Archive for July, 2011

Women who eat lots of fiber have less breast cancer

Last Updated on Friday, 29 July 2011 11:35 Written by admin Friday, 29 July 2011 11:35

(Reuters Health) – A fresh look at the medical evidence shows women who eat more fiber are less likely to get breast cancer.

Chinese researchers found those who ate the most of the healthy plant components were 11 percent less likely to develop breast cancer than women who ate the least.

Their findings don’t prove fiber itself lowers cancer risk, however, because women who consume a lot of it might be healthier overall than those who don’t.

The results “can identify associations but cannot tell us what will happen if people change their behavior,” said John Pierce, a cancer research at the University of California, San Diego, who was not involved in the work.

While earlier research has yielded mixed conclusions on the link between cancer and fiber, it would make scientific sense: According to the Chinese researchers, people who eat high-fiber diets have lower levels of estrogen, which is a risk factor for breast tumors.

So to get more clarity, the researchers combined 10 earlier studies that looked at women’s diets and followed them over seven to 18 years to see who developed cancer.

Of more than 710,000 women, 2.4 percent ended up with breast cancer. And those in the top fifth of fiber intake were 11 percent less likely to do so than women in the bottom fifth.

That was after accounting for differences in risk factors like alcohol drinking, weight, hormone replacement therapy and family members with the disease.

Still, it’s impossible to rule out that big fiber eaters had healthier habits overall that would cut their risk, Jia-Yi Dong of Soochow University in Suzhou and his colleagues write in the American Journal of Clinical Nutrition.

And the potential effect was “very small,” Dr. Eleni Linos of Stanford University, who wasn’t involved in the research, told Reuters Health in an email.

About one in eight American women get breast cancer at some point, with less than a quarter of them dying from it.

Although the connection between breast cancer risk and fiber is a small one, fiber is “something that we know is healthy for you anyway,” said Christina Clarke, a research scientist at the Cancer Prevention Institute of California in Fremont.

Known benefits of a high-fiber diet include lower cholesterol and weight loss. If it turns out to cut cancer risk as well, that would be an extra bonus, Clarke said.

Fruits, vegetables, beans, and whole grains are all high in fiber.

According to the U.S. Department of Agriculture’s 2010 Dietary Guidelines, most Americans don’t get enough fiber. The guidelines recommend that women eat 25 grams of fiber per day and men eat 38 grams, while the average Americans gets just 15 grams a day.

“Increasing dietary fiber intake in the general public is of great public health significance,” the Chinese team concludes.

Source: http://www.reuters.com/article/2011/07/28/us-fiber-breast-cancer-idUSTRE76R6YM20110728

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‘Super antibody’ fights off flu

Last Updated on Friday, 29 July 2011 11:22 Written by admin Friday, 29 July 2011 11:22

The first antibody which can fight all types of the influenza A virus has been discovered, researchers claim.

Experiments on flu-infected mice, published in Science Express, showed the antibody could be used as an “emergency treatment”.

It is hoped the development will lead to a “universal vaccine” – currently a new jab has to be made for each winter as viruses change.

Virologists described the finding as a “good step forward”.

Many research groups around the world are trying to develop a universal vaccine. They need to attack something common to all influenza which does not change or mutate.

Human source

It has already been suggested that some people who had swine flu may develop ‘super immunity’ to other infections.

Scientists from the Medical Research Council’s National Institute for Medical Research at Mill Hill and colleagues in Switzerland looked at more than 100,000 samples of immune cells from patients who had flu or a flu vaccine.

They isolated an antibody – called FI6 – which targeted a protein found on the surface of all influenza A viruses called haemagglutinin.

Sir John Skehel, MRC scientist at Mill Hill, said: “We’ve tried every subtype of influenza A and it interacts with them all.

“We eventually hope it can be used as a therapy by injecting the antibody to stop the infection.”

Professor Antonio Lanzavecchia, director of the Institute for Research in Biomedicine, Switzerland, said: “As the first and only antibody which targets all known subtypes of the influenza A virus, FI6 represents an important new treatment option.”

When mice were given FI6, the antibody was “fully protective” against a later lethal doses of H1N1 virus.

Mice injected with the antibody up to two days after being given a lethal dose of the virus recovered and survived.

This is only the antibody, however, not the vaccine.

A vaccine would need to trigger the human body’s immune system to produce the antibody itself.

