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HEMA is a Dutch department store. The first store opened on November 4, 1926, in Amsterdam. Now there are 150 stores all over the Netherlands. HEMA also has stores in Belgium, Luxemburg, and Germany. In June of this year, HEMA was sold to a British investment company, Lion Capital.

Take a look at HEMA’s product page. You can’t order anything and it’s in Dutch, but just wait a couple of seconds and watch what happens. Don’t click on any of the products pictured, just wait and see what happens. And be sure you have your sound turned up.


Strains of bacteria that are resistant to the antibiotic vancomycin grow easily in its presence (top), but are completely eliminated (bottom) when exposed to Ceftobiprole

September 2, 2008, Rockefeller University – The problem with antibiotics is that, eventually, bacteria outsmart them and become resistant. But by targeting the gene that confers such resistance, a new drug may be able to finally outwit them. Rockefeller University scientists tested the new drug, called Ceftobiprole, against some of the deadliest strains of multidrug-resistant Staphylococcus aureus (MRSA) bacteria, which are responsible for the great majority of staphylococcal infections worldwide, both in hospitals and in the community.

The problem with antibiotics is that, eventually, bacteria outsmart them and become resistant. But by targeting the gene that confers such resistance, a new drug may be able to finally outwit them. Rockefeller University scientists tested the new drug, called Ceftobiprole, against some of the deadliest strains of multidrug-resistant Staphylococcus aureus (MRSA) bacteria, which are responsible for the great majority of staphylococcal infections worldwide, both in hospitals and in the community.

The research, to be published in the August 2008 issue of the journal Antimicrobial Agents and Chemotherapy and available online now, looked at how well Ceftobiprole worked against bacterial clones that had already developed resistance to other drugs. In every case, Ceftobiprole won. “It just knocked out the cells 100 percent,” says the study’s lead investigator, Alexander Tomasz, head of the Laboratory of Microbiology at Rockefeller.

Previous research had already shown that — in general — Ceftobiprole was highly effective against most clinical isolates of S. aureus. “Instead, we looked more carefully at the highly resistant cells that already occur in such clinical isolates at very low frequency — maybe in one bacterium in every 1,000,” says Tomasz. Ceftobiprole was able to kill these resistant cells.

Never before has an antibiotic been tested this way. “In the history of antibiotic development, an antibiotic arrives on the scene, and sooner or later resistant bacteria emerge,” Tomasz says. “We sought to test in advance which would win this particular chess game: the new drug, or the bacteria that now cause human deaths.”

In an ominous new “move” in this chess game, S. aureus strains with resistance to vancomycin (VRSA), a different class of antibiotics, also began to appear in hospitals in the United States. Ceftobiprole was also able to kill these new resistant VRSA strains.

The drug is effective because the chemists who developed Ceftobiprole managed to outwit the bacteria at their own game, Tomasz says. The broad-spectrum antibiotic was discovered by Basilea Pharmaceuticals, based in Basel, Switzerland, and is being developed in the U.S. and worldwide by Johnson & Johnson. The research was supported by Johnson & Johnson along with a grant from the U.S. Public Health Service.

Source : Rockefeller University

Information for Healthcare Professionals
Cimzia (certolizumab pegol), Enbrel (etanercept),
Humira (adalimumab), and Remicade (infliximab)

FDA ALERT [9/4/2008]: FDA is notifying healthcare professionals that histoplasmosis and other invasive fungal infections are not consistently recognized in patients taking tumor necrosis factor-α blockers (TNF blockers), Cimzia (certolizumab pegol), Enbrel (etanercept), Humira (adalimumab), and Remicade (infliximab). This has resulted in delays in appropriate treatment, sometimes resulting in death.

FDA has received reports of patients developing pulmonary and disseminated histoplasmosis, coccidioidomycosis, blastomycosis and other opportunistic infections while taking TNF blockers. In some patients, the diagnosis of histoplasmosis was initially unrecognized and antifungal treatment was delayed. Some of these patients died from histoplasmosis. There were also deaths in patients with coccidioidomycosis and blastomycosis.

