Indoor Tanning: The Risks of Ultraviolet Rays

Theres no such thing as a safe tan. Regardless of the source, UV rays pose a health risk. Learn more at http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm186687.htm

Published by: USFoodandDrugAdmin

DIA 2012 Annual Meeting: Collaborate to Innovate

DIA 2012 is the premier global event that brings together more than 8,000 global professionals who are involved in every aspect of the discovery, development, and life cycle management of pharmaceuticals, biotechnology, medical devices, and related products.

Published by: DrugInfoAssoc

Generics, Pseudo-Generics and the Race for Consumer Dollars

 

Author: Saaqshi Sharma

The release of pseudo-generics or ‘fake’ generic drugs is common practice in Canada. This allows drug developers to maintain market share over a niche market of drug consumers, but also challenges generic companies’ ability to compete in the industry.

According to Health Canada Regulations, generic drugs have the same active pharmaceutical ingredients (APIs) and therapeutic effects as the corresponding brand name drugs, and differ only in their non-medicinal ingredients (aka excipients). Generic drugs sell at a fraction of the price of brand name drugs because they do not bear the extreme financial burden of extensive research and development phases, clinical trials, and brand marketing.

Generic drugs were first implemented following the Hatch-Waxman Act in 1984 which allowed generic drug manufactures to produce drug products with less fear of litigation from the drug’s innovators. This can only take place after the drug patent for the active ingredients has expired. Since the drug development process can take over 15 years from the original idea to the final drug product, drugs that have been approved by Health Canada and the FDA are awarded a 20 year patent that provides the manufacturer exclusive rights to sell the drug. This gives the innovator time to have sole marketing rights to their product, referred to as market exclusivity, and hopefully make back some of the money they have spent over the phases of research and development before other companies can enter the market with a generic version. When a drug patent expires all other companies are free to produce their own generic versions.

Patents can be extended when new uses for the drug are presented. Drug companies often scramble to find such indications so that they can extend their patent life and as a result be the sole providers of the drug for a longer amount of time. Competing companies similarly move quickly to release generic versions of drugs with closing patents in order capitalize on consumers looking for generic alternatives. In another attempt to maintain their market exclusivity, manufacturers of the brand name drug will release pseudo-generics which are identical to the brand name drug and manufactured on the same production line, but marketed and sold under a different name. Basically it is a ‘generic drug’ that is being produced by the brand name company.

This way, manufacturers can move quickly to infiltrate the generic drug market with little to no competition before the actual generic companies even have time to produce their products. This is beneficial for consumers who can get the same drug for 20-90% of its original cost. On the other hand, it is discouraging for competing generic companies because the market is already saturated with both the brand name drug and the pseudo-generic drugs, both made by the same company.

As a result there is a divide between innovation and competition. Innovator drug companies strive to maintain their market share and recoup costs associated with the development process; and generic companies fight to remain competitive in the industry.

 

Credits: Saaqshi Sharma  Canadian Centre for Clinical Trials

Paralyzed individuals use thought-controlled robotic arm to reach and grasp

 

NIH-funded study shows progress in brain-computer interface technology

In an ongoing clinical trial, a paralyzed woman was able to reach for and sip from a drink on her own – for the first time in nearly 15 years – by using her thoughts to direct a robotic arm. The trial, funded in part by the National Institutes of Health, is evaluating the safety and feasibility of an investigational device called the BrainGate neural interface system. This is a type of brain-computer interface (BCI) intended to put robotics and other assistive technology under the brain's control.

A report published today in Nature describes how two individuals — both paralyzed by stroke — learned to use the BrainGate system to make reach-and-grasp movements with a robotic arm, as part of the BrainGate2 clinical trial. The report highlights the potential for long-term use and durability of the BrainGate system, part of which is implanted in the brain to capture the signals underlying intentional movement. It also describes the most complex functions to date that anyone has been able to perform using a BCI.

For the woman, it was the first time since her stroke that she was able to sip a drink without help from a caregiver.

