Shawn's Health Blog: Jan 24, 2009

1/24/2009

Scientists learning more about cancer-initiating properties of stem cells

Recent discoveries about the role of stem cells in cancer have altered the landscape of cancer research. With each new study, scientists are learning more about cancer-initiating properties of stem cells at organ sites and throughout the body. Increasingly, stem cells are examined as the cause %26#8211; and potential target of treatment %26#8211; for many, if not all, cancers. At the 2007 Annual Meeting of the American Association for Cancer Research, researchers present new discoveries about stem cells in leukemia, breast and colon cancer that add to the growing evidence that perhaps cancer is, fundamentally, a stem cell problem.

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PTEN and HER2 regulate self-renewal and invasion of human mammary stem cells: Abstract 1287

Two genes associated with aggressive breast cancer are linked to a key property of mammary stem cell function, according to researchers at the University of Michigan. The genes, PTEN and HER2, both are involved in the biochemical pathways that mediate stem cell self-renewal, a defining property of stem cells.

According to the researchers, understanding the pathways that regulate stem cell self-renewal is important in developing therapeutics that target the tumor stem cell pool. These genes might also become targets of interest in the treatment of tumors resistant to the drug Herceptin.

"We now believe that our results show further evidence that breast cancer arises from signaling errors in the biochemical pathways that control mammary stem cell self-renewal" said Hasan Korkaya, D.V.M., Ph.D., a research fellow at the University of Michigan%26#8217;s Comprehensive Cancer Center. "Since only stem cells have the ability to self-renew, deregulation of either PTEN or HER2 expands the stem cell populations with self-renewing ability."

According to Korkaya, cells with deregulated %26#8211; or increased %26#8211; self-renewing ability will then initiate and maintain tumors that are resistant to current therapies.

The two genes appear to influence stem cell self-renewal by controlling two different arms of the pathway, says Korkaya. In breast cancer, the loss of PTEN is linked to nearly a quarter of all cases, while the overproduction of HER2 is associated with nearly 40 percent of all cases. Patients with a combined defect of PTEN loss and HER2 amplification represent worse prognosis than either defect alone.

To replicate this clinical phenomenon and study the link between stem cell self-renewal and tumorigenesis, the researchers altered the expression of the two genes in a line of human breast carcinoma cells. In experimental settings, their results confirmed this clinical data that either defect increases stem cell population by three to five times. Furthermore, Korkaya observed an additive effect and an approximate 10-fold increase in stem cell population when they created a cell line with deleted PTEN and HER2 overexpression. Another property of aggressive tumors is metastasis; the team also found that these cells had increased invasive capacity in a matrigel invasion assay.

"In general, tumors are heterogeneous including stem and non-stem cell populations in a given malignancy," Korkaya said. "If the stem cells acquired mutations in their self-renewing pathways, they will then begin reproducing at an accelerated rate, leading to a particularly aggressive form of cancer."

The researchers believe further studies will identify new biomarkers that will enable physicians to clinically screen patients for mammary stem cells and provide specific treatments designed to target these cells.

Local Radiotherapy Might Contribute to Leukemia Risk in Breast Cancer by Recruitment of Hematopoietic Stem Cells: Abstract 5050

Radiation therapy affects not only the cancer mass, but also the surrounding tissues, including the bone marrow. Signals from the cells in the bone marrow damaged by cancer radiotherapy could be involved in the development of secondary acute myeloma by drawing hematopoietic stem cells, the blood-producing cells of the bone marrow, from distant sites into the irradiated bone marrow, according to researchers from the Ontario Cancer Institute. Their findings suggest that local radiotherapy leads to leukemia, even though radiotherapy directly affects only a small fraction of the bone marrow.

While often effective in treating breast cancer, localized radiation therapy increases the risk of developing secondary cancer, which most frequently manifests in the form of acute myeloid leukemia. In breast cancer, less than 10 percent of bone marrow is exposed to radiation therapy, yet a much higher percentage of hematopoietic stem cells could be affected.

To understand this effect, the researchers labeled and tracked the movement of hematopoietic stem cells in an animal model. Following local radiation therapy, they found that more than four times more hematopoietic stem cells accumulated in the irradiated bone marrow, compared to the non-irradiated bone marrow. Through molecular screening, they found that cells in the area were creating an overabundance of three protein signals known to recruit hematopoietic stem cells: SDF1, MMP2 and MMP9.

"Cells within the bone marrow send out these chemical signals as a sort of call for help, which recruits a large number of hematopoietic stem cells into the affected areas, supposedly to replace damaged cells," said Carlo Bastianutto, Ph.D., a scientific associate at the Ontario Cancer Institute. "In effect, this becomes a trap for this specific population of stem cells, drawing them into the bone marrow present in the radiation field and getting them exposed to the following radiation cycles. This story might repeat at every cycle of radiation therapy, therefore increasing the chance of producing a leukemic stem cell."

According to the OCI researchers, the recruiting signal might be stopped by chemical blockers, which was shown to inhibit the signals experimentally. "Conceivably, it could be possible to inhibit these chemical signals, and this could reduce the risk of secondary acute myeloid leukemia, but much more research needs to be done," Bastianutto said.

The researchers believe this model could help prevent acute myeloid leukemia in patients with malignancies other than breast cancer.

Prospective identification of highly tumorigenic colon adenocarcinoma cells enriched for stem-like properties: Abstract 1288

Colon cancer could join the growing list of stem cell-related cancers with the discovery of a population of highly tumorigenic primary human colon tumor cells, according to researchers from Biogen Idec.

"Such stem cells could be responsible for the perpetuation of colon cancer and its relapse following successful therapy," said Peter Chu, Ph.D., researcher at Biogen Idec. "Our goal is to improve cancer survival rates by identifying these cancer stem cells in order to pave the way for therapeutics to prevent the relapse or metastasis of cancer."

To identify potential cancer stem cells, also known as cancer-initiating cells, the researchers screened a population of human colon cancer cells for molecular markers that differentiated some cells from others. They found a certain subset of cells produced an exceptional amount of CD44 cell surface receptor protein, a well-studied protein involved in many forms of cancer.

According to Chu, to be identified as cancer stem cells, they had to be highly tumorigenic, creating new tumors quickly and from very few starting cells; had to be self-renewing, possessing a capacity to regenerate; and they had to produce tumors similar to the tumor of origin. "These CD44-producing cells fit the bill, although there is evidence to believe that CD44 overexpression is not the sole marker for colon cancer stem cells," said Chu.

Chu and his colleagues discovered that as few as 10 cells producing high amounts of CD44 were capable of creating tumors in an animal model. In contrast, other tumor cells were 10 to 50 times less tumorigenic. The fact that they were tumorigenic at all, the researchers say, indicates that CD44 alone is unlikely to be the sole indicator of stem cell-ness among the tumor cell population. However, according to Chu, the discovery that high CD44 producing cells have cancer stem cell properties provides an entry point into further research into cancer-causing stem cells.

BRCA1 regulates human mammary stem cell self-renewal and differentiation: Abstract 5700

Mutations in the well-known breast cancer susceptibility gene BRCA1 have a role in the propagation of aggressive stem cell-driven cancer. The findings, according to researchers at the University of Michigan, offer further evidence that breast cancer treatment strategies require a stronger focus on the stem cells that drive the disease.

"Our lab previously identified the presence of mammary stem cells and, since BRCA1 is such a strong predictor of breast cancer, we were interested in the involvement of the gene in stem cells," said Suling Liu, Ph.D., a researcher at the University of Michigan%26#8217;s Comprehensive Cancer Center. "If mammary stem cells are, indeed, the driving force of breast cancer, then we need to know more about their function if we hope to create more effective therapies."

To investigate the role of the gene in stem cells, the team engineered a lentivirus to carry small interfering RNA segments that, in effect, silence the BRCA1 gene. They then observed how a population of mammary stem cells functioned without the ability to produce BRCA1. When BRCA1 was inhibited, the number of stem cells was increased by 75 percent. These new cells, in turn, produced three times the normal amount of a stem cell marker protein ALDH1.

In an animal model of the disease, the knockdown of the BRCA1 gene increased the number of stem cells, which then propagated in the fatty tissues of the breast.

These studies suggest that loss of BRCA1 function leads to a block in cell differentiation, expanding the stem cell pool. Since BRCA1 also regulates DNA repair, this may then produce genetically unstable stem cells which in turn generate tumors in these women.

According to Liu, the loss of a single BRCA1 gene can lead to stem cell propagation. The researchers believe their findings might lead to better BRCA1 screening in women with a family history of breast cancer.

Source: American Association for Cancer Research

Omega-3 fatty acid may slow growth of two brain lesions in Alzheimer’s disease

A type of omega-3 fatty acid may slow the growth of two brain lesions that are hallmarks of Alzheimers disease, UC Irvine scientists have discovered. The finding suggests that diets rich in docosahexaenoic acid (DHA) can help prevent the development of Alzheimers disease later in life.This study wit...

A type of omega-3 fatty acid may slow the growth of two brain lesions that are hallmarks of Alzheimer%26#8217;s disease, UC Irvine scientists have discovered. The finding suggests that diets rich in docosahexaenoic acid (DHA) can help prevent the development of Alzheimer%26#8217;s disease later in life.

This study with genetically modified mice is the first to show that DHA, an omega-3 fatty acid, can slow the accumulation of tau, a protein that leads to the development of neurofibrillary tangles. Such tangles are one of two signature brain lesions of Alzheimer%26#8217;s disease. DHA also was found to reduce levels of the protein beta amyloid, which can clump in the brain and form plaques, the other Alzheimer%26#8217;s lesion.

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Previous studies have shown that DHA may have therapeutic value for Alzheimer%26#8217;s patients, but this research is among the first to show that it may delay the onset of the disease. DHA is found in fish, eggs, organ meats, micro-algae, fortified foods and food supplements.

