Category: Health

{Having a healthy skin gives a woman the kind of glow that makes her the envy of others. It’s not impossible for a woman to have a beautiful skin; besides gene, it all depends on how well she takes care of herself.}

Every lady must observe these top 7 beauty rules if they want that healthy skin that glows.

1. Try as much as possible to protect yourself from the sun. The sun is probably the number one factor that can hurt a beautiful skin and cause wrinkles, patches, fine lines and sun spots.

According to the American Academy of Dermatology, the sun plays a major role in premature ageing of the skin.

2. Eat lots of fruits and vegetables. If you want that healthy skin that glows, then you must replace junk foods with fruits and vegetables. Fruits and vegetables are rich in nutrients that nourish your skin and antioxidants that help protect the skin.

3. Try as much as possible to sleep on your back. Sleeping with your face against the pillow can cause dark circles and patches around the eyes and face. It can restrict blood flow and result in poor blood circulation.

4. Wash your face every night. This will help remove the makeups and pollutants and other things that your skin might have collected during the day.

5. Moisturise your skin at least within 3 minutes of having your bath. It’ll help protect the skin from drying out and from the impact of the weather.

6. Avoid smoking; it doesn’t add any benefit to your life, rather it has so many detrimental effect on your skin. It could cause the skin to dry, damage the outer layer of the skin, constrict blood vessels, thereby depleting the skin of oxygen and vital nutrients.

7. Have enough sleep. All these tips mentioned above will be less effective if you don’t observe enough sleep. The quality of your sleep is very important. A 2015 study published in Clinical Experiments in Dermatology found that chronic poor sleep quality is associated with increased signs of intrinsic ageing, diminished skin barrier function and lower satisfaction with appearance.

Source:Elcrema

{A study from Massachusetts General Hospital (MGH) researchers has found that a pattern of gene variants associated with an “apple-shaped” body type, in which weight is deposited around the abdomen, rather than in the hips and thighs, increases the risk for type 2 diabetes and coronary heart disease, as well as the incidence of several cardiovascular risk factors. The report appears in the February 14 issue of JAMA.}

“People vary in their distribution of body fat — some put fat in their belly, which we call abdominal adiposity, and some in their hips and thighs,” says Sekar Kathiresan, MD, director of the MGH Center for Genomic Medicine, associate professor of Medicine at Harvard Medical School, and senior author of the JAMA report. “Abdominal adiposity has been correlated with cardiometabolic disease, but whether it actually has a role in causing those conditions was unknown. We tested whether genetic predisposition to abdominal adiposity was associated with the risk for type 2 diabetes and coronary heart disease and found that the answer was a firm ‘yes’.”

While several observational studies have reported greater incidence of type 2 diabetes and heart disease among individuals with abdominal adiposity, they could not rule out the possibility that lifestyle factors — such as diet, smoking and a lack of exercise — were the actual causes of increased disease risk. It also could have been possible that individuals in the early stages of heart disease might develop abdominal adiposity because of a limited ability to exercise. The current study was designed to determine whether body type really could increase cardiometabolic risk.

To answer that question, the research team applied a genetic approach called mendelian randomization, which measures whether inherited gene variants actually cause outcomes such as the development of a disease. Using data from a previous study that identified 48 gene variants associated with waist-to-hip ratio adjusted for body mass index — an established measure for abdominal adiposity — they developed a genetic risk score. They then applied that score to data from six major genome-wide association studies and to individual data from the U.K. Biobank — a total research group of more than 400,000 individuals — to determine any association between a genetic predisposition to abdominal adiposity and cardiometabolic disease and its risk factors.

The results clearly indicated that genetic predisposition to abdominal adiposity is associated with significant increases in the incidence of type 2 diabetes and coronary heart disease, along with increases in blood lipids, blood glucose and systolic blood pressure. No association was found between the genetic risk score and lifestyle factors, and testing confirmed that only the abdominal adiposity effects of the identified gene variants were associated with cardiometabolic risk.

“These results illustrate the power of using genetics as a method of determining the effects of a characteristic like abdominal adiposity on cardiometabolic outcomes,” says lead author Connor Emdin, DPhil, of the MGH Center for Genomic Medicine and the Cardiology Division. “The lack of association between the body type genetic risk score and confounding factors such as diet and smoking provides strong evidence that abdominal adiposity itself contributes to causing type 2 diabetes and heart disease.”

