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Scientists are focusing on a new concept in fighting airborne pathogens by manipulating what is called the “switching time,” the point at which a highly regulated immune response gives way to powerful cells that specialize in fighting a specific invading bug.

In the case of tuberculosis, Ohio State University researchers are using mathematical modeling to determine whether a change to the natural switching time would result in a more effective immune response. They also are analyzing which parts of the immune response are most important to striking a balance between properly timing the switch and completing the task at hand – killing the microbe.

The complex modeling takes into account the huge assortment of cells and molecules at work in the human immune response to Mycobacterium tuberculosis, the microbe that causes TB. The response to all airborne pathogens is particularly complicated because it takes place in the highly protective environment of the lung. Human lungs are programmed to minimize immune responses as a way to avoid inflammation, which could interfere with breathing.

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A low dose of oral interferon alpha shows promise in preserving beta cell function for patients with newly diagnosed type 1 diabetes, or juvenile diabetes, according to researchers at The University of Texas Medical School at Houston.

The results of the Phase II trial are published today in Diabetes Care, a journal of the American Diabetes Association.

“It shows a strong trend in preserving insulin-producing beta cell function that is significantly better than placebo,” said Staley Brod, M.D., principal investigator of the trial, which includes the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). “It can extend the ‘honeymoon phase’ of the disease, allowing the body to still produce insulin from beta cells, which correlates with decreased complication rates.”

As many as 3 million Americans may have type I diabetes, formerly called juvenile diabetes, according to the Juvenile Diabetes Research Foundation International. Each year, 15,000 children are diagnosed with the autoimmune disease, in which the pancreas stops producing the insulin needed to transfer glucose from the blood to cells for energy. The result is too much glucose in the blood, which can lead to kidney failure, blindness, nerve damage, amputations, heart attack and stroke.

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Hoping to prevent ear infections for the more than 15 million children in the United States who suffer from them, a promising new vaccine candidate to prevent middle ear infections (otitis media) is being developed by researchers at the Columbus Children’s Research Institute (CCRI) on the campus of Columbus Children’s Hospital.

According to Lauren Bakaletz, PhD, director of the CCRI Microbial Pathogenesis Center, a faculty member of The Ohio State University College of Medicine and Public Health, and the principle investigator for the CCRI vaccine, the CCRI researchers recently partnered with the National Institutes for Health (NIH), the Food and Drug Administration (FDA), pharmaceutical companies and other scientists in an effort to expedite the process of developing what they believe is a long-overdue vaccine for ear infections.

“An alliance of this nature has not been formed since the development of the pertussis vaccine for whooping cough,” said Bakaletz.  “Through the collaboration, human trials of a vaccine candidate are expected to begin within a year.”

Inner ear infections are the number one reason young children see their pediatricians, present to emergency departments, require surgery and lose their hearing. Further, it’s the number one reason physicians prescribe antibiotics—a growing concern because antibiotic resistance in children will make treating ear and other infections more difficult in the future.  A vaccine to prevent ear infections could alleviate these problems.

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A UCSF study for the treatment of heart failure after heart attack found that the extract derived from bone marrow cells is as effective as therapy using bone marrow stem cells for improving cardiac function, decreasing the formation of scar tissue and improving cardiac pumping capacity after heart attack.

Findings were published online and in the July 2009 issue of the Journal of Molecular Therapy. The cover of the journal features a microscope image of cells from the UCSF study.

The studies were done in mice using a novel stem cell delivery method developed by UCSF researchers to show that the extract from bone marrow cells is as beneficial to cardiac function as are intact, whole cells.  Both the cell and cell extract therapies resulted in the presence of more blood vessels and less cardiac cell death, or apoptosis, than no therapy.  The study also showed that heart function benefitted despite the finding that few of the injected cells remained in the heart at one month after therapy.

“Peer-reviewed medical literature is controversial as to whether bone marrow cells differentiate into cardiomyocytes, or cardiac muscle cells, but there is general agreement that stem cell therapy with these cells results in some level of functional improvement after a heart attack. The exact mechanism for this is not yet clear. Our results confirm that whole cells are not necessarily required in order to see the beneficial effects of bone marrow cell therapy,” said Yerem Yeghiazarians, MD, study author, cardiologist and director of UCSF’s Translational Cardiac Stem Cell Development Program.

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A new computer model developed at MIT can help solve a problem that has plagued drug companies trying to develop promising new treatments made of antibodies: Such drugs have a relatively short shelf life because they tend to clump together, rendering them ineffective.

Antibodies are the most rapidly growing class of human drugs, with the potential to treat cancer, arthritis and other chronic inflammatory and infectious diseases. About 200 such drugs are now in clinical trials, and a few are already on the market.

Patients can administer these drugs to themselves, but this requires high doses – and the drugs must therefore be stored at high concentrations. However, under these conditions the drugs tend to clump, or aggregate. Even if they are stored at lower concentrations and administered by a doctor intravenously, they often have stability issues. Addressing such issues typically takes place later in the drug development process, and the cost – both in time and money – is often high.

