Category: Health

{Taking a bottle of a cola drink or energy drink regularly is like a ritual to most people these days but how healthy are these drinks to our teeth?}

According to Dr Tom Bierman, a dentist at the San Diego Dental Studio in the United States, sugary drinks can cause irreparable damage to our teeth.

The image above shows the staining caused by a cola drink on a tooth after just two weeks.

The image below shows the destructive effect of an energy drink on a tooth.

Dr Bierman, 34, decided to check the effect of sugary drinks on the teeth after reading a book, Rust: The Longest War by Jonathan Waldman, which claims that one in seven energy drinks are too corrosive to put in aluminum cans, according to a Daily Mail report.

“I thought: If that’s what these things do to a can, what on earth are they doing to our teeth?” Bierman told Good Health.

To perform the experiment, Bierman put a tooth into a bottle of a popular energy drink, another into cola, a third in diet cola and the fourth into water as control.

After two weeks, the tooth placed in diet cola didn’t do much damage but it was stained while the tooth in the cola drink was stained nearly black.

The biggest damage was caused by the energy drink. The energy drink was a lot more destructive to the enamel than the cola drink.

“Even more concerning is that this was the sugar-free version of the energy drink. It’s very potent stuff,” Bierman added.

However, Biermam admitted the experiment wasn’t the same as consuming the drinks regularly but he insists the damage to the tooth can be the same in the long run if these drinks are consumed daily or almost every day.

Source:Elcrema

{A chemical found in tumors may help stop tumor growth, according to a new study.

Researchers at the University of Illinois at Chicago report that increasing expression of a chemical cytokine called LIGHT in mice with colon cancer activated the immune system’s natural cancer-killing T-cells and caused primary tumors and metastatic tumors in the liver to shrink.}

LIGHT is an immune-stimulating chemical messenger previously found to have low levels of expression in patients with colon cancer metastases.

The results are published in Cancer Research.

Colon cancer is the second-leading cause of cancer-related death in the U.S. and, despite advances in treatment, long-term survival of patients with liver metastases is rare.

“For most patients with colon cancer that has spread to the liver, current treatments are palliative and not curative,” says Dr. Ajay Maker, associate professor of surgery in the UIC College of Medicine and corresponding author on the paper. “And while studies have suggested that immunotherapy may be a promising approach for advanced cancers, the use of such treatments for advanced gastrointestinal metastases have not yet been very successful.”

Maker, a surgical oncologist, says that this study is exciting because it looks at an immunotherapy intervention for a previously unresponsive gastrointestinal cancer. The intervention, he says, essentially trains the immune system to recognize and attack the tumor, and to protect against additional tumor formation — a significant issue in colon cancer.

Maker and his colleagues established colon cancer tumors in a mouse model, in which the animals had an intact and unedited immune system. Once tumors were sizable, the mice were randomized into two groups — one group had the cytokine LIGHT turned on in the tumors, and the other served as a control group for comparison.

Tumors exposed to LIGHT showed an influx of T-cells that resulted in rapid and sustained diminishment in size, even after expression of the cytokine stopped. In mice with liver metastases, expression of LIGHT similarly provoked a potent immune response that resulted in a significant decrease in tumor burden.

“We demonstrated that delivery of a therapeutic immune-stimulating cytokine caused T-cells to traffic to tumors and to become activated tumor-killing cells,” Maker said. “This activity is especially exciting because it resulted in a profound anti-tumor immune response without any other chemotherapy or intervention. The treatment manipulates our natural defenses to fight off the tumor in the same way it has been trained to attack other foreign invaders in our body.”

“Not only did we find that LIGHT expression promoted tumor regression, upon further study we also identified the specific type of T-cell — CD8 — that was responsible for shrinking the tumor,” Maker said. “These findings are powerful and have great clinical potential.”

Co-authors on the paper are Guilin Qiao, Jianzhong Qin, Nicholas Kunda, Jed Calata, Dolores Mahmud, Peter Gann and Bellur Prabhakar of UIC; Yang-Xin Fu of the University of Texas Southwestern; and Steven Rosenberg of the National Cancer Institute.

