Diabetes drug increases the weight of fetus

When pregnant women take the common diabetes medication metformin throughout pregnancy, it can positioned their kids at increased hazard of having weight problems or obese. Many pregnant women are taking metformin to deal with gestational diabetes or polycystic ovary syndrome PCOS. PCOS increases the risk of developing diabetes and other metabolic problems.

When pregnant women with PCOS or gestational diabetes take metformin, it crosses the placenta and passed to the fetus. According to Liv Guro Engen Hanem, M.D., of the Norwegian University of Science and Technology in Trondheim, Norway, the children of pregnant women who took metformin or placebo during pregnancy are at risk of weight gain.

Researchers invited parents of 292 children who participated in previous randomized scientific trials to be part of the study. In the preceding trials, pregnant women with PCOS were assigned to take either metformin or a placebo during pregnancy, the researchers wound up reviewing frame mass index BMI and other measurements for 161 children born following the advance studies.

At age four, the children whose mothers had been randomized to metformin at some point of being pregnant tended to weigh greater than the children whose mother took the placebo despite the fact that metformin did not appear to have an effect on birth weight, the trend became apparent whilst children reached six months of age. At age four, the children in metformin group had higher BMI scores and were much more likely to satisfy the criteria for weight problems or overweight than children in placebo group.
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Cannabis substance reduces seizures

Epilepsy is a disorder that causes unprovoked, recurrent seizures. Seizure is a sudden electrical activities in the brain.  Some patients treated for epilepsy continue to have seizures after the treatment.

Cannabidiol (CBD), one of the many active compounds in the cannabis (marijuana) plant can be effective for treating epilepsy. Purified CBD is being tested, but artisanal formulations of CBD (oils) are already available and being used by some patients.

To evaluate the efficacy of artisanal CBD for patients with epilepsy, Robert Carson, MD, PhD, and colleagues performed a retrospective study of medical records obtained from Vanderbilt's BioVU resource.

They found that among 108 pediatric patients with epilepsy, 39 percent who added CBD oil to their treatments experienced a 50 percent reduction in seizures, 10 percent became seizure-free, and 22 percent were able to decrease doses of other anti-seizure medications.
CBD oil can be used for treating seizure reduction with few side effects.
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Apadaz for treating acute pain

FDA approves Apadaz (benzhydrocodone and acetaminophen) for the short-term management of acute pain. It contains an opioid agonist and acetaminophen and is indicated for the short-term (not more than 14 days) management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate.

Because of the risks of addiction, abuse, and misuse with opioids, even at recommended doses, reserve Apadaz for use in patients for whom alternative treatment options have not been or are not expected tolerated, or have not provided adequate analgesia, or are not expected to provide adequate analgesia.

Apadaz is contraindicated in patients with: significant respiratory depression; acute or severe bronchial asthma in an unmonitored setting or in absence of resuscitative equipment; known or suspected gastrointestinal obstruction, including paralytic ileus; and hypersensitivity to hydrocodone or acetaminophen.

Apadaz contains benzhydrocodone, a Schedule II controlled substance. Apadaz can be abused and is subject to misuse, addiction, and criminal diversion. Potential risks associated with Apadaz include addiction, abuse, and misuse, life-threatening respiratory depression, neonatal opioid withdrawal syndrome, risks of concomitant use or discontinuation of cytochrome P450 CYP3A4 inhibitors and inducers, acetaminophen hepatoxicity risks from concomitant use with benzodiazepines or other CNS depressants.

Others are risk of life-threatening respiratory depression in patients with chronic pulmonary disease or in elderly, cachectic, or debilitated patients, adrenal insufficiency, severe hypotension, serious skin reactions, risks of use in patients with increased intracranial pressure, brain tumors, head injury, or impaired consciousness, hypersensitivity/anaphylaxis, risks of use in patients with gastrointestinal conditions, risk of use in patients with seizure disorders, and withdrawal, risks of driving and operating machinery.
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Urine test for detecting aging

Researchers find that a substance indicating oxidative damage increases in urine as people get older. Aging Neuroscience described a way to measure levels of this marker in human urine samples. The new marker potentially provides a method to measure how much human body has aged-biological rather than chronological age.

Everyone born in the same year has the same chronological age,  the bodies of different people age at different rates. This means that the risk of many diseases increases with age, the link between age in years and our health and lifespan is relatively loose. Many people enjoy long lives, relatively free of disease, while others suffer chronic illness and premature death.

The rate of cellular damage can vary from person to person, and may be dictated by genetics, lifestyle and the environment we live in. This cellular damage may be a more accurate indication of  biological age than the number of years. Measuring biological age could predict the risk of developing age-related diseases and death.

One mechanism thought to underlie biological aging involves a molecule vital to human survival- oxygen-the free radical theory of aging. Oxygen by-products produced during normal metabolism can cause oxidative damage to biomolecules in cells, such as DNA and RNA," explains Jian-Ping Cai, a researcher involved in the study. "As we age, we suffer increasing oxidative damage , and so the levels of oxidative markers increase in our body."

One such marker, with the catchy name of 8-oxo-7,8-dihydroguanosine-or 8-oxoGsn for short-results from oxidation of a crucial molecule in our cells called RNA. In previous studies in animals, Cai and colleagues found that 8-oxoGsn levels increase in urine with age. To see if this is true for humans as well, the researchers measured 8-oxoGsn in urine samples from 1,228 Chinese residents aged 2-90 years old, using a rapid analysis technique called ultra-high-performance liquid chromatography. Age-dependent increase in urinary 8-oxoGsn in participants 21 years old and older."

Therefore, urinary 8-oxoGsn is promising as a new marker of aging. Levels of 8-oxoGsn were roughly the same between men and women, except in post-menopausal women, who showed higher levels. This may have been caused by the decrease in estrogen levels that happens during menopause, as estrogen is known to have anti-oxidant effects. Urinary 8-oxoGsn may reflect the real condition of human body better than chronological age, and may help us to predict the risk of age-related diseases.
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Depression linked to brain inflammation

Years of depression can cause brain inflammation that has been linked to degenerative diseases like Alzheimer's and Parkinson's, an analysis of brain-changes among people whose depression lasted more than 10 years, done by the Canadian Centre for Addiction and Mental Health, suggested doctors may need to treat both depression and inflammation in these patients.

The average, untreated bout of depression typically lasts a few months, according to Harvard University. Everyone's symptoms vary in type, severity, and duration. Depression may look like irritability or simply a 'low mood.' But the staying power of depression may make it even more difficult to diagnose, as years of the disorder come to be seen as 'normal' for the person suffering the symptoms.

This may be why the average age of diagnosis for persistent depressive disorder (PDD) is relatively late, at 31 years old. The condition is also known to affect eating habits and experiences. Some tend to overeat when they are depressed, others lose their appetites, and still others will experience upset stomachs.

