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Can cancer itself damage the heart?

Jan 12, 2016

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It has been found by the researchers at the UK's first dedicated cardio-oncology clinic that impaired heart function is common to both treated and untreated cancer patients. A research concluding the same was presented at the recently held EuroEcho-Imaging 2015 seminar. It states the possibility that cancer itself may damage heart muscle irrespective of exposure to cancer drug therapies. The annual meeting of the European Association of Cardiovascular Imaging (EACVI), a registered branch of the European Society of Cardiology (ESC) was recently held in Seville, Spain.

Dr. Rajdeep S. Khattar, consultant cardiologist at the Royal Brompton Hospital in London, UK and last author of the abstract opined that it is well known that chemotherapy is potentially toxic to the heart, making cancer patients more prone to cardiovascular complications such as heart failure, hypertension or myocardial ischaemia. He added that the study is significant as it raises the possibility that tumour growth itself may also damage the heart which could have important implications for monitoring.

Cardiotoxicity is defined based on a reduced ejection fraction (less than 55%) and symptoms of heart failure. Echocardiography is needed to assess ejection fraction – coarse measure of left ventricular function. In simple words, it refers to the percentage of blood pumped into the circulation when the heart contracts. For an example, say there is 100 ml of blood in the left ventricle and 60 ml is pumped out, the ejection fraction is said to be 60%.

For this study, the researchers applied an even more subtle measure of left ventricular function using echocardiography called strain. This measure indicate how well the myocardial fibres contract. It has been known from previous studies that cancer patients who have undergone chemotherapy may have a normal ejection fraction but reduced strain and that this may be the onset of subsequent cardiotoxicity. Khattar remarked that through their study they wanted to see if cancer patients who have not been through chemotherapy and have a normal ejection fraction, can have reduced strain measurements.

As a part of the study, myocardial strain in three groups with a normal ejection fraction (55% or more) were compared: 43 patients with cancer who were currently being treated or had received treatment in the past, 36 patients with as yet untreated cancer, and 20 healthy individuals matched to the cancer groups for age and gender. The study revealed that both groups of cancer patients had similarly reduced strain measurements which indicated impaired heart function as compared to the healthy individuals.

Dr. Khattar said that it is interesting to note that all the cancer patients had a preserved ejection fraction. So, if one went by that coarse measure their hearts were functioning normally. However, the strain measurements indicated that they did have myocardial dysfunction. This finding is something new and it needs to be taken into account with all seriousness while treating cancer patients. It raises the possibility that the tumour itself may have a significant undesirable effect on the function of the heart.

Dr. Khattar said that patients with reduced strain before they start their cancer drug therapies may be predisposed to developing heart failure during the course of their treatment and hence there is a need for closer monitoring in such patients. It will be a real change as presently it is not mandatory for them to have a cardiovascular risk assessment by a cardiologist.”

The patients in the current study will be followed upon by the researchers in the days and years to come to find out if their rates of heart failure and death are predicted by the strain measurements. Dr. Khattar opined that if it turns out that the patients with reduced strain prior to cancer treatment are more prone to heart failure and death then implementing closer monitoring of patients with cancer will be of great importance.

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Reference Links:

https://medicalxpress.com/news/2015-12-cancer-heart.html

https://healthmanagement.org/c/cardio/news/can-cancer-damage-the-heart

A Step towards Gene Therapy against Intractable Epilepsy

Jan 11, 2016

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Epilepsy is one of the most common neurological disorders that affects people of all ages and is characterized by unpredictable seizures. There are many existing drugs to treat the condition. However, many patients with epilepsy have not experienced any improvements in the symptoms from the existing drugs. In severe conditions, surgery is recommended in cases where it is possible to localize and remove the epileptic focus in the brain where seizures arise.

A group of researchers at the Lund University in Sweden along with colleagues at University of Copenhagen Denmark have been experimenting and studying the effects of delivering genes for a certain signal substance and its receptor into the brain of test animals with chronic epilepsy. The good news is that their efforts seem to have succeeded as it has considerably reduced the number of epileptic seizures among the animals. The test has been designed to as far as possible mimic a future situation involving treatment of human patients.

