Health News Today

AAMC Pleased That Health Care Reform Is Top Priority In Obama Budget

2009-03-02T13:00:00.000+02:00

AAMC (Association of American Medical Colleges) President and CEO Darrell G. Kirch, M.D., issued the following comments on President Obama's budget blueprint, released :

"America's medical schools and teaching hospitals are pleased that President Obama views health care reform as one of the nation's top priorities this year. We agree that the current challenges of cost, quality, and access facing our health care system must be addressed immediately. This includes making vital investments to ensure that our nation's health care workforce has both the skills and the capacity to care for all Americans.

It was gratifying to see that the new administration will use eight principles to guide its health care reform efforts. These principles adhere very closely to those developed by the nation's medical schools and teaching hospitals last year to guide America's discussion of health care reform. We concur that affordable health care coverage should be available to all, that our system should be restructured to promote wellness and prevention while still providing high-quality, cost-effective treatment, and, most importantly, that health care financing should be sustainable, equitable, and accountable.

The AAMC and its members also believe the key to achieving comprehensive reform is to support and preserve the greatest strengths of our current system, while making improvements to health care delivery and financing. We agree with the need to reduce waste and inefficiency in our system, but at the same time, these savings should not undermine the ability of our teaching hospitals and physicians to care for their communities.

U.S. medical schools and teaching hospitals play a pivotal role in improving the health of our nation. These institutions train tomorrow's doctors, treat large numbers of uninsured Americans, and advance care through groundbreaking cures and treatments. With a concerted national effort from the public and private sectors, we believe the goal of affordable, quality health care can be achieved in the coming years. We stand ready to work with Congress and President Obama to attain the positive changes needed for successful reform."

For a copy of the "AAMC's Principles for Reform of U.S. Health Care: A Guide for Policymakers," go to: http://www.aamc.org/reformprinciples

The Association of American Medical Colleges is a not-for-profit association representing all 130 accredited U.S. and 17 accredited Canadian medical schools; nearly 400 major teaching hospitals and health systems, including 68 Department of Veterans Affairs medical centers; and nearly 90 academic and scientific societies. Through these institutions and organizations, the AAMC represents 125,000 faculty members, 70,000 medical students, and 104,000 resident physicians. Additional information about the AAMC and U.S. medical schools and teaching hospitals is available at http://www.aamc.org/newsroom.

Association of American Medical Colleges

Don't Confuse FEN Death And Investigation With Aid In Dying

2009-02-28T13:00:00.000+02:00

The media has recently reported the arrest of individuals associated with a group known as Final Exit Network (FEN) on charges of assisting a suicide in Arizona, and attempting to engage in similar activity in Georgia. The cases reported in the media this week involving FEN ought not be confused with the choice of aid in dying.

Media accounts of the facts suggest that the Arizona decedent was not terminally ill and may have suffered from impaired judgment and/or mental illness.

It is important to recognize the difference between the choice of a mentally competent, terminally ill patient for a peaceful death via self-administering medications prescribed for this purpose, and the act of a distraught individual who is not dying, who may be suffering from impaired judgment or mental illness, to precipitate death. The former is a practice known as aid in dying, which has strong and growing support among the public and among medical and health policy professionals. The latter is suicide. It is essential to recognize the difference between these.

In 2008, four major national medical professional and health policy organizations adopted policy in support of aid in dying, the practice of a physician providing a prescription to a mentally competent, terminally ill patient that brings about a peaceful death. This represents a significant turning point in American society's evolution to empower terminally ill patients with information and choices about how they will die.

The organizations adopting policy in support of aid in dying include the American Medical Women's Association (AMWA), the American Medical Students' Association (AMSA), the American College of Legal Medicine (ACLM), and the American Public Health Association (APHA).

The Oregon Death with Dignity Act (Dignity Act) began implementation in 1998. This law permits mentally competent individuals who have less than six months to live to obtain a prescription for medication that can be self-administered to bring about a peaceful death. It has been implemented without interruption since 1998.

Under the Dignity Act, patients must follow a strict set of procedures to establish eligibility. A physician must determine that the patient has a life expectancy of less than six months; this diagnosis must be confirmed by a second opinion. The patient must make multiple requests, waiting at least fifteen days between the first and last request, must establish capacity to make medical decisions, and must be informed of palliative care options such as hospice, if not already receiving such services. If all of these procedures are followed, and the patient is deemed eligible by the physician to obtain the life-ending medication, an Oregon physician can provide the requested prescription. During the decade that aid in dying has been legal in Oregon, close to 30 terminally ill individuals each year have gone through the process, obtained and taken the medication, and died peacefully. Those present at these deaths, usually close family members, report that the patient was enormously relieved to be able to make this choice. On a date chosen by the patient, loved ones may gather around for a final goodbye.

The patient consumes the medication, becomes drowsy, falls deeply asleep, and after a short period of time ceases to breathe. The long road from diagnosis to curative treatment to palliative care to death has ended on terms acceptable to the patient. More patients obtain the medication than go on to use it: some fraction each year receive the medication, put it in the medicine cabinet, feel comforted to know it is there, and never take it.

Demographic data about the patients who choose to use the Dignity Act show that most are dying of cancer. The next most common terminal illness is amyotrophic lateral sclerosis (ALS). Those using the law are insured, well educated, and are receiving comprehensive pain and symptom management, typically through hospice services. Opponents of the Dignity Act legislation had argued that such a law would be forced upon the uninsured, the poor, minorities, persons without access to hospice, or disabled persons. The data have disproved this conjecture.

In addition, a number of unexpected but significant developments occurred in Oregon following implementation of the Dignity Act. Referral of patients to hospice care increased dramatically, as did physician enrollment in continuing education courses on how to treat pain and symptoms associated with terminal illness. It is likely that physicians want to ensure that no patient makes use of the Dignity Act due to inadequate pain and symptom management. This galvanized both the increase in hospice referrals and physician efforts to learn more about treating pain and symptoms.

Voters in the state of Washington considered the issue in 2008 and adopted the Washington Death with Dignity Act by the significant margin of 59% to 41%. The Washington measure is virtually identical to Oregon's and will begin implementation on March 5, 2009.

