Blood clots made visible by nanoparticles

Every year, millions of people come into emergency rooms complaining of chest pains, yet those pains are only sometimes due to heart attacks. Unfortunately in many of those cases, the only way to be sure of what’s going on is to admit the patient for an overnight stay, and administer time-consuming and costly tests. Now, however, a new procedure could reveal the presence and location of a blood clot within hours. It’s made possible by the injection of nanoparticles, each containing a million atoms of bismuth – a toxic heavy metal.
The particles were developed by Dr. Dipanjan Pan, at the Washington University School of Medicine in St. Louis, Missouri.

He used bismuth because it shows up on a spectral CT scanner, which is itself a new type of technology. Whereas regular CT scanners only provide black and white images, spectral scanners use the entire spectrum of the X-ray beam to differentiate objects, and display metals (such as bismuth) in color.
Injecting a straight-up shot of toxic heavy metals into a patient’s bloodstream would have dire consequences. To keep the nanoparticles harmless, they were created from a compound in which bismuth atoms were attached to fatty acid chains that won’t come apart in the body. This compound was dissolved in a detergent, which was then combined with phospholipids – a key component of cell membranes. Like oil droplets in vinegar, the nanoparticles proceeded to self-assemble, with the bismuth compound at the core and a phospholipid membrane on the outside. Trials on mice showed that the body was able to release the bismuth from within the membrane, in a safe form.

Pan also added a molecule to the nanoparticles’ surface that is attracted to fibrin, a protein that is found in blood clots but not elsewhere in the vascular system. That molecule draws the particles to blood clots, where the bismuth shows up as a color such as green or yellow on a spectral CT scan image.
Not only could the technology be used to locate blood clots, but it could possibly even treat their cause – ruptures in artery walls. If the nanoparticles contained some sort of healing agent, then once they attached to the fibrin in a blood clot, they could set about sealing any weak spots.

Lasers to combat AIDS..New developments in laser treatment

November 7, 2007 Current laser treatments for virus and disease can be more harmful than effective, sometimes causing damage to DNA and even skin cancer. Now groundbreaking research has developed a new technique that uses lasers to destroy viruses and bacteria, including AIDS and Hepatitis, without causing harm to the human cells of the infected person.

The research was conducted by Physicists from Arizona State University and published in the Institute of Physics' Journal of Physics: Condensed Matter. It discusses how pulses from an infrared laser can be fine-tuned to discriminate between problem microorganisms and human cells.

The research was based on putting femtosecond (one billionth of one millionth of a second.) laser pulses through a process which then produces lethal vibrations in the protein coat of microorganisms. In doing so, the vibrations destroy the microorganisms and thereby can work to disinfect blood and treat blood-borne diseases.

The physicists involved in the research believe the treatment destroys the virus but not the human cells due to the different structural compositions on the protein coats of the human cells and the bacteria and viruses. Beyond being a treatment for disease, the technique may also be effective in reducing the spread of infections such as MRSA in hospitals.

Starve yourself and live longer

Researchers at Mount Sinai School of Medicine have unraveled a molecular puzzle to reveal why a lower-calorie diet slows the development of some age-related conditions such as Alzheimer’s disease, as well as the aging process itself. In their search for an answer they discovered that it doesn’t seem to matter how the diet is restricted – whether fats, proteins or carbohydrates are cut – to produce protective effects against aging and disease.

A two-part study led by Charles Mobbs, PhD, Professor of Neuroscience and of Geriatrics and Palliative Medicine at Mount Sinai School of Medicine, indicates that a reduction of dietary intake blocks a person’s glucose metabolism, which contributes to oxidative stress - a cellular process that leads to tissue damage and also promotes cancer cell growth. Conversely, high calorie diet may accelerate age-related disease by promoting oxidative stress.
Dietary restriction induces a transcription factor called CREB-binding protein (CBP), which controls the activity of genes that regulate cellular function. By developing drugs that mimic the protective effects of CBP – those usually caused by dietary restriction – scientists may be able to extend lifespan and reduce vulnerability to age-related illnesses.
“We discovered that CBP predicts lifespan and accounts for 80 percent of lifespan variation in mammals,” said Dr. Mobbs. “Finding the right balance is key; only a 10 percent restriction will produce a small increase in lifespan, whereas an 80 percent restriction will lead to a shorter life due to starvation.”
The team found an optimal dietary restriction, estimated to be equivalent to a 30 percent caloric reduction in mammals, increased lifespan over 50 percent while slowing the development of an age-related pathology similar to Alzheimer’s disease.
The first part of the study looked at c. elegans, a species of roundworm, that were genetically altered to develop Alzheimer’s disease-like symptoms. Dr. Mobbs and his team reduced the roundworms’ dietary intake by diluting the bacteria the worms consume. They found that when dietary restriction was maintained throughout the worms’ adulthood, lifespan increased by 65 percent and the Alzheimer's disease-related paralysis decreased by about 50 percent.
In the second part of study, Dr. Mobbs and his team looked at the other end of this process: What happens to CBP in a high-calorie diet that has led to diabetes, a disease in which glucose metabolism is impaired? Researchers examined mice and found that diabetes reduces activation of CBP, leading Dr. Mobbs to conclude that a high-calorie diet that leads to diabetes would have the opposite effect of dietary restriction and would accelerate aging.
Interestingly, dietary restriction triggers CBP for as long as the restriction is maintained, suggesting that the protective effects may wear off if higher dietary intake resumes. CBP responds to changes in glucose within hours, indicating genetic communications respond quickly to fluctuations in dietary intake. “Our next step is to understand the exact interactions of CBP with other transcription factors that mediate its protective effects with age,” said Dr. Mobbs. “If we can map out these interactions, we could then begin to produce more targeted drugs that mimic the protective effects of CBP.”

