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Scientists Identify DNA Alterations As Among Earliest To Occur In Lung Cancer Development

Nov 2, 2015

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Lungs Cancer

In a report published recently in Nature Communications, researchers from John Hopkins have revealed that they have discovered what they believe to be among the very earliest premalignant genetic changes that mark the potential onset of the deadly lung cancer.

The team of scientists was working with tissue, blood and DNA from six people with precancerous and cancerous lung lesions. The DNA alterations they have uncovered were in premalignant lung lesions known as atypical adenomatous hyperplasia, or AAH. These alterations took place long before the lesions would become malignant and invade surrounding tissue and fulfill the definition of adenocarcinoma of the lung.

Mariana Brait, Ph.D., a member of the research team, an assistant professor of otolaryngology-head and neck surgery at the Johns Hopkins University School of Medicine said that they believe that what they have detected for the first time is the DNA circulating in the blood from precancerous lesions of the lung. This discovery could give a chance to find people at risk of lung cancer early. Their analysis also revealed that different regions of the same lesion had various mutations distinctly associated with good and poor outcomes, and that in patients for whom blood samples were available, circulating DNA evidence of the mutations showed up clearly.

David Sidransky, M.D., professor of oncology and pathology at the Johns Hopkins University School of Medicine and the director of head and neck cancer research at Johns Hopkins opined that this study takes detection to a whole new level. Sidransky cautions that even though the findings are preliminary and involved only a few patients, it shows promise about how DNA testing might be used to detect precancerous changes at their earliest stages.

Statistics from the American Lung Association reveal that adenocarcinomas are the most frequent subtype of lung cancer and are typically diagnosed after they have spread. Even with the most advanced chemotherapy, surgery and other treatments, average five-year survival rate for people with adenocarcinoma is merely 15 percent. It is believed by experts that adenocarcinomas of the lung develop from microscopic lesions that accumulate multiple genetic alterations over time that then lead to malignancy.

Evgeny Izumchenko, Ph.D., a postdoctoral fellow in Sidransky’s laboratory and the lead author of the study said that in many cases the precancerous lesions regress and disappear after a few years, but some will progress to cancer. To find out which factors make the lesions turn into cancer, the team studied tissue samples from six patients undergoing surgical removal of lung tumors. Then William Westra, M.D., professor of pathology, went through the tissue samples to single out tiny precancerous AAH lesions in the lung tissue for study. The scientists then extracted and sequenced DNA from these AAH lesions, as well as from other adenocarcinomas in situ, minimally invasive adenocarcinomas and fully invasive adenocarcinomas�an array of lesions that represent the progression from AAH to fully invasive adenocarcinoma.

Using a DNA sequencing technique they next looked for mutations in 125 genes known to play a significant role in cancer development and advancement. When the DNA of the premalignant lesions was compared with DNA isolated from primary invasive cancer within each patient, the sequencing showed that in three of the patients, the same mutations were shared between the premalignant lesions and the tumor from the same patient. Izumchenko opined that it suggests that these mutations could be the drivers of tumor progression.

Their study also revealed that lung cancer can be initiated by disturbances in different molecular pathways since they found that different AAH lesions from different patients had unique patterns of mutations. Also, it was found that there could be differences even within the same lesion. Further findings also suggest that a blood or sputum test could better represent the overall composition of a tumor than a single biopsy sample. The results of the study are promising � further studies are planned involving more lung cancer patients to confirm the findings.

References

https://medicalxpress.com/news/2015-09-scientists-dna-earliest-lung-cancer.html

https://www.hopkinsmedicine.org/news/media/releases/scientists_identify_dna_alterations_as_among_earliest_to_occur_in_lung_cancer_development_

Maternal Protein Deficiency during Pregnancy Memorized By Fetal Muscle Cells

Nov 1, 2015

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A new study by the researchers at the University of Illinois published in the British Journal of Nutrition, has discovered the genetic processes that show the link between insufficient protein intake during pregnancy with the development of muscle problems in mothers and their male offspring. The study also reveals the metabolic pathway through which these genetic changes are transferred to the fetus, thereby triggering the development of chronic health problems in adulthood such as obesity, cardiovascular disease, and Type 2 diabetes.