As a result of a court case, Montana recently recognized that the freedom of its terminally ill citizens to choose aid in dying is a fundamental right protected by its state constitution's guarantees of privacy and dignity.

Public support for empowering dying patients with the freedom to choose aid in dying is strong. A Harris poll in 2005 found that 70% of U.S. adults favor a law that would "allow doctors to comply with the wishes of a dying patient in severe distress who asks to have his or her life ended."

When a patient does not feel able to discuss the desire for aid in dying with his or her physician, or cannot find a physician willing to provide it, the patient may seek assistance in hastening death from a family member or loved one. Unfortunately, these incidents often involve a violent means to death, such as gunshot.

A fraction of terminally ill patients - including those who have excellent pain and symptom management - confront a dying process so prolonged and marked by such extreme suffering and deterioration that they decide aid in dying is preferable to the alternatives. Having this option harms no one, and greatly benefits both the relatively few patients in extremis who make use of it and many more who draw comfort from knowing it is available should their dying process become intolerable. The trend in policy among mainstream medical and health policy associations is clearly in favor of supporting this compassionate option.

For more information please visit http://www.compassionandchoices.org.

NHS Plan For Rare Diseases Must Be A Priority For Government - Campaign Group Launched On Rare Disease Day 2009, UK

2009-02-27T13:00:00.000+02:00

A coalition of patient charities, medical professionals and industry representatives have called on Department of Health Ministers to move forward with EU proposals to develop a national plan for the treatment of rare diseases.

Rare Disease UK is formally launched today on Rare Disease Day 2009 in the House of Commons. Alastair Kent, Chair of Rare Disease UK, said: "It is a national disgrace that the NHS does not have a coordinated plan to treat the many thousands of people who are every year affected by rare diseases. Currently patients, families and individuals affected by rare diseases are denied their right to high quality care and support, due to a lack of coordination and information provision to both health professionals and patients.

Finding expert help is too often a matter of chance rather than planning by the NHS. A national plan would help to bring together expertise and skill to ensure that patients with rare conditions are not denied high quality care".

He added: "The paradox of rare diseases is that they collectively affect over 3.5 million people in the UK but that all too often patients go undiagnosed and misdiagnosed with appalling consequences. Ministers can do more and must do more to make the NHS fit for the purpose of treating rare conditions."

Dr Peter Corry, a leading Paediatrician at St Luke's Hospital, Bradford, said: "Many rare diseases are severe, or even life-threatening. Diagnosis is often difficult and the complex treatments required may involve several specialists. Frontline medical staff need good sources of up-to-date information, clear pathways and access to the appropriate experts."

There are over 6000 rare conditions identified, and they affect over 3.5 million people in the UK and over 30 million people in the EU at some point in their life.

A European survey of patients with rare diseases published today shows:

- 40% of respondents to a recent survey of patients said they received the incorrect diagnosis

- 25% of patients waited between 5 - 30 years for a correct diagnosis.

- 50% of respondents seeking social services reported that their expectations were only met "somewhat" or even "not at all"

The report can be downloaded by clicking here

Note

1. Rare Disease UK is a joint initiative of the Genetic Interest Group, (the UK alliance of patient organisations with a membership of over 130 charities which support children, families and individuals affected by genetic disorders) and others in response to unmet health care needs of families who currently strugglee to get access to integrated care and support from the NHS.

3. Rare Disease Day is being marked on 28th February. It is an international day to raise awareness of rare conditions http://www.rarediseaseday.org

4. 1 in 17 people will develop a rare condition at some point during their life. There are over 30 million people living in the European Union affected by a rare disease and 3.5 million in the UK.

5. The European Council of Ministers is expected to ratify a European Commission communication later this year requiring all Member States to develop national plans for the treatment of rare diseases.

6. Further information and reports will appear on the Rare Disease website: http://www.raredisease.org.uk Rare Disease UK is registered at Unit 4D, Leroy House, 436 Essex Road, London, N1 3QP.

Rare Disease

Compounds Protect Against Cerebral Palsy - A Stunning Finding:

2009-02-26T13:00:00.000+02:00

Two compounds developed by Northwestern University chemists have been shown to be effective in pre-clinical trials in protecting against cerebral palsy, a condition caused by neurodegeneration that affects body movement and muscle coordination.

"The results were just stunning, absolutely amazing," said Richard B. Silverman, John Evans Professor of Chemistry in the Weinberg College of Arts and Sciences at Northwestern, who led the drug development effort. "There was a remarkable difference between animals treated with a small dose of one of our compounds and those that were not."

The findings, which are published online by the journal Annals of Neurology, suggest that a preventive strategy for cerebral palsy may be feasible for humans in the future. (The paper also will appear in the journal's February issue, in print the week of March 2.)

None of the fetuses born to animals treated with the two compounds died; more than half of those born to untreated animals died. Eighty-three percent of animals treated with one of the compounds were born normal, with no cerebral palsy characteristics. Sixty-nine percent of animals treated with the other compound were born normal. There was no sign of toxicity in the treated animals, and their blood pressure was normal.

Cerebral palsy is caused by an injury to the brain before, during or shortly after birth, although it typically is not diagnosed until after the age of one. Approximately 750,000 children and adults in the United States have a form of cerebral palsy, with the majority having been born with the condition.

The new compounds Silverman and his team developed inhibit an enzyme found in brain cells that produces nitric oxide, thus lowering nitric oxide levels. At normal levels, nitric oxide acts as a neurotransmitter and is important to neuronal functioning, but at high levels it has been shown to damage brain tissue. An overabundance of nitric oxide is believed to play a role in cerebral palsy.

After a lengthy drug development process, Silverman went to his collaborator Sidhartha Tan, M.D., a neonatologist from NorthShore University HealthSystem, to test the two best compounds on Tan's cerebral palsy animal model. A diminished supply of oxygen (hypoxia) from mother to fetus causes an increase in nitric oxide levels in the brain, which leads to brain damage and newborns with cerebral palsy characteristics.