New 3D Imaging technology promises early detection of Alzheimer’s and Dementia

The older people become, the greater risk they have of sharing the tragic fate of those who remain alive yet are increasingly unaware of the world around them. In industrialised countries, one to six percent of the population over the age of 65 and an even more alarming ten to twenty percent over the age of 80 suffer a progressive loss of their cognitive abilities. Alzheimer disease is the most common cause, affecting 50 to 60 percent of all cases, followed by circulatory disorders in small blood vessels, capillaries and venules (calcifications), which make up about 20 percent. These disorders cause ever larger parts of the brain to become necrotic due to an insufficient supply of blood.

The earlier these disorders and their causes are detected, the more effective the therapies can be for preventing the disease or at least substantially slowing down its progress. Increasingly higher-resolution imaging techniques making major contributions to early detection are now being presented at the European Congress of Radiology (ECR 2007), held in Vienna from March 9 to 13, 2007, and attended by some 16,000 participants from 92 countries. University Professor Dr. Daniela Prayer from the Clinical Department for Neuroradiology at the Vienna University of Medicine states, “Although we cannot yet depict individual cells, we can image ultra-tiny bundles of fibre with high resolution. That is a spectacular breakthrough!”
Voxel-based morphometry allows for the volume of grey matter and white matter in the brain to be determined to the nearest cubic millimetre.
A reduction in brain mass (atrophy) in certain areas indicates Alzheimer’s disease and in other areas, other forms of dementia, according to Professor Prayer. An MR study by Professor Dr. Riccardo della Nave and his colleagues at the University of Florence, for instance, found that certain degenerative phenomena occurring in the left thalamus and in a zone in the left cerebral cortex are the first signs of family-related Alzheimer’s disease. “These findings are quite valuable. They enable us not only to differentiate precisely but also to detect the patterns of the disease before symptoms even occur and to check the efficacy of new drugs, namely, whether they can really stop the loss of brain mass.”
Another advance allows insights into the circuitry architecture of individual bundles of cerebral fibre. It is based on special techniques applicable with modern magnetic resonance devices to render visible the movements of water molecules in the space between fibres. Professor Prayer explains, “Wherever protons change direction, there has to be an obstacle, a cell wall or a fibre connection. Applying the reverse conclusion, we obtain a picture of these structures and see early on where swelling occurs or cells die off.”
No less fascinating are the prospects opened up by magnetic resonance spectroscopy (MRS). It allows a non-contact x-ray view of biochemical processes within the regions of the brain under examination.
All in all, Professor Prayer notes, “the new methodological advances of magnetic resonance technology provide us with a hopeful view of the future in terms of the early diagnosis and efficacy testing of therapies for dementias. If this happens in the near future, the spectre of old-age dementia will lose much of its threatening effect.”

Early detection of Alzheimer’s disease using x-rays!!

A highly detailed x-ray imaging technique previously been used to examine tumors in breast tissue and cartilage in knee and ankle joints could used for early diagnosis of Alzheimer’s disease. Researchers at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory are the first to test the technique’s ability to visualize a class of minuscule plaques that are a hallmark feature of Alzheimer’s disease.
Scientists have long known that Alzheimer’s disease is associated with plaques - areas of dense built-up proteins in the affected brain. Many also believe that these plaques actually cause the disease. Before drug therapies that remove the plaques from the brain can be tested, researchers need a non-invasive, safe, and cost-effective way to track the plaques’ number and size.

That is no easy task as the plaques are on the micrometer scale, or one millionth of a meter. Conventional techniques such as computed tomography (CT) poorly distinguish between the plaques and other soft tissue such as cartilage or blood vessels. The new technique developed at Brookhaven, called diffraction-enhanced imaging (DEI), might provide the extra imaging power researchers crave.
DEI, which makes use of extremely bright beams of x-rays available at synchrotron sources such as Brookhaven’s National Synchrotron Light Source, is used to visualize not only bone, but also soft tissue in a way that is not possible using standard x-rays. In contrast to conventional sources, synchrotron x-ray beams are thousands of times more intense and extremely concentrated into a narrow beam. The result is typically a lower x-ray dose with a higher image quality.