A high number of physical complaints may also be, in some cases, a warning sign that someone is depressed or in the throes of another mental health issue. Depression typically involves a shortage of serotonin, a neurochemical that nerve cells use to communicate a command for blood vessels to constrict. This is particularly important to the way that the digestive tract functions, as well as to the experience of pain.

Depression is a physical illness that could be treated with anti-inflammatory drugs, an overactive immune system may trigger the mental health condition by causing widespread inflammation that leads to feelings of hopelessness and unhappiness. The immune system may fail to 'switch off' after an illness or traumatic event. Previous research has shown people who suffer severe emotional trauma have signs of inflammation, which suggests their immune system is constantly 'fired-up'.

Researchers from the Center for Addiction and Mental Health (CAMH) found evidence that longer bouts of depression increased brain inflammation. To determine whether or not the duration of depression made a difference for its inflammatory effects, the research team, led by senior study author Dr Jeff Meyer of CAMH's Campbell Family Mental Health Research Institute recruited three groups of 25 people.

The first group had experienced more than a decade of depression, the second had experienced less than a decade, and the third had never experienced any depression, by their own reports. The difference between the PDD sufferers and the other two groups was dramatic. Those who had been depressed for more than 10 years had 30 percent more of a protein marker of brain-inflammation than those who had experienced depression, but for shorter amounts of time.

Their inflammation levels were also higher than the control group that had never been depressed. Greater inflammation in the brain is a common response with degenerative brain diseases as they progress, such as with Alzheimer's disease and Parkinson´s diseases.
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Low magnesium levels makes Vitamin D ineffective

Vitamin D can't be metabolized without sufficient magnesium levels. Without magnesium, Vitamin D is not really useful or safe," says study co-author Mohammed S. Razzaque, MBBS, PhD, a professor of pathology at Lake Erie College of Osteopathic Medicine. Razzaque explains that consumption of Vitamin D supplements can increase calcium and phosphate levels even if Vitamin D is deficient. People may suffer from vascular calcification if their magnesium levels aren't high enough to prevent the complication.

Patients with optimum magnesium levels require less Vitamin D supplementation to achieve sufficient Vitamin D levels. Magnesium also reduces osteoporosis, helping to mitigate the risk of bone fracture that can be attributed to low levels of Vitamin D. Deficiency in either of these nutrients is reported to be associated with various disorders, including skeletal deformities, cardiovascular diseases, and metabolic syndrome.

While the recommended daily allowance for magnesium is 420 mg for males and 320 mg for females. Magnesium status is low in people who consume processed foods that are high in refined grains, fat, phosphate, and sugar. Consuming an optimal amount of magnesium may lower the risks of Vitamin D deficiency, and reduce the dependency on Vitamin D supplements.

Magnesium is the fourth most abundant mineral in the human body after calcium, potassium, and sodium. Foods high in magnesium are almonds, bananas, beans, broccoli, brown rice, cashews, egg yolk, fish oil, flaxseed, green vegetables, milk, mushrooms, nuts, oatmeal, pumpkin seeds, sesame seeds, soybeans, sunflower seeds, sweet corn, tofu, and whole grains.
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Talk therapy for opioid crisis

Recent study found people who received psychotherapy, such as simplified pain education and cognitive behavioral therapy, had a greater reduction in pain intensity than those who received usual care such as opioids and other pain medications. Opioids are commonly prescribed for chronic pain.

The new study, conducted by researchers from the University of Alabama, suggests talk therapy could provide a new approach to pain management. 'We need more than just medication and surgery for chronic pain because they do not eradicate the problem or increase physical function,' Dr Beverly Thorn, professor of clinical health psychology.

For the study, Dr Thorn and her colleagues collected data from 290 patients. They either received cognitive-behavioral therapy (CBT), simplified pain education (EDU) or usual care. CBT and EDU therapies were delivered in 10 weekly 90-minute group sessions, with all information and materials modified to be accessible to patients reading at or even below the fifth grade level.

Researchers found that CBT and EDU interventions significantly improved pain and physical function between pre- and post-treatment. Patients enrolled in the talk therapies decreased their pain ratings by 1.5 points, which met the threshold of being a 'clinically meaningful effect.'
These talk therapies were so effective in reducing pain because physical issues are also psychological. Pain involves emotions and thoughts, and all of these are processed by the brain.
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Daffodils can fight cancer

A research describes the anti-cancer effects of a natural alkaloid extracted from Daffodils. Led by Denis Lafontaine, affiliated with the Faculty of Sciences at the ULB, the researchers have discovered that this compound triggers the activation of an anti-tumoral surveillance pathway.

 The researchers extracted a natural anti-cancer compound from Daffodils (Amaryllidaceae Narcissus). They established that this compound, an alkaloid named haemanthamine, binds to the ribosome. Ribosomes are nanomachines essential to the survival of humans cells because they synthesize all the required proteins. To sustain their unrestrained growth, cancer cells rely on increased protein synthesis: they are therefore particularly sensitive to treatments that inhibit the production and the function of ribosomes.

Haemanthamine blocks the production of protein by ribosomes, thus slowing growth of cancer cells. Haemanthamine also inhibits the production of these nanomachines in the nucleolus (the "ribosome factory"): this nucleolar stress triggers the activation of an anti-tumoral surveillance pathway leading to the stabilization of the protein p53 and to the elimination of cancer cells.

This study provides a molecular explanation to the anti-tumoral activity of Daffodils used for centuries in folk medicine. Haemanthamine belongs to a large family of therapeutic molecules of natural origin: numerous other alkaloids, used in human health, are extracted from plants, such as morphine (potent pain killer), quinine (anti-malarial agent), and ephedrine (anti-asthmatic).
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Anxiety can help memory

According to  a study from the University of Waterloo, anxiety can help people to remember things. The study of undergraduate students found that manageable levels of anxiety actually aided people in being able to recall the details of events. It also found that when anxiety levels got too high or descended into fear, it could lead to the colouring of memories where people begin to associate otherwise neutral elements of an experience to the negative context.

There is an optimal level of anxiety that is going to benefit memory, high levels of anxiety can cause people to reach a tipping point, which impacts their memories and performance. The study saw 80 undergraduate students from the University of Waterloo (64 females) complete the experiment. Half of the participants were randomly assigned to a deep encoding instruction group while the other half were randomly assigned to a shallow encoding group. All participants completed the Depression Anxiety Stress Scales.

It was discovered that individuals high in anxiety showed a heightened sensitivity to the influences of emotional context on their memory, with neutral information becoming tainted, or coloured by the emotion with which it was associated during encoding. Thinking about emotional events or about negative events might put the mind in a negative mindset that can change way of perceiving the environment.
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Antibiotics linked to higher death rate

A common antibiotic used to treat infections could be deadly for heart disease patients years after taking the drug. Clarithromycin, sold under the brand name Biaxin, is used to treat many skin, ear, sinus and lung infections.