The study was funded by grant number K08CA190855 from the National Cancer Institute, one of the National Institutes of Health.

Source:Science Daily

{Head injuries can harm hundreds of genes in the brain in a way that increases people’s risk for a wide range of neurological and psychiatric disorders, UCLA life scientists report.}

The researchers identified for the first time master genes that they believe control hundreds of other genes which are linked to Alzheimer’s disease, Parkinson’s disease, post-traumatic stress disorder, stroke, attention deficit hyperactivity disorder, autism, depression, schizophrenia and other disorders.

Knowing what the master genes are could give scientists targets for new pharmaceuticals to treat brain diseases. Eventually, scientists might even be able to learn how to re-modify damaged genes to reduce the risk for diseases, and the finding could help researchers identify chemical compounds and foods that fight disease by repairing those genes.

“We believe these master genes are responsible for traumatic brain injury adversely triggering changes in many other genes,” said Xia Yang, a senior author of the study and a UCLA associate professor of integrative biology and physiology.

Genes have the potential to become any of several types of proteins, and traumatic brain injury can damage the master genes, which can then lead to damage of other genes.

That process can happen in a couple of ways, said Yang, who is a member of UCLA’s Institute for Quantitative and Computational Biosciences. One is that the injury can ultimately lead the genes to produce proteins of irregular forms. Another is to change the number of expressed copies of a gene in each cell. Either change can prevent a gene from working properly. If a gene turns into the wrong form of protein, it could lead to Alzheimer’s disease, for example.

“Very little is known about how people with brain trauma — like football players and soldiers — develop neurological disorders later in life,” said Fernando Gomez-Pinilla, a UCLA professor of neurosurgery and of integrative biology and physiology, and co-senior author of the new study. “We hope to learn much more about how this occurs.”

The research appears in EBioMedicine, a journal published by Cell and The Lancet.

The researchers trained 20 rats to escape from a maze. They then used a fluid to produce a concussion-like brain injury in 10 of the rats; the 10 others did not receive brain injuries. When the rats were placed in the maze again, those that had been injured took approximately 25 percent longer than the non-injured rats to solve it.

To learn how the rats’ genes had changed in response to the brain injury, the researchers analyzed genes from five animals in each group. Specifically, they drew RNA from the hippocampus, which is the part of the brain that helps regulate learning and memory, and from leukocytes, white blood cells that play a key role in the immune system.

In the rats that had sustained brain injuries, there was a core group of 268 genes in the hippocampus that the researchers found had been altered, and a core group of 1,215 genes in the leukocytes that they found to have been changed.

“A surprise was how many major changes occurred to genes in the blood cells,” Yang said. “The changes in the brain were less surprising. It’s such a critical region, so it makes sense that when it’s damaged, it signals to the body that it’s under attack.”

Nearly two dozen of the altered genes are present in both the hippocampus and the blood, which presents the possibility that scientists could develop a gene-based blood test to determine whether a brain injury has occurred, and that measuring some of those genes could help doctors predict whether a person is likely to develop Alzheimer’s or other disorders. The research could also lead to a better way to diagnose mild traumatic brain injury.

More than 100 of the genes that changed after the brain injury have counterparts in humans that have been linked to neurological and psychiatric disorders, the researchers report. For example, 16 of the genes affected in the rats have analogs in humans, and those genes are linked to a predisposition for Alzheimer’s, the study reports. The researchers also found that four of the affected genes in the hippocampus and one in leukocytes are similar to genes in humans that are linked to PTSD.

Yang said the study not only indicated which genes are affected by traumatic brain injury and linked to serious disease, but also might point to the genes that govern metabolism, cell communication and inflammation — which might make them the best targets for new treatments for brain disorders.

The researchers now are studying some of the master genes to determine whether modifying them also causes changes in large numbers of other genes. If so, the master genes would be even more promising as targets for new treatments. They also plan to study the phenomenon in people who have suffered traumatic brain injury.