In their study study, researchers from Brookhaven and Stony Brook University used DEI in a high-resolution mode called micro-computed tomography to visualize individual plaques in a mouse-brain model of Alzheimer’s disease. The results not only revealed detailed images of the plaques, but also proved that DEI can be used on whole brains to visualize a wide range of anatomical structures without the use of a contrast agent. The images are similar to those produced by high-resolution magnetic resonance imaging (MRI), with the potential to even exceed MRI pictures in resolution.
Although the radiation dose used for the study is too high to safely image individual plaques in humans, it did show that images could be produced from live animal brains to learn how the plaques grow. The ultimate goal for the researchers is to find a way to develop a safe imaging technique for humans.

Human blood stem cells engineered to kill HIV

A proof-of-principle study has demonstrated that it is possible to engineer human blood stem cells into cells that can target and kill HIV-infected cells. The result is the equivalent of a genetic vaccine which is not only good news in the fight against HIV - the process could also be used against a range of chronic viral diseases.

In the study researchers from the UCLA AIDS Institute and colleagues took the “killer” T cells that help fight infection, known as CD8 cytotoxic T lymphocytes, from an HIV-infected individual. The researchers then identified the molecule known as the T-cell receptor – the molecule that guides the T cell in recognizing and killing HIV-infected cells. Although these cells are able to destroy HIV-infected cells, they do not exist in enough quantities to clear the virus from the body. So the researchers cloned the receptor and genetically engineered human blood stem cells, then placed the stem cells into human thymus tissue that had been implanted in mice, allowing them to study the reaction in a living organism.

The engineered stem cells developed into a large population of mature, multifunctional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also found that HIV-specific T-cell receptors have to be matched to an individual in much the same way that an organ is matched to a transplant patient.
The next step is to test this strategy in a more advanced model to determine if it would work in the human body, said co-author Jerome A. Zack, UCLA professor of medicine in the division of hematology and oncology and associate director of the UCLA AIDS Institute. And with the results of the study suggesting the strategy could be an effective weapon in the fight against AIDS, the researchers also hope to expand the range of viruses against which this approach could be used.

"We have demonstrated in this proof-of-principle study that this type of approach can be used to engineer the human immune system, particularly the T-cell response, to specifically target HIV-infected cells," said lead investigator Scott G. Kitchen, assistant professor of medicine in the division of hematology and oncology at the David Geffen School of Medicine at UCLA and a member of the UCLA AIDS Institute. "These studies lay the foundation for further therapeutic development that involves restoring damaged or defective immune responses toward a variety of viruses that cause chronic disease, or even different types of tumors."

Love as pain relief ....

As science continues to unravel the mysteries of ourselves and the world around us at a furious pace, it can sometimes feel like the boffins are proving things that many of us feel we already know or take for granted. This interesting example comes from the Stanford University School of Medicine, where scientists have found that intense feelings of love are as effective at relieving pain as painkillers or even illicit drugs.
The last few decades have shown us that pain is not simply a symptom of trauma, but is a discreet disease entity in its own right that can affect the entire nervous system. Advances in neuro-imaging have allowed scientists a better look at the areas in which pain is processed, how the brain is affected and how it changes our thoughts and emotions, in an effort to create a multi-disciplinary treatment for pain.

Neuroimaging was able to link the activation of reward systems in the brain with the feelings of euphoria and contentment that are often distinguished by the early stages of a relationship. With Functional Magnetic Resonance Imaging (fMRI) they found that the area of the brain that processes pain and the area of the brain that is involved in reward-processing are situated close together. Close neurological ties between the two areas meant activation of the reward-processing area could affect the pain-processing area.

Stanford study
Fifteen lovesick individuals were tested in the first nine months of their relationship. They were subjected to moderate and high thermal pain, and shown pictures of their partner, pictures of another attractive and familiar friend, and underwent a word-association task designed to be distracting. Both the partner pictures and distraction technique reported a significant reduction in pain, or analgesia, and only the partner pictures activated the brain's reward-processing areas; the caudate head, nucleus accumbens, lateral orbitofrontal cortex, amygdala, and dorsolateral prefrontal cortex.

The study suggests that neural activation of the reward-processing areas via non-pharmacological means could be a powerful action on the pain experience, and could help future work with pain management in humans.
"When people are in this passionate, all-consuming phase of love, there are significant alterations in their mood that are impacting their experience of pain," said Sean Mackey, MD, PhD, chief of the Division of Pain Management, associate professor of anesthesia and senior author of the study. "We're beginning to tease apart some of these reward systems in the brain and how they influence pain. These are very deep, old systems in our brain that involve dopamine — a primary neurotransmitter that influences mood, reward and motivation."

