Small molecule reduce the spread of cancer

One small molecule that regulate gene expression plays a big role in keeping human safe from the machinations of cancer. In human lung cancer cells, low levels of the microRNA, miR-125a-5p, which enables the death of aberrant cells like cancer cells, correlates with high levels of the protein TIMP-1, which is already associated with a poor prognosis in patients with cancer.

Conversely, when they decrease TIMP-1 levels in these highly lethal cancer cells, tumor spread goes down while rates of cell death go up along with expression of miR-125a-5p, says Dr. Mumtaz V. Rojiani, cancer biologist in the Department of Medicine at the Medical College of Georgia and a member of the Molecular Oncology and Biomarkers Program at the Georgia Cancer Center at Augusta University.

While increasing microRNA levels is technically difficult, further delineating how cancer hijacks these normal body systems may help identify new treatment targets. TIMP-1 has a positive role in a healthy body to balance levels of enzymes the body makes to ease cell movement for things like wound healing or reproduction.

The healthy body and cancer make these enzymes, matrix metalloproteinases, or MMPs, to break down the surrounding matrix that helps keep cells stable. While it's critical to positives like wound healing, when the matrix breakdown is usurped by cancer, it also gives cancer cells this freedom to move.

In cancer, TIMP-1 levels rise dramatically and it has a distinctive role enabling both growth of new blood vessels and inhibition of apoptosis, a cell's natural inclination to die if something unfixable is wrong. In cancer, what the tumor cells do is start secreting a lot more of these enzymes so they can break down the matrix and start migrating and metastasizing.

Classically, TIMP-1 should be inhibiting MMPs but over the years it has been found to have other functions that actually increase tumor aggressiveness. In their studies of TIMP-1 expression in human lung cancer cells, they saw this aggressive response. It turned out that TIMP-1 is like a two-faced individual smiling at cancer sometimes and other times cutting it off.

Increased levels of two-faced TIMP-1 have been found in increased tumor spread and poor prognosis in breast, gastric and colorectal cancers as well as the non-small cell lung cancer the MCG scientists studied, which accounts for about 85 percent of all lung cancers and has a five-year survival rate of under 20 percent.

TIMP-1 overexpression also is associated with increased upregulation of Bcl-2, a protein which can prevent apoptosis, or cell death. To make bad matters worse, a key way chemotherapy works is by inducing apoptosis and TIMP-1 has been associated with potentially deadly drug resistance.
However, with high expression of miR-125a-5p, TIMP-1 becomes the target. One result is increased expression of the gene p53, a known tumor suppressor, which enables cell death.

When ressearchers knocked down TIMP-1 expression, it significantly increased expression of miR-125a-5p. Conversely, when they restored higher levels of TIMP-1, miR-125a-5p expression went down. The look of the cancer cells changed with the level of TIMP-1. At high levels they looked more like cells unshackled from their current location and able to migrate and invade. When they decreased TIMP-1 levels, the cells pretty much stayed put.

 Adding more synthetic miR-125a-5p to the cancer cells, and the lung cancer cells moved more toward a stationary normal look and cell death increased. When they inhibited miR-125a-5p, the cells were ready to roam. Looking at the biopsies of lung cancer patients, they found as expected TIMP-1 expression much higher in the lung cancer tissue than nearby healthy tissue. But they also saw an inverse relationship between high levels of TIMP-1 and miR-125a-5p levels. In fact, tumor cells had almost no miR-125a-5p.
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How to prevent opioid addiction after surgery

The American Society of Anesthesiologists recommends using prescription painkillers sparingly, if at all, after surgery. There are effective alternatives and many people don't need opioids at all or at least should drastically reduce the amount they take. Opioid painkillers like OxyContin (oxycodone) and Vicodin (hydrocodone/acetaminophen) are addictive, the addiction can develop after taking just a few of them.

Post-surgical prescription have played a role in opioid epidemic. Despite the risk of dependence, many surgery patients receive prescriptions for a month's supply or more of opioid pills. And some of the patients are still using them three months or longer after their surgery.

More than 2 million Americans abuse opioids, according to the U.S. Centers for Disease Control and Prevention. Since 2000, opioid overdose deaths in the United States have increased 200 percent. To reduce reliance on painkillers, the anesthesiologists' group offers advice for coping with discomfort as you recover from surgery:
Only take opioids when in extreme pain . Medications such as ibuprofen (Motrin), naproxen (Aleve) and acetaminophen (Tylenol) can manage pain and soreness. These medications are not addictive and are far less risky than opioids.

Understand that soreness and discomfort after surgery are normal and will improve within a day or two. These sensations are different than pain, which is typically sharp or intense. While in recovery after surgery, try to be clear when asked if you are in pain. Specify if you are sore, uncomfortable or in serious pain.

If you have significant pain, ask that an opioid prescription be limited to a small amount, such as five pills. If you do take opioids, take them only for a day or two after surgery, three days at most. Your pain will improve significantly within a few days whether or not you take opioids. Those who are in continued severe pain after surgery can engage in exercise, use nerve blocks and non-opioid medications.
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Bacteria in milk linked to rheumatoid arthritis

A strain of bacteria found in milk and beef may be a trigger for developing rheumatoid arthritis in people who are at risk, according to a new study from the University of Central Florida. A team of UCF College of Medicine researchers has discovered a link between rheumatoid arthritis and Mycobacterium avium subspecies paratuberculosis, known as MAP, a bacteria found in about half the cows in the United States. The bacteria can be spread to humans through the consumption of infected milk, beef and produce fertilized by cow manure.

