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November 5, 2007, 10:18 PM CT

Albuferon for chronic hepatitis C

Albuferon for chronic hepatitis C
Human Genome Sciences, Inc. today announced the final results of a Phase 2b clinical trial of the investigational drug, Albuferon (albinterferon alfa-2b), in combination with ribavirin in therapy-naive patients with genotype 1 chronic hepatitis C. This Phase 2b study demonstrated that, with half as a number of injections as Pegasys (peginterferon alfa 2a), Albuferon was just as effective in achieving sustained virologic response (SVR) an undetectable amount of virus in the blood at 24 weeks following the end of therapy with comparable safety and less impairment of health-related quality of life on therapy. Albuferon is administered every two weeks, while peginterferon alfa-2a requires administration every week.

The final Phase 2b data are being presented this week at the 58 th AASLD Annual Meeting in Boston. In two additional press releases also issued by HGS today, the Company announced the full presentations at AASLD of quality-of-life data from the Phase 2b trial, and results from the Phase 2 trial of Albuferon in combination with ribavirin in patients with chronic hepatitis C who had not responded to prior interferon-based therapy regimens.

The final Phase 2b results suggest that the every-two-week dosing regimen of Albuferon halves the number of injections that are mandatory with peginterferon alfa-2a, while providing at least comparable efficacy, comparable safety and the potential for less impairment of quality of life and daily activity, said Stefan Zeuzem, M.D., Professor of Medicine and Chief, Department of Medicine, J.W. Goethe University Hospital, Frankfurt, Gera number of. We are continuing the evaluation of the 900-mcg and 1200-mcg doses of Albuferon in larger populations in Phase 3 trials. We also conclude that monthly dosing of Albuferon deserves further evaluation.........

Posted by: Emily      Read more         Source


November 5, 2007, 9:03 PM CT

Marijuana-like brain chemicals work as antidepressant

Marijuana-like brain chemicals work as antidepressant
Daniele Piomelli
American and Italian scientists have observed that boosting the amounts of a marijuana-like brain transmitter called anandamide produces antidepressant effects in test rats.

Led by Daniele Piomelli, the Louise Turner Arnold Chair in Neurosciences and director of the Center for Drug Discovery at the University of California, Irvine, the scientists used a drug they created, called URB597, which blocks anandamide degradation in the brain, thereby increasing the levels of this chemical.

"These findings raise the hope that the mood-elevating properties of marijuana can be harnessed to treat depression," Piomelli said. "Marijuana itself has shown no clinical use for depression. However, specific drugs that amplify the actions of natural marijuana-like transmitters in the brain are showing great promise".

The scientists administered URB597 to chronically stressed rats which showed behaviors similar to those seen in depressed human patients. After five weeks of therapy, the stressed rats treated with the drug were behaving similarly to a comparison group of unstressed animals. The study appears in the Nov. 15 issue of Biological Psychiatry.

URB597 works by inhibiting FAAH, an enzyme in the body that breaks down anandamide. Dubbed "the bliss molecule" for its similarities to the active ingredient in marijuana, anandamide is a neurotransmitter that is part of the brain's endocannabinoid system and it has been shown in studies by Piomelli and others to play analgesic, anti-anxiety and antidepressant roles. It also is involved in regulating feeding and obesity. Blocking FAAH activity boosts the effects of anandamide without producing the "high" seen with marijuana.........

Posted by: Emily      Read more         Source


November 5, 2007, 8:42 PM CT

Predicting survival after liver transplantation

Predicting survival after liver transplantation
Patients awaiting liver transplantation who also suffer from other medical problems may face poorer survival after transplantation. These comorbid problems, which include coronary disease, diabetes, chronic obstructive pulmonary disease (COPD), connective tissue disease and renal insufficiency, have been incorporated into a new modified comorbidity index which helps predict post-transplant survival. These findings appear in the recent issue of Liver Transplantation, a journal by John Wiley & Sons. The article is also available online via Wiley Interscience (http://www.interscience.wiley.com/journal/livertransplantation).