Professor Merab Kokaia remarked that there is a period between the detection of this focus and the operation when the gene therapy alternative could be tested. If the therapy works well, the patient can avoid the hassle of a surgery. In case it doesn’t, surgery will go ahead as initially planned and the affected part can then be removed. With this approach, the experimental treatment will be more secure for the patient.

For the study, the researchers are working on a rat model that mimics temporal lobe epilepsy- the most common type of epilepsy. As a part of the study, these test animals are given injections of the epilepsy-inducing substance, kainate, in the temporal lobe of one the cerebral hemispheres. It was seen that most of these animals had seizures of varying degrees, but some had no seizures. Merab Kokaia opines that it is a good result, as it mimics the situation among people. Brain damage resulting from various accidents has varying consequences for different patients, as some develop epilepsy, whereas others do not.

Gene therapy was given to the rats that developed epilepsy. The genes were delivered to that part of the brain where kainate had been injected, and where the seizures arose. For best results genes were delivered for both the signal substance (neuropeptide Y) and one of its receptors. The idea behind it was that the combination would create a larger effect than only delivering the gene for the signal substance itself. Neuropeptide Y can bind to several different receptors and in worst cases it has been observed that it binds to a receptor that promotes an increase in seizures instead of decreasing it.

The results of the study have been encouraging so far. The increase in the frequency of seizures among the control animals treated with inactive genes diminished after the treatment with combination of active genes, and for as many as 80 % of the animals the number of seizures was reduced by almost half.

Merab Kokaia opined that there is a need to repeat the test in more animal studies, so that the possible side effects, like on memory can be studied. He added that this study should be regarded as promising proof of concept that the method works.

Kokaia is hopeful that the first gene therapy treatments will be carried out on patients who have already been selected for surgical procedures. But in the long run, he thinks that the gene therapy will be most helpful for those patients who cannot be operated on. In some patients with severe epilepsy the epileptic focus can be so badly placed that an operation is out of question as it can impair e.g. speech or movement. Since, a surgery is out of question for them, they could benefit from gene therapy in the future.

Reference Links:

https://medicalxpress.com/news/2015-12-gene-therapy-intractable-epilepsy.html

https://www.sciencenewsline.com/news/2015120318480025.html

Lucentis Proves Effective against Proliferative Diabetic Retinopathy

Jan 10, 2016

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The results of a new research conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), published in the Journal of the American Medical Association have found that that the drug ranibizumab (Lucentis) is highly effective in treating proliferative diabetic retinopathy (PDR), a complication of diabetes that can significantly damage eyesight. This clinical trial funded by the National Eye Institute (NEI) involved 300 patients and demonstrates the first major therapy advance for the condition in nearly 40 years.

Blood vessels in the light sensitive retina in the back of the eye are damaged in PDR and as the condition worsens these blood vessels stop functioning properly. When this condition becomes proliferative, the retina produces a protein called vascular endothelial growth factor (VEGF) that stimulates the growth of abnormal blood vessels. It can induce bleeding in the center of the eye that might need surgical intervention. If PDR is untreated, it can lead to vision loss. As many as 7.7 million U.S. residents have diabetic retinopathy, of which about 1.5 percent cases have progressed to PDR.

Lucentis is among several drugs that block the effects of VEGF. The golden standard for PDR since the mid-1970s has been a laser therapy called panretinal photocoagulation. Even though this laser therapy preserves central vision, it can damage night and side vision, so researchers have been on the lookout for therapies that lack these side effects. The results of the Lucentis injections were compared with the laser therapy and it is found that Lucentis is a safe and effective alternative to laser therapy against PDR.

Lloyd Paul Aiello, M.D., Ph.D., director of the Beetham Eye Institute at Joslin Diabetes Center and Professor of Ophthalmology at Harvard Medical School said that patients who received Lucentis showed a little bit better central vision, much less loss of their side vision, and substantially less risk for surgery than patients who received laser treatment.

