[x]

"وقـل اعمـلوا فسـيرى الله عـملكم ورسـوله والمؤمنـون"


..لمحة عن كليات جامعة دمشق و فروعها... شاركنا تجربتك وكلمنا عن اختصاصك



المحـاضـرات
برنـامج الـدوام
برنـامج الامتحــان
النتـائج الامتحـانيـة
أسـئلة دورات
أفكـار ومشــاريع
حلقــات بحـث
مشــاريع تخـرّج
"وقـل اعمـلوا فسـيرى الله عـملكم ورسـوله والمؤمنـون"
كلية الصيدلة

مواضيع مميزة..


مواضيع ننصح بزيارتها .:Pharmacy:. عش متعة الصيدلة .:Pharmacy:. تقنية الويكي: معاً نحو محتوى عربي رقمي علمي نصنعه معاً .:Pharmacy:. ساحة مشروع ترجمة موسوعة التكنولوجيا الصيدلية .:Pharmacy:. تعو نلازم كلنا سوا .:Pharmacy:. معلومة عالماشي يا صـــــــيــــــــدلــــــي .:Pharmacy:. كل شـــي جـــديــــد .:Pharmacy:. مواقع الشركات الدوائية
مواضيع مميزة:
مـنـتـدى تـرجـمــة وتـدقـيـق أقــســام الـمـوســـوعـة
للتواصل مع الهيئة الإدارية في كلية الصيدلة اضغط هنا
ويكـي فـارما

المركز الإخباري الــصــيدلاني

مشروع ترجمة الموسوعة التكنلوجية الصيدلانية

موسوعة العلوم العربية

مشروع المجلة الطبية Medical Journal

مشروع الأختام الجماعية الدورية

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19-05-2011 08:23 PM




السلام عليكم:

Errors in Protein Structure Sparked Evolution of Biological Complexity

Newswise — Over four billion years of evolution, plants and animals grew far more complex than their single-celled ancestors. But a new comparison of proteins shared across species finds that complex organisms, including humans, have accumulated structural weaknesses that may have
actually launched the long journey from microbe to man.
The study, published in Nature, suggests that the random introduction of errors into proteins, rather than traditional natural selection, may have boosted the evolution of biological complexity. Flaws in the "packing" of proteins that make them more unstable in water could have promoted protein
interactions and intracellular teamwork, expanding the possibilities of life.

"Everybody wants to say that evolution is equivalent to natural selection and that things that are sophisticated and complex have been absolutely selected for," said study co-author Ariel Fernández, PhD, a visiting scholar at the University of Chicago and senior researcher at the Mathematics Institute of Argentina (IAM) in Buenos Aires. "What we are claiming here is that inefficient selection creates a niche or an opportunity to evolve complexity."

"This is a novel bridge between protein chemistry and evolutionary biology," said co-author Michael Lynch, PhD, professor of biology at Indiana University. "I hope that it causes us to pause and think about how evolution operates in new ways that we haven't thought about before."
When mildly negative mutations arise in a species with a large population, such as the trillions of bacterial organisms that can fill a small area, they are quickly cleared out by selective forces. But when a new mutation appears in a species with a relatively small population, as in large mammals and humans, selection against the error is slower and less efficient, allowing the mutation to spread through the population.

To look at whether these mild defects accumulate in species with small populations, Fernández and Lynch compared over 100 proteins shared by 36 species of varying population size. Though these shared, "orthologous" proteins are identical in shape and function, genetic differences alter them in more subtle ways.

Fernández and Lynch focused on design flaws called "dehydrons," sites where the protein structure is vulnerable to chemical reactions with water. Proteins with more dehydrons are more "unwrapped" - unstable in an aqueous environment, and therefore prone to bind with another protein to protect their vulnerable regions.
A computational analysis of 106 orthologous proteins confirmed their hypothesis that proteins from species with smaller populations were more vulnerable in water. The result suggests that structural errors accumulate in large organisms such as humans due to random genetic drift.

"We hate to hear that our structures are actually lousier," Fernández said. "But that has a good side to it. Because they are lousier, they are more likely to participate in complexes, and we have a much better chance of achieving more sophisticated function through teamwork. Instead of being a loner, the protein is a team player."

On their own, these unstable proteins might be expected to perform their cellular duties more poorly, possibly causing harm to the organism. But unstable proteins are also "stickier," more likely to form associations with other proteins that could introduce more flexibility and complexity into the cell. If these complexes create a survival advantage for the organism, forces of natural selection should take over and spread the new protein complex through the population.

"It's not an argument against selection, it's an argument for non-adaptive mechanisms opening up new evolutionary pathways that wouldn't have been there before," Lynch said. "It's those first little nicks getting into the protein armor that essentially open up a new selective environment."