"The smile on her face was a remarkable thing to see. For all of us involved, we were encouraged that the research is making the kind of progress that we had all hoped," said the trial's lead investigator, Leigh Hochberg, M.D., Ph.D., who is an associate professor of engineering at Brown University in Providence, R.I. and a critical care neurologist at Massachusetts General Hospital (MGH)/Harvard Medical School in Boston.

"Years after the onset of paralysis, we found that it was still possible to record brain signals that carry multi-dimensional information about movement and that those signals could be used to move an external device," Dr. Hochberg said.

He noted that the technology is years away from practical use and that the trial participants used the BrainGate system under controlled conditions in their homes with a technician present to calibrate it.

The BrainGate neural interface system consists of a sensor to monitor brain signals and computer software and hardware that turns these signals into digital commands for external devices. The sensor is a baby aspirin-sized square of silicon containing 100 hair-thin electrodes, which can record the activity of small groups of brain cells. It is implanted into the motor cortex, a part of the brain that directs movement.

"This technology was made possible by decades of investment and research into how the brain controls movement. It’s been thrilling to see the technology evolve from studies of basic neurophysiology and move into clinical trials, where it is showing significant promise for people with brain injuries and disorders," said Story Landis, Ph.D., director of NIH's National Institute of Neurological Disorders and Stroke (NINDS). The institute funds BCI research in hopes of restoring function and improving quality of life for people coping with limb amputations or paralysis from spinal cord injury, stroke or neuromuscular disorders.

NIH has supported basic and applied research in this area for more than 30 years. In 2009 and 2010, an additional $3.8 million in NIH funding was made possible through the Recovery Act.

The latest analysis from the BrainGate2 trial focused on two participants — a 58-year-old woman and a 66-year-old man. Both individuals are unable to speak or move their limbs because of brainstem strokes they had years ago — the woman's in 1996 and the man's in 2006. In the trial, both participants learned to perform complex tasks with a robotic arm by imagining the movements of their own arms and hands.

In one task, several foam targets were mounted on levers on a tabletop and programmed to pop up one at a time, at different positions and heights. The participants had less than 30 seconds to grasp each target using the DEKA Arm System (Generation 2), which is designed to work as a prosthetic limb for people with arm amputations. One participant was able to grasp the targets 62 percent of the time, and the other had a 46 percent success rate.

This YouTube video describes how two trial participants were able to use the BrainGate system to make complex reach-and-grasp movements with a robotic arm, simply by imagining they were using their own arms. Credit: The BrainGate Collaboration.

In some sessions, the woman controlled a DLR Light-Weight Robot III arm, which is heavier than the DEKA arm and designed to be used as an external assistive device. She used this arm prior to the DEKA arm in the foam target task, and had a success rate of 21 percent. In other sessions with the DLR arm, her task was to reach for a bottled drink, bring it to her mouth and sip from a straw. She was able to complete four out of six attempts.

This is not the first glimmer of hope from human BCI research. Participants in the BrainGate trial and other studies have also used BCI technology to perform point-and-click actions with a computer cursor, a level of control that has been used for communication.

"This is another big jump forward to control the movements of a robotic arm in three-dimensional space. We’re getting closer to restoring some level of everyday function to people with limb paralysis," said John Donoghue, Ph.D., who leads the development of BrainGate technology and is the director of the Institute for Brain Science at Brown University.

Dr. Donoghue said the woman's ability to use the BrainGate was especially encouraging because her stroke occurred nearly 15 years ago and her sensor was implanted more than five years ago. Some researchers have wondered whether neurons in the motor cortex might die or stop generating meaningful signals after years of disuse. Researchers in the field have also worried that years after implantation, the sensor might break down and become less effective at enabling complex motor functions.

Roderic Pettigrew, M.D., Ph.D., director of NIH's National Institute of Biomedical Imaging and Bioengineering (NIBIB), which supports the research, indicated that the technology is promising, but at present is still undergoing development and evaluation. "The researchers have begun the long, difficult process of testing and refining the system with feedback from patients, and they've found that it is possible for a person to mentally control a robotic limb in three-dimensional space. This represents a remarkable advance," he said.