Sir John said the structure of the antibody and how it interacted with haemagglutinin had been worked out, which would help in the search for a vaccine, but that was “definitely years away”.

Professor John Oxford, a virologist at Queen Mary, University of London, said: “It’s pretty good if you’ve got one against the whole shebang, that’s a good step forward.”

Source: http://www.bbc.co.uk/news/health-14324901

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Proteus Syndrom Gene Variant Identified

Last Updated on Thursday, 28 July 2011 11:34 Written by admin Thursday, 28 July 2011 11:34

Researchers have discovered the gene mutation that leads to Proteus syndrome, a condition that causes different parts of the body to grow faster and larger than others, HealthDay reports.

With only about 500 cases known in the developed world, Proteus syndrome is rare. The condition is marked by a partial enlargement of the hands or feet, an enlarged head and overgrowth of one side of the face, body or limbs. It is thought to be the cause of the disabilities of 19th century Englishman Joseph Merrick, popularly known as the “Elephant Man.”

According to HealthDay, Proteus syndrome is a mosaic disorder, one in which some cells in the body have the genetic mutation and some don’t. Working on identifying the specific gene variant since 1996, researchers at the U.S. National Human Genome Research Institute were finally able to compare tissue samples from affected areas of the body to unaffected areas in 29 Proteus syndrome patients. They were able to identify the same mutation in 26 patients.

The mutation occurred in the AKT1 gene, they said. HealthDay explains the mutation as “a single ‘misspelling’ in the billions of letters that make up the human genome.”

HealthDay noted that the gene mutation in Proteus syndrome creates an oncogene, which drives the uncontrolled cell division. Oncogenes are usually associated with cancer, the website reported.

Researchers hope that finding the gene will be able to lead to better treatment for people with Proteus syndrome.

“It may become possible to treat those with Proteus syndrome with a drug originally developed for cancer,” said the study’s senior author Leslie Biesecker. “This allows us to leapfrog a number of steps. But, Proteus syndrome is not an overgrowth syndrome so we would have to adapt cancer treatments.”

Source: http://www.thirdage.com/news/proteus-syndrom-gene-variant-identified_07-28-2011

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Studies Show Natural Protein May Provide Benefits Against Stroke up to 12 Hours After Onset

Last Updated on Wednesday, 27 July 2011 04:38 Written by admin Wednesday, 27 July 2011 04:38

Scientists suggest that treating stoke patients with an endogenous immunomodulatory neuroprotectant protein, ?B-crystallin (Cryab), could help limit brain damage even if first administered 12 hours after the onset of stroke. Studies by a Stanford University School of Medicine team in a mouse model of stroke found that administering Cryab to animals 12 hours after stroke induction led to significantly reduced stroke volume and lower levels of inflammatory cytokines associated with stroke pathology than untreated mice.

Conversely, animals in which the Cryab gene had been knocked out demonstrated increased lesion size and diminished neurologic function after stroke than wild-type mice. The research team, led by Gary K. Steinberg, M.D., director of Stanford’s Institute for Neuro-Innovation and Translational Neurosciences, reports its findings in PNAS in a paper titled “Systemic augmentation of ?B-crystallin provides therapeutic benefit twelve hours post-stroke onset via immune modulation.”

Tissue plasminogen activator (tPA) is currently the only FDA-approved treatment for stroke, and must be given within 4.5 hours of stroke onset to be effective, the researchers note. tPA acts through the conversion of plasminogen into active plasmin, to cleave the blood clot, and exemplifies strategies that aim to alter the obstructive blood clot rather than actually protect the damaged brain.

Cryab, meanwhile, is a small heat shock protein (designated sHSP B5) that is constitutively expressed in the lens of the eye and muscle, and is induced in many types of brain injury. Previous studies have shown the protein has both anti-apoptotic and immunomodulatory properties; it is also the most abundant induced transcript in multiple sclerosis lesions and is highly expressed in areas of inflammation, the authors add.

Previous studies by a group led by co-author Lawrence Steinman, M.D., George A. Zimmermann professor of neurology and neurological sciences and pediatrics at Stanford, had found that Cryab reduces the severity of brain damage caused by multiple sclerosis, and that the protein can also limit the damage caused by reduced blood supply to heart tissue and to the retina. These findings, coupled with other research suggesting that Cryab has neuroprotective properties, led Drs. Steinberg, Steinman, and colleagues to evaluate the effects of Cryab deficiency on cerebral ischemia.