For the study, researchers recruited 100 of her patients who volunteered clinical samples for testing. Seventy-eight percent of the patients with rheumatoid arthritis were found to have a mutation in the PTPN2/22 gene, the same genetic mutation found in Crohn's patients, and 40 percent of that number tested positive for MAP. People born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis.

Rheumatoid arthritis is an autoimmune and inflammatory disease that causes the immune system to attack a person's joints, muscles, bones and organs. Patients suffer from pain and deformities mostly in the hands and feet. It can occur at any age but the most common onset is between 40 and 60 years old and is three times more prevalent in women. Some RA patients suffer from Crohn's disease and vice versa, the researchers say a national study needs to investigate the incidence of the two diseases in the same patients.
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How gene mutation triggers the immune system

Scientists discovered how a gene mutation affects T cell function to promote immune disorders and then tested a treatment based on the discovery-successfully fixing donated immune cells from a 16-year-old boy with an abnormally low level of white blood cells called lymphopenia. The discovery centers on mutation of the gene Gimap5, which is important to the healthy formation and function of CD4+ T cells, one of the immune system's super soldiers against infection and disease.

The protein associated with the Gimap5 gene (also Gimap5), is important because it regulates a protein that inactivates an enzyme called GSK3, researchers said. If GSK3 isn't inactivated it causes DNA damage in T cells that are expanding, causing the cells not to survive or function properly. In mice and human blood cells, the researchers tested drugs that inhibit GSK3, improving immune system function in mice and restoring normal T cell function in the human cells.

GSK3 inhibitors are used to treat other diseases like Alzheimer's, mood disorders and diabetes mellitus. GSK3 inhibitors will improve T cell survival and function and may prevent or correct immune-related disorders in people with Gimap5 loss-of-function mutations.Therapeutically targeting this pathway may be relevant for treating people with Gimap5 mutations linked to autoimmunity in Type 1 diabetes, systemic lupus erythematosus or asthma.

Hoebe led the study, together with Andrew Patterson, a PhD student in Hoebe's lab, and Jack Bleesing, MD, PhD, in the Division of Bone Marrow Transplantation and Immune Deficiency. Immune system disorders lead to abnormally low immune activity (deficiency) or overactivity (autoimmunity). Immune deficiency diseases decrease the body's ability to fight infection, while autoimmunity prompts the body to attack its own tissues. Both are common causes of illness, and malfunctioning T cells are linked to both.

The Gimap5 gene controls its associated protein Gimap5 (GTPase of immunity associated protein 5). As the name suggests, its role is mainly linked to immune system function, lymphocyte white blood cell survival and T cell formation in the thymus. Genetic variants in Gimap5 were already associated with autoimmunity and colitis.
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Genetic basis of glaucoma

Northwestern Medicine scientists and international collaborators discovered mutations that cause improper drainage and a buildup of ocular pressure leading to one form of congenital glaucoma, and identified a path towards future treatments for the disease. Susan Quaggin, MD, chief of Nephrology and Hypertension in the Department of Medicine and director of the Feinberg Cardiovascular Research Institute, was senior author on the studies.

Glaucoma is a leading cause of blindness around the globe, and elevated intraocular pressure (IOP) is an important risk factor for the disease. Developmental defects in the anterior chamber of the eye, including a drainage vessel called Schlemm's canal, can lead to a particularly severe form of glaucoma in children known as primary congenital glaucoma (PCG).

Previous studies from Quaggin and her collaborators have shown loss-of-function mutations in the angiopoietin (ANGPT) receptor TIE2/TEK in families with PCG, and that ANGPT/TIE2 pathway activity is critical for Schlemm's canal development.

 In the JCI study, Quaggin and her colleagues used mice models to explore the importance of individual components of the ANGPT/TEK pathway, finding mice without the growth factor ANGPT1 had severely deformed and small Schelmm's canals. In addition, loss of TIE2/TEK, the angiopoietin receptor, had a similar effect.

Both ANGPT1 and TIE2/TEK are essential to form the drainage system of the eye to regulate intraocular pressure and prevent Glaucoma. Researchers found two human subjects with loss-of-function mutations in ANGPT1 within an international group of PCG patients, further supporting a causative role for ANGPT1 in the disease.

In the PNAS study, Quaggin and her colleagues searched for ways to influence the molecular pathway they'd identified. In particular, inhibition of TIE2/TEK has been linked to vessel leakage and inflammation, so finding a way to activate TIE2/TEK was a priority. Using mouse models, investigators found inhibition of a protein called VEPTP allowed ANGPT2 to be used as a TIE2/TEK activator, providing a blueprint for a pharmacological solution.
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Vitamin D could prevent cardiovascular damage

A new study conducted by Ohio University scientists suggests that a little more sunlight might restore damage to cardiovascular system. The study shows that vitamin D3 which is made by the body naturally when skin is exposed to the sun can significantly restore the damage to the cardiovascular system caused by several diseases like hypertension, diabetes and atherosclerosis.

Vitamin D3 is associated with the bones. However, in recent years, in clinical settings people recognize that many patients who have a heart attack will have a deficiency of D3. It doesn't mean that the deficiency caused the heart attack, but it increased the risk of heart attack. Nanosensors shows that vitamin D3 can be beneficial, especially for the function and restoration of the cardiovascular system.