As the trial continues, the BrainGate research team needs to test the technology in more individuals, they said. They envision a system that would be stable for decades, wireless and fully automated. For now, the sensor — and therefore the user — must be connected via cables to the rest of the system. Prior to each session with the robotic arms, a technician had to perform a calibration procedure that lasted 31 minutes on average. Improvements are also needed to enhance the precision and speed of control. In the foam target task, for example, a successful reach-and-grasp motion typically took almost 10 seconds.

The ultimate goal for helping people with paralysis is to reconnect the brain directly to paralyzed limbs rather than robotic ones, the researchers said. In the future, the BrainGate system might be used to control a functional electrical stimulation (FES) device, which delivers electrical stimulation to paralyzed muscles. Such technology has shown promise in monkeys. The Eunice Kennedy Shriver National Institute for Child Health and Human Development (NICHD) has long supported the clinical trial research for BrainGate, with the goal of enabling mental control of an FES system for limb movement. In previous reports from the BrainGate2 trial, a participant was able to use the BrainGate system to direct the movements of a virtual, computer-animated arm designed to simulate FES control of a real arm.

To support this research, NIH has worked closely with the Department of Veterans Affairs (VA) and the Defense Advanced Research Projects Agency (DARPA), the research arm of the Department of Defense. DARPA supports development of the DEKA arm. Development of the DLR arm is funded by the German aerospace agency DLR. NIH has supported the fundamental neuroscience and BCI development, and the clinical research in collaboration with the VA. Drs. Hochberg and Donoghue hold research positions with the Providence VA Medical Center.

Dr. Donoghue is supported by a Javits Neuroscience Investigator award (NS025074) from NINDS, and by a grant (EB007401) from NIBIB and NICHD. The research is also supported by contracts (HD53403, HD100018) from NICHD's National Center for Medical Rehabilitation Research to Robert Kirsch, Ph.D., at Case Western Reserve University, Cleveland. Additional support came from an NIH Challenge grant (HD063931) to Dr. Donoghue and a grant (DC009899) from the National Institute on Deafness and other Communication Disorders (NIDCD) to Dr. Hochberg, which were funded all or in part through the Recovery Act.

The BrainGate trial began in 2004 and was run by Cyberkinetics Inc., in collaboration with Brown University and MGH. NICHD began funding the trial in 2005. After Cyberkinetics withdrew from the research for financial reasons, funding continued through this NICHD contract, MGH became the clinical trial and administrative lead, and the trial was renamed BrainGate2. The trial is currently recruiting. For more information, visit:http://www.clinicaltrials.gov/ct2/show/NCT00912041 or http://www.braingate2.org.

NIBIB (http://www.nibib.nih.gov) is dedicated to improving health by bridging the physical and biological sciences to develop and apply new biomedical technologies.

NICHD (http://www.nichd.nih.gov) sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation.

NIDCD (http://www.nidcd.nih.gov) supports and conducts research and research training on the normal and disordered processes of hearing, balance, taste, smell, voice, speech and language and provides health information, based upon scientific discovery, to the public.

NINDS (http://www.ninds.nih.gov) is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease — a burden borne by every age group, by every segment of society, by people all over the world.

Source:NIH

NIH study finds that coffee drinkers have lower risk of death

 

Older adults who drank coffee — caffeinated or decaffeinated — had a lower risk of death overall than others who did not drink coffee, according a study by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, and AARP.

Coffee drinkers were less likely to die from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections, although the association was not seen for cancer. These results from a large study of older adults were observed after adjustment for the effects of other risk factors on mortality, such as smoking and alcohol consumption. Researchers caution, however, that they can't be sure whether these associations mean that drinking coffee actually makes people live longer. The results of the study were published in the May 17, 2012 edition of the New England Journal of Medicine.

Neal Freedman, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and his colleagues examined the association between coffee drinking and risk of death in 400,000 U.S. men and women ages 50 to 71 who participated in the NIH-AARP Diet and Health Study. Information about coffee intake was collected once by questionnaire at study entry in 1995-1996. The participants were followed until the date they died or Dec. 31, 2008, whichever came first.