Determining who receives the limited supply of donor organs is one of the greatest challenges facing the transplant community. Severity of illness is the main criteria for hopeful liver recipients, however it is not the only factor that influences post-transplant survival. In other medical fields, co-morbidities have been considered as relevant predictors of survival, but never among the liver transplant community.

To address this paucity in the literature, researchers, led by Michael Volk of the University of Michigan sought to determine if the Charlson Comorbidity Index (CCI) would predict long-term survival after liver transplantation.

They conducted a retrospective study of 624 patients who underwent liver transplantation at the University of Michigan Hospital between 1994 and 2005 (to obtain a median follow-up of 5 years). They collected demographic, clinical and laboratory data for each patient, but focused on the nine comorbidities comprising the Charlson Comorbidity Index. These include congestive heart failure, coronary artery disease, diabetes mellitus, peripheral vascular disease, cerebral vascular accident, COPD, connective tissue disease, renal insufficiency and malignancy.........

Posted by: Emily      Read more         Source


November 4, 2007, 7:58 PM CT

Epilepsy genes may cancel each other

Epilepsy genes may cancel each other
Inheriting two genetic mutations that can individually cause epilepsy might actually be seizure-protective, said Baylor College of Medicine scientists in a report that appears online today in the journal Nature Neuroscience.

In the genetics of the brain, two wrongs can make a right, said Dr. Jeffrey L. Noebels, professor of neurology, neuroscience and molecular and human genetics at BCM. We believe these findings have great significance to clinicians as we move toward relying upon genes to predict neurological disease.

In addition, the finding might point the way to new ways of treating epilepsy using gene-directed treatment.

If you have a potassium channel defect, then a drug blocking certain calcium channels might also benefit you, said Noebels.

Noebels and colleagues, who included first author Dr. Ed Glasscock, a post-doctoral researcher at BCM, tested this hypothesis by breeding mice with two defective genes that govern ion channels, tiny pores in cells that allow molecules such as potassium and calcium to flow in and out.

The genes were known to cause epilepsy when inherited singly within families. They have also been found in a large-scale screen of people with non-familial seizure disorders being performed in collaboration with the Baylor Human Genome Sequencing Center.........

Posted by: Emily      Read more         Source


November 1, 2007, 10:10 PM CT

PET for Alzheime Disease Diagnosis

PET for Alzheime Disease Diagnosis
A PET scan (positron emission tomography) that measures uptake of sugar in the brain significantly improves the accuracy of diagnosing a type of dementia often mistaken for Alzheimers disease, a study led by a University of Utah dementia expert has found.

The scan, FDG-PET, helped six doctors from three national Alzheimers disease centers correctly diagnose frontotemporal dementia (FTD) and Alzheimers in almost 90 percent of cases in the studyan improvement of as much as 14 percent from usual clinical diagnostic methods. FDG stands for fluorodeoxyglucose, a short-lived radioactive form of sugar injected into people during PET scans to show activity levels in different parts of the brain. In Alzheimers, low activity is mostly in the back part of the brain; in FTD, low activity is mostly in the front of the brain.

FDG-PET is an particularly powerful tool in early therapy of FTD, said the studys lead author, Norman L. Foster, M.D., professor of neurology and director of the Center for Alzheimers Care, Imaging and Research at the University of Utah School of Medicine.

FTD is a common cause of early onset dementia among people 45-64 years old and is marked by behavioral changes and language difficulties. Like Alzheimers, it can take years to develop and, for now, is incurable. Eventhough FTD is a separate disorder, it often meets clinical diagnostic criteria for Alzheimers and often is misdiagnosed even by dementia experts.........