Other studies running concurrently are using brain imaging to train patients to control the experience of pain; to identify the changes in the brain experienced during chronic pain that amplify the pain experience, and how to reverse them; to examine distraction techniques as a viable method of pain management; to study pain-processing via the spinal cord; the use of neurotoxins as a novel method of pain management; the use of intravenous lidocaine as an effective pain relief; the pain experience and contributing factors; and sensitization to pain following repeated use of opiates.
The study was published online in PLoS ONE.

Ancient body clock discovered that helps to keep all living things on time

A group of Cambridge scientists have successfully identified the mechanism that drives our internal 24-hour clock, or circadian rhythm. It occurs not only in human cells, but has also been found in other life forms such as algae, and has been dated back millions of years. Whilst the research promises a better understanding of the problems associated with shift-work and jet-lag, this mechanism has also been proven to be responsible for sleep patterns, seasonal shifts and even the migration of butterflies.

The study from the Institute of Metabolic Science at the University of Cambridge discovered that red blood cells contain this 24-hour rhythm. In the past, scientists assumed this rhythm came from DNA and gene activity but unlike most cells, red blood cells do not contain DNA.
During this study, the Cambridge scientists incubated healthy red blood cells in the dark at body temperature for several days, sampling them at regular intervals. It was discovered that the levels of peroxiredoxins (proteins that are produced in blood), underwent a 24-hour cycle. Virtually all known organisms contain peroxiredoxins.
"The implications of this for health are manifold," said Akhilesh Reddy, lead author of the study. "We already know that disrupted clocks – for example, caused by shift-work and jet-lag – are associated with metabolic disorders such as diabetes, mental health problems and even cancer. By furthering our knowledge of how the 24-hour clock in cells works, we hope that the links to these disorders – and others – will be made clearer. This will, in the longer term, lead to new therapies that we couldn't even have thought about a couple of years ago."

A second study by scientists working together at the Universities of Edinburgh and Cambridge, and the Observatoire Oceanologique in Banyuls, France, identified a similar 24-hour rhythm in marine algae. Once again, the scientists held a previous belief that the circadian clock was driven by gene activity, but both the algae and the red blood cells proved this theory wrong.
"This groundbreaking research shows that body clocks are ancient mechanisms that have stayed with us through a billion years of evolution," said Andrew Millar of the University of Edinburgh's School of Biological Sciences. "They must be far more important and sophisticated than we previously realized. More work is needed to determine how and why these clocks developed in people – and most likely all other living things on Earth – and what role they play in controlling our bodies."

Cell reprogramming breakthrough could mend broken hearts

Heart disease remains one the biggest killers in the Western world. When a heart attack or heart failure occurs, permanent damage often affects the heart, destroying live cells and leaving the patient with irreversible scarring. This scarring can often lead to a terminal condition or increase the risk of danger of future heart attacks. Now scientists at the Gladstone Institute of Cardiovascular Disease (GICD) have discovered a new technique to create healthy beating heart cells from structural cells. These advancements mean that in the future doctors could be able to repair damaged hearts.

Our human heart comprises of cardiomyocytes (beating heart cells) and cardiac fibroblasts, which provide a support structure and secrete signals. In research published in the current issue of the Journal Cell, scientists were able to successfully reprogram fibroblasts within the heart to transform them into cardiomyocytes.

"Scientists have tried for 20 years to convert nonmuscle cells into heart muscle, but it turns out we just needed the right combination of genes at the right dose," said lead researcher Dr. Masaki Ieda.
With this success of these trials the researchers have discovered evidence which would suggest that independent adult cells within the body can be reprogrammed from one cell type to another whilst by-passing the stem cell state. This discovery could have repercussions in all areas of medicine. Whilst direct cellular reprogramming may erase the issues involving the use of stem cells, it could also remove the risk that some stem cells may later develop into tumors.

The first stage of the cellular reprogramming occurs over three days, before the cells start to adopt the characteristics of cardiac muscle. However it may take up to seven weeks before the cells are fully reprogrammed into healthy beating heart cells.
"The ability to reprogram fibroblasts into cardiomyocytes has many therapeutic implications," said GICD director Dr. Deepak Srivastava. "Half of the cells in the heart are fibroblasts, so the ability to call upon this reservoir of cells already in the organ to become beating heart cells has tremendous promise for cardiac regeneration. Introducing the defined factors, or factors that mimic their effect, directly into the heart to create new heart muscle would avoid the need to inject stem cells into the heart and all the obstacles that go along with such cell-based therapies."

