Researchers at the University of Rochester Medical Center in New York gave teriparatide (Forteo) to 145 people who had bone fractures that had not healed, many for six months or more. They found that 93 percent of them showed significant healing and pain control after eight to 12 weeks.

Teriparatide speeds the healing of fractures by changing the behavior and number of cartilage and bone stem cells involved in the healing process, the researchers found.

“The decreased healing time is significant, especially when fractures are in hard-to-heal areas like the pelvis and the spine, where you can’t easily immobilize the bone — and stop the pain,” Dr. Susan V. Bukata, medical director of the university’s Center for Bone Health, said in a news release from the center.

“Typically, a pelvic fracture will take months to heal, and people are in extreme pain for the first eight to 12 weeks,” she said. “This time was more than cut in half. We saw complete pain relief, callus formation and stability of the fracture in people who had fractures that up to that point had not healed.”

Based on the findings, the news release said, the U.S. National Institutes of Health has funded a clinical trial of the drug’s use on fractures. The study will include men and post-menopausal women older than 50 who have what’s called a low-energy pelvic fracture and who are admitted to the emergency department of Strong Memorial Hospital in Rochester.

Participants in the study will be given either teriparatide or a placebo and will be followed for 16 weeks to measure fracture healing in a number of ways, including pain levels, microscopic bone growth determined through CT scans and functional testing of bone strength.

Teriparatide was approved by the U.S. Food and Drug Administration in 2002 as a treatment for osteoporosis.

If clinical trials prove that the drug speeds bone healing, it could prove especially important for older adults, who suffer the majority of broken bones that heal slowly.

“In many people, as they get older, their skeleton loses the ability to heal fractures and repair itself,” J. Edward Puzas, head of orthopedic bone research at the medical center and the lead investigator for the clinical trial, said in the news release. “With careful application of teriparatide, we believe we’ve found a way to turn back the clock on fracture healing through a simple, in-body stem cell therapy.”

Bracing and immobilization cannot be used for the approximately 60,000 Americans who suffer a pelvic fracture each year.

“It takes three to four months for a typical pelvis fracture to heal,” Bukata said. “But, during those three months, patients can be in excruciating pain, because there are no medical devices or other treatments that can provide relief to the patient.”

“Imagine if we can give patients a way to cut the time of their pain and immobility in half?” she said.

Speeding the healing time for pelvic fractures could also reduce the risk of death and medical costs.

Pelvic fractures carry the same risk of death as hip fractures. About “one-quarter of all older women with pelvic fractures will die from complications,” Bukata said. “And during that year of recovery, a patient typically puts a greater strain on our health-care system, not to mention their pain and suffering.”

Slow-Healing Bones May Get Boost From Drug

The technique, which leaves healthy cells unaffected, could potentially offer hope to people with hard-to-treat cancers where surgery is not possible.

Although it has only been tested in mice so far, the researchers hope for human trials in two years.

The UK study is published online by the journal Cancer Research.

The genes were wrapped up in microscopic nano-particles which were taken up by cancer cells, but not their healthy neighbours.

Once inside, the genes stimulated production of a protein which destroys the cancer.

The researchers say the technology could potentially be particularly relevant for people with cancers that are inoperable because they are close to vital organs.

They hope it will eventually also be used to treat cancer that has spread.

‘Exciting step’

Lead researcher Dr Andreas Schatzlein, from the School of Pharmacy in London, said: “Gene therapy has a great potential to create safe and effective cancer treatments but getting the genes into cancer cells remains one of the big challenges in this area.

“This is the first time that nanoparticles have been shown to target tumours in such a selective way, and this is an exciting step forward in the field.

“Once inside the cell, the gene enclosed in the particle recognises the cancerous environment and switches on. The result is toxic, but only to the offending cells, leaving healthy tissue unaffected.

“We hope this therapy will be used to treat cancer patients in clinical trials in a couple of years.”

Traditional chemotherapy indiscriminately kills cells in the affected area of the body, which can cause side effects like fatigue, hair loss or nausea.