People suffering from heart disease that took a two-week course of it had a significantly higher risk of heart attack or sudden death a year or more after they were treated for infection.

Clarithromycin belongs to a family of antibiotics called macrolides, which fight infections by blocking protein production in bacteria. Both clarithromycin and azithromycin-another common drug in the same family, sold as Z-Pak-are broad-spectrum antibiotics.

Respiratory infections have been shown, in some studies, to raise the risk of heart attack by as much as 17 percent, so it is key that heart disease patients get effective treatment for them quickly, but the FDA's trial suggests that clarithromycin could pose a similar risk to infection.
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Autoimmune kidney disease

Monash researchers have solved a mystery, revealing how certain immune cells work together to instigate autoimmune kidney disease.The study, led by Professor Michael Hickey and Professor Richard Kitching from Monash University's Centre for Inflammatory Diseases. In glomerulonephritis, an immune disease of the kidney, rogue immune cells damage the kidney via a misdirected inflammatory attack.

Special cells called monocytes continuously patrol the glomeruli by crawling within its blood vessels. Monocytes are very good at 'picking up and removing rubbish' and being on the lookout for signs of infection and tissue injury. However in autoimmunity, some immune cells in the circulation are highly reactive to molecules picked up in the kidney.

Patrolling monocytes can display these molecules to the reactive immune cells in the bloodstream, resulting in the rogue cells remaining in the kidney and turning on an unnecessary and damaging inflammatory attack. This autoimmune damage to the kidney can severely impact on the normal function of the kidney, if left untreated.

 This damage occurs while the cells are moving around in the kidney blood vessels. This process, known as intravascular antigen recognition, has never been described before for the key helper T cells that direct and control the immune response.
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Helping the immune system thwart infections

Yale researchers have developed a set of synthetic molecules that may boost the strength of a key, virus-fighting protein. The protein, RIG-I, is an important sensor in the immune system of humans and other animals. It recognizes and responds to viral RNA by surrounding it, latching onto it, and launching the immune system into action.

The Yale team, led by biologists Anna Pyle and Akiko Iwasaki, has designed molecules that jump-start the process. These synthetic, stem-loop RNA (SLR) molecules can be visualized as short cords with a knot at one end. The configuration enables the SLRs to bind with RIG-I molecules in a way that prompts an aggressive response.

"When you tickle RIG-I with this small, RNA hairpin, it alerts the body that it's time to respond," said Pyle, professor of molecular, cellular, and developmental biology, and of chemistry. This gives a tool that can help with everything from the design of better vaccines to better antivirals and anti-cancer therapies.The new study represents the first time scientists have been able to specifically manipulate and analyze the RIG-I biosensor in a living animal-mice.
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Anesthesia may triggers asymptomatic brain changes

Patients who were given general anesthesia before surgery performed slightly worse on memory tests, this was due to cognitive changes in the brain related to immediate memory, or the ability to remember information over a brief period. 'The cognitive changes after surgery are small-probably asymptomatic and beneath a person's awareness,' said senior author Dr Kirk Hogan, a professor of anesthesiology at the University of Wisconsin-Madison.

For the study, Dr Hogan and his colleagues measured memory and executive function in 964 participants, with the average age of 54, who had no signs of Alzheimer's disease, dementia, or cognitive impairment before surgery. Of the participants, 312 of them had at least one surgical procedure performed and 652 of them did not. Researchers found there was a decline in immediate memory over the course of four years in participants who had surgery.

Memory became abnormal in 18 percent of those who had at least one surgical procedure compared with 10 percent of those who had not. Regarding the working memory test, surgery and anesthesia were associated with a decline in immediate memory by one point out of a possible maximum test score of 30 points. They found no differences in other measures of memory and executive function between those who had surgery and their counterparts.

 Patients having surgery and anesthesia are likely to experience impaired performance on neuropsychological tests of memory and executive function, an association that might be causal. Researchers found the activity of memory loss receptors remains high long after the drugs have been eliminated from the patient's body. Other risk factors like the sort of disease or illness a person have could impact brain function. Diseases like hypertension and diabetes may also be responsible for cognitive decline in patients who have had surgery.
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Genetic defect may cause rare movement disorders

A Massachusetts General Hospital (MGH)-led research team has found that a defect in transcription of the TAF1 gene may be the cause of X-linked dystonia parkinsonism (XDP), a rare and severe neurodegenerative disease. Symptoms begin around age 40 with dystonia-involuntary muscle contractions that can force the body into abnormal, sometimes twisted positions and eventually proceed to Parkinson's-like symptoms, such as slowness of movement and a shuffling gait. Patients become progressively more disabled as the disease progresses and often die from complications such as infections or pneumonia.

Individuals with XDP share seven DNA sequence changes, which cluster within a region of the X-chromosome that includes the TAF1 gene. These sequence changes have always appeared to be inherited together. The largest genomics study ever performed for XDP, analyzing a total of 792 DNA samples from individuals with XDP and their unaffected relatives, as well as historical samples from studies dating back to the initial descriptions of the disease.

The analysis of these samples revealed a far greater genetic diversity among XDP patients than was previously known. While most shared a total of 54 unique sequence changes in a collection of variants known as a haplotype, in some individuals the haplotype had been broken apart due to genetic recombination. By comparing these recombination events, it was possible to narrow the disease-causing genomic segment to a smaller region that contained only the TAF1 gene.

Researchers reprogramed skin cells from patients with XDP and their healthy relatives back into stem cells, which differentiated into neural progenitor cells and then mature neurons. The team used RNA sequencing to characterize TAF1 expression patterns and found a defect in how the DNA sequence is transcribed into RNA in neural cells from XDP patients. In those cells, a portion of the TAF1 RNA appeared to terminate prematurely, which reduced expression of the full-length RNA. The truncated TAF1 RNA ended close to a known XDP-specific sequence variants - a large DNA insertion known as a retrotransposon.

 To determine whether the retrotransposon caused the transcriptional defect, t used genome they used editing tools to remove the sequence, which restored RNA transcription and normalized TAF1 expression. In a separate study, they analyzed the sequence of the retrotransposon in patients with XDP and found that it contained a segment of repetitive DNA that was longer in patients who developed symptoms at an earlier age and shorter in those whose symptoms appeared later.
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Beetroot for treating heart failure

Beetroot juice supplements may enhance exercise capacity in patients with heart failure, according to a new proof-of-concept study. The study examined the impact of dietary nitrate in the form of beetroot juice supplements on the exercise capacity of eight heart failure patients with reduced ejection fraction, a condition in which the heart muscle doesn't contract effectively and can't get enough oxygenated blood to the body.