The researchers found that the association between coffee and reduction in risk of death increased with the amount of coffee consumed. Relative to men and women who did not drink coffee, those who consumed three or more cups of coffee per day had approximately a 10 percent lower risk of death. Coffee drinking was not associated with cancer mortality among women, but there was a slight and only marginally statistically significant association of heavier coffee intake with increased risk of cancer death among men.

"Coffee is one of the most widely consumed beverages in America, but the association between coffee consumption and risk of death has been unclear. We found coffee consumption to be associated with lower risk of death overall, and of death from a number of different causes," said Freedman. "Although we cannot infer a causal relationship between coffee drinking and lower risk of death, we believe these results do provide some reassurance that coffee drinking does not adversely affect health."

The investigators caution that coffee intake was assessed by self-report at a single time point and therefore might not reflect long-term patterns of intake. Also, information was not available on how the coffee was prepared (espresso, boiled, filtered, etc.); the researchers consider it possible that preparation methods may affect the levels of any protective components in coffee.

"The mechanism by which coffee protects against risk of death — if indeed the finding reflects a causal relationship — is not clear, because coffee contains more than 1,000 compounds that might potentially affect health," said Freedman. "The most studied compound is caffeine, although our findings were similar in those who reported the majority of their coffee intake to be caffeinated or decaffeinated."

The National Cancer Institute (NCI) leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI Web site at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

Source: NIH

FDA approves generic versions of blood thinner Plavix

For Immediate Release: May 17, 2012

The U.S. Food and Drug Administration today approved generic versions of the blood thinning drug Plavix (clopidogrel bisulfate), which helps reduce the risk of heart attack and stroke by making it less likely that platelets in the blood will clump and form clots in the arteries.

Clopidogrel is FDA-approved to treat patients who have had a recent heart attack or a recent stroke, or have partial or total blockage of an artery (peripheral artery disease).

“For people who must manage chronic health conditions, having effective and affordable treatment options is important,” said Keith Webber, Ph.D., deputy director of the Office of Pharmaceutical Science in the FDA’s Center for Drug Evaluation and Research. “The generic products approved today will expand those options for patients.”

Clopidogrel has a boxed warning to alert health care professionals and patients that the drug may not work well for those with certain genetic factors that affect how the body metabolizes the drug. Patients can be tested for these genetic factors to ensure that clopidogrel is the right choice for them. Also, certain medicines, such as proton pump inhibitors Prilosec (omeprazole) and Nexium (esomeprazole), reduce the effect of clopidogrel, leaving a person at greater risk for heart attack and stroke.

Clopidogrel may cause bleeding, which can be serious and sometimes lead to death. While taking the drug, people may bruise and bleed more easily, be more likely to have nose bleeds, and it may take longer for all bleeding to stop. Clopidogrel is dispensed with a patient Medication Guide that provides important instructions on its use and drug safety information.

Dr. Reddy's Laboratories, Gate Pharmaceuticals, Mylan Pharmaceuticals, and Teva Pharmaceuticals have gained FDA approval for 300 milligram (mg) clopidogrel. Apotex Corporation, Aurobindo Pharma, Mylan Pharmaceuticals, Roxane Laboratories, Sun Pharma, Teva Pharmaceuticals, and Torrent Pharmaceuticals have received approval for 75 mg clopidogrel.

Generic drugs approved by FDA are of the same high quality and strength as brand-name drugs. The generic manufacturing and packaging sites must pass the same quality standards as those for brand-name drugs.

Information about the availability of generic clopidogrel can be obtained from the manufacturers.

For more information:

FDA: Understanding Generic Drugs

Source: FDA

The meaning of life at the cellular level: detecting apoptosis with fluorescence

In this webinar, experts from Life Technologies will demonstrate several solutions using fluorescent probes to study key components of the apoptotic machinery.

