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In normal human beings the intake of food is converted in to a form of sugar which is called as glucose and the glucose is carried in the blood stream and reaches the cells of the body. The cells keeps the sugar and convert it in to energy by using insulin and throughout these changes the sugar level in the blood is kept constant at normal levels. The condition of high glucose level in the blood develops by inefficient use of insulin by the cells of liver, muscles and fat. Gestational form of diabetes is developed in the pregnant women during the later stage of pregnancy and it disappears after child birth and it is caused by want of insulin temporarily. Many people have diabetes and they do not know it and many may not have any symptoms at all. Aged, overweight people, people with high blood pressure are coming under the high risk group for having diabetes. Pre-diabetes group of people would have a slight elevation of blood glucose level but less than the levels of diabetes. Body weight, blood pressure and cholesterol could be controlled by changing the eating habits. Increase the amount of fruits and vegetables in the diet and reduce the fat diets like meat and desserts. Alcoholic drinks to be avoided or it should be given up immediately.  Reduce the number of calories you have each day.
Regular practice of exercise will keep the body’s cholesterol level and blood pressure at normal. You can increase your physical activities by walking, running, cycling and climbing up through stairs.
The food for the last 30 years has drugs and chemicals that make BILLION$$$ for the drug makers and destroy the peoples gut(insulin)and the FDA allows this.
I totally agree with the first comment, the pharmaceutical industry and our supposed watchdog of them are complicit in the proliferation of compounds that do tremendous harm to the human body beyond the near term result of the compund’s intended effect.
The pancreas is about 6 inches long and sits across the back of the abdomen, behind the stomach. Diabetes, type 1: The body’s immune system attacks and destroys the pancreas’ insulin-producing cells.
Diabetes, type 2: The pancreas loses the ability to appropriately produce and release insulin.
Cystic fibrosis: A genetic disorder that affects multiple body systems, usually including the lungs and the pancreas.
Pancreatic cancer: The pancreas has many different types of cells, each of which can give rise to a different type of tumor.
Pancreatic pseudocyst: After a bout of pancreatitis, a fluid-filled cavity called a pseudocyst can form. Islet cell tumor: The hormone-producing cells of the pancreas multiply abnormally, creating a benign or cancerous tumor. If a single magnetic resonance image is worth a thousand words, the time-lapse videos on Charles Guttmann’s laptop are worth a million.
As a result, the abnormal amount of glucose is maintained at blood for want of insulin or by inefficient use of insulin by the cells.
In this type, the beta cells of the pancreas is affected by the immune system and it is damaged and hence the beta cells unable to produce insulin. But some have only mild  symptoms and they ignore it since they do not know as them for symptoms for diabetes.
Testing the glucose level by oral glucose tolerance test will reveal normal blood glucose level people, pre-diabetic and diabetes group of people. When insulin is not properly used over weight attributes to high blood pressure also and losing a small body weight will prevent you from developing diabetes type 2 disease. This non-insulin dependent diabetes mellitus (NIDDM) is primarily characterized by insulin resistance, relative insulin deficiency and hyperglycemia. Insulin resistance and declined ?-cell function are the core consequences of T2DM (Rhodes et al, 2002). Obesity has also been reported as a major factor in the development of insulin resistance and T2DM (Steinberger et al, 2003). In the first phase of insulin secretion, the level of glucose-stimulated insulin release is impaired in Type 2 diabetes condition and decreased in the second phase (Ward et al., 1986). The Endoplasmic reticulum stress pathway which is active in adipose tissue and liver has a molecular link between obesity, decreased insulin sensitivity and type 2 diabetes. Many candidate genes and the susceptible loci responsible for Type 2 diabetes mellitus have already been reported and this list is being increased as the research on genetic variation in this metabolic disorder progresses all over the world. The various factors contributing to the development of T2DM have been depicted in Figure 2.
