سویچ متابولیک: عامل سندرم خستگی مزمن

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شواهد جدید نشان می دهد که در سندرم خستگی مزمن بدن به مسیرهای کمتر بهینه برای تولید انرژی منحرف شده است.

 

در گذشته تصور می شد که این حالت ناشی از اختلالات روحی و عصبی می باشد. حال آن که محققین اکنون به شواهدی دست یافته اند که نشان می دهد در افراد مبتلا سلول های بدن بیشتر از آن که از قند به تولید انرژی بپردازند بیش از پیش وابسته به تولید انرژی از پربی و پروتئین می شوند. این نکته به نوبه خود منجر به تولید لاکتات می شود که منجر به ایجاد خستگی و درد در عضلات می شود.

این نکته هم توجیه کننده علت خستگی و هم ایجاد درد و عدم تحمل حتی با ورزش های کم است.

این دانشمندان اکنون این مطالعه را در جمعیتی بزرگ تر در نروژ ادامه می دهند تا با ثبت شواهد جدید و دقیقتر در پی درمان آن باشند.

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تغذیه با شیر مادر برای کودکان مبتلا به آسم مفید است

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B

کودکانی که از شیر مادر تغذیه می‌کنند ریسک پایین‌تری از عفونت‌ها استفراغ و اسهال و نیز احتمال کمتری از بیماری‌های دوران بزرگسالی دارند.

 

در یک مطالعه که اخیراً به چاپ رسیده است نشان داده شده است که کودکانی که از  شیر مادر استفاده می‌کنند و از نظر ژنتیکی در معرض بیماری آسم هستند در مقایسه با آنانیاز شیر مادر استفاده نکردند خطر کمتری برایشان ایجاد می شود.

این مطالعه که نتایج آن در کنفرانس انجمن تنفس و ۹ اخیراً در لندن برگزار شد منتشر شده است در د ۳۶۸ شیرخوار سوئیسی انجام گرفته است .

, Interaction of 17q21 variants with breast-feeding in relation to respiratory symptoms in infancy]

در این مطالعه آن دسته از شیرخوارانی که از نظر ژنتیکی در معرضآسم بودند  در صورتی که از شیر مادر استفاده نموده بودند ۲۷% کاهش خطر ابتلا به بیماری در آنها مشاهده گردید . اما انانی که از شیر مادر ستفاده نکرده بودند خطر ابتلا به آسم در آنها بیشتر بود.   این مطالعه بار دیگر  تأثیر متقابل بین محیط و ژن‌ها  رابه روشنی ارائه نموده است

 

 

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تردید های جدید در مورد موفقیت روش های لقاح مصنوعی سه والدی

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این شیوه کمک باروری که به منظور پیشگیری از انتقال بیماری های میتوکندریایی از مادر به فرزند طراحی شده ممکن است بر خلاف امید های اولیه موثر نباشد.

Mitochondrial replacement therapy involves swapping faulty mitochondria for those of a healthy donor. But if even a small number of mutant mitochondria are retained after the transfer — a common occurrence — they can outcompete healthy mitochondria in a child’s cells and potentially cause the disease the therapy was designed to avoid, experi ments suggest.

“It would defeat the purpose of doing mitochondrial replacement,” says Dieter Egli, a stem-cell scientist at the New York Stem Cell Foundation Research Institute who led the work. Egli says that the finding could guide ways to surmount this hurdle, but he recommends that the procedure not be used in the meantime.

The UK government last year legalized mitochondrial replacement therapy, although the country’s fertility regulator has yet to green-light its use in the clinic. In the United States, a panel convened by the National Academies of Sciences, Engineering, and Medicine has this year recommended that clinical trials of the technique be approved if preclinical data suggest that it is safe.

Faults carried over

As many as 1 in 5,000 children are born with diseases caused by harmful genetic mutations in the DNA of their mitochondria; the diseases typically affect the heart, muscles and other power-hungry organs. Children inherit all their mitochondria from their mothers.

To prevent a mother who has harmful mitochondrial mutations from passing them to her children, the proposed remedy is to transplant the nuclear DNA of her egg into another, donor egg that has healthy mitochondria (and which has been emptied of its own nucleus). The resulting embryo would carry the mitochondrial genes of the donor woman, and the nuclear DNA of their father and mother. These are sometimes called three-person embryos.