To confirm that the accumulation of structural flaws in proteins preceded, rather than resulted from, the formation of complexes, Fernández and Lynch turned to a natural experiment. Some bacterial species have two types of populations: communities that live inside other organisms and larger populations living free in the environment. When orthologous proteins were compared between these two populations, the same pattern emerged – proteins from the smaller populations were more flawed than those from the free-living bacteria of the same species.

Despite these accidental benefits, the accumulation of too many structural flaws can be dangerous to an organism. When highly reactive proteins such as prions, amyloid-beta, or tau are too sticky, they can clump into aggregates that kill cells and cause diseases such as Alzheimer’s and encephalopathy.

The implication that complexity initially arose by accident may be provocative within the field of evolutionary biology, the authors said. The discovery that flawed proteins are more likely to form complexes could also revolutionize the growing field of bioengineering, where the tools of evolution are used to create stronger, self-assembling, or self-reparing materials.

"Natural designs are often one notch more sophisticated than the best engineering," Fernández said. "This is another example: Nature doesn't change the molecular machinery, but somehow it tinkers with it in subtle ways through the wrapping."

The paper, "Nonadaptive origins of interactome complexity," will be published online May 18 by Nature (doi: 10.1038/nature09992). Fernández performed the initial phase of the work as the Hasselmann Chair in Bioengineering at Rice University. The research was supported by the National Institutes of Health and the National Science Foundation





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*ZAID*

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رب اجعل هذا البلد آمناً




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19-05-2011 09:04 PM




Gene for Alzheimer's Risk May Affect Brain Early


May 18, 2011 -- Young adults who carry a so-called Alzheimer's risk gene show disruption in their brains as early as their 20s, according to new research.

Researchers from the University of California, Los Angeles used a special MRI scan that maps brain connections to examine 398 healthy young adults. Some carried the variant of the gene linked with Alzheimer's risk and some did not.

"The people who carry this gene have severely impaired wiring in most of their brain, even when they are young," says researcher Paul M. Thompson, PhD, professor of neurology at the University of California, Los Angeles David Geffen School of Medicine.

Even so, they don't notice symptoms of Alzheimer's disease, such as memory loss at this time, he tells WebMD. Following a healthy lifestyle early can offset the genetic risk, he says.

The study is published in The Journal of Neuroscience.

WebMD Health News





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20-05-2011 07:50 AM




السلام عليكم:

Weighty Issues for Alzheimer’s: How Weight Affects Alzheimer's Disease

Dr. Cynthia D. Haines, M.D.
Wednesday, May 18, 2011


Piling on the pounds as the years go by may pose more of a threat to your long-term health and well-being than you realize. In fact, being overweight during middle age may increase your risk of developing dementia in your golden years, a recent Swedish study published in the journal Neurology suggests.
We have already seen that midlife obesity (body mass index [BMI] at or above 30) has been linked to a heightened risk of dementia later on. This new research adds that simply overweight status may have the same implications. Overweight is defined by a BMI of 25 up to 30.

The researchers found that being overweight at midlife increased one's risk of dementia in late life by over 70 percent. Obesity posed an even bigger risk: nearly four-fold.

The global impact of this is huge, as 1.6 billion adults worldwide are obese or overweight - including approximately two-thirds of Americans.
The reasons for the weight-dementia connection have not been definitively identified, to date. Possibilities include:

• A higher BMI is known to raise risk of other dementia-related diseases, such as diabetes and cardiovascular disease. These diseases could then impact the likelihood of dementia.

• There is evidence that adipose tissue (fat) produces inflammatory chemicals that could have an effect on brain health. Having excess fat at midlife could mean a longer duration of exposure to these potentially harmful and memory-robbing chemicals.

The science is not exact in other ways as well. BMI is an estimate of body fat. It can overestimate fat in very muscular individuals and can underestimate in the elderly or others who have lost muscle.

In any case, weight is a factor that we each have the power to do something about - unlike genetics or certain environmental exposures. We can strive to get unwanted and excess pounds off and keep them off as we age.
The authors also importantly noted that it is never too late to start in terms of reducing one's risk of dementia through weight reduction and maintenance.
Here are some tips to get you started:

1. Know your numbers. It's easy to check your BMI. The NIH has a chart to do just that. Aim for a BMI less than 25 but above 18. If you have question about how the BMI chart may or may not be applicable to you and your body habitus, talk to your doctor. They may have other numbers for you to track (such as weight measured by scale or waist circumference).

