Dr Penna

Recently UK government announced the increasing safety measures to decrease sex offenders. Of the proposals one is quite interesting. This is the use of chemicals to decrease the sex drive or libido. They suggested use of anti depressants, which in turn has causation for decrease in sexual drive. According to government the whole process is entirely voluntary. Few of the issues are will the patients/subjects take these medications regularly (compliance) if not how government is going to supervise taking of this tablets by patients.

Sex crime drug treatments planned

Plans to offer more drug treatments to child sex offenders to try to stop them committing further crimes have been announced by the Home Office.

The treatment involving libido-reducing drugs or anti-depressants would be taken on a voluntary basis.

Parents will also be able to ask for checks on whether new partners or people dealing with their children are known sex offenders.

It would be an offence to disclose the information to others.

Sarah’s Law

Convicted paedophiles will also be subjected to lie detector tests if there is a suspicion they are targeting children.

Home Secretary John Reid said he was introducing 20 measures aimed at strengthening the way child sex offenders were dealt with.

He said the law was being updated to allow parents and guardians who had a relationship with someone who had unsupervised access to their children to register concerns about their child’s safety with the police.

If that person was a convicted sex offender, the presumption would be that the parent or guardian should be informed, said Mr Reid.

The scheme will be piloted in three areas, at a cost of £2m, as soon as legislation can be introduced - from around April 2008.

Mr Reid said allowing everyone to have access to information about sex offenders could drive paedophiles underground.

At the moment, employers can request a Criminal Records Bureau (CRB) check if a potential employee is going to work with children, while private citizens cannot.

Some of the most persistent sex offenders are already offered drug treatment, but the Home Office says this provision could be increased.

Mr Reid said more sex offenders would be offered drug treatment on a voluntary basis as part of a £1.2m package of improvements to treatment and supervision.

Lie-detector tests

Offenders will have to provide more information including their e-mail, internet and passport details to the authorities as well as informing them if they begin a new relationship with a single parent.

And the Home Office will also introduce trials of compulsory lie-detector tests in the supervision of offenders.

David Davis, the shadow home secretary, questioned how the government would ensure that information passed to parents would remain private.

He also suggested that voluntary drug treatment was ineffective.

“The headlines today are about chemical castration. The reality is that while a voluntary scheme may be useful in some cases, it will not deal with the worst offenders who do not wish to conform,” said Mr Davis.

He also complained that a national computer system, which was promised by the government in 2004 after the inquiry into the deaths of Holly Wells and Jessica Chapman, had been delayed until 2010 or 2011.

Nick Clegg, the Liberal Democrats home affairs spokesman, said he broadly welcomed the proposals as long as they could be made to work in practice.

‘No honour’

Dr Donald Findlater, director of research and development at the child protection charity the Lucy Faithfull Foundation, said: “I think we have this notion that all sex offenders want to do bad things all the time. Some of them are desperately struggling with what’s going on in their lives, and want help to be stopped.

“Some of them have been very enthusiastic about participating in lie-detector tests, and indeed would happily take pills if that will help.”

Sara Payne, whose daughter Sarah was murdered by paedophile Roy Whiting seven years ago, welcomed plans to share information on sex offenders with parents but told the BBC that drug treatment should be compulsory.

“You’re placing an honour based system on people that have already shown they have absolutely no honour.

Sarah Payne
The murder of Sarah Payne in 2000 prompted calls for new laws

“These are people that rape, molest our children, take photographs of what they’re doing.

“They’ve already shown that they are the nastiest, I think the nastiest, people in the world because of what they do to children.”

The US law, known as Megan’s Law, named after Megan Kanka, seven, who was killed by a convicted sex offender, gives parents access to names and addresses of known paedophiles.

A campaign to launch a “Sarah’s Law” - a UK version of the legislation - was launched after Sarah Payne’s murder in 2000.

Source: Home Office

Children’s charity NSPCC said it was pleased there would be no Sarah’s Law because it could drive paedophiles underground.

But Steve Bevan, from Survivors Swindon, which helps men who have been sexually abused, said people had a right to know where sex offenders were living.

Harry Fletcher, assistant general secretary of probation union Napo, said Mr Reid’s move to give parents information about sex offenders sounded “like a sop to certain tabloid papers”.

“The information is not a commodity; it is highly sensitive and must be kept confidential,” said Mr Fletcher.