It is hoped that gene therapy will have fewer associated side effects by targeting cancer cells.

Dr Lesley Walker, of the charity Cancer Research UK, said: “These results are encouraging, and we look forward to seeing if this method can be used to treat cancer in people.

“Gene therapy is an exciting area of research, but targeting genetic changes to cancer cells has been a major challenge.

“This is the first time a solution has been proposed, so it’s exciting news.”

Nano-treatment to torpedo cancer

The hippocampus is widely known to be integral to memory, but researchers say they now see just how images are stored and recalled in this part of the brain.

Wellcome Trust scientists trained four participants to recognise several virtual reality environments.

Discernible patterns in brain activity then signalled where they were, they wrote in the journal Current Biology.

Neurons in the hippocampus, also known as “place cells”, activate when we move around to tell us where we are.

The team, based at University College London, then used specialised scanning equipment which measures changes in blood flow in the brain.

This allowed them to examine the activity of these cells as the participants – all young men with experience of playing videogames – moved around the virtual reality environment. The data was then passed through a computer.

“We asked whether we could see any interesting patterns in the neural activity that could tell us what the participants were thinking, or in this case where they were,” said Professor Eleanor Maguire.

Are you lying?

“Surprisingly, just by looking at the brain data we could predict exactly where they were in the virtual reality environment. In other words we could ‘read’ their spatial memories.”

“By looking at activity over tens of thousands of neurons, we can see that there must be a functional structure – a pattern – to how these memories are encoded.”

But they stressed that the prospect of genuinely reading someone’s most intimate thoughts – or working out if they were lying – was still a long way off.

Their participants were all willing subjects who allowed their brains to be trained and monitoring to take place.

“It would be very easy not to co-operate, and then it wouldn’t work,” said Demis Hassabis, who developed the computer programme to read the data. “These kind of scenarios would require a great technological leap.”

It is brain diseases such as Alzheimer’s which could stand to benefit from such research.

“Understanding how we learn and store memories could aid our understanding of conditions in which memory is compromised and potentially help patients in the rehabilitation process,” said Professor Maguire.

Professor Clive Ballard, director of research at the Alzheimer’s Society, said: “This exciting development will boost our understanding of the hippocampus, a key area affected in Alzheimer’s disease and the most important part of the brain for memory.

“Learning more about how the brain works could help us work out which types of nerve cells are lost in Alzheimer’s.”

Rebecca Wood, of the Alzheimer’s Research Trust, said the research was “fascinating”.

She said: “Understanding how memories are formed may help researchers discover how this process goes wrong in diseases like Alzheimer’s.”

A step closer to reading the mind

A wheelchair-mounted robotic arm controlled by thought alone has been created by scientists at the University of South Florida.

The device could give people with amytrophic lateral sclerosis (ALS) or full body paralysis the ability to perform simple day to day functions that would otherwise be impossible.

“We aren’t reading people’s thoughts,” said Redwan Alqasemi, a scientist at the University of South Florida who, along with Rajiv Dubey and Emanuel Donchin of USF, helped develop the software and hardware. “This is the first time a person with severe disabilities like ALS can perform daily activities for themselves.”

Over time, patients with ALS slowly lose control over their muscle movement, losing the ability to move their arms, legs and eventually all muscles except those around the eye. Patients with ALS have fully functional brains, but have no way to express their thoughts.

EEG scans offer one way for patients with ALS to communicate with the outside world. By fitting patients with a head cap equipped with electrodes and filled with an electrically conductive gel, scientists can monitor particular kinds of electrical impulses coursing through the brain.

In this case, the scientists monitor a particular brain wave called P300, so-called because it lasts about one-third of a second. Reading P300 waves is basically like reading a person’s thoughts, but only in the most coarse kind of way.

For the wheelchair-mounted robotic arm, the person in the wheelchair looks at directional arrows flashing across a small screen. When the arrow points in the direction that they want to go, their brain lights up on the EEG, and the wheelchair or robotic arm moves accordingly.