Emdin continues, “Not only do these results allow us to use body shape as a marker for increased cardiometabolic risk, they also suggest that developing drugs that modify fat distribution may help prevent these diseases. Future research also could identify individual genes that could be targeted to improve body fat distribution to reduce these risks.”

Source:Science Daily

{There’s a multi-billion-dollar industry devoted to products that fight signs of aging, but moisturizers only go skin deep. Aging occurs deeper — at a cellular level — and scientists have found that eating less can slow this cellular process.}

Recent research published in Molecular & Cellular Proteomics offers one glimpse into how cutting calories impacts aging inside a cell. The researchers found that when ribosomes — the cell’s protein makers — slow down, the aging process slows too. The decreased speed lowers production but gives ribosomes extra time to repair themselves.

“The ribosome is a very complex machine, sort of like your car, and it periodically needs maintenance to replace the parts that wear out the fastest,” said Brigham Young University biochemistry professor and senior author John Price. “When tires wear out, you don’t throw the whole car away and buy new ones. It’s cheaper to replace the tires.”

So what causes ribosome production to slow down in the first place? At least for mice: reduced calorie consumption.

Price and his fellow researchers observed two groups of mice. One group had unlimited access to food while the other was restricted to consume 35 percent fewer calories, though still receiving all the necessary nutrients for survival.

“When you restrict calorie consumption, there’s almost a linear increase in lifespan,” Price said. “We inferred that the restriction caused real biochemical changes that slowed down the rate of aging.”

Price’s team isn’t the first to make the connection between cut calories and lifespan, but they were the first to show that general protein synthesis slows down and to recognize the ribosome’s role in facilitating those youth-extending biochemical changes.

“The calorie-restricted mice are more energetic and suffered fewer diseases,” Price said. “And it’s not just that they’re living longer, but because they’re better at maintaining their bodies, they’re younger for longer as well.”

Ribosomes, like cars, are expensive and important — they use 10-20 percent of the cell’s total energy to build all the proteins necessary for the cell to operate. Because of this, it’s impractical to destroy an entire ribosome when it starts to malfunction. But repairing individual parts of the ribosome on a regular basis enables ribosomes to continue producing high-quality proteins for longer than they would otherwise. This top-quality production in turn keeps cells and the entire body functioning well.

Despite this study’s observed connection between consuming fewer calories and improved lifespan, Price assured that people shouldn’t start counting calories and expect to stay forever young. Calorie restriction has not been tested in humans as an anti-aging strategy, and the essential message is understanding the importance of taking care of our bodies.

“Food isn’t just material to be burned — it’s a signal that tells our body and cells how to respond,” Price said. “We’re getting down to the mechanisms of aging, which may help us make more educated decisions about what we eat.”

Source:Science Daily

{Scientists have warned men against wearing underpants to bed. This is because wearing underpants to bed can make the crotch area too warm.}

Men are being urged to go to bed naked as it could boost their chances of becoming a father.

Dr Brian Steixner, director of the Institute for Men’s Health at Jersey Urology Group told The Sun: “Your nether regions need to be just the right temperature in order to optimise sperm production.

“More bacteria makes for a higher likelihood that any chafed or irritated skin down there becomes infected.”

Sleeping naked helps lower the body temperature which increases a man’s sperm production by keeping his scrotum at a specific temperature.

Sleeping naked is also good for couples because skin-to-skin contact releases oxytocin in the brain which strengthens emotional bond.

Source:Elcrema

{Women have claimed for years that their bodies react differently whether they’re pregnant with a male or female baby. Some studies suggest that a baby’s sex could play a role in why some women report differences with morning sickness, cravings and other symptoms based on the sex of their baby.}

Now evidence, published in the February issue of the journal Brain, Behavior and Immunity, shows the sex of a baby is associated with pregnant women’s immune responses. Researchers from The Ohio State University Wexner Medical Center followed 80 pregnant women across the course of their pregnancy and examined whether women exhibited different levels of immune markers called cytokines based on fetal sex. Analyses were conducted on levels of cytokines in the blood and levels produced by a sample of immune cells that were exposed to bacteria in the lab.