The study has a huge significance said Huan Wang, the principal investigator on the study. During the course of pregnancy, women must consume an additional 25 grams of protein every day If insufficiency of protein intake is detected during the early stages of pregnancy, the consequences can be averted by treating it through dietary changes or other strategies,. It can significantly avert many serious health conditions in the next generation.

Wang carried out her study in rats, but evidences from prior research show that the implications are similar for humans. During the study, Wang found that inadequate protein intake during pregnancy activates the amino acid response (AAR) pathway, triggering cell destruction – a process called autophagy or atrophy, which simply means wasting, of the mother’s skeletal muscles.

Under stress conditions, cell resorts to autophagy – a survival mechanism whereby cells degrade unnecessary or dysfunctional components to maintain homeostasis in the body. These genetic changes get transferred through the placenta and are “memorized” in the skeletal muscles of the fetus, which can result in low birth weight and stunted growth in male offspring.

Wang conducted the research while completing her doctorate in food science and human nutrition at Illinois. She says that it is the link that scientists have been seeking for years, which shows transduction from the mom through the placenta to the child. She points out that it should be noted that there is a gender specificity as the cell autophagy is activated in the skeletal muscles of the male offspring only. It seems the female offspring have more resistance to low-protein exposure during gestation and to cell autophagy.

For this study, Wang experimented on 2 groups of pregnant rats � one group consumed food that contained 8 or 9 percent protein, while the other one consumed about two times of it – 18 to 20 percent. After delivery, all of the rats consumed the control diet during lactation, so did their pups after weaning. The body weights and food intake of the rats were recorded every other day. It was found that the mother rats on the low-protein diet gained significantly less weight during pregnancy, and their babies were smaller at birth. It was also found that the rats on low protein diet had lower levels of threonine and histidine, and higher levels of alanine, lysine and serine, which suggests of potential disturbances in their protein metabolism.

When the skeletal muscles of the mother rats were examined after delivery, evidence of muscle atrophy, such as smaller fiber size, greater variation in fiber diameter and split fibers were found by Wang.

Among other findings of the study were increased activation of several AAR pathway downstream genes in both the mothers’ with low protein intake and their male pups’ skeletal muscles. Surprisingly, it was found that their other tissues – and those of the female pups – were unaffected. It was also discovered that rats on the low-protein diet showed higher expression of the ATF4 gene, a key regulatory protein within the AAR pathway known to play a critical role in muscle dystrophy caused by fasting. ATF4 is also linked with cell autophagy.

The study confirms a molecular link between the activation of the AAR signal and the autophagy pathway, Wang said. It is understood that the AAR- and autophagy-related genes remained activated in the skeletal muscles of the male pups, signifying that the amino acid limitation signal within the pregnant mothers’ skeletal muscles was transferred to the offspring through the placenta.

The findings stresses on the importance of adequate protein intake in women during pregnancy to protect the health of their children.

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References

https://medicalxpress.com/news/2015-09-maternal-protein-deficiency-pregnancy-fetal.html

https://www.biosciencetechnology.com/news/2015/09/maternal-protein-deficiency-during-pregnancy-memorized-fetal-muscle-cells

Alzheimer’s Drug Could Prevent Bone Fractures

Oct 31, 2015

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Increasing cases of Alzheimer’s disease in our aging population is a cause of great concern. It is one of the most common forms of dementia that affects our elderly. In its early stages, Alzheimer's disease is characterized by decreasing bone density, which puts patients at a higher risk of bone fractures.

A new research article published in the new open access journal Heliyon, has revealed that the most common drug used for treating Alzheimer’s disease increases bone mass in mice. This is good news as the authors of the study from Saitama Medical University in Japan point out. The results of the study signify that following further clinical research, the drug could also be used to treat bone loss diseases like osteoporosis and periodontitis.

Donepezil is the commonly used drug to treat Alzheimer's disease. As per the new Heliyon disease, this drug can improve cognitive function as well as increase bone density, thereby reducing the risk of fractures.

Dr. Tsuyoshi Sato, Associate Professor in the Department of Oral and Maxillofacial Surgery, Saitama Medical University and also the lead author of the study said that they are of the opinion that donepezil can improve cognitive function and increase bone mass, making it a very useful drug for patients with dementia and osteoporosis. Since, this drug serves dual purpose, from the viewpoint of medical economics; it will reduce the cost of treating these diseases.