In a 2016 study, Yang, Gomez-Pinilla and colleagues reported that hundreds of genes can be damaged by fructose and that an omega-3 fatty acid called docosahexaenoic acid, or DHA, seems to reverse the harmful changes produced by fructose. One of the genes they identified in that study, Fmod, also was among the master regulator genes identified in the new research.

Not everyone with traumatic brain injuries develops the same diseases, but more severe injuries can damage more genes, said Gomez-Pinilla, who also is a member of UCLA’s Brain Injury Research Center.

Source:Science Daily

{An epidemiological analysis of data from more than 6,000 American and Canadian women with breast cancer finds that post-diagnosis consumption of foods containing isoflavones — estrogen-like compounds primarily found in soy food — is associated with a 21 percent decrease in all-cause mortality. This decrease was seen only in women with hormone-receptor-negative tumors, and in women who were not treated with endocrine therapy such as tamoxifen.}

The study, led by nutrition and cancer epidemiologist Fang Fang Zhang, M.D., Ph.D., from the Friedman School of Nutrition Science and Policy at Tufts University, was published March 6 in Cancer.

“At the population level, we see an association between isoflavone consumption and reduced risk of death in certain groups of women with breast cancer. Our results suggest, in specific circumstances, there may be a potential benefit to eating more soy foods as part of an overall healthy diet and lifestyle,” said Zhang, who is also the 2016-2017 Miriam E. Nelson Tisch Faculty Fellow at the Jonathan M. Tisch College of Civic Life and an adjunct scientist in nutritional epidemiology at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts.

“Since we only examined naturally occurring dietary isoflavone, we do not know the effect of isoflavone from supplements. We recommend that readers keep in mind that soy foods can potentially have an impact, but only as a component of an overall healthy diet,” she adds.

Isoflavones have been shown to slow the growth of breast cancer cells in laboratory studies, and epidemiological analyses in East Asian women with breast cancer found links between higher isoflavone intake and reduced mortality. However, other research has suggested that the estrogen-like effects of isoflavones may reduce the effectiveness of endocrine therapies used to treat breast cancer. Because of this double effect, it remains unknown whether isoflavone consumption should be encouraged or avoided by breast cancer patients.

In the current study, Zhang and her colleagues, including Esther John, Ph.D., senior cancer epidemiologist at the Cancer Prevention Institute of California, analyzed data on 6,235 American and Canadian breast cancer patients from the Breast Cancer Family Registry, a National Cancer Institute-funded program that has collected clinical and questionnaire data on enrolled participants and their families since 1995. Women were sorted into four quartile groups based on the amount of isoflavone they were estimated to have consumed, calculated from self-reported food frequency questionnaires. Mortality was examined after a median follow-up of 9.4 years.

The team found a 21 percent decrease in all-cause mortality among women in the highest quartile of intake, when compared to those in the lowest quartile. The association between isoflavone intake and reduced mortality was strongest in women with tumors that lacked estrogen and progesterone receptors. Women who did not receive endocrine therapy as a treatment for their breast cancer had a weaker, but still significant association. No associations were found for women with hormone-receptor-positive tumors and for women who received endocrine therapy.

While the study categorized women in the highest quartile as those who consumed 1.5 milligrams or more of isoflavone per day — equivalent to a few dried soybeans — the authors caution that individuals tend to underestimate their food intake when filling out questionnaires.

“The comparisons between high and low consumption in our study are valid, but our findings should not be interpreted as a prescription,” Zhang said. “However, based on our results, we do not see a detrimental effect of soy intake among women who were treated with endocrine therapy, which has been hypothesized to be a concern. Especially for women with hormone-receptor-negative breast cancer, soy food products may potentially have a beneficial effect and increase survival.”