%26#8220;We are greatly excited by these results, which show us that simple changes in diet can positively alter the way the brain works and lead to protection from Alzheimer%26#8217;s disease pathology,%26#8221; said Frank LaFerla, professor of neurobiology and behavior and co-author of the study.

This research appears in the April 18 issue of The Journal of Neuroscience.

LaFerla and his research team studied the effects of DHA in mice bred to develop the plaques and tangles associated with Alzheimer%26#8217;s disease. Mice in the control group were given food that mimics a typical American diet, with the ratio of omega-6 fatty acids to omega-3 fatty acids being 10:1. Studies indicate that a proper ratio is important to maintain health, with the ideal being 3:1 to 5:1. Typical Western diets contain unhealthy ratios ranging from 10:1 to 30:1. Omega-6 fatty acids are found in corn, peanut and sunflower oils.

Mice in three test groups were given food with a 1:1 ratio of omega-6 fatty acids to omega-3 fatty acids. One of these groups received supplemental DHA only, and two groups received DHA plus additional omega-6 fatty acids. After three months, mice in all of the test groups had lower levels of beta amyloid and tau than mice in the control group, but at nine months, only mice on the DHA diet had lower levels of both proteins. These results suggest that DHA works better on its own than when paired with omega-6 fatty acids.

The scientists also determined the mechanism by which DHA leads to lower levels of beta amyloid. DHA, they found, leads to lower levels of presenilin, an enzyme responsible for cutting beta amyloid from its parent, the amyloid precursor protein. Without presenilin, beta amyloid cannot be generated. When clumped into plaques, beta amyloid disrupts communication between cells and leads to symptoms of Alzheimer%26#8217;s disease.

This latest study adds to growing evidence that diet and lifestyle changes may reduce the risk of developing Alzheimer%26#8217;s disease. LaFerla and his team have previously shown that short but repeated learning sessions can slow the physical progression of Alzheimer%26#8217;s in mice, suggesting that the elderly can delay onset of the disease by keeping their minds active. The team also found that stress hormones appear to rapidly exacerbate the formation of plaques and tangles, suggesting that managing stress could slow the progression of Alzheimer%26#8217;s.

%26#8220;Combined with mental stimulation, exercise, other dietary intakes, and avoiding stress and smoking, we believe that people can significantly improve their odds against this disease,%26#8221; said Kim Green, scientist and lead author on the DHA, learning and stress studies.

Alzheimer%26#8217;s is a progressive neurodegenerative disorder that affects more than 4.5 million adults in the United States. With an aging population, that number could approach 20 million by 2050. Five percent of people older than 65 have Alzheimer%26#8217;s, and up to one-half of people are affected by age 80.

Source: University of California, Irvine

Robotic "caterpillar" crawls around heart to deliver treatment without surgery

A device that sounds like a 21st century version of a medicinal leech may soon be set loose inside the chests of heart patients. Resembling a robotic caterpillar, it will crawl across the surface of their beating heart, delivering treatment without the need for major surgery.The device, called Heart...

The device, called HeartLander, can be inserted using minimally invasive keyhole surgery. Once in place, it will attach itself to the heart and begin inching its way across the outside of the organ, injecting drugs or attaching medical devices. In tests on live pigs, the HeartLander has fitted pacemaker leads and injected dye into the heart.

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The 20-millimetre-long robot has two suckers for feet, each pierced with 20 holes connected to a vacuum line, which hold it onto the outside of the heart. By moving its two body segments back and forth relative to one another it can crawl across the heart at up to 18 centimetres per minute. This back-and-forth movement is generated by pushing and pulling wires that run back to motors outside the patient's body. The robot is being developed by Cameron Riviere and colleagues at Carnegie Mellon University in Pittsburgh, Pennsylvania.

The plan is to insert the HeartLander through an incision below the ribcage, and pass it through a further incision in the membrane that encloses the heart. Surgeons keep track of the device using X-ray video or a magnetic tracker, and control its movements via a joystick.

Traditional open-heart surgery requires a massive incision, and the heart usually has to be stopped to make it easier to operate safely. Though minimally invasive procedures on a beating heart are sometimes possible, some areas of the heart are out of reach to instruments inserted through the keyhole incisions, and the limited space in the chest cavity makes operating difficult.

"HeartLander can reach all parts of the heart's surface," Riviere says. And because it is stationary relative to the heart's surface, there is no need to interfere with the organ's movement.

Entering the body from a single small incision could even allow some heart procedures to be performed without a general anaesthetic, he says. "It avoids having to disturb the ribcage, or to deflate the left lung to access the heart."

"This device is certainly like nothing else I've seen," says Andrew Rankin, a cardiologist at the University of Glasgow in the UK. Many procedures can be performed by passing instruments into the heart through blood vessels, but this is not possible where damaged or diseased tissue is close to the heart's surface. "This device could be useful in those cases," Rankin says.

He suggests it might come into its own for future treatments such as stem cell therapies to encourage regeneration of heart tissue. "You can imagine this device moving around the surface of a scarred heart to deliver treatments."

The researchers are now working on adding a radiofrequency probe to the device, to treat arrhythmias by selectively killing malfunctioning heart tissue. They also plan to add a camera.

Source: New Scientist

Studying how antioxidants and herbal supplements can be useful in promotion of health and prevention of chronic diseases

Nutrition: It's not just the four basic food groups any more.Researcher Dr. Susanne Mertens-Talcott of Texas A&M University is looking into how plant-based phytochemicals, including antioxidants and herbal supplements, can be useful in the promotion of health and prevention of chronic diseases.This ...

Nutrition: It's not just the four basic food groups any more.

Researcher Dr. Susanne Mertens-Talcott of Texas A%26amp;M University is looking into how plant-based phytochemicals, including antioxidants and herbal supplements, can be useful in the promotion of health and prevention of chronic diseases.

This field is still growing. In the U.S. more than $20 billion was spent on dietary supplements in 2005, said Talcott, who is in a joint research and teaching position with the department of nutrition and food science and the department of veterinary physiology and pharmacology.

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"Over $7 billion was spent on herbal dietary supplements in 2005." These supplements are plant-based, including grape seed extract, St. John's wort, ginseng and biloba extract, she added.

"In addition to that there is the segment of so-called %26#8216;functional foods,' including antioxidant foods %26#8211; for example, fruit juices and beverages and grain-based products," Talcott said.

The amount spent on these foods each year "has increased drastically; however, we do not know yet how efficacious these different antioxidants really are in the prevention of chronic diseases such as cardiovascular disease and cancer," she said. "We also do not know very much about the mechanisms, which appear to include antioxidant and anti-inflammatory effects of these phytochemicals."

This can be important to health since these reactive oxygen species or %26#8216;free radicals' may play a role in some diseases, including Alzheimer's, cancer and atherosclerosis, she said.

"However, other mechanisms, including the prevention of chronic inflammation and interaction with intracellular mechanisms, may be as important in the prevention of chronic diseases," she said. But are they safe? Are they efficient? How much is required? And how much is too much? Talcott is looking for the answers to these questions through her research.

"My overall goal is to find out more about the safety and efficacy of phytochemical dietary supplements," she said. Because these items are already popular with consumers, "we need to follow up with research. We know very little about (dose) recommendations and how safe (they are)."

Phytochemicals, also called secondary plant compounds %26#8211; including antioxidants %26#8211; have been defined as chemicals found in plants that have protective or disease-fighting properties ( http://phytochemicals.info/ ).

Pomegranate juice and extract have been the focus of much of her studies. Because these are used in different food products, they are found as ingredients in many different items in supermarkets, Talcott said.

She has also done research on the properties of muscadine grapes and acai, a palm fruit from Brazil, as well as isolated compounds including quercetin and ellagic acid, which are also sold as dietary supplements.

The results of some of her studies were published in the Oct. 13, 2006, edition of the Journal of Agricultural and Food Chemistry. The article was titled "Absorption, Metabolism and Antioxidant Effects of Pomegranate (Punica granatum L.) Polyphenols after Ingestion of a Standardized Extract in Healthy Human Volunteers."

In addition to her research, Talcott teaches a class on "Special Topics in Phytochemicals of Fruits and Vegetables" for students who are majoring in nutrition and food science. Many of the students are planning to enter medical or pharmacy school, she added.

"It is my goal to give students as much relevant information, which they directly can apply in their desired profession," Talcott said. "Consumers and patients have many questions about herbal dietary supplements, and health care professionals and (members of the) food industry are and will be even more confronted with these questions."

For example, Dr. Joseph M. Betz was a recent guest lecturer in Talcott's class. Betz is the director of the Dietary Supplement Methods and Reference Materials Program Office of Dietary Supplements at the National Institutes of Health in Bethesda, Md. He discussed Food and Drug Administration rules as to the differences between foods and drugs and how each must be labeled. With regard to herbal supplements, this can sometimes be a little tricky, he said.

During the question and answer period at the end of his talk, one of the students asked about a recent study on antioxidants. According to news reports, the study seemed to find that antioxidants %26#8211; especially vitamins A and E %26#8211; don't have the beneficial properties they are thought to have and may even increase mortality.

Talcott offered this clarification in regard to the study: "This study statistically analyzed many different clinical studies with vitamins A, E (and) C, beta-carotene and selenium. The performed statistical analysis indicated that vitamin A and E and beta-caraotene may increase mortality in some of the selected studies. The meaning of this study currently is being discussed."

The study looked at synthetic antioxidants, she said, which are not the same compounds that she is researching.

"Even though we still have a lot to learn about the efficacy, safety and dosing recommendations for herbal supplements and antioxidant foods, we can be confident to recommend a healthy balanced diet according to the food-pyramid rich in fresh fruits and vegetables. I also would not see a problem with the intake of reasonable amounts of standardized high-quality antioxidant dietary supplements," she said

"It is my long-term goal to see science-based intake recommendations developed for those herbal plant compounds which have a proven potential in the promotion of health and prevention of chronic disease."