They found that Cryab-knockout animals demonstrated significantly larger lesions two days after an induced cerebral artery occlusion than wild-type mice. This increased damage in the Cryab-deficient animals persisted at seven days, indicating that Cryab deficiency affects both the early and delayed phases of ischemic damage. The Cryab-knockout mice also scored significantly worse in terms of functional assessment.

Interestingly, granulocyte and macrophage populations, and the subpopulation of monocytes, were significantly higher in the Cryab-deficient mice at the two-day post-stroke stage, but not at seven days. The numbers of lymphoid cells, however, were significantly increased in the knockout animals at seven days. More specifically, there were increased numbers of granulocytes and activated macrophages in the Cryab-deficient mice than in the wild-type controls at two days. There were also marked increases in the numbers of T cells in the brains of Cryab knockouts than wild-type mice at seven days and, in particular, increased levels of IL-17-producing ??-TCR⁺(??-T) cells. The overall data suggested that “a deficiency of Cryab might lead to a more vigorous inflammatory response to stroke,” the authors note.

Because some research has previously suggested that Cryab expression is upregulated in neurons and astrocytes after cerebral ischemia, the researchers moved on to analyze levels of Cryab in the plasma of wild-type mice before stroke, and at various time points after the induction of stroke. This showed that Cryab levels were significantly increased at the 12 hour time point, and decreased gradually over the next seven days.

When they analyzed the plasma concentrations of Cryab in human patients with ischemic stroke, they found increased levels of the protein in younger patients within four hours of stroke symptom onset, but surprisingly not in older patients. In younger patients only, lesion volume also correlated with plasma Cryab levels, “perhaps indicating that the body’s endogenous response to stroke is age dependent,” the team suggests.

To test the notion that increased plasma Cryab after stroke is beneficial, Cryab-knockout mice were given intraperitoneal injections of recombinant Cryab protein, starting one hour before stroke onset and continuing at 12 hours, 24 hours, and then daily for seven days in total. Lesion sizes in the Cryab-treated knockout mice were significantly smaller than those of the knockout animals that weren’t given exogenous Cryab. Evaluation of splenocytes from PBS-treated wild-type mice, Cryab-deficient animals, and Cryab-treated Cryab-knockout animals showed that those of PBS-treated knockouts produced more proinflammatory IL-2, IL-17, and TNF than both PBS-treated wild-type mice and Cryab-treated Cryab-deficient mice. The animals receiving exogenous Cryab also produced more anti-inflammatory IL-10. “These data indicate that restoration of plasma Cryab by systemic treatment modulates the peripheral inflammatory response and is sufficient to decrease the lesion sizes in Cryab?/? mice to the levels of wild-type mice after stroke,” the researchers note.

They progressed to evaluate whether Cryab therapy could benefit wild-type mice after stroke onset. When Cryab was administered one hour before and 12 hours after stroke onset, the lesion size at two days was not different between PBS- and Cryab-treated wild-type mice groups. In contrast, when it was administered 1 hour before, 12 hours and 24 hours after, and then daily for seven days, the lesion sizes were significantly reduced in the Cryab-treated group compared with the PBS-treated group. “Moreover, starting the initial treatment even 12 hours after the stroke onset—making the treatment highly relevant if translated into the clinic—conferred neuroprotection in the Cryab-treated group,” the team claims. Analysis of splenocytes cytokines seven days after stroke in wild-type mice again showed that the Cryab-treated animals produced less proinflammatory IL-2, IL-17, IFN-?, IL-12p40, and IL-6, and more anti-inflammatory IL-10, than the PBS-treated animals.

“Our findings describe a therapeutic role for Cryab in stroke, and emphasize how it functions as an endogenous neuroprotectant by modulating the immune system,” the authors conclude. “Its presence as an endogenous protectant can be exploited by administering it in larger quantities as a therapeutic agent. Its benefit seen with starting the treatment 12 hours after stroke would represent a significant improvement over tPA if translated to the clinic.”

Source: http://genengnews.com/gen-news-highlights/studies-show-natural-protein-may-provide-benefits-against-stroke-up-to-12-hours-after-onset/81245471/

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Smelly socks tested in Tanzania as way to prevent malaria

Last Updated on Thursday, 14 July 2011 11:49 Written by admin Thursday, 14 July 2011 11:49

In global public health, disease-fighting tools that are cheap, available and sustainable are the Holy Grail. It might be hard to top the one being tested in Tanzania as a way to prevent malaria: smelly socks.

