An enzyme (protein) found in a “Superbug” found in United Kingdom and other parts of the world is now famed as joining the ranks of the deadly Methicillin-Resistant Staphylococcus Aureus (MRSA) and has scientist worried.  The New Delhi Metallo-beta-lactamase (NDM-1) is an enzyme that gets embedded into a bacteria and makes it so powerful of a bug that it becomes resistant to the latest antibiotics, including Carbapenem.  Regardless of whether the Indian government can admit that this Superbug originated from that country, it is now reported that the bug is found in several countries including the United States.

The majority of cases seem to be in populations of those who have traveled to India recently.  In fact the UK’s Cardiff University has reported that approximately 17 out of the 37 cases had visited India or Pakistan when they were infected with the Superbug.

India has a booming medical tourism, predominantly consisting of plastic surgery.  Some believe that the Indian government’s recent attacks on the British scientists who claimed that the Superbug currently of concern in the UK originated in India might have a lot to do with protecting the medical tourism in that country.

The CDC issues the following statement in its Mortality and Morbidity Weekly Report (MMWR) of June 24th, 2010 about the NDM-1 enzyme:

Antimicrobial resistance in Gram-negative bacteria is a well-recognized problem, and a new resistance mechanism found in three U.S. Enterobacteriaceae could compound this challenge. This new mechanism, New Delhi Metalol-beta-lactamase (NDM-1), is linked to receipt of medical care in India or Pakistan, where it is common among enteric bacteria. NDM-1 is an enzyme that destroys many commonly used antibiotics, rendering them ineffective. It is carried on a mobile element that can readily spread to other bacteria. In order to prevent transmission of bacteria possessing NDM-1 in the U.S., CDC is alerting clinicians to be aware of NDM-1 in patients who have recently received medical care in India or Pakistan and requesting that carbapenem-resistant enteric bacteria from these patients be sent to CDC for further investigation. Also, CDC is reiterating the importance of implementing CDC recommendations to prevent the spread of these highly resistant organisms.

The underlying reason as to why (and perhaps more importantly why) some bacteria become resistant to antibiotics remains the same.  Typically, when antibiotics are overused in a population mainly because they are unregulated, the bacterial become accustomed to their mechanism of action.  This is particularly true when antibiotics are not used properly – meaning the patient discontinues them before the typical course of that drug is completed.

According to the Pulmonologist Dr. Horovitz this sort of thing isn’t really that out of the ordinary considering the moisture and the warmth inside the lungs make for perfect conditions to grow seeds!

Here is a lesson to you: chew your food well and when a seed  goes down the wrong tube, get help!

The agency is working with the drug’s manufacturer, GlaxoSmithKline, to update the prescribing information and patient medication guide to include this risk.

Aseptic meningitis has a number of causes including, but not limited to, viruses, toxic agents, some vaccines, autoimmune diseases, and certain medications, including Lamictal. Symptoms can include headache, fever, chills, nausea, vomiting, stiff neck and sensitivity to light. Hospitalization may be required.

In suspected cases of meningitis, the underlying cause should be rapidly diagnosed so that treatment can be promptly initiated. Discontinuation of Lamictal should be considered if no other clear cause of meningitis is identified.

“Aseptic meningitis is a rare but serious side effect of Lamictal use,” said Russell Katz, M.D., director of the Division of Neurology Products in the FDA’s Center for Drug Evaluation and Research. “Patients that experience symptoms should consult their health care professional immediately.”

The FDA became aware of the association between Lamictal and aseptic meningitis through routine adverse event monitoring and communications with the drug’s manufacturer. Since the drug’s approval in December 1994 through November 2009, there were 40 cases of aseptic meningitis identified in patients taking Lamictal. The symptoms were reported to occur within one to 42 days after starting Lamictal. Thirty-five of the 40 patients required hospitalization. In most cases, symptoms ended after Lamictal was discontinued. In 15 cases, symptoms, often more severe, returned when patients restarted the drug.

source: http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm222212.htm

Much of the research on overeating has focused on food’s pleasurable effects, which scientists call positive reinforcement. A team of researchers led by Dr. Pietro Cottone and Dr. Valentina Sabino at the Boston University School of Medicine and Dr. Eric Zorrilla at the Scripps Research Institute wanted to explore the role of negative reinforcement. That’s the idea that the stress of not having certain foods might drive dieters to overeat those foods once they become available.

The researchers recently found that rats given intermittent access to sugary food ate less of their normal food when the sweet food wasn’t available, and they overate the sweet food when it was available again. The scientists hypothesized that the brain’s stress system might be behind the behavior. Funded by several NIH institutes, along with the Ellison Medical Foundation and the Pearson Center for Alcoholism and Addiction Research at Scripps, the team?which included NIH researcher Dr. Kenner C. Rice?set out to investigate.