Source: Texas A%26amp;M University

Deep brain stimulation successfully treats depression

A study at the University Clinics of Bonn and Cologne gives people with therapy-resistant depression reason for hope. The doctors treated two men and a woman with what is known as deep brain stimulation. All three patients have been suffering from very severe depression for several years which could neither be brought under control using medication nor by other therapies. During the simulation the condition of two of the three patients improved within a few days. Initial changes were even noticeable in a matter of minutes. The research team warn against exaggerated expectations in view of the small number of patients involved. Nevertheless, the results of the preliminary study are so sensational that they have now been published in the renowned journal Neuropsychopharmacology.

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In deep brain stimulation (DBS) electrodes are implanted selectively in certain areas of the brain and are stimulated using an electric pulse generator. Up to now the procedure has mainly been used in the treatment of Parkinson's. It is currently being investigated whether it also helps with certain psychiatric diseases such as compulsive behavioural disorders. Initial tests on about two dozen patients worldwide also show that it could possibly also have an effect in the case of severe depression.

Previous tests have concentrated mainly on two areas of the brain in particular. "By contrast we stimulated a third region, the nucleus accumbens," the Bonn Professor of Psychiatry, Thomas E. Schl%26#195;%26#164;pfer, explains. The nucleus accumbens is an important part of what is known as the "reward system". It ensures that we remember good experiences and puts us in a state of pleasurable anticipation. Without the reward system we would not make plans for the future, simply because we could not enjoy the fruits of these plans. "Inactivity and inability to enjoy things are two important signs of depression," Profesor Schl%26#195;%26#164;pfer emphasises. "The conclusion is therefore obvious that the nucleus accumbens plays a key role in the genesis of the disease."

Initial effects minutes after onset of therapy

In their study the researchers report on two men and a woman who have been suffering from very severe depression for years. The researchers implanted electrodes in the nucleus accumbens, which they were able to stimulate using an electric pulse generator in the chest. Some of the effects were observable instantly. "One of the patients expressed the desire to go to the top of Cologne Cathedral a minute after the start of the stimulation and put this into practice the next day," Thomas Schl%26#195;%26#164;pfer says. "The woman treated was similar. She said she would enjoy going bowling again." Nevertheless, the patients did not notice a direct improvement in their mood. Nor could they tell whether the pulse generator was switched on or off.

In the first few days of the DBS the symptoms of depression improved significantly in two of the three patients. Their condition remained constant for as long as they were undergoing treatment. However, as soon as the pulse generator was switched off, the depression recurred with full intensity. "The recurring symptoms were so severe that for ethical reasons we could not permit the treatment to be interrupted for as long as we had originally planned," Professor Schl%26#195;%26#164;pfer emphasises.

While psychotropics generally interfere with the biochemistry of the brain, DBS acts locally in the affected areas. The doctors did not observe any side effects like those occurring after the use of antidepressants. The patients only complained about post-operative pain at the site of implantation. In the long term DBS does not seem to pose any major risks. There have been patients with Parkinson"s who have been using this kind of brain pacemaker for more than ten years without experiencing any problems.

Preliminary results

Even so, the research team caution against exaggerated expectations. "Of course, with so few patients, these are only fairly preliminary results," Professor Schl%26#195;%26#164;pfer says. "Our follow-up experiments are showing even now that by no means every patient will respond to this therapy." In the case of operations on the brain, in particular, ethical factors also need to be taken into account, not least because such operations are always risky. For that reason, there were particularly stringent conditions attached to the patients" consent. "One thing has certainly been demonstrated by our research and that of others: DBS can help some people with depression even in cases which were assumed to be resistant to therapy."

Source: University of Bonn

Treating strawberries with alcohol makes them healthier

Strawberries are good for you, but serving them in daiquiri form may make them even healthier, scientists show.While exploring ways to help keep strawberries fresh during storage, researchers from Thailand and the US discovered that treating the berries with alcohol led to an increase in antioxidant...

Strawberries are good for you, but serving them in daiquiri form may make them even healthier, scientists show.

While exploring ways to help keep strawberries fresh during storage, researchers from Thailand and the US discovered that treating the berries with alcohol led to an increase in antioxidant capacity and free radical scavenging activity within the fruit. While such a boost helped the berries resist decay, the same compounds would also be expected to make the strawberries healthier to eat.

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Dr Korakot Chanjirakul and colleagues at Kasetsart University in Thailand, in collaboration with scientists at the United States Department of Agriculture, tested the berries with ethanol and found that the treatment improved the physiology of the fruit as measured by several different laboratory tests for antioxidant activity.

Coloured berry fruits like strawberries contain compounds known as polyphenols and anthocyanins. Consumption of these compounds has been linked to the prevention of diseases ranging from cancer to neurodegenerative disorders. They work by helping to mop up damaging free radicals produced naturally during a person%26#8217;s normal metabolism.

Those who aren%26#8217;t keen on strawberry daiquiris might be relieved to know that the scientists found similar results with blackberries, meaning that a blackberry-crowned champagne cocktail might achieve the same effect.

Source: Society of Chemical Industry

Cutting back on salt reduces chances of heart disease by 25 percent

People who significantly cut back on the amount of salt in their diet could reduce their chances of developing cardiovascular disease by a quarter, according to a report on bmj.com today.Researchers in Boston also found a reduction in salt intake could lower the risk of death from cardiovascular dis...

People who significantly cut back on the amount of salt in their diet could reduce their chances of developing cardiovascular disease by a quarter, according to a report on bmj.com today.

Researchers in Boston also found a reduction in salt intake could lower the risk of death from cardiovascular disease by up to a fifth.

Cardiovascular disease refers to the group of diseases linked to the heart or arteries, for example a stroke or heart disease. While there is already a substantial body of evidence showing that cutting back on salt lowers blood pressure, studies showing subsequent levels of cardiovascular disease in the population have been limited and inconclusive.

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This research provides some of the strongest objective evidence to date that lowering the amount of salt in the diet reduces the long term risk of future cardiovascular disease, say the authors of the report.

Researchers followed up participants from two trials completed in the nineties which had been conducted to analyse the effect that reducing salt in the diet had on blood pressure.

All the participants had high-normal blood pressure (pre-hypertension). They were therefore at greater risk of developing cardiovascular disease. 744 people took part in the first Trial of Hypertension Prevention which was completed in 1990, 2382 in the second, which ended in 1995. In both trials participants reduced their sodium intake by approximately 25% - 35% alongside a control group who didn%26#8217;t cut back on their salt intake.

Detailed information about cardiovascular and other health problems was sought from participants in the earlier trials. As part of this researchers found that participants who had cut back on salt during the trials tended to stick to a lower salt diet compared to those who had been in the control group. In total the researchers obtained information from 2415 (77.3%) participants, 200 of whom had reported some sort of cardiovascular problem.

The reduction in the risk of developing cardiovascular problems as a result of the sodium reduction intervention was substantial. The results showed these pre-hypertensive individuals were 25% less likely to develop cardiovascular problems over the course of the 10-15 years post-trial. There was also a 20% lower mortality rate. This risk reduction was evident in each trial.

To the authors knowledge this study is the first and only study of sufficient size and duration to assess the effects of a low salt diet on cardiovascular problems based on randomised trial data. It provides unique evidence that lowering salt in the diet might prevent cardiovascular disease.

Source: BMJ

Miscue of body’s genetic repair system may cause Huntington’s disease

Mayo Clinic researchers, along with collaborators from the National Institutes of Health (NIH) and University of Oslo, Norway, have discovered that a miscue of the bodys genetic repair system may cause Huntingtons disease, a fatal condition that affects 30,000 Americans annually by destroying their ...

Mayo Clinic researchers, along with collaborators from the National Institutes of Health (NIH) and University of Oslo, Norway, have discovered that a miscue of the body%26#8217;s genetic repair system may cause Huntington%26#8217;s disease, a fatal condition that affects 30,000 Americans annually by destroying their nervous system. Until now, no one knew how Huntington%26#8217;s begins, only that it is incurable. The findings appear in the online issue of the journal Nature.

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"We showed that when single-strand breaks in DNA caused by oxidative lesions were repaired, the Huntington%26#8217;s gene continued to add extra replacement segments," explains Cynthia McMurray, Ph.D., a Mayo Clinic molecular biologist who led the study team. "Over time, this expansion -- especially in nerve cells -- becomes toxic."

The finding is significant because so little is known about Huntington%26#8217;s. According to Dr. McMurray, the finding is the first confirmed connection between the DNA repair and progression of the disease. Leaders at the NIH, which sponsored the study, are optimistic the findings will lead to advances.

"As so often happens, basic research on a fundamental biological process -- in this case, enzymes involved in DNA repair -- leads to new insights about how diseases arise and new approaches for treating or preventing them," said NIH Director Elias Zerhouni, M.D.

In their study of transgenic mice that carried the human Huntington%26#8217;s gene, the researchers noted that the repeated tracts of replacement repair segments seem stable until the animals reach about 4 months of age. After that point -- which represents middle age for a mouse -- the segments expand and continue to do so as the animals age. Researchers also showed that the expansion of the tracts -- an inherited characteristic -- also caused toxicity in cells that cannot expand, such as nerve cells. The result is that cell death acceleration is directly proportional to the additional repeated lengths.

In a further step, the team eliminated a key enzyme (OGG1) related to DNA repair for oxidative lesions and found that it stopped or greatly reduced segment growth. This may position OGG1 as a target candidate for interventional therapies to disrupt the onset of the disease.