A £150,000 publicity campaign has also been promised by the government to remind people that 90% of child sex abuse is carried out by someone known to the family.

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Researchers from Duke University Medical centre report that lapatinib, one of the newer agents useful in treating breast cancer protects heart. They report that drug protect by preventing apoptosis (Programmed cell death) especially when heart is under stress.

Study Suggests Newer Breast Cancer Drug May Protect Heart

By uncovering how one breast cancer drug protects the heart and another does not, Duke University Medical Center researchers believe they may have opened up a new way to screen drugs for possible heart-related side effects and to develop new drugs.

The Duke researches compared the actions of two breast cancer drugs in experiments involving human cells and rats. The drugs in question were the older drug trastuzumab, whose trade name is Herceptin, and the newer drug lapatinib, whose trade name is Tykerb.

The results of the study appear early online in the journal Proceedings of the National Academy of Science.

The main side effect of trastuzumab is that it can damage heart muscle cells. Heart abnormalities have been detected in 2 to 7 percent of women taking the drug, and about one in ten women cannot take the drug because preexisting heart problems put them at greater risk for heart damage. To date, there appear to be fewer cardiac effects associated with lapatinib therapy.

Both drugs are prescribed to women whose cancerous breast cells have HER2 genes that are overactive. Approximately one in four women with breast cancer have this overactive gene, which is associated with increased cancer recurrence and worse outcomes. Lapatinib was approved earlier in March for use in women who have not responded to trastuzumab therapy.

“Trastuzumab revolutionized the treatment of HER2-positive breast cancers and represents an effective therapy for some women with one of the most aggressive forms of breast cancer,” said Duke oncologist Neil Spector, M.D., first author of the paper.. “However, now we have two agents that go after the same target and both have an effect against the cancer, but one appears to have a greater potential – based on this preliminary work – for causing cardiovascular damage.

“It is important to be clear that we are reporting findings from pre-clinical experiments, so while they suggest a difference between these two agents, it would be over-interpreting the study to conclude that women taking trastuzumab should consider any treatment change,” Spector said. “However, it may be important to conduct well-controlled clinical trials to answer this question.”

In addition to its association with breast cancer, HER2 is also essential for the early development and later sustenance of heart muscle cells. It appears that trastuzumab’s mechanism for blocking HER2 is different.

“We found that lapatinib activates a critical pathway that protects heart cells from ‘committing suicide’ as a result of stress,” Spector continued. “Heart muscle cells require a tremendous amount of energy to function properly and are therefore extremely sensitive to energy deprivation as a consequence of reduced oxygen or nutrient supply. In addition, heart muscle cells appear to be sensitive to the death promoting effects of inflammation.

“Our experiments in isolated human heart muscle cells indicate that lapatinib activates a pathway that protects cardiac muscle cells from the death-promoting effects of mediators of inflammation, which are activated in cancer patients, particularly those who have received chemotherapies that damage heart tissue,” Spector said. “In contrast, trastuzumab does not activate this protective pathway.”

With clinical trials currently investigating the combination of lapatinib with trastuzumab, there is a possibility that the effects of lapatinib in cardiac muscle cells might protect the heart against potential toxicity associated with trastuzumab, Spector added.

More broadly, Spector said that these findings of how lapatinib bestows cardiovascular protection during times of stress – whether from chemotherapy or heart muscle cells deprived of oxygen during a heart attack — could be used in other situations.

“Using this system, we could theoretically screen drugs that are in the development phase to see what their effects may be on heart muscle cells,” Spector said. “We may be able to select the drug candidates that have the fewest cardiovascular side effects and theoretically would be safer for patients. This way, we could find out about some of these potential problems long before the drugs even make it to market.”

Additionally, Spector said there is the potential for the development of similar drugs that can be used as protective agents in situations where the heart is stressed for periods of time, such as during heart attacks, coronary artery bypass surgery or angioplasty. Such a drug could even be used to preserve cardiac function in hearts being harvested for transplant, he said.

The study was supported in part by the Duke Comprehensive Cancer Center.

Other members of the team were Wenle Xia, Duke; Yosef Yarden and Rony Seger, Weizman Institute, Rehovot, Israel; Bradley Smith, Cell Signaling Technologies, Beverly, Mass.; and Ljuba Lyass, Patricia Trusk, Karen Pry, Jason Hill and Sarah Bacus, Targeted Molecular Diagnostics, Westmont, Ill.