Posted by: Emily      Read more         Source


November 1, 2007, 9:57 PM CT

Carotid Artery Stenting Risk In Elderly

Carotid Artery Stenting Risk In Elderly
Image courtesy of lucid-echo.com
New Orleans, LA Dr. Hernan Bazan, Assistant Professor of Surgery, Section of Vascular Surgery, at Louisiana State University Health Sciences Center New Orleans School of Medicine, is the lead author of a research paper which may help physicians decide which patients with carotid artery occlusive disease should have carotid surgery or carotid stenting. The research sheds light on characteristics of the aortic arch that could help explain why octogenarians, patients over the age of 80 years, have a higher risk of embolization and stroke during carotid artery stenting (CAS), an artery expanding procedure promoting blood flow done to prevent stroke, and how early identification may allow planning of alternative techniques to reduce risk. Increased aortic calcification in patients older than 75 years: Implications for carotid artery stenting in elderly patients is reported in the November 2007 issue of the Journal of Vascular Surgery.

We hypothesized that elderly patients have more heavily calcified arches than younger patients, noted Dr. Bazan. It is possible that heavily calcified aortic arches could be a source of increased embolization during wire manipulation and catheter exchanges at some stage in carotid artery stenting. We also sought to define what the arches look like or what their morphology is and observed that in patients over the age of 75 years, there was a dramatic increase in calcium content and more complex aortic arches.........

Posted by: Emily      Read more         Source


Fri, 02 Nov 2007 00:53:19 GMT

Are We Programmed to Laugh When Tickled?

Are We Programmed to Laugh When Tickled?
Do we learn to laugh when tickled or is it an innate response? That is the question psychologist Professor Clarence Leuba set himself to examine using his own children, no less, as experimental subjects.

In 1933 he decided that he would not laugh in the presence of his first child while tickling him (Leuba, 1941). Everyday life in the Leuba household, therefore, was devoid of tickling except for one special experimental period. During this period he would cover his own face with a mask while tickling his son so his facial expression was hidden.

Even the tickling was experimentally controlled. First he would tickle lightly, then more vigorously. First under the armpit, then the ribs, followed by chin, neck, knees and feet.

Mrs Leuba slips up
Reportedly all went well until late April 1933 when his wife suddenly forgot all the protocols. After her son''s bath she accidentally administered a short bout of bouncing up and down on her knee with laughter while using the words: "Bouncy, bouncy"!

Was the experiment ruined? Leuba wasn''t sure. But after seven months, with only one bout of laughter associated with tickling the results were in. His son happily laughed away when tickled. It appeared that laughing when tickled is an innate response.

Leuba wasn''t satisfied with this, though, and set about carrying out the same test on his next child, a girl. This time the same experimental procedure was administered and Mrs Leuba''s "Bouncy, bouncy" tendencies were apparently kept at bay for seven months. At the end Leuba got the same results - his daughter began to spontaneously laugh when tickled despite never having been shown how.

Tickling tips
But it wasn''t all experimental procedures and faces hidden behind masks in the Leuba household, indeed Professor Leuba must have become an expert tickler.

He found the best way to make his children laugh was to tickle them along the ribs and under the arms. The element of surprise was also important in producing maximum giggling response. He observed that his children would control the level of tickling by holding his finger, but would then demand more tickling.

Who says science isn''t a laugh?

Posted by: Jerry      Read more     Source


October 30, 2007, 9:54 PM CT

Blocks bacterial communication system

Blocks bacterial communication system
In hopes of combating the growing scourge of antibiotic-resistant bacteria, in particular drug-resistant staph bacteria, a team of researchers from the Scripps Research Institute has designed a new type of vaccine that could one day be used in humans to block the onset of infection. The advantage of the new vaccine is that it would work not only on current bacterial resistant stains but also would not induce the potential for new bacterial resistance because, rather than killing bacterial cells, it blocks their communication system, preventing the shift from harmless to virulent, thus allowing the bodys natural defenses to combat the bacteria.

The work was reported in the October 29 issue of the journal Chemistry and Biology.