Source: Mayo Clinic

Muscle function restored in Duchenne's muscular dystrophy

Using a new type of drug that targets a specific genetic defect, researchers at the University of Pennsylvania School of Medicine, along with colleagues at PTC Therapeutics Inc. and the University of Massachusetts Medical School, have for the first time demonstrated restoration of muscle function in a mouse model of Duchenne's muscular dystrophy (DMD). The research appears ahead of print in an advanced online publication of Nature.

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"This new class of treatment has the potential to help a large number of patients with different genetic diseases that have the same type of mutation," says senior author H. Lee Sweeney, PhD, chair of the Department of Physiology at Penn. This genetic flaw causes from 5 to 15 percent (and in a few instances up to 70 percent) of individual cases of most inherited diseases, including DMD, cystic fibrosis, and hemophilia.

The new drug, developed by the South Plainfield, NJ-biotech firm and called PTC124, binds to the ribosome, a cellular component where the genetic code is translated into proteins, one amino acid at a time. The drug allows the ribosome to read through a mistake in the genetic code called a premature stop codon in order to properly make whole proteins.

In DMD, patients are missing dystrophin, a protein that helps keep muscle cells intact. About 15 percent of DMD patients do not make dystrophin because of the mutation. DMD eventually affects all voluntary muscles, as well as heart and breathing muscles.

PTC124 attaches to ribosomes in all cell types within the MD mouse model, overriding the mutation in the dystrophin gene that tells it to halt production of the protein. Instead of stopping, the full-length dystrophin protein is made. The drug enables enough protein to be made to correct defects in the muscle of the DMD mouse, and at the same time the drug does not prevent the ribosome from reading correct "stop" signals in the genetic code to make other necessary proteins.

"Enough dystrophin accumulated in the muscles of the MD mice so that we could no longer find defects in the muscles when we examined them," says Sweeney. "For all intents and purposes the disease was corrected by treatment with PTC124." The drug allowed dystrophin to be made in cells in which it was previously absent, to be delivered to the proper location at the cell membrane, and to induce restoration of muscle function in rodent muscles.

Source: University of Pennsylvania

First evidence of a molecular mechanism that dynamically alters the strength of higher brain network connections

Yale School of Medicine and University of Crete School of Medicine researchers report in Cell April 20 the first evidence of a molecular mechanism that dynamically alters the strength of higher brain network connections.This discovery may help the development of drug therapies for the cognitive defi...

This discovery may help the development of drug therapies for the cognitive deficits of normal aging, and for cognitive changes in schizophrenia, bipolar disorder, or attention deficit hyperactivity disorder (ADHD).

"Our data reveal how the brain%26#8217;s arousal systems influence the cognitive networks that subserve working memory%26#8212;which plays a key role in abstract thinking, planning, and organizing, as well as suppressing attention to distracting stimuli," said Amy Arnsten, lead author and neurobiology professor at Yale.

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The brain%26#8217;s prefrontal cortex (PFC) normally is responsible for so-called executive functions. The ability of the PFC to maintain such memory-based functions declines with normal aging, is weakened in people with ADHD, and is severely disrupted in disorders such as schizophrenia and bipolar disorder.

The current study found that brain cells in PFC contain ion channels called hyperpolarization-activated cyclic nucleotide-gated channels (HCN), that reside on dendritic spines, the tiny protrusions on neurons that are specialized for receiving information. These channels can open when they are exposed to cAMP (cyclic adenosine monophosphate). When open, the information can no longer flow into the cell, and thus the network is effectively disconnected. Arnsten said inhibiting cAMP closes the channels and allows the network to reconnect.

The study also found alpha-2A adrenergic receptors near the channels that inhibit the production of cAMP and allow the information to pass through into the cell, connecting the network. These receptors are stimulated by a natural brain chemical-norepinephrine-or by medications like guanfacine.

"Guanfacine can strengthen the connectivity of these networks by keeping these channels closed, thus improving working memory and reducing distractibility," she said. "This is the first time we have observed the mechanism of action of a psychotropic medication in such depth, at the level of ion channels." Arnsten said the excessive opening of HCN channels may underlie many lapses in higher cognitive function. Stress, for example, appears to flood PFC neurons with cAMP, which opens HCN channels, temporarily disconnects networks, and impairs higher cognitive abilities.

There is also evidence that this pathway may not be properly regulated with advancing age, resulting in destruction of cAMP. The dysregulation of the pathway may contribute to increased forgetfulness and susceptibility to distraction as we grow older.

The research is also relevant to common disorders such as ADHD, which is associated with weaker regulation of attention and behavior. ADHD is highly heritable, and some patients with ADHD may have genetic changes in molecules that weaken the production of norepinephrine. Treatments for ADHD all enhance stimulation of the norepinephrine receptors.

These new data also have important implications for the researchers%26#8217; studies of more severe mental illnesses like schizophrenia and bipolar disorder, which can involve mutations of a molecule called DISC1 (Disrupted in Schizophrenia) that normally regulates cAMP. Loss of function of DISC1 in patients with schizophrenia or bipolar disorder would increase vulnerability to cortical network disconnection and profound PFC deficits. This may be especially problematic during exposure to even mild stress, which may explain the frequent worsening of symptoms following stress exposure. "We find it remarkable to relate a genetic mutation in patients to the regulation by an ion channel of PFC neuronal networks," said Arnsten.

Source: Yale School of Medicine

Heart defect may be cause of some forms of migraine headaches

Researchers of the heart and headaches at Thomas Jefferson University Hospital are combining efforts to determine if a common heart defect may be the cause of some forms of migraine headaches.Investigators from the Jefferson Heart Institute and the Jefferson Headache Center are enrolling participant...

Researchers of the heart and headaches at Thomas Jefferson University Hospital are combining efforts to determine if a common heart defect may be the cause of some forms of migraine headaches.

Investigators from the Jefferson Heart Institute and the Jefferson Headache Center are enrolling participants in a blinded study to determine if closing a Patent Foramen Ovale (PFO), a small hole or flap that can allow blood to flow between the right and left sides of the heart, can stop migraines. In newborns, the PFO closes at or shortly after birth, but in 20 percent of adults the gap remains open to some degree.

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More than 28 million Americans suffer from migraine headaches. Debilitating migraine headaches cause major disruption in individual's lives and cost billions of dollars in lost work, school and medical treatment each year. More than one quarter of the people who struggle with migraines have the heart defect.

Most people who have a PFO are never screened for it because doctors rarely suspect it of causing health problems but new evidence suggests that individuals with PFO are more susceptible to migraine. This susceptibility is believed to be due to the passage of material from the right side of the heart to the left side of the heart via the PFO. Blood and material that travels through the PFO is not filtered or oxygenated and in this form may travel to the brain, which can trigger the changes in the blood vessels that underlies migraine.

"Strokes, for example are sometimes triggered when blood clots passing through the PFO travel to the brain," said one of the study's primary investigators, David Fischman, M.D., Co-Director of the Cardiac Catherization Laboratory at Thomas Jefferson University Hospital, and Associate Professor of Medicine, Jefferson Medical College of Thomas Jefferson University.

"Up until now cardiologists have told us that patients with migraine get better when they have their PFO closed for other reasons," said Stephen Silberstein, M.D., director of the Jefferson Headache Center, the study's other primary investigator.

"We need to be able to prove that closure of a PFO by itself will actually diminish migraines," said Dr. Silberstein, Professor of Neurology, Jefferson.

In this study, participants will be randomly assigned to one of two groups. One group will undergo a minimally-invasive procedure to close their PFO. An interventional cardiologist will insert a catheter into the heart and release a device which will form a seal around the PFO to prevent the incorrect blood flow. Typically, the procedure lasts one to two hours under local anesthesia.

The other group will not have their PFO closed but will undergo a procedure that only mimics the closure and will continue medical therapy for their migraines. But none of the participants will know to which group they have been assigned to. However, all participants will receive the same post-operative care and will leave the hospital within 24 hours.

Source: Thomas Jefferson University

New method for detecting cancer very early in its development

Researchers at the Moores Cancer Center at the University of California, San Diego report that they have developed a new method for detecting cancer very early in its development, when it consists of just a few cells. The best existing detection methods are not able to detect a tumor until it consis...

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The paper, published in the April 18 issue of the online journal PLoS ONE, describes a series of proof-of-concept experiments in which the researchers, working with two cancer cell lines, were able to select out and amplify tiny amounts of cancer-causing DNA in the presence of more than 99.9 percent of normal DNA. Current methods for identifying deleted DNA would not work in clinical settings because they require isolation of relatively pure cancer cells. This is not feasible for clinical samples, which typically contain large amounts of the person%26#8217;s normal cells.

%26#8220;We have developed a new technology for very early detection of virtually any type of solid-tumor cancer based upon damaged DNA, which is where all cancers begin,%26#8221; said co-author Dennis A. Carson, M.D., professor of medicine and director of the Moores Cancer Center. %26#8220;We are now working with engineers toward the fabrication of the clinical devices that will enable this to be widely used in patients.%26#8221;

Carson said they are several years away from clinical testing, but ultimately individuals will be able to be screened for DNA markers of cancer cells using simple clinical samples such as blood or urine. Using this same technology, physicians will be able to easily and inexpensively monitor the status of patients by looking for the DNA markers. If the treatment worked, there would be no mutated DNA and the patient would be cured. Such monitoring would also shorten the time needed to determine if the treatment is not working so another approach could be instituted.

The technology, called Primer Approximation Multiplex PCR (PAMP), is based upon an enzyme reaction that only works when a piece of DNA has been deleted or is abnormally joined to another piece of DNA, according to co-author Yu-Tsueng Liu, M.D., Ph.D., assistant project scientist and director of the biomarker laboratory at the Moores Cancer Center. The exact location of the mutation does not matter. The method will detect any mutated DNA in the presence of normal DNA, and amplify only the mutant molecules.