The large size and diverse racial/ethnic makeup of the Breast Cancer Family Registry allowed the researchers to evaluate mortality risk across different subtypes of breast cancer and subgroups of patients, and adjust for confounding factors. However, the authors note that dietary isoflavone intake was correlated with socioeconomic and lifestyle factors, which may also play a role in lowering mortality. In particular, women who consumed higher levels of dietary isoflavone were more likely to be Asian Americans, young, physically active, more educated, not overweight, never smokers, and drink no alcohol. Although the team controlled for these factors in the analyses, the possibility of a partial confounding effect on the associations identified in the study cannot be ruled out.

“Whether lifestyle factors can improve survival after diagnosis is an important question for women diagnosed with hormone-receptor negative breast cancer, a more aggressive type of breast cancer. Our findings suggest that survival may be better in patients with a higher consumption of isoflavones from soy food,” John said.

Source:Science Daily

{The World Health Organisation (WHO) report has revealed that more than one in four deaths of children under five-years are attributable to unhealthy environments.}

According to the first WHO report dubbed,” Inheriting a Sustainable World Atlas on Children’s Health and the Environment” stated that a large portion of the most common causes of death among children aged one month to five- years are diarrhoea, malaria and pneumonia which are preventable by interventions known to reduce environmental risks, such as access to safe water and clean cooking fuels.

Dr Margaret Chan, the WHO Director-General, said: “A polluted environment is a deadly one particularly for young children.” adding that this is because their developing organs and immune systems, and smaller bodies and airways, make them especially vulnerable to dirty air and water.

She said harmful exposures can start in the mother’s womb and increase the risk of premature birth. Additionally, when infants and preschoolers are exposed to indoor and outdoor air pollution and second-hand smoke they have an increased risk of pneumonia in childhood, and a lifelong increased risk of chronic respiratory diseases, such as asthma. Exposure to air pollution may also increase their lifelong risk of heart disease, stroke and cancer.

The WHO report findings correspond with those of researchers from Makerere University Medical School which confirmed that in Uganda, pneumonia which is attributed to the unhealthy environment is a leading cause of death among children under five-years of age.

“Pneumonia deaths could be averted if caretakers recognised the danger signs and sought appropriate treatment promptly,” the finding from researchers at Makerere University Medical School read in part.

The research finding are derived from interviewing 278 caretakers in Mukono District Uganda, whose under-five children had suffered from probable pneumonia two weeks prior to the evaluation. Through structured questionnaires they assessed caretaker’s knowledge about danger signs among under-five children with pneumonia and the actions taken to manage probable pneumonia using descriptive statistics. They also conducted in-depth interviews with caretakers and community health workers.

{{Utility:}}

Top 5 causes of death in children under five-years linked to the environment
A companion report, Don’t pollute my future! The impact of the environment on children’s health, provides a comprehensive overview of the environment’s impact on children’s health, illustrating the scale of the challenge. Every year:
570 000 children under 5 years die from respiratory infections, such as pneumonia, attributable to indoor and outdoor air pollution, and second-hand smoke.

361 000 children under 5 years die due to diarrhoea, as a result of poor access to clean water, sanitation, and hygiene.

270 000 children die during their first month of life from conditions, including prematurity, which could be prevented through access to clean water, sanitation, and hygiene in health facilities as well as reducing air pollution.

200 000 deaths of children under 5 years from malaria could be prevented through environmental actions, such as reducing breeding sites of mosquitoes or covering drinking-water storage.

200 000 children under 5 years die from unintentional injuries attributable to the environment, such as poisoning, falls, and drowning.

Source:Daily Monitor

{People who suffer from depression should participate in yoga and deep (coherent) breathing classes at least twice weekly plus practice at home to receive a significant reduction in their symptoms.}

The findings, which appear in the Journal of Alternative and Complementary Medicine, provide preliminary support for the use of yoga-based interventions as an alternative or supplement to pharmacologic treatments for depression.

Major depressive disorder (MDD) is common, recurrent, chronic and disabling. Due in part to its prevalence, depression is globally responsible for more years lost to disability than any other disease. Up to 40 percent of individuals treated with antidepressant medications for MDD do not achieve full remission. This study used lyengar yoga that has an emphasis on detail, precision and alignment in the performance of posture and breath control.