For this study the DRCR.net enrolled 305 participants (394 eyes) with PDR in one or both eyes at 55 clinical sites across the country. The participants' eyes were assigned randomly to treatment with Lucentis or laser. About half of the eyes assigned to the laser group required more than one round of laser treatment. In the other group, Lucentis was injected into the eye once per month for three consecutive months, and then as needed until the disease resolved or stabilized.

At two years, vision in the Lucentis group improved by an average of about half a line on an eye chart, compared with virtually no change in the laser group. It was also noted that participants treated with laser generally lost substantial peripheral vision, but those given injections did not. The benefits of anti-VEGF medication were clear. Many of the patients who had laser treatment noticed that they have more tunnel vision, which can lead to difficulties as they go about activities of daily life. The use of anti-VEGF treatment rather than laser for PDR could help prevent these symptoms. Also, the need for vitrectomy surgery was lower in the Lucentis group (8 of 191 eyes) than in the laser group (30 of 203 eyes).

Dr. Aiello noted that the drug’s benefits are particularly clear for people with both PDR and DME � diabetic macular edema, a condition when fluid builds up in the center of the retina. Since, it can help treat both conditions at the same time it can be an appealing treatment alternative for patients.

Dr. Aiello also added that in a separate clinical trial they are going to examine whether anti-VEGF injections given at an earlier stage of diabetic eye disease can help prevent people from developing both DME and the sight-threatening PDR stage of the disease.

Here's how you can reverse your diabetes starting today.

Reference Links:

https://medicalxpress.com/news/2015-11-lucentis-effective-proliferative-diabetic-retinopathy.html

https://www.justdiabetesnews.com/lucentis-proves-effective-against-proliferative-diabetic-retinopathy/

FDA To Review Fortifying Corn Flour with Folic Acid to Prevent Birth Defects

Jan 9, 2016

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The lack of folic acid can lead to severe birth defects. There has been a rise is such defects in an ongoing cluster of cases in Washington state and other cases in the nation’s growing Hispanic population. In order to curtail it the federal Food and Drug Administration has agreed to review a long-delayed petition to fortify corn masa flour with folic acid, a move advocates say will be significant in preventing devastating birth defects associated with lack of folic acid in women of child bearing age.

The petition to fortify corn flour was co-sponsored by the officials with the March of Dimes in 2012. They have revealed that the FDA has received results of recent tests that validate the stability of the B vitamin when added to foods such as tortillas and corn chips.

Cynthia Pellegrini, March of Dimes senior vice president of public policy and government affairs, said in an email that they were pleased to have moved the process forward on our citizen petition to fortify corn masa flour with folic acid. She added that they along with their co-petitioners would work with the FDA on this critically important issue for mom and baby health, especially in Hispanic communities.

The required tests were conducted by Utah food scientists in June and only after that the agency considered the petition that would help in curtailing severe birth defects such as spina bifida and anencephaly, particularly in Hispanic communities.

Since 2010, there have been at least 40 cases of anencephaly in the three of Washington state counties – a condition in which babies develop in utero missing all or part of the brain and skull. The irony is state and federal health officials have found no cause for it and no way to halt the rare and fatal disorder.

It is known that adequate amount of folic acid is important for the proper formation of the neural tube, which creates the brain and spinal cord early in fetal development. In cases where the tube doesn’t close properly, it can lead to spina bifida, or, in extreme cases, anencephaly. The only way known to reduce or prevent such defects is through folic acid supplements and fortification of foods.

Since 1996, the cereal-grain products identified as enriched has been fortified with folic acid after an intervention from FDA. Since then the cases of neural-tube defects in the U.S. have lowered by 35 percent. As per an estimate, this fortification eliminated about 10,000 defects in a decade, thereby making it one of the top 10 public-health interventions of the 21st century’s first decade. However, at that time as corn flour was not as common in the U.S as it is now. So, this staple grain in the Hispanic Diet was overlooked and was not classified as an enriched grain.

The U.S. Hispanic population is on the rise now and a quarter of all U.S. babies are now born to Hispanic mothers. These babies have a 20 percent increased risk of neural-tube defects.

According to the Centers for Disease Control and Prevention (CDC), by fortifying corn masa flour with folic acid, an average of 40 neural-tube defects a year in Hispanic women and perhaps as many as 120 nationwide could be prevented.