While direct cellular reprogramming hopes to offer many advantages, further laboratory work will need to be carried out before this technique can be used easily and effectively within our hospital systems.
"Direct reprogramming has not yet been done in human cells," Dr. Srivastava added. "And, the hope is still to find small molecules, rather than genetic factors, that can be used to direct the cell-fate switch."

Creation of liver cells from skin cells gives hope in fight against liver disease

Researching liver disorders is extremely difficult because liver cells (hepatocytes) cannot be grown in the laboratory. However, researchers at the University of Cambridge have now managed to create diseased liver cells from a small sample of human skin. The research shows that stem cells can be used to model a diverse range of inherited disorders and paves the way for new liver disease research and possible cell-based therapy.

Liver disease on the rise

In the UK, liver disease is the fifth largest cause of death after cardiovascular, cancer, stroke, and respiratory diseases. Over the past 30 years mortality from liver disease in young and middle-aged people has increased over six times, with the number of individuals dying from the disease increasing at a rate of 8-10 percent every year.
By 2012, the UK is expected to have the highest liver disease death rates in Europe and, without action to tackle the disease, it could overtake stroke and coronary heart disease as the leading cause of death within the next 10-20 years. In the United States, it accounts for approximately 25,000 deaths a year.


Cell-based therapy?

By replicating the liver cells, researchers can not only investigate exactly what is happening in a diseased cell, they can also test the effectiveness of new therapies to treat these conditions. It is hoped that their discovery will lead to tailored treatments for specific individuals and eventually cell-based therapy – when cells from patients with genetic diseases are 'cured' and transplanted back. Additionally, as the process could be used to model cells from other parts of the body, their findings could have implications for conditions affecting other

For their research, the scientists took skin biopsies from seven patients who suffered from a variety of inherited liver diseases and three healthy individuals (the control group). They then reprogrammed cells from the skin samples back into stem cells. These stem cells were then used to generate liver cells which mimicked a broad range of liver diseases – the first time patient-specific liver diseases have been modeled using stem cells – and to create 'healthy' liver cells from the control group. Importantly, the three diseases the scientists modeled covered a diverse range of pathological mechanisms, thereby demonstrating the potential application of their research on a wide variety of disorders.

 Dr Tamir Rashid of the Laboratory for Regenerative Medicine, University of Cambridge, lead author of the paper detailing the team’s findings, said: "We know that given the shortage of donor liver organs alternative strategies must urgently be sought. Our study improves the possibility that such alternatives will be found – either using new drugs or a cell-based therapeutic approach."

The University of Cambridge.

Handyscope turns an iPhone into a digital dermoscope

Call me crazy, but I’ve always found some peace of mind knowing that the latest medical gadget scanning some worrisome part of my body isn’t an accessory for a smartphone, but costs in the millions of dollars and is the result of years of expensive research and development.

However, as someone who has more than their fair share of moles dotted all over their body, I’m willing to make an exception for the handyscope. Consisting of an optical attachment and an accompanying app, the handyscope turns an iPhone into a digital dermoscope to provide an instantaneous up close look at potential skin cancers.

One of the big pluses of the device, aside from its portability, is the ease with which images of suspicious moles can be shared with colleagues or uploaded to a second opinion service where world-renowned specialists can weigh in with their view.

"We developed the handyscope for all doctors who want to have the possibility to take pictures of the skin and work with them later. It is an alternative for those who miss the ‛capture-and-save-function’ when using conventional handheld dermatoscopes,” explains Andreas Mayer, chief executive officer of FotoFinder.

 The handyscope has its own in-built 2400mAh battery pack, which will keep the LEDs running for up to eight hours and can be recharged with the standard iPhone USB cable.

FotoFinder will launch the handyscope in February at the 69th Annual Meeting of the American Academy of Dermatology in New Orleans. Health professionals can order the handyscope for 1,166.20 euro (approx. US$1,590), while the app costs US$11.99 through the iTunes App Store.

Axolotl eggs could provide a potent weapon in fight against cancer

A common cause of cancer is when cells are altered or mutated and the body’s tumor suppressor genes are switched off. Scientists at the University of Nottingham have managed to bring cancer cells back under control by reactivating the cells’ cancer suppressor genes using an extract from axolotl oocytes. The scientists say the discovery could form a powerful new technology platform for the treatment of a variety of cancers.

The process of cell division is controlled by specific genes and these are turned “on” or “off” depending on their function. Among the most important of these genes are tumor suppressor genes. These genes repress the development of cancers and normally act as a control point in the cell division cycle. Therefore, the switching off of tumor suppressor genes is a common cause of cancers.

The on/off switch in genes is controlled by the modification of proteins that are bound to the DNA in a cell, which are known as epigenetic modifications. Tumour suppressor genes in many cancers are switched off by epigenetic marks, which is the underlying cause of tumors.