Researchers found that the beetroot supplement resulted in significant increases in exercise duration, peak power and peak oxygen uptake while exercising. The improvements were not accompanied by any changes in the breathing responses of the patients, and there was no change in their exercise efficiency, a measure of how much external work a person gets for a certain input of energy.

Abnormalities in aerobic exercise responses play a major role in the disability, loss of independence and reduced quality of life that accompany heart failure, elevations in ventilatory demand and decreases in peak oxygen uptake are highly predictive of mortality in patients with heart failure. Dietary supplementation may be a valuable addition to treatment for exercise intolerance among heart failure patients with reduced ejection fraction.
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Impacts of genetics on snacking patterns

Researcher Elie Chamoun investigated whether genetic variants in taste receptors related to sweet preference, fat taste sensitivity and aversion to bitter green leafy vegetables influence the snacks chosen by children. He found that nearly 80 per cent of children in the study carried at least one of these potential at-risk genotypes that could predispose them to poor snacking habits.

Chidren are eating a lot more snacks now than they used to, looking at how genetics can be related to snacking behaviour, it  is important to understanding increased obesity among children, the study looked at connections between the genes of the three at-risk taste receptors and linked them to snacking patterns among children.

The study entailed tracking the day-to-day diets of children and found that one-third of the children's diets were made up of snacks, children with a sweet tooth, who have the gene related to sweet taste preference, ate snacks with significantly more calories from sugar. The children with the genetic variant related to fat taste sensitivity were found to consume snacks with higher energy density.

People with this genetic variant may have low oral sensitivity to fat and therefore consume more fatty foods without sensing it. Higher-energy density snacks, such as cookies with lots of sugar and fat, have a higher number of calories for their weight. The children with the genetic variant related to avoiding bitter vegetables also consumed snacks with high energy density.
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Anti-addiction medication

Drug addiction continues to plague vast numbers of people across the world, destroying and ending lives, while attempts to develop more effective pharmaceutical addiction treatments continue.
Vigabatrin is an anti-epilepsy medication approved by the Food and Drug Administration that has also been shown to be effective against addiction to cocaine, nicotine, methamphetamine, heroin and alcohol in animal models.

In humans, vigabatrin eliminates cocaine addiction in 28 percent of patients. It works by blocking an enzyme-aminobutyric acid (GABA) aminotransferase, which breaks down GABA. The result is higher levels of this neurotransmitter in the brain and diminished narcotic-activated release of dopamine. Long-term vigabatrin therapy can have serious side effects however, causing eye damage in up to 40 percent of those treated.

In previous work, the researchers designed a compound, CPP-115, that is 186 times more efficient in inactivating GABA aminotransferase than vigabatrin. In this study, they used computational molecular dynamics simulations of CPP-115 in complex with the enzyme to develop a new and improved agent with 10 times greater efficiency.

The drug should also be less likely to cause side effects, as it has fewer off-target activities in in vitro tests. In initial rat experiments, the new compound was far better at blocking dopamine release after a cocaine or nicotine stimulus than CPP-115.
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Links between depression and arginine levels

People suffering from major depressive disorder, MDD, have reduced arginine levels, a new study from the University of Eastern Finland shows. Arginine is an amino acid which the body uses to produce nitric oxide. Nitric oxide is a nervous system and immune defence mediator, and it also plays a role in vascular regulation.

The global arginine bioavailability ratio, GABR, is an indicator of the body's arginine levels, and the ratio has previously been used to measure the body's capacity to produce nitric oxide. Reduced arginine bioavailability is also known to be an independent risk factor of cardiovascular diseases. The study shows that people suffering from MDD have reduced arginine bioavailability.

"It is possible that depression-induced inflammatory responses lead to reduced arginine levels. This may result in insufficient production of nitric oxide for the needs of the nervous system and circulation. However, we don't know yet what exactly causes reduced arginine bioavailability in people with depression," says Doctoral Student Toni Ali-Sisto, the lead author of the study.

The research carried out by the University of Eastern Finland and Kuopio University Hospital involved 99 adults with diagnosed major depressive disorder and 253 non-depressed controls. The concentrations of three amino acids, namely arginine, citrulline and ornithine, were analysed from their fasting glucose samples, and this data was used to calculate their GABRs. Symmetric and asymmetric dimethylarginine concentrations were also measured, as they both play a role in the production of nitric oxide.

The findings were then compared between the depressed and the non-depressed controls. The study also analysed whether these concentrations changed in people with depression during a follow-up of eight months, and whether remission of depression had an effect on the concentrations. The study shows that people with depression have reduced arginine bioavailability, this doesn't mean that taking an arginine supplement would protect against depression.

People with depression had weaker arginine bioavailability than their non-depressed controls. The study did not find significant differences in the symmetric and asymmetric dimethylarginine concentrations. The use of anti-depressants or anti-psychotics did not affect the concentrations, either. Contrary to the researchers' expectations, there were no clear differences in the concentrations measured from people who had recovered from depression and people who remained depressed. Arginine bioavailability was slightly higher in people who had recovered from depression than in people who remained depressed.
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Hormone that support early pregnancy

Scientists have discovered a fertility hormone that prepares the womb's lining for pregnancy. The discovery made by testing tissue from women aged in their forties could help scientists develop ways to improve fertility. Each month, as part of the menstrual cycle, hormones send chemical signals to cells in the womb lining to create conditions to support pregnancy.

Fertilised eggs are extremely sensitive to changes in the womb lining, but the exact environment needed for healthy implantation is unknown. The hormone helps prime cells for implantation, a vital stage in early pregnancy when a fertilised egg attaches to the womb lining. Researchers at the University of Edinburgh tested the effects of a hormone known as DHEA on healthy tissue donated by women undergoing unrelated surgery.

 DHEA may boost pregnancy, rates in women trying to conceive naturally or through IVF. They found that treating womb lining cells with DHEA in a dish doubled the level of key proteins associated with healthy implantation in the tissue. DHEA treatment also increased the production of active androgens hormones found in high levels in men.

The study also suggests that levels of DHEA-which are known to decline significantly with age could play a role in infertility in later life. A fertilised egg will implant only if the conditions are just right and DHEA and androgens might improve this environment in cells.
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How to stop snoring

Research has revealed that people who snore have obstructive sleep apnea, which could increase the risk of developing heart disease. Snoring can be minimized or stopped in different ways. Sleeping on  side stops the base of  tongue and soft palate from collapsing to the back wall of throat that usually happens when sleeping on the back. This usually results in a vibrating sound when a person is asleep.

If sleeping on the side is difficult, a body pillow or taping tennis balls to the back of pyjamas can be a solution. Losing weight can help people who have recently gained weight and have started to snore as a result. Thin people do snore, but weight gain can occasionally squeeze the diameter of the throat, again causing it to collapse during sleep.