Silverman and Tan wanted to see if they could prevent brain damage in the fetuses by administering one of the compounds to the mother before the hypoxic event. They expected some degree of success but were surprised by how effective the treatment was. The researchers attribute the protection from cerebral palsy to the decrease in the brain enzyme and the nitric oxide that is produced.

"We still have to bring the phenomenon to humans, which would be very exciting," said Tan, who has been investigating the impact of nitric oxide on neuronal damage. "There is such a dire need. If we could safely give the drug early to mothers in at-risk situations, we could prevent the fetal brain injury that results in cerebral palsy."

In developing the potential drugs, Silverman and his team were able to produce something that pharmaceutical companies so far have not: highly selective compounds that inhibit the enzyme found in brain cells that produces nitric oxide but that do not affect similar nitric oxide-producing enzymes found in endothelial and macrophage cells.

Endothelial cells regulate blood pressure, and macrophage cells play an important role in the immune system. Reducing their production of nitric oxide would have deleterious effects on an animal, such as increasing blood pressure or compromising the immune system.

"The challenge was to lower only the nitric oxide in the brain and not in the other cells where the nitric oxide is very important," said Silverman, a member of Northwestern's Center for Drug Discovery and Chemical Biology.

"Early compounds developed by drug companies to target the brain enzyme actually bound to all three nitric oxide enzymes," he said. "This made me think that the three enzymes must be very similar in structure. We decided to look for differences away from the normal binding site to get selectivity for only the brain enzyme."

This approach paid off. Silverman and his team started with a molecule that showed good selectivity of the brain enzyme over the macrophage enzyme but with no selectivity over the endothelial enzyme. The researchers then made modifications to the molecule and built a library of 185 different compounds that could be tested for the selectivity they wanted. They found 10 good ones. More modifications were made until they had a few compounds that were very selective and very potent for the brain enzyme.

Silverman then started collaborating with Thomas Poulos, Chancellor's Professor of Molecular Biology and Biochemistry and a crystallographer from University of California, Irvine, who had been working on the structure of the neuronal brain enzyme. Silverman sent him several potent and selective compounds, and Poulos produced crystal structures showing each compound bound to the brain enzyme.

"Thanks to the talents of Tom and his associate Huiying Li we could, for the first time, see visually why these compounds were selective and also see the difference between them," said Silverman.

Haitao Ji, a postdoctoral fellow who is an expert in structure-based design, joined Silverman's team. Ji took the crystal structures of their molecules bound to the enzyme and, using computer modeling, designed new structures with even better properties.

These compounds were more potent and much more selective than earlier ones. Poulos produced crystal structures of the new compounds. These are the compounds that Tan tested on his cerebral palsy animal model with such promising results, as reported by the research team in the Annals of Neurology paper.

"This is a great example of a multi-institutional collaboration that could not have been done without each of the parts -- we each contributed something different," said Silverman. "Science is going in that direction these days."

The researchers caution that taking the compounds to human clinical trials is a lengthy and complicated process. Silverman says they next plan to make the compounds even more potent, selective and bioavailable and then envision partnering with a company that would want to develop the drugs further.

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Article adapted by Medical News Today from original press release.

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Silverman, Tan, Poulos, Li and Ji (lead author) are all authors of the paper, titled "Selective Neuronal Nitric Oxide Synthase Inhibitors and the Prevention of Cerebral Palsy." Other authors are Jotaro Igarashi, from the University of California, Irvine; Matthew Derrick, M.D., from NorthShore University HealthSystem (formerly Evanston Northwestern Healthcare); Pavel Martasek, M.D., and Linda J. Roman, from the University of Texas Health Science Center; and Jeannette Vasquez-Vivar, from the Medical College of Wisconsin.

Source: Megan Fellman

Northwestern University

Poorer Canadians More Likely To Be Hospitalized For Depression But Have Similar Hospital Experiences

2009-02-25T13:00:00.000+02:00

In 2004-2005, people in Canada's poorest neighbourhoods were 85% more likely to be hospitalized for depression than people living in better-off neighbourhoods, according to a new analysis from the Canadian Institute for Health Information (CIHI). The analysis examines the relationship between neighbourhood income and general hospital use for depression for persons aged 15 to 64 in 13 Canadian cities. The analysis examines hospitalization rates, lengths of stay and readmission rates. Depression is the most common cause of hospitalization for mental illness in Canada, with a rate of 100 per 100,000 population (2005-2006).

CIHI's analysis found that, whereas poorer Canadians were more likely to be hospitalized for depression, there were no differences between income groups in the duration of hospital stays (average of 16 days). This suggests patients had similar hospital experiences regardless of their income.

Similarly, CIHI's analysis found no differences between income groups in the likelihood of readmission. Just more than 7% of patients admitted to hospital because of depression were readmitted within 30 days of their initial discharge.

The Association Between Socio-Economic Status and Inpatient Hospital Service Use for Depression

About CIHI

The Canadian Institute for Health Information (CIHI) collects and analyzes information on health and health care in Canada and makes it publicly available. Canada's federal, provincial and territorial governments created CIHI as a not-for-profit, independent organization dedicated to forging a common approach to Canadian health information. CIHI's goal: to provide timely, accurate and comparable information. CIHI's data and reports inform health policies, support the effective delivery of health services and raise awareness among Canadians of the factors that contribute to good health.

Canadian Institute for Health Information

Clue To Potential New Anthrax Treatment discovered in Houseplant Pest

2009-02-24T13:00:00.000+02:00

Researchers at the University of Warwick have found how a citric acid-based Achilles heel used by a pathogen that attacks the popular African Violet house plant could be exploited not just to save African Violets but also to provide a potentially effective treatment for Anthrax.

The researchers examined how a chemical structure is assembled in a bacterial pathogen called Pectobacterium chrysanthemi (Dickya dadantii) that afflicts plants - particularly the African Violet which often appears in many homes as a decorative houseplant.