Liu explains: %26#8220;When a cancer cell mutates, it often brings together two pieces of DNA that are normally apart. We have developed an enzyme reaction that works well only when two DNA pieces that are normally separated are close together. This technology amplifies the mutant DNA and then uses a microarray to identify the specific mutation. Our experiments were conducted on a specific gene mutation that is well-known for its role in cancer, called CDKN2A, but this technology would work on any DNA abnormality.%26#8221;

Source: University of California, San Diego

Biotextiles play greater role in medical treatment

If youve ever had a broken armor a paper cutyou probably appreciated the healing role textiles played in your recovery. New types of materials are now being used to treat internal illnesses and injuries, making surgeries less invasive, for example, and delivering drugs with greater efficiency.Dr. Ma...

If you%26#8217;ve ever had a broken arm %26#8211; or a paper cut %26#8211; you probably appreciated the healing role textiles played in your recovery. New types of materials are now being used to treat internal illnesses and injuries, making surgeries less invasive, for example, and delivering drugs with greater efficiency.

Dr. Martin King, professor of biotextiles and textile technology in North Carolina State University%26#8217;s College of Textiles, is playing a leading role in the growing field of biomedical textiles, or biotextiles.

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%26#8220;Many companies that make medical devices have a lot of experience working with materials like plastics, metals and ceramics,%26#8221; says King, who also holds an appointment at Laval University medical school in Quebec City, Canada. %26#8220;Many of them don%26#8217;t have a lot of experience working with textiles, so we have a unique role in assisting with the development of new medical textile products.%26#8221;

Such products include artificial arteries, stents, heart valves, blood filters, spinal column cushions that can be inserted between vertebrae to replace degenerative discs, or heart support devices for people who suffer from congestive heart failure.

%26#8220;The amazing thing about some of these devices is you can deliver them where they%26#8217;re supposed to go in the body by using surgical procedures that are less invasive,%26#8221; King says.

For example, a small incision on the thigh and the insertion of a catheter probe, which can be viewed radiologically, can position a stent in the right place in an artery, rather than having to make long, deep incisions as was common in the past using open surgery.

%26#8220;If you can do this, the patient can walk out of the hospital the next day with a Band-Aid over the incision, rather than spending several days in the hospital recovering,%26#8221; King says. %26#8220;Medical textile devices help reduce trauma, shorten the time of the operation and reduce recovery time for the patient.%26#8221;

King%26#8217;s work on biotextile devices involves testing their lifespan and how compatible the materials will be with the body. The next wave of innovations will involve creating devices that will aid in the healing process through materials that foster cell growth.

%26#8220;In this new paradigm of tissue engineering, we%26#8217;d like the body to form new tissue around these devices so it%26#8217;s not relying solely on synthetic foreign implanted material,%26#8221; King says. %26#8220;Now that we know more about molecular biology and how cells behave and interact with each other, we are beginning to understand how we can create certain markers that will encourage functional cells to migrate and grow on these surfaces.%26#8221;

King and other researchers are already seeing progress in cell growth research, through a partnership with Dr. David Gerber%26#8217;s liver implantation team at the University of North Carolina at Chapel Hill%26#8217;s School of Medicine. One of King%26#8217;s graduate students, Jessica Gluck, has demonstrated that viable and functioning liver cells can be grown on textile scaffolds.

%26#8220;In the future, this approach may allow surgeons like Dr. Gerber to re-establish liver function in patients with liver disease by implanting living and functional liver tissue that has been grown in the laboratory,%26#8221; King says. %26#8220;We are only just beginning to understand how these types of textile scaffolds can support cell growth, and we are just scratching the surface on how textiles may be used in many different internal and external medical applications.%26#8221;

Source: North Carolina State University

Green tea may help protect against autoimmune disease

Green tea may help protect against autoimmune disease, Medical College of Georgia researchers say.Researchers studied an animal model for type I diabetes and primary Sjogren's Syndrome, which damages the glands that produce tears and saliva.They found significantly less salivary gland damage in a gr...

Green tea may help protect against autoimmune disease, Medical College of Georgia researchers say.

Researchers studied an animal model for type I diabetes and primary Sjogren's Syndrome, which damages the glands that produce tears and saliva.

They found significantly less salivary gland damage in a group treated with green tea extract, suggesting a reduction of the Sjogren's symptom commonly referred to as dry mouth. Dry mouth can also be caused by certain drugs, radiation and other diseases.

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Approximately 30 percent of elderly Americans suffer from degrees of dry mouth, says Dr. Stephen Hsu, a researcher in the MCG School of Dentistry and lead investigator on the study. Only 5 percent of the elderly in China, where green tea is widely consumed, suffer from the problem.

"Since it is an autoimmune disease, Sjogren's Syndrome causes the body to attack itself and produce extra antibodies that mistakenly target the salivary and lacrimal glands," he says.

There is no cure or prevention for Sjogren's Syndrome.

Researchers studied the salivary glands of the water-consuming group and a green tea extract-consuming group to look for inflammation and the number of lymphocytes, a type of white blood cells that gather at sites of inflammation to fend off foreign cells.

The group treated with green tea had significantly fewer lymphocytes, Dr. Hsu says. Their blood also showed lower levels of autoantibodies, protein weapons produced when the immune system attacks itself, he says.

Researchers already know that one component of green tea %26#8211; EGCG %26#8211; helps suppress inflammation, according to Dr. Hsu.

"So, we suspected that green tea would suppress the inflammatory response of this disease. Those treated with the green tea extract beginning at three weeks, showed significantly less damage to those glands over time."

These results, published in a recent issue of Autoimmunity, reinforced findings of a 2005 study showing a similar phenomenon in a Petrie dish, Dr. Hsu says.

Researchers also suspect that the EGCG in green tea can turn on the body's defense system against TNF-alpha %26#8211; a group of proteins and molecules involved in systemic inflammation.

TNF-alpha, which is produced by white blood cells, can reach out to target and kill cells.

"The salivary gland cells treated with EGCG had much fewer signs of cell death caused by TNF-alpha," Dr. Hsu says. "We don't yet know exactly how EGCG makes that happen. That will require further study. In some ways, this study gives us more questions than answers."

Further study could help determine green tea's protective role in other autoimmune diseases, including lupus, psoriasis, scleroderma and rheumatoid arthritis, he says.

Source: Medical College of Georgia

Genetically inactivating a protein can protect nerve fibers in a mouse model of multiple sclerosis

Oregon Health & Science University neuroscientists are eyeing a protein as a potential therapeutic target for multiple sclerosis because de-activating it protects nerve fibers from damage.OHSU researchers, working with colleagues at the Portland Veterans Affairs Medical Center and the University of ...

Oregon Health %26amp; Science University neuroscientists are eyeing a protein as a potential therapeutic target for multiple sclerosis because de-activating it protects nerve fibers from damage.

OHSU researchers, working with colleagues at the Portland Veterans Affairs Medical Center and the University of Padova in Italy, have shown that genetically inactivating a protein called cyclophilin D can protect nerve fibers in a mouse model of multiple sclerosis. Cyclophin D is a key regulator of molecular processes in the nerve cell's powerhouse, the mitochondrion, and can participate in nerve fiber death. Inactivating cyclophilin D strengthens the mitochondrion, helping to protect nerve fibers from injury. The findings are published today in Proceedings of the National Academy of Sciences.

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"We're extremely excited," said Michael Forte, Ph.D., senior scientist at the Vollum Institute at OHSU and the study's lead author. "While we can't genetically inactivate cyclophilin D in people, there are drugs out there that can block the protein. Our research predicts that drugs that block cyclophilin D should protect nerve fibers from damage in MS."

Such a drug would be the first therapy specifically for secondary-progressive MS, one of the more debilitating forms of MS involving an initial period of relapsing and remitting, followed by a steady worsening of symptoms. It affects half of the estimated 2 million people with MS.

The only available therapies for MS are anti-inflammatory drugs, which reduce the inflammation believed to spur certain T-cells in the body to attack myelin, the fatty sheath insulating nerve fibers in the brain and spinal cord. The fibers can't conduct impulses, leading to paralysis, memory loss, dizziness, fatigue, pain and imbalance. Over time, the nerve fibers themselves degenerate, leading to permanent functional deficits.

"All MS drugs available right now are anti-inflammatory," said study co-author Dennis Bourdette, M.D., professor and chairman of neurology in the OHSU School of Medicine, and director of the OHSU MS Center of Oregon. "What is desperately needed is a therapeutic that protects the nerve fibers from degeneration."

In recent years, scientists have increasingly viewed MS as a neurodegenerative disorder rather than simply an inflammatory one. Loss of nerve cells, injury to nerve fibers and atrophy within the central nervous system occur progressively from the start of the disease, eventually leading to permanent disability, especially in patients who've had MS for many years.

"What puts people in wheelchairs from MS is not an inflammatory attack on myelin of the central nervous system. It's the severing of the axons (nerve fibers), which is a permanent thing," Forte said.

Inflammation triggers a chain of molecular events that leads to progressive nerve fiber deterioration in MS, including the development of free radicals such as reactive oxygen and nitrogen that slow the cell's energy generation capability. It also throws off mitochondrial function by causing calcium to build up in the cell, reducing levels of ATP that serves as the cell's fuel source.

But scientists believe that cyclophilin D is responsible for causing the unregulated opening of a pore in the mitochondrion's membrane that allows the calcium overload. The OHSU team showed that mice lacking cyclophilin D still developed an MS-like disease, but unlike their counterparts possessing the protein, the mutant mice partially recovered. Scientists found their nerve fibers remained intact, and they resisted the free radicals and calcium overload.

"What we've done is make it so the mitochondria can tolerate higher loads of calcium before they die," Forte said. "The mutant mice are protected from axonal damage associated with this MS-like disease in mice."