This doesn’t happen at the speed of thought, however. Turning the wheelchair or moving the robotic arm takes about seven seconds as the arrows cycle across the screen. The wheel chair or arm continues in that direction until it receives a new command.

The wheelchair or arm could move faster, but it might not move as accurately, said Alaqsemi. The next step for the USF scientists is to refine the model’s hardware and software, to increase speed and reliability while cutting down on weight.

“Every pound you take off the robotic arm is another pound of payload that can be lifted,” said Alqasemi.

Right now the robotic arm can lift about four pounds, about the weight of a gallon of milk. In the next version Alqasemi hopes to double the payload.

Lifting a door handle or moving a gallon of milk may seem like simple tasks, but according to Jonathan Wolpaw, who builds brain computer interfaces at the Wadsworth Center in New York, using thought-controlled devices is harder than simply just thinking.

“Our normal muscle movements require practiced skill and control,” said Walpaw. “Controlling brain activity is also a skill that requires practice.”

Reading P300 brain waves is a good system, argues Walpaw, because it doesn’t take a lot of practice to train the brain. With only one WMRA built so far and no current plans to commercialize the design, not many people will get the chance for their brain to learn the new skill. But when commercial models appear in several years, even slow brain computer interfaces could make the impossible, possible.

“It would allow patients with severe disabilities the ability to control their own environment and have some form of independent mobility,” said William Heetderks, Director of the National Institute of Biomedical Imaging and Bioengineering. “It would be very valuable to these individuals.”

Wheelchair arm controlled by thought alone

Researchers have discovered human antibodies that neutralise not only H5N1 bird flu, but other strains of influenza as well. They now hope to develop them into life-saving treatments.

The antibodies — immune system proteins that attach to invaders such as viruses —also might be used to protect frontline workers and others at high risk in case a pandemic of flu broke out, the researchers said.

Several types

In tests on mice, the viruses neutralised several types of influenza A viruses, including the H5N1 avian influenza virus, the researchers reported in Sunday’s issue of the journal Nature Structural & Molecular Biology.

“We were surprised and actually delighted to find that these antibodies neutralised a majority of other influenza viruses, including the regular seasonal (H1N1 strain of) flu,” Robert Liddington of the Burnham Institute for Medical Research in La Jolla, California, told reporters in a telephone briefing.

Influenza is especially difficult to fight because it cloaks itself in lollipop-shaped proteins called hemagglutinin and neuraminidase, which mutate regularly.

Bird flu war could soon be won

Colds are difficult to treat and prevent because the rhinovirus that causes them takes many forms, becoming elusive targets for drugs, said Stephen Liggett, a geneticist at the University of Maryland School of Medicine’s Institute for Genome Sciences in Baltimore who led the study.

Liggett and his team sequenced all 99 known strains of the rhinovirus in a report in the journal Science that traced the evolution of the germ.

The full sets of genes, or genomes, described in the study show the viruses have a few regions that consistently appear and may be vulnerable to medications, the researchers said in Sciencexpress, the online version of the journal.

The analysis also found a potential new species of the virus for the first time.

“I’m hoping this will lead to interventions that can be fast-tracked and applied to a very practical and worthy cause,” Liggett said yesterday in a telephone interview. “All these genome sequences are in the public domain now so they can be mined by interested people.”

Colds and their complications, such as asthma attacks, cost as much as US$100 billion annually in care and lost work, Liggett said.

He became interested in tracking down the gene sequences of cold germs because of his interest in finding the connection between colds and asthma.

“It became clear that there was a missing link here,” he said. “About 50 percent of all asthma attacks are caused by rhinovirus infections. So we needed to understand more about it. Like it or not, it’s part of the equation.”

Only eight rhinovirus genomes had been sequenced when he started the study, Liggett said.

New sequencing technology from Illumina Inc, Roche Holding AG’s 454 unit, and Applied Biosystems Inc, helped speed the three-year effort.

The study showed that viruses within divisions of the rhinovirus family, such as its B group, are far more diverse than had been thought.

He also found a potential new species of rhinovirus, called HRV-D.