Like many bacteria Pectobacterium chrysanthemi competes with its host for iron. Without a supply of this essential nutrient the bacterium cannot grow. The University of Warwick researchers Dr Nadia Kadi, Dr Daniel Oves-Costales, Dr Lijiang Song and Professor Gregory Challis worked with colleagues at St Andrews University to examine how a "siderophore", one of the key tools the bacterium uses to harvest iron is assembled. They discovered how an enzyme catalyst in the assembly of this particular siderophore - called achromobactin - binds citric acid, a vital iron-binding component of the structure. Their findings show that this chemical pathway could be blocked or inhibited to prevent the bacterium from harvesting iron, essentially starving it.

While an interesting piece of science in itself and of even more interest to owners of African Violet houseplants the Warwick research team found that this work also has major implications for the treatment of several virulent and even deadly mammalian infections including Anthrax.

A second piece of research conducted by three of the University of Warwick researchers (Dr Daniel Oves-Costales, Dr Lijiang Song and Professor Gregory L. Challis ) found that the deadly pathogen which causes Anthrax in humans uses an enzyme to incorporate citric acid into another siderophore that is very similar to the one used by the African Violet pathogen. The researchers showed that both enzymes recognise citric acid in the same way. This means a common strategy could be used to block both the Anthrax and African Violet pathogen siderophore synthesis pathways.

Professor Greg Challis University of Warwick said:

"Inhibiting this citric acid-based process could be even more effective in combating an anthrax infection than it would be in combating the African violet pathogen, because the African Violet pathogen has a second siderophore that can harvest iron from the host and could attempt to struggle on with just this, whereas the anthrax pathogen appears not to have such a back up mechanism."

This new discovery could lead to the design of drugs that might eliminate the anthrax pathogen's ability to harvest iron and stop an infection dead in its tracks. A respiratory anthrax infection is nearly always fatal but this discovery opens new possibilities for combating such infections.

The benefits of the discovery may even go beyond treatments for Anthrax. The researchers are now looking at similar enzymes involved in the assembly of citric acid-derived siderophores in E. coli and MRSA, which may offer further targets for drug development.

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Article adapted by Medical News Today from original press release.

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Funding for the research reported in both papers was provided by the Biotechnology and Biological Sciences Research Council (BBSRC)

The African violet pathogen research "AcsD catalyzes enantioselective citrate desymmetrization in siderophore biosynthesis" is published in Nature Chemical Biology, 2009, 5, 174-182. The paper on Anthrax entitled "Enantioselective desymmetrisation of citric acid catalysed by the substrate-tolerant petrobactin biosynthetic enzyme AsbA" is published in Chemical Communications, 2009, doi: 10.1039/b823147h

For further information please contact:

Professor Greg Challis, Professor of Chemical Biology, Department of Chemistry, University of Warwick

PR21 PJD 23rd February 2009

Source: Professor Greg Challis

University of Warwick

UK Blood Inquiry Blames Procrastination For "Horrific Human Tragedy"

2009-02-23T19:00:00.000+02:00

A two-year privately funded independent inquiry into how nearly 5,000 UK citizens who were given blood transfusions over 20 years ago were infected with Hepatitis C and HIV, found that procrastination on the part of government and scientific agencies was to blame for the "horrific human tragedy".

Led by Labour Peer Lord Archer of Sandwell, the inquiry authors, who released their findings earlier today, Monday 23 February, concluded that:

"Commercial priorities should never again override the interests of public health."

4,670 people who were given blood transfusions using NHS supplied blood in the 1970s and 1980s were infected with Hepatitis C, and a quarter of them also became infected with HIV.

According to the Telegraph, the authors said although it was difficult to say exactly who was responsible, they were "dismayed" at how long it took the UK government and scientific advisers to act. In Ireland it took only 5 years for the country to become self-sufficient in blood products, whereas in England and Wales it took 13 years, a rate of progress that the authors described as "lethargic".

A speedier response on the dangers of Hepatitis C and HIV could have saved many lives. In order to meet the demand, the NHS bought blood products from US suppliers, whose sources included prison inmates, a population known to have a higher prevalence of HIV and Hepatitis C carriers. Lord Archer said it would have been highly unlikely that UK sourced supplies would have come from such a population of donors.

The authors said it was hard not to conclude that "commercial interests took precedence over public health concerns" and that a full public inquiry should have taken place much earlier.

The inquiry was set up after decades of campaiging by victims and their families. Many of the victims included hemophiliacs, nearly 2,000 of whom have died since receiving contaminated blood from the tainted supplies.

52-year old Haydn Lewis, a hemophiliac who lives in Cardiff, told the BBC that he became infected with HIV and Hepatitis C from contaminated blood products. He is waiting for a liver transplant and said he thinks he also infected his wife because doctors delayed telling him he was infected.

Lewis told the BBC the report should have criticized the government more. He said he wants closure, after 20 years of having "a ball and chain around my ankle".

Lord Archer told the BBC that is was too late to say who is to blame and what the government needs to do is "address is the needs of people now".

The report authors recommend that the government should set up a compensation scheme for the victims who so far have only received money from charities.

For the full report, visit the website Public inquiry into contaminated blood and blood products.

Sources: Telegraph, BBC News.

Written by: Catharine Paddock, PhD

Copyright: Medical News Today

Not to be reproduced without permission of Medical News Today

Thermo Fisher Scientific Introduces New Pipette Tip Packaging Systems

2009-02-23T13:00:00.000+02:00

Thermo Fisher Scientific, Inc., the world leader in serving science, announced today the addition of its MBP brand ART barrier tips in two new packaging configurations. The ART Reload System combines individually packaged barrier tip reload inserts with space-saving hinged racks, offering an innovative and environmentally-friendly alternative to ordinary tip packaging.

This sterile, barrier tip reload system features a "push down" blister tub that clips the inserts securely into the hinged rack without exposure to the environment for a completely contamination-free transfer of the pipette tips into the tip racks. Effortless removal of the inserts from the racks after tips have been used makes this space-saving reload system a compact alternative. Simply reload the existing rack with new inserts. Purchasing inexpensive empty hinged racks allows for simple conversion to the blister tubs, while covers may be used as hinged or lift-off style, to fit specific laboratory needs. The Reload System components utilize recycled materials to package virgin polypropylene barrier tips, making the Reload System a contamination-free, environmentally-friendly choice.