In an effort to reverse this process the researchers looked to the axolotl salamander – an animal well known for its ability to regenerate most of its body parts. The scientists found that humans evolved from animals that closely resemble axolotls and therefore, proteins in axolotls are very similar to those in humans. Axolotl oocytes – eggs prior to ovulation – are also packed with molecules that have very powerful epigenetic modifying activity and a powerful capacity to change epigenetic marks on the DNA of human cells.

By treating the cancerous cells with axolotl oocyte extract, the researchers were able to reactivate the tumor suppressor genes and stop the cancer from growing. After 60 days there was still no evidence of cancerous growth.
The researchers say the identification of the proteins in axolotl oocytes responsible for this tumor reversing activity is a major goal of future research, and could form a powerful weapon in the fight against cancer.


Human protein may help muscular dystrophy patients

Duchenne Muscular Dystrophy is the most common and severe childhood form of muscular dystrophy (MD), affecting one in 3,500 boys. The disease progressively weakens muscles cells and tissues until muscle degradation is so severe that the patient dies, most often in their late teens or twenties. Scientists at Brown University in Providence, Rhode Island and the University of Pennsylvania, hope their research into the human protein, biglycan, will ultimately improve the condition of muscular dystrophy sufferers. Their studies have shown that biglycan significantly slows muscle damage and improves function in mice with the Duchenne genetic mutation. Human clinical trials will be the next step.

Boys with the genetic mutation causing Duchenne MD (as the gene is on the X chromosome MD mostly affects males; female carriers have milder symptoms) are unable to produce dystrophin, a protein that keeps muscles strong.

Dystrophin is part of a complex protein that connects the cytoskeleton of a muscle fiber to the tissue framework surrounding each cell through the cell membrane. In cases of muscular dystrophy, contraction of the muscle leads to disruption of the outer membrane of the muscle cells and eventual weakening and wasting of the muscle.
 The research, published online on 27 December in Proceedings of the National Academy of Sciences, found that biglycan delivered to the bloodstream restores the muscle-strengthening presence of another protein called utrophin. Utrophin is prevalent in very young children and although it still exists to a far lesser degree in adults, it is not available in a way that can benefit those with muscular dystrophy.

The muscle-strengthening effect of biglycan continued through the testing and there were no indications of side effects on kidney or liver function.
In one experiment there was a 50-percent reduction in “centrally nucleated” fibers in the muscle tissue of mice treated with biglycan treated compared to untreated mice. Biologists recognize the fibers as indicators of recent tissue damage and repair, so a reduction suggests that the muscle tissue is suffering less damage.

In addition, a standardized stress test simultaneously stretched and contracted mouse muscle. Eventually even healthy muscle is weakened however the muscles of muscular dystrophy mice treated with biglycan lost their strength 50 percent more slowly in some muscles than in untreated mice.
“This is all aimed at getting a therapy that will meaningfully improve the condition of patients,” said Justin Fallon, professor of neuroscience at Brown University and the senior author of the Paper.

Multiple sclerosis-Definition, Causes & Risk factors-By Mayo Clinic staff


Multiple sclerosis (MS) is a potentially debilitating disease in which your body's immune system eats away at the protective sheath that covers your nerves. This interferes with the communication between your brain and the rest of your body. Ultimately, this may result in deterioration of the nerves themselves, a process that's not reversible.
Symptoms vary widely, depending on the amount of damage and which nerves are affected. People with severe cases of multiple sclerosis may lose the ability to walk or speak. Multiple sclerosis can be difficult to diagnose early in the course of the disease because symptoms often come and go sometimes disappearing for months.
There's no cure for multiple sclerosis. However treatments can help treat attacks, modify the course of the disease and treat symptoms


The cause of multiple sclerosis is unknown. It's believed to be an autoimmune disease, in which the body's immune system attacks its own tissues. In multiple sclerosis, this process destroys myelin - the fatty substance that coats and protects nerve fibers in the brain and spinal cord.
Myelin can be compared to the insulation on electrical wires. When myelin is damaged, the messages that travel along that nerve may be slowed or blocked.
Doctors and researchers don't understand why multiple sclerosis develops in some people and not others. A combination of factors, ranging from genetics to childhood infections, may play a role

Risk factors

These factors may increase your risk of developing multiple sclerosis:

■Being between the ages of 20 and 40. Multiple sclerosis can occur at any age, but most commonly affects people between these ages.