2. Track your weight (but not too often). Consider weighing yourself no more than once a week. Weight tends to fluctuate from day to day, so this can lead to frustration. But less often will hamper your opportunity to address smaller gains.

3. Exercise daily. In addition to helping you get your weight in check, regular exercise has numerous other benefits, including a lower risk of heart disease and colon cancer.





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20-05-2011 06:25 PM




السلام عليكم:

Scientists Discover New Drug Target for Squamous Cell Carcinoma


Newswise — SEATTLE – Researchers at Fred Hutchinson Cancer Research Center have discovered a new drug target for squamous cell carcinoma – the second most common form of skin cancer. Scientists in the laboratory of Valeri Vasioukhin, Ph.D., have found that a protein called alpha-catenin acts as a tumor suppressor and they also have unlocked the mechanism by which this protein controls cell proliferation.
The findings by Vasioukhin and colleagues will be published May 24 in Science Signaling.
For the study, the researchers studied mice that were bred to lack a copy of the gene that makes the protein alpha-catenin in hair follicle stem cells. The researchers found that these mice developed a type of skin cancer called squamous cell carcinoma.
“The fact that alpha-catenin-deficient mice developed skin cancer led us to conclude that the loss of this protein is an important event in cancer development, and that alpha-catenin functions as a tumor suppressor,” said Vasioukhin, an associate member of the Hutchinson Center’s Human Biology Division. “We also found that unlike normal cells, alpha-catenin-mutant cells cannot stop dividing when they become very crowded in the Petri dish – this characteristic is one of the hallmarks of cancer cells.”
The researchers also teased out the mechanisms by which the protein suppresses tumor growth. They found that alpha-catenin controls the activity of a protein called Yap1, which, if activated, can cause cancer.
“We found that alpha-catenin controls cell proliferation by regulating Yap1, which is active in cells missing alpha-catenin. Therefore, Yap1 is likely to be an excellent target for the treatment of patients with squamous cell carcinoma,” Vasioukhin said.
More than 700,000 new cases of squamous cell carcinoma are diagnosed each year. This form of skin cancer arises in the cells that make up most of the skin’s upper layers (epidermis). Squamous cell malignancies may arise in many areas of the body including the mucous membranes and genitals, but are most common in areas frequently exposed to the sun, such as the rim of the ear, lower lip, face, scalp, neck, hands, arms and legs.
The National Cancer Institute funded this research, which was also supported in part by a Chromosome and Metabolism and Cancer Training Grant from the National Institutes of Health. In addition to researchers in the Hutchinson Center’s Human Biology Division, co-authors included investigators from Dermatopathology Northwest in Bellevue, Wash.; Harvard University; and the University of Pennsylvania Medical School.
Note for media only: To obtain an embargoed copy of the Science Signaling paper by Vasioukhin and colleagues, “A-catenin is a Tumor Suppressor that Controls Cell Accumulation by Regulating the Localization and Activity of the Transcriptional Coactivator Yap1,”.





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22-05-2011 06:17 PM




السلام عليكم:

Study Identifies Novel Role for a Protein That Could Lead To New Treatments for Rheumatoid Arthritis


Newswise — A new study by rheumatologists at Hospital for Special Surgery in New York has shown that a powerful pro-inflammatory protein, tumor necrosis factor (TNF), can also suppress aspects of inflammation. The researchers say the identification of the mechanism of how this occurs could potentially lead to new treatments for diseases such as rheumatoid arthritis. The study was published May 22 online in advance of publication in the journal Nature Immunology.

“Prior to this study, TNF has long been known as a potent pro-inflammatory cytokine, but if you look carefully through the literature, there are hints that it also has some suppressive functions, but nothing was known about the mechanisms,” said Lionel Ivashkiv, M.D., associate chief scientific officer and physician in the Arthritis and Tissue Degeneration Program at Hospital for Special Surgery who led the study. “This is really the first mechanism showing how TNF can turn inflammation down.”

Because many proteins have homeostatic functions, both driving and suppressing certain actions so a cell can maintain internal equilibrium, researchers thought TNF might not be an exception. “Most strong activators in the immune system trigger a feedback response to restrain the amount of inflammation,” Dr. Ivashkiv said.

To find out, researchers designed experiments stimulating macrophages with lipopolysaccharide (LPS), a prototypical inflammatory factor that stimulates receptors important in inflammation. In test tube studies, the researchers treated human monocytes and macrophages, cells that have a key role in inflammatory diseases, with TNF and then challenged these cells with LPS. They found that the TNF suppressed the inflammatory response of the macrophages and monocytes. They then gave mice low doses of TNF followed by high doses of LPS and found that the mice were protected from the effects of high dose LPS, which is usually lethal.