Current techniques can’t avoid dragging a small number of the mother’s mitochondria into the donor egg, totalling less than 2% of the resulting embryo’s total mitochondria. This isn’t enough to cause health problems. But researchers have worried that the proportion of faulty, ‘carried-over’ mitochondria may rise as the embryo develops. The UK Human Fertilisation and Embryology Authority (HFEA) — which will oversee clinical applications of mitochondrial replacement — has called for research into this possibility.

Egli’s study, published today in Cell Stem Cell, offers some clarity. His team used eggs from women with healthy mitochondria, but otherwise followed a procedure similar to a real therapy: transplanting nuclear DNA from one set of egg cells into another woman’s egg cells. The team then converted these eggs into embryos with two copies of the maternal genome, a process called parthenogenesis. (Mitochondrial replacement is normally performed on eggs fertilized with sperm, but Egli’s team wanted to discount any role for paternal DNA.) The researchers then extracted stem cells from the embryos and grew the cells in dishes in the lab.

The embryos, on average, had just 0.2% of carried-over mitochondrial DNA (mtDNA), and the resulting embryonic stem cells at first harboured similarly minuscule levels. But one stem-cell culture showed a dramatic change: as the cells grew and divided, levels of the carried-over mtDNA jumped from 1.3% to 53.2%, only to later plummet down to 1%. When the team split this cell line into different dishes, sometimes the donor egg’s mtDNA won out; but in others, the carried-over mtDNA dominated.

In another set of experiments, the low levels of carried-over mtDNA consistently outcompeted the donor mtDNA, both in embryonic stem cells and in tissues made from these cells.

Competing DNA

Exactly how the carried-over mitochondria rose to dominance is hazy. Egli’s team found no evidence that they helped cells to divide any faster — for instance, by delivering extra energy. Egli suspects that the resurgence happened because one mitochondrion was able to copy its DNA faster than the others could, which he says is more likely to occur when large DNA-sequence differences exist between the two populations of mitochondria. In his team’s study, the most dramatic rebound in carried-over mtDNA occurred when the nucleus of a woman with mitochondria common among Europeans was inserted into the egg cell of a woman with mitochondria usually found in people with African ancestry.

Iain Johnston, a biomathematician at the University of Birmingham, UK, says that this theory makes sense. He was part of a team that found that, in mice with mitochondria from both lab and distantly related wild populations, one mitochondrial lineage tended to dominate. If mitochondrial replacement does reach the clinic, Johnston says that donors should be chosen such that their mitochondria closely match those of the recipient mother.

But Mary Herbert, a reproductive biologist at the University of Newcastle, UK, who is part of a team pursuing mitochondrial replacement, says that mitochondria behave very differently in embryonic stem cells compared to normal human development. Levels of mutant mitochondria can fluctuate wildly in stem cells. “They are peculiar cells, and they seem to be a law unto themselves,” she says, calling the biological relevance of the latest report “questionable”. She thinks that data from embryos cultured for nearly two weeks in the laboratory will provide more useful information than Egli’s stem cell studies.

An HFEA spokesperson says that the agency is waiting for further experiments on the safety and efficacy of mitochondrial replacement (including data from Herbert’s team) before approving what could be the world’s first mitochondrial replacement in humans.

Egli hopes that the HFEA considers his team’s data. He thinks the problem they identified can be surmounted, for instance, by improving techniques to reduce the level of carried-over mitochondria or matching donors such that their mitochondria are unlikely to compete. Until this is shown for sure, he advocates caution. “I don’t think it would be a wise decision to go forward with this uncertainty.”

This article is reproduced with permission and was first published on May 19, 2016.

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مغز مي تواند خاطرات بد را عامدانه پاك كند

در يك مطالعه كه نتايج آن در بولتن سيكونونيك چاپ شده است محققان كالج دارموث در نيوهامپشاير آمريكا دريافتند كه مغز انسان مي تواند به صورت عمدي مطالبي را كه نمي خواهد به ياد داشته باشد از حافظه پاك كند. 

بعضی ژن ها در محیط سالم موجب افزایش طول عمر می شوند

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BUFFALO, N.Y. – Researchers at the University at Buffalo Research Institute on Addictions have discovered how a gene in the brain’s dopamine system can play an important role in prolonging lifespan: it must be coupled with a healthy environment that includes exercise.

The study, led by Panayotis (Peter) K. Thanos, senior research scientist at RIA, appears in the current, online version of Oncotarget Aging, a top-ranked aging journal.

Thanos and his team studied the genes in dopamine to assess their impact on lifespan and behavior in mice. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centers and helps regulate physical mobility and emotional response.