The head of the pancreas is on the right side of the abdomen and is connected to the duodenum (the first section of the small intestine) through a small tube called the pancreatic duct.
Each was created by a colleague, Dominik Meier, based on a time-series analysis of 24 brain magnetic resonance imaging scans taken in a man with relapsing-remitting multiple sclerosis (RRMS) over 12 months (Meier et al., 2007).
Over the time, this condition damages all the systems of the body including nerves and blood vessels and leading to the complications such as kidney disease, stroke, heart disease, infection, nerve damage and damage to the extremities. This condition could be treated by insulin with necessary exercise and with proper food choices. This disease appears at any stage of the life and it may appear in the younger ages in which the body does not able to use the insulin properly though there is enough availability of insulin.
Even if you are inactive, plan your self to get started to be active by having master plan for daily exercises. It contains flouride and will damage beyond its ability to kill a few bugs that you probably could have killed otherwise – try raw garlic! Diabetes develops due to the genetic predisposition and environmental factors, such as improper food-habit, obesity, sedentary lifestyle, urbanization etc.
Abnormalities in ?-cell function that results in T2DM include reduced non-glucose insulin secretagogues stimulation, asynchronous insulin release, a decreased conversion of proinsulin to insulin and a significant decrease in ?-cell mass (Mahler et al., 1999). This endoplasmic reticulum stress in obese individuals leads to suppression of insulin receptor signaling by increased activation of c-Jun N-terminal kinase (JNK) and phosphorylation of insulin receptor substrate–1 (IRS-1) on serine residues (Ozcan et al., 2004).
Because there are usually few or no early symptoms, pancreatic cancer is often advanced by the time it’s discovered. Numerous abnormal bright spots blossom and grow or shrink, as if the disease is waging a fierce territorial war in the brain.
Cholesterol and blood pressure should also be controlled while treating this disease of type 1 diabetes.
People who are obese and do not have necessary physical activity acquires this form of diabetes. Alterations in glucose metabolism by skeletal muscle and liver, the key insulin-responsive organs that monitors normal glucose homeostasis are seen in Type 2 Diabetes condition (Lowell et al, 2005). Adiponectin, an insulin sensitizing hormone from adipocytes, is a key factor for predicting T2DM (Hara et al., 2005). The treatment includes taking medicine, exercise, maintaining the cholesterol and blood pressure at normal level with wise food choices. In the initial stages, insulin resistance is compensated by the hyper-secretion of insulin by the pancreatic ? cells. The increased levels of non-esterified fatty acid (NEFA), glycerol, Tumor Necrosis Factor-? (TNF-?), and cytokines in the blood plasma lead to the increased level of insulin resistance and reduced insulin sensitivity (Steven et al., 2006).
And yet the 38-year-old man was, “according to the clinical measures, stable during that year,” Guttmann says.  MRI research over the past few decades has opened a visual window into the pathology and puzzle of MS, a scourge traditionally infamous for its attack on white matter of the central nervous system. As insulin resistance increases, the plasma glucose level increases due to the lower insulin sensitivity and the normal functionality of the pancreatic ? cells is lost, leading to hyperglycemia (Weir et al, 2004). Many investigators view MRI measures as the best prospect for a biological indicator—or biomarker—that can help them understand the disease process, diagnose patients, monitor treatment response, and predict prognosis.

MRI tests have indeed sped up diagnosis, and they’ve become a ubiquitous tool in clinical drug trials. Yet, shortcomings of current MRI technology have hindered it from fully living up to the imaging field’s high hopes, particularly as a prognostic tool.
For starters, Meier’s time-lapse movies can’t tell anyone exactly what’s going on inside the patient’s lesions. Now investigators are on the brink of various imaging-related advances that might allow them to peer more closely at the brain’s cells.
With those innovations—plus cutting-edge imaging of the whole spinal cord and the recent epiphany that MS also ravages gray matter—the full scope of the damage is emerging. A fundamental complication, however, is that MRI pictures and movies raise more questions than they answer.