There are two types of cell at work to control bone mass and density in our bodies – osteoblasts make bone and osteoclasts absorb it. A molecule named acetylcholine causes osteoclasts to die in vitro. Although an enzyme called acetylcholinesterase breaks this molecule down, the effect of this enzyme on osteoclasts remains unclear.

It is seen that donepezil, stops acetylcholinesterase from working, leading to an increase in the amount of acetylcholine in the brain. Recent clinical studies seem to suggest that patients who are on donepezil for Alzheimer’s disease have a lower risk of hip fracture. The researchers wanted to further their study and understand how donepezil prevents bone degradation. They observed the drug’s activity in vitro using mouse bone marrow cells, and it was found that more acetylcholinesterase is produced when osteoclasts are being made, which leads to even more osteoclasts being made. Donepezil stops acetylcholinesterase from working, which in turn prevents osteoclasts from being made.

The team then studied the effect this drug has in a mouse model with bone loss. It was found that by preventing the production of osteoclasts, donepezil increases bone mass in mice. Dr. Sato said that it was indeed surprising to find that donepezil directly inhibits the production of osteoclasts and subsequently increases bone mass in vivo. Some of the researches done previously have shown that acetylcholinesterase activity increases continuously with age, and that is the reason why elderly people are at an accelerated risk of bone loss.

The researchers also noted that the concentration of acetylcholinesterase in macrophages was higher when the tissue was inflamed. It suggests that inflammation causes bone to be degraded in part due to acetylcholinesterase production. Dr. Sato seemed very positive about the findings of the study as they are very promising and suggest that there is a role for donepezil in increasing bone mass in elderly patients with inflammation and dementia. Of course, more research is needed to observe the effect of this drug in patients.

To further their studies, the team now plans to work with the Department of Neurology at Saitama Medical University on clinical research. They will study if taking donepezil reduces patients’ risk of bone fracture by looking at its effect in a group of patients compared to a control group.

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References

https://medicalxpress.com/news/2015-09-alzheimer-drug-bone-fractures.html

https://www.sciencenewsline.com/summary/2015092115420016.html

A High Fat Diet Leads To Overeating Because Of Faulty Brain Signaling

Oct 30, 2015

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Our body is designed to perform the balancing act when it comes to food. It controls the food intake by striking a balance between the body's need for food to survive and its desire for food for pleasure. However, a new study published in the new open access journal Heliyon, has revealed that faulty brain signaling can cause overeating of high fat foods in mice, leading to obesity. Due to a tweak in the balance of the brain signaling system, pleasure can override need and it can lead to overeating and subsequently to obesity.

The researchers at the Neuroscience Program in Substance Abuse (N-PISA) at Vanderbilt University, USA opines that if we can understand the mechanisms behind overeating, incidences of obesity could be reduced or prevented.

Dr. Aurelio Galli, one of the authors of the study said that scientists have observed that animals as well as humans tend to over-consume tasty high-fat foods, even though they have a feeling of being full. One of the important factor in this phenomenon is a high fat diet – it causes obese people to eat more, which skyrockets their caloric intake and their weight loss goals goes for a toss. Several studies have been conducted to understand why a high fat diet has such an effect.

Since 1980, obesity has doubled worldwide. It is estimated that 2 billion people are overweight of weight 600 million people are obese. Economic stresses, changes in environment and changing food trends � all contribute to obesity.

Obesity occurs when due to faults in the central nervous system; our body can’t match its energy intake through food with its energy expenditure. The new study reveals a novel mechanism that leads to overeating high fat foods for pleasure. A specific signaling pathway in brain cells that is in charge of controlling motivation, movement and attention determines the amount of high fat foods consumed. When there is a fault in this signal, the person only overeat high fat foods.

Dr. Kevin Niswender, one of the authors of the study said that they distilled the neurobiological mechanisms involved specifically in overeating for fat. They defined the basics of ‘hedonic’ obesity and found that disrupting a specific signaling pathway in the brain can lead to overeating specifically food high in fat. That specific signaling pathway in the brain is insulin signaling. Study revealed that insulin signaling can override the body’s natural homeostatic mechanisms in favor of the reward mechanisms, leading to obesity.