Michael Dunn, the Brigham Young University food scientist who led the study opined that the test results are positive and promising. He remarked that the folic acid remained quite stable in stored corn flour, baked tortillas and even in fried chips. While the new review is no guarantee of FDA approval, advocates opine that it’s a move long overdue.

Check this out for holistic remedies for pregnancy and natural childbirth.

Reference Links:

https://medicalxpress.com/news/2015-11-fda-fortifying-corn-flour-folic.html

https://www.seattletimes.com/seattle-news/health/fda-agrees-to-review-folic-acid-in-corn-flour-to-halt-birth-defects/

How to Eliminate Pain Tied To Tooth Decay

Jan 8, 2016

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Tooth decay is in fact the most prevalent chronic disease says the National Institutes of Health. There is some good news for all those who have experienced tooth pain due to decay at some point in their life. Dual discoveries at USC propose a promising method that can regrow nonliving hard tissue, lessening or even eliminating pain associated with tooth decay.

For the past two decades, Janet Moradian-Oldak, a professor at the Herman Ostrow School of Dentistry of USC, has been researching ways to regrow tooth enamel. The process is not an easy one because tooth enamel is a nonliving tissue and unlike bone, mature enamel cannot rejuvenate. Janet in collaboration with lead author Sauma Prajapati of USC and other colleagues published a study in the Biomaterials journal stating matrix metalloproteinase-20, an enzyme found only in teeth, chops up amelogenin proteins, which in turn facilitate organized enamel crystal formation. MMP-20 clears the way for hard material to take up the vacated space. This is the first time the function of an enzyme for preventing protein occlusion inside a crystal has been described.

Janet who is also the study’s senior author added that MMP-20 is released at a very early stage of enamel formation. MMP-20 chops up proteins during the crystallization of enamel. Together with other enzymes, it gets rid of ‘sludge’ so the enamel making cells in the body can add more mineral and make enamel, the hardest bioceramic in the human body.

The discovery by Janet Moradian-Oldak will be coupled with another study published in the Journal of Biomedical Engineering and Informatics, which concluded an amelogenin-chitosan hydrogel could repair early tooth decay by growing an enamel-like layer that reduces lesions by up to 70 percent.

Qichao Ruan, lead author of the hydrogel study and a postdoctoral research associate in the Center for Craniofacial Molecular Biology at USC remarked that recognizing MMP-20’s function in biomineralization is one of the first steps to learning how dental enamel forms in nature. He added that the findings about MMP-20 are significant as they can not only help to further understand the mechanisms of enamel formation but these findings can also be applied in the design of novel biomaterials for future clinical applications in dental restoration or repair.

Any type of enamel re-growing gel has not been approved by the Food and Drug Administration yet. Even USC is in pre-clinical trials. However, Janet is hopeful that that day is not far when people may be able to use an overnight mouth guard or teeth strips saturated with hydrogel to regrow enamel-like substances and reduce teeth sensitivity.

There are products like toothpaste and mouthwash containing fluoride and casein phosphopeptide-amorphous calcium phosphate that promote remineralization of initial enamel lesions; but the thing is they need to be used regularly to plug up the problem. It is more of a tire patch than a real solution that minimizes the feeling of tooth pain. This gel is different as it fills the cracks and holes with an enamel-like substance making the solution more durable.

Grinding teeth at night, gum recession and the disappearance of enamel over a lifetime due to demineralizing acidic food and drink are all common problems people everywhere face. Statistics reveal that in the United States, about 92 percent of adults between the ages of 20 to 64 have had dental decay in their permanent teeth.

Ruan remarked that when tested in an environment that mimics an oral cavity’s biochemical processes, the hydrogel was able to create a robust attachment, thereby eliminating the threat of secondary cavities in the same spot. It is very likely that the gel could be more effective than traditional crowns that weaken over time. Not just biocompatibility and biodegradability, the gel has unique antimicrobial and adhesion properties that are important for dental applications.

Struggling with dental problems? Try this.