For patients taking TNF blockers who present with signs and symptoms of possible systemic fungal infection, such as fever, malaise, weight loss, sweats, cough, dypsnea, and/or pulmonary infiltrates, or other serious systemic illness with or without concomitant shock, healthcare professionals should ascertain if patients live in or have traveled to areas of endemic mycoses. For patients at risk of histoplasmosis and other invasive fungal infections, clinicians should consider empiric antifungal treatment until the pathogen(s) are identified. Consultation with an infectious diseases specialist should be sought when feasible. As with any serious infection, consider stopping the TNF blocker until the infection has been diagnosed and adequately treated.

FDA will require the makers of the tumor necrosis factor-α blockers (TNF blockers) to further highlight the information about the risk of invasive fungal infections, such as histoplasmosis, in the Boxed Warning and Warnings sections of the drugs’ prescribing information and the Medication Guide for patients. FDA will also require that the makers of the TNF blockers educate prescribers about this risk.

This information reflects FDA’s current analysis of data available to FDA concerning this drug. FDA intends to update this sheet when additional information or analyses become available.

To report any unexpected adverse or serious events associated with the use of these drugs, please contact the FDA MedWatch program and complete a form on line at http://www.fda.gov/medwatch/report/hcp.htm or report by fax to 1-800-FDA-0178, by mail using the postage-paid address form provided on line, or by telephone to 1-800-FDA-1088.

Considerations for Healthcare Professionals

* TNF blockers are immunosuppressants. Patients taking TNF blockers are at risk for developing invasive fungal infections such as histoplasmosis, coccidioidomycosis, blastomycosis, aspergillosis, candidiasis, and other opportunistic infections. Healthcare practitioners should be alert to these risks of TNF blockers in patients who live in regions of endemic mycoses.
* Patients should be closely monitored during and after treatment with TNF blockers for the development of signs and symptoms of possible systemic fungal infection including fever, malaise, weight loss, sweats, cough, dypsnea, pulmonary infiltrates on X-ray, or serious systemic illness including shock. Patients who develop an infection should have their TNF blocker discontinued and undergo a complete diagnostic workup, which may include fungal cultures, histopathological or cytological evaluations, antigen detection and serum antibody titers.
* For patients who reside or travel in regions where mycoses are endemic, invasive fungal infections should be suspected if they develop the signs and symptoms of possible systemic fungal infection. The decision to administer empiric antifungal therapy in these patients should be made in consultation with an infectious diseases specialist with expertise in the diagnosis and treatment of invasive fungal infections when feasible.
* TNF blockers may be restarted after recovery from the infection. The decision to restart the TNF blocker should include a reevaluation of the benefits and risks of TNF blockers, especially in patients who live in regions of endemic mycoses. Both the decision to restart TNF blocker therapy and the duration of antifungal therapy should be made in consultation with an infectious disease specialist, when feasible.

Information for the Patient

Prescribers should discuss the following information with patients and their caregivers:

* Patients treated with TNF blockers have an increased risk for infections. Some patients have had serious infections while receiving TNF blockers. In some cases, patients needed to be hospitalized for treatment. These serious infections include infections caused by viruses, fungi, or bacteria including tuberculosis (TB), including infections that have spread throughout the body. Some patients have died from these infections.
* If you have weight loss, persistent fever, sweating, cough, shortness of breath, or fatigue, promptly seek medical attention.
* Tell your doctor where you live and about recent travel in and outside the USA. The risk of some infections is greater in regions where different microorganisms (bacteria, fungi, viruses, parasites) are more common.
* Tell your doctors that you are taking a TNF blocker. A doctor may make different decisions about your medical treatment if he or she knows that you are taking a TNF blocker.
* Tell your doctor about all of your medical conditions, including if you have an infection that won’t go away or a history of an infection that keeps coming back.