A major discovery from these studies is that vitamin D3 is a powerful stimulator of nitric oxide (NO), which is a major signaling molecule in the regulation of blood flow and the prevention of the formation of clots in the cardiovasculature. Additionally, vitamin D3 significantly reduced the level of oxidative stress in the cardiovascular system. Treatment with vitamin D3 can significantly restore the damage to the cardiovascular system caused by several diseases, including hypertension, atherosclerosis, and diabetes, while also reducing the risk of heart attack.

These studies, performed at Ohio University, are the first to identify the molecular mechanism of vitamin D3-triggered restoration of the function of damaged endothelium in the cardiovasculature. While these studies were performed using a cellular model of hypertension, the implication of vitamin D3 on dysfunctional endothelium is broader. The dysfunction of endothelium is a common denominator of several cardiovascular diseases, particularly those associated with ischemic events.

Vitamin D3 may be of clinical importance in the restoration of dysfunctional cardiac endothelium after heart attack, capillary endothelium after brain ischemia (stroke), hypovolemia, vasculopathy, diabetes and atherosclerosis. This suggestion is strongly supported by several clinical studies which indicate that vitamin D3 at doses higher than those currently used for the treatment of bone diseases, may be highly beneficial for the treatment of the dysfunctional cardiovascular system.
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E-cigarettes flavours are toxic

Sugar and spice are not healthy when it comes to vaping or inhalation. Exposure to e-cigarette flavoring chemicals and liquids can cause significant inflammation to monocytes, a type of white blood cell and many flavoring compounds are also toxic, with cinnamon, vanilla and buttery flavors among the worst. That's the finding of new research published in open-access journal
Frontiers in Physiology, which also found that mixing e-cigarette flavors has a much worse effect than exposure to just one.

The use of e-cigarettes has exploded in the past decade as traditional cigarette consumption has declined. Vaping exposes the lungs to flavoring chemicals when the e-liquids are heated and inhaled. Since the flavoring chemicals are considered safe to eat, e-cigarettes are often considered and advertised as a healthier alternative to traditional cigarettes.

This new study, led by researchers at the University of Rochester Medical Centre in the United States, wanted to test the assumption that vaping nicotine-free flavored e-liquids is safer than smoking conventional cigarettes. Previous studies show that flavors used in e-cigarettes cause inflammatory and oxidative stress responses in lung cells.

Users of e-cigarettes also show increased levels oxidative stress markers in the blood compared to non-smokers. The new study extends this to assess the effects of commonly used flavoring chemicals, as well as e-liquids without nicotine, directly on immune cells-a type of white blood cell called monocytes.

Exposure to the e-cigarette flavoring chemicals and e-liquids led to higher production of two well-established biomarkers for inflammation and tissue damage mediated by oxidative stress. Furthermore, many of the flavoring chemicals caused significant cell death with some flavors being more toxic than others.
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Lutathera for treating gastroenteropancreatic neuroendocrine tumours

The U.S. Food and Drug Administration had approved Lutathera (lutetium Lu 177 dotatate) for the treatment of a type of cancer that affects the pancreas or gastrointestinal tract called gastroenteropancreatic neuroendocrine tumors (GEP-NETs). This is the first time a radioactive drug, or radiopharmaceutical, has been approved for the treatment of GEP-NETs. Lutathera is indicated for adult patients with somatostatin receptor-positive GEP-NETs.

GEP-NETs are a rare group of cancers with limited treatment options after initial therapy fails to keep the cancer from growing. GEP-NETs can be present in the pancreas and in different parts of the gastrointestinal tract such as the stomach, intestines, colon and rectum. Lutathera is a radioactive drug that works by binding to a part of a cell called a somatostatin receptor, which may be present on certain tumors. After binding to the receptor, the drug enters the cell allowing radiation to cause damage to the tumor cells.

The approval of Lutathera was supported by two studies. The first was a randomized clinical trial in 229 patients with a certain type of advanced somatostatin receptor-positive GEP-NET. Patients in the trial either received Lutathera in combination with the drug octreotide or octreotide alone. The study measured the length of time the tumors did not grow after treatment (progression-free survival).

Progression-free survival was longer for patients taking Lutathera with octreotide compared to patients who received octreotide alone. This means the risk of tumor growth or patient death was lower for patients who received Lutathera with octreotide compared to that of patients who received only octreotide.

The second study was based on data from 1,214 patients with somatostatin receptor-positive tumors, including GEP-NETS, who received Lutathera at a single site in the Netherlands. Complete or partial tumor shrinkage was reported in 16 percent of a subset of 360 patients with GEP-NETs who were evaluated for response by the FDA.

Patients initially enrolled in the study received Lutathera as part of an expanded access program. Expanded access is a way for patients with serious or immediately life-threatening diseases or conditions who lack therapeutic alternatives to gain access to investigational drugs for treatment use.

Common side effects of Lutathera include low levels of white blood cells (lymphopenia), high levels of enzymes in certain organs (increased GGT, AST and/or ALT), vomiting, nausea, high levels of blood sugar (hyperglycemia) and low levels of potassium in the blood (hypokalemia).

Serious side effects of Lutathera include low levels of blood cells (myelosuppression), development of certain blood or bone marrow cancers (secondary myelodysplastic syndrome and leukemia), kidney damage (renal toxicity), liver damage (hepatotoxicity), abnormal levels of hormones in the body (neuroendocrine hormonal crises) and infertility.