Drinking alcohol four or five hours before sleeping can make snoring worse and louder as it can reduce the resting tone of the muscle in the back of the throat. Some people who do not usually snore can sometimes snore after drinking. Lack of sleep can also play a significant part in the increase of snoring as, when a tired person goes into a deep sleep, muscles become floppier.

Opening nasal passages can minimize snoring if you have  cold or if your nose is blocked. A hot shower, a neti pot or nasal strips can help clear passages before bed. Replacing pillows can reduce allergens and dust mites that are present in the bedroom that may be contributing to snoring.

Sleep apnea, or obstructive sleep apnea OSA is a long-term condition and may require lifelong treatment for people who suffer from it. In most cases, this would mean losing weight, stopping smoking, limiting alcohol consumption and avoiding sedation and sleeping tablets, as well as sleeping on side instead of back.

People with moderate to severe OSA may have to use a continuous positive airway pressure CPAP device, which is a small pump that provides a continuous supply of compressed air through a mask that covers the nose and the mouth. Another treatment method is the mandibular advancement device MAD which is a dental appliance similar to a gum shield. It is worn over the teeth when you are asleep and aims to hold the jaw and tongue forward to increase the space at the back of the throat.
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Molecular biomarkers for preeclampsia

Preeclampsia is a sudden pregnancy complication that can interfere with the blood flow to the placenta and possibly to the fetus, it can lead to low birth weight, prematurity and death. It is also a leading cause of maternal mortality. A new Tel Aviv University study identifies novel molecular biomarkers of preeclampsia, signaling the potential for an early diagnostic blood test.

Research for the study was led by Dr. Noam Shomron and Prof. Moshe Hod and conducted by Liron Yoffe and other lab members, all affiliated with TAU's Sackler School of Medicine, and in collaboration with Prof. Kypros Nicolaides of King's College, London. Preeclampsia is a serious disease that endangers the health, sometimes even the lives, of the mother and the fetus.

The causes of  preeclampsia is unknown if caught in time it has a simple and proven remedy: low doses of aspirin administered from the 16th week until the end of pregnancy. Medical practitioners have assessed a woman's risk of preeclampsia by referring to previous pregnancies, blood pressure levels and other general symptoms. Blood test could predict preeclampsia and, in turn, allow doctors to provide treatment that would prevent the  onset of the disease.

Researchers examined the blood samples from thousands of pregnant women in their first trimester, the team then narrowed their focused to 75 specific blood samples: 35 taken from women who eventually contracted preeclampsia, and 40 taken from those who completed their pregnancies in full health. The researchers extracted the RNA molecules (snippets of molecular information present in human cells) from the plasma of the samples and sequenced these using Next Generation Sequencing (NGS).

The scientists discovered the new biomarkers by analyzing the data using computational methods that included statistical analyses and machine learning algorithms. They identified 25 small RNA molecules that were differentially expressed between the preeclampsia and the control groups. Based on those RNA molecules, they developed a model for the classification of preeclampsia samples.

These findings indicate the predictive value of circulating small RNA molecules in the first trimester, and lay the foundation for producing a novel early non-invasive diagnostic tool for preeclampsia, which could reduce the life-threatening risk for the mother and fetus.
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E-cigarette contains toxic metals

Significant amounts of toxic metals, including lead, leak from some e-cigarette heating coils are present in the aerosols inhaled by users, according to a study from scientists at Johns Hopkins Bloomberg School of Public Health. In the study, the scientists examined e-cigarette devices owned by a sample of 56 users. They found that significant numbers of the devices generated aerosols with potentially unsafe levels of lead, chromium, manganese and nickel.

Chronic inhalation of these metals has been linked to lung, liver, immune, cardiovascular and brain damage, and even cancers. E-cigarettes typically use a battery-supplied electric current that passes through a metal coil to heat nicotine-containing "e-liquids," creating an aerosol-a mix including vaporized e-liquid and tiny liquid droplets.

Vaping is popular in part because it provides the nicotine "hit" and the look and feel of tobacco-smoking but without smoking's extreme health risks. Evidence that vaping isn't entirely safe continues to accumulate. Recent studies have found that e-cigarette liquids contain flavorings and other chemicals that harm cells in standard toxicology tests.

Of the metals significantly present in the aerosols, lead, chromium, nickel and manganese were the ones of most concern, as all are toxic when inhaled. The median lead concentration in the aerosols, for example, was about 15 μg/kg, or more than 25 times greater than the median level in the refill dispensers. Almost 50 percent of aerosol samples had lead concentrations higher than health-based limits defined by the Environmental Protection Agency. Similarly, median aerosol concentrations of nickel, chromium and manganese approached or exceeded safe limits.

E-cigarette heating coils typically are made of nickel, chromium and a few other elements, making them the most obvious sources of metal contamination. Aerosol metal concentrations tended to be higher for e-cigarettes with more frequently changed coils-suggesting that fresher coils give off metals more readily.
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MicroRNA for treating cancer and asthma

A microRNA that regulates inflammation shows promise as a treatment for inflammatory diseases such as asthma and cancer. The microRNA, known as miR-223, is highly expressed in blood cells that cause inflammation (neutrophils). When they're working correctly, those blood cells protect the body against infections, but sometimes they damage host tissue instead of microbes, causing chronic inflammation and disease.

To uncover the link between miR-223 and inflammation, a Purdue University research team created a zebrafish totally deficient of miR-223. Then they cut off a small chunk of its fin. "The inflammation was really robust," said Qing Deng, a professor of biological sciences at Purdue and corresponding author of the paper. "Neutrophils accumulated at the wound and they just kept coming. This is consistent with the literature, but we wanted to understand why."

Extensive gene expression analysis led them to pathway NF-kB, a protein complex found in nearly all animal cell types that regulates inflammation and cell proliferation. Heightened activation of this pathway is the cause of increased inflammation, although it's limited to the deeper, or basal, layer of the epithelium. This means any therapeutics would need to reach the basal layer to work.

The same pathway plays an important role in human bronchial epithelial cells, which are critical in the development of asthma, according to the study. MiR-223 suppresses the pathway, which means supplementing it to epithelial cells could help control inflammatory disease.
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Gout drug for treating heart failure

Researchers at the University of Cincinnati (UC) College of Medicine have shown that probenecid, a drug long used to treat gout, may be able to improve heart function in adult patients who experience heart failure. The drug improved the two main ways in how the heart functions. It improves how the heart contracts and how it relaxes.

Patients were offered probenecid as part of a randomized, double-blind, crossover and placebo-controlled single-center clinical trial. Patients, who averaged 57 years of age, were enrolled during four-week periods. They were required to undergo an echocardiogram, an electrocardiogram and six-minute endurance test along with other assessments, explains Rubinstein, a UC Health cardiologist and member of the UC Heart, Lung and Vascular Institute.