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Researchers define a new implant that can be inserted to auditory nerve, and they claim it is superior to Cochlear nerve implants. But the research is still at animal studies and not yet come to humans. Questions still remain include feasibility of the procedure compared to insertion of Cochlear implants (based on technical aspects). But it is a good welcome to a new era of research and hope it is useful.

More than three decades ago, scientists pursued the then-radical idea of implanting tiny electronic hearing devices in the inner ear to help profoundly deaf people. An even bolder alternative that promised superior results — implanting a device directly in the auditory nerve — was set aside as too difficult, given the technology of the day.
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Shown here is the portion of a device that, when inserted in the auditory nerve, transmitted a wide range of sounds to the brain in a University of Michigan animal study. The 16 stimulating sites are spaced 1/10 of a millimetre apart.

Now, however, scientists have shown in animals that it’s possible to implant a tiny, ultra-thin electrode array in the auditory nerve that can successfully transmit a wide range of sounds to the brain. The studies took place at the University of Michigan Kresge Hearing Research Institute.

If the idea pans out in further animal and human studies, profoundly and severely deaf people would have another option that could allow them to hear low-pitched sounds common in speech, converse in a noisy room, identify high and low voices, and appreciate music — areas where cochlea implants, though a boon, have significant limitations.

“In nearly every measure, these work better than cochlear implants,” says U-M researcher John C. Middlebrooks. He led a study requested by the National Institutes of Health to re-evaluate the potential of auditory nerve implants. Middlebrooks is a U-M Medical School professor of otolaryngology and biomedical engineering. He collaborated with Russell L. Snyder of the University of California, San Francisco and Utah State University. The two co-authored an article on the results in the June issue of Journal of the Association for Research in Otolaryngology.

The possible auditory nerve implants likely would be suitable for the same people who are candidates today for cochlear implants: the profoundly deaf, who can’t hear at all, and the severely deaf, whose hearing ability is greatly reduced. Also, the animal studies suggest that implantation of the devices has little impact on normal hearing, offering the possibility of restoring sensitivity to high frequencies while preserving remaining low-frequency hearing.

Middlebrooks says it’s possible that the low power requirements of the auditory nerve implants might lead to development of totally implantable devices. That would be an improvement over the external speech processor and battery pack cochlear implant users need to wear and often have to recharge daily.

If the initial success in animals is borne out in further tests, a human auditory nerve implant is probably five to 10 years away, he says.

The researchers used cats bred for laboratory use in their experiments. They measured brain processing of auditory signals in normal conditions, then compared deaf animals’ brain responses to sounds using cochlear implants and then the direct auditory nerve implants. These measurements employed neuron -monitoring technology developed earlier at U-M. The scientists found their sensitive 16-electrode microarray resulted in several advantages over cochlear implants.

Approved by the Food and Drug Administration in 1984, cochlear implants have greatly benefited profoundly and severely deaf people. More than 100,000 implants have been performed worldwide in the last two decades, including more than 1,000 at U-M.

Like the new device, cochlear implants are small electrode arrays that receive signals from an external sound processor… They are designed to stimulate the auditory nerve and other cells to produce a sensation of hearing. But their location, separated from auditory nerve fibers by fluid and a bony wall, is a limitation.

“Access to specific nerve fibers is blunted,” Middlebrooks says. “The effect is rather like talking to someone through a closed door.”

With the new intraneural stimulation procedure, that effect is eliminated, and there are other technical advantages, too. “The intimate contact of the array with the nerve fibers achieves more precise activation of fibers signaling specific frequencies, reduced electrical current requirements and dramatically reduced interference among electrodes when they are stimulated simultaneously,” Middlebrooks says.

Middlebrooks has talked with U-M surgeons in otolaryngology about surgical approaches in humans, and is working with U-M biomedical engineers on an intraneural device that can remain in place and be tested further in animals over the next two years. The devices need to be studied over time to see if they are safely tolerated by the auditory nerve.

“If our work continues to go very well, we might begin human trials in no less than five years,” Middleton says.

Such a device might be used first in people whose cochleas are filled with bone and therefore aren’t eligible for a cochlear implant, or people whose cochlear implants are no longer effective.

The University of Michigan has submitted a patent application for the procedure. Through its Office of Technology Transfer, it is seeking a commercialization partner to assist in bringing the technology to market.

