.eurekalert.org/pub_releases/2010-01/fo1b-ana122309.php:
A new ally in the battle against cocaine addiction

A recent study shows that a bacterial protein may help cocaine addicts break the habit.
Cocaine esterase (CocE) is a naturally-occurring bacterial enzyme that breaks down cocaine, thereby reducing its addictive properties. The efficacy of CocE in animals and its suitability for treatment of addiction has been limited by its short half-life in the body.

A recent study, published in the Journal of Pharmacology and Experimental Therapeutics and reviewed by Faculty of 1000 Medicine's Friedbert Weiss, demonstrates that a more stable version of CocE, double mutant or DM CocE, significantly decreased the desire for cocaine and prevented death from cocaine overdose.
In the study, rats were trained to self-administer cocaine by pressing a button in their cage, mimicking the need for regular doses of the drug during addiction. Rats treated with the double mutant form of CocE pressed the button to receive cocaine less often, suggesting that DM-CocE broke down the drug and dampened addiction.

DM-CocE decreased the rats' urge for cocaine but not for an addictive analogue, highlighting the degree of specificity for cocaine. Weiss notes that the DM-CocE enzyme also provides "long-lasting protection" against the toxic effects of a potentially lethal dose.

Though the effects of CocE can be overcome by a sufficiently large dose of cocaine, the present findings suggest that CocE has great promise as a drug abuse treatment.
Weiss says, "These therapeutic approaches may therefore not be "fail-safe" for reducing cocaine intake by determined users" but "long-acting forms of CocE represent potentially valuable treatment approaches not only for the prevention of cocaine-induced toxicity but also for ongoing cocaine abuse in humans."


Две чудесных статьи о привыкании к кофеину

Ещё о дозировании витаминов

Интересная статья на http://www.scienceblog.com/cms/putting-limits-vitamin-e-28815.html:
Vitamin-fortified foods and dietary health supplements can ease health worries. But what kinds of vitamins are right for you? And how much of them should you take, and how often?
A research group from Tel Aviv University has done the most comprehensive and accurate study of clinical data on Vitamin E use and heart disease to date, and it warns that indiscriminate use of high-dose Vitamin E supplementation does more harm than good. Their results were recently reported in ATVB, a leading journal of cardiology, and discussed in the journal BioFactors.
"There were so many conflicting reports about Vitamin E and its effect on various diseases, particularly heart disease, that we wanted to set the record straight," says Prof. Dov Lichtenberg of TAU's Sackler School of Medicine.
"Our new study shows that some people may be harmed by the treatment, whereas others may benefit from it. Now we're trying to identify groups of people that are most likely to benefit from the effects of Vitamin E," adds study co-researcher Dr. Ilya Pinchuk. The TAU research team also included decision analyst Dr. Moshe Leshno of the Sackler Faculty of Medicine and the Leon Recanati Faculty of Management and Dr. Yedidya (Didi) Dotan, whose PhD thesis is the basis for this analysis.
A longer life without it?
Applying a very different approach than any previous study, the team of researchers put their heads together to draw definitive conclusions about Vitamin E. In their publication in ATVB the Tel Aviv University researchers evaluated the results of the prominent studies measuring the health benefits of Vitamin E but reached varying conclusions. There have been many previous publications on the subject. Analysis of the results of all these past publications together revealed that subjects who did not take a Vitamin E supplement enjoyed more quality-adjusted-life-years (QALY), a standard parameter used in medicine to assess the effect of medical interventions.
"To explain the meaning of this parameter," says Dr. Pinchuk, "consider a participant who was healthy during the first 10 out of 20 years of the study, but then suffered a stroke and became dependent on others throughout the following 10 years. The QALY during the first 10 years of healthy life is 10, but after the stroke the quality of life is only half of what this person had before. Therefore, the second decade is considered the equivalent of merely 5 years of healthy life and in sum a person's QALY is 15.
The researchers examined data from more than 300,000 subjects in the US, Europe and Israel. "Our major finding," says Dr. Pinchuk, "was that the average quality-adjusted life years (QALY) of Vitamin E- supplemented individuals was 0.30 less than that of untreated people. This, of course, does not mean that everybody consuming Vitamin E shortens their life by almost 4 months. But on average, the quality-adjusted longevity is lower for vitamin-treated people. This says something significant."
Overturning earlier studies
In the BioFactors article, the TAU researchers defined "the real challenge as being able to identify who is likely to benefit taking Vitamin E." They also explored the first hypothesis of the oxidative theory of atherosclerosis published more than 20 years ago, which was the basis for the widespread use of antioxidants today. At first, this hypothesis raised great enthusiasm that anti-oxidants like Vitamins E and C and flavonoids could be used to prevent disease or its progression. In this respect, the new findings are very disappointing.
"We've now concluded that going to the grocery or to a health food store to buy Vitamin E supplements, for the most part, won't do you good. In some cases it can do harm," says Dr. Pinchuk. "A doctor wouldn't prescribe anti-hypertension drugs to the whole population, only to those with low blood pressure. It seems this is true for antioxidants, too. When you give them to everybody, you may be doing more harm than good. Some people may benefit from it, but more may be harmed."
The researchers are now building sets of criteria that detail under what conditions Vitamin E supplements should be taken. They are also investigating the chemical mechanisms of antioxidants in general to better understand how they work.
American Friends of Tel Aviv University (www.aftau.org) supports Israel's leading and most comprehensive center of higher learning. In independent rankings, TAU's innovations and discoveries are cited more often by the global scientific community than all but 20 other universities worldwide.
Internationally recognized for the scope and groundbreaking nature of its research programs, Tel Aviv University consistently produces work with profound implications for the future.