Experiments in three villages where people get about 350 bites a year from malaria-infected mosquitoes are using dirty socks to lure the insects into traps, where they become contaminated with poisons and ultimately die.

Researchers hope that if the strategy works, it will eventually complement insecticide-treated bed nets as a low-tech way to prevent malaria, which kills nearly 900,000 people a year worldwide, most of them children.

“It’s a bold idea. Who would have thought there was a life-saving technology working in your laundry basket?” said Peter A. Singer, a physician who heads Grand Challenges Canada, a development agency of the Canadian government that is helping fund the research.

Previous lab studies have shown that smelly socks work well in attracting mosquitoes. Field experiments have shown that synthetic bait is more attractive than people, at least until the insects get close enough to realize there’s no blood waiting for them.

The new experiments, however, are the first head-to-head field tests of footwear vs. chemistry. The researchers hope the footwear wins.

“It is simply a cost issue and an expediency issue,” said Fredros O. Okumu, the Tanzanian entomologist leading the research. “Socks are more readily available, and you don’t have to mix any chemicals. It is the sort of thing that could be set up in a cottage factory.”

The traps are square boxes that look a little like commercial beehives. Some will contain the human-odor bait, which consists of simple chemicals (including lactic acid, ammonia and propionic acid) that are exuded by people, especially from the legs and feet. Some will contain socks worn for a day by adults. Others will contain cotton pads that schoolchildren will put inside their socks for a day and then deliver to researchers.

The researchers will compare the number of mosquitoes caught with each method.

Earlier work by Okumu and his colleagues at the Ifakara Health Institute in Tanzania showed that the chemical bait attracted four times as many mosquitoes as live people and that dirty socks worked just as well, at least in the lab. If the sock pads prove adequate, they will be the preferred bait.

The inside surfaces of some traps are coated with an organophosphate pesticide. Mosquitoes that land there will die within 24 hours. Other traps contain a fungus that infects the insects and kills them in five days — roughly half the time needed for the complicated cycle that enables a newly infected mosquito to transmit the malaria parasite to a person.

The bait-and-kill strategy is a new one in malaria prevention efforts.

Normally, attempts to prevent malaria by controlling mosquitoes, known as vector control, have aimed at driving the insects away from people or killing them once natural attraction has brought them into proximity.

Insecticide-treated bed nets, millions of which have been sold or given away in Africa in the past decade, have a long-acting repellant, permethrin. In many malaria-endemic areas, people spray the inside walls of dwellings with insecticide that kills mosquitoes when they land.

Bed nets have cut childhood deaths by about 20 percent in malaria-endemic areas. Modeling suggests that traps could reduce malaria transmission about as much as bed nets do in villages where half the households use them.

Despite its low-tech appearance, the strategy Okumu is testing is far more complicated, and potentially fraught with hazard, than it seems.

A key question is where to place traps. They need to be close enough to dwellings to attract mosquitoes, but not so close that they will increase people’s exposure to the disease-carrying insects. Okumu’s research suggests that the traps should be at least 100 feet from houses.

Another question is how many traps a village might need. Okumu has calculated the minimum number at 20 per 1,000 people, although in places where malaria transmission is especially intense and in certain village configurations, 130 traps per 1,000 people might be needed.

Despite these challenges, Singer said, projects such as these are what Grand Challenges Canada is looking to support. It is providing $388,000 for the research, and the Bill and Melinda Gates Foundation is providing a similar amount. The Gates Foundation gave Okumu $100,000 for preliminary studies, as well.

“We are inspired by people like Fredros,” Singer said. “We strongly believe that innovators in low-income countries are best situated to solve their own problems. He is an African researcher with an African innovation for an African problem.”

Okumu, who is a doctoral candidate at the London School of Hygiene and Tropical Medicine, said he is “working on the premise that this is a global problem — a global problem in a flat world.”

He said he doubted that there might be an application for his strategy — should it prove successful — in non-malarious places such as the United States. A pair of socks from a recent 10K run at the corner of a patio will only briefly divert mosquitoes. They’ll soon find the bare legs under the picnic table.

“Mosquitoes are still fairly clever animals,” he said. “What they are looking for is blood. They might be attracted to the socks, but they will not spend much time there.”