Lutathera can cause harm to a developing fetus; women should be advised of the potential risk to the fetus and to use effective contraception. Patients taking Lutathera are exposed to radiation. Exposure of other patients, medical personnel, and household members should be limited in accordance with radiation safety practices.
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Oestrogen changes neuroblastoma cells into neurons

The female sex hormone oestrogen can perform an important role in neuroblastoma, a form of cancer mainly affecting young children. In laboratory experiments, researchers at Karolinska Institutet in Sweden demonstrate that oestrogen treatment and overexpression of the oestrogen receptor cause malignant neuroblastoma cells to mature into neuron-like cells.

Neuroblastoma forms in the peripheral nervous system and is one of the most common forms of solid cancer in young children. The disease mainly affects babies and young children, and while in some cases the tumours can disappear of their own accord, the majority are aggressive, metastasising cancer tumours that are resistant to modern combinations of surgery, radiotherapy and intensive chemotherapy.

The most aggressive forms of neuroblastoma are often associated with a more active MYCN gene, which drives tumour cell growth and spread and inhibits the maturation of the cells. Researchers focus on the activity of this gene and how it relates to neuroblastoma. MYCN is often seen only as a marker for a poor prognosis, but it's critical to the disease and is a possible target for new drugs.

In a previous study, the group discovered that activation of MYCN results in the formation of specific microRNAs, which are relatively small RNA molecules that regulate proteins. Some of these microRNAs disable the oestrogen receptor ERalpha. The present study shows that the inhibition of these microRNA molecules or oestrogen therapy in combination with an overexpression of the oestrogen receptor can cause aggressive neuroblastoma cells with MYCN activation to mature into neuron-like cells which behave more like normal cells.

The researchers studied tumour tissue from patients, cultivated human tumour cells and tumours in mouse models for neuroblastoma. In the mice, the neuron-like cells did not grow as quickly as the original cancer cells, and analyses of the tumour tissue from patients show that those with a high level of the oestrogen receptor have a better survival rate than those with a low. Oestrogen could be a therapeutic method for patients who express high levels of the oestrogen receptor. Another therapy could involve deregulating MYCN or upregulating the oestrogen receptor and then treating with oestrogen.
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Nicotine in E-cigarettes may cause cancer

The nicotine in e-cigarettes seems to damage DNA in ways that may increase cancer risk, the damage was seen both to DNA and its ability to repair itself, making cells more likely to mutate and develop into cancer, said lead researcher Moon-shong Tang, a professor of environmental medicine at New York University School of Medicine.

Reseachers exposed laboratory mice to e-cigarette vapor, which contains both nicotine and liquid solvents. They also exposed mice to the nicotine and the solvents separately. The vapors were produced using 4.2 volts of electricity, at or below the level at which most commercial e-cigarettes function.

Prior studies have shown that e-liquid heated using higher levels of electricity could produce harmful chemicals. This research team wanted to investigate the risk posed to people using a typical e-cigarette. They found the solvent alone does not cause DNA damage, nicotine with e-cigarette solvent caused the same damage as nicotine alone. The researchers also exposed cultured human lung and bladder cells to nicotine, and found the same effects-DNA damage and suppressed DNA repair.
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How intestine repairs itself

Researchers at Baylor College of Medicine, Johns Hopkins University School of Medicine and the University of California, San Francisco have gained new insights into how the small intestine, one of the fastest renewing tissues in the human body, repairs itself after injury caused by intestinal rotavirus infection. Their findings have led them to propose that, contrary to the current thinking, how the intestine repairs itself seems to depend on the type of damage, and they found that triggers that were previously thought to be unimportant are actually essential for repairing virus-caused injury.

They studied different damage model, damage caused by rotavirus, a common small intestinal viral infection that affects young children. Repair and turnover of the epithelium, the most external cellular layer of the small intestine responsible for absorption of nutrients and other functions, depend on the intestinal stem cells, regardless of the cause of the damage. There are two types of intestinal stem cells: CBCs (crypt-based columnar cells) and reserve intestinal stem cells. The type of injuries studied until now damages the highly proliferative CBCs, and when these stem cells are destroyed, the reserve intestinal stem cells respond to restore the damage. The response to injury caused by rotavirus, however, is different.

Rotavirus is an infection and has a very specific damage pattern, the virus specifically infects epithelial cells, but not the stem cells. The first finding refers to the type of stem cell involved in the repair of the epithelial cells damaged by the virus. Previous studies had shown that when CBC stem cells are damaged, the reserve stem cells come to their rescue leading the reconstitution of the damaged epithelium. When rotavirus damages the epithelium, but not the stem cells,  the CBCs, not the reserve stem cells, are the primary cell type involved in the restoration of the intestinal epithelium.

 CBCs were not considered important for the repair of intestinal epithelium, but the results show that they are crucial for injury repair after rotavirus-induced epithelial cell damage in contrast to previous studies supporting the reserve intestinal stem cells as the cell type involved in epithelial restitution. The second finding refers to the source of the signaling molecules-called WNTs that trigger the growth and activation of stem cells leading to injury repair. Scientists have described two sources of WNT molecules, epithelial cells and mesenchymal cells. Epithelial WNT molecules were essential to signal the stem cells to repair the damage caused by rotavirus infection.
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Effects of brain tickle on memory

Tickling the brain with low-intensity electrical stimulation in a specific area can improve verbal short-term memory. Mayo Clinic researchers report their findings in Brain. The researchers found word recall was enhanced with stimulation of the brain's lateral temporal cortex, the regions on the sides of the head by the temples and ears.