Webinar Details

We will provide you with:

• An overview of the features of apoptosis
• Key parameters that can be measured to assay apoptosis
• A comprehensive guide to available labeling and detection technologies for apoptosis research
• Tips and tricks to best implement those technologies

Register for the webinar session that is convenient for you:

Session 1:

• North America: May 24, 2012 at 10:00 am EDT (7:00 am PDT)
• Europe: May 24, 2012 at 2:00 pm GMT
• Bangalore: May 24, 2012 at 7:30 pm IST

Session 2:

• North America: May 24, 2012 at 7:00 pm EDT(4:00 pm PDT)
• Beijing: May 25, 2012 at 7:00 am CST
• Singapore: May 25, 2012 at 7:00 am SGT
• Sydney: May 25, 2012 at 9:00 am EST

Source: www.lifetechnologies.com

Uncovering the Molecular Basis of Learning and Memory

 

Researchers have developed a way to pinpoint the molecules involved in forming a specific memory. The finding, in genetically engineered mice, gives scientists new insight into how memories are formed.

Newly synthesized proteins (green) traveled to mushroom-shaped spines in mouse hippocampus neurons. Researchers believe this process is key to strengthening a memory. Images after 1 (left), and 6 (right) hours of fear conditioning. Image courtesy of Drs. Mark Mayford and Naoki Matsuo, Scripps Research Institute.

For a memory to last long-term, the neural connections holding it need to be strengthened by incorporating new proteins. Some researchers have proposed that an experience creates a molecular “tag” at activated synapses, the connections between neurons. The tag allows synapses to capture newly made proteins and thus solidify a memory. But the molecular details of the process have been a mystery.

Previous studies suggested that proteins called AMPA-type glutamate receptors (AMPARs) strengthen memories by becoming part of the synapses that encode new memories. Drs. Mark Mayford and Naoki Matsuo of the Scripps Research Institute, supported in part by NIH's National Institute of Mental Health (NIMH), decided to explore the proteins further. They genetically engineered a strain of mice to make AMPARs that could be traced by their green glow.

The transgenic mice were taught to associate a specific environment with a foot shock, a process known as fear conditioning. This brief training produces a long-lasting memory that requires the brain’s hippocampus region. After fear conditioning had triggered new AMPARs deep in the neuron's nucleus, the researchers tracked where the newly made proteins went.

In the February 22, 2008, issue of the journal Science, the researchers reported that the newly synthesized AMPARs travel to and become captured by only certain hippocampus synapses—presumably the ones holding the new memory—within hours.

Synaptic connections are made onto small nubs on the neuron called spines. These spines come in 3 different shapes called thin, stubby and mushroom. The researchers found that the synapses receiving the new AMPARs were limited to the mushroom type.

The mushroom spines also figured prominently in the same neurons when fear conditioning was reversed by repeatedly exposing the animals to the feared situation without getting shocked—a procedure called extinction learning. This result shows that the same neurons activated when a fear is learned are also deactivated when it is lost.

The surge of receptors in mushroom spines appeared within hours of learning, suggesting that when mice learn something new, there are changes in some mushroom spines that allow them to capture newly synthesized AMPARs. The receptor surge was gone within 3 days, however, so other changes likely solidify the memory for the long term.

"Remarkably, this research demonstrates a way to untangle precisely which cells and connections are activated by a particular memory," said NIMH Director Dr. Thomas Insel. "We are actually learning the molecular basis of learning and memory."

Source: NIH

What is Type 1 Diabetes?

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Protease Inhibitors for Recurrent Hepatitis C after Liver Transplantation- When Less is More

^*Corresponding author:
Dr. Sandeep Mukherjee
Section of Gastroenterology and Hepatology
Nebraska Medical Center
Omaha, NE 68198-3285, USA
E-mail: smukherj@unmc.edu

Citation: Mukherjee S (2012) Protease Inhibitors for Recurrent Hepatitis C after Liver Transplantation-When Less is More. J Antivir Antiretrovir 4: i-i. doi:10.4172/ jaa.1000e101

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The approval of boceprevir and telaprevir, two protease inhibitors for hepatitis C (HCV) treatment earlier this year, was met with virtually universal optimism as the addition of these medications will lead to a significantly improved chance of viral eradication in HCV genotype 1 patients [1]. However, this enthusiasm is yet to be embraced by the liver transplant community primarily due to the interaction between protease inhibitors and calcineurin inhibitors such as cyclosporine and tacrolimus. Boceprevir and telaprevir inhibit cytochrome P450 3A which metabolizes cyclosporine and tacrolimus leading to elevated and potentially lethal levels of these calcineurin inhibitors [2,3].