They discovered that the mechanism by which TNF suppressed the inflammatory response involved a protein known as GSK3 (glycogen synthase kinase 3-alpha) and a gene known as TNFAIP3 that encodes the A20 protein. Experiments with a drug that can inhibit GSK3 as well as experiments with RNA interference of A20, which can block A20 gene function, helped identify the roles of this protein and gene.

The researchers say the findings could be used to develop potential therapies for diseases, such as rheumatoid arthritis. “We think it is relevant to rheumatoid arthritis, not only because the cells we are studying (the macrophages) are exactly the same cells that migrate into joints and make the inflammatory cytokines involved in rheumatoid arthritis, but because A20 is involved. TNFAIP3 is one of the best linked genes to rheumatoid arthritis,” Dr. Ivashkiv said. “There are polymorphisms in the A20 gene that have been linked to RA pathogenesis.”

The researchers hypothesize that patients who make less A20 are more susceptible to inflammation and thus rheumatoid arthritis. One approach to treating RA could be to increase A20 levels in patients who naturally make less A20 by manipulating GSK-3, since this study showed that GSK-3 influences A20. “The study sort of opens a line of investigation to understanding how A20 levels can be manipulated in patients with various diseases,” Dr. Ivashkiv said.

The findings could be applied to other diseases besides arthritis. In conditions such as rheumatoid arthritis, you may want to boost A20, but in other settings such as cancer, where the macrophages are suppressed, you may want to inhibit A20 expression.

“What the study shows that is new is that TNF has suppressive functions in addition to its well-known activating functions,” Dr. Ivashkiv said. “Before this study, people thought it might suppress adaptive immunity, but surprisingly we found that it actually suppresses a cell of the innate immune system, the macrophage, which is the same cell that makes it and, by doing that, it regulates its own production.”





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22-05-2011 06:22 PM




السلام عليكم:

Human Brain’s Most Ubiquitous Cell Cultivated in Lab Dish

Newswise — MADISON – Pity the lowly astrocyte, the most common cell in the human nervous system.

Long considered to be little more than putty in the brain and spinal cord, the star-shaped astrocyte has found new respect among neuroscientists who have begun to recognize its many functions in the brain, not to mention its role in a range of disorders of the central nervous system.

Now, writing in the current (May 22) issue of the journal Nature Biotechnology, a group led by University of Wisconsin-Madison stem cell researcher Su-Chun Zhang reports it has been able to direct embryonic and induced human stem cells to become astrocytes in the lab dish.

The ability to make large, uniform batches of astrocytes, explains Zhang, opens a new avenue to more fully understanding the functional roles of the brain’s most commonplace cell, as well as its involvement in a host of central nervous system disorders ranging from headaches to dementia. What’s more, the ability to culture the cells gives researchers a powerful tool to devise new therapies and drugs for neurological disorders.

“Not a lot of attention has been paid to these cells because human astrocytes have been hard to get,” says Zhang, a researcher at UW-Madison’s Waisman Center and a professor of neuroscience in the UW-Madison School of Medicine and Public Health. “But we can make billions or trillions of them from a single stem cell.”

Although astrocytes have gotten short shrift from science compared to neurons, the large filamentous cells that process and transmit information, scientists are turning their attention to the more common cells as their roles in the brain become better understood. There are a variety of astrocyte cell types and they perform such basic housekeeping tasks as helping to regulate blood flow, soaking up excess chemicals produced by interacting neurons and controlling the blood-brain barrier, a protective filter that keeps dangerous molecules from entering the brain.

Astrocytes, some studies suggest, may even play a role in human intelligence given that their volume is much greater in the human brain than any other species of animal.

“Without the astrocyte, neurons can’t function,” Zhang notes. “Astrocytes wrap around nerve cells to protect them and keep them healthy. They participate in virtually every function or disorder of the brain.”

The ability to forge astrocytes in the lab has several potential practical outcomes, according to Zhang. They could be used as screens to identify new drugs for treating diseases of the brain, they can be used to model disease in the lab dish and, in the more distant future, it may be possible to transplant the cells to treat a variety of neurological conditions, including brain trauma, Parkinson’s disease and spinal cord injury. It is possible that astrocytes prepared for clinical use could be among the first cells transplanted to intervene in a neurological condition as the motor neurons affected by the fatal amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, are swathed in astrocytes.

“With an injury or neurological condition, neurons in the brain have to work harder, and doing so they make more neurotransmitters,” chemicals that in excess can be toxic to other cells in the brain, Zhang says.

“One idea is that it may be possible to rescue motor neurons by putting normal, healthy astrocytes in the brain,” according to Zhang. “These cells are really useful as a therapeutic target.”