Patients recalled more words from a previously viewed list when low-amplitude electrical stimulation was delivered to the brain. One patient reported that it was easier to picture the words in his mind for remembering.

Human memory for language information can be improved by directly stimulating this underexplored brain area. Memory impairments are a prevalent, costly problem in many brain diseases. Medication and behavioral therapies have limited effectiveness in many cases. While electrical stimulation of the brain is emerging as potential therapy for a wide range of neurological and psychiatric diseases, little is known about its effect on memory.

The memory testing was done with patients undergoing evaluation for surgery to address seizures. These patients agreed to have their memory investigated using the electrodes implanted in their brains for surgical evaluation. It is common for people with epilepsy to have memory problems because the brain circuits that underlie memory function often are affected by epilepsy.

In the study, patients were instructed to read a list of words-one at a time from a computer screen. Electrical stimulation was applied some of this time. Patients then attempted to freely recall the words in any order. The researchers found enhanced memory performance in the patients with stimulation of the lateral temporal cortex but not among those with the other brain regions stimulated.
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Mediterranean diet may increase the success rate of IVF

New research has found that women who follow a "Mediterranean" diet in the six months before assisted reproductive treatment have a significantly better chance of becoming pregnant and giving birth to a live baby than women who did not.

Researchers asked women about their diet before in vitro fertilisation (IVF) treatment and found that those who ate more fresh vegetables, fruit, whole grains, legumes, fish and olive oil, and less red meat, had a 65-68% greater likelihood of achieving a successful pregnancy and birth compared to women with the lowest adherence to the Mediterranean-style diet.

Researchers assessed the diet of different women through a food frequency questionnaire when they enrolled at an Assisted Conception Unity in Athens, Greece, for their first IVF treatment. The questionnaire asked them about how often they ate certain groups of food in the preceding six months; the results gave the women a MedDiet Score, which ranged from 0-55 with higher scores indicating greater adherence to the Mediterranean diet. The women were aged between 22-41 and were non-obese (body mass index of less than 30 kg/m 2 ).

Researchers, led by Associate Professor Nikos Yiannakouris at the Department of Nutrition and Dietetics at Harokopio University of Athens, divided the women into three groups depending on their MedDiet Score: the first group had scores between 18 to 30, the second scored between 31-35 and the third group scored between 36 to 47.

They found that compared to the 86 women in the highest scoring group, the 79 women in the lowest scoring group had significantly lower rates of pregnancies (29% versus 50%) and live births (26.6% versus 48.8%). When the researchers looked at women younger than 35 years old, they found that every five-point improvement in the MedDiet Score was linked with an approximately 2.7 times higher likelihood of achieving a successful pregnancy and live birth.

Overall, 229 women (93.9%) had at least one embryo transferred to their wombs; 138 (56%) had a successful implantation; 104 (42.6%) achieved a clinical pregnancy (one that can be confirmed by ultrasound); and 99 (40.5%) gave birth to a live baby. Women attempting fertility should be encouraged to eat a healthy diet, such as the Mediterranean diet, because greater adherence to this healthy dietary pattern may increase the chances of successful pregnancy and delivering healthy baby.

Adherence to the Mediterranean diet may also help improve semen quality. Taken together, these findings highlight the importance of dietary influences and diet quality on fertility, and support a favourable role for the Mediterranean diet on assisted reproduction performance. The researchers did not find any association between diet and the chances of successful pregnancies and live births among women aged 35 and older. However, they believe this is because hormonal changes, fewer available eggs and other changes that women experience as they get older could mask the influences of environmental factors such as diet.
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Cure for skin cancer

The newly discovered drugs combination for skin cancer can help if chemotherapy fails, extending patients’ lives by at least a year. In almost half of kidney cancer patients, by the time the disease is diagnosed it has already spread to other areas of the body due to a lack of symptoms, slashing life expectancy from five years to two. While chemotherapy, which kills both cancer and healthy cells, is used to treat most other advanced cancers, the treatment does not work for most kidney cancers.

The established treatment for the condition is either radiotherapy-which shrinks tumours or tyrosine-kinase inhibitor drugs, including one called sunitinib, which interrupt the blood supply to cancer. However, these only hinder the growth of tumours for four or five months. The drugs, ipilimumab and nivolumab, are already used with remarkable success in the treatment of deadly melanoma skin cancer.

Nivolumab is also used to treat advanced lung tumours. The new trial found that the combination achieved significant kidney tumour shrinkage in 42 per cent of the 425 patients in a trial and reduced the risk of death within two years by 37 per cent. Ipilimumab and nivolumab are immunotherapy drugs that work by enhancing the ability of the body’s immune system cells to attack and destroy cancer. Rather than just putting the cancer into remission for a period, like standard treatments, they appear to carry on working even after treatment has stopped

During the trial, 840 kidney cancer patients were given either sunitinib or the combination immunotherapy. Those on the combination had four infusions of the two drugs at three-weekly intervals. One-fifth of patients experienced severe side effects such as inflammation of the bowel or liver, and had to stop early. The median overall survival rate [the time at which 50 per cent of patients have died after treatment] for sunitinib was 26 months, but for the combination immunotherapy arm, it has still not been reached 36 months on. More than half the patients are still alive.
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Source of Huntington's disease

Huntington's disease is a fatal hereditary disorder for which there is currently no treatment, it is associated with jerky movements and as these patients increasingly lose brain neurons, they slide into dementia. But the new research suggests that these symptoms may be a late manifestation of a disease that originates much earlier, in the first steps of embryonic development.