Funding for the study came from the National Institute on Deafness and Other Communication Disorders, National Institutes of Health.

Journal citation: “Auditory Prosthesis with a Penetrating Nerve Array,” Journal of the Association for Research in Otolaryngology, Volume 8, Number 2 / June, 2007; 10.1007/s10162-007-0070-2 (DOI)

Written by: Anne Rueter

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Researchers are debating the link between low oxygen delivery conditions relating to Alzheimer’s dementia. But is this the relation between dementia related to vascular causes which is well reported in the literature.

University of Leeds scientists have shown how stroke victims could be more vulnerable to Alzheimer’s disease - years or even decades after making a full recovery.

It has been known for some time that the two conditions were linked, but now the Leeds team has shown how an incident of reduced oxygen to the brain - caused by the stroke - can leave the patient vulnerable to the gradual build-up of toxic chemicals which can cause Alzheimer’s.

The research was led by Professor Chris Peers of the University’s school of medicine, who explained: “Our research is looking into what happens when oxygen levels in the brain are reduced by a number of factors, from long-term conditions like emphysema and angina, to sudden incidents such as a heart attack, stroke or even head trauma. Even though the patient may outwardly recover, the hidden cell damage may be irreversible.

“It could even be an issue for people who snore heavily, whose sleep patterns are such that there will be times in the night when their brain is hypoxic - deprived of sufficient oxygen. It can be anything that stops the heart and lungs working together to their optimal capabilities.”

The research centred on the damage done by these low-oxygen incidents to a group of brain cells called astrocytes. When the brain is functioning normally, it makes connections through the release of tiny amounts of chemical across the synapses. Once the chemical has been transmitted, it is “mopped up” by the astrocytes.

The Leeds team - which also includes Dr John Boyle in the Faculty of Medicine and Health and Dr Hugh Pearson of the Faculty of Biological Sciences - has shown that if at some point the astrocytes have become hypoxic, they are less able to mop up these transmitters, allowing the residual chemicals to accumulate and become toxic.

“This is an important factor in what’s going on in hypoxic brains,” said Prof Peers, whose work received funding from the Alzheimer’s Society and the Alzheimer’s Research Trust. “Astrocytes are just as essential as neurones for normal brain function - and we have ten times as many of them.”

Professor Susanne Sorensen, head of research at the Alzheimer’s Society, added: “The team examined the role of cells that support neurones in the brain. This is exciting because rather than focussing on neurones they looked at processes in the brain, which until now have not be researched in so much detail.”

In another project, the team is investigating two key signalling molecules which are very sensitive to fluctuations in oxygen levels. The scientists suspect that in low oxygen conditions these molecules could begin the increased production of a toxic protein called amyloid which builds up in the brains of people with Alzheimer’s.

The work at Leeds is part of a network of research projects nationally and internationally, which are adding to the sum of knowledge about a disease which costs the UK more than cancer, heart disease and stroke combined.

There are around 700,000 people in the UK currently suffering with dementia - a figure that is set to more than double by 2050, simply because we are living longer. And the disparity between funding levels for research into different conditions is stark, as Prof Peers explained: “For every cancer patient in this country, between £300 and £400 is spent every year on research. For Alzheimer’s sufferers it is closer to £15, yet sufferers can need full-time care for the last 20 to 30 years of their lives, so any research into intervention can be really cost-effective in the long term.”

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Further information

Around 700,000 people in the UK - including 20 per cent of those aged over 80 - have a form of dementia. Alzheimer’s disease accounts for more than half of these. Alzheimer’s is not a normal, unavoidable part of getting older, but a fatal and incurable brain disease. It can take 30 years to develop. Beyond the age of 65, your chance of developing Alzheimer’s doubles every five years.

The Alzheimer’s Research Trust is a UK dementia research charity dedicated to finding ways to treat, cure or prevent Alzheimer’s disease, vascular dementia, Lewy Body disease and fronto-temporal dementias. With no government funding it relies on public donations to fund its vital research. The Trust provides free information to the public on dementia and the treatments currently available. Visit http://www.alzheimers-research.org.uk/

The Alzheimer’s Society works across the UK to champion the rights of people living with dementia and those who care for them. As a charity, the society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now by visiting http://www.alzheimers.org.uk/. Visit http://www.alzheimers.org.uk/

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New evidence and research points to use of non embryonic cells to generate stem cells. They report use of fibroblasts which are found plentiful in whole body, to be precursors for stem cells.