Rapamycin complex 2 (mTORC2) is a group of proteins involved in insulin signaling in the brain. The researchers researched further to find out how insulin signaling and mTORC2 affect overeating of high fat foods. For this the researchers genetically altered brain cells in mice by taking out a part of mTORC2 and found that the mice without a functioning mTORC2 ate high-fat food excessively. But, when provided only with low-fat food they did not overeat. They also found that the mice whose mTORC2 does not function also had less dopamine in specific regions of the brain. It is known that lower dopamine transmission in brain cells is associated with obesity in humans and animals, and also in escalating substance abuse.

Dr. Galli opined that their studies reveal that the system designed to control eating high fat food in the brain can be hijacked by the very foods that it is designed to control. This can lead to a vicious cycle of increase in high-fat diet intake which further cements changes in these brain areas. The next step in the researcher's study is to find out if disrupting the signaling system works. And also to find out what happens when they restore mTORC2 signaling in obese mice. Does it lead to them eating a normal amount of calories? Only further research can reveal it.

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References

https://medicalxpress.com/news/2015-09-high-fat-diet-overeating-faulty.html

https://www.sciencedaily.com/releases/2015/09/150921090147.htm

Why Walking To Improve Your Health Is Not Quite As Straightforward As It Seems

Oct 29, 2015

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Statistics reveal that 50% of the US adult population suffers from chronic diseases or cancer. So, it comes as no surprise that from time to time the US Surgeon General urges the nation to get walking and to engage in some physical activity. Any increase in activity will definitely bring significant public health benefits. Walking seems to be one of the easiest and most effective ways of achieving this goal.

Even though walking sounds fairly easy in principle, getting people to walk the right way and in the right amount is somehow a challenging task. The physical activity guidelines in 2008 advocated at least 2.5 hours a week of moderate intensity physical activity, like brisk walking.

Reports reveal that only 54% of adult men and 46% of adult women in the US meet the physical activity goal. Not just that 28% of men and 32% of women report to not have done any physical activity that lasted more than 10 minutes in the previous week of being asked. So, the potential benefit of walking if these people got active in terms of public health are quite obvious.

For walking to reap the desired health benefit, the pace at which the walking should be done needs to be above certain intensity. However, it is not specifically mentioned in the US Surgeon General’s “Step it Up” programme to promote walking, wearables like the ones from Jawbone, Fitbit and others, are one way of tracking the number of steps walked in a day. Most people make it a target to get 10,000 steps a day. But, the point is only those steps achieve the health benefit which are above a certain pace.

In order to measure the intensity of activity, a measure called metabolic Equivalent or MET is used. A person resting consumes energy at the rate of 1 MET. 3-5.9 MET signifies moderate intensity activity. In walking it translates to 4.8 km per hour or 3 miles per hour. It is recommended that a person should engage himself in about 500 to 1000 MET minutes a week to reap the health benefits. Only 2.5 hours a week will make a person reach only the bottom of the range. In reality doing 5 active hours of walking would be better.

It should be noted increased level of activity does not actually mean linear increase in health benefits. Some health benefits hit a plateau after a particular level of activity.

The health benefits of walking are known since long. However, there is a lack of scientific studies which uses objective measures to measure activity. Today, consumer wearables can now provide us with such data � a thing that was not possible earlier.

In his recent call to action announcement, the US Surgeon General has made clear that, much more research is needed. It can help in making evidence for the exact nature of the benefits clear and can also aid in investigating how people can be persuaded to start and stick with a programme of walking to achieve the recommended amounts of exercise. As compared to running, walking typically results in fewer injuries but it is not totally free of risk. So, this is another area that requires more research.

If you are a user of devices like Fitbit or other such wearable), it will make more sense to concentrate on the active minute target than on the number of steps. 2.5 to 5 hours of active walking a week should be ideal. Another way of measuring the right level of intensity when walking without using a pedometer is that you should have enough breath to be able to talk to someone but not be able to sing.