The researchers found that the dopamine D2 receptor gene (D2R) significantly influences lifespan, body weight and locomotor activity, but only when combined with an enriched environment that included social interaction, sensory and cognitive stimulation and, most critically, exercise.

“The incorporation of exercise is an important component of an enriched environment and its benefits have been shown to be a powerful mediator of brain function and behavior,” Thanos says.

PHOTO: http://www. buffalo. edu/ news/ releases/ 2016/ 04/ 056. html.

The mice in the enriched environment lived anywhere from 16 to 22 percent longer than those in a deprived environment, depending on the level of D2R expression.

“These results provide the first evidence of D2R gene-environment interaction playing an important role in longevity and aging,” Thanos says. “The dichotomy over genes versus environment has provided a rigorous and long debate in deciphering individual differences in longevity. In truth, there exists a complex interaction between the two which contribute to the differences.”

Research exploring this genetic-environmental interaction should lead to a better understanding and prediction of the potential benefits of specific environments, such as those including exercise, on longevity and health during aging.

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The study’s authors include Thanos, John Hamilton, MA, and Joseph R. O’Rourke, MA, UB Research Institute on Addictions; Anthony Napoli, PhD, Suffolk Community College; Marcelo Febo, PhD, Kenneth Blum, PhD, and Mark Gold, MD, University of Florida, and Nora Volkow, MD, National Institute on Drug Abuse.

RIA is a research center of the University at Buffalo and a national leader in the study of alcohol and substance abuse issues. RIA’s research programs, most of which have multiple-year funding, are supported by federal, state and private foundation grants. Located on UB’s Downtown Campus, RIA is a member of the Buffalo Niagara Medical Campus and a key contributor to UB’s reputation for research excellence. To learn more, visit buffalo.edu/ria.

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بالا بودن حجم عضلاني منجر به كاهش خطر مرگ در بيماران قلبي مي شود. 

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FINDINGS

صرف تظر از حجم و نسبت چربي بالا بودن نسبت عضلاني منجر به كاهش خطر مرگ مي شود.

These findings indicate the importance of assessing body composition as a way to help predict cardiovascular and total mortality in people with cardiovascular disease.

BACKGROUND

In previous studies on the relationship between body composition and mortality, the researchers used a simpler clinical measure of body composition called the bio electrical impedance scale. They noted a possible protective effect of muscle mass on both mortality and metabolism in healthy people. The new study extends the findings from the earlier research using dual X-ray absorptiometry, a more rigorous method of measuring body composition.

The researchers examined data from the National Health and Nutrition Examination Survey, 1999 to 2004, of 6,451 participants who had prevalent cardiovascular disease. Each subject was categorized into one of four groups:

  • low muscle/low fat mass
  • low muscle/high fat mass
  • high muscle/low fat mass
  • high muscle/high fat mass

Those with high muscle mass and low fat mass had the lowest risk of cardiovascular and total mortality.

IMPACT

Because people with higher muscle mass were more likely to have a high body mass index, the findings could explain the “obesity paradox,” which holds that people with a higher BMI have lower mortality levels.

The findings also highlight the importance of maintaining muscle mass, rather than focusing on weight loss, in order to prolong life, even in people who have a higher cardiovascular risk. The authors suggest that clinicians encourage their patients to participate in resistance exercises as a part of healthy lifestyle changes, rather than focusing primarily on, and monitoring, weight loss.

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AUTHORS

Dr. Preethi Srikanthan, associate clinical professor of medicine in the division of endocrinology at the David Geffen School of Medicine, is the study’s primary investigator. The study’s co-authors are Dr. Tamara Horwich, health sciences clinical professor of medicine, division of cardiology, and Dr. Chi-hong Tseng, adjunct associate professor of medicine in the division of general internal medicine and health services research.

JOURNAL

The study was published in the American Journal of Cardiology.

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 بيماران روماتيسم بايد از نظر شنوايي هم بررسي شوند

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روماتيسم بر ارگانهاي شنوايي هم اثر مخرب دارد
RA is the commonest autoimmune arthritis affecting 1% of the general population. Despite its main articular manifestations, RA caninvolveextra-articular organs including the auditory system.

HI in RA is multifactorial. Mechanism of injury and predisposing factors are not clearly understood. Sensorineural hearing loss is the most common type in RA patients with a prevalence of 25-72%. Possible pathologies are including: Synovial destruction of incudostapedial and incudomalleolar joints, rheumatoid nodules, auditory neuropathy, destruction of the cochlear hair cells and drug-induced ototoxicity. “Elderly Patients and those with long disease duration, active disease, seropositivity, elevatedacute phase reactants and rheumatoid nodules are more likely to have HI”, demonstrated a recent study by Amir Emamifar, Kristine Bjørndal and Inger Marie Jensen Hansen.