“While women didn’t exhibit differences in blood cytokine levels based on fetal sex, we did find that the immune cells of women carrying female fetuses produced more pro-inflammatory cytokines when exposed to bacteria. This means that women carrying female fetuses exhibited a heightened inflammatory response when their immune system was challenged, compared to women carrying male fetuses,” said Amanda Mitchell, a postdoctoral researcher in the Institute for Behavioral Medicine Research at Ohio State’s Wexner Medical Center and principal investigator of the study.

Inflammation is a critical part of the immune response involved in wound healing and responses to viruses, bacteria and chronic illnesses. However, excessive inflammation is stressful to the body and can contribute to sickness-related symptoms, such as achiness and fatigue. While more research is needed, the heightened inflammation observed among women carrying female fetuses could play a role in why women tend to experience exacerbated symptoms of some medical conditions, including asthma, when carrying a female versus a male fetus.

“This research helps women and their obstetricians recognize that fetal sex is one factor that may impact how a woman’s body responds to everyday immune challenges and can lead to further research into how differences in immune function may affect how a women responds to different viruses, infections or chronic health conditions (such as asthma), including whether these responses affect the health of the fetus,” Mitchell said.

While maternal inflammation can affect outcomes related to the fetus, like timing of birth, more research is necessary to understand how fetal sex is associated with maternal inflammation. It’s possible the sex hormones or other hormones in the placenta affect maternal inflammation levels, Mitchell said.

“It’s important to think about supporting healthy immune function, which doesn’t necessarily mean boosting it — it’s problematic to have too little or too great of an immune response. That being said, research has shown that exercise supports healthy immune functioning, as does eating some foods, like leafy greens, and relaxing with activities like meditation. Of course, it’s always important to check with your healthcare provider before making any changes to your routine or diet,” she said.

Source:Science Daily

{Model kidney could replace animal, human testing.}

{Instead of running tests on live kidneys, researchers at Binghamton, University State University of New York have developed a model kidney for working out the kinks in medicines and treatments.
}
Developed by Assistant Professor Gretchen Mahler and Binghamton biomedical engineering alumna Courtney Sakolish PhD ’16, the reusable, multi-layered and microfluidic device incorporates a porous growth substrate, with a physiological fluid flow, and the passive filtration of the capillaries around the end of a kidney, called the glomerulus, where waste is filtered from blood.

“This is a unique platform to study interactions between drugs and cells or tissues, specifically in the kidney, where current models were lacking,” said Sakolish. “These platforms will, hopefully, in the future, be used as an animal alternative during pre-clinical testing to more accurately direct these studies toward successful results in humans.”‘

“This is tissue engineering, but not for the purpose or replacing an organ or tissue in a person,” said Mahler. “The idea is that we can recreate the major organ functions in a simplified way for use as a drug screening tool. Finding new drugs is very hard, expensive and inefficient. We hope that by using human cells in a physiological environment we can help to direct resources toward the most promising new drug candidates and determine that other new drug candidates will fail, faster.”

Results suggest that cells grown in the device exhibit more natural behaviors than when grown in traditional culturing methods, and the filtration by the glomerulus is necessary for healthy cell function.

“We found that the more complex, dynamic culturing conditions (like those used in this project) are necessary to accurately predict renal drug toxicity in human systems,” said Sakolish. “When we compared physiological renal function and drug toxicity in traditional static culturing against our new model, we found significant differences in the ways that cells behaved. In our platform, cells looked and acted like those that you would find in the body, showing more sensitive responses to drugs than traditional static culturing.”

Mahler said that while others have developed microfluidic models of the proximal tubule before, this is the first to offer glomerular filtration.

“This type of device uses human cells in a dynamic, more physiologic environment, potentially making it better at predicting the body’s response to drugs than animals (animal effectiveness studies often don’t translate to humans) or static cell cultures, which are the most commonly used preclinical screening tools,” said Mahler.

{Northwestern Medicine scientists have discovered a cell in the retina that may cause myopia when it dysfunctions. The dysfunction may be linked to the amount of time a child spends indoors and away from natural light.}

“This discovery could lead to a new therapeutic target to control myopia,” said Greg Schwartz, lead investigator and assistant professor of ophthalmology at Northwestern University Feinberg School of Medicine.