Background Information and Data

TNF blockers suppress the immune system by blocking the activity of TNF, a substance in the body that can cause inflammation and lead to immune system-related diseases. There are currently four TNF blockers available in the United States: Cimzia, Enbrel, Humira, and Remicade. The TNF blockers have demonstrated benefit and are each approved to treat one or more of a number of immune system diseases including juvenile idiopathic arthritis (JIA), rheumatoid arthritis, psoriatic arthritis, plaque psoriasis, Crohn’s disease, and ankylosing spondylitis. Remicade is approved for use in children to treat Crohn’s disease. Enbrel and Humira are approved for use in children to treat JIA.

Since TNF blockers are immunosuppressants, patients that take these drugs are at increased risk of serious infections, including invasive fungal infections such as histoplasmosis, coccidioidomycosis, blastomycosis, aspergillosis, candidiasis, cryptococcosis, as well as other opportunistic infections. Since the initial approval of the four TNF blockers, the prescribing information for these drugs has included information about the risk of serious infections, including fungal infections. However, based on the reports reviewed by FDA, healthcare professionals are not consistently recognizing cases of histoplasmosis and other invasive fungal infections, leading to delays in treatment. Some patients with invasive fungal infections have died.

FDA reviewed 240 reports of histoplasmosis in patients receiving Remicade (207 cases), Enbrel (17 cases), or Humira (16 cases). The majority of cases were from Histoplasma capsulatum-endemic areas in the Ohio and Mississippi River valleys. In at least 21 of the reports, histoplasmosis was initially unrecognized and antifungal treatment was delayed. Twelve of these 21 patients died. FDA has reviewed 1 reported case of histoplasmosis in a patient taking Cimzia, which was approved in April 2008. FDA has also received reports of cases, including deaths, of coccidioidomycosis and blastomycosis in patients receiving TNF blockers.

August 2008 — Albert Einstein College of Medicine — As people age, their cells become less efficient at getting rid of damaged protein — resulting in a buildup of toxic material that is especially pronounced in Alzheimer’s, Parkinson’s disease, and other neurodegenerative disorders.

34D9C775-23FB-4EE1-A148-CD02BD6D5BBA.jpgNow, for the first time, scientists at the Albert Einstein College of Medicine of Yeshiva University, have prevented this age-related decline in an entire organ — the liver — and shown that, as a result, the livers of older animals functioned as well as they did when the animals were much younger. Published in the online edition of Nature Medicine, these findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompany old age. The study’s senior author was Dr. Ana Maria Cuervo, associate professor in the departments of developmental & molecular biology, medicine and anatomy & structural biology at Einstein.

The cells of all organisms have several surveillance systems designed to find, digest and recycle damaged proteins. Many studies have documented that these processes become less efficient with age, allowing protein to gradually accumulate inside cells. But researchers continue debating whether this protein buildup actually contributes to the functional losses of aging or instead is merely associated with those losses. The Einstein study was aimed at resolving the controversy.

1A784E40-7722-412B-9734-B596146C732F.jpgOne of these surveillance systems — responsible for handling 30 percent or more of damaged cellular protein — uses molecules known as chaperones to seek out damaged proteins. After finding such a protein, the chaperone ferries it towards one of the cell’s many lysosomes — membrane-bound sacs filled with enzymes. When the chaperone and its cargo “dock” on a receptor molecule on the lysosome’s surface, the damaged protein is drawn into the lysosome and rapidly digested by its enzymes.

In previous work, Dr. Cuervo found that the chaperone surveillance system, in particular, becomes less efficient as cells become older, resulting in a buildup of undigested proteins within the cells. She also detected the primary cause for this age-related decline: a fall-off in the number of lysosomal receptors capable of binding chaperones and their damaged proteins. Could replenishing lost receptors in older animals maintain the efficiency of this protein-removal system throughout an animal’s lifespan and, perhaps, maintain the function of the animal’s cells and organs as well?

To find out, Dr. Cuervo created a transgenic mouse model equipped with an extra gene — one that codes for the receptor that normally declines in number with increasing age. Another genetic manipulation allowed Dr. Cuervo to turn on this extra gene only in the liver and at a time of her choosing, merely by removing the antibiotic doxycycline from the animals’ diet.