Environmental factors for instance smoking, alcohol and noise can deteriorate the condition. Passive smokers are also at risk of HI. Long-term exposure to alcohol affects hearing in RA, causing harmful effects on the cochlear function.

Results of pure tone audiometry revealed that RA patients have high prevalence of HI for all frequencies.Transiently Evoked Otoacoustic Emissions (TEOAEs) test has been used widely to evaluate cochlear function, and is capable of detecting various amounts of decreases in RA patients at an early stage of the disease.

Treatment of HI in RA is empirical. Oral steroids and intensifying Disease-Modifying Antirheumatic Drugs might be an option. Anti-oxidants (eg. vitamin E) may play a protective role for the inner ear. Regular audiometric test and TEOAEs should be performed. Patients will also benefit from the cessation of smoking and alcohol. Like other causes of HI in healthy individuals, HI in RA can also be managed by use of different types of hearing aids and implantable devices.

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Contact: amir.emamifar@rsyd.dk

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خطر سرطان كيد در هپاتيت ب حتي بعد از حذف ويروس هم وجود دارد

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Long-term infection with hepatitis B virus (HBV) can cause liver inflammation and increase the risk of liver cancer. Researchers from the US Centers for Disease Control and Prevention, however, found that resolving HBV infection was not associated with reduced rates of liver cancer.

A total of 238 patients who resolved HBV infection and 435 patients who did not were selected from among 1346 patients with chronic HBV infection followed for up to 31 years. The liver cancer risk, measured as a hazard ratio (HR), in patients after resolving HBV infection was similar compared with the risk in patients who did not resolve infection (HR: 0.7; 95% confidence interval: 0.2-2.4).

“Since the risk of liver cancer persists among adults with apparent cure of the infection, they might still need to be followed closely,” said Dr. Prabhu Gounder, lead author of the Alimentary Pharmacology & Therapeutics article.

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مشكل در مسير يابي شايد  اولين علامت آلزايمر باشد

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IMAGE

IMAGE: Participants in this Alzheimer’s disease study used a joystick to navigate a virtual maze and locate landmarks, such as this bookcase. view more

Credit: Courtesy of Denise Head

Long before Alzheimer’s disease can be diagnosed clinically, increasing difficulties building cognitive maps of new surroundings may herald the eventual clinical onset of the disorder, finds new research from Washington University in St. Louis.

“These findings suggest that navigational tasks designed to assess a cognitive mapping strategy could represent a powerful new tool for detecting the very earliest Alzheimer’s disease-related changes in cognition,” said senior author Denise Head, associate professor of psychological and brain sciences in Arts & Sciences.

“The spatial navigation task used in this study to assess cognitive map skills was more sensitive at detecting preclinical Alzheimer’s disease than the standard psychometric task of episodic memory,” she said.

Preclinical Alzheimer’s disease denotes the presence of Alzheimer-related changes in the brain that occur prior to the development of symptoms that lead to the diagnosis.

The cognitive findings from this study, published in the April issue of the Journal of Alzheimer’s Disease, are consistent with where in the brain the ill effects of Alzheimer’s disease first surface, as well as with the progression of the disease to other brain regions.

Previous research has shown that navigation problems crop up early in individuals with Alzheimer’s disease. These deficits may be associated with the build up of amyloid plaques and tau tangles and other signs of deterioration and shrinkage in the brain’s prefrontal cortex, hippocampus and caudate.

The hippocampus, which is associated with long-term memory storage, the recognition of new surroundings and the creation of cognitive maps, is well-established as an early target for Alzheimer’s-related damage. Similar damage also turns up in the caudate, which is associated with learning as well as voluntary movement.

“Our observations suggest a progression such that preclinical Alzheimer’s disease is characterized by hippocampal atrophy and associated cognitive mapping difficulties, particularly during the learning phase,” said first author Samantha Allison, a psychology doctoral student at Washington University. “As the disease progresses, cognitive mapping deficits worsen, the caudate becomes involved, and route learning deficits emerge.”

Making a mental map

While these deficits are well documented in patients with early stage Alzheimer’s disease, they have not been well studied in seemingly normal patients who may be progressing toward identifiable early stages of the disease, a status known as preclinical Alzheimer’s disease.