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References

https://medicalxpress.com/news/2015-09-health-straightforward.html

https://theconversation.com/why-walking-to-improve-your-health-is-not-quite-as-straightforward-as-it-seems-47463

Study Highlights Possible Knowledge Gap over Effects of Some Diabetes Drugs

Oct 28, 2015

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A scientific paper published in the Journal of Biological Chemistry reveals that it is likely that there is a gap in scientific knowledge about a family of drugs used to treat Type 2 diabetes. While researchers warn that the results are speculative at this stage and that more research is needed before definitive conclusions can be drawn, there is a lack of complete information about the potential impact of GLP-1 agonists, or incretin mimetics often prescribed in type2 diabetes to patients who have not been able to bring their condition under control through lifestyle changes or with first-stage, tablet treatments.

Their research found one hitherto unknown effect of such treatment and that is it activates receptor sites for the hormone, glucagon which in turn can promote the release of sugars into the blood. That is something GLP-1 agonists are meant to prevent.

The researchers have also said that while there is no evidence that the existing GLP-1 agonists are harmful for patients, however there should be more comprehensive tests before such drugs are launched in the market.

Academics from the University of Cambridge and the University of Warwick lead the team of researchers. Dr. Graham Ladds, from St John’s College, University of Cambridge, opined that there is a need for complete understanding of how anti-diabetic drugs interact with receptors in different parts of our bodies.

Diabetes is characterized by an increase in the blood sugar levels and it results in complications as the body doesn't produce enough of the hormone which enables uptake of sugar from food � insulin. As per WHO, about 347 million people suffer from this disease and cases of type 2 diabetes are on the rise among adults.

GLP-1 agonists work by imitating the effects of a naturally-occurring hormone, called a Glucagon-like peptide (GLP-1). This regulates blood sugar levels both by stimulating the release of insulin, and also by inhibiting glucagon, another hormone which allows the liver to release stored sugar into the bloodstream.

GLP-1 takes effect by binding to specific receptor sites in the cells of our bodies. GLP-1 agonists are synthetic molecules which are designed to bind to these receptors in the same way. The new study investigated the possibility that instead of activating these receptors, GLP-1, might bind to the receptor for glucagon instead. Activating that could cause an unwanted side-effect for people with diabetes as it can lead to the release of more sugar into the bloodstream.

Some of the previous studies have suggested that such a thing was not possible. However, the present study team discovered that under certain circumstances, GLP-1 can bind to the glucagon receptor.

When initial experiments, carried out on yeast containing the receptor, found that it was activated not only by GLP-1, but also by a GLP-1 agonist, they carried out further experiments on a mammalian cell culture, and got similar results. Upon further investigation, it was found that another protein called receptor activity-modifying protein (RAMP2) was of key importance. When RAMP2 was present, it prevented the peptides from binding to the glucagon receptors. But in its absence, binding became possible.

Not much is known about RAMP2. Experiments were carried out in mice and it was found that its level can vary in different parts of the body. Like in liver, levels of RAMP2 appear to be lower than in other parts of the body. Dr. Ladds opined that this study shows that there is a possibility that, glucagon receptors can potentially be activated by anti-diabetic treatments. It is clear that RAMPS have a big role to play in the process of regulating blood sugar, but more research is needed to find more about them.

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References

https://medicalxpress.com/news/2015-09-highlights-knowledge-gap-effects-diabetes.html

https://www.cam.ac.uk/research/news/study-highlights-possible-knowledge-gap-over-effects-of-some-diabetes-drugs

New drug approach could offer relief to patients, hospitals fighting antibiotic resistance

Oct 27, 2015

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Antibiotic resistance has become a problem of epic proportion. In the United States alone, it affects about 2 million people. A new research by the scientists at Virginia Tech has found a new group of antibiotics which may provide relief to people who are suffering from it.

Bacteria Staphylococcus aureus, or staph, and the antibiotic resistant strains commonly known as MRSA (methicillin-resistant Staphylococcus aureus) are the new targets of this new antibiotics group. The results of the study were published in Medicinal Chemistry Communications recently.

In the year 2013, an estimated 9,937 people had died in the United States due to invasive MRSA infections. Even though the current infection rate have declined, as per the Active Bacterial Core surveillance report by the Centers for Disease Control and Prevention, as many as 8150 deaths were associated with inpatient stays in health care facilities.