Intuition tells us that lesions, or plaques, can’t be good for the brain, but their meaning for a person’s functional status and future is unclear. The stumbling block is the so-called clinicoradiological paradox: Abnormal spots on MRI often don’t manifest in physical or cognitive symptoms. As the movies from Boston illustrate, brain scans can be red herrings, pinpointing neural-tissue changes that don’t match up with how a patient feels. And physicians cannot always trace symptoms to a particular spot on a scan. Of all its uses in the MS field, MRI’s current ability to predict short- or long-term clinical outcomes is most controversial (Goodin, 2006). Louis. Sensitive in some ways, imprecise in othersMS-treating physicians and investigators rely upon conventional MRI scans, which include so-called T1-weighted or T2-weighted images, as well as gadolinium (Gd)-enhanced T1 images. Although brain lesions often don’t correlate with clinical symptoms, that discrepancy can partly be understood as a function of where in the nervous system those plaques hit, experts say, and of whether anatomical redundancies and adaptive mechanisms in a given person’s brain can compensate.
For instance, a white spot (or hyperintensity) on a T2 brain scan means excess water, which accompanies inflammation or swelling that can result from various causes, such as a tumor or infection—or an MS lesion.
But the standard imaging techniques reveal only rough details of what underlies those changes, somewhat like a smoke detector that wails at the slightest whiff, but that doesn’t indicate whether the problem is a burning pot roast or an electrical fire. MRI can’t parse what’s happening inside a lesion, Guttmann says. In MS, lesions arise when white blood cells, having crossed the blood-brain barrier, infiltrate an area and fuel inflammation that strips the fatty myelin insulation from the axon nerve fiber, thus letting additional water in to fill the breach, on top of the fluid of the initial swelling. MRI can’t even distinguish a neuron from other brain cells such as the oligodendrocytes that compose the myelin insulation.
Complicating the picture further, the plaque is not necessarily all bad news: Within it, some remyelination can be occurring. T1 scans—which are like photo negatives of T2 images, with increased water showing up dark, not white—are likewise limited in the details they can provide. However, chronic black spots (T1 hypointensities, or “black holes”) indicate extreme and permanent tissue destruction of both myelin and axons.
These techniques include diffusion tensor imaging (DTI), magnetization transfer imaging, and magnetic resonance spectroscopy, among others.
That year, imaging measures were first incorporated into the McDonald diagnostic criteria, which have since become the gold standard worldwide for identifying the illness. In decades past, if a patient experienced an initial neurologic attack (called a clinically isolated syndrome), doctors had to wait for a second episode before they could confirm MS. With the 2001 criteria, however, that diagnosis could be clinched if brain images taken a few months apart revealed that new lesions had formed. And under criteria revised in 2010 (Polman et al., 2011), a single Gd-enhanced scan can confirm MS in some cases.
That lesson comes from MS research centers, such as Guttmann’s, where patients often undergo imaging more than once a year and where advanced image-analysis software tools have made it easier to align and compare a person’s brain scans taken at different visits. A more sensitive method can now “subtract” an older scan from a newer one to identify recent changes in the brain, Guttmann says, provided that the images were taken with similar scanners and protocols. Any difference identified by this technique, called subtraction imaging (sMRI), immediately “bangs you in the eye,” he says. In a small study, Guttmann and colleagues in Boston and Amsterdam found that two-thirds of MS patients showed no Gd-enhanced lesions at their initial visit or 1 year later (Liguori et al., 2011). If clinicians relied on Gd-enhanced scans as a primary indicator of active disease, they might conclude that those patients were stable, Guttmann says; although doctors also look for whether new lesions have formed on T2 scans since the previous year’s visit, he adds, they tend to eyeball the images in a cursory manner. In Guttmann’s study, 83% of those apparently “stable” patients showed disease activity on subtraction imaging of T2-weighted scans taken at the same two time points. Clinicians traditionally view plaques detected on T2 images—or on another type of conventional T2-weighted scan called fluid-attenuated inversion recovery imaging (FLAIR)—as a fixed record of disease.