Liggett said he is conducting a nationwide sampling of rhinovirus infections to find more genomes and further expand the list of known rhinoviruses.

With current technology, each virus genome can be sequenced at a cost of about US$100, he said.
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Taipei Times – archives

Far more potent than similar compounds already in clinical trial, the drug short-circuits the normal ability of cells to sense the need to grow and divide — a signal that cancer cells exploit to spread in the body.

The scientists are working with clinicians to test the drug’s effectiveness against a range of cancers that have proven difficult to treat.

The discovery is reported in the Feb. 10, 2009 edition of PLoS Biology, a journal published by the Public Library of Science.

The research was led by scientists at the University of California, San Francisco (UCSF) and the UCSF Helen Diller Family Comprehensive Cancer Center. Senior author of the paper is Kevan Shokat, PhD, Howard Hughes Medical Investigator and professor of cellular and molecular pharmacology at UCSF.

Normally, in response to growth signals, a multi-protein unit in cells called mTOR integrates information about the cell’s nutritional and energy needs, and prompts the cell to manufacture key proteins for cell growth. But cancer exploits this signal for its own growth.

Clinical trials are underway to stymie cancer proliferation by using a drug called rapamycin—marketed as Rapamune–or related compounds to block the growth signal cycle. The new drug greatly improves on rapamycin’s effectiveness, the scientists reported. The name mTOR stands for “mammalian target of rapamycin.”

Of serious concern to clinicians, rapamycin and related drugs can actually promote cancer at the same time they thwart it. This happens, the scientists found, because the drugs only partially block the cells response to a growth signal. When this happens, the drugs end up augmenting the growth signal itself because a feedback process in the cell kicks in to assure adequate nutrition. With the feedback system in play, cancer cells can regain needed nutrients and continue to proliferate.

The new drug totally blocks this feedback loop, said Shokat, who also is a faculty affiliate at the California Institute for Quantitative Biosciences, known as QB3, which is headquartered at UCSF.

“We were trying to synthesize compounds that could help us learn more about how cancer exploits normal growth controls,” he explained. “Once we made it, though, we found it was even better than we thought it would be at blocking mTor signaling. It does everything that rapamycin does and more.”

The new drug succeeds because there are two mTOR signal pathways, and it blocks both, the scientists found. Rapamycin only blocks one, and so allows the growth-signaling system to still function.

The scientists think that the drug’s total blockage of the nutrient-sensitive mTOR and its feedback loop offer a major advance over rapamycin based drugs, which have been approved to treat only renal call carcinoma effectively.

“I hope the new drug can be used to treat a range of cancers,” Shokat said. “We will work with clinicians to test it against a number of types of cancer – colorectal, lung, breast, multiple myeloma and others. We want to first find the cancer that is most sensitive to it.”

The new compound has been dubbed a TORKinib because it inhibits the mTOR signal. UCSF has applied for a patent and licensed the patent to a startup biotech company, co-founded by Shokat and colleagues, to advance its use in clinical trials to treat cancer.

mTOR is known as a kinase, a ubiquitous type of signaling molecule – there are more than 500 different kinases in the body – that essentially switches proteins on or off. The switch is one of the most common interactions in the body. The kinase adds a small molecule known as a phosphate group to the protein, and that single action either turns on the protein or dampens its activity.

Like all signaling systems in the body, the one involving mTOR goes through many steps to accomplish its duties. The different steps form a cascade that can ramp the signal up or down, depending on the conditions of the cells or tissues. These kinase cascades are embedded within complicated feedback loops, such as the one activated by rapamycin.

Research on the mTOR pathway is of increasing interest to drug companies, Shokat said.

Since mTOR acts “upstream” and “downstream” of other key kinases that are found to cause cancer– such as the much-studied kinases PI3K and Akt– he thinks blocking it will short-circuit the many feedback loops cancer cells use to generate and maintain a growth signal.

“We are extremely excited about the potential of targeting mTOR in this way to treat a number of cancers, although we are aware that there are many hurdles to reaching the finish line,” Shokat said.

Lead author on the paper is Morris E. Feldman, a graduate student in Shokat’s lab.