The scientists are now testing drugs that could be used to shut down the cyclophilin D protein and the mitochondrion pore it activates. "If you basically inhibited that protein with a drug, you would see the same axonal preservation that you saw in the mutant mouse," Forte said.

One class of compounds Forte and Bourdette are particularly interested in is non-immunosuppressive derivative of cyclosporin A (CsA). Some nonimmunsuppressive derivatives of cyclosporin A are in human trials for other conditions. Because these drugs are already being tested in humans, they could be rapidly tested in MS. Bourdette believes that a cyclophilin D antagonist could potentially become available as a treatment for MS within five years.

"We don't have to invent the drugs to target this protein. They already exist," Bourdette said.

Such a therapy can't come soon enough for 36-year-old West Linn, Ore. resident Laura Wieden, who has suffered since 1995 from relapsing-remitting MS that's caused weakness in both legs and forced her to ride a Segway personal transportation device or a wheelchair. "For me, it's fabulous," she said. "If you can prevent MS, that's great, but what about the millions of people who have it? They need something that keeps the cells from dying. This just holds so much promise."

Wieden's father, Dan Wieden, co-founder of Portland-based Wieden + Kennedy advertising agency, set up a fund in his daughter's name %26#8211; the Laura Fund for Innovation in Multiple Sclerosis Research %26#8211; to support MS research that pushes traditional boundaries to discovery. The discovery by Forte, Bourdette and their team, which was funded in part by the foundation, fits the bill, he said.

"It goes to prove that sometimes the big breakthroughs do not come from the more traditional lines of inquiry," he said. "What I appreciate about our relationship with OHSU is that there seems to be a sense of urgency about these projects. And it's been beneficial for us to develop a more personal relationship with the researchers. That way it becomes not just an academic exercise, but a very passionate inquiry on their part."

Source: Oregon Health %26amp; Science University

Naturally occurring compound found in fruits, vegetables, and red wine selectively kills leukemia cells

A naturally occurring compound found in many fruits and vegetables as well as red wine, selectively kills leukemia cells in culture while showing no discernible toxicity against healthy cells, according to a study by researchers at the University of Pittsburgh School of Medicine. These findings, which were published online March 20 in the Journal of Biological Chemistry and will be in press on May 4, offer hope for a more selective, less toxic therapy for leukemia.

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%26#8220;Current treatments for leukemia, such as chemotherapy and radiation, often damage healthy cells and tissues and can produce unwanted side effects for many years afterward. So, there is an intensive search for more targeted therapies for leukemia worldwide,%26#8221; said corresponding author Xiao-Ming Yin, M.D., Ph.D., associate professor of pathology, University of Pittsburgh School of Medicine.

Leukemia is not a single disease but a number of related cancers that start in the blood-forming cells of the bone marrow. Meaning literally %26#8220;white blood%26#8221; in Greek, leukemia occurs when there is an excess of abnormal white blood cells. There are both acute and chronic forms of leukemia, each with many subtypes that vary in their response to treatment. According to the National Cancer Institute, about 44,000 new leukemia cases will be diagnosed in the United States in 2007, and there will be about 22,000 leukemia-related deaths.

Based on previous reports that anthocyanidins, a group of naturally occurring compounds widely available in fruits and vegetables as well as red wine, have chemopreventive properties, Dr. Yin and his collaborators studied the effects and the mechanisms of the most common type of a naturally modified anthocyanidin, known as cyanidin-3-rutinoside, or C-3-R, which was extracted and purified from black raspberries, in several leukemia and lymphoma cell lines.

They found that C-3-R caused about 50 percent of a human leukemia cell line known as HL-60 to undergo programmed cell death, or apoptosis, within about 18 hours of treatment at low doses. When they more than doubled the concentration of C-3-R, virtually all of the leukemia cells became apoptotic and died. C-3-R also induced apoptosis in other human leukemia and lymphoma cell lines.

When the investigators studied the mechanism of cell death in the leukemia cells, they found that C-3-R induced the accumulation of peroxides, a highly reactive form of oxygen, which, in turn, activated a mitochondria-mediated apoptotic pathway. Mitochondria are specialized structures located within all cells in the body that contain enzymes needed by the cell to metabolize foodstuffs into energy sources. In contrast, when the researchers treated normal human blood cells with C-3-R, they did not find any increased accumulation of reactive oxygen species and there were no apparent toxic effects on these cells.

Previous studies have shown that C-3-R possesses strong antioxidant activities, a characteristic shared by other polyphenols, such as those found in green tea, which could be responsible for their chemoprevention effects. Dr. Yin%26#8217;s work suggests that although C-3-R demonstrates antioxidant effects in the normal cells, it paradoxically induces an oxidative %26#8220;stress%26#8221; in the tumor cells. It is possible that this differential effect of C-3-R may account for its selective toxicity in the tumor cells.

According to Dr. Yin, these results indicate that C-3-R has the promising potential to be used in leukemia therapy with the advantages of being highly selective against cancer cells. %26#8220;Because this compound is widely available in foods, it is very likely that it is not toxic even in purified form. Therefore, if we can reproduce these anti-cancer effects in animal studies, this will present a very promising approach for treating a variety of human leukemias and, perhaps, lymphomas as well.%26#8221;

Source: University of Pittsburgh Schools of the Health Sciences

Chronic depression may cause diabetes in older adults

Chronic depression or depression that worsens over time may cause diabetes in older adults, according to new Northwestern University research.This is the first national study to suggest that depression alone -- and not lifestyle factors like being overweight can trigger Type 2 diabetes in adults 65 ...

Chronic depression or depression that worsens over time may cause diabetes in older adults, according to new Northwestern University research.

This is the first national study to suggest that depression alone -- and not lifestyle factors like being overweight %26#8211;can trigger Type 2 diabetes in adults 65 and older, a population with a high prevalence of diabetes and depression. The report will be published April 23 in Archives of Internal Medicine.

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The study examined 4,681 men and women 65 and older from Forsyth County, N.C.; Sacramento County, Calif.; Washington County, Md.; and Pittsburgh, Pa., annually for 10 years.

"This means doctors need to take depressive symptoms in older adults very seriously because of the effect it has on the likelihood of developing diabetes," said Mercedes Carnethon, lead author of the study and assistant professor of preventive medicine at Northwestern%26#8217;s Feinberg School of Medicine.

An estimated 2 million older adults suffer from clinical depression, the second highest incidence of any age group. People 65 and older also have the highest prevalence of Type 2 diabetes.

"Diabetes is a scourge," said Carnethon. "It causes heart disease, blindness, kidney disease, leg amputations and lowered cognitive function because it essentially degrades the small and large blood vessels."

The study differed from prior research in several ways. It is the first to examine the connection between increasing symptoms of depression over time and the incidence of diabetes.

Previous studies linking diabetes to depression have been based on a one-time measure of depressive symptoms. A single measure could be based on an episode or event that has caused a person to feel blue for a limited amount of time.

Carnethon's study measured depressive symptoms at a single point in time as well as depressive symptoms over time. This approach paints a more accurate depiction of depressive symptoms. By measuring depressive symptoms before diabetes developed, she and colleagues were better able to investigate the causal effect between mood and diabetes.

The Northwestern study also factored out other known lifestyle causes of diabetes such as being overweight or getting little physical exercise.

"We know that overweight and obesity are the primary risk factors for diabetes and most people with Type 2 diabetes are overweight or obese," Carnethon said. "But even after we adjusted for [statistically accounted for] body mass index (measure of height versus weight), we still saw a residual association between depression and diabetes."

In addition, the study considered a key biological factor %26#8211; a high level of inflammation common in depressed people -- that might have explained the link between depression and diabetes. Inflammation is estimated by the levels of an inflammatory protein in the blood called C-reactive protein. But even after accounting for levels of the protein, depressive symptoms were still associated with the development of diabetes.

Carnethon theorizes that the culprit responsible for diabetes in persons who are depressed is a high level of a stress hormone, cortisol. High levels of cortisol may decrease insulin sensitivity and increase fat deposits around the waist (a risk factor for diabetes). While her study was limited to older adults, she believes high cortisol levels in depressed younger adults may also put them at risk for diabetes.

Insulin enables glucose (sugar) to enter the body%26#8217;s cells to be used as fuel. When people are under acute stress or are depressed, the cells in the pancreas are suppressed and secrete less insulin to enable the body to sweep glucose out of the bloodstream. Compounding the problem, high cortisol levels decrease the muscles%26#8217; sensitivity to insulin, which also could result in elevated glucose levels, Carnethon said.

"When you%26#8217;re depressed or under stress your body is trying to keep glucose in the bloodstream because it needs it for immediate energy," Carnethon noted. "So, it%26#8217;s blocking insulin action. And you may even be producing more glucose because your body thinks it needs the sugar."

Carnethon said the study shows the importance of screening older adults for depressive symptoms. "It%26#8217;s not a normal condition for older adults to be depressed," she said. "I think a lot of people say, %26#8216;Oh, they%26#8217;re old, they should be depressed. What does it matter if they%26#8217;re a little bit down?%26#8217; Well, it does matter and you should treat it aggressively because it has effects on health beyond that of mood."

Source: Northwestern University

Junk DNA may be not be "junk" afterall

Large swaths of garbled human DNA once dismissed as junk appear to contain some valuable sections, according to a new study by researchers at the Stanford University School of Medicine and the University of California-Santa Cruz. The scientists propose that this redeemed DNA plays a role in controll...

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Gill Bejerano, PhD, assistant professor of developmental biology and of computer science at Stanford, found more than 10,000 nearly identical genetic snippets dotting the human chromosomes. Many of those snippets were located in gene-free chromosomal expanses once described by geneticists as "gene deserts." These sections are, in fact, so clogged with useful DNA bits - including the ones Bejerano and his colleagues describe - that they've been renamed "regulatory jungles."