But many of those lesions can heal in such a way that they disappear from that record, according to unpublished results from Naismith and Stuart Cook of the University of Medicine and Dentistry of New Jersey in Newark (Qian et al., 2011). Tracking 75 RRMS patients, the team took monthly MRIs of various types—such as T1, T2, FLAIR, and DTI—on an advanced brain scanner with a magnet twice as powerful as in conventional machines (3 tesla versus 1.5 tesla). However, an examination of tissue integrity within those lesions—using DTI—revealed that traces of injury persisted (although leaving less damage than in permanent FLAIR lesions). Lesions that were transient on FLAIR persisted longer on other types of T2 scans, but a significant subset of plaques still vanished from detection by those techniques too. Such findings are disturbing, says neurologist Benjamin Greenberg of the University of Texas Southwestern Medical Center in Dallas (who is an Accelerated Cure Project scientific adviser). Many of his own MS patients on treatments look good, feel good, and have T2 lesions that appear stable on MRI from year to year, but they could have plaques “coming and going, coming and going, and I just didn't catch 'em,” he says. Clinical trials have shown that when drugs reduce relapses of MS symptoms, lesion activity on scans decreases, says neurologist Daniel Reich, chief of the translational neuroradiology unit at NINDS. What patients tend to fear most is the potential for permanent disability that confines them to a wheelchair, Reich says.
But disability from MS is unpredictable and takes years or decades to emerge. Thus, the ultimate vision is that MRI scans could someday help forecast whether an individual newly diagnosed with MS will experience a significant physical decline in, say, 5 or 15 years or sail through the next 3 decades without trouble, and whether treatment might change that prognosis.
But right now, controversy persists about how helpful conventional MRI scans are in projecting disability.
Research so far has mostly focused not on individual patients but on groups of them, which is plenty challenging in itself. Evidence indicates that on average, people with MS who suffer many clinical attacks or show a large burden of lesions on MRI early in their disease tend to fare worse, years later, than those who don’t. In addition, many clinical studies and drug trials in MS have found simple correlations, when analyzing averaged results from groups of patients, between conventional MRI measures and relapse rates or scores of disability on the Expanded Disability Status Scale (EDSS).
However, the EDSS itself is generally considered an insensitive short-term yardstick (Ebers et al., 2008). To justify the time and expense of costly MRI scans, he says, the important question is whether imaging contributes value “independently of everything else” in predicting disability, particularly in the long run.
The answer is “no” for changes in T2 lesion volume and Gd-enhanced lesions, say Ebers and Martin Daumer, director of the nonprofit Sylvia Lawry Centre for Multiple Sclerosis Research in Munich. The strongest predictors of short-term, on-study relapse rate or EDSS changes were patients’ disease duration and past relapse rate. “In a nutshell, MRI as it is used is not a good investment” for predicting outcomes, Daumer says.
Pooling data sets “is very dangerous if you cannot control for all the sources of variability,” says statistician Maria Pia Sormani of the University of Genoa in Italy.
Many of their studies have demonstrated simple correlations, however, and do not satisfy Ebers’s desire to see a demonstration that MRI provides predictive value independent of other indicators. The arguments and counterarguments about predicting outcomes with MRI can be downright dizzying. But in December 2011, neurologist Douglas Goodin of the University of California, San Francisco, published a 16-year follow-up analysis of 260 MS patients in the clinical trial of interferon-?-1b that led to the drug’s 1993 approval by the U.S. Yet, in Goodin’s view, the analysis shows that such measures are “pretty weakly associated” with long-term physical function, he says. After the initial interferon trial, many things could have happened in the patients’ treatment histories that might muddy the picture, Sormani says.