■Being female. Women are about twice as likely as men are to develop multiple sclerosis.
■Having a family history. If one of your parents or siblings has had multiple sclerosis, you have a 1 to 3 percent chance of developing the disease — as compared with the risk in the general population, which is just a tenth of 1 percent. But the experiences of identical twins show that heredity can't be the only factor involved. If multiple sclerosis was determined solely by genetics, identical twins would have identical risks. However, an identical twin has only a 30 percent chance of developing multiple sclerosis if his or her twin already has the disease.
■Having certain infections. A variety of viruses have been linked to multiple sclerosis. Currently the greatest interest is in the association of multiple sclerosis with Epstein-Barr virus, the virus that causes infectious mononucleosis. How Epstein-Barr virus might result in a higher rate of MS remains to be clarified.
■Being white. White people, particularly those whose families originated in northern Europe, are at highest risk of developing multiple sclerosis. People of Asian, African or Native American descent have the lowest risk.
■Living in countries with temperate climes. Multiple sclerosis is far more common in Europe,
southern Canada, northern United States, New Zealand and southeastern Australia. The risk seems to increase with latitude.
A child who moves from a high-risk area to a low-risk area, or vice versa, tends to have the risk level associated with his or her new home area. But if the move occurs after puberty, the young adult usually retains the risk level associated with his or her first home.
■Having certain other autoimmune diseases. You're very slightly more likely to develop multiple sclerosis if you have thyroid disease, type 1 diabetes or inflammatory bowel disease

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Multiple sclerosis-Symptoms & Complications-By Mayo Clinic staff


Signs and symptoms of multiple sclerosis vary widely, depending on the location of affected nerve fibers. Multiple sclerosis signs and symptoms may include:

■Numbness or weakness in one or more limbs, which typically occurs on one side of your body at a time or the bottom half of your body
■Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement (optic neuritis)
■Double vision or blurring of vision
■Tingling or pain in parts of your body
■Electric-shock sensations that occur with certain head movements
■Tremor, lack of coordination or unsteady gait
Most people with multiple sclerosis, particularly in the beginning stages of the disease, experience relapses of symptoms, which are followed by periods of complete or partial remission. Signs and symptoms of multiple sclerosis often are triggered or worsened by an increase in body temperature


In some cases, people with multiple sclerosis may also develop:
■Muscle stiffness or spasms
■Paralysis, most typically in the legs
■Problems with bladder, bowel or sexual function
■Mental changes, such as forgetfulness or difficulties concentrating

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Multiple sclerosis-Tests and diagnosis-By Mayo Clinic staff

Tests and diagnosis

There are no specific tests for multiple sclerosis. Ultimately, the diagnosis relies on ruling out other conditions that might produce similar symptoms. Your doctor may base a multiple sclerosis diagnosis on the following:

Blood tests
Analysis of your blood can help rule out some infectious or inflammatory diseases that have symptoms similar to multiple sclerosis.

Spinal tap (lumbar puncture)
In this procedure, a doctor or nurse removes a small sample of cerebrospinal fluid from within your spinal canal for laboratory analysis. This sample can show abnormalities associated with multiple sclerosis, such as abnormal levels of white blood cells or proteins. This procedure can also help rule out viral infections and other conditions that can cause neurological symptoms similar to those of multiple sclerosis.

This test uses a powerful magnetic field and radio waves to produce detailed images of internal organs. MRI can reveal lesions, indicative of the myelin loss on your brain and spinal cord. However, these types of lesions can also be caused by other conditions, such as lupus or Lyme disease, so the presence of these lesions isn't definitive proof that you have multiple sclerosis.
During an MRI test, you lie on a movable table that slides into a large, tube-shaped machine, which makes loud tapping or banging noises during the scans. Most MRIs take at least an hour. While the test is painless, some people feel claustrophobic inside the machine. Your doctor can arrange for a sedative if necessary.

You may also receive an intravenous dye that may help highlight "active" lesions. This helps doctors know whether your disease is in an active phase, even if no symptoms are present. Newer MRI techniques can provide even greater detail about the degree of nerve fiber injury or permanent myelin loss and recovery.
Newer MRI techniques may help with diagnosing multiple sclerosis. They include:

■Magnetic resonance spectroscopy (MRS). This provides information about the brain's biochemistry.
■Magnetization transfer imaging (MTI). MTI can detect abnormalities before lesions are visible on standard MRI scans.
■Diffusion tensor imaging (DTI). This technology provides 3-D images of demyelinated areas of the brain, which are useful in determining disease progression.
■Functional MRI (fMRI). This is used during cognitive performance tests.
Evoked potential test
This test measures the electrical signals sent by your brain in response to stimuli. An evoked potential test may use visual stimuli or electrical stimuli, in which short electrical impulses are applied to your legs or arms

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Multiple sclerosis-Treatments and drugs-By Mayo Clinic staff

Treatments and drugs

There is no cure for multiple sclerosis. Treatment typically focuses on strategies to treat attacks, to modify the course of the disease and to treat symptoms. Some people have such mild symptoms that no treatment is necessary

Strategies to treat attacks

Corticosteroids. The most common treatment for multiple sclerosis, corticosteroids reduce the inflammation that spikes during a relapse. Examples include oral prednisone and intravenous methylprednisolone. Side effects may include increased blood pressure, mood swings and weight gain. Long-term use can lead to cataracts, high blood sugar and increased risk of infections.
Plasma exchange (plasmapheresis). This procedure looks a little like dialysis as it mechanically separates your blood cells from your plasma, the liquid part of your blood. Plasma exchange is sometimes used to help combat severe symptoms of multiple sclerosis relapses in people who aren't responding to intravenous steroids.