More than a billion people in the world have myopia, whose incidence is rising and is linked to how much time people spend indoors as children.

The newly discovered retinal cell — which is highly sensitive to light — controls how the eye grows and develops. If the cell instructs the eye to grow too long, images fail to be focused on the retina, causing nearsighted vision and a lifetime of corrective glasses or contact lenses.

“The eye needs to stop growing at precisely the right time during childhood,” Schwartz said.

It has long been long known the retina contains a signal to focus the image in the eye, and this signal is important for properly regulating eye growth during childhood.

“But for years no one knew what cell carried the signal,” Schwartz said. “We potentially found the key missing link, which is the cell that actually does that task and the neural circuit that enables this important visual function.”

Schwartz named the cell, “ON Delayed,” in reference to its slow responses to lights becoming brighter. The cell was unique among many other cell types tested in its exquisite sensitivity to whether an image was in focus.

He described the neural circuit as the diagram that reveals how this cell is wired to other cells in the retina to acquire this unique sensitivity.

How too much time indoors may trigger myopia

The indoor light spectrum has high red/green contrast, which activates these clusters of photoreceptors in the human eye, creating the equivalent of an artificial contrast image on the retina. It’s likely the human version of the ON Delayed retinal ganglion cell would be overstimulated by such patterns, causing aberrant over-growth of the eye, leading to myopia, Schwartz said.

The study will appear in the Feb. 20 print issue of Current Biology. It was published online Jan. 26.

To conduct the study, Schwartz and co-author Adam Mani, a postdoctoral fellow in ophthalmology at Feinberg, used microscopic glass electrodes to record electrical signals from cells in a mouse retina while presenting patterns of light on a digital projector.

The next goal is to find a gene specific to this cell. Then scientists can turn its activity up or down in a genetic mouse model to try to induce or cure myopia.

The study is part of Schwartz’s larger body of research to reverse engineer the retina by identifying new retinal cell types in mice. The retina has about 50 types of retinal ganglion cells, which together convey all the information we use to perceive the visual world. Each of these cells provides different visual information — such as color or motion — about any point in space.

Schwartz, who is funded by the National Institutes of Health (NIH), wants to identify the new cells by their specific function, analyze their genetic signatures and understand how the cells are interconnected within the retina and to their targets in the brain. His research could lead to gene therapy to treat blindness and to improve the function of artificial retinal prosthetics.

The article is titled “Circuit Mechanisms of a Retinal Ganglion Cell with Stimulus-Dependent Response Latency and Activation Beyond Its Dendrites.”

{A study published in JAMA Cardiology has added to growing evidence that electronic cigarettes (e-cigarettes) are not harmless.}

“Studies like this give further confirmation that e-cigarettes are not harmless,” said European Society of Cardiology cardiovascular prevention spokesperson Professor Joep Perk.

“If I was a minister of health I would put my efforts into public anti-smoking campaigns especially directed towards the younger generation, and not promote e-cigarettes as an alternative to smoking,” he continued. “There are studies also showing that people that start with e-cigarettes have a tendency to become persistent tobacco cigarette smokers as well.”

The 2016 European guidelines on cardiovascular disease prevention flagged up the need for further research on the long-term effects of e-cigarettes.

The current study included 23 habitual e-cigarette users (used most days for at least one year) and 19 non-users between the ages of 21 and 45 years. It found that habitual e-cigarette users were more likely than non-users to have increased cardiac sympathetic activity (increased adrenaline levels in the heart) and increased oxidative stress — known mechanisms by which tobacco cigarettes increase cardiovascular risk.

The authors said the findings “have critical implications for the long-term cardiac risks associated with habitual e-cigarette use” and “mandate a re-examination of aerosolized nicotine and its metabolites.” They added that causality could not be confirmed on the basis of this single, small study, and that further research into the potential adverse cardiovascular health effects of e-cigarettes is warranted.

“Nicotine stimulates the central nervous system, so it’s not at all surprising that people continuously taking nicotine get this sympathetic stimulation,” said Professor Perk. “This then might lead to irregular heartbeat and raised blood pressure, and probably has long-term deleterious effects on the blood vessel walls.”