Source: http://www.washingtonpost.com/national/health-science/smelly-socks-tested-in-tanzania-as-way-to-prevent-malaria/2011/07/12/gIQAshifBI_story.html

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Daily pill can prevent HIV infection

Last Updated on Thursday, 14 July 2011 11:36 Written by admin Thursday, 14 July 2011 11:36

The partners of people who have HIV can protect themselves from infection by taking a once-daily pill, two groundbreaking studies in Botswana, Kenya and Uganda have shown.

The discovery could bring work to combat Aids close to a “tipping point”, experts say. Attempts to promote condom use to protect against HIV in the hardest-hit parts of the world, and particularly Africa, have hit cultural barriers and had limited success.

But now it appears that men or women who know – or suspect – their partner has HIV could protect themselves, secretly if necessary. The larger study, involving 4,758 “discordant” couples (where one has HIV but the other has not) in Kenya and Uganda, led by the University of Washington’s International Clinical Research Centre, shows that those taking a single daily tablet of the Aids drug tenofovir had 62% fewer infections and those who took a pill combining tenofovir and emtricitabine had 73% fewer infections than those who took a placebo pill.

The drugs have few side-effects, which is important if they are to be given to healthy individuals. Both are made by Gilead, which has licensed their manufacture to generic companies in the developing world, allowing them to produce cheap copies – so this is a relatively inexpensive intervention.

“This study demonstrates that antiretrovirals are a highly potent and fundamental cornerstone for HIV prevention and should become an integral part of global efforts for HIV prevention,” said Dr Connie Celum, professor of global health and medicine at the university and principal investigator of the study, known as the Partners PrEP Study, which was funded by the Bill and Melinda Gates Foundation.

The second study in Botswana was conducted by the United States Centres for Disease Control. It followed 1,200 heterosexual men and women without HIV who received either a once-daily tenofovir/emtricitabine tablet or a placebo pill. The antiretroviral tablet reduced the risk of acquiring HIV infection by roughly 63% overall.

“This is a major scientific breakthrough which re-confirms the essential role that antiretroviral medicine has to play in the Aids response,” said Michel Sidibé, Executive Director of the Joint United Nations Programme on HIV/Aids (UNAids). “These studies could help us to reach the tipping point in the HIV epidemic.”

The news follows hard on the heels of another very significant finding – that people with HIV who are taking combinations of antiretroviral drugs not only stay healthy themselves but are unlikely to infect their partner.

The two pieces of research give a massive boost to the cause of rolling out more Aids drugs and treating people at the earliest stage of their illness.

“Effective new HIV prevention tools are urgently needed, and these studies could have enormous impact in preventing heterosexual transmission,” said Dr Margaret Chan, WHO’s director general. “WHO will be working with countries to use the new findings to protect more men and women from HIV infection.”

Source: http://www.guardian.co.uk/world/2011/jul/14/hiv-daily-pill-breakthrough

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Scientists Discover Gonorrhea Resistant to Antibiotics

Last Updated on Tuesday, 12 July 2011 11:11 Written by admin Tuesday, 12 July 2011 11:11

(EndPlay Staff Reports) – A new untreatable strain of gonorrhea has been discovered in Japan and is causing concern in the United States.

Scientists reported that the strain, which is named H041, is resistant to all known forms of antibiotics. The researchers discussed the findings at a Monday meeting in Canada about three days after the CDC warned on July 8 that gonorrhea samples in the U.S. are also showing signs of drug resistance.

The concern is that the new strain of Neisseria gonorrhoeae is resistant to the cephalosporin family of antibiotics such as ceftriaxone, cefixime and cefpodoxime, which are widely used to treat the sexually transmitted disease in the United States. The CDC warned that this is a concern because it only leaves a few antibiotic options that are “simple, well-studied, and highly effective.”

The resistance to antibiotics, according to the CDC , was first documented in Asia before emerging in Hawaii and other western states then spreading elsewhere.

“This is a large public health problem and the era of untreatable gonorrhea may now have been initiated,” the team of researchers said at the Quebec City meeting of the International Society for Sexually Transmitted Disease Research, The Los Angeles Times reported.

The US Gonococcal Isolate Surveillance Project launched in 1986 has not discovered any U.S. cases in which treatment with cephalosporin antibiotics was a complete failure. The Times, though, reported there have been more cases that required unusually high doses of the antibiotic to cure them.

The majority of samples showing this trend were obtained from men having sex with men, the newspaper stated. The largest growth in cases noticed between 2000 and 2010 have been in Hawaii and California.