Reference Links:

https://medicalxpress.com/news/2015-11-pain-tied-tooth.html

https://news.usc.edu/88721/how-to-eliminate-pain-associated-with-tooth-decay/

Brain Structure May Be Root of Apathy

Jan 7, 2016

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A new brain study by the neuroscientists at Oxford has revealed a very interesting connection between apathy and brain structure. The results of their study seem to suggest that the reasons why some people typically said to be lazy are due to the biology of their brain and not attitude.

This study carried out by a team of neuroscientists at Oxford is funded by The Wellcome Trust. As a part of the study the researchers studied young people to see if there were any differences in the brains of those who were motivated compared to those who were apathetic.

Masud Husain, Professor of Neurology and Cognitive Neuroscience remarked that it is known that in certain cases people can become pathologically apathetic, say after a stroke or with Alzheimer’s disease. Many of these patients can be physically capable and not depressed, but they can become so demotivated that they don't care about caring for themselves. In this study, the researchers studied healthy people with the aim to find out if there are any significant differences in their brains that could shed light on apathy.

Forty healthy volunteers were asked to complete a questionnaire and were then scored on how motivated they were. As a part of the study, they were then made to play a game in which they were given rewards – each needed different level of physical effort to win the reward. It was not surprising to find that offers with high rewards that needed low effort were more popular, while low rewards requiring high effort were less popular.

The volunteers were made to play the game in an MRI machine, so that the researchers could study their brains. In the process of studying the brain, a surprising finding emerged. It is seen that apathetic people are typically less likely to accept effortful offers; however, it was found that one area of their brains actually showed more activity than in motivated individuals. The pre-motor cortex is a major area involved in taking actions and it becomes active just before those areas of the brain that control our movement. It is a paradox that in more apathetic people it was more active when they chose to take an offer than it was in motivated people.

Husain says that it was expected that that area would be less active as apathetic people were less likely to accept effortful choices but just the opposite was found. The likely reason could be that their brain structure is less efficient, so it’s more of an effort for apathetic people to turn decisions into actions. Brain scanning techniques were employed to find that connections in the front part of the brains of apathetic people are less effective. Typically, the brain uses around a fifth of the energy one burns each day. Since, it takes more energy to plan an action; it becomes more costly for apathetic people to make actions.

Dr. Raliza Stoyanova, Senior Portfolio Developer in the Neuroscience and Mental Health team at the Wellcome Trust remarked that lack of motivation to act towards achieving even simple goals is a characteristic of some brain disorders but it also varies naturally within the population. The biological basis of such apathy is not well known. This study shares new insights, showing us that the brain systems involved in motivation and preparing for action are important components.

This is the first time a biological basis for apathy in healthy people has been found. It can't be said that it account for apathy in everyone but it can give us more information about the brain processes underlying normal motivation, and aid in designing treatment for those pathological conditions of extreme apathy.

Reference Links:

https://www.ox.ac.uk/news/2015-11-13-brain-structure-may-be-root-apathy-1

https://medicalxpress.com/news/2015-11-brain-root-apathy.html

Molecular Clocks Control Mutation Rate in Human Cells

Jan 6, 2016

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A copy of the human genome is present in each and every cell in the human body. It is believed that during a person's lifetime all cells acquire mutations. While some of these mutations are through external exposure like tobacco smoking or sunbathing, there are certain other mutational processes that happen internally and occur continuously at a constant rate over years. Such mutations are typically clock-like � that is for a certain age of a person, there are likely to be certain number of mutations.

In a new research published in Nature Genetics two clock-like mutational processes have been discovered in human cells and the rates at which the two clocks tick in different human cell types have been determined. It is understood that these mutational processes could have a significant role to play in many human cancers and in human ageing.

Previous studies on cancer cells have found that mutations often leave a molecular fingerprint, called a mutational signature, on the genome of a cancer cell. In order to identify the mutational signatures of clock-like mutational processes in the human body, the researchers of this study looked at the DNA sequences of 10,250 cancer genomes, from 36 different types of cancer. 33 mutational signatures were found in the cancer genomes by the researchers of which only two exhibited clock-like features. Named Signature 1 and Signature 5, these signatures showed a correlation between the age of the patient when the cancer was diagnosed and the number of mutations found in each cancer sample.