Shokat’s colleague, Davide Ruggero, PhD, who studies cancer’s effect on protein synthesis, is also a coauthor. Ruggero is assistant professor of urology in the UCSF Helen Family Comprehensive Cancer Center. Other coauthors are Beth Apsel, PhD, a graduate student in chemistry and chemical biology; and Zachary Knight, PhD, a postdoctoral scientist in Shokat’s lab during the research project. Also: Aino Uotila and Robbie Loewith in the department of molecular biology, University of Geneva.

The research was funded by the Howard Hughes Medical Institute.

The private company co-founded by Shokat is called Intellikine. He is the chairman of its scientific advisory board and holds stock options in the company.

Drug Discovery Short-circuits Cancer Growth

The move comes three days after the inauguration of President Barack Obama who has been a strong supporter of embryonic stem cell research.

Since 2001 there have been limits on federal funding for stem cells.

Geron Corp, the biotech company behind the research, plans to initiate a clinical trial in patients paralysed due to spinal cord injury.

The BBC predicted last week that the White House would reverse the restrictions placed on stem cell research once President Obama took office.

The US Food and Drug Administration gave the go ahead for the research on Friday.

Under President Bush, federal funding had been limited to around sixty stem cell lines created from embryos destroyed prior to August 2001.

Scientists had warned that only twenty eligible cell lines remain useful for research and many of these are problematic.

Researchers had told the BBC that the restrictions had slowed down their work.

Controversy

Interest in use of embryonic stem cells is due to their ability to turn into any of the body’s two hundred cell types.

Using embryos donated through IVF treatment scientists have coaxed the stem cells inside into many types of tissue. One embryo can provide a limitless supply because the cell lines can be grown indefinitely.

But the use of human embryonic stem cells in research is controversial with come campaigners saying it is unethical.

Geron, a biotech company based in “silicon valley” south of San Francisco, has spent $170m on developing a stem cell treatment for spinal cord injury.

The research will use cells coaxed to become nerve cells which are injected into the spinal cord.

In animal trials of the treatment, paralysed rats regained some movement.

Company chief Dr Tom Okarma said: “What stem cells promise for a heart attack or spinal cord injury or diabetes is that you go to the hospital, you receive these cells and you go home with a repaired organ, that has been repaired by new heart cells or new new nerve cells or new islet cells that have been made from embryonic stem cells.”

‘Pivotal decision’

Professor Chris Mason, an expert in regenerative medicine at University College London, described the FSA decision as “historic” and a “pivotal milestone in the development of embryonic stem cell therapies.

He said: “The knowledge that will be gained in this first clinical trial deploying embryonic stem cell derived material will accelerated the development of all future stem cell therapies.”

Professor Pete Coffey, director of the London Project to cure blindness, said: “It’s great news for the field.

“This strengthens our recent call for regulators in the UK to help provide a clear process for researchers to take this forward.

“It’s also exciting for me because it brings our own moves towards clinical trials with embryonic stem cells for age-related macular degeneration a step forward.”

Professor Robin Lovell-Badge, head the MRC National Institute for Medical Research, said it often takes 15 to 20 years to develop a therapy.

“It takes a long time and much work to derive processes that will efficiently and reproducibly give an appropriate cell type for grafting and many animal experiments to test efficacy and safety.

“An appropriate set of patients have to be identified for the first tests and clinicians willing to participate in trials.

“And the regulatory hurdle is, understandably, a huge one – in this case it required 21,000 pages of documents.”

He added that for those patients desperate for treatment, and for their families, the news showed the research is moving in the right direction.

BBC NEWS | Health | Green light for US stem cell work

Craig, a public relations specialist who works at Columbia University in New York City, knew that Roger’s medications could cause weight gain. But she had never been told that the drugs he was taking might be harming his heart.

“We were never counseled by his psychiatrist or his primary care provider to watch for symptoms of heart disease or any risk of sudden death at all,” Craig says. There’s no evidence that Roger’s medications caused his death, but his family might have been able to get him help sooner if they had known about the risks, Craig explains.