As a precaution, the CDC is suggesting dual treatment with another antibiotic such as azithromycin or doxycycline.

Gonorrhea, ABC News reported, is one of the most common STDs with about 700,000 new cases each year in the United States. It is spread through direct contact with the penis, vagina, mouth or anus and can also be transmitted from mother to baby during birth.

Only about half of infected women and less than five percent of infected men develop symptoms including a burning sensation and discharge. ABC News said it can spread to the skin, blood and other organs and cause pain, infertility and death if not treated.

Scientists are concerned that such a strain could spread quickly if new ways are not found to stop it. Dr. William Schaffner, chair of preventive medicine at Vanderbilt University Medical Center in Nashville, Tenn., told ABC News that this coincides with cutbacks in research as pharmaceutical companies invest less in the search for new antibiotics.

While the strain that did not respond at all to antibiotics was discovered in Kyoto, Japan, he warned, such bacteria “don’t need a passport” to spread.

Source: http://www.myfoxboston.com/dpps/health/scientists-discover-gonorrhea-resistant-to-antibiotics-dpgoha-20110712-fc_14088790

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A deadly new reason to avoid deer ticks

Last Updated on Monday, 11 July 2011 02:35 Written by admin Monday, 11 July 2011 02:35

Move over, Lyme disease: Another tick-borne illness is on the rise in various parts of the country, and this one can kill.

Known as babesiosis, the disease is caused by a microscopic parasite that attacks blood cells, causing flu-like symptoms that can make it difficult to accurately diagnose. Like Lyme disease, which is caused by bacteria, babesia microti parasites are carried by deer ticks.

First documented in Massachusetts in 1969, the once-obscure babesiosis has surfaced as a significant public health threat in parts of the Northeast and Upper Midwest over the last several years. A recent study in the journal Emerging Infectious Diseases, published by the U.S. Centers for Disease Control and Prevention, revealed that between 2001 and 2008 cases climbed from six to 119 in New York’s Lower Hudson Valley — a 20-fold regional increase.

And many cases may be escaping detection, experts say.

“I think it’s underreported. One of the reasons we’re seeing more about it is because people are becoming more aware,” said Dr. Peter Krause, a babesiosis researcher and senior research scientist at the Yale University School of Public Health. “The theory is that it’s spreading from east to west, as if you were dropping a pebble in a pond and it spread outward geographically.”

About 1,000 cases are reported annually in affected locales, Krause said, but many people with babesiosis have no symptoms and never know they’re harboring the parasite. For others, symptoms can include high fever, severe headache, fatigue, chills, and muscle aches and pains. It is treated with antimicrobial drugs, such as antibiotics.

People with compromised immune systems — including the elderly and those with cancer, HIV or no spleens — are especially at risk of potentially deadly complications such as organ failure. Between 10 percent and 20 percent of patients in those populations die as a result, Krause said.

The more prolific Lyme disease causes similar symptoms in early stage cases but is easier to diagnose by its telltale bullseye rash, said Dr. Barbara Herwaldt, a medical epidemiologist at the CDC who specializes in parasitic conditions.

Deer are pivotal to the life cycle of ticks carrying the babesia microti parasite by serving as a blood meal, shelter and a place to mate, Krause said. Ticks also feed on birds, who serve as carriers for Lyme disease, which affects the entire continental United States. Fortunately for humans, birds don’t carry babesia microti.

Krause noted that ticks need a moist climate to thrive, so dry states such as Arizona are not likely to see babesiosis cases caused by tick bites. But the disease can potentially spread to all states in an even sneakier way — through the blood supply.

Although a blood screening test is in trials, Krause said, donors are currently only asked if they have had babesiosis, and those who harbored it but never showed symptoms can pass it through their donated blood. And because most blood recipients are already physically compromised, babesiosis has about a 30 percent mortality rate in that group, he said.

“Getting babesiosis through the blood supply is a rare event and people shouldn’t panic,” he said. “I don’t think it will reach a crisis level, but it’s still a concern.”

To help prevent babesiosis, the CDC advises people with compromised immune systems or other vulnerabilities to avoid tick-infested wooded areas, particularly during warm months. The agency also recommends that everyone walk in the middle of trails and avoid bushy areas with lots of leaves or tall grasses and to use the repellent DEET and pre-treat clothes with an insect repellent containing permethrin before going outdoors.

The CDC also recommends doing full-body checks and showering within a few hours of being in the woods, as well as tossing used clothes in the dryer to kill any ticks that might be hiding there.