The newly discovered potential new antibiotic group is different from the contemporary antibiotics as they contain iridium – a silvery-white transition metal. Since, the new transition metal complexes do not easily breakdown, it makes the delivery of antibiotics to where they are needed to fight infections in the body more precise and accurate. Researchers have experimented about the toxicity of these iridium containing compounds and have found them to be nontoxic to animals and animal cells. So, it is very likely that they are also safe for human use.

Joseph Merola, a corresponding author of the study, a professor of chemistry in the College of Science and a Fralin Life Science Institute affiliate said that their study have found that these compounds are safer than other compounds made from transition metals. Researchers have experimented to find that the antibiotics effectively kill the bacteria without inhibiting mammalian cells. One version of the said antibiotic was also tested for toxicity in mice with no harmful effects. The compounds are also being tested in human cell lines and till now the cells have remained normal and healthy.

Joseph Falkinham, a professor of microbiology in the College of Science and an affiliate of the Virginia Tech Center for Drug Discovery said that even though the development of the antibiotic is at a very early stage, the preliminary results till now show that they are safe and effective as well. The researchers hope that in the coming few years, they would be able to identify various characteristics of these antibiotics �like its stability, distribution and concentration in animal tissue, penetration into white blood cells, and its metabolism in animals.

Staphylococcus aureus is a bacterium commonly found on the skin and nose – that is how it spreads into hospitals and other medical facilities. When people contract the bacteria in a hospital setting, the infection can be life-threatening. It can cause pneumonia and infections in the bloodstream and in surgical wounds.

In September last year, the U.S. Federal government has issued an executive order to combat the rise of antibiotic-resistant bacteria in a statement that said � it represents a serious threat to public health and the economy”. Following that announcement in March this year, a National Action Plan sketched out the next critical steps for key federal agencies and departments.

Merola said that it is good news for us that we have discovered the organometallic antibiotics when bacteria have not evolved to resist them.

The spread of MRSA is a major threat to people in hospitals and other health care facilities not only in the U.S. but also in Europe and around the world. As per an estimate provided by the Centers for Disease Control and Prevention, antibiotic resistance is a problem that adds around $20 billion annually to health care costs in the U.S.

Here’s how you can fight a common infection without the use of antibiotics.

References

https://medicalxpress.com/news/2015-09-drug-approach-relief-patients-hospitals.html

https://www.nzhealthtec.com/new-drug-approach-could-offer-relief-to-patients-hospitals-fighting-antibiotic-resistance/

Mediterranean Diet plus Olive Oil Associated With Reduced Breast Cancer Risk

Oct 26, 2015

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Breast Cancer is one of the frequently diagnosed form of cancer and also one of the leading causes of death in women. Researchers have extensively researched diet as a modifiable factor in the development of breast cancer. However, there is inconsistency in the epidemiologic evidence on the effect of specific dietary factors.

An article recently published online by JAMA Medicine revealed that eating a Mediterranean diet supplemented with extra virgin olive oil was associated with a relatively lower risk of breast cancer in a study of women in Spain.

A Mediterranean diet is rich in plant food sources, fish and particularly olive oil. Miguel A. Martínez-González, M.D., of the University of Navarra in Pamplona and CIBEROBN in Madrid, Spain, and coauthors analyzed the effects of two interventions with the Mediterranean diet- one supplemented with extra virgin olive oil [EVOO] or nuts, and compared it with advice to women to follow a low-fat diet. The study was conducted within the framework of the large PREDIMED (Prevención con Dieta Mediterránea) trial, meant to test the effects of the Mediterranean diet on the primary prevention of cardiovascular disease.

The participants in the two intervention groups were given EVOO (one liter per week for the participants and their families) or mixed nuts (30 grams per day: 15 grams of walnuts, 7.5 grams of hazelnuts and 7.5 grams of almonds).

4282 women between the ages of 60 to 80 and those at high risk of cardiovascular disease were recruited between 2003 and 2009. One part of the recruited women (1476) was assigned Mediterranean diet supplemented with EVOO, another part's (1285) Mediterranean diet was supplemented with nuts and another part (1391) was advised control diet with advice to reduce their dietary intake of fat.