For example, those who originally received a placebo treatment were later offered interferon; any differences in MRI lesions that the drug triggered between the treated and untreated groups during the trial’s 3 years would tend to disappear, since everyone ended up on interferon. After 16 years, all correlations “tend to be diluted,” Sormani says, making it harder to detect any predictive power of MRI for long-term events.
As many studies, including Sormani’s work, have shown, inflammation-inhibiting medications such as interferon that suppress new lesions on conventional MRI generally curb the number of relapses in the 2- to 3-year time frame of clinical trials. That being the case, Sicotte says, an experimental anti-inflammatory agent that fails to reduce new Gd-enhanced lesions in small, early-stage studies might not be developed further.
This practice saves the effort and cost of proceeding with a compound that probably will not benefit patients. In contrast, positive early results give the green light for the larger, longer phase III trials for establishing a drug’s clinical benefits to win FDA approval. Nearly all MS drug trials now also track changes in whole-brain tissue volume as a gauge of atrophy. Brain volume gradually dwindles in MS, but measurements can be confounded by other processes, says neurologist Richard Rudick of the Cleveland Clinic in Ohio. For example, inflammatory activity of the disease can swell the white matter and increase its volume, whereas beneficial drug therapy can shrink it by quelling inflammation.
A crucial unanswered question is how MS treatments affect abnormalities in gray matter, which are more extensive in MS than experts once thought (see “Revealing what’s below the tip of the MS-pathology iceberg”).

Few clinical trials specifically monitor gray-matter pathology because researchers are still struggling to image it, Rudick says. In the next couple of years, Rudick and others say, the FDA might move toward accepting the use of T2 lesions and Gd-enhanced lesions as primary surrogate markers of relapse-reducing efficacy when assessing drugs—starting with generic forms of anti-inflammatory therapies. If a generic cousin of interferon shows similar effects on MRI to the already-approved drug, “why would you need to do a long, expensive study to show that it has clinical benefits?” Rudick says.
However, regulatory agencies are unlikely to accept those MRI measures as universal surrogate markers when it comes to testing new medication classes that work through different mechanisms, Wolinsky says. It’s possible that some novel therapies might not inhibit MRI lesion activity, yet could still quell flare-ups by, say, counteracting the downstream consequences of the plaques; or they could protect neurons in a way that prevents disease progression.
In such scenarios, investigators and drug developers would need to come up with more relevant predictors of clinical benefit in phase II testing—or take a leap of faith in proceeding to phase III studies. The findings suggest that structural damage unfolds independently in the two areas—meaning that even when no new changes show up on brain scans, MS could be progressing in the spinal cord without the patient knowing it, Bakshi says. Spinal cord disease in MS might partly account for the mismatch between brain MRI measures and current (or future) clinical status. Likewise, another potential explanation for the clinicoradiological paradox is that white-matter lesions in the brain are just the tip of the iceberg in MS. Although experts traditionally thought that the illness primarily targets white matter, which is mostly made up of myelin-covered nerve axons, the brain’s gray matter contains not just nerve cell bodies but plenty of axons too. The recognition that MS also triggers substantial demyelination and neuronal injury in gray matter—in the cortex and certain deeper structures—has made the research area a hotbed of inquiry (Hulst and Geurts, 2011). Gray-matter pathology is “the Trojan horse of multiple sclerosis,” Rudick says. Unlike white-matter lesions, gray-matter lesions often aren’t visible on conventional T2 scans because they don’t involve as much infiltration by inflammation-provoking white blood cells, Sicotte says. It was only by using FLAIR scans (which adjust T2 scans for the brightness of background water signals from fluid in nearby brain ventricles) that investigators first noticed cortical lesions. Improved histological staining techniques confirmed that the cortex is “chock-full of demyelinated areas,” Sicotte says.