 Researchers examined probenecid in animal heart cells and found it improved how well the heart uses calcium, an important component in cardiac muscle contraction. Heart failure occurs when the heart pump is not strong enough to move blood throughout the body and meet the body's needs for oxygen.

Left ventricular assist devices, pacemakers, heart transplants and medications are available to treat heart failure patients, but outcomes for patients with heart failure are still worse than outcomes for the vast majority of cancer patients, probenecid drug may change this.
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Amantadine for treating Parkinson's disease

FDA Approves Osmolex ER (amantadine) for the treatment of Parkinson’s disease and drug-Induced extrapyramidal reactions. Amantadine is an antiviral medicine that blocks the actions of viruses in the body. It is used to treat or prevent influenza A in adults and children. It may not be effective during every flu season because certain strains of the virus may be resistant to this medicine. It should not be used in place of getting a yearly flu shot.

Amantadine is also used to treat "Parkinson-like" symptoms such as stiffness or tremors, shaking, and repetitive uncontrolled muscle movements that may be caused by the use of certain drugs.

Amantadine side effects
Get emergency medical help if you have signs of an allergic reaction: hives ; difficult breathing; swelling of your face, lips, tongue, or throat. Call your doctor at once if you have: extreme drowsiness, falling asleep suddenly even after feeling alert; a light-headed feeling, like you might pass out; shortness of breath (even with mild exertion), swelling in your hands or feet;
painful or difficult urination; depression, agitation, aggression, behavior changes, hallucinations, thoughts of hurting yourself; a seizure; or severe nervous system reaction-very stiff (rigid) muscles, high fever, sweating, confusion, fast or uneven heartbeats and tremors.
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How alcohol causes dementia

Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study of over one million adults diagnosed with dementia in France.

This study looked specifically at the effect of alcohol use disorders and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol. Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.

The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men and 40 grams per day for women. Heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm.

Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths. Alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death. For early-onset dementia, there was a significant gender split.

Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.
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How infection site affects the immune system

A new study by scientists at the Gladstone Institutes shows that infection sites could affect the immune system's response to a virus and the way the virus spreads through the body. The researchers focused on common routes of sexual transmission of viruses, such as the lower female reproductive tract and the lower gastrointestinal tract that includes the large intestine and the anus.

These mucosal barriers-the body's openings lined with a membrane called mucosa are responsible for distinguishing between harmless bacteria that normally reside in human and potentially dangerous pathogens, as well as other substances, such as food or sperm. Human body is constantly trying to balance between tolerating harmless elements and defending against the threats.

Reseachers discovered that the body's reaction is different based on the infection site. They showed that the vaginal and rectal cavities activate a distinct immune response to the same pathogen. To conduct the study, research team created a new model of viral infection through the rectum that uses lymphocytic choriomeningitis virus (LCMV), a rodent virus often used in research to model other pathogens. They then compared their findings to their previous work on vaginal infection by LCMV.

In 2016, they showed that vaginal infection causes a delayed response by protective cells. As a result, the immune system takes longer to clear the virus from the female reproductive tract. They also noticed that the virus stayed in the vagina and didn't spread to other parts of the body. In contrast, the new study indicates that, after infection through the rectum, the virus rapidly spreads throughout the body. The scientists also found that the virus wasn't being carried through the blood. Instead, LCMV infects the body's own immune cells, which in turn spread the virus systemically. Interestingly, this is the same dissemination process used by the HIV virus.

The initial immune response elicited depends on the route of infection, and can actually dictate the dissemination of the virus. The researchers revealed that mucosal barriers have different tolerance mechanisms that affect the immune system's response to invading pathogens. Once a virus breaches one of the barriers, early events in the body's response to that virus can play a key role in determining the outcome of an infection.
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How insulin receptor works

The researchers from the Paul Langerhans Institute Dresden of the Helmholtz Zentrum München at the University Hospital Carl Gustav Carus of TU Dresden together with colleagues from Rockefeller University New York succeeded for the first time in the visualization of the insulin receptor activation.

Insulin exerts multiple effects on cellular metabolism and growth. The biological actions of insulin are mediated by a cell-surface receptor, called insulin receptor, which is present on the surface, i.e. the plasma membrane, of virtually all mammalian cells. The dysfunction of insulin receptor has been linked to severe pathologies including diabetes mellitus or cancer. Insulin binds outside the cell to the extracellular domain of its receptor and induces a structural change that is propagated across the membrane to the intracellular kinase domains inside the cell, causing them to activate each other, thus initiating signaling cascades.

The nature of this structural change remained a mystery for decades, resulting in mutually exclusive models for insulin receptor activation being put forward. To obtain insights into receptor activation, researchers purified full-length insulin receptors and embedded them into nanodiscs, which are nanoscale disc-shaped membrane patches. Those could then be directly visualized by single-particle electron microscopy.

This technology enables researchers to directly study the cell-surface receptors in an artificial membrane environment. In the absence of insulin, the receptor displays an inverted U-shaped ectodomain, which is consistent with previous crystallographic studies of isolated ectodomains, implying that the membrane-passing transmembrane domains and thus kinase domains are held well apart from each other. Upon insulin binding, the ectodomain of the receptor undergoes a dramatic reorganization, changing from a U-shaped to a T-shaped structure and also causing a rearrangement of the transmembrane domains. These now come together likely facilitating kinase domain interactions and thus their activation.

These nanodisc-embedded receptors provide a novel platform to address further questions regarding insulin receptor regulation and eventually to test therapeutic agents. The results directly demonstrate the structural transition in the full-length receptor upon insulin binding and offer an answer to the longstanding question concerning the mechanism by which insulin activates its receptor, thus improving understanding of the receptor.
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How running preserves the memory

Exercise has long been known to combats stress, but a study by Brigham Young University suggests that it can also combat forgetfulness. The researchers found that running protects against the negative effects of stress on the hippocampus-the part of the brain responsible for learning and memory.

Within the hippocampus, memory formation and recall work best when the connections between neurons-synapses, are strengthened over time, a process called long-term potentiation (LTP). Chronic or prolonged stress, however, weakens the synapses and with them the LTP, negatively impacting memory.

The ideal situation for improving learning and memory would be to experience no stress and to exercise. To study the link between memory, stress and exercise, researchers divided mice into four groups: sedentary no stress, exercise no stress, exercise with stress, and sedentary with stress. The mice were then exposed to stress inducing situations, such as walking on an elevated platform or swimming in cold water, or put on a running wheel depending on their grouping.

To determine how the variables affected each group's memory, the researchers used electrophysiology to measure the LTP in the animals' brains. They found that the stressed mice who exercised had considerable higher LTP rates than those who had not exercised. The researchers also used a maze-running experiment to test the mice's memories. The stressed mice who exercised performed just as well as non-stressed mice who exercised.