News report from BBC

New experiments carried out on mice suggest it may be possible to replicate embryonic stem cells from skin patches, rather than having to use embryos.

Japanese and US researchers made the discovery, which represents a key breakthrough in stem cell research.

If the same can be done in humans, it could lessen or remove the need for the controversial use of embryos.

It is hoped stem cells will one day be used to replace tissue damaged by diseases like Parkinson’s and MS.

They are the body’s “master” cells, and can in theory be transformed into any type of tissue in the body.

Until recently, the most obvious source of this type of cell was from human embryos themselves - but the use of embryos is fiercely opposed in some quarters as unethcial.

Embryonic stem cells can turn, stage by stage, into any cell type in the body, but the process is extremely difficult to research, and has produced only limited success.

The latest research, published in the journal Nature, used a cell called a fibroblast, which can be found just under the skin surface.

By genetically manipulating fibroblasts from mice, the scientists “switched” them back to an embryonic state, and were able to develop them into a variety of different tissue types.

Joint finding

The advance was strengthened further by the fact that three different teams of researchers - from the Whitehead Institute in Cambridge, Massachusetts, the Harvard Stem Cell Institute, and Kyoto University in Japan - produced exactly the same result using the same technique.

Professor Rudolf Jaenisch, who led the Whitehead team, said: “These reprogrammed cells, by all criteria that we can apply, are indistinguishable from embryonic stem cells.”

Dr Lyle Armstrong, a lecturer in stem cell biology at the University of Newcastle, described the findings as a “valuable and important” development.

He said: “If the same technique works for human cells we can find out a lot about how their genomes were reprogrammed.”

However, he said that the technique would need to be refined to be safe to use in human treatments, as the mouse experiment used a retrovirus to make the genetic tweaks to the cells.

Embryo takeover

Elsewhere, scientists are developing another method of stem cell research - by potentially eliminating the need for an unfertilised human egg in cloning experiments.

At present, a cloned embryo of the patient would have to be produced to supply embryonic stem cells for treatment.

Each of those embryos requires a human egg to carry the patient’s genetic material, and these are scarce.

The Harvard University research - also published in Nature - managed to convert the “genetic identity” of a mouse embryo by temporarily halting its development at a very early stage, then inserting the genetic components from a different mouse.

This opens the possibility of using unrelated human embryos, which are in theory more plentiful, as many are created but never implanted during the IVF process, and either discarded or frozen.

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Targeted and regulated drug release will probably help the prevent blocking of shunt.

From Forschungszentrum Dresden-Rossendorf

Stents are medical implants that, for example, prevent the blocking of arteries after surgery. One of the problems using stents is the biocompatibility as the human body rejects and attacks foreign material. The Forschungszentrum Dresden-Rossendorf (FZD) developed a new method for making the surface of metal stents highly nano porous by producing millions of nano bubbles underneath. This enlarged surface allows depositing and slowly releasing drugs over a longer period of time than with usual drug eluting stents. The market leader for stents, the Boston Scientific Corporation in the US, focuses on this route to prevent the rejection of cardiovascular stents as this allows the targeted release of the drug right at the walls of the blood vessels.

Stents are implanted in certain organs as a supporting scaffold that reinforces the organ walls. Vascular stents act as small tubes made of metal or plastic mesh. The major problem in the application of stents is their compatibility with the human tissue: About 20 to 30 percent of the patients react with the rejection and the shut-down of the vessel. During the 1990’s, vascular stents, which are coated with different substances, have been developed in order to solve this problem. This kind of drug eluting stent releases small amounts of a certain drug that constrains the regeneration of cells. In addition to the more conventional bare metal stent, more and more coated stents are used in Germany since 2002, especially for the treatment of coronary heart disease. Drug eluting stents are particularly effective in the treatment of diabetic patients, which make up 30% of the interventionally treated coronary patients and also carry the highest risk for renewed narrowing.