A team at Rockefeller led by Ali Brivanlou, the Robert and Harriet Heilbrunn Professor, developed a system to model Huntington's in human embryonic stem cells for the first time. Researchers describe early abnormalities in the way Huntington's neurons look, and how these cells form larger structures that had not previously been associated with the disease.

Huntington's is one of the few diseases with a straightforward genetic culprit: One hundred percent of people with a mutated form of the Huntingtin (HTT) gene develop the disease. The mutation takes the form of extra DNA, and causes the gene to produce a longer-than-normal protein. The DNA itself appears in the form of a repeating sequence, and the more repeats there are, the earlier the disease sets in.

Research on Huntington's has thus far relied heavily on animal models of the disease, and has left many key questions unanswered. For example, scientists have not been able to resolve what function the HTT gene serves normally, or how its mutation creates problems in the brain. Suspecting that the disease works differently in humans, whose brains are much bigger and more complex than those of lab animals, researchers developed a cell-based human system for their research. They used the gene editing technology CRISPR to engineer a series of human embryonic stem cell lines, which were identical apart from the number of DNA repeats that occurred at the ends of their HTT genes.

In cell lines with mutated HTT, we saw giant cells. It looked like a jungle of disorganization. When cells divide, they typically each retain one nuclei. However, some of these enlarged, mutated cells flaunted up to 12 nuclei-suggesting that neurogenesis, or the generation of new neurons, was affected. The disruption was directly proportional to how many repeats were present in the mutation: The more repeats there were, the more multinucleated neurons appeared.

There is an unrecognized developmental aspect to the pathology. Huntington's may not be just a neurodegenerative disease, but also a neurodevelopmental disease. Treatments for Huntington's have typically focused on blocking the activity of the mutant HTT protein, the assumption being that the altered form of the protein was more active than normal, and therefore toxic to neurons. However, Brivanlou's work shows that the brain disruption may actually be due to a lack of HTT protein activity.

To test its function, the researchers created cell lines that completely lacked the HTT protein. These cells turned out to be very similar to those with Huntington's pathology, corroborating the idea that a lack of the protein not an excess of it is driving the disease. The findings are significant because existing treatments that were designed to block HTT activity may actually do more harm than good.
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How diabetes causes fracture

Type 2 diabetes is known to be a risk factor for bone fractures. New research in animal models by a team of scientists at UC San Francisco, UC Davis, and UC Berkeley suggests that the disease compromises the collagen within bones, making the bones less flexible and more likely to break.
Journal of Bone and Mineral Research.

Adults with Type 2 diabetes have a higher fracture risk for a given bone density, which is otherwise the main clinical predictor of fracture risk. This is a widespread and growing issue now that these individuals are living longer with better insulin management.

Fields and colleagues looked at factors outside of bone density that could explain bone fragility in diabetes. In healthy bones, networks of collagen fibers stretch and slide in response to strain, which helps the bones resist cracking. But hyperglycemia in diabetes leads to the accumulation of advanced glycation end products, which bind collagen fibers to each other and impair their stretching and sliding, according to the new findings.

The researchers examined bones from the lower back and forearm of lean, obese and diabetic obese rat models. They imaged the bones with high-resolution CT scans, tested their biomechanical properties, and measured the collagen networks' response to strain using small-angle X-ray scattering at the Lawrence Berkeley National Laboratory Advanced Light Source.

They then simulated the contribution of these various factors to bone strength using supercomputers at the Texas Advanced Computing Center at the University of Texas. Both the obese rats and the diabetic obese rats had overall weaker bones for a given bone mineral content. In obese rats, the reduced strength was attributable to structural deficits, such as changes to the microarchitecture of the bones and inefficient distribution of bone mass.

In the diabetic obese rats, however, these structural deficits were compounded by material deficits -changes to the collagen networks that were previously not well documented. By comparing the obese rats with the diabetic obese rats, the researchers could isolate the effect of hyperglycemia on bone fragility. In the forearm bones, for example, the collagen changes were responsible for significant reductions in the elastic, yield and ultimate tensile properties of the bone tissue.

The researchers note that they did not study animals with an advanced duration and severity of diabetes, which may limit generalizability, but they expect that long-term diabetes would only further impair bone strength.
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Roles of brain protein

A protein called AKT, is ubiquitous in brain tissue and instrumental in enabling the brain to adapt to new experiences and lay down new memories. AKT comes in three distinct varieties residing in different kinds of brain cells and affecting brain health in very distinct ways. It is a central protein that has been implicated in a bevy of neurological diseases.

Discovered in the 1970s and known best as an "oncogene" (one that, when mutated, can promote cancer), AKT has more recently been identified as a key player in promoting "synaptic plasticity," the brain's ability to strengthen cellular connections in response to experience. AKT is one of the first proteins to come up after observing scary objects, it is a central switch that turns on the memory factory.

For the study, Hoeffer's team silenced the three different isoforms, or varieties, of AKT in mice and observed their brain activity. They made a number of key discoveries: AKT2 is found exclusively in astroglia, the supportive, star-shaped cells in the brain and spinal cord that are often impacted in brain cancer and brain injury.