“It is too large a step to say that these negative effects are proof that people are going to die early because they used e-cigarettes,” he continued. “To prove this you have to put people on e-cigarettes for 10 to 15 years and see how many die early — a study that will not be done for ethical reasons. The weakness of all studies in this field is that they are observational and small, and they look at indicators of vascular wall damage rather than incidence of cardiovascular disease or death.”

Professor Perk said that, even after this study, e-cigarettes could still be used to help people stop smoking tobacco cigarettes, but they should be used with caution and other methods should preferably be tried first.

He said: “E-cigarettes are one of the tools we have in nicotine replacement therapy but as clinicians we should be cautious of putting people on large amounts of central nervous system stimulant drugs. Other smoking cessation schemes, such as chewing gum or patches, always include the decision to taper off use and eventually stop. This is not in general the case with e-cigarettes, which tend to be seen as a replacement and not a weaning off nicotine addiction. In fact they prolong the addiction.”

“This is an area where we need more knowledge,” continued Professor Perk. “The more data we collect, the more it seems that nicotine replacement strategies that taper off and ultimately end nicotine use are the way to go.”

“At the end of the day the best thing is simply to prevent people ever getting into the vicinity of nicotine,” he concluded.

{Chemical recalibration of brain cells during sleep is crucial for learning, and sleeping pills may sabotage it.}

Studying mice, scientists at Johns Hopkins have fortified evidence that a key purpose of sleep is to recalibrate the brain cells responsible for learning and memory so the animals can “solidify” lessons learned and use them when they awaken — in the case of nocturnal mice, the next evening.

The researchers, all of the Johns Hopkins University School of Medicine, also report they have discovered several important molecules that govern the recalibration process, as well as evidence that sleep deprivation, sleep disorders and sleeping pills can interfere with the process.

“Our findings solidly advance the idea that the mouse and presumably the human brain can only store so much information before it needs to recalibrate,” says Graham Diering, Ph.D., the postdoctoral fellow who led the study. “Without sleep and the recalibration that goes on during sleep, memories are in danger of being lost.”

A summary of their study appears online in the journal Science on Feb. 3.

Diering explains that current scientific understanding of learning suggests that information is “contained” in synapses, the connections among neurons through which they communicate.

On the “sending side” of a synapse, signaling molecules called neurotransmitters are released by a brain cell as it “fires”; on the “receiving side,” those molecules are captured by receptor proteins, which pass the “message” along. If a cell receives enough input through its synapses, it fires off its own neurotransmitters.

More specifically, experiments in animals have shown that the synapses on the receiving neuron can be toggled by adding or removing receptor proteins, thereby strengthening or weakening them and allowing the receiving neuron to receive more or less input from nearby signaling neurons.

Scientists believe memories are encoded through these synaptic changes. But there’s a hitch in this thinking, Diering says, because while mice and other mammals are awake, the synapses throughout its brain tend to be strengthened, not weakened, pushing the system toward its maximum load. When neurons are “maxed out” and constantly firing, they lose their capacity to convey information, stymying learning and memory.

One possible reason that neurons don’t usually max out is a process that has been well-studied in lab-grown neurons but not in living animals, asleep or awake. Known as homeostatic scaling down, it is a process that uniformly weakens synapses in a neural network by a small percentage, leaving their relative strengths intact and allowing learning and memory formation to continue.

To find out if the process does occur in sleeping mammals, Diering focused on the areas of the mouse brain responsible for learning and memory: the hippocampus and the cortex. He purified proteins from receiving synapses in sleeping and awake mice, looking for the same changes seen in lab-grown cells during scaling down.

Results showed a 20 percent drop in receptor protein levels in sleeping mice, indicating an overall weakening of their synapses, compared to mice that were awake.

“That was the first evidence of homeostatic scaling down in live animals,” says Richard Huganir, Ph.D., professor of neuroscience, director of the Department of Neuroscience and lead author of the study. “It suggests that synapses are restructured throughout the mouse brain every 12 hours or so, which is quite remarkable.”

To learn specifically which molecules were responsible for the phenomenon, the team turned to a protein called Homer1a, discovered in 1997 by Paul Worley, M.D., professor of neuroscience, who was also part of the team conducting the new study. Studies showed that Homer1a — named for the ancient Greek author and the scientific “odyssey” required to identify it — is important for the regulation of sleep and wakefulness, and for homeostatic scaling down in lab-grown neurons.