To keep the level of the receptor constant throughout life, Dr. Cuervo waited until mice were six months old (the age that the chaperone system’s efficiency begins to decline) before turning on the added receptor gene. When the mice were examined at 22 to 26 months of age (equivalent to approximately 80 years old in humans), the liver cells of transgenic mice digested and recycled protein far more efficiently than in their normal counterparts of the same age — and, in fact, just as efficiently as in normal six-month old mice.

Does maintaining efficient protein clearance in liver cells of an older animal translate into better functioning for the liver as a whole? Since a key function of the liver is metabolizing chemicals, Dr. Cuervo answered this question by injecting a muscle relaxant into very old transgenic mice and very old normal mice. The very old transgenic mice metabolized the muscle relaxant much more quickly than very old normal mice and at a rate comparable to young normal mice.

“Our study showed that functions can be maintained in older animals so long as damaged proteins continue to be efficiently removed — strongly supporting the idea that protein buildup in cells plays an important role in aging itself,” says Dr. Cuervo. “Even more important, these results show that it’s possible to correct this protein ‘logjam’ that occurs in our cells as we get older, thereby perhaps helping us to enjoy healthier lives well into old age.”

Dr. Cuervo next plans to study animal models of Alzheimer’s, Parkinson’s and other neurodegenerative brain diseases to see whether maintaining efficient protein clearance in the brain might help in treating them. “Most people with these conditions are born with a mutation that gives rise to defective proteins, but they don’t experience symptoms until later in life,” says Dr. Cuervo. “We think that’s because their protein-clearance systems can handle abnormal proteins when the person is younger but get overwhelmed as their efficiency falls with age. By preventing this decline in protein clearance, we may be able to keep these people free of symptoms for a longer time.”

Dr. Cuervo will also investigate whether maintaining efficient protein clearance in all the body’s tissues will influence longevity and prevent the functional losses associated with growing old. “There’s reason to hope that drugs exerting a similar effect throughout the body may help us enjoy healthier lives well into old age,” says Dr. Cuervo. Meanwhile, she notes, evidence is mounting that two dietary interventions —low-fat and calorie-restricted diets — help cells to maintain efficient protein clearance.

Cong Zhang, a graduate student working in Dr. Cuervo’s laboratory, was the lead author of the Nature Medicine study. The research was supported by grants from the National Institute on Aging, an Ellison Medical Foundation Award and a Glenn Foundation Award.

2F1596A7-7CA0-47F4-A67E-B7E3D31752F0.jpgGood News At Last About Looking Younger

By Nicholas Bakalar, August 2008, The New York Times – Nostrums that promise to smooth wrinkled skin are a staple of snake-oil salesmen everywhere, but now there is strong evidence that certain kinds of treatment are effective. Over the past decade, researchers have been learning which treatments work, and why.

The key is a growing understanding of the skin’s connective tissue, called the dermal collagen, and a recognition that damage to the mechanical properties of the collagen outside the skin cells, and not necessarily genetic damage to the cells themselves, causes wrinkled skin.

A recent review in The Archives of Dermatology concludes that three anti-aging treatments are proven clinically effective: the topical application of retinol; carbon dioxide laser resurfacing; and injection of hyaluronic acid, a moisture-retaining acid that occurs naturally in the skin. Each depends on the same mechanism, the interaction of skin cells called fibroblasts with the collagen they produce.

“This is an area where there’s a lot of hype and not much substance,” said David J. Leffell, a professor of dermatology and surgery at Yale who was not involved in the review. But, he said, this study is “good science.”

Theory and experiment back these treatments, the authors write. Fibroblasts — connective tissue cells — secrete a complex group of polysaccharides and proteins that creates collagen, which gives the skin shape and elasticity and supports the blood vessels that permeate it. The network of collagen tissue is maintained by its mechanical tension with these skin cells.

Skin deteriorates as it ages, but its exposure to sunlight inhibits the ability of fibroblasts to produce collagen. The hands, face, neck and upper chest all suffer more than unexposed skin, and light-pigmented people wrinkle more readily than others. This damage, the authors write, is essentially an accelerated version of chronological aging. Ultraviolet radiation induces production of the same enzymes that degrade collagen with age.