 AKT1 is ubiquitous in neurons and appears to be the most important form in promoting the strengthening of synapses in response to experience-memory formation. (This finding is in line with previous research showing that mutations in AKT1 boost risk of schizophrenia and other brain disorders associated with a flaw in the way a patient perceives or remembers experiences.)
AKT3 appears to play a key role in brain growth, with mice whose AKT3 gene is silenced showing smaller brain size.
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Links between colonoscopy and appendicitis

Colonoscopy is the examination of the colon- the large intestine by a gastroenterologist. It is is associated with increased risk of appendicitis, there is an evidence to suggest that colonoscopy can cause appendicitis up to one week after colonoscopy in some patients. The rate of appendicitis and appendectomy in the first week after a colonoscopy is high.

The colon must be completely cleaned before colonoscopy, if bacteria within the colon are altered as the bowel is prepared prior to colonoscopy in ways that increase the likelihood of inflammation, or if the increased air pressure caused by colonoscopy, it may have effects on the colonic mucosa that can predispose people to appendicitis.

Appendicitis is a condition when the appendix becomes inflamed and filled with pus, colonoscopy is valuable and the appendicitis rate is still very low, right-lower abdominal pain after colonoscopy may be a sign of appendicitis.
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Reversing insulin resistance

Researchers at Vanderbilt University have discovered how insulin crosses the capillary endothelium to exit blood vessels and stimulate skeletal muscle cells-a major finding that may lead to new ways to reverse insulin resistance, a hallmark of type 2 diabetes. This was made possible by the development of a novel microscopy technique which allowed measurement of insulin movement across the endothelial wall of skeletal muscle capillaries in the mouse.

One of insulin's key functions is to stimulate glucose uptake by muscle, where it is stored or used as fuel. To stimulate glucose uptake insulin must cross the endothelial barrier into muscle tissue. Impaired delivery of insulin into tissue is a key feature of insulin resistance and type 2 diabetes.

Using a quantitative intravital fluorescence microscopy technique they developed combined mathematical modeling, the researchers showed that insulin moves across the endothelium by fluid-phase transport. Such movement is not dependent on the presence of endothelial insulin receptors or limited by saturation of endothelial transport processes, as had been hypothesized previously.

Better understanding of the variables controlling insulin movement across the endothelial wall could lead to improved strategies for reversing insulin resistance, including development of small molecules that enhance insulin delivery or novel insulin analogs that can access muscle more easily. The fluorescence microscopy technique developed for these studies can be applied to other drugs and hormones to study molecular access to a range of tissues.
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Roles of Mesp1 gene

Researchers at the Université libre de Bruxelles and University of Cambridge identified the role of key gene Mesp1 in the earliest step of cardiovascular lineage segregation. This discovery may help to better understand congenital heart defects. The heart is the first organ that forms during development and contains four regions (ventricles and atria), which contain cells that perform specialized functions: the beating cardiomyocytes ensure the pumping activity, vascular cells represent the inner lining and blood vessels, and the pacemaker cells regulate the heartbeat.

Unless the progenitor cells are specified at the correct time, migrate to the correct location, and differentiate into the correct cell types, severe malformations of the heart occur. In human patients, these are recognized as congenital heart diseases, which represent the most common cause of severe birth defects in newborn babies. Previous studies had shown that a diverse range of heart progenitor cells arises from different pools of cells expressing the Mesp1 gene. However, it remained unclear how the various progenitors can be distinguished at the molecular level, and what molecular mechanisms promote specification into a particular heart region or cardiac lineage.

Researchers led by Pr. Cédric Blanpain, Laboratory of Stem Cells and Cancer, Université libre de Bruxelles, Belgium, and Pr. Berthold Göttgens, the University of Cambridge, identified the role of Mesp1 in the earliest step of cardiovascular lineage segregation by single cell molecular profiling and lineage tracking. Fabienne Lescroart and colleagues isolated Mesp1 expressing cells at different stages of embryonic development and performed single cell transcriptomic analysis of these early cardiac progenitors to identify the molecular features associated with regional and cell type identity of cardiac progenitors.

They demonstrated that the different populations of cardiac progenitors are molecularly distinct. To determine the role of the transcription factor Mesp1 in regulating the cardiovascular differentiation program and the heterogeneity of early cardiovascular progenitors, they also performed single cell molecular profiling of these early progenitors in a Mesp1 deficient context. These experiments showed that Mesp1 is required for the exit from the pluripotent state and the induction of the cardiovascular gene expression program.

Bioinformatic analysis identified, among these early Mesp1 progenitors, distinct populations of cells corresponding to progenitors committed to different cell lineages and regions of the heart, identifying the molecular features associated with early lineage restriction and regional segregation of the heart. While progenitor cells are not yet differentiated, this new analysis shows that cardiovascular progenitors are already "primed" or pre-specified to give rise to cardiac muscle cells or vascular cells. The researchers found that these different populations are also born at different time points and are located at specific locations at this early stage of development.