The technology developed by the Wisconsin group lays a foundation to make all the different species of astrocytes. What’s more, it is possible to genetically engineer them to mimic disease so that previously inaccessible neurological conditions can be studied in the lab.

In addition to Zhang, co-authors of the new Nature Biotechnology paper include Robert Krencik, Jason Weick and Zhijian Zhang, all of UW-Madison, and Yan Liu of Fudan University Shanghai Medical School. The work was supported by the ALS Foundation, the National Institute of Neurological Disorders and Stroke, the National Multiple Sclerosis Society, the Bleser Family Foundation and the Busta Family Foundation.





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....{SalaM}....

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23-05-2011 07:21 AM




السلام عليكم


الجرافين... مادة ستغير مستقبل الحاسبات

بعد أن استنفد السيليكون الذي تبنى عليه المعالجات الإلكترونية في الكمبيوترات قدراته

الفيزيائية، بدأ الباحثون البحث عن بديل آخر نظراً لأن الحاسبات المبنية على السيليكون تقوم

بعمليات عديدة في الثانية من دون أن ترتفع حرارتها ولكن لحد معين.

ومنذ عدة سنوات لم يتوان الفيزيائيون عن أن يتخيلوا ويجربوا كل ما عرفوا وما لم يعرفوا من

مواد للتوصل إلى مادة تزيد من سرعة المعالجات بنسبة كبيرة وفتح آفاق جديدة في صنع

الترانزستورات التي تتكون منها هذه المعالجات.

كانت نتيجة هذه الأبحاث توصل الباحثين إلى مادة الجرافين التي تستخدم في تصنيع العديد من

المواد مثل أقلام الرصاص، ومن مميزات الجرافين أنه من الناحية البنيوية الشبكية يعتبر المادة

المتبلرة الوحيدة ذات البعدين في الفراغ بمعنى أن ذرات الكربون فيها مرتبة على شكل

مسدس الزوايا والأضلاع كخلية النحل تماماً. هذا الأمر يجعله يكون جزيئاً مسطحاً وبسمك ذرة

واحدة أي ما يعادل 0،1 نانومتر.

وكان الباحثان الأمريكيان ديفيد مرمين وهربرت واجنر توصلا في 1966 إلى أن الجرافيت الذي

تصنع منه أقلام الرصاص، يتأثر بعامل الحرارة أو الاستثارة الحرارية، أي أن طبقة واحدة من

الذرات يمكن أن تضطرب في بنيتها الشكلية، وبالتالي فإن المادة نفسها يمكن أن تتحول إلى

سائل أو مادة مائعة نظراً لأنه لا يمكن عزلها.

هذا الأمر لم يمنع الفيزيائي الهولندي ذا الأصل الروسي أندريه جايم وفريقه العلمي من جامعة

مانشستر، من أن ينجحوا في عزل بلورة الجرافين، اللهم إلا أن الجرافين ليس مسطحاً تماماً

ويظهر عن تموجات دقيقة جداً قادرة على امتصاص طاقة الاستثارة الحرارية.

ومنذ اكتشافه لم يكف الجرافين عن إظهار خصائص جديدة غير مسبوقة، فخصائصه تبين أنه

مادة شفافة وموصلة ومثالية في مجال صناعة الألواح الشمسية أو البلورات السائلة كما أن

مقاومته الميكانيكية تبشر بأنه سيكون من المواد فائقة الصلابة، فضلاً عن ذلك فإن خواصه

الإلكترونية أثارت دهشة العلماء بالفعل لأن سرعة النقل الإلكتروني فيه مرتفعة بشكل لا

يصدق أي أن الإلكترونات تمر عبره من دون مقاومة تقريباً وترتفع درجة حرارته بنسبة قليلة جداً

وذلك لأنه موصل جيد للحرارة وفقده لها سريع جداً الأمر الذي يجعله مناسباً للاستخدام في

الإلكترونيات.

ويشير الباحثون إلى أن سرعة انتقال الإلكترونات فيه تزيد على سرعتها في السيليكون بثلاثين

مرة. علاوة على ذلك فإن سرعة المعالجات المبنية على السيليكون ستبقى محصورة في

نطاق الجيفاهرتز أما الجرافين فسيمكنها من اختراق نطاق السيتراهرتز.