A newer MRI method called double inversion recovery (DIR) provides a more sensitive way to find gray-matter lesions. Cortical lesions may be “extremely important” as an underlying cause of disability and disease progression, Rudick says. The field is now heading “as fast as it can go” toward developing sensitive measures of gray-matter pathology, Rudick says. For example, Bakshi, colleague Mohit Neema, and other associates are testing a tool called the Magnetic Resonance Disease Severity Scale (MRDSS) on a 3-tesla scanner platform in 200 patients to determine whether it can predict EDSS status, cognitive function, and quality-of-life changes 5 years later (Moodie et al., 2012). The latest version of MRDSS will factor in white-matter abnormalities by measuring T2 lesion and T1 black hole volumes as well as diffuse damage (as detected by diffusion tensor imaging). But the tool will also scrutinize atrophy, from T1 scan data, in the brain’s gray matter as well as in the spinal cord. Can next-generation methods help fill in the gaps?Everybody agrees that conventional MRI tells just part of the story of how MS patients are faring. It’s like watching a movie about a complex crime from the viewpoint of the most obvious suspect. The complete story, encompassing an entire gangster ring, would entail not just whether and where T2 or Gd-enhanced lesions are present, but also whether other kinds of damage are ravaging the brain or spinal cord. Water molecules generally diffuse within the lengths of healthy axons but tend to move outward (perpendicular to the axon fibers) if nerve tissue has been damaged. Scientists thus are trying to harness DTI as a way to assess myelin or axon integrity in the brain and spinal cord.
Reich has been using DTI to explore the links between disability and tissue damage in specific nerve tracts.
However, DTI is still experimental and limited by the fact that “we don’t quite know what we’re measuring on the tissue level,” he says.  By comparison, magnetization transfer MRI gauges myelin integrity in brain tissue by measuring how much water is linked with myelin (which, despite its high content of fatty molecules, contains some water) rather than unattached. Demyelinated areas show increased amounts of “free” water; the less water-linked, healthy myelin present, the lower the magnetization transfer ratio (MTR). The approach scrutinizes myelin increases or decreases in each voxel, or three-dimensional pixel, within an MTR brain map, rather than taking an average of the changes in a region of interest as other, histogram-based analysis methods do. As such, Zivadinov says, the voxel-wise MTR strategy is more sensitive to detecting demyelination and remyelination within an area—competing processes that could cancel each other out if regionally averaged on MTR images (Dwyer et al., 2009).
By tracking myelin changes, MTR reveals “another aspect of the disease that might be extremely important, especially as we move from drugs that are stopping the inflammation to drugs that are promoting remyelination,” he says. Meanwhile, magnetic resonance spectroscopy uses standard MRI scanners to detect other molecules, such as N-acetyl aspartate (NAA), choline, or creatine. But one downside of spectroscopy and MTR, Sicotte says, is that they require a fair amount of postprocessing data analysis, which radiologists usually don’t have time for in the clinic. Other types of imaging technology are also emerging. Correlations with tissue pathology and long-term studies are needed to confirm the meaning and prognostic significance of these measures—which take considerable time and money. Instead of a “free-for-all” where everybody is racing to pursue the hottest new methods without pausing to do a thorough assessment of their utility, MS imaging leaders should identify the most promising MRI techniques and then validate them, Greenberg says. National Multiple Sclerosis Society to get uniform imaging protocols into clinical trials, so that MRI results can be gathered and pooled across different studies for analysis. Indeed, inconsistencies in MRI data gathering have challenged the imaging field because scan acquisition isn’t identical from site to site, even within a multicenter clinical study that uses a single MRI analysis center. To fully exploit MRI’s potential as a screening and prognostic tool would require a major effort to standardize equipment, acquisition protocols, and image-analysis software across manufacturing vendors, says Daumer of the Sylvia Lawry Centre. National Multiple Sclerosis Society, and the Multiple Sclerosis Society of Canada, with funding from Bayer Schering Pharma (Barkhof et al., 2012). In the United States, the Common Data Elements (CDE) Project—sponsored by NINDS—aims to establish standards for collecting data in clinical studies of neurologic diseases. But standardizing an imaging approach might “fossilize” it before it has fully evolved—which could mean losing an opportunity to learn new things, says Wolinsky, chair of the imaging subgroup for the MS CDEs.