Ещё один метод исследования активности мозга

МИТовцы, как обычно, доисследовались до интересных штук. Читаем на http://www.biologynews.net/archives/2010/01/06/mit_neuroengineers_silence_brain_cells_with_multiple_colors_of_light.html
Neuroscientists at MIT have developed a powerful new class of tools to reversibly shut down brain activity using different colors of light. When targeted to specific neurons, these tools could potentially lead to new treatments for the abnormal brain activity associated with disorders such as chronic pain, epilepsy, brain injury, and Parkinson's disease.

The tools work on the principle that such disorders might be best treated by silencing, rather than stimulating, brain activity. These "super silencers" exert exquisite control over the timing of the shutdown of overactive neural circuits – an effect that's impossible with existing drugs or other conventional therapies.

"Silencing different sets of neurons with different colors of light allows us to understand how they work together to implement brain functions," explains Ed Boyden, senior author of the study, to be published in the Jan. 7 issue of Nature. "Using these new tools, we can look at two neural pathways and study how they compute together. These tools will help us understand how to control neural circuits, leading to new understandings and treatments for brain disorders – some of the biggest unmet medical needs in the world." Boyden is the Benesse Career Development Professor in the MIT Media Lab and an associate member of the McGovern Institute for Brain Research at MIT.

Boyden's super silencers are developed from two genes found in different natural organisms such as bacteria and fungi. These genes, called Arch and Mac, encode for light-activated proteins that help the organisms make energy. When neurons are engineered to express Arch and Mac, researchers can inhibit their activity by shining light on them. Light activates the proteins, which lowers the voltage in the neurons and safely and effectively prevents them from firing. In this way, light can bathe the entire brain and selectively affect only those neurons sensitized to specific colors of light. Neurons engineered to express Arch are specifically silenced by yellow light, while those expressing Mac are silenced by blue light.

"In this way the brain can be programmed with different colors of light to identify and possibly correct the corrupted neural computations that lead to disease," explains co-author Brian Chow, postdoctoral associate in Boyden's lab.

In 2005, Boyden, in collaboration with investigators at Stanford University and the Max Planck Institute, introduced the first such "optogenetic" technique, so called because it combines the use of optics with gene delivery. The 2005 tool, now widely used, involves a light-activated ion channel, ChR2, which allows light to selectively turn on neurons in the brain.

Two years later, Boyden demonstrated that halorhodopsin, another light-sensitive protein, could inhibit the activity of neurons when illuminated. "But the genomic diversity of the world suggested that more powerful tools were out there waiting to be discovered," Boyden says. His group accordingly screened a diverse set of microbial light-sensitive proteins, and found the new multicolor silencers. The newly discovered tools are much better than the old. Arch-expressing neurons were switched off with greater precision and recovered faster than halorhodopsin-expressing neurons, allowing researchers to manipulate different neurons with different colors of light.

"Multicolor silencing dramatically increases the complexity with which you can study neural circuits," says co-author Xue Han, postdoctoral researcher in Boyden's lab. "We will use these tools to parse out the neural mechanisms of cognition."

How they did it: MIT researchers loaded the Arch and Mac genes into viruses that inserted their genetic cargo into mouse neurons. Optical fibers attached to lasers flashed light onto the neurons, and electrodes measured the resulting neural activity. [See graphic]

Next steps: Boyden's team recently demonstrated the efficacy of ChR2 in monkeys with no apparent side effects. Determining whether Arch and Mac are safe and effective in monkeys will be a critical next step toward the potential use of these optical silencing tools in humans. Boyden plans to use these super silencers to examine the neural circuits of cognition and emotion and to find targets in the brain that, when shut down, could relieve pain and treat epilepsy. His group continues to mine the natural world for new and even more powerful tools to manipulate brain cell activity – tools that, he hopes, will empower scientists to explore neural circuits in ways never before possible.

Source : Massachusetts Institute of Technology