في هذه الآونة تنشط المختبرات العلمية لإنتاج الجرافين بكميات تجارية بطريقتين: الأولى منها

يديرها معهد جورجيا التكنولوجي بولاية أتلانتا الأمريكية وتتمثل في رفع حرارة بلورة كربيد

السيليسيوم (السيليكون) إلى أكثر من 1000 درجة مئوية إلى أن تتفكك وتتبخر. وينتج عن

هذه العملية بقاء ذرات الكربون التي ترتبط فيما بينها بشكل تلقائي مشكلة شبكة سداسية

من الجرافين. وتقول كلير برجيه التي تعمل في هذا المعهد بفخر: “يبلغ عرض وريقات الجرافين

التي ينتجها المختبر بضع عشرات من الميكرومتر، لكن الأهم من ذلك هو أننا استطعنا خلال

هذه السنة أن نثبت أن نقاوة العينات التي أنتجناها كانت كافية لاستخدامها في التطبيقات

الميكروإلكترونية، ما يعني أن مرحلة الإنتاج على المستوى التجاري قد انطلقت بالفعل في

ديسمبر/ كانون الأول 2008 في أتلانتا”.

الطريقة الثانية التي يسعى إلى التحضير لها الباحث تيري بوارو من مختبر الأبحاث التطبيقية

في مجال الإلكترونيات بمدينة غرونوبل الفرنسية، تستفيد من اكتشاف الباحثين الفرنسيين أنه

عندما نؤكسد الجرافيت في وسط حمضي فإن وريقاته تتفكك وتتحول إلى جرافين وبالتالي فإنه

يكفي تنقية البلورة باستخدام محلول مختزل. وفي الآونة الأخيرة، تمكن فريق من الباحثين من

جامعة كاليفورنيا من اكتشاف أن مادة الهيدرازين (مركب من الآزوت والهيدروجين) قادرة على أن

تقوم بالدور الذي تقوم به الجرافين بشكل ممتاز حيث يمكن للباحثين الحصول على طبقات ذات

درجة توصيل عالية وبسعر أرخص من الطريقة الأولى.

استخدامات الجرافين لن تبقى محصورة في المعالجات والترانزستورات بل ستمتد إلى تقنيات

أخرى كالاتصالات والتصوير والكشف الموجي والكشف عن الأسلحة والبيولوجيا للكشف عن

متتاليات الحمض النووي وذلك لأن جميع هذه التطبيقات تتطلب سرعة فائقة.

ويقول الباحث أندريه جايم إن الجرافين بمثابة الرحمة للفيزيائي لأنه من الناحية النظرية يمكنه

من خلال ذرة واحدة الحوصل على مادة ثنائية الأبعاد وفائقة التوصل، ففي وريقة واحدة من

الجرافين تتحرك الشحنات الكهربية كالجسيمات الكمومية النسبوية وكأنها في الحقيقة فقدت

كتلتها مما يجعلها تتحرك بسرعة الضوء. ويضيف جايم أن هذا النوع من الفيزياء الذرية كان بعيد

المنال، ولذا يمكنني تشبيه الجرافين بأنه يعمل كمعجل للجسيمات، وستكون السنوات

الخمس عشرة المقبلة فاصلة في موضوع التطورات التي سيشهدها عالم الكمبيوتر بشكل

خاص.. كيف لا وهو أشد مقاومة من الفولاذ بمائتي مرة؟





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....{SalaM}....

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مسجل منذ: 31-07-2009
عدد المشاركات: 3855
تقييمات العضو: 532
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23-05-2011 09:34 AM




السلام عليكم



ديلي تلغراف :علماء بريطانيون يكتشفون مادة هلامية يمكن أن تصلح الأقراص النخاعية للعمود الفقري   


لندن-سانا

ذكرت صحيفة ديلي تلغراف البريطانية أن علماء بريطانيين اكتشفوا مادة هلامية (جل) يمكن أن

تصلح الأقراص النخاعية للعمود الفقري ولاسيما أن آلام الظهر تؤثر في نحو 80 بالمئة من

الناس عند مرحلة معينة في حياتهم مضيفة أنه في الولايات المتحدة وحدها يعد ألم الظهر

السبب الأكثر شيوعا للعجز الوظيفي حيث إنه عامل رئيسي في جعل الناس يخسرون

وظائفهم.

ونقلت الصحيفة عن علماء جامعة مانشستر البريطانية قولهم إنهم اكتشفوا كيفية استبدال

طريقة عمل القرص بين الفقرات بطريقة دائمة من خلال جزيئات مجهرية إسفنجية الشكل

تتجمع مع بعضها لتصلح الأقراص المتآكلة.

وأضافت الصحيفة أن رئيس البحث الدكتور براين سوندرز وفريقه نجحوا في ربط جزيئات المادة

الهلامية المتناهية الصغر مع بعضها لتكوين مواد هلامية قابلة للحقن وشديدة التحمل ومرنة

وقادرة على تحمل التغيرات الكبيرة الدائمة في الشكل بدون تكسر.