New research published Wednesday in the New England Journal of Medicine shows that antipsychotic drugs are not risk free, and the study’s authors are urging much more caution in their use. The drugs are associated with a risk of sudden cardiac death, particularly at higher doses. Health.com 10 best foods for your heart

Craig’s brother was taking haloperidol, which belongs to an older class of drugs called typical antipsychotics, which have long been known to increase the risk of sudden death due to cardiac causes. He was also on risperidone, a member of a newer class of drugs called atypical antipsychotics, which had been considered safer.

Doctors prescribe these newer medications, originally developed to treat schizophrenia, for a wide variety of problems — from conduct disorder in kids to aggressive behavior in Alzheimer’s patients. In fact, they’ve become so popular that three of them — olanzapine, risperidone, and quetiapine — are among the 10 top-selling drugs worldwide, with $14.5 billion in sales in 2007.

The new study suggests that among patients taking high doses of atypical antipsychotics, there are about 3.3 cases of sudden cardiac death per 1,000 patients per year, which an editorial characterizes as a risk that’s “between ‘moderate’ and ‘low,’ but not ‘rare.’” Health.com: Heart drug may be a cancer fighter

About 325,000 people in the United States each year die of sudden cardiac death, which has an incidence of 0.1 to 0.2 percent per year in adults.

“[The drugs] have potentially very serious side effects,” says Wayne A. Ray, Ph.D., the director of the division of pharmacoepidemiology at Vanderbilt University School of Medicine, in Nashville. “So whenever a decision is made to use one, consideration of potential side effects needs to be made.” Ray and his colleagues found that atypical antipsychotics doubled the risk of sudden death from heart-related causes, most likely by causing disturbances in heart rhythms.

First introduced in the mid-nineties, atypical antipsychotics were praised for having none of the troublesome side effects of their predecessors, including frequent, involuntary movements of the face and mouth that were in some cases irreversible.

But the new study shows that the increased risk of sudden cardiac death seen with the older drugs is nearly identical to that of the newer medications. There had been suspicions that the drugs were risky, especially when used in older patients, but the current study is the first to systematically investigate their association with sudden cardiac death.

Ray and his colleagues reviewed data on Tennessee Medicaid patients, comparing 44,218 people using older typical antipsychotics and 46,089 taking the newer atypical antipsychotics to 186,600 people who had never used the drugs. People with schizophrenia may have a higher rate of cardiac problems, due to smoking and other factors. To account for this, researchers also compared antipsychotic drug users without schizophrenia to non-drug users who had characteristics (in most cases, mood disorders) that made them likely candidates for the drugs.

Overall, people taking typical antipsychotics were at 1.99-times greater risk of sudden cardiac death, while the risk for those on atypical antipsychotics was increased 2.26 times. The increased risk was greater for people on higher doses of the drugs. People who had used the drugs in the past but stopped weren’t at greater risk of sudden cardiac death.

“The drugs are still very effective for conditions that there’s proven evidence for,” says Jeffrey A. Lieberman, M.D., a professor and chair of psychiatry at Columbia University, in New York City, and the director of the New York State Psychiatric Institute, who was not involved with Ray’s research. “They clearly need to still be able to be used. I think this [study] really underscores the need to be very judicious about how these medications are used and whom they’re given to.”

While atypical antipsychotics have been used to ease aggressive behavior for patients with Alzheimer’s disease, for example, they are not approved for this purpose by the U.S. Food and Drug Administration; in fact, in 2005, the FDA issued a warning that these drugs increased the risk of death among elderly people, extending the warning to all antipsychotic drugs last year, notes Sebastian Schneeweiss, M.D., Sc.D., an associate professor of medicine at Harvard Medical School, in Boston, who coauthored an editorial accompanying the current study. Health.com: How is depression in the elderly different from dementia?

Given the lack of better alternatives, these drugs are still widely used in patients with dementia despite the warnings, he adds. But while there’s anecdotal evidence that they will “cool these patients down” and reduce their aggressive behaviors, there’s no scientific evidence that they really help patients or their caregivers, Dr. Schneeweiss says.