Repeating his previous analysis of synaptic proteins, Diering indeed found much higher levels of Homer1a — 250 percent more — in the synapses of sleeping mice than awake mice. And in genetically engineered mice missing Homer1a, the previous decrease of synaptic receptor proteins associated with sleep was no longer present.

To sort out how Homer1a senses when the mice are sleeping or awake, the researchers looked to the neurotransmitter noradrenaline, which drives the brain to arousal and wakefulness. By blocking or enhancing noradrenaline levels, both in lab-grown neurons and in mice, the researchers confirmed that when noradrenaline levels were high, Homer1a stayed away from synapses; when it was low, it collected there.

To directly test whether the location of Homer1a was related to sleep, the team kept mice awake for four extra hours by placing them in an unfamiliar cage. Some then got two and a half hours of “recovery sleep.” As predicted, levels of Homer1a in the receiving synapses were much higher in the sleep-deprived mice than in those that got recovery sleep. That suggests, says Diering, that Homer1a is sensitive to an animal’s “sleep need,” not just what time of day it is.

Diering emphasizes that sleep need is controlled by adenosine, a chemical that accumulates in the brain as an animal stays awake, provoking sleepiness. (Caffeine, the world’s most widely consumed psychoactive drug, directly interferes with adenosine.) When mice were given a drug during sleep deprivation that blocks adenosine, Homer1a levels no longer increased in their synapses.

“We think that Homer1a is a traffic cop of sorts,” says Huganir. “It evaluates the levels of noradrenaline and adenosine to determine when the brain is sufficiently quiet to begin scaling down.”

As the final test of their hypothesis that scaling down during sleep is crucial for learning and memory, the researchers tested the mice’s ability to learn without scaling down. Individual mice were placed in an unfamiliar arena and given a mild electrical shock, either as they woke up or right before they went to sleep. Some mice then received a drug known to prevent scaling down.

When an undrugged mouse received a shock just before sleep, its brain went through the scaling-down process and formed an association between that arena and the shock. When placed in that same arena, those mice spent about 25 percent of their time motionless, in fear of another shock. When placed in a different unfamiliar arena, they froze sometimes, but only about 9 percent of their time there, probably because they were relatively good a telling the difference between the two unfamiliar arenas.

Expecting that drugged mice that couldn’t scale down during sleep would have weaker memories and therefore freeze less than undrugged mice, Diering was surprised that they were motionless longer (40 percent of their time) when returned to the arena where they were shocked. But the drugged mice were also motionless longer (13 percent of their time) when in a new arena. When the shock was given after the mice woke up, the drug made no difference in how long the mice froze in either arena, confirming that scaling down only occurs during sleep.

“We think that the memory of the shock was stronger in the drugged mice because their synapses couldn’t undergo scaling down, but all kinds of other memories also remained strong, so the mice were confused and couldn’t easily distinguish the two arenas,” says Diering. “This demonstrates why ‘sleeping on it’ can actually clarify your ideas.”

“The bottom line,” he says, “is that sleep is not really downtime for the brain. It has important work to do then, and we in the developed world are shortchanging ourselves by skimping on it.”

Huganir says that sleep is still a big mystery. “In this study, we only examined what goes on in two areas of the brain during sleep. There are probably equally important processes happening in other areas, and throughout the body, for that matter,” he adds.

Among the events that require further exploration is how learning and memory are affected by sleep disorders and other diseases known to disrupt sleep in humans, like Alzheimer’s disease and autism. Huganir also says that benzodiazapines and other drugs that are commonly prescribed as sedatives, such as muscle relaxants and other sleep aids, are known to prevent homeostatic scaling down and are likely to interfere with learning and memory, though that idea has yet to be tested experimentally.

Other authors of the report include Raja Nirujogi, Richard Roth and Akhilesh Pandey of the Johns Hopkins University School of Medicine.

This work was supported by grants from the Canadian Institutes for Health Research, the Johns Hopkins Center for Proteomics Discovery, the National Institutes of Health Office of the Director (S10OD021844) and the National Institute of Mental Health (5P50MH100024).