The authors of the study also advised clinicians to consider babesiosis in patients who have been exposed to ticks or received blood products and who show up for treatment with a fever and anemia resulting from the destruction of red blood cells.

Source: http://yourlife.usatoday.com/health/story/2011/07/A-deadly-new-reason-to-avoid-deer-ticks/49212700/1

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Stem cell research and use in veterinary medicine

Last Updated on Thursday, 7 July 2011 01:09 Written by admin Thursday, 7 July 2011 01:09

Stem cells show so much promise in human medicine. Cells that have the ability to become anything that the body needs is nothing short of a miracle. What is the role of stem cells in veterinary medicine? Do stem cells have a place? Many say they very much do.

Stem cells are able to be harvested from animals and are primarily used in horses, dogs, and cats for arthritic conditions.

There is much less controversy in veterinary medicine over the use of stem cells (at least at the present time) because of where they are harvested, or obtained. Rather than take stem cells from an umbilical cord or from an unborn fetus, the cells are harvested from the host itself.

How is this possible? Right now we know there is a certain amount of stem cells that exists in adult animals in either fat or bone marrow. These stem cells are considered adult stem cells and are somewhat limited in there ability to become “any cell” as compared to embryonic stem cells. However, adult stem cells can become cells similar to themselves.

What does this mean? There are individual reports of stem cells being used in veterinary medicine for conditions like ligament and tendon injuries in horses, as well as to treat a condition called laminitis. Everyone knows what tendons and ligaments are but what is laminitis?

Laminitis is a condition in horses that affects the blood supply and connective tissue from the bone to the hoof. In mild cases of laminitis there is just pain and inflammation which can be treated with rest, anti-inflammatories and special shoes to fit on the hoof.

Unfortunately, many times mild cases can progress to severe cases. There are also specific causes of laminitis that skip the mild phase and go right to the severe phase. The more severe phase can permanently damage the blood supply and the hoof would actually start to separate from the bone. If this happens many times it is irreversible and the only option for this is humane euthanasia. Stem cell therapy has been used to help to regrow the blood supply and connective tissue.

There are also reports that injecting adult stem cells harvested from bone marrow or fat can be used to treat arthritis in dogs and cats. There is a thin layer of cartilage that covers the bone at the joint called synovial cartilage. Synovial cartilage cushions the bone at the joint, as well as produces joint fluid. Joint fluid not only acts as a lubricant allowing the bones to slide back and forth, but also contains natural antioxidants and immune defenses.

When arthritis occurs in dogs the thin layers of synovial cartilage begin to degrade, or break down. It doesn’t happen all at once but when the cartilage is lost it does not grow back naturally. This is when you will hear orthopedists talk about “bone-on-bone” contact, and bone-on-bone contact is intensely painful.

The injection of stem cells into the joint has shown promise in regrowing this thin layer of synovial cartilage. No controlled studies have been performed to substantiate this claim. However, there are reports from various veterinarians using stem cells for this purpose that they see an improvement in their patients after receiving a stem cell treatment.

Using stem cells in veterinary patients to regrow tissue of any organ in the body is a long way off and even the use of stem cells for specific conditions like arthritis and laminitis has not been completely proven successful but there is hope on the horizon.

Source: http://www.northshoreoflongisland.com/Articles-i-2011-07-07-88828.112114-sub-Stem-cell-research-and-use-in-veterinary-medicine.html

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Who wants to live forever? Scientist sees aging cured

Last Updated on Tuesday, 5 July 2011 11:56 Written by admin Tuesday, 5 July 2011 11:56

(Reuters) – If Aubrey de Grey’s predictions are right, the first person who will live to see their 150th birthday has already been born. And the first person to live for 1,000 years could be less than 20 years younger.

A biomedical gerontologist and chief scientist of a foundation dedicated to longevity research, de Grey reckons that within his own lifetime doctors could have all the tools they need to “cure” aging — banishing diseases that come with it and extending life indefinitely.

“I’d say we have a 50/50 chance of bringing aging under what I’d call a decisive level of medical control within the next 25 years or so,” de Grey said in an interview before delivering a lecture at Britain’s Royal Institution academy of science.

“And what I mean by decisive is the same sort of medical control that we have over most infectious diseases today.”

De Grey sees a time when people will go to their doctors for regular “maintenance,” which by then will include gene therapies, stem cell therapies, immune stimulation and a range of other advanced medical techniques to keep them in good shape.