Additionally, the exercising mice made significantly fewer memory errors in the maze than the sedentary mice. The findings suggest exercise is an effective way to protect learning and memory mechanisms from the negative cognitive impacts of chronic stress on the brain.
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How gene shaped human face

Researchers from KU Leuven (Belgium) and the universities of Pittsburgh, Stanford, and Penn State (US) have identified fifteen genes that determine human facial features. Human DNA determines what an individual look like, including facial features. That appeals to the popular imagination, as the potential applications are obvious. Doctors could use DNA for skull and facial reconstructive surgery, forensic examiners could sketch a perpetrator's face on the basis of DNA retrieved from a crime scene, and historians would be able to reconstruct facial features using DNA from days long gone.

In a new study conducted by KU Leuven in collaboration with the universities of Pittsburgh, Stanford and Penn State, the researchers adopted a different approach. "Our search doesn't focus on specific traits," lead author Peter Claes (KU Leuven) explains. "My colleagues from Pittsburgh and Penn State each provided a database with 3D images of faces and the corresponding DNA of these people. Each face was automatically subdivided into smaller modules. Next, we examined whether any locations in the DNA matched these modules. This modular division technique made it possible for the first time to check for an unprecedented number of facial features."

The scientists were able to identify fifteen locations in human DNA. The Stanford team found out that genomic loci linked to these modular facial features are active when human face develops in the womb. "Furthermore, we also discovered that different genetic variants identified in the study are associated with regions of the genome that influence when, where and how much genes are expressed," says Joanna Wysocka (Stanford). Seven of the fifteen identified genes are linked to the nose, and that's good news, Peter Claes (KU Leuven) continues. "

A skull doesn't contain any traces of the nose, which only consists of soft tissue and cartilage. Therefore, when forensic scientists want to reconstruct a face on the basis of a skull, the nose is the main obstacle. If the skull also yields DNA, it would become much easier to determine the shape of the nose. Age, environment, and lifestyle have an impact on what human face looks like, this could provide genetic insight into the shape and functioning of human brain, as well as in neurodegenerative diseases such as Alzheimer's."
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Using smartphone app for detecting bacteria in food

Researchers have developed a smartphone app that alerts users of bacteria in their food using only a microscope attachment. There are very few methods for preventing food poisoning in part because testing for harmful bacteria such as E.Coli and salmonella requires specialized equipment and can take up to two days to show results.

 New technology from researchers at the University of Massachusetts Amherst changes that, delivering bacteria results in minutes using a smartphone app. Current methods for identifying bacteria associated with food poisoning are time-consuming because it is challenging to collect enough material.

The most common method involves rinsing potentially risky food, collecting small amounts of bacteria from the water and giving it 24 hours to multiply so there's enough to test.The tool developed at UMass uses a chemically-coated chip that binds to even the smallest amounts of bacteria. The university created a video showing how the prototype works: They rinse a potentially contaminated product with water and then place the chip into the water. Within half an hour, the microscope, which can attach to any type of smartphone camera, reveals the bacteria on the screen.

If you don't have the app, you can prevent food poisoning by: keeping the cooking area and your hands clean. Avoiding cross-contamination-raw meat, poultry, seafood and eggs can spread germs to ready-to-eat foods if not kept separate. Use separate cutting boards and plates when handling different foods. To cook food safely, the internal temperature must be high to kill the germs that could cause food poisoning-use a food thermometer.

Store foods properly-storing food properly is essential to combating harmful bacteria, expiration dates may not be accurate for some foods-strange smell or color may indicate that the food is not safe, frozen foods should be thawed in the refrigerator, in cold water, or in the microwave.
          haleplushearty.blogspot.com

Blood and urine tests to indicate autism in children

Autism spectrum disorders ASDs are defined as developmental disorders mainly affecting social interaction and they can include a wide spectrum of behavioural problems like-speech disturbances, repetitive or compulsive behaviour, hyperactivity, anxiety, and difficulty to adapt to new environments, some with or without cognitive impairment. Since there is a wide range of ASD symptoms diagnosis can be difficult and uncertain at the early stages of development.

The research team which is based at the University's Warwick Medical School involves academics at the University of Warwick's Warwick Systems Biology group, the University of Birmingham, the University of Bologna, the Institute of Neurological Sciences, Bologna, and the Don Carlo Gnocchi Foundation ONLUS. They found a link between ASD and damage to proteins in blood plasma by oxidation and glycation-processes where reactive oxygen species (ROS) and sugar molecules spontaneously modify proteins.

They found the most reliable of the tests they developed was examining protein in blood plasma where, when tested, children with ASD were found to have higher levels of the oxidation marker dityrosine (DT) and certain sugar-modified compounds called "advanced glycation endproducts" (AGEs). Genetic causes have been found in 30-35% of cases of ASD and the remaining 65-70% of cases are thought to be caused by a combination of environmental factors, multiple mutations, and rare genetic variants. However the research team also believe that the new tests could reveal yet to be identified causes of ASD.

The team's research also confirmed the previously held belief that mutations of amino acid transporters are a genetic variant associated with ASD. The Warwick team worked with collaborators at the University of Bologna, Italy, who recruited locally 38 children who were diagnosed as having with ASD (29 boys and nine girls) and a control group of 31 healthy children (23 boys and eight girls) between the ages of five and 12. Blood and urine samples were taken from the children for analysis.

They discovered that there were chemical differences between the two groups. Working with a further collaborator at the University of Birmingham, the changes in multiple compounds were combined together using artificial intelligence algorithms techniques to develop a mathematical equation or "algorithm" to distinguish between ASD and healthy controls. The outcome was a diagnostic test better than any method currently available.
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Calcium may cause Parkinson's disease

The international team, led by the University of Cambridge, found that calcium can mediate the interaction between small membranous structures inside nerve endings, which are important for neuronal signalling in the brain, and alpha-synuclein, the protein associated with Parkinson's disease. Excess levels of either calcium or alpha-synuclein may be what starts the chain reaction that leads to the death of brain cells.

Parkinson's disease is one of a number of neurodegenerative diseases caused when naturally occurring proteins fold into the wrong shape and stick together with other proteins, eventually forming thin filament-like structures called amyloid fibrils. These amyloid deposits of aggregated alpha-synuclein, also known as Lewy bodies, are the sign of Parkinson's disease.

Curiously, it hasn't been clear until now what alpha-synuclein actually does in the cell: why it's there and what it's meant to do. It is implicated in various processes, such as the smooth flow of chemical signals in the brain and the movement of molecules in and out of nerve endings, but exactly how it behaves is unclear.

"Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study," said senior author Dr Gabriele Kaminski Schierle from Cambridge's Department of Chemical Engineering and Biotechnology.

Super-resolution microscopy techniques makes it possible to look inside cells to observe the behaviour of alpha-synuclein. To do so, researchers isolated synaptic vesicles, part of the nerve cells that store the neurotransmitters which send signals from one nerve cell to another.