For more information about the new ART Reload System, please visit http://www.mbpinc.com.

Molecular BioProducts is part of Thermo Fisher Scientific, the world leader in serving science.

About Thermo Fisher Scientific

Thermo Fisher Scientific Inc. (NYSE: TMO) is the world leader in serving science, enabling our customers to make the world healthier, cleaner and safer. With annual revenues of $10.5 billion, we have more than 34,000 employees and serve over 350,000 customers within pharmaceutical and biotech companies, hospitals and clinical diagnostic labs, universities, research institutions and government agencies, as well as environmental and industrial process control settings. Serving customers through two premier brands, Thermo Scientific and Fisher Scientific, we help solve analytical challenges from routine testing to complex research and discovery. Thermo Scientific offers customers a complete range of high-end analytical instruments as well as laboratory equipment, software, services, consumables and reagents to enable integrated laboratory workflow solutions. Fisher Scientific provides a complete portfolio of laboratory equipment, chemicals, supplies and services used in healthcare, scientific research, safety and education. Together, we offer the most convenient purchasing options to customers and continuously advance our technologies to accelerate the pace of scientific discovery, enhance value for customers and fuel growth for shareholders and employees alike. Visit http://www.thermofisher.com.

Thermo Fisher Scientific acquired Molecular BioProducts (MBP), a leading manufacturer of high quality pipette tips within the liquid handling market, who has made continual innovations and patents focused in the area of controlling contamination associated with handling samples in the molecular biology workplace.

Thermo Fisher Scientific Inc

Drug A-002 Could Be Effective Anti-Atherosclerotic Agent

2009-02-20T13:00:00.000+02:00

The secretory phospholipase A2 enzyme (sPL A2) inhibitor A-002 could be an effective anti-athersclerotic agent, concludes an Article in this week's edition of The Lancet, written by Professor Robert S Rosenson, University of Michigan, USA, and colleagues.

Atherosclerosis is a disease of the arteries in which they become blocked and inflamed by a build-up of white blood cells and fatty (lipid) material within. Phospolipid molecules in the blood and vessel wall are broken down by sPLA2 , producing two potentially bioactive fats that can be involved in atheroscelroisis. There are ten separate groups in the family of sPLA2 enzymes, of which groups IIA, V, and X are highly expressed in atherosclerotic lesions in both humans and mice. Thus any potential treatment would need to target these three groups. The authors tested the effect of A-002, an sPLA2 enzyme inhibitor that targets these three groups, on sPLA2 and on plasma lipoproteins and inflammatory biomarkers in patients with coronary heart disease, specifically examining the effect on sPLA2 IIA. Groups V and X sPLA2 are more highly concentrated in the vessel wall, so these were not specifically analysed.

In this phase II randomised controlled trial, 393 patients from the USA and Ukraine were randomised to receive placebo (79), or one of four does of A-002: 50mg (79), 100mg (80), 250mg (78) or 500mg (77). All groups received their treatment twice daily for eight weeks. The researchers found that mean sPLA2 IIA concentration fell by 87% in the overall A-002 group, compared with a fall of only 5% in the placebo group. The reductions for A-002 patients were does dependent, ranging from 69% in the 50mg group to 96% in the 500mg group. Mean LDL (bad) cholesterol concentrations decreased by 8.0% in the overall A-002 treatment group, compared with 1.7% in the placebo group. C-reactive protein (an inflammatory marker) concentrations decreased by 56% in the overall A-002 treatment group, and by only 25% in the placebo group.

The authors say*: "Our study demonstrates that sPLA2 inhibition produces favorable changes in plasma lipids, oxidized LDL and inflammatory markers, and the magnitude of these changes was larger in statin-treated patients. Proof of concept for sPLA2 inhibition has been established in experimental animal studies. These studies have demonstrated that sPLA2 inhibition with varespladib reduced atherosclerosis progression and improved histopathological features associated with plaque stability. The clinical utility of sPLA will require a randomized, double-blind clinical trial that investigates the effects of sPLA2 inhibition on reducing atherosclerosis progression and cardiovascular events."

The authors conclude: "The reductions in sPLA2 concentration suggest that A-002 might be an effective anti-atherosclerotic agent."

In an accompanying Comment, Dr Marshall A Corson, University of Washington/Harborview Medical Center, Seattle, Washington, says that these enzymes are promising targets for therapeutic interventions. But he also cautions that recent attempts to develop selective anti-inflammatory or antioxidant therapies initially showed favourable effects on biomarkers and measures of efficacy, but were subsequently found to be adverse or neutral for cardiovascular disease events. He concludes: "[This difficulty] suggests that challenges might lie ahead for sPLA2 inhibitors. These difficulties could increase the regulatory hurdles that need to be cleared for these, or other, novel antiatherosclerotic therapies."

The Lancet

In The Most Lethal Brain Cancer Newly Discovered Gene Could Be A Prime Target

2009-02-19T13:00:00.000+02:00

Scientists at Duke University Medical Center and Johns Hopkins University have discovered mutations in two genes that could become therapeutic targets in malignant glioma, a dangerous class of brain tumors.

"The fact that the defective genes code for metabolic enzymes found only in malignant glioma, and not in normal tissue, could make the gene products therapeutic targets," says Hai Yan, M.D., Ph.D., lead author, an assistant professor in the Duke Department of Pathology. The findings are published in the Feb. 19 issue of the New England Journal of Medicine.

These genetic flaws might also help distinguish between primary and secondary glioblastoma multiforme (GBM), two subtypes of especially deadly malignant gliomas, with survival of only months after their diagnosis. Patients that have mutation of the genes, isocitrate dehydrogenase 1, gene 1 and 2 (IDH1 and IDH2), also had a longer survival time.