Such potential conflicts of interest have become common across the clinical research world, which continues to grapple with them. A second trend will be a move toward assessing gray-matter damage in routine clinical imaging. To fathom how the affliction manifests itself in patients, he says, researchers must consider imaging findings along with genetic, environmental, and other factors. MRI technology has transformed the practice of medicine for MS in accelerating diagnoses and helping to inform some treatment decisions, but it “doesn’t show us everything, and sometimes it shows us things that are not important,” says UT Southwestern’s Greenberg.
Recent advances in MRI techniques have allowed better detection of damage in gray matter and the spinal cord. Do abnormalities in those areas correlate better with clinical status?In a paradigm shift, research has shown that MS is not merely a white-matter disease; gray-matter damage in the cortex is also often extensive.
Can these quantitative methods provide reliable measures of the amounts of myelin loss or nerve damage?Differences in how MRI scans are acquired and analyzed create challenges in pooling and assessing data from different clinical studies and drug trials.
What standards should be set for MRI protocols and image-analysis software in research to allow for meaningful comparisons among data sets?MS is a complex disease that appears to be influenced by numerous genetic and environmental factors, including key immune-system genes and vitamin D levels.
How do these factors correlate with MRI measures of MS activity, and what might that reveal about mechanisms of the disease? Image creditsThumbnail image on landing page. Courtesy of Daniel Reich, NINDS. Conflict-of-Interest Disclosures as of February 2012The following is a list, not necessarily complete, of recent industry-related disclosures for experts interviewed for this MS Discovery Forum News Synthesis article, as reported in their research publications. MS Discovery Forum is funded with a grant from EMD Serono, an affiliate of Merck KGaA, to Massachusetts General Hospital. The forum operates completely independently of its funders, who have no influence over the site's content or operations. Rohit Bakshi of Brigham and Women's Hospital has received consulting fees from Biogen Idec, Novartis, Questcor, and Teva Neuroscience. He has received research support from Biogen, EMD Serono, and Teva Neuroscience. Martin Daumer is scientific director of the Sylvia Lawry Centre and a managing director of Trium Analysis Online GmbH.
He has received research grant support from Bayer Schering Pharma. Douglas Goodin has received fees from Merck Serono, Novartis, Berlex Laboratories, Bayer Pharmaceuticals Corporation, Biogen Idec, Schering AG, and Teva Neuroscience for speaking, consulting, and work on clinical trials.
He has received research support from Bayer HealthCare and Novartis. Benjamin Greenberg of the University of Texas Southwestern Medical Center has received honoraria or consulting fees from Biogen Idec, EMD Serono, Sanofi-Aventis Pharmaceuticals, and Teva Neuroscience. He holds ownership interest in Roche and Novartis. Robert Naismith of Washington University in St.
He has consulted for or received speaker fees from Acorda Therapeutics, Actelion Pharmaceuticals, Bayer HealthCare, Biogen Idec, EMD Serono, Facet Biotech, Hoffmann-LaRoche, Novartis, Peptimmune, Pfizer, Sanofi-Aventis, Serono Symposia International Foundation, Teva Neuroscience, and Teva Pharmaceuticals. Wolinsky has received research or contractual support from Sanofi-Aventis and the NIH as principal investigator of a subcontract to UTHSCH for image analysis in MS drug trials.
He also receives royalties from Millipore (Chemicon) for monoclonal antibody technology. Robert Zivadinov of the University at Buffalo School of Medicine and Biomedical Sciences has consulted for or received speaker honoraria from Biogen Idec, EMD Serono, Genzyme, Questcor, and Teva Neuroscience.

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