The scientists tested a drug that blocks the action of corticotropin-releasing factor (CRF), a signaling molecule involved in the brain’s response to fear, anxiety and stress. CRF has been tied to withdrawal syndromes for every major drug of abuse, including alcohol, nicotine, cocaine, opiates, amphetamines and marijuana.

The team divided 20 rats into 2 groups. One group was fed alternating diets of 5 days of regular chow and 2 days of sweet chow. The other was given only regular food. All rats could eat as much as they wanted. After 7 weeks, the rats were given the CRF-blocker.

The researchers reported on November 24, 2009, in Proceedings of the National Academy of Sciences that blocking CRF blunted the rats’ bingeing. The diet-cycled rats ate more of the regular chow and less of the sweet food when it was available. The drug had no effect on the rats eating only normal chow. The drug also blocked the diet-cycled rats’ anxious behavior when their sweet food was withdrawn, without affecting control rats.

To explore where CRF was at work, the team measured CRF levels in the central amygdala, a brain area involved in fear, anxiety and stress responses. Diet-cycled rats had significantly higher CRF levels when eating normal chow. Their levels were normal when the rats were fed sweet food. These results show that withdrawal from tasty food, at least in rats, leads to an increase in stress.

“People will often say they are eating bad foods or fail a diet because they’re stressed,” Zorrilla says. “Our findings suggest that intermittently eating sweet food changes the brain’s stress system so that you might feel stressed?In other words, you might be self-medicating stress-like symptoms of abstinence with that piece of pie.”

“The findings suggest that frequent dieting with frequent relapse is worse than dieting by itself,” Cottone says. On and off, yo-yo dieting may actually be a risky habit.

“This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties,” explained Steven McKnight, Ph.D., who co-led the research with Andrew Pieper, M.D., Ph.D., both of University of Texas Southwestern Medical Center, Dallas. “It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development.”

The researchers report on their findings July 9, 2010 in the journal Cell. Their work was funded, in part, by the NIHÂ’s National Institute of Mental Health (NIMH), a NIH DirectorÂ’s Pioneer Award (http://commonfund.nih.gov/pioneer/Profiles04/McKnight.aspx) supported through the Common Fund (http://nihroadmap.nih.gov/) and managed by the National Institute of General Medical Sciences, and National Cancer Institute.
“This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in AlzheimerÂ’s disease,” said NIMH Director Thomas Insel, M.D.

Physical activity, social, or other enriching experiences promote neurogenesis — the birth and maturation of new neurons. This growth takes place in the dentate gyrus, a key area of the brain’s memory hub, the hippocampus. But even in the normal adult brain, most of these newborn neurons die during the month it takes to develop and get wired into brain circuitry. To survive, the cells must run a gauntlet of challenges. Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer’s, marked by runaway cell death.
Photo of a mouse and a compound discovered living in mice.
The neuroprotective compound P7C3 was discovered by testing more than 1000 small molecules in living mice. Source: Andrew Pieper, M.D., Ph.D., UT Southwestern Medical Center.

In hopes of finding compounds that might protect such vulnerable neurons during this process, Pieper, McKnight and colleagues tested more than 1000 small molecules in living mice. One of the compounds, designated P7C3, corrected deficits in the brains of adult mice engineered to lack a gene required for the survival of newborn neurons in the hippocampus. Giving P7C3 to the mice reduced programmed death of newborn cells – normalizing stunted growth of branch-like neuronal extensions and thickening an abnormally thin layer of cells by 40 percent. Among clues to the mechanism by which P7C3 works, the researchers discovered that it protects the integrity of machinery for maintaining a cell’s energy level.

To find out if P7C3 could similarly stem aging-associated neuronal death and cognitive decline, the researchers gave the compound to aged rats. Rodents treated with P7C3 for two months significantly outperformed their placebo-treated peers on a water maze task, a standard assay of hippocampus-dependent learning. This was traced to a threefold higher-than-normal level of newborn neurons in the dentate gyrus of the treated animals. Rats were used instead of mice for this phase of the study because the genetically engineered mice could not swim.
Image of Rat Dentate Gyrus: Newborn Neurons
Aged rats treated with P7C3 performed significantly better on a memory test than control rats treated with an inactive substance (veh). This was traced to a three-fold higher number of newborn neurons in the dentate gyrus area of the hippocampus. Source: Andrew Pieper, M.D., Ph.D., UT Southwestern Medical Center

The researchers pinpointed a derivative of P7C3, called A20, which is even more protective than the parent compound. They also produced evidence suggesting that two other neuroprotective compounds eyed as possible Alzheimer’s cures may work through the same mechanism as P7C3. The A20 derivative proved 300 times more potent than one of these compounds currently in clinical trials for Alzheimer’s disease. This suggested that even more potent neuroprotective agents could potentially be discovered using the same methods. Following up on these leads, the researchers are now searching for the molecular target of P7C3 — key to discovering the underlying neuroprotective mechanism.