"It's funny how quickly the field is now evolving," Bejerano said. His work picking out these snippets and describing why they might exist will be published in the April 23 advance online issue of the Proceedings of the National Academy of Sciences.

It turns out that most of the segments described in the research paper cluster near genes that play a carefully orchestrated role during an animal's first few weeks after conception. Bejerano and his colleagues think that these sequences help in the intricate choreography of when and where those genes flip on as the animal lays out its body plan. In particular, the group found the sequences to be especially abundant near genes that help cells stick together. These genes play a crucial role early in an animal's life, helping cells migrate to the correct location or form into organs and tissues of the correct shape.

The 10,402 sequences studied by Bejerano, along with David Haussler, PhD, professor of biomolecular engineering at UC-Santa Cruz, are remnants of unusual DNA pieces called transposons that duplicate themselves and hop around the genome. "We used to think they were mostly messing things up. Here is a case where they are actually useful," Bejerano said.

He suspects that when a transposon is plopped down in a region where it wasn't needed, it slowly accumulated mutations until it no longer resembled its original sequence. The genome is littered with these decaying transposons. When a transposon dropped into a location where it was useful, however, it held on to much of the original sequence, making it possible for Bejerano to pick out.

In past work, Bejerano and his co-workers had identified a handful of transposons that seemed to regulate nearby genes. However, it wasn't clear how common the phenomenon might be. "Now we've shown that transposons may be a major vehicle for evolutionary novelty," he said.

The paper's first author, Craig Lowe, a graduate student in Haussler's lab at UC-Santa Cruz, said finding the transposons was just the first step. "Now we are trying to nail down exactly what the elements are doing," he said.

Bejerano's work wouldn't have been possible without two things that became available over the past few years: the complete gene sequence of many vertebrate species, and fast computers running sophisticated new genetic analysis software. "Right now it's like being a kid in a candy warehouse," Bejerano said. Computer-savvy biologists have the tools to ask questions about how genes and chromosomes evolve and change, questions that just a few years ago were unanswerable.

Bejerano and his colleagues aren't the first to suggest that transposons play a role in regulating nearby genes. In fact, Nobel laureate Barbara McClintock, PhD, who first discovered transposons, proposed in 1956 that they could help determine the timing for when nearby genes turn on and off.

Source: Stanford University Medical Center

Risk of developing Parkinson’s disease may be reduced with exercise

The risk of developing Parkinsons disease may be reduced with moderate to vigorous exercise or other recreational activities, according to research that will be presented at the American Academy of Neurologys 59th Annual Meeting in Boston, April 28May 5, 2007.The study followed more than 143,000 peo...

The risk of developing Parkinson%26#8217;s disease may be reduced with moderate to vigorous exercise or other recreational activities, according to research that will be presented at the American Academy of Neurology%26#8217;s 59th Annual Meeting in Boston, April 28 %26#8211; May 5, 2007.

The study followed more than 143,000 people with an average age of 63 over 10 years. In that time, 413 people developed Parkinson%26#8217;s disease. Researchers found that those with moderate to vigorous activity levels were 40 percent less likely to develop Parkinson%26#8217;s disease than those with no or light activity levels. Those with moderate to vigorous activity were exercising an average of a half hour per day or more.

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"This study does not prove that exercise caused the lowered risk of Parkinson%26#8217;s disease %26#8211; it%26#8217;s possible that something else lowers the risk," said the study%26#8217;s lead author Evan L. Thacker, SM, from the Harvard School of Public Health in Boston, MA. "But considering all of the other benefits of exercise, it certainly doesn%26#8217;t hurt to make sure you get some moderate or vigorous exercise several times a week."

The researchers also looked at the participants%26#8217; activity level at age 40 and found that there was no significant relationship between the level of physical activity at age 40 and the risk of developing Parkinson%26#8217;s disease.

"If exercise truly does provide some protection against Parkinson%26#8217;s disease, the protection may be relatively short term," Thacker said. "However, in a previous study with a similar prospective design activity in early adulthood was related to lower risk for Parkinson%26#8217;s disease, so the jury%26#8217;s still out on this one."

Source: American Academy of Neurology

First step toward major revolution in human regenerative medicine

Findings described in a new study by Stanford scientists may be the first step toward a major revolution in human regenerative medicinea future where advanced organ damage can be repaired by the body itself. In the May 2007 issue of The FASEB Journal, researchers show that a human evolutionary ances...

Findings described in a new study by Stanford scientists may be the first step toward a major revolution in human regenerative medicine%26#8212;a future where advanced organ damage can be repaired by the body itself. In the May 2007 issue of The FASEB Journal, researchers show that a human evolutionary ancestor, the sea squirt, can correct abnormalities over a series of generations, suggesting that a similar regenerative process might be possible in people.

"We hope the mechanisms underlying this phenomenon will ultimately lead to new insights regarding the potential of cells and tissues to be reprogrammed and regenerate compromised organs in humans," said Ayelet Voskoboynik, Ph.D., of Stanford University and first author of the study.

[More:]

Missing limbs, scarred hearts, broken spines, and wounded muscles always try to repair themselves, but often the result is invalidism or disease. Even some tumors try to revert to normal, but are unsuccessful. If the genetic sequence described in the sea squirt applies to humans, this study represents a major step for regenerative medicine.

The sea squirt is more closely related to humans than many would expect. It may appear similar to a sea sponge, worm, or plant, but it is actually not closely related to any of these organisms. Sea squirt larvae have primitive spinal cords, distinguishing them in the greater chain of life and on the evolutionary ladder. Specifically, sea squirts, like humans, belong to a group of animals called chordates (organisms with some level of spinal cord development), and many scientists believe that sea squirts approximate what the very first human chordate ancestor may have been like 550 million years ago. By studying this modern day representative of our evolutionary ancestor, researchers are able to identify fundamental principles of complex processes, such as healing and organ regeneration, on which new treatments are based.

"The aim of biomedical science is to understand life so we can defend our bodies against injury, deformity, and disease. The ultimate medical treatment would be to change an abnormal organ or tissue back to its vibrant, normal state," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This study is a landmark in regenerative medicine; the Stanford group has accomplished the biological equivalent of turning a sow%26#8217;s ear into a silk purse and back again."

Source: Federation of American Societies for Experimental Biology

3D ultrasound

Parents-to-be might soon don 3-D glasses in the ultrasound lab to see their developing fetuses in the womb "in living 3-D, just like at the IMAX movies," according to researchers at Duke University's Pratt School of Engineering.The same Duke team that first developed real-time, three-dimensional ult...

The same Duke team that first developed real-time, three-dimensional ultrasound imaging says it has now modified the commercial version of the scanner to produce an even more realistic perception of depth. Paired images seem to pop out of the screen when viewed with the special glasses.

[More:]

The researchers created an updated version of the image-viewing software found on clinical ultrasound scanners, making it possible to achieve a stereo display with no additional hardware.

"To our knowledge, this is the first time it's been made possible to display real-time stereo image pairs on a clinical scanner," said Stephen Smith, a professor of biomedical engineering at Duke. "We believe all 3-D scanners could be modified in this way with only minor software changes."

The new imaging capability can improve the early diagnosis of certain kinds of birth defects of the face and skull and improve surgeons' depth perception during ultrasound-guided medical procedures, including tumor biopsies and robot-assisted surgeries done through tiny "keyhole" incisions.

The Duke team, which also includes Joanna Noble, an undergraduate student, and Matthew Fronheiser, a graduate student in Smith's laboratory, reported the findings in an issue of the journal Ultrasonic Imaging dated July 2006, but published in April 2007. The research was supported by the National Institutes of Health.

Human depth perception is largely the result of stereo vision -- the slightly different perspectives of the same scene that are observed by the left and right eyes, Smith said. The brain processes the information to produce a sense of depth, a phenomenon that can't be achieved when viewing a single, flat image.

Stereoscopic images solve that problem by taking two "snapshots" of the same object from slightly different angles, mimicking the normal difference between left and right eye views.

Special glasses or goggles can then be used to fuse the two images into one, gaining a 3-D effect. This principle lies behind 3-D movies and the familiar Fisher Price View-Master toy. With practice, some people can "defocus" their eyes and fuse the paired images without the aid of any special viewing device. (Find out how at http://en.wikipedia.org/wiki/Stereoscopy.)

To demonstrate the new capability, the researchers first generated stereo ultrasound images of a small metal cage. They then advanced to ultrasound images in living animals of a heart valve and blood vessels and needle biopsies of the animals' brains and esophagi.

The researchers have since recorded ultrasound images of a model human fetus that is traditionally used in the testing of fetal ultrasound imaging devices. (Watch the video, including paired images of both the cage and model fetus, at http://youtube.com/watch?v=4VSRlH01mzg. See if you can fuse them without goggles.)

"Thousands of 3-D ultrasound systems in clinics could be upgraded with such new software, and stereoscopic goggles could be issued to them as well," Smith said. "Keepsake DVDs of the fetal exam could also be viewed at home in 3-D stereo."

The goggles would soon become obsolete, he added. New monitors capable of fusing stereo 3-D images without them are now in development.

Source: Duke University

Corn, oats, cherries and red wine’s high melatonin content can help delay ageing

A study carried out by researchers from the University of Granadas Institute of Biotechnology proves that consuming melatonin neutralizes oxidative damage and delays the neurodegenerative process of ageing.
- In this study researchers used normal and genetically-modified mice which were subjected to...

A study carried out by researchers from the University of Granada%26#8217;s Institute of Biotechnology proves that consuming melatonin neutralizes oxidative damage and delays the neurodegenerative process of ageing.

- In this study researchers used normal and genetically-modified mice which were subjected to accelerated cell ageing, although their results can also be applied to humans.