Physicists and chemists at the Forschungszentrum Dresden-Rossendorf developed an innovative method to create a large number of tiny pores with a diameter of a few ten to a few hundred nano meters (one nano meter being one millionth of a millimeter) on the surface of stainless steel. Dr. Natalia Shevchenko and Dr. Andreas Kolitsch from the FZD Ion-Beam Center bombard the surface of a stent from all sides with a high dose of noble gas ions. This generates a scaffold of nano pores in the material below the surface. Tuning the ion energy, the flux and the temperature during the process, the desired porosity can be precisely engineered. A larger amount of the highly effective drugs can be deposited on the enlarged noble metal surface, due to this nano porous structure, which enhances the biocompatibility of the implants in the human body. Thus, this treatment results in the release of drugs over a longer period of time. The method developed by the FZD is currently assessed as a platform technology for the next generation of drug eluting stents by the Boston Scientific Corporation. The Forschungszentrum Dresden-Rossendorf and the Boston Scientific Corporation signed joint cooperation contracts with patent sharing. The objective of this research is to further develop this technique and to establish this method for surface modification in the private sector.

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Check the details about an anti-aging formula being researched.

Update from University of Michigan Health systems

Male mice get a longevity boost from compound found in creosote bush

Federal study’s early results suggest male mice fed a normal diet plus anti-inflammatory substance may live longer than control mice

ANN ARBOR, Mich. — Aspirin didn’t pan out. Neither did two other potential anti-aging agents. But a synthetic derivative of a pungent desert shrub is now a front- runner in ongoing animal experiments to find out if certain chemicals, known to inhibit inflammation, cancer and other destructive processes, can boost the odds of living longer.

Today at the annual meeting of the American Aging Association, University of Michigan scientist Richard A. Miller reports early results from a mouse study his lab and two others are conducting for the National Institute on Aging. The study, now in its fourth year, will test as many as two dozen possible anti-aging agents in animals in the next five years. The other centers are the University of Texas Health Science Center in San Antonio, Texas, and the Jackson Laboratory in Bar Harbor, Maine.

The scientists were surprised to find so quickly that one agent showed promise: NDGA, a compound derived from creosote bushes. These common North American desert shrubs have been traditionally used by Native Americans as healing remedies.

The preliminary results, to be published in August in the journal Aging Cell, show that male mice fed a normal diet and NDGA so far have survived in significantly greater numbers than mice on a normal diet. Scientists measured the difference at a point called median lifespan, when half the control mice had died of natural causes associated with aging.

“This is the first time to my knowledge when an agent has been shown to extend median life span in three laboratories,” says Miller, professor of pathology at the U-M Medical School and associate director of the U-M Geriatrics Center. Miller is also a research scientist at the Ann Arbor VA Medical Center.

No significant difference occurred in female mice. The scientists can’t explain why at this point. “We don’t know how NDGA is having its effect on survival in this first analysis,” Miller says.

“It may be that the female mice because of their hormonal status have other pathways to death and disability, or need higher or lower levels of NDGA to see an effect.”

The large, carefully controlled study at three sites, called the NIA Interventions Testing Program, is intended to provide some of the first reliable data on potential drugs to slow aging and its accompanying ills.

Miller says prior studies typically have been too small and their results hard to confirm in subsequent studies. “The National Institute on Aging decided to fund grants at three institutions to do studies of this sort in the right way,” he says.

In six to 10 months, once all the mice in the control group have died, the scientists will get answers to the really burning question: Will the mice fed NDGA, already well past middle age, live past the normal outer limit of old age? The longest that mice of this type usually live is around 1,000 to 1,100 days.

“If NDGA turns out to extend maximal lifespan by 20 or 30 percent, people would accept that as an important finding,” Miller says.

No one excited by these early results in mice is advised to bulk up on creosote bush leaves as a way to defy old age. If NDGA pushes the aging envelope in the final results of this study, other labs will likely try to repeat the results in animals. Much more research is needed before any possible human anti-aging drug could emerge, Miller says.

“Even if this agent turns out to be good for mice, it won’t be possible to tell without careful studies of humans whether NDGA is beneficial, useless, or harmful to people. Occasionally, something that is harmless in mice turns out to be highly toxic for people,” Miller cautions, adding that the Food and Drug Administration doesn’t evaluate the safety of such herbal remedies.

Randy Strong of the University of Texas Health Science Center, David E. Harrison of the Jackson Laboratory and Miller are chief collaborators in the National Institute on Aging project, which includes scientists at Oklahoma Medical Research Foundation, the University of Florida, and Milan, Italy.

The research is funded by the National Institute on Aging, part of the National Institutes of Health.