Collagen fibers last as long as 30 years. But with age and ultraviolet exposure, they deteriorate and fragment, and fragmented collagen impairs the collagen-producing function of the fibroblasts that created it. As the fragmented collagen accumulates, new collagen production declines, the connections between the fibroblasts and the collagen weaken, and the skin, now lacking support, begins to wrinkle.

But there are treatments that counter this process. Topical application of retinol, a form of vitamin A, was the first to be proved useful. Although the molecular pathways are not well understood, retinol causes new collagen to form in chronologically aged skin and in skin damaged by ultraviolet light.

Skin creams with retinol are available over the counter, but many do not indicate the concentration of the active ingredient. “Many products just refer to retinol or vitamin A as a buzzword,” said Gary J. Fisher, the lead author of the review and a professor of dermatology at the University of Michigan.

Concentrations of 0.2 to 0.6 percent are enough, Dr. Fisher said, but preparations strong enough to have an effect can also have a side effect, a rash called retinoid dermatitis. Dr. Fisher’s advice is to stop using it if a rash occurs. The rash can sometimes be avoided if the concentration is increased gradually.

Retinol also makes the skin more sensitive to damage from ultraviolet light, so protection from the sun while using it is essential. “O.T.C. products tend to try to walk the line between effects and side effects,” Dr. Fisher said. “But many intentionally keep the concentration too low to have any benefit.”

Dr. Robyn S. Gmyrek, an assistant professor of dermatology at Columbia University, is also skeptical of over-the-counter wrinkle creams. “If something shows true biological activity, it’s regulated as a drug,” she said. “A cream bought over the counter is certainly not going to do what prescription-strength retinol will do.” Dr. Gmyrek was not involved in the study.

Carbon dioxide laser resurfacing is another well-tested treatment for wrinkles. The laser removes thin layers of skin without damaging surrounding tissue. As the wound heals, new collagen is produced. The treatment works first by inducing high levels of matrix metalloproteinase, or MMP, an enzyme that destroys fragmented collagen. Then it reduces MMP and increases the production of new and undamaged replacement material. The procedure is also used for removing scars, warts and birthmarks.

Healing takes two to three weeks, and the wound has to be cleaned with saline or diluted vinegar and treated with ointments to prevent scarring. In most cases, the procedure is done only once, Dr. Fisher said, and lasts many years.

There are now some less invasive laser procedures, the authors write, but their effectiveness is doubtful.

The third effective treatment is injecting a form of hyaluronic acid, similar to a substance the skin normally produces, into the dermis that underlies the wrinkles. This was originally designed as a space filler, with no intended physiological effect. But as the injection stretches the dermis, the fibroblasts respond by producing more collagen and less MMP. The authors cite studies that have demonstrated that increased collagen production is visible within a month after the injection. The benefit lasts about six months, Dr. Fisher said.

This type of hyaluronic acid, he said, should not be confused with hyaluronic acid in some topical cosmetic products. Rubbing such products on the skin will not stimulate collagen production.

Do the benefits of these treatments outweigh the risks?

“It’s a matter of the kind of problem a person perceives and how he wants to deal with it,” Dr. Fisher said. “For these treatments, which have sound research behind them, and for people who want to improve their appearance, the benefits far outweigh any problems.”

The authors have no ties to companies that make skin care products, but the University of Michigan, where they teach, has patents on the use of matrix metalloproteinase inhibitors in the treatment and prevention of aging skin.

This article has been revised to reflect the following correction:

Correction: August 21, 2008
Because of an editing error, an article on Tuesday about three treatments proved to be effective against wrinkles described incorrectly part of the process of one of those treatments, carbon dioxide laser resurfacing. After the laser removes thin layers of skin, the healing wound produces more collagen, not less.

September 4, 2008, ChinaCSR.com – Bayer is providing sustainable support for the reconstruction of Sichuan Technology and Business College in Dujiangyan — one of the three colleges most heavily damaged by the earthquake in Sichuan.

The donation of classrooms, homes and a mobile clinic by the Bayer Cares Foundation is valued at around EUR825,000, and brings the Bayer group’s total donations to earthquake relief – including medical supplies, cash donations by employees and the company, and vector control – to more than EUR2.2 million.