Dr. Ludmil Alexandrov, Oppenheimer Fellow at Los Alamos National Laboratory in the USA and author of the study said that this finding is very significant as it solves a longstanding question. This study shows that mutational molecular clocks exist and that there are two separate clock processes that are constantly degrading DNA. The rate at which these clocks tick may determine the ageing of this cell and the likelihood for it to become cancerous.

The researchers investigated 7,329,860 somatic mutations from the cancer genomes calculated which mutations each cell had had before it became a cancer cell. It helped them understand the rate at which the mutational clocks had generated the mutations. This information could be crucial to understand biology of cancer development and metastasis.

Dr. Julian Sale, an author on the paper and group leader at the MRC Laboratory of Molecular Biology opined that this study have practical implications for cancer patients. It could lead to clinicians being able to compare the genomes of a primary tumour and any metastases, and find out how long it took to spread. It can also assist doctors in predicting for new patients how quickly a cancer may change, like how fast it can spread or acquire resistance to a drug. It will help doctors in planning the best course of treatment.

It was found that both Signature 1 and Signature 5 clock-like processes accumulated mutations at a constant rate over time and operated in essentially all cell types in the human body. But, it was also seen that they exhibited different mutation rates in the different tumour types and surprisingly they also had different rates to each other, even in the same type of tumour. This suggests that they are likely to be due to two different biological processes.

Signature 1 had the highest mutation rate in cells with high turnover rates, like stomach and colorectal cells, and seemed to be due to certain methylated cytosine bases transforming into thymine, leading to mismatches in the genome that get converted into mutations when a cell divides. The mutational process for Signature 5 is still not very clear. Unlike Signature 1, the Signature 5 mutation rate did not correlate with the number of cell divisions. Further study is needed on both these processes to understand their full roles in the cell.

Professor Sir Michael Stratton, corresponding author and Director of the Wellcome Trust Sanger Institute remarked that it is the first identification and quantification of mutational molecular clocks, and was carried out by looking through the “cracked lens” of cancer genomes. In future research large-scale sequencing of all types of normal cells to refine this clock-like mutation rates is planned.

Reference Links:

https://medicalxpress.com/news/2015-11-molecular-clocks-mutation-human-cells.html

https://www.sanger.ac.uk/news/view/molecular-clocks-control-mutation-rate-human-cells

Antiangiogenic breast cancer treatment may benefit only patients with well-perfused tumors

Jan 4, 2016

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In a report published online in PNAS Early Edition, a research team from Massachusetts General Hospital (MGH), in collaboration with investigators at the Dana-Farber Cancer Institute has revealed the possible reason why the use of antiangiogenesis drugs – which has improved outcomes for patients with several types of cancer – fails to benefit some breast cancer patients. In their report, researchers have described how preoperative treatment with the antiangiogenic drug bevacizumab was found to be beneficial for patients whose tumors were highly perfused with blood vessels before treatment.

Rakesh K. Jain, PhD, co-senior author of the current report and director of the Steele Laboratory of Tumor Biology in the MGH Radiation Oncology Department remarked that as was expected, the bevacizumab treatment did reduce pressure within tumors and the density of tumor vasculature, but the pathologic response to therapy – whether or not it actually eradicated the tumor – seems to depend on the microvascular density of the tumor before treatment. That is to say, the results of the study point to a fact that a significant percentage of breast cancers do not have a blood supply sufficient to benefit from the vascular normalization provided by antiangiogenic drugs.

The use of antiangiogenesis drugs helps in suppressing the action of factors that induces the formation of blood vessels and it is seen that it has beneficial results in the treatment of several types of cancer. However, studies of their use in treating breast cancer have had inconsistent results. The mechanism through which antiangiogenesis drugs produce their effects is unclear – one hypothesis proposes that they reduce the supply of blood to tumor making it difficult for them to survive and another one says that they actually improve the delivery of oxygen to the tumor � a requisite for the beneficial effects of radiation and chemotherapy. The later theory was proposed by Jain, and has been supported by imaging studies even though it is not been conclusive yet.