De Grey lives near Cambridge University where he won his doctorate in 2000 and is chief scientific officer of the non-profit California-based SENS (Strategies for Engineered Negligible Senescence) Foundation, which he co-founded in 2009.

He describes aging as the lifelong accumulation of various types of molecular and cellular damage throughout the body.

“The idea is to engage in what you might call preventative geriatrics, where you go in to periodically repair that molecular and cellular damage before it gets to the level of abundance that is pathogenic,” he explained.

CHALLENGE

Exactly how far and how fast life expectancy will increase in the future is a subject of some debate, but the trend is clear. An average of three months is being added to life expectancy every year at the moment and experts estimate there could be a million centenarians across the world by 2030.

To date, the world’s longest-living person on record lived to 122 and in Japan alone there were more than 44,000 centenarians in 2010.

Some researchers say, however, that the trend toward longer lifespan may falter due to an epidemic of obesity now spilling over from rich nations into the developing world.

De Grey’s ideas may seem far-fetched, but $20,000 offered in 2005 by the Massachusetts Institute of Technology (MIT) Technology Review journal for any molecular biologist who showed that de Grey’s SENS theory was “so wrong that it was unworthy of learned debate” was never won.

The judges on that panel were prompted into action by an angry put-down of de Grey from a group of nine leading scientists who dismissed his work as “pseudo science.”

They concluded that this label was not fair, arguing instead that SENS “exists in a middle ground of yet-to-be-tested ideas that some people may find intriguing but which others are free to doubt.”

CELL THERAPY

For some, the prospect of living for hundreds of years is not particularly attractive, either, as it conjures up an image of generations of sick, weak old people and societies increasingly less able to cope.

But de Grey says that’s not what he’s working for. Keeping the killer diseases of old age at bay is the primary focus.

“This is absolutely not a matter of keeping people alive in a bad state of health,” he told Reuters. “This is about preventing people from getting sick as a result of old age. The particular therapies that we are working on will only deliver long life as a side effect of delivering better health.”

De Grey divides the damage caused by aging into seven main categories for which repair techniques need to be developed if his prediction for continual maintenance is to come true.

He notes that while for some categories, the science is still in its earliest stages, there are others where it’s already almost there.

“Stem cell therapy is a big part of this. It’s designed to reverse one type of damage, namely the loss of cells when cells die and are not automatically replaced, and it’s already in clinical trials (in humans),” he said.

Stem cell therapies are currently being trialed in people with spinal cord injuries, and de Grey and others say they may one day be used to find ways to repair disease-damaged brains and hearts.

NO AGE LIMIT

Cardiovascular diseases are the world’s biggest age-related killers and de Grey says there is a long way to go on these though researchers have figured out the path to follow.

Heart diseases that cause heart failure, heart attacks and strokes are brought about by the accumulation of certain types of what de Grey calls “molecular garbage” — byproducts of the body’s metabolic processes — which our bodies are not able to break down or excrete.

“The garbage accumulates inside the cell, and eventually it gets in the way of the cell’s workings,” he said.

De Grey is working with colleagues in the United States to identify enzymes in other species that can break down the garbage and clean out the cells — and the aim then is to devise genetic therapies to give this capability to humans.

“If we could do that in the case of certain modified forms of cholesterol which accumulate in cells of the artery wall, then we simply would not get cardiovascular disease,” he said.

De Grey is reluctant to make firm predictions about how long people will be able to live in future, but he does say that with each major advance in longevity, scientists will buy more time to make yet more scientific progress.

In his view, this means that the first person who will live to 1,000 is likely to be born less than 20 years after the first person to reach 150.

“I call it longevity escape velocity — where we have a sufficiently comprehensive panel of therapies to enable us to push back the ill health of old age faster than time is passing. And that way, we buy ourselves enough time to develop more therapies further as time goes on,” he said.

“What we can actually predict in terms of how long people will live is absolutely nothing, because it will be determined by the risk of death from other causes like accidents,” he said.

“But there really shouldn’t be any limit imposed by how long ago you were born. The whole point of maintenance is that it works indefinitely.”

Source: http://www.reuters.com/article/2011/07/04/us-ageing-cure-idUSTRE7632ID20110704

Posted under Cell Analysis, Discoveries, Innovations and Patents, DNA Reasearch, Medicinal Chemistry, Research Projects, Stem Cell Research | Comments Off

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