At the beginning of the study, it was noted that the average age of the women was 67.7 years, with an average body mass index of 30.4. It was also noted that most of them had undergone menopause before the age of 55 and less than 3 percent had opted for hormone therapy. When a median follow-up was carried out nearly five years later, the authors identified 35 confirmed new cases of malignant breast cancer.

It is reported by the authors that the women eating a Mediterranean diet supplemented with EVOO showed a 68 percent (multivariable-adjusted hazard ratio of 0.32) relatively lower risk of malignant breast cancer than those asked to follow a control diet. Women eating a Mediterranean diet supplemented with nuts did not show much significant risk reduction compared with women in the control group.

However, there are a number of limitations of the study observed by the authors. They say that breast cancer was not the primary end point of the trial for which the women were recruited. Agreed, the number of observed breast cancer cases was low, however, the authors do not have information on an individual basis on whether and when women in the trial underwent mammography. Also, it cannot be established with confidence that the observed beneficial effect was attributable mainly to the EVOO or to its consumption within the context of the Mediterranean diet.

Still, in general it is known that consumption of a diet that is based on plant foods, fish and extra virgin olive oil, is known to reduce the risk of cardiovascular disease and is safe. That is why it is possible that Mediterranean diet may also prevent breast cancer.

The results of the PREDIMED study do suggest a beneficial effect of a Mediterranean diet supplemented with EVOO in the primary prevention of breast cancer. However it was also concluded by the authors that these results need confirmation by long-term studies with a higher number of incident cases.

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References

https://medicalxpress.com/news/2015-09-mediterranean-diet-olive-oil-breast.html

https://www.sciencedaily.com/releases/2015/09/150914092837.htm

Filtered Sunlight a Safe, Low-Tech Treatment for Newborn Jaundice

Oct 25, 2015

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A new study by researchers at the Stanford University School of Medicine published recently in The New England Journal of Medicine reveals that newborn jaundice can be treated with filtered sunlight. This finding has global impact as it can be instrumental in providing a safe, inexpensive, low-tech solution to a health problem that now causes permanent brain damage or death in more than 150,000 babies in developing countries each year.

In the study which was conducted in Nigeria, some mothers and babies sat under outdoor canopies that filtered out harmful wavelengths from sunlight, and allowed jaundice-treating blue wavelengths to reach the babies’ skin. The filtered-sunlight treatment was as safe and effective as the blue-light lamps traditionally used to treat infant jaundice.

David Stevenson, MD, the Harold K. Faber Professor in Pediatrics and senior associate dean for maternal and child health at Stanford and study’s senior author said that all babies can get jaundice. In such circumstances where there is no access to modern devices, this study shows that there is something that can be used all around the planet�sunlight�to treat this dangerous condition.

Jaundice is quite common in newborns � it is due to a compound called bilirubin which is released during the normal breakdown of red blood cells. ��Baby's body needs a few days after birth to develop the enzymes that enable excretion of bilirubin. In case too much bilirubin builds up in the blood, the skin and eyes acquire the typical yellow tinge of jaundice. �If high bilirubin levels are left untreated for long, it can cause lasting brain damage or infant death.

Since the 1960s, the most common treatment for newborn jaundice has been phototherapy with lamps that emit blue wavelengths. However, in developing countries many hospitals and health clinics do not have the funds, expertise and reliable electricity needed to operate the equipment.

Commercially available plastic films were used by the researchers to build the outdoor canopies. These canopies could filter out sunburn-causing ultraviolet rays and infrared rays that could make infants overheat. But, it would let the blue wavelengths that treat jaundice to pass through filters. Different types of canopies were built for sunny days and for overcast days.

Hendrik Vreman, PhD, a senior research scientist in pediatrics at Stanford and a study author who developed and tested the canopies opined that even on an overcast sky, good light transmission and phototherapy is possible. The clinical trial was carried out in a large inner-city hospital in Lagos, Nigeria where the scientists enrolled 447 infants with jaundice. 224 of the infants were randomly assigned to treatment with filtered sunlight and 223 were treated with conventional phototherapy.

The infants were given at least five hours per day of their assigned treatment, and were evaluated hourly during the span of the treatment for signs of hypothermia, overheating, dehydration and sunburn. The infants who were treated with filtered sunlight were rested in their mother's lap under the canopies. Breastfeeding was allowed while receiving the treatment.