In order to understand the mechanism of antiangiogenic therapy in breast cancer – the researchers studied the effects of an initial dose of bevacizumab, followed by a standard chemotherapy in combination with bevacizumab before surgical removal of the tumor. This approach is termed as neoadjuvant therapy, and it helps in reducing the size and growth of the primary tumors. 91 patients with HER2-negative breast cancer followed the protocol and only 16 had no active cancer cells within their tumors at the time of surgery � a situation called pathologic complete response.

When the biopsy samples taken before and after bevacizumab administration were examined, it was found that achieving a pathologic complete response happened in patients whose tumors had a dense blood supply before treatment. Also, it was seen that patients who had a larger number of mature, normalized blood tumor vessels after bevacizumab treatment had an even better pathologic response. These results indicate that, in breast cancer, the benefits of antiangiogenesis-induced vascular normalization need a sufficient pretreatment level of vascularization.

Jain remarked that their findings provide the first direct evidence of a relationship between structural vascular normalization and the extent of tumor regression after neoadjuvant bevacizumab treatment in breast cancer. He added that they have also identified several potential blood biomarkers of treatment response, which need to be validated in prospective, randomized trials.

Ian Krop, MD, PhD, co-senior author and director of Breast Cancer Clinical Research for the Susan F. Smith Center for Women’s Cancer at Dana-Farber added that for years breast cancer investigators have struggled to determine which cancers may respond to bevacizumab. The present research identifies the potential breast cancer patient population that can benefit from combined bevacizumab/chemotherapy treatment and suggest new strategies to improve outcome.

Reference Links:

https://medicalxpress.com/news/2015-11-antiangiogenic-breast-cancer-treatment-benefit.html

https://www.cancercommons.org/news/?rtag=breast-cancer&ctag=pc

Obese People Need More Vitamin E but Actually Get Less

Jan 3, 2016

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One in every three adults in the United States suffer from metabolic syndrome � a condition that is characterized by at least three of five common issues that raise health concerns – excess abdominal fat, high blood pressure, low “good” cholesterol, and/or high levels of blood sugar and triglycerides.

A new study by experts in the Linus Pauling Institute at Oregon State University indicate that obese people with metabolic syndrome face an unexpected shortage of vitamin E. Due to their weight and other problems there is an increase in oxidative stress, hence, they need more than normal levels of the vitamin. But, these same problems actually cause their effective use of vitamin E to be reduced.

The researchers involved in the study are of the opinion that a huge number of Americans may be chronically deficient in vitamin E, and it could compound the wide range of diseases known to be associated with metabolic syndrome, such as heart disease, diabetes, Alzheimer’s disease and cancer. The findings of the study are counterintuitive in certain instances – like since, vitamin E is a fat soluble micronutrient so in theory it should be available at increased levels in people who are overweight and eat large amounts of fatty foods. But, a study in the American Journal of Clinical Nutrition has suggested that even though circulating vitamin E in the bloodstream may be high in obese people, it is not in effect finding its way into tissues where it is most needed.

Maret Traber, a principal investigator in the Linus Pauling Institute and a professor in the College of Public Health and Human Science at OSU opined that Vitamin E is associated with lipids, or the fats found in the blood, but it’s mostly just a micronutrient that’s going along for the ride. She added that what this study has found is that the tissues of obese people are rejecting intake of some of these lipids because they already have enough fat. In doing so, they also reject the associated vitamin E. That is why even though the tissues are facing serious oxidative stress, the delivery of vitamin E to the tissues is hampered and as a result of it they are not getting enough of this important micronutrient.

Excess fat in the body causes oxidative stress. Vitamin E is among the body's natural defenses that fight this problem. . Some foods that are rich in this micronutrient include nuts, seeds, and olive oil. But, most Americans � almost 92 percent consume a diet that is 50% deficient in Vitamin E.

Traber added that most people who suffer from weight issues and want to reduce weight limit their fat intake. This makes some sense if you are trying to reduce calories, but the fact is – fat is the most common source of vitamin E in our diets, so, in trying to lose weight most people often harm themselves and it can sometimes actually worsen a nutrient deficiency.