وأضاف سوندرز أن فريقه تقدم خطوة هامة إلى الأمام على طريق تصميم مواد مبتكرة من مادة

هلامية قابلة للحقن لمعالجة تدهور الأقراص بين الفقرات.

وأوضح أن تدهور الأقراص بين الفقرات يؤدي إلى ألم مزمن في الظهر يكلف البلد مليارات

الدولارات سنويا ويسبب معاناة كبيرة للمصابين وأسرهم.

وأشارت الصحيفة إلى أن الحقنة التي هي نتاج عمل متواصل منذ 25 عاما على مليارات

الجزيئات الدقيقة التي تشكل سائلا في المحقنة وبمجرد دخولها إلى الجسم تتحول إلى (جل).

وتعد آلام أسفل الظهر من أكثر المشكلات الصحية شيوعا بين الناس و تأتي في المرتبة الثانية

بعد نزلات البرد وأسبابها كثيرة جداً و متفرعة أهمها أسباب ميكانيكية وروماتيزمية و أسباب

أيضية أو لها علاقة بالغدد الصماء و الضغط النفسي و أسباب بكتيرية و بعض أمراض الجهاز

البولي التناسلي و بعض أمراض الجهاز الهضمي وبعض الأورام الحميدة والخبيثة.





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مسجل منذ: 31-07-2009
عدد المشاركات: 3855
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23-05-2011 07:28 PM




السلام عليكم


Does Eating Give You Pleasure, Or Make You Anxious?


New study reveals biological reasons for feelings of anxiety instead of reward in patients with anorexia

Newswise — Perhaps the most puzzling symptom of anorexia nervosa – a disorder that tends to occur in young women – is the refusal to eat, resulting in extreme weight loss. While most people have a great deal of difficulty in dieting and losing weight, particularly if a diet extends over many months or years, individuals with anorexia nervosa can literally diet themselves to death. In fact, this disorder has a very high death rate from starvation. A new study, now online in the journal International Journal of Eating Disorders, sheds light on why these symptoms occur in anorexia nervosa.

Most people find eating to be a pleasant and rewarding experience. In contrast, people with anorexia nervosa often say that eating makes them more anxious, and food refusal makes them feel better. Research over the past decade has provided new insights into the brain mechanisms that are associated with the rewarding aspects of eating. One of these brain chemicals is dopamine, which is released when people or animals eat tasty foods.

A study led by Walter Kaye, MD, professor of psychiatry and director of the Eating Disorder Treatment and Research Program at the University of California, San Diego School of Medicine, used a brain imaging technology called positron emission tomography (PET), which permits visualization of dopamine function in the brain. In order to provoke dopamine levels in the brain, scientists administered a one-time dose of the drug amphetamine, which releases dopamine in the brain.

In healthy women without an eating disorder, amphetamine-induced release of dopamine was related to feelings of extreme pleasure in a part of the brain known as a “reward” center. However, in people who had anorexia nervosa, amphetamine made them feel anxious, and the part of the brain that was activated was, instead, a part of the brain that worries about consequences.

“This is the first study to demonstrate a biological reason why individuals with anorexia nervosa have a paradoxical response to food,” said Kaye. “It’s possible that when people with anorexia nervosa eat, the related release of the neurotransmitter dopamine makes them anxious, rather than experiencing a normal feeling of reward. It is understandable why it is so difficult to get people with anorexia nervosa to eat and gain weight, because food generates intensely uncomfortable feelings of anxiety.”

Importantly, this study was of people who have recovered from anorexia nervosa for at least a year, suggesting that the feeling provoked may be due to pre-existing traits, rather than a response to being at an extremely low weight.

In terms of impact on treatment strategies, there are no currently proven treatments that reduce core symptoms in anorexia nervosa, such as eating-induced anxiety. According to the researchers, even though food is accompanied by severe anxiety, it is still critical to eat and gain weight in order to effectively treat this disorder.

Contributors to the study include Ursula F. Bailer, MD, Medical University of Vienna and UCSD Department of Psychiatry; Vikas Duvvuri, MD, PhD, UCSD Department of Psychiatry; and Rajesh Narendran, MD, W. Gordon Frankle, MD, Michael L. Himes and Chester A. Mathis, PhD, University of Pittsburgh School of Medicine. These results have been published on line in the International Journal of Eating Disorders.

The study was supported in part by the National Institute of Mental Health and the Prince





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آية الرحمن

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مسجل منذ: 02-07-2009
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23-05-2011 08:09 PM




السلام عليكم:

Common Test Could Help Predict Early Death in Diabetes


Newswise — WINSTON-SALEM, N.C. – Monday, May 23, 2011 – New findings out of Wake Forest Baptist Medical Center reveal that a common test may be useful in predicting early death in individuals with diabetes.