Individuals with MDD were randomized to the high dose group, three 90-minute classes a week along with home practice, or the low dose group, two 90-minute classes a week, plus home practice. Both groups had significant decreases in their depressive symptoms and no significant differences in compliance. Although a greater number of subjects in the high dose group had less depressive symptoms, the researchers believe attending twice weekly classes (plus home practice) may constitute a less burdensome but still effective way to gain the mood benefits from the intervention.

“This study supports the use of a yoga and coherent breathing intervention in major depressive disorder in people who are not on antidepressants and in those who have been on a stable dose of antidepressants and have not achieved a resolution of their symptoms,” explained corresponding author Chris Streeter, MD, associate professor of psychiatry and neurology at Boston University School of Medicine and a psychiatrist at Boston Medical Center.

According to Streeter compared with mood altering medications, this intervention has the advantages of avoiding additional drug side effects and drug interactions. “While most pharmacologic treatment for depression target monoamine systems, such as serotonin, dopamine and norepinephrine, this intervention targets the parasympathetic and gamma aminobutyric acid system and provides a new avenue for treatment.”

Source:Science Daily

{Scientists have revealed for the first time how immature mouse immune cells, called T cells, choose which type of skills they will develop to fight malaria infection. Reported today in Science Immunology, researchers from the Wellcome Trust Sanger Institute, European Bioinformatics Institute and QIMR Berghofer Medical Research Institute, Australia, tracked individual T cells during infection with malaria parasites. They discovered a whole network of chemical conversations between different types of cells that influenced T cell specialisation.}

Using the latest single-cell genomics technology and computational modelling, the study also discovered genes within the T cells that may be involved in controlling antibody production during malaria infection. One of these, Galectin 1, encouraged development of a particular type of T cell when active. These genes are possible drug targets to boost immunity to malaria and other infections.

The immune system is extremely complex and responds to disease by developing specific types of immune cells. Two different types of T cell — T helper1 (Th1) and T follicular helper (Tfh) — develop and help fight infection. The researchers discovered that more Th1 cells were produced when a gene called Galectin 1 was active. These Th1 cells help remove parasites from the bloodstream and are needed early on in an infection, however for longer-term immunity, more Tfh cells are needed.

Dr Ashraful Haque, joint lead author from the QIMR Berghofer Medical Research Institute, Brisbane, Australia, said: “This is the first time that Galectin 1 acting inside T cells has been seen to influence Th1 fate, and has shown that Galectin 1 is a possible therapeutic target for malaria. An important next step will be to test many of the new gene targets identified by our studies, to see if they can be targeted by drugs to boost immunity to malaria.”

The exact molecules that encourage the T cells to develop into one or the other form are poorly understood. The researchers used single-cell RNA sequencing to take ‘snapshots’ of the active genes produced by each individual T cell after the mouse was infected with malaria. With these snapshots of data, the researchers identified all the different stages between immature T cells and fully specialised Th1 or Tfh cells.

Dr Sarah Teichmann, Head of Cellular Genetics at the Sanger Institute and joint lead author on the paper, said: “This is the first high resolution time-course of cells using a pathogen in mice, where we have used cutting edge genomics coupled with computational methods to reconstruct how cells evolve and develop over infection. With methods from machine learning, we have simplified really complex biological processes into something we can understand. This approach could be applied to resolve any biological developmental process.”

The team also developed a new computer modelling system called GPfates* which allowed them to see how all the cells related to each other. This uses methods from spatio-temporal statistics, to show which genes were switched on in each of the two distinct cell states (Th1 and Tfh).

Dr Oliver Stegle, joint lead author from the European Bioinformatics Institute, said: “Using genomics we uncovered the inter-cellular conversation that is taking place between immune cells such as monocytes and Th1 cells. This has not been seen before, and our data have allowed us to uncover tens or hundreds of new genes that may be involved in controlling the production of antibodies. Activity in these genes may help the body, for example in curing an infection, or may hinder by allowing cancerous cells to flourish. The principles and the computational methods we have developed here could be applied to future studies to explore these questions.”