The study revealed that both therapies worked equally well and were equally safe. Filtered sunlight was effective on 93 percent of treatment days, and conventional phototherapy on 90 percent of treatment days. �To further their study, the team is now studying greenhouse-like structures that incorporate the filters. Such structures could be used in places which are rainy, windy or colder than Nigeria.

Stevenson, who is a member of the Stanford Child Health Research Institute, said that they were happy and excited about the fact that they could use their understanding of the biology of jaundice and adapt treatment to the local context of a developing country and with the resources available there.

References

https://medicalxpress.com/news/2015-09-filtered-sunlight-safe-low-tech-treatment.html

https://www.nlm.nih.gov/medlineplus/news/fullstory_154667.html

Study Finds Viral Protein That Causes Dengue Shock

Oct 24, 2015

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Vaccine

An effective vaccine against dengue has remained elusive for quite a while. While we are still a long way from finding an effective solution, there is some good news in our fight against dengue. Researchers at the University of California, Berkeley, have identified the thing responsible for the fluid loss and resulting shock that are the hallmark of severe and potentially fatal dengue virus infections.

Eva Harris, a molecular virologist and a UC Berkeley professor in the Division of Infectious Diseases and Vaccinology lead the team of researchers who found that the culprit is a protein secreted by cells infected with mosquito-borne dengue virus. This protein is called nonstructural protein 1 (NS1) and it is the only one of the 10 viral proteins secreted by infected cells to circulate freely in the bloodstream. Through their experiment on human lung endothelial cells and in mice, the researchers discovered that NS1 cause permeability of the endothelium, which lines the walls of blood and lymph vessels making it leak fluid. Another remarkable discovery made by the researchers is that by blocking this protein in mice, the lethal effects of the dengue virus infection on the mice could be prevented.

The results of the study were published recently in the journal Science Translational Medicine.

Harris, senior author of the study said that this was the missing part in the pathogenesis of dengue. �Till now, the role of NS1 itself was overlooked in severe forms of dengue disease, but since it is known now that has an important role to play, it is a prime target for drugs, and vaccine development.

As per statistics every year 390 million people are infected with this virus and because of lack of vaccine or treatment, reducing mosquito breeding sites and supportive care, such as fluid replacement, for patients with severe dengue has been the focus for treating the disease. The most severe symptoms of dengue range from fever, joint and muscle pain, dengue hemorrhagic fever and dengue shock syndrome caused by the loss of fluids from blood vessels. Dengue hemorrhagic fever and dengue shock syndrome can be fatal and result in the death of 22,000 people annually.

Harris said that if fluid loss begins in a patient infected with dengue, it can get fatal in just a day or two. Dengue is caused by 4 serotypes of the virus, so people who have had prior infection are more prone to get a more severe dengue infection the second time. An initial infection can impart long-term immunity for that one of the four virus type, but only temporary immunity against the rest. The dominant hypothesis to explain this has been that the antibodies from the first infection react with the new serotype in a way that worsens the damage.

P. Robert Beatty, an assistant research scientist at UC Berkeley’s School of Public Health and study's lead author said that the interaction with the antibodies might be happening, but it never fully explained all cases of dengue hemorrhagic fever. The toxicity of NS1 makes more sense than just having an over-reactive immune response.

NS1 is produced by all serotypes of dengue virus. The researchers zeroed in on this viral protein after they observed that the pathogenic effects of dengue virus infection were blocked in mice that had generated antibodies to NS1. In fact, the team found that when they injected the mice with NS1 alone, without the virus present, it developed symptoms of dengue disease. When the researchers added a sublethal dose of dengue virus type 2, the resulting infection was fatal. It was also found that immunization of mice with recombinant NS1 from each of the four serotypes protected mice against vascular leak and the lethal effects of dengue virus. These finding can surely pave the way for the nipping the disease at an early stage.

References

https://medicalxpress.com/news/2015-09-viral-protein-dengue.html

https://www.livemint.com/Politics/ngraH92wDDHF7rcEzftKzI/Scientists-discover-viral-protein-that-makes-dengue-fatal.html

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