Because the researchers found this genetic mutation in several different stages of glioma development, "the results suggested that the IDH mutations are the earliest genetic changes that start glioma progression," said Darell Bigner, M.D., Ph.D., a co-author and director of the Preston Robert Tisch Brain Tumor Center at Duke University. Yet, patients with GBM or anaplastic astrocytoma who had the IDH mutations also were found to live longer than patients with those two cancers who lacked the mutations.

Malignant glioma appears to be two diseases, one that involves IDH mutations and one that doesn't, Yan explained. "As a cancer culprit gene, IDH mutations do contribute to cancer," he said. "Meanwhile, patients with the IDH mutation live longer with their cancer. The IDH mutation could serve as a biomarker that would help single out individuals who are likely to have better outcomes and receive different treatment."

He said that IDH mutations appear to define a specific subtype of GBMs, which is important so that physicians can plan specific treatment strategies to target this specific subtype of GBMs. "All GBMs are basically considered the same and are treated in the same way," Yan said. "Our studies clearly demonstrate that we need to start thinking about them as different. It is entirely possible that treatments that work for the IDH-mutation subtype would not work for the rest of GBMs, or vice versa." Knowing the tumor subtype has significant implications for how we plan future clinical trials for patients with GBMs, he added.

"I can say this is potentially one of the most important discoveries in genetic studies on malignant gliomas, in the low-grade to high-grade forms of the tumor," Yan said. "The results are so clear cut. I have been doing intensive genetic studies in brain cancers for six years, and I have never seen gene mutations as striking as in this study."

The researchers found IDH1 mutations in more than 70 percent of astrocytomas and olidgodendrogliomas (WHO grade II and III), as well as in secondary GBMs (WHO grade IV). Those without the IDH1 mutation had similar mutations in the closely related IDH2 gene. The mutations decreased IDH enzymatic activity. This signaled that IDH mutations are likely important in initiating malignant gliomas, but it is not known yet how they contribute to glioma development.

The findings are important in many ways. IDH can be used to distinguish primary GBMs, which do not arise from an existing tumor, from secondary GBMs, which arise from low-grade glioma tumors. The IDH1 mutation is missing in pilocytic astrocytomas, which means these particular brain tumors arise through a different mechanism.

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Article adapted by Medical News Today from original press release.

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Dr. William Parsons of Johns Hopkins Kimmel Cancer Center contributed equally with Dr. Yan to the article. Other authors included Genglin Jin, Ph.D., Roger McLendon, M.D., and B. Ahmed Rasheed, Ph.D., from the Duke Department of Pathology; Ivan Kos, Ph.D., and Ines Batinic-Haberle, Ph.D., of the Duke Department of Radiation Oncology; Henry Friedman, M.D., of Duke Neuro-Oncology; and Allan Friedman, M.D., and David Reardon, M.D., of the Duke Department of Surgery, members of the Pediatric Brain Tumor Foundation Institute and the Preston Robert Tisch Brain Tumor Center; and James Herndon, Ph.D., of the Duke Cancer Statistical Center. The remaining authors came from the Ludwig Center for Cancer Genetics and Therapeutics and the Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, the Johns Hopkins Department of Neurosurgery, the Department of Pediatrics at Baylor College of Medicine, and the Center for Drug Evaluation and Research of the U.S. Food and Drug Administration.

Funding came from the Pediatric Brain Tumor Foundation Institute, a Damon Runyon Foundation Scholar Award, a grant from the Southeastern Brain Tumor Foundation, Alex's Lemonade Stand Foundation, a grant from the V Foundation for Cancer Research, the Virginia and D.K. Ludwig Fund for Cancer Research, the Pew Charitable Trusts, the American Brain Tumor Association, the Brain Tumor Research Fund at Johns Hopkins, grants from Beckman Coulter, grants from the Accelerate Brain Cancer Cure Foundation, and several National Institutes of Health grants. Drs. Yan, Bigner and Parsons plus four Johns Hopkins scientists reported being eligible for royalties received by Johns Hopkins University on sales of products related to research described in this study, under licensing agreements between the university and Beckman Coulter.

Source: Mary Jane Gore

Duke University Medical Center

Cancer Survivors Less Likely To Be In Employment

2009-02-18T19:00:00.000+02:00

Breast cancer survivors are less likely to have jobs, says a new study published in JAMA (Journal of the American Medical Association) . The report explains that this is especially the case for breast and gastrointestinal cancer survivors.

The authors explain that the long-term effects of cancer and its treatment may impair social functioning, including getting or keeping employment. Nearly a half of all cancer survivors are under 65.

"Many cancer survivors want and are able to return to work after diagnosis and treatment. Relatively few studies have assessed the association of cancer survivorship with unemployment," the researchers write. Several factors can make unemployment more probable, including job discrimination, finding it hard to work while receiving treatment at the same time, as well as physical and/or mental limitations.

Angela G. E. M. de Boer, Ph.D., Coronel Institute of Occupational Health, Academic Medical Center, Amsterdam, The Netherlands, and team carried out a meta-analysis to identify unemployment risks for cancer survivors, compared to healthy control participants.

Alter looking through several databases, they found 26 articles which reported the results from 36 studies - all of them met the criteria in the analysis. This included 16 studies from the USA, 15 from Europe and 5 from other parts of the world. All the studies involved 177,969 participants, 20,366 of whom were cancer survivors, while 157,603 were healthy control participants.

Cancer survivors were 1.37 times more likely to be without a job, compared to the healthy control participants, according to the study (33.8% vs 15.2%). Here are some further figures showing a higher risk of unemployment for cancer survivors, according to cancer type:

-- Breast cancer (35.6% compared to 31.7%)

-- Gastrointestinal cancer ( 48.8% compared to 33.4%)

-- Cancers of the female reproductive organs (49.1% compared to 38.3%)

The researchers did not gather any data on survivors of blood, prostate and testicular cancers.

In countries with a fairly high background unemployment rate, the diference between cancer survivors and healthy participants is smaller.

Seven of the studies indicated that the main factor limiting a survivor´s chances of finding or keeping a job was disability - in fact, disability increased the risk of unemployment by a factor of three.

The authors write "..the mechanism behind the higher unemployment rate among cancer survivors is likely to be a higher disability rate."