Staph and other infections are becoming increasingly deadly because a number of strains of the bacteria that cause disease develop resistance to the array of antibiotics used to control them. A Centers for Disease Control (CDC) report released last week estimated that more than 94,000 Americans were infected in 1995 by a drug-resistant staph superbug called methicillin-resistant Staphylococcus aureus (MRSA), and more than 18,000 Americans died that year during hospital stays involving this type of infection.

The bacterial infection process is dependent on a sort of chemical conversation between individual bacterial cells, referred to as quorum sensing. In their free-living state, bacteria are typically easy to kill and non-virulent. The shift to virulence is dependent on small molecules emitted by bacteria known as autoinducers, because bacteria sense when concentrations of these autoinducers are high enough to suggest a large number of other bacteria are present.........

Posted by: Emily      Read more         Source


October 29, 2007, 10:12 PM CT

'Memory' in cells and molecules

'Memory' in cells and molecules
Veronika Zarnitsyna, Cheng Zhu and Jun Huang (l-r) use a biomembrane force probe for experiments on single-molecule mechanics.

Credit: Gary Meek
Research to be reported October 29 in the journal Proceedings of the National Academy of Sciences (PNAS) provides evidence that some molecular interactions on cell surfaces may have a memory that affects their future interactions. The report could lead to a re-examination of results from certain single-molecule research.

Scientists who use sequentially repeated tests to obtain statistical samples of molecular properties commonly assume that each test is identical to and independent of any other tests in the sequence. In their article, however, scientists at the Georgia Institute of Technology provide examples of test sequences that may not be composed of independent and identically-distributed (i.i.d.) random variables.

If you are probing a cell to get a bit of information, how do you know that the cell is not going to respond by changing the information it reveals the next time you probe it? asked Cheng Zhu, a Regents Professor in the Coulter Department of Biomedical Engineering at Georgia Tech and Emory University. If you are probing a molecule, can you assume that the molecule will return to its original configuration before you test it the next time? We didnt think about this until we had been doing these kinds of experiments for more than ten years.........

Posted by: Emily      Read more         Source


Sun, 28 Oct 2007 16:03:52 GMT

How to Avoid a Bad Bargain

How to Avoid a Bad Bargain
[Photo by Dplanet]
An award-winning social psychology experiment reveals why we often fail to bargain effectively with each other. This deceptively simple experiment examines the effect of two vital aspects of bargaining: threat and communication.

Bargaining is one of those activities we often engage in without quite realising it. It doesn''t just happen in the boardroom, or when we ask our boss for a raise or down at the market, it happens every time we want to reach an agreement with someone. This agreement could be as simple as choosing a restaurant with a friend, or deciding which TV channel to watch. At the other end of the scale, bargaining can affect the fate of nations.

Big-scale or small-scale, bargaining is a central part of our lives. Understanding the psychological processes involved in bargaining can provide us with huge benefits in our everyday lives. In a classic, award-winning series of studies, Morgan Deutsch and Robert Krauss investigated two central factors in bargaining: how we communicate with each other and how we use threats (Deutsch & Krauss, 1962).

To do this, they used a game which forces two people to bargain with each other. Although Deutsch and Krauss used a series of different conditions - nine in fact - once you understand the basic game, all the conditions are only slight variations.

So, imagine you were a clerical worker at the Bell Telephone Laboratories in the late 1950s and you''ve been asked to take part in a psychology study. Every psychology study has a story, and this one revolves around two trucking companies....

Experiment 1: Keep on trucking
Before the experiment proper starts, the researcher explains that you''ll be playing a game against another participant. In the game you will run a trucking company. The object of the game is the same as a real trucking company: to make as much money as possible.

Like the real-life trucking company you have to deliver as many of your goods as possible to their destination in the shortest possible time. But in this game you only have one starting point, one destination and one competitor. It looks like a pretty simple game.

Here''s the catch.

The road map your one truck has to travel across presents you with a dilemma. You are the ''Acme'' trucking company and your fellow participant is the ''Bolt'' trucking company, although both of you have an identical problem. Have a look below.

Posted by: Jerry      Read more     Source


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