The study appears in the May issue of Diabetes Care.
“People with diabetes are already at high risk of developing heart disease and experiencing an early death,” said Donald W. Bowden, Ph.D., the director of the Center for Diabetes Research at Wake Forest Baptist and lead investigator. “With this study, we’ve discovered that we can identify a subset of individuals within this high risk group who are at even higher risk, and the means to do this is already widely available in the form of a computed tomography (CT) scan – a relatively inexpensive and non-invasive test.”

More than 25 million Americans – 8.3 percent of the population – are currently living with diabetes, according to the National Institutes of Health. People with the condition are at increased risk of developing heart and vascular disease and, while vascular disease is common in the general population, it is twice as common in people with diabetes. At least 60 percent of diabetes patients – even those on dialysis for kidney failure – ultimately die of a vascular event, such as heart attack or stroke. However, Bowden said, questions about why so many diabetes patients die early have remained unanswered in the medical community’s understanding of the disease.

For the Diabetes Heart Study, Bowden and colleagues have been following nearly 1,500 patients with diabetes in North Carolina for about 13 years, gathering data on various aspects of the disease and how it affects individual health. As original study participants began to die, the researchers sought to understand why.

“When we reviewed the data last year, we were shocked by the number of participants who had already died during this study,” Bowden said. “We wanted to find out if there were any predictors of who would succumb versus those who are still living. In a group of people who are already at high risk, we were looking for a way to identify which individuals were at even higher risk for early death, with the goal of finding interventions or ways to focus medical care and attention toward those individuals at highest risk.”

A high coronary artery calcium (CAC) score is known to be a strong indicator of coronary heart disease. The score provides a measure of how much coronary artery disease, or calcified “plaque” is present in the blood vessels of the heart. Plaque plays a major role in heart attacks and other vascular events and can be measured by taking a special “gated” CT scan which, in comparison to typical CT scans, uses very few X-rays, does not require any injections and generally takes less than 10 minutes to perform. At Wake Forest Baptist, the test costs just over $200 and some insurance companies will cover the exam in appropriate situations.

Within the diabetes-affected population, there is a very wide range of calcified plaque buildup in the arteries and the heart, from individuals with none at all, to people whose entire vessels are nearly completely calcified. The researchers separated more than 1,000 study participants into five groups, according to the amount of calcified plaque they had in their blood vessels at the beginning of the study. The health of those participants was then followed for an average of 7.4 years before researchers compared the data from those who died during the study to those who are still living.

“We saw a dramatic risk of dying earlier in the people with highest levels of calcified plaque in their blood vessels,” Bowden said. “When comparing the group with the highest amount of plaque to the group that had the lowest amount of calcified plaque, the risk of dying was more than six times greater in the group with high levels of calcified plaque. The difference in risk that we revealed is striking. It’s in a group of people who are already at risk, but the CAC level really rather dramatically differentiates risk between people within this high risk group. This finding could have novel clinical implications.”
Diabetes is associated with many other medical problems, Bowden said, so identifying a way to determine who is at highest risk and who needs the most intensive medical monitoring and care is especially important.
“The striking magnitude of the risk suggests very strongly that other research samples should be evaluated, especially in individuals with diabetes,” he said.
The study was funded by the National Heart, Lung, and Blood Institute, as well as the General Clinical Research Center of Wake Forest Baptist. Co-authors are: Subhashish Agarwal, M.D., Timothy Morgan, Ph.D., David M. Herrington, M.D., M.H.S., Jianzhao Xu, B.S., Amanda J. Cox, Ph.D., Barry I. Freedman, M.D., and J. Jeffrey Carr, M.D., M.S.C.E., all of Wake Forest Baptist.
Wake Forest Baptist Medical Center (www.wakehealth.edu) is a fully integrated academic medical center located in Winston-Salem, N.C. Wake Forest School of Medicine directs the education and research components, with the medical school ranked among the nation’s best and recognized as a leading research center in regenerative medicine, cancer, the neurosciences, aging, addiction and public health sciences. Piedmont Triad Research Park, a division of Wake Forest Baptist, fosters biotechnology innovation in an urban park community. Wake Forest Baptist Health, the clinical enterprise, includes a flagship tertiary care hospital for adults, Brenner Children’s Hospital, a network of affiliated community-based hospitals, physician practices and outpatient services. The institution’s clinical programs and the medical school are consistently recognized as among the best in the country by U.S.News & World Report





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