The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery and cure. For more information, visit www.nimh.nih.gov.

The NIH Common Fund encourages collaboration and supports a series of exceptionally high impact, trans-NIH programs. These new programs are funded through the Common Fund, and managed by the NIH Office of the Director in partnership with the various NIH Institutes, Centers and Offices. Common Fund programs are designed to pursue major opportunities and gaps in biomedical research that no single NIH Institute could tackle alone, but that the agency as a whole can address to make the biggest impact possible on the progress of medical research. Additional information about the NIH Common Fund can be found at http://commonfund.nih.gov.

NIGMS is a part of NIH that supports basic research to increase our understanding of life processes and lay the foundation for advances in disease diagnosis, treatment and prevention. For more information on the Institute’s research and training programs, see http://www.nigms.nih.gov.

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).

Your liver’s job is to help fight infections and clean your blood. It also helps digest food and stores energy for when you need it. People needing a liver transplant are placed on a national waiting list kept at the United Network for Organ Sharing. Their blood type, body size and severity of sickness all play a role in when they?ll receive a liver. Whole livers can come only from people who have just died. Currently, there?s an estimated shortfall of about 4,000 livers per year.

Liver cell transplantation has shown some promise, but has limited uses. To be successful, an artificial transplant must be sufficiently large to provide enough liver function. That requires a network of small blood vessels?called a microvascular network?to transport oxygen and nutrients throughout the structure.

Decellularization?the process of removing cells from a structure but leaving a scaffold with the architecture of the original tissue?has shown some success in other organs. One group of scientists reported the decellularization of an entire heart that preserved the original architecture and microvascular network. A research team led by Dr. Korkut Uygun at Massachusetts General Hospital tried a similar approach for the liver. Their work was supported by NIH?s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and others.

In the June 13, 2010, advance online edition of Nature Medicine, the team explained the process they developed. They used a gentle detergent over 3 days to decellularize the liver while preserving its structure. A matrix of proteins remained behind to hold the liver?s shape. Using a dye, the researchers showed that the microvascular network in each eerily translucent liver was intact.

The researchers were then able to successfully introduce functional hepatocytes?a type of liver cell?back into the matrix. When they tested the recellularized matrix, they found that it carried out liver-specific functions at levels comparable to a normal liver.

Grafts transplanted into rats maintained their functional hepatocytes as well, for a few hours. The researchers note, however, that successful engineering of an entire functional liver will require other types of cells.

“As far as we know, a transplantable liver graft has never been constructed in a laboratory setting before,” Uygun says. “Even though this is very exciting and promising, it is a proof-of-concept study only. Much more work will be required to make long-term functional liver grafts that can actually be transplanted into humans.”

That said, the study highlights the feasibility of using this approach. There is currently a large pool of livers that are unsuitable for transplantation, including livers from people who have died of heart attacks. These could potentially be used to make decellularized liver matrices.

Research suggests that Alzheimer’s disease is up to 80% heritable, but until recently only one gene, known as APOE, had been linked to disease risk and age at onset. Last year, genome-wide association studies identified 3 additional chromosome regions, or loci, that affect Alzheimer’s risk. Still, the underlying causes of the disease remain mostly unknown.

In the new study, reported in the June 2010 issue of the Archives of Neurology, scientists searched for connections between gene variants and specific brain changes typical of Alzheimer’s disease. The researchers drew on publicly available data collected for the Alzheimer’s Disease Neuroimaging Initiative. This research consortium conducts genome-wide analyses and collects neuroimaging and other data on older adults from across North America. The initiative is a public-private partnership funded primarily by NIH?s National Institute on Aging (NIA) and National Institute of Biomedical Imaging and Bioengineering (NIBIB), along with pharmaceutical companies and other organizations.

The scientists analyzed data on 168 Alzheimer’s patients, 357 people with mild cognitive impairment (a precursor to Alzheimer’s disease) and 215 who were cognitively normal. They scoured MRIs for structural traits in 6 brain regions linked to Alzheimer’s disease, including changes in the size of the amygdala and hippocampus.

The researchers found that APOE had the strongest association with clinical Alzheimer’s disease and was linked to all the neuroimaging traits except one. The 3 genes identified last year, along with 2 new target genes, had a significant cumulative effect on all 6 neuroimaging traits. The newly identified genes?BIN1 and CNTN5?are known to contribute to neuron function, although their roles are poorly understood.

“The genes we identified, and other genes that they interact with, will provide good targets for drug development in the future,” says study coauthor Dr. Alessandro Biffi of Massachusetts General Hospital and the Broad Institute. “Still, with the information we have, we’re not able to provide any type of personalized medicine for Alzheimer’s disease, mainly because the effects of these gene variants are very weak.”

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Stay tuned while we get all of our ducks in a row and get started!