In his editorial, Dr. Schneeweiss and coauthor Jerry Avorn, M.D., also of Harvard, call for patients to undergo an electrocardiogram before and shortly after being placed on atypical antipsychotics, to determine if the drugs are causing any heart rhythm disturbances.

For people who must be on these medications, Ray says, it’s essential for their doctors to treat any other conditions, such as high blood pressure, that can harm the heart. “Sudden cardiac death usually occurs when multiple risk factors are present,” he explains. “When you add one, it’s kind of like the straw that broke the camel’s back.”

“Absolutely the lowest dose that works should be used, because we found a strong dose response,” Ray says.

Jamaison Schuler, a spokesperson for Eli Lilly and Company, the maker of Zyprexa, says, “Although the study appears to have important limitations, it provides additional information for practicing physicians to consider as they decide how to treat very complex diseases such as schizophrenia and bipolar disorder.”

The FDA has approved atypical antipsychotics for treating bipolar disorder, Ray adds. But the researcher recommends that physicians first try safer alternatives, such as the mood stabilizer lithium. “That’s a very serious illness, and it has important consequences for patients’ quality of life and relationships,” Ray notes. “If the mood stabilizer doesn’t work, I think it’s very reasonable to consider an antipsychotic, but…other drugs should be considered first.”

Finally, he says, a patient should never stop taking any drug without consulting his or her physician. Nevertheless, anyone taking an atypical antipsychotic for a non-FDA-approved use should consult his physician. “I think off-label use should be undertaken very cautiously, and its frequency should be much less than it is currently,” Ray says. Health.com: Superfoods that can save your health

For Susan Craig, the new research makes it clear that treating serious mental illness must go far beyond just prescribing pills. “We need to be supporting these people in a better, more systematic way,” she says. “There’s no magic pill. It’s treating the whole person.”

Antipsychotic Drugs Linked to Sudden Cardiac Death – CNN.com

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“Our research findings reveal that Baxß protein levels are normally kept at essentially undetectable levels in healthy cells by the protein degradation machine in cells known as proteasomes,” said Dr Victor Yu, who led the Institute of Molecular and Cell Biology (IMCB) research team.

In a researcher article in the journal Molecular Cell, the researchers describe proteasomes as “protein-digesting machines” that regulate cellular levels of various proteins, including that of the lethal Baxß, by breaking them into smaller components within the cell.

“Thus, the proteasomes are there to keep the lethal Baxß in check. This is exciting — if the proteasome-mediated degradation of Baxß could be inhibited specifically in cancer cells, it could cause the harmful cancer cells to go through apoptosis,” Dr Victor Yu said.

In apoptosis, unwanted, damaged and infected cells are eliminated. Before the discovery of Baxß, only one single protein called Bax-alpha (Baxa) had been extensively studied in cells.

The researchers have now found that Baxß is able to associate with, and promote, Baxa activation, and that Baxß, in its native form, is 100 times more potent than its sibling Baxa in triggering a key step in apoptosis.

They believe that the development of such compounds as can elevate levels of Baxß, or stimulate its interaction with Baxa, may pave the way for new drug approaches to cancer treatment, as these compounds are likely to enhance the apoptotic signals triggered by many conventional cancer drugs, which frequently cause toxic side effects in patients when higher doses of drugs are needed.

Dr David Andrews, Professor of Biochemistry and Biomedical Sciences at McMaster University, Canada said: “The beta-isoform4 of Bax has been enigmatic for several years. Although earlier research had hinted at its existence, the protein has proven extremely difficult to detect or examine functionally. Even attempts to produce the protein in the laboratory have been largely unsuccessful.

In this study the Yu group resolves these issues by demonstrating that in cells Baxß is normally rapidly degraded and kept at low levels, and when it is not degraded, it is profoundly apoptotic on its own and works in concert with Baxa. These studies provide information necessary for the elucidation of the importance of Baxß in cell physiology.”

Protein for cancer cell death discovered-Science-Health & Science-The Times of India