Source:Science Daily

{Researchers from Charité — Universitätsmedizin Berlin have discovered a new way of developing painkillers. The team of researchers used computational simulation to analyze interactions at opioid receptors — the cell’s docking sites for painkillers. }

When used in an animal model, their prototype of a morphine-like molecule was able to produce substantial pain relief in inflamed tissues. However, healthy tissues remained unaffected, suggesting that the severe side effects currently associated with these types of painkillers might be avoided. This research has been published in the current issue of the journal Science.

Opioids are a class of strong pain killers. They are mainly used to treat pain associated with tissue damage and inflammation, such as that caused by surgery, nerve damage, arthritis or cancer. Common side effects associated with their use include drowsiness, nausea, constipation and dependency and, in some cases, respiratory arrest. “By analyzing drug-opioid receptor interactions in damaged tissues, as opposed to healthy tissues, we were hoping to provide useful information for the design of new painkillers without harmful side effects,” explains Prof. Dr. Christoph Stein, Head of the Department of Anesthesiology and Surgical Critical Care Medicine on Campus Benjamin Franklin. In cooperation with PD Dr. Marcus Weber from the Zuse Institute Berlin, and with the help of innovative computational simulations, the researchers were able to analyze morphine-like molecules and their interactions with opioid receptors. They were able to successfully identify a new mechanism of action, which is capable of producing pain relief only in the desired target tissues — those affected by inflammation.

Treating postoperative and chronic inflammatory pain should now be possible without causing side effects. Doing so would substantially improve patient quality of life. The study’s first authors, Dr. Viola Spahn and Dr. Giovanna Del Vecchio, explain: “In contrast to conventional opioids, our NFEPP-prototype appears to only bind to, and activate, opioid receptors in an acidic environment. This means it produces pain relief only in injured tissues, and without causing respiratory depression, drowsiness, the risk of dependency, or constipation.” After designing and synthesizing the drug prototype, the researchers subjected it to experimental testing. Using computer modeling, the researchers simulated an increased concentration of protons, thereby mimicking the acidic conditions found in inflamed tissues. “We were able to show that the protonation of drugs is a key requirement for the activation of opioid receptors,” conclude the authors.

Their findings, which may also apply to other types of pain, may even find application in other areas of receptor research. Thereby, the benefits of improved drug efficacy and tolerability are not limited to painkillers, but may include other drugs as well.

Source:Science Daily

{A female brain’s resident immune cells are more active in regions involved in pain processing relative to males, according to a recent study by Georgia State University researchers.}

The study, published in the Journal of Neuroscience, found that when microglia, the brain’s resident immune cells, were blocked, female response to opioid pain medication improved and matched the levels of pain relief normally seen in males.

Women suffer from a higher incidence of chronic and inflammatory pain conditions such as fibromyalgia and osteoarthritis. While morphine continues to be one of the primary drugs used for the treatment of severe or chronic pain, it is often less effective in females.

“Indeed, both clinical and preclinical studies report that females require almost twice as much morphine as males to produce comparable pain relief,” said Hillary Doyle, graduate student in the Murphy Laboratory in the Neuroscience Institute of Georgia State. “Our research team examined a potential explanation for this phenomenon, the sex differences in brain microglia.”

In healthy individuals, microglia survey the brain, looking for signs of infection or pathogens. In the absence of pain, morphine interferes with normal body function and is viewed as a pathogen, activating the brain’s innate immune cells and causing the release of inflammatory chemicals such as cytokines.

To test how this sex difference affects morphine analgesia, Doyle gave male and female rats a drug that inhibits microglia activation.

“The results of the study have important implications for the treatment of pain, and suggests that microglia may be an important drug target to improve opioid pain relief in women,” said Dr. Anne Murphy, co-author on the study and associate professor in the Neuroscience Institute at Georgia State.

The research team’s finding that microglia are more active in brain regions involved in pain processing may contribute to why the incidence rates for various chronic pain syndromes are significantly higher in females than males.

Source:Science Daily