The researchers added that physical limitation(s), and/or cancer-related symptoms were the main reasons for survivors not keeping or finding employment.

"Apart from the effects on employment, there are probably long-term effects of cancer on work ability, work capacity, and wage losses for a large group of survivors. Employment outcomes can be improved with innovations in treatment and with clinical and supportive services aimed at better management of symptoms, rehabilitation, and accommodation for disabilities. Moreover, workplace interventions are needed that are aimed at realizing workplace accommodations and paid sick leave during treatment. The development and evaluation of such interventions is urgently needed because they could mitigate the economic impact of surviving cancer and improve the quality of life for survivors," the researchers concluded.

JAMA. 2009;301[7]:753-762.

http://jama.ama-assn.org

Written by - Christian Nordqvist and Stephanie Brunner

Copyright: Medical News Today

Not to be reproduced without permission of Medical News Today

Study Shows Patients Unable To Read Or Understand Their Rights

2009-02-18T13:00:00.000+02:00

Patients hoping to find out about their rights are unlikely to get the information they need from hospital documents designed precisely for that purpose. In reality, patients are presented with information written in legal jargon that the majority of them can neither read nor understand. These findings1 by Dr. Michael Paasche-Orlow from Boston University's School of Medicine in the US, and his team, were just published online in Springer's Journal of General Internal Medicine.

Some forty years ago, notions of informed consent and autonomy were first officially endorsed and the concept of patients' rights emerged. In 1990, a condition of hospital accreditation was to inform every patient about their rights. Then in 2001, the US House of Representatives and US Senate passed bills to create a Federal Patients' Bill of Rights (PBOR). Many states now have Patients' Bill of Rights laws in place.

Ironically, these efforts to progress patients' rights are being held back by the use of overly complex language which far exceeds patients' average reading capacity, which is at the 8th grade level. Paasche-Orlow and his team analyzed PBOR statutes for general patient populations in 23 states and 240 hospital PBOR documents from 50 states. They assessed their readability by looking at a combination of reading level, complexity of sentences and vocabulary, and quality of writing style.

The hospital PBOR documents had an average readability at the level of the second year of college. In the nine states that stipulate that PBOR texts are to be distributed to patients, the average reading grade level of the materials was that of a college junior. Not only was the language patients are presented with extremely complex, it was also usually exclusively in English.

These findings show that an advanced college reading level is routinely required to read PBOR documents. Bearing in mind that the average reading level of an American adult is 8th grade, it is clear that the written information patients are given in US hospitals far exceeds their reading capacity.

The authors highlight several reasons why clinicians and patient advocates should be concerned about the readability and accessibility of the language in PBOR documents. In essence, giving patients unreadable legal jargon is a missed opportunity to present the patient care mission in a clear manner.

Paasche-Orlow concludes that: "Patients' rights statutes are designed to promote the ethical and humane treatment of patients. These goals will not be realized by presenting patients with documents they are not able to read and understand."

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Article adapted by Medical News Today from original press release.

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Reference

1. Paasche-Orlow MK et al (2009). National Survey of Patients' Bill of Rights Statutes.

Journal of General Internal Medicine. DOI 10.1007/s11606-009-0914-z

Source: Renate Bayaz

Springer

Forcing Evolution: Boosting Its Infectivity Turns Benign Virus Into Good Gene Therapy Carrier For Cystic Fibrosis

2009-02-17T13:00:00.000+02:00

Researchers from the University of California, Berkeley, and the University of Iowa have turned a relatively benign virus into a highly infectious form that is ideal as a carrier for gene therapy.

In its first gene therapy test, it completely cured human cystic fibrosis lung tissue in culture.

This success with the benign adeno-associated virus (AAV), published this week in the online early edition of the journal Proceedings of the National Academy of Sciences, overcomes a major problem of earlier virus-based gene therapy for cystic fibrosis, and sets the stage for tests in advanced animal models of the disease.

"I think it is worthwhile thinking about clinical therapy at the levels of infection we are achieving," said coauthor David Schaffer, professor of chemical engineering at UC Berkeley.

A new pig model of cystic fibrosis developed last year by Schaffer's colleague, pulmonologist Joseph Zabner of the University of Iowa Hospitals and Clinics in Iowa City, will provide a key test of the virus as a carrier of a gene to replace the mutated gene responsible for the disease.

"If we are able to show that efficient gene transfer can result in gene therapy, if we can cure the lung disease of pigs that have been genetically engineered to have cystic fibrosis lung disease, we should have a real chance of curing cystic fibrosis in humans," Zabner said in an e-mail.

Schaffer's lab is collaborating with groups elsewhere to adapt the virus to gene therapy for other diseases, including Alzheimer's disease and amyotrophic lateral sclerosis (Lou Gehrig's disease).

"Both of those are situations where improvements in the properties of the vehicle can have a significant impact on the success of the therapy," Schaffer said.

Cystic fibrosis (CF) is a common hereditary disease that affects the body's mucus membranes, in particular the lungs, resulting in difficulty breathing and typically in death before the age of 40 from lung or organ failure. One in 4,000 children in the United States is born with CF.

Schaffer and his UC Berkeley colleagues collaborated with Zabner's laboratory to test a technique developed by Schaffer to force the evolution of a virus in ways that make it more effective in gene therapy.

Two years ago, Schaffer and colleagues used the technique to create a variant of AAV that more easily avoids the immune system, allowing the virus to remain in the body long enough to deliver a gene to its intended target.

Using the same technique, the team produced a variant of AAV that is several hundred times more effective at entering lung cells than the natural virus.

Schaffer's technique involves making many mutations in AAV, culturing these variants with cells, and then taking those with specific improved properties - in this case, the ability to infect lung cells - and repeating the process.

"We probably conducted about six rounds of evolution in which we infected the lung epithelial cultures in Iowa, they sent it back to us, we recovered the viral sequences, made new viruses and sent them back again," Schaffer said. "It was iterative rounds of infection and selection for improved infection that finally led to this enhancement of function."