Strategies to modify the course of the disease

Beta interferons. These types of drugs — such as Avonex, Betaseron, Extavia and Rebif — appear to slow the rate at which multiple sclerosis symptoms worsen over time. Interferons can cause side effects, including liver damage, so you'll need blood tests to monitor your liver enzymes.
Glatiramer (Copaxone). Doctors believe that glatiramer works by blocking your immune system's attack on myelin. You must inject this drug subcutaneously once daily. Side effects may include flushing and shortness of breath after injection.
Fingolimod (Gilenya). An oral medication given once daily, this works by trapping immune cells in lymph nodes. It reduces attacks of MS and short-term disability. To take this drug, you'll need to have your heart rate monitored for six hours after the first dose because the first dose can slow your heartbeat (bradycardia). You'll also need to be immune to the chickenpox virus (varicella-zoster virus). Other side effects include high blood pressure and visual blurring.
Natalizumab (Tysabri). This drug is designed to work by interfering with the movement of potentially damaging immune cells from your bloodstream to your brain and spinal cord. Tysabri is generally reserved for people who see no results from or can't tolerate other types of treatments.
This is because Tysabri increases the risk of progressive multifocal leukoencephalopathy — a brain infection that is usually fatal.
Mitoxantrone (Novantrone). This immunosuppressant drug can be harmful to the heart, and it's associated with development of blood cancers like leukemia, so it's usually used only to treat severe, advanced multiple sclerosis.
Strategies to treat symptoms
Physical therapy. A physical or occupational therapist can teach you stretching and strengthening exercises, and show you how to use devices that can make it easier to perform daily tasks.
Muscle relaxants. If you have multiple sclerosis, you may experience painful or uncontrollable muscle stiffness or spasms, particularly in your legs. Muscle relaxants such as baclofen (Lioresal) and tizanidine (Zanaflex) may improve muscle spasticity. Baclofen may increase weakness in the legs.
Tizanidine may cause drowsiness or a dry mouth.
Medications to reduce fatigue. Drugs such as amantadine (Symmetrel) may help reduce fatigue.
Other medications. Medications may also be prescribed for depression, pain and bladder or bowel control problems that may be associated with multiple sclerosis.

A number of other drugs and procedures such as stem cell transplantation to treat multiple sclerosis are under investigation

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Multiple sclerosis-Lifestyle and home remedies-By Mayo Clinic staff

These steps may help relieve some symptoms of multiple sclerosis:

■Get plenty of rest. Fatigue is a common symptom of multiple sclerosis, and although it's generally unrelated to your activity level, resting may make you feel less tired.
■Exercise. Regular aerobic exercise may offer some benefits if you have mild to moderate multiple sclerosis. Benefits include improved strength, muscle tone, balance and coordination, and help with
depression. Swimming is a good option for people who are bothered by heat.
■Cool down. Multiple sclerosis symptoms often worsen when your body temperature increases. Cool baths can reduce your core temperature, especially if you submerge your upper torso.
■Eat a balanced diet. Eating a healthy, balanced diet can help keep your immune system strong.
■Relieve stress. Because stress may trigger or worsen signs and symptoms, try to learn to relax.

Activities such as yoga, tai chi, massage, meditation or deep breathing — or just listening to music — might help

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Antioxidants .. Are they really helpful to us

What are antioxidants? Essentially, they are substances that reduce, neutralize, and prevent the damage done to the body by free radicals. Free radicals are simply electrons that are no longer attached to atoms. Instead of circling the nucleus of an atom (much like the earth circles the sun), free radicals are both free and radical enough to go careening through our cells, inflicting damage as they go

What causes free radicals to be formed? A process called oxidation creates free radicals and this process happens in the context of normal metabolic processes and our everyday exposure to our environment. In other words, eating, breathing, and going out in the sun all contribute to the the process of oxidation, free radical formation, and the resulting damage that is caused to the cells of our bodies

What kind of damage are we talking about? Pretty much every kind you can think of: the deterioration of bone, joints and connective tissue; the wearing out of organs; the decline of the immune system; the irritating advance of the visible effects of aging; and even, possibly, to some extent, the aging process itelf

List of known Antioxidants
Alpha Lipoic Acid
Beta Carotene
Coenzyme Q10
Ginkgo Biloba
Grape Seed
Green Tea
Pine Bark
Superoxide Dismutase
Vitamin C
Vitamin E