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The influenza virus that wreaked worldwide havoc in 1918-1919 founded a viral dynasty that persists to this day, according to scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. In an article published online on June 29 by the New England Journal of Medicine, authors Anthony S. Fauci, M.D., Jeffery K. Taubenberger, M.D., Ph.D., and David M. Morens, M.D., argue that we have lived in an influenza pandemic era since 1918, and they describe how the novel 2009 H1N1 virus now circling the globe is yet another manifestation of this enduring viral family.

“The 1918-1919 influenza pandemic was a defining event in the history of public health,” says NIAID Director Dr. Fauci. “The legacy of that pandemic lives on in many ways, including the fact that the descendents of the 1918 virus have continued to circulate for nine decades.”

Influenza viruses have eight genes, two of which code for virus surface proteins—hemagglutinin (H) and neuraminidase (N)—that allow the virus to enter a host cell and spread from cell to cell. There are 16 H subtypes and 9 N subtypes, and, therefore, 144 possible HN combinations. However, only three (H1N1, H2N2 and H3N2) have ever been found in influenza viruses that are fully adapted to infect humans. Other combinations, such as avian influenza H5N1, occasionally infect people, but they are bird viruses, not human viruses.

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Medical scientists at the University of Leicester are investigating how signalling molecules known to control blood pressure and penile erection act to regulate brain function and which have potential for treatments of migraine, chronic pain, epilepsy and Alzheimer’s disease.

The study in the MRC Toxicology Unit at the University of Leicester is being funded by the Medical Research Council (MRC).
The team is interested in the action of the molecule Nitric Oxide – made famous when it was discovered that its action could be exploited in the treatment of erectile dysfunction, notably by pharmaceutical drugs such as Viagra or Cialis.

The Leicester research is exploring how brain cells communicate by examining the junctions between brain cells – termed the “synapse”. The group, ‘Neurotoxicity at the Synapse’, led by Professor Ian Forsythe in the MRC Toxicology Unit, is interested in the action of Nitric Oxide at these synapses.

Researcher Adam Tozer said: “The brain is a communication station and understanding how the cells ‘talk’ to each other will help in the treatment of neurodegenerative disease.

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Stimulant medications, such as Ritalin and Adderall, are the accepted treatment to stem hyperactivity in children with attention deficit-hyperactive disorder (ADHD) and improve their behavior.

Now a recent review of research by University at Buffalo pediatric psychologists suggests that such medication, or the assumption of medication, may produce a placebo effect — not in the children, but in their teachers, parents or other adults who evaluate them.

A placebo effect is a positive change in symptoms or behavior after a patient receives a “fake” medication or procedure; in other words, the belief can become the medicine. In this case, the review suggested that when caregivers believed their ADHD patients were receiving ADHD medication, they tended to view those children more favorably and treat them more positively, whether or not medication was actually involved.

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The pharmaceutical company Pfizer is concealing data on the effect of a drug (Edronax® containing the agent reboxetine) for the treatment of depression. Despite repeated requests by the Institute for Quality and Efficiency in Health Care (IQWiG), Pfizer has refused to provide a complete list of all published and unpublished trials on reboxetine. The Institute discovered through its own literature search that the drug approved in Germany has been tested in at least 16 trials. However, in 9 of these 16 trials, key information is missing that would enable an evaluation of reboxetine’s performance.

According to Peter T. Sawicki, IQWiG’s Director, “By concealing study data, the manufacturer is depriving patients and doctors of the opportunity to make an informed decision on different therapy options.” Furthermore, it hinders the work of institutions such as IQWiG. IQWiG’s aim is to draw reliable conclusions concerning the benefit and harm of drugs.

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The risk of cancer possibly increases if patients with diabetes use the long-acting insulin analogue glargine instead of human insulin. The Institute for Quality and Efficiency in Health Care (IQWiG), in collaboration with the “Wissenschaftliches Institut der AOK” (WIdO), the research institute of the German Local Health Care Fund, analysed the data of almost 130,000 patients with diabetes in Germany who had been treated with either human insulin or the insulin analogues lispro (trade name: Humalog), aspart (Novorapid) or glargine (Lantus) between January 2001 and June 2005.

The analysis has now been published together with further studies in the scientific journal Diabetologia, the official organ of the European Association for the Study of Diabetes (EASD). The disturbing result is that malignancies were found more frequently in patients treated with glargine than in those prescribed a comparable dose of human insulin. “Our analysis does not provide absolute proof that glargine promotes cancer,” says Peter T. Sawicki, IQWiG’s Director and co-author of the study. “Our study does, however, arouse an urgent suspicion which should have consequences for the treatment of patients.”

No difference was found between the short-acting insulin analogues, lispro and aspart, and human insulin. Insulin analogues are synthetic molecules that do not occur naturally, whereas human insulin matches the insulin that the human body manufactures itself.

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