[More:]

The Spanish Ageing Research Network (Red Nacional de Investigaci%26#243;n del Envejecimiento), funded by Carlos III Health Institute and headed by professor Dar%26#237;o Acu%26#241;a Castroviejo, from the University of Granada (Universidad de Granada), is very near to achieving one of today%26#8217;s Science greatest goals: allowing humans to age in the best possible health conditions.

As well as from the UGR, researchers from the Spanish universities of Seville, Oviedo, Saragossa, Barcelona and Reus also took part in this study, concluding that the consumption of melatonin %26#8211; a natural substance produced in small amounts by human beings and present in many types of food %26#8211; delays the oxidative damage and inflammatory processes typical of the old age. Melatonin can be found in small amounts in some fruits and vegetables, like onions, cherries and bananas, and in cereals like corn, oats and rice, as well as in some aromatic plants, such as mint, lemon verbena, sage or thyme, and in red wine.

UGR participation in this study was leaded by professor Dar%26#237;o Acu%26#241;a Castroviejo, member of the Institute of Biotechnology and lecturer at this University%26#8217;s department of Physiology. Professor Acu%26#241;a Castroviejo also coordinates the Spanish Ageing Research Network. Both normal and genetically-modified mice, with an accelerated cell ageing, were analysed. "We proved", says professor Acu%26#241;a Castroviejo, %26#8220;that the first signs of ageing in animal tissues start at the age of five months [in mice] %26#8211; equivalent to 30 human years of age %26#8211; due to an increase in free radicals (oxygen and nitrogen), which cause an inflammatory reaction.%26#8221;

The UGR researcher points out that such oxidative stress also has effects in animals%26#8217; blood, as blood cells have been proven to be %26#8220;more fragile with the years and, therefore, their cell membranes become easier to break".

Use in mice

The authors of this innovative finding administered small amounts of melatonin to mice and observed that not only did this substance neutralize the oxidative stress and the inflammatory process caused by ageing, but it also delayed its effects, thus increasing longevity. In particular, the University of Granada%26#8217;s goal was to analyse the mitochondrial function in mice and check their mitochondrial capacity to produce ATP %26#8211; adenosine triphosphate %26#8211; a molecule whose mission is to store the energy every cell needs to carry out its functions.

Professor Acu%26#241;a Castroviejo highlights that chronic administration of melatonin in animals from the moment they stop producing this substance %26#8211; five months of age in mice %26#8211; helps counteract all age-related processes. Therefore, daily melatonin intake in humans from the age of 30 or 40 could prevent %26#8211; or, at least, delay %26#8211; illnesses related to ageing, free radicals and inflammatory processes, such as many neurodegenerative disorders (e.g. Parkinson's disease) and complications linked to other illnesses, like diabetes.

The researcher is confident that the Spanish Ministry of Health will soon legalise the use of melatonin since, being a substance naturally produced by the body, it cannot be patented and the drug industry would not make much profit out of its artificial production. However, %26#8220;while the substance becomes legalised, humans should try to increase melatonin consumption through food", recommends professor Acu%26#241;a Castroviejo.

Source: Universidad de Granada

How your food is cooked may be as important to your health as the food itself - Grilled, fried, broiled meat linked to disease

How your food is cooked may be as important to your health as the food itself. Researchers now know more about a new class of toxins that might soon become as important a risk factor for heart disease and metabolic disorders as trans fats.This class of toxins, called advanced glycation end products ...

This class of toxins, called advanced glycation end products (AGEs), are absorbed into the body through the consumption of grilled, fried, or broiled animal products, such as meats and cheeses. AGEs, which are also produced when food products are sterilized and pasteurized, have been linked to inflammation, insulin resistance, diabetes, vascular and kidney disease, and Alzheimer%26#8217;s disease.

[More:]

A new study at Mount Sinai School of Medicine reveals that AGE levels are elevated in the blood of healthy people, and even more so in older individuals than in younger people. Of particular interest was the finding that a major determinant of the blood levels of AGEs is the amount of AGEs in the diet, not dietary calories, sugar, or fat. The study, which was done in collaboration with, and supported by, the National Institute on Aging (NIA), is published in the April issue of the Journal of Gerontology: Medical Sciences.

"AGEs are quite deceptive, since they also give our food desirable tastes and smells," says Helen Vlassara, MD, senior study author, Director of the Division of Experimental Diabetes and Aging, and Professor of Medicine and Geriatrics at Mount Sinai School of Medicine. "So, consuming high amounts of grilled, broiled, or fried food means consuming significant amounts of AGEs, and AGEs in excess are toxic. People should be given information about their AGE intake and be advised to consider their intake in the same way they would think about their trans fats and salt intake. They should be warned about their AGE levels the way they are about their cholesterol levels or cigarette smoking."

Inflammation and oxidative stress are more common in older age, so the goal of the study was to assess whether AGEs played a significant role in age-related inflammation and oxidative stress by measuring AGE levels in both young and older individuals. The study involved 172 healthy men and women who were divided into two age groups%26#8212;those between the ages of 18 and 45 and those between the ages of 60 and 80. Dr. Vlassara and her team also wanted to assess whether AGE levels correlated with dietary intake. To do this, her team recorded the patient%26#8217;s body weight, body fat, three-day dietary information, and collected blood samples to measure biomarkers of inflammation, such as C-reactive protein (CRP). Blood samples were used to test for two common AGEs, called carboxymethyllysine (CML) and methylglyoxal (MG), which latch on to proteins and fats.

The blood tests showed that AGE levels were 35 percent higher in individuals age 65 and older compared with those younger than age 45. The study also showed that in all of the participants, the higher the consumption of foods rich in AGEs, the higher the blood levels of AGEs, and higher the levels of CRP and other markers of inflammation.

Much to the researchers%26#8217; surprise, the study also showed that AGE levels could be very high in young healthy people. In fact, high AGE levels found in some healthy adults in this study were on par with AGE levels observed in diabetic patients in their earlier studies. The fact that healthy adults had levels similar to those seen in diabetic patients may suggest that early and prolonged exposure to these substances in the diet could accelerate the onset of diseases. Dr. Vlassara notes that the availability and consumption of AGE-rich foods is high and correlates with rising rates of diabetes and heart disease.

"Excessive intake of fried, broiled, and grilled foods can overload the body%26#8217;s natural capacity to remove AGEs," Dr. Vlassara notes, "so they accumulate in our tissues, and take over the body%26#8217;s own built-in defenses, pushing them toward a state of inflammation. Over time, this can precipitate disease or early aging." Once AGEs enter the body, it becomes more difficult to get them out, especially as people age. Older people have a reduced capacity for removing AGEs from the body, the researchers explain, most likely because kidney function slows down as the body ages.

As Dr. Vlassara cautions, "although the accumulation of AGEs pose an immediate and significant health threat to the older adult population, they are also an invisible, lingering danger especially for younger people and this needs to be addressed. AGE levels should be shown on nutrition labels so everyone is aware of them when buying or preparing meals %26#8211; and our studies explain why."

A Simple Solution: Steam, Boil, Stew Despite the ubiquity of AGEs, Dr. Vlassara and her team offer simple, safe, and economic solutions that echo the recommendations given concerning trans fats%26#8212;watch what you eat. New methods of cooking to reduce AGE intake, particularly steaming, boiling or making stews, can make a difference. "Keeping the heat down and maintaining the water content in food reduces AGE levels," Dr. Vlassara says. A 50 percent reduction in AGE intake could have a significant and positive impact on overall health and may even help extend one%26#8217;s lifespan, according to Dr. Vlassara. In other studies, the team has found that cutting AGE intake in half, but maintaining a diet comprised of the same calories and fat, increased the lifespan of animals when compared with animals fed their usual diet.

At the moment, changing one%26#8217;s approaches to cooking is the only defense against excessive AGE consumption. There is no routine clinical test to inform individuals of their blood or dietary AGE levels nor established treatment to reduce high AGE blood levels. "The concept that food-related AGE intake is harmful is new to the general public," says Dr. Vlassara, "and scientists are now seeing how AGE intake fits with the current trends of disease epidemics. Hopefully, these wake-up signals, together with other gathering evidence at the cellular and molecular level, will accelerate our efforts to develop effective measures against excessive dietary AGEs. This issue, however, should be dealt with as an important health hazard now, rather than later."

Source: Mount Sinai School of Medicine

Shawn's Health Blog

1/24/2009

Scientists learning more about cancer-initiating properties of stem cells

Omega-3 fatty acid may slow growth of two brain lesions in Alzheimer’s disease

Robotic "caterpillar" crawls around heart to deliver treatment without surgery

Studying how antioxidants and herbal supplements can be useful in promotion of health and prevention of chronic diseases

Deep brain stimulation successfully treats depression

Treating strawberries with alcohol makes them healthier

Cutting back on salt reduces chances of heart disease by 25 percent

Miscue of body’s genetic repair system may cause Huntington’s disease

Muscle function restored in Duchenne's muscular dystrophy

First evidence of a molecular mechanism that dynamically alters the strength of higher brain network connections

Heart defect may be cause of some forms of migraine headaches

New method for detecting cancer very early in its development

Biotextiles play greater role in medical treatment

Green tea may help protect against autoimmune disease

Genetically inactivating a protein can protect nerve fibers in a mouse model of multiple sclerosis

Naturally occurring compound found in fruits, vegetables, and red wine selectively kills leukemia cells

Chronic depression may cause diabetes in older adults

Junk DNA may be not be "junk" afterall

Risk of developing Parkinson’s disease may be reduced with exercise

First step toward major revolution in human regenerative medicine

3D ultrasound

Corn, oats, cherries and red wine’s high melatonin content can help delay ageing

How your food is cooked may be as important to your health as the food itself - Grilled, fried, broiled meat linked to disease

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