This was confirmed in an important phase I, open-label randomized, single sequence study earlier this year by Garg et al. [4] which merits further review. In part A of the study, ten healthy volunteers were administered a single 100mg oral dose of cyclosporine followed by an 8 day washout period before they were administered a single 10mg dose of cyclosporine and either a single dose of telapervir 750 mg or steadystate teleparevir 750mg every 8 hours. In part B, ten volunteers were administered a single dose of tacrolimus 0.5mg followed by a 14 day wash-out period before they were administerd a single 0.5mg dose of tacrolimus with telaprevir 750mg every 8 hours. Blood samples were obtained throughout the study for pharmacokinetic assessment and analysis. The investigators reported that co-administration of telaprevir with cyclosporine and tacrolimus, respectively, led to increased cyclosporine by 4.6 fold and tacrolimus by 70 fold, levels that are toxic and life-threatening.

This important study has confirmed the concerns of many transplant hepatologists. Despite the study’s findings, there were some important limitations, notably that it was conducted in healthy volunteers and not in liver transplant recipients with recurrent HCV. Extrapolating these results to a different patient population may be hard to justify. However, it seems more rather than less likely that HCV protease inhibitors should be prescribed with extreme caution in transplant patients-not only may drug metabolism be different from healthy volunteers but transplant recipients are also exposed to a variety of other medications that may interact with protease inhibitors independent of calcineurin inhibitors.

The concerns with HCV protease inhibitors were eloquently outlined by Michael Charlton, MD in an accompanying editorial this year [5]. Before we prescribe these medications, we need to inform patients and their families the following:

(a) Treatment is experimental as there are no studies in liver transplant patients

(b) Side effects may include organ failure and death from severe calcineurin toxicity

(c) Hepatic allograft rejection is a possibility as the dose and frequency for either calcineurin inhibitor has yet to be established

(d) Drug-Drug interactions between protease inhibitors and other medications used in transplant recipients are not fully recognized

(e) Only physicians well-versed with the management of liver transplant recipients and drug-drug interactions should care for these patients

(f) Treatment should only be reserved for patients with aggressive histological evidence of recurrent HCV in an attempt to prevent retransplantation [6].

Until the appropriate randomized trials are performed, transplant physicians should be extremely wary of prescribing these medications for patients with recurrent HCV. Human nature is such that it is inevitable that these medications will be used (or already have), in some cases probably appropriately as in patients where retransplantation or even re-retransplantation is to be avoided or contraindicated. Under these circumstances, adhering to the above check-list may lessen morbidity and mortality in this vulnerable group of patients.

References

1. Ferenci P, Reddy KR (2011) Impact of HCV protease-inhibitor-based triple therapy for chronic HCV genotype1 infection. Antivir Ther 16: 1187-1201.
2. Boceprevir (Victrelis) US Package Insert 2011.
3. Telaprevir (Incivek) US Package Insert 2011.
4. Garg V, Van Heeswijk R, Eun Lee J, Alves K, Nadkarni A, et al. (2011) Effect of telaprevir on the pharmacokinetics of cyclosporine and tacrolimus. Hepatology 54: 20-27.
5. Charlton M (2011) Telaprevir, boceprevir, cytochrome P450 and immunosuppressive agents-a potentially lethal cocktail. Hepatology 54: 3-5.
6. Limaye A, Firpi RJ (2011) Management of recurrent hepatitis C after liver transplantation. Clin Liv Dis 15: 845-858.