In neurons, calcium plays a role in the release of neurotransmitters. The researchers observed that when calcium levels in the nerve cell increase, such as upon neuronal signalling, the alpha-synuclein binds to synaptic vesicles at multiple points causing the vesicles to come together. This may indicate that the normal role of alpha-synuclein is to help the chemical transmission of information across nerve cells.

There is a fine balance of calcium and alpha-synuclein in the cell, and when there is too much of one or the other, the balance is tipped and aggregation begins, leading to Parkinson's disease. The imbalance can be caused by a genetic doubling of the amount of alpha-synuclein (gene duplication), by an age-related slowing of the breakdown of excess protein, by an increased level of calcium in neurons that are sensitive to Parkinson's, or an associated lack of calcium buffering capacity in these neurons.

Understanding the role of alpha-synuclein in physiological or pathological processes may aid in the development of new treatments for Parkinson's disease. One possibility is that drug candidates developed to block calcium, for use in heart disease for instance, might also have potential against Parkinson's disease.
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Link between gut and type 1 diabetes

Scientists have found that targeting micro-organisms in the gut, known as microbiota, could have the potential to prevent type 1 diabetes. University of Queensland researcher Dr. Emma Hamilton-Williams investigated differences in the gut microbiota, comparing those susceptible to type 1diabetes to those protected against the autoimmune disease.

This research has shown there is a genetic component to microbiota and the immune response involved in regulating it, this means that changes in the microbiota in type 1 diabetes occur before symptoms develop, and are not just a side-effect of the disease. Therapies targeting the microbiota could therefore have the potential to help prevent type 1 diabetes in the future.

An immunotherapy targeting T-cells associated with type 1 diabetes resulted in dramatic changes in the gut biology and altered the microbiota in mice models. Genetic susceptibility and change in immune system function led to alterations in the microbiota. The implications are that a person's genetics contribute to an unhealthy microbiota as well as their diet.
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Effects of stress on sperm

Children of stressed fathers are at greater risk of developing PTSD and depression, according to a new study. Researchers found life's pressures can change the DNA of a man's sperm - leading to brain development changes in his yet unborn baby. It's widely known that a mother's environment during pregnancy, including factors such as poor diet, stress and infection, can negatively impact the offspring.

Learning how a father's behavior and environment can impact his child's development could lead to the detection and prevention of many mental health disorders. Researchers have known for years that stress can increase the risk of mental disorders,' Dr Tracy Bale, professor of neuroscience at the University of Maryland School of Medicine, told Daily Mail Online. 'What’s interesting here is that we are finding intergenerational effects.'

Researchers, led by Dr Bale, conducted a mice experiment to examine how a father's lifestyle impacts his children. Previously, the team has found male mice experiencing chronic periods of mild stress passed down genetic coding for a less effective hormonal response to stress in children. Three major hormones are released by the nervous system when the body is under stress. These are adrenaline, cortisol and norepinephrine. Collectively, these hormones send human bodies into ''fight''mode, which is important to the body's ability to cope with the effects of stress.

Stress resulted in changes in sperms genetic material known as microRNA, which plays a key role in which genes become functional proteins. These changes in stress reactivity have been linked to some mental disorders, including depression and PTSD.

In the new study, presented at the 2018 AAAS annual meeting in Austin, Texas, Dr Bale and her colleagues unraveled new details about the microRNA changes in the sperm. The caput epididymis, the structure where sperm matures, release vesicles which contain microRNA that can fuse with sperm to change its cargo delivered to the egg. When males mice were stressed, the caput epididymis responded by altering the content of these vesicles.

This suggests even mild environmental stress, such as workplace stress, can have a significant impact on the development and potentially the health of future offspring. This is through a process known as epigenetics where DNA is changed through lifestyle factors such as diet, exercise - or even stress. Scientists have known a mother's environment during pregnancy can damage a fetus by diet, stress or infection affecting the expression of certain genes in the same way.

Father's stress can affect offspring development by altering important aspects of his sperm. Her previous studies on the placenta have revealed novel sex differences during pregnancy that may predict increased pre-natal risk for neurodevelopmental disorders in males. Historically, most research on how a parent's lifestyle, behavior and environment can affect their children has focused on the mother. But scientists have recently been paying increasing attention to how a father's health impacts his children.
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Immune signature predicts asthma susceptibility

Asthma is a chronic inflammatory disease driven by the interplay of genetics, environmental factors and a diverse cast of immune cells. Researchers at La Jolla Institute for Allergy and Immunology (LJI) identified a subset of T cells, whose frequency serves as early childhood immune signature that predicts the risk of developing asthma later on.

Children who, at the age of one, had a higher frequency of MAIT cells appear to be less likely to develop asthma by the age of seven. Consistent with the "hygiene hypothesis," which holds that increased microbial exposure in the first years of life is protective for asthma, the team's findings also indicate that the presence of house dust components that stimulate the innate immune system decreases asthma risk.

Unlike conventional T cells, which belong to the adaptive arm of the immune response and take a few days before they are fully trained on a single, specific protein fragment or peptide antigen, MAIT and iNKT cells recognize molecular components common to many microbes. The team analyzed the frequency of different types of immune cells in blood collected from 110 one year-old study participants, the presence of immune-stimulatory components in the subjects' house dust and asked whether any of the factors correlated with an increased of asthma at age seven.

Certain immune signatures such as having more MAITs that are protective in humans MAIT cells are unique in that they are borne to make gamma interferon, which could help skew the immune system toward an asthma-protective. And while the absolute numbers of iNKT cells had no bearing on asthma risk, the iNKT cell antigenic content in house dust from subjects' houses did. iNKT activity reflects a home environment with increased microbe exposure and prevents asthma.
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Calcium and Vitamin D supplements not responsible for heart attack

New research from the University of Southampton has found no association between the use of calcium or vitamin D supplementation and cardiovascular events such as heart attacks. Calcium and vitamin D supplements, which usually come in the forms of tablets, are widely used and have been generally viewed as relatively safe, but some researchers have previously raised concerns over potential links with cardiovascular disease.

Investigators from the Medical Research Council Lifecourse Epidemiology Unit, University of Southampton (MRC LEU), used the internationally unique UK Biobank cohort, comprising over 500,000 men and women aged between 40 and 69 years, to explore relationships between use of calcium and vitamin D supplementation and the risk of cardiovascular events such as heart attacks.

The analysis accounted for a wide range of other potential influences, and did not detect any statistically significant associations between use of the supplements and events such as heart attacks, hospital admission for angina, or related deaths.

Calcium and vitamin D supplements are widely used in the population, and are particularly appropriate for those at risk of deficiency in either nutrient. In this situation there is good evidence that they provide a modest reduction in fracture risk, although do not replace medications specifically licensed for the treatment of osteoporosis.
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