Traber suggested that in such cases the best approach is to try and eat a balanced diet. People should also make it a point to take a daily multivitamin that includes 100 percent of the recommended daily allowance of vitamin E – 15 milligrams per day. It’s also necessary to eat some food that contains at least a little fat when taking a supplement. That because Vitamin E is a fat-soluble vitamin � and without some fat in the diet it will not be well-absorbed.

The participants of the study were a mixture of adults � some of them were healthy and some were suffering from metabolic syndrome. The authors of the study concluded that higher intake of dietary vitamin E is important for adults with metabolic syndrome.

Want to learn more about fighting obesity? Click here.

Reference Links:

https://medicalxpress.com/news/2015-11-obese-people-vitamin.html

https://oregonstate.edu/ua/ncs/archives/2015/nov/obese-people-need-more-vitamin-e-actually-get-less

Dengue – Asymptomatic people transmit the virus to mosquitoes

Jan 2, 2016

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Every year about 390 million people are infected with dengue virus through the bite of mosquitoes of the Aedes genus. As per an estimate of these infected people about 300 million are asymptomatic � which means they do not have clinical symptoms that are severe enough to be detected by health care systems. Previously, it was assumed that these asymptomatic or mildly symptomatic infections did not have high enough level of viremia (the concentration of the virus in the blood) to infect mosquitoes.

A new study by researchers at the Institut Pasteur in Cambodia, the Institut Pasteur in Paris and the CNRS published in the journal PNAS, have revealed that people infected by dengue virus but showing no clinical symptoms have the ability to infect mosquitoes that bite them.

The results of the study suggest that these asymptomatic people � who along with mildly symptomatic patients, represent three-quarters of all dengue infection and these people have a significant role to play in the transmission chain of the virus. The findings of the study put a question mark on the established theories concerning the epidemiology of dengue.

For this study, the researchers from the Institut Pasteur in Cambodia, the Institut Pasteur in Paris, and the CNRS studied the people with few or no symptoms that represent 75% of all dengue infections, and experimented to test if whether these people could actually infect mosquitoes that bite them.

The researchers chose the participants of the study from a human population at risk of dengue infection in Cambodia, in the town of Kampong Cham, roughly 100km northeast of Phnom Penh. Their research strategy depended on their ability to detect dengue infections that had not been identified by traditional health care systems because the participants were asymptomatic. Blood tests were carried out on people living in close proximity – like in the same household or in the immediate neighborhood – to patients with confirmed symptomatic dengue. Those people who tested positive for dengue virus in their blood tests but showed no clinical symptoms were then put into contact with healthy laboratory-bred mosquitoes.

When these mosquitos were later analysed it was found that they were infected and had become capable of transmitting the virus the next time they bit a human. It was also found through the research data that the viremia level has a significant role to play in transmission of dengue virus from a human to a mosquito.

Louis Lambrechts, a CNRS scientist in charge of the Insect-Virus Interactions Group at the Institut Pasteur in Paris opined that the findings of the study are significant.� It raises the possibility that asymptomatic people with dengue – the ones that form a majority of people infected by dengue – may have a big contribution to the spread of the virus without realizing it.

Also, people who are virtually or completely unaffected by the virus have a greater chance to be exposed to more mosquitoes during their daily routines than those who are severely ill, bed-ridden or hospitalized.

Veasna Duong, a scientist in the Virology Unit directed by Philippe Buchy at the Institut Pasteur in Cambodia, when this work had been done remarked that these findings should make us review and reconsider our approach to the early management of dengue epidemics. There is also a need to check and adjust the transmission rate estimates to ensure sufficient vaccination coverage for the vaccines currently under development. Meanwhile, in another leg of the study at the Institut Pasteur in Paris, the DENFREE European project, coordinated by Anavaj Sakuntabhai, investigation about the specific biological characteristics of asymptomatic infections is underway.

References:

https://medicalxpress.com/news/2015-11-dengue-asymptomatic-people-transmit-virus.html

https://www.pnas.org/content/early/2015/11/04/1508114112

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