To help restore normal schooling at the college, Bayer has donated 20 standard classrooms, 50 houses and a clinic, including design, production, transport and on-site assembly. The total construction area exceeds 2,000 square meters. The company also provided all the necessary equipment for the completion and immediate functioning of the buildings, such as whiteboards, beds, and medicines.

NEW YORK, NY (August 27, 2008) – The New York Stem Cell Foundation (NYSCF) – a privately-funded non-profit organization dedicated to advancing cures for major diseases through stem cell research – today hailed the announcement by Harvard Stem Cell Institute (HSCI) Co-Director Douglas Melton, PhD, and his colleagues that they have succeeded in reprogramming adult pancreatic cells into insulin-producing beta cells in mice. The new research is a major step forward in understanding the process of reprogramming one cell type into another and could have implications for the treatment of multiple degenerative diseases. Dr. Melton is a founding member of NYSCF’s Medical Advisory Board.

In a paper published in the online edition of the journal Nature, Melton and colleagues at the Harvard Stem Cell Institute reported that they were able to convert one type of mature, differentiated somatic cell into another without first reverting the cell to an undifferentiated pluripotent state. Using a strategy similar to that employed to reprogram adult cells to pluripotent iPS cells, the researchers introduced viruses carrying three genes involved in pancreas development into adult diabetic mice. While the new cells were not able to fully correct the diabetic state, these genes were able to convert some of the remaining mature pancreatic cells into the insulin producing beta cells that are normally destroyed in diabetes. As the technique requires viruses to introduce the genes, much work remains to make the strategy ready for the clinic. However, future improvements could make similar approaches generally useful for converting abundant adult cell types into other cell types needed for repair of damaged tissues.

The work adds to a growing array of tools available to researchers studying regenerative medicine. “The pace of regenerative medicine research is breathtaking – we are reading about major, new discoveries literally every week,” said Susan L. Solomon, CEO of the New York Stem Cell Foundation. “Dr. Melton and his colleagues have achieved a remarkable result that brings us that much closer to understanding how we might better combat or even prevent diabetes.”

Dr. Kevin Eggan, Associate Professor, Department of Stem Cell and Regenerative Biology, Harvard University, and Assistant Investigator, Stowers Medical Institute, noted: “This is a major advance that once again demonstrates that a sophisticated understanding of how humans develop can be leveraged for the discovery of new approaches to replace cells that are destroyed through aging and disease. In this case, the discovery of methods for directly turning other cells in the pancreas into the insulin-producing cells that are destroyed by diabetes suggests a brand new, never imagined means for treating diabetes, which affects millions of people. However, results like this would never have been possible without basic investigations into embryonic cell development and underscores the importance of pushing forward on all fronts – through direct reprogramming and other methods for trying to replace diseased cells, for instance with embryonic stem cells. I think it’s important to point out that this development in no way supplants the need for research on human embryonic stem cells, which are still one of our best options for coming to a better understanding of – and treatments for – human disease.”

“The work reported by Dr. Melton and his colleagues is an important step forward in the long and arduous process of developing cell-based treatments for diabetes,” said Dr. Zach W. Hall, a former Institute Director at the NIH, and former President of the California State Stem Cell Initiative. “Our rapidly growing understanding of how cells differentiate through continued research on embryonic stem cells, iPS cells and the conversion of adult cells will dramatically increase our chances for devising the optimal treatment for each of a wide range of diseases.”

About The New York Stem Cell Foundation
Founded in 2005, The New York Stem Cell Foundation is a privately funded foundation dedicated to furthering stem cell research to advance the search for cures of the major diseases of our time. The foundation opened the first privately funded stem cell laboratory in New York City in March 2006 to serve as a “safe haven” where scientists can conduct advanced stem cell research free of federal restrictions. The organization supports scientists engaged in stem cell research through grants, fellowships and symposia; runs collaborative, state-of-the-art research facilities supported entirely with private funds and directly focused on curing disease; and educates the public about the importance and potential benefits of stem cell research.