The main problem in CF is a mutation in the CFTR (cystic fibrosis transmembrane conductance regulator) gene that results in a defective chloride ion channel in the body's cells. This, in turn, creates a chloride ion imbalance in the cell, which interferes with water transport in and out of the cell. In the lungs, this causes the mucus that lines the lung surface to become thick and sticky. Breathing becomes difficult if the mucus is not loosened, often by vigorous pounding on the chest, and coughed out. Respiratory infections are common, and lung failure often results. The ion channel defect also affects digestion, leading to nutritional deficiency.

According to Schaffer, previous attempts to deliver a normal CFTR gene to lung cells by means of a virus failed either because the immune system mopped up the virus before it had a chance to deliver its cargo, as was the case with adenovirus; or because the virus was inefficient at delivering the gene to cells, the case with adeno-associated virus. Most respiratory viruses tend to have low infection rates, apparently because they would otherwise quickly wipe out their host, Schaffer said.

Schaffer's technique forced the normally benign AAV, which has already infected over 90 percent of people without any harmful side effects, through rounds of directed evolution to increase its infectivity several hundred-fold.

"We devised a way to evolve viruses that are released from the natural constraints of evolution and have the freedom or ability to evolve toward properties that are more useful for medical application," he said. "In human lung tissue, it completely rescued the chloride ion transport properties of the cells after delivering the correct copy of the CFTR gene to replace the mutated copy of the gene that is present in cystic fibrosis patients."

In this case, the infectious AAV strain developed two major changes: Thanks to a mutation on the viral surface, it was able to bind to different receptors or bind to a more plentiful receptor on the cell surface; and it also acquired a mutation that gave the virus an enhanced ability to make it past the cell surface membrane, slip past the lipid bilayer and reach the inside the cell.

"Neither change alone was enough; it had to be the combination of the two that resulted in the improved properties," said Schaffer. "If we decided to use rational design, we wouldn't have known this. So, we left it up to evolution to discover the answer."

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Article adapted by Medical News Today from original press release.

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Coauthors with Schaffer and Zabner were James T. Koerber, a graduate student with UC Berkeley's chemical engineering and bioengineering departments and with the Helen Wills Neuroscience Institute; research scientist Katherine J. D. A. Excoffon and David D. Dickey of the University of Iowa; Matthew Murtha and Brian K. Kaspar of The Research Institute at Nationwide Children's Hospital in Columbus, Ohio; and Saf Keshavjee of Toronto General Hospital and the University of Toronto.

The research was funded by the National Institutes of Health and the Cystic Fibrosis Foundation.

Source: Robert Sandes

University of California - Berkeley

Unexplained Infertility: The Culprit Could Be Celiac Disease - Now Much Easier To Diagnose With A New Home Screening Test

2009-02-16T13:00:00.000+02:00

Health studies suggest that celiac disease, a hereditary condition that often goes undiagnosed, can lead to infertility. Experts acknowledge that without treatment, celiac disease can cause repeated miscarriages and early menopause.

For women facing no explanation for their infertility, now there is a simple, accurate way to find out if undiagnosed celiac disease might be the cause. For the first time in Canada, Health Canada has approved the Biocard™ Celiac Test Kit, an at-home test that measures gluten antibodies from a fingertip blood sample.

According to health officials, about one per cent or one out of 100 Canadians are affected by celiac disease, which occurs when gluten--a protein found in wheat, rye and barley--triggers damage to the lining of the small intestine, interfering with your absorption of nutrients. But that estimate increases to as much as six per cent for women with unexplained infertility.

Infertility affects as many as one in six couples in their reproductive years in America. Of those, about 15 per cent are from no apparent cause. At the same time, the symptoms of celiac disease are not always obvious. It may be years before symptoms worsen and the disease is diagnosed, and by then child-bearing years may be over. The Biocard™ Celiac Test Kit, first developed in Finland, gives these couples an easy way to find out if celiac disease is a possible cause for their infertility.

Celiac disease affects people differently and not all symptoms are obvious. Classic celiac symptoms include diarrhea, stomach pain, weight loss and, in children, delayed growth. For others, the symptoms are subtler, such as such as bloating, or excess gas. Fatigue, weakness, joint pain and migraines -- symptoms typically not associated with the gut -- are also reported, and the diagnosis is often anemia, stress, irritable bowel syndrome or chronic fatigue syndrome. Without treatment, celiac disease increases the risk of malnutrition, osteoporosis (because of poor absorption of calcium and vitamin D), certain digestive tract cancers and other disorders such as Type 1 diabetes and thyroid disease.

Average time for correct diagnosis of celiac disease - 12 years: According to a 2007 survey of the Canadian Celiac Association's more than 5000 members, the average time it took to be diagnosed was 12 years. Many reported consulting with three or more doctors before their diagnosis was confirmed. In fact, health research experts estimate that some 97 per cent of those affected by the disorder remain undiagnosed.

Home Screening Test Now Available

The Biocard™ Celiac Test Kit is an at-home test that measures IgA antibodies from a fingertip blood sample. While this easy test gives a high degree of certainty that you are either developing celiac disease or already have celiac disease, you still need to see your doctor for a confirmation. Confirming a diagnosis requires a small bowel biopsy in which an endoscope is passed through the mouth into the stomach's upper intestine so that the lining can be examined and a biopsy taken.

The only treatment for celiac disease is a gluten-free diet for life. Still, the day you're confirmed celiac and start your diet, is the day you're on the road to recovery.

Information on celiac disease, the Biocard™ Celiac Test Kit, and links to key informational sites can be found at http://www.celiachometest.com/. The kit can be purchased online, or at London Drugs, Rexall Pharma Plus, and other major Canadian retail chains.

About 2G Pharma Inc.

Founded by Karina Nelimarkka and Janet Monk, 2G Pharma markets the unique, patient-friendly celiac disease test kit first developed by AniBiotech in Finland. This kit has been redesigned for the Canadian market and is currently the only Health Canada approved point-of-care celiac disease test kit available. Information on celiac disease, the Biocard™ Celiac Test and links to key informational sites can be found at http://www.celiachometest.com/.

2G Pharma Inc.