Visit www.americanaging.org for more information on the American Aging Association and its annual meeting.

Written by: Anne Rueter

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Recent research showed arsenic to be useful in extending the survival of patients with acute promyelocytic lukemia as reported in reuters.

Arsenic, the poison of choice for many a murder mystery, can significantly extend survival in patients with a rare form of leukemia, U.S. researchers said on Saturday.

“It’s a much smaller dose than you would use to poison people,” added Dr. Bayard Powell of Wake Forest University Baptist Medical Center.

Adding arsenic to standard treatment can extend patients’ lives and prevent relapse, Powell said. The effect is so impressive that patients may some day be able to skip chemotherapy — but that will take more testing.

“This study has redefined the standard of care,” said Powell, who presented results from the large, three-year study at a meeting of the American Society of Clinical Oncology in Chicago.

“The people who took arsenic lived longer,” Dr. Nancy Davidson, president-elect of the American Society of Clinical Oncology, told Reuters.

The drug, arsenic trioxide, which is made by Pennsylvania- based Cephalon Inc. and sold under the brand Trisenox, is approved for people with acute promyelocytic leukemia, or APL, whose disease has returned.

Standard treatment for APL — a form of acute myeloid leukemia that strikes 1,500 people a year in the United States — involves chemotherapy and a form of vitamin A called all-trans retinoic acid, which helps 70 to 80 percent of patients gain long-term remission.

About 25 percent of those patients, however, relapse and no longer respond to treatment. Those patients often get arsenic trioxide.

But in a study sponsored by The National Cancer Institute, Powell and colleagues paired arsenic with standard treatment in newly diagnosed patients.

They found that 81 of 261 patients in the arsenic group were free of disease after three years, compared with 66 of 257 patients in the group who got the standard regimen alone.

“Among those who actually got arsenic, only five patients, or 2 percent, relapsed,” Powell said. “This is very impressive.”

Doctors at the meeting believe the drug will be used as a first treatment right after chemotherapy.

“This really brings what has been a salvage treatment up front and actually improves survival,” said Dr. Joseph Moore of Duke University Medical Center.

“The next question is how far do we move it forward?” Powell asked.

He said future studies would test whether patients can skip chemotherapy and just take arsenic.

Dr. Mitchell Smith, director of the lymphoma service at Fox Chase Cancer Center in Philadelphia, said the therapy’s effect was compelling but he was not ready to rule out chemotherapy, at least not without more study.

While most chemo treatments are toxic and work by killing cells, arsenic trioxide zeros in on disease-causing cells

“It seems to kill preferentially,” Smith said.

Arsenic has been used as a traditional therapy in China for more than 2,000 years, but its use in the United States is still rather novel.

“Patients look up and pay attention when you mention you are going to treat them with arsenic,” Powell said.

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Reuters reports a link between smoking and risk of depression.

Persistent smokers appear to be at increased risk for becoming depressed compared to never smokers, results of a long-term study of Finnish twins suggest. On the other hand, this association was not seen in individuals who stopped smoking many years ago.

“Although nicotine in cigarettes has some mood-elevating properties, in the long-run chronic exposure to cigarette smoke may have a more important role in the etiology of depressive symptoms,” lead author Dr. Tellervo Korhonen from the University of Helsinki told Reuters Health.

The results are based on 4,000 male and 5,000 female Finnish twins, whose health and health behavior were monitored for 15 years. The results suggest that persistent chronic smoking predicts the development of depressive symptoms.

However, when adjusted for other factors associated with depression, the elevated risk of depression with persistent smoking remained significant only among men.

There was also evidence that smokers who had quit were also at increased risk of depression, but only in the short term. Smokers who quit and remained off cigarettes in the long run did not have an increased risk for depression compared with never smokers. “This may reflect a relatively long recovery process from the adverse effects of cigarette smoking, Korhonen said in a statement.

“When people start smoking, the immediate effects of nicotine in the brain are rewarding and pleasurable,” Korhonen explained. “This suggests self-medication, where a person who has mood problems seeks relief via cigarette.”

Because addiction to nicotine is as strong as an addiction to heroin, abstinence is difficult.

“Smokers who are vulnerable to depression may need specific pharmacological treatment and behavioral support to overcome the earlier phase of abstinence,” Korhonen said. After that, “their chances to quit successfully improve.”

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