In this study, researchers used a virtual maze navigation experiment to examine whether specific problems with route learning and cognitive map building, which involve the caudate and the hippocampus, respectively, could be detected in preclinical Alzheimer’s. The experiment’s design plays on the fact that humans generally find their way in life using two distinct forms of spatial representation and navigation.

With egocentric navigation, people rely on past knowledge to follow well-worn routes, moving sequentially from one landmark to another until they reach their target destination. In allocentric navigation, people become familiar with their big picture surroundings and create a mental map of existing landmarks, allowing them to plot best available routes and find shortcuts to new destinations.

Participants in this study were separated into three groups based on a test of brain and spinal fluids that can detect biomarkers shown to predict the future development of Alzheimer’s-related plaques and tangles in the brain. People who are clinically normal with these markers are considered to have preclinical Alzheimer’s disease.

This study included 42 clinically normal individuals who lacked the cerebrospinal fluid markers for Alzheimer’s, 13 clinically normal individuals who were positive for these markers and thus had preclinical Alzheimer’s, and 16 individuals with documented behavioral symptoms of early stage Alzheimer’s.

All 71 study participants spent about two hours on a desktop computer being tested on their ability to navigate a virtual maze consisting of a series of interconnected hallways with four wallpaper patterns and 20 landmarks. Participants were tested on two navigation skills: how well they could learn and follow a pre-set route, and how well they could form and use a cognitive map of the environment. Participants were given 20 minutes to either learn a specified route, or to study and explore the maze with a navigation joystick. They were then tested on their ability to recreate the route or find their way to specific landmarks in the environment.

“People with cerebrospinal markers for preclinical Alzheimer’s disease demonstrated significant difficulties only when they had to form a cognitive map of the environment — an allocentric, place-learning navigation process associated with hippocampal function,” Head said. “This same preclinical Alzheimer’s disease group showed little or no impairment on route learning tasks — an egocentric navigation process more closely associated with caudate function.”

When compared with cognitively normal study participants who lacked the cerebrospinal fluid markers of Alzheimer’s, those with preclinical Alzheimer’s disease scored lower on their ability to learn the locations of objects in the environment in relation to each other during the initial study phase.

While these results suggest deficits in the ability to form a cognitive map, preclinical Alzheimer’s disease participants eventually managed to overcome these map-learning deficits, performing almost as well as cognitively normal participants during a subsequent wayfinding navigation task.

“These findings suggest that the wayfinding difficulties experienced by people with preclinical Alzheimer’s disease are in part related to trouble acquiring the environmental information,” Head said. “While they may require additional training to learn new environments, the good news here is that they seem to retain sufficient information to use a cognitive map almost as well as their cognitively normal counterparts.”

A more sensitive diagnostic?

Head cautions that the current study has several limitations, including a relatively small sample size and a lack of direct information about brain regions and networks that have a role in spatial navigation and wayfinding.

However, Allison notes, “We are currently investigating how brain regions impacted early during the course of the disease are related to cognitive mapping deficits in a larger sample of individuals with preclinical Alzheimer’s disease.”

Within the context of these limitations, the current investigation demonstrates significant preclinical Alzheimer’s disease-related deficits in aspects of cognitive mapping with relative preservation in route learning. In contrast, people experiencing memory lapses and other behavioral problems associated with early stage Alzheimer’s disease had clear difficulties both in learning an established route and in finding their own way to new landmarks.

“This pattern is consistent with decrements in hippocampal integrity prior to changes in the caudate,” Head said. “These findings suggest that navigational tasks designed to assess a cognitive mapping strategy could represent a powerful tool for detecting the very earliest Alzheimer’s disease-related changes in cognition.”

Participants in the study came from an ongoing study at Washington University’s Charles F. and Joanne Knight Alzheimer’s Disease Research Center. Scientists have been following participants with and without a family history of the disease, with the aim of identifying Alzheimer’s disease biomarkers most closely associated with the development of full-blown disease years later.

The research team notes that the presence of cerebrospinal fluid markers for preclinical Alzheimer’s does not guarantee that a person will go on to develop full blown Alzheimer’s. “Future research should examine whether cognitive mapping deficits in individuals in preclinical Alzheimer’s are associated with an increased risk of developing symptomatic Alzheimer’s,” they said.

Other study co-authors, both from Washington University School of Medicine, include Anne M. Fagan, professor of neurology, and John C. Morris, MD, director of the Charles F. and Joanne Knight Alzheimer’s Disease Research Center and the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology.

This work was supported by NIH grants P50 AG05861, P01 AG03991, and P01 AG026276. Samantha Allison was supported by National Institute on Aging 5T32AG00030.

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