The researchers have identified the earliest branching point between the cardiac and vascular lineages, and shown that Notch1 marks the early progenitor committed to the vascular lineage during early embryonic development. Understanding the molecular features associated with early cardiovascular lineage commitment and heart regions will be important to design new strategies to instruct cardiovascular progenitors to adopt cardiac or vascular identity from different heart regions that can be used for cellular therapy of cardiac diseases.
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Bacteria prevent transmission of Zika and Dengue viruses

Scientists at the University of Glasgow's MRC Centre for Virus Research opens in new window (CVR) have found a bacterial strain which blocks dengue and Zika virus transmission from mosquitoes. In a new study, published in PLOS Pathogens opens in new window, the scientists show that a novel strain of the inherited bacteria, called Wolbachia, strongly blocks transmission of dengue and Zika virus in infected mosquitoes. This finding could offer a potential alternative to strains already being tested as virus control tools.

The scientists have already carried out the research in the mosquito species Aedes aegypti, notorious for spreading several dangerous human viruses, including dengue, Zika and chikungunya. Previous research in the scientific community has shown that transmission of these viruses among mosquitoes is stalled if the flies are deliberately infected with one strain of Wolbachia bacteria. With this knowledge, several countries are testing whether infecting local mosquito populations with Wolbachia could lead to lower rates of viral disease in humans.

The MRC scientists in Glasgow found that a novel strain-called 'wAu' – is more effective for virus transmission blocking than the strains currently being used. The effect is emphasised in hot, tropical climates where there is a high prevalence of these diseases. The Wolbachia transmission blocking strategy shows great promise for the control of mosquito-borne viruses, and is now starting to be deployed on a large scale in a number of tropical countries.

The results with the wAu strain showed by far the effective transmission blocking for all the viruses we tested, and it provides an exciting new option to explore for disease control programmes. Several Wolbachia strains have already been tested in the field, but there is evidence to suggest that some strains may not block transmission very effectively or may not be inherited efficiently at high ambient temperatures. In the new study, the research team performed laboratory experiments to test the potential promise of alternative Wolbachia strains.

The researchers introduced four Wolbachia strains into Aedes aegypti mosquitoes, which do not naturally carry these anthropod-infecting bacteria. Two of the strains, wMel and wAlbB had already been evaluated in prior studies, and the scientists wanted to compare their effects with those of two novel strains, wAu and wAlbA.

The analysis revealed particularly promising results for strain wAu. After feeding on blood infected with dengue or Zika virus, mosquitoes infected with wAu had lower levels of viral RNA in their body tissue than did mosquitoes infected with the other strains. wAu also showed very high rates of inheritance, including under high-temperature conditions. The aim is to reduce and block the transmission of pathogens by releasing specific insect disease vectors.
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Omega-3s for cancer prevention

Omega-3s from fish is better than flaxseed and other oils for cancer prevention, according to a first-ever University of Guelph study. Prof. David Ma has discovered that marine-based omega-3s are eight times more effective at inhibiting tumour development and growth. This study is the first to compare the cancer-fighting potency of plant- versus marine-derived omega-3s on breast tumour development.

There is evidence that both omega-3s from plants and marine sources are protective against cancer and we wanted to determine which form is more effective. There are three types of omega-3 fatty acids : a-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). ALA is plant-based and found in such edible seeds as flaxseed and in oils, such as soy, canola and hemp oil. EPA and DHA are found in marine life, such as fish, algae and phytoplankton.

The study involved feeding the different types of omega-3s to mice with a highly aggressive form of human breast cancer called HER-2. HER-2 affects 25per cent of women and has a poor prognosis. Researchers exposed the mice to either the plant-based or the marine-based omega-3s, beginning in utero. The mice were exposed to the different omega-3s even before tumours developed, which allowed comparing how effective the fatty acids are at prevention.

EPA and DHA can inhibit breast tumour growth, but no one has looked directly at how effective these omega-3s are compared to ALA, exposure to marine-based omega-3s reduced the size of the tumours by 60 to 70 per cent and the number of tumours by 30 per cent. However, higher doses of the plant-based fatty acid were required to deliver the same impact as the marine-based omega-3s.

Omega-3s prevent and fight cancer by turning on genes associated with the immune system and blocking tumour growth pathways. Humans should consume two to three servings of fish a week to have the same effect. Besides certain foods containing EPA and DHA, supplements and functional foods, such as omega-3 eggs or DHA milk, can offer similar cancer prevention effects.
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Vitamin D supplements could ease irritable bowel syndrome

Vitamin D supplements could ease painful Irritable Bowel Syndrome IBS symptoms. Scientists from the University's Department of Oncology and Metabolism reviewed and integrated all available research on vitamin D and IBS. The study showed a high prevalence of vitamin D deficiency in IBS patients. They also assessed the possible benefits of vitamin D supplements on IBS symptoms. Their findings suggested supplements may help to ease symptoms which can include abdominal pain, bloating, diarrhea and constipation. Vitamin D was shown to have the most benefit on quality of life in IBS.

People with IBS should have their vitamin D levels tested and a large majority of them would benefit from supplements. IBS is a poor condition which impacts severely on the quality of life of sufferers. There is no single known cause and no cure. IBS is a debilitating functional disorder of the gastrointestinal (GI) tract. Little is known about why and how the condition develops, although it is known that diet and stress can make symptoms worse.

Vitamin D is essential for general wellbeing, including bone health, immune function, mental health as well as gut health. Vitamin D inadequacy can be remedied relatively easily with supplements if diagnosed. Low vitamin D status has already been associated with the risk of colorectal cancer and has been implicated in inflammatory bowel disease.
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Low carbohydrate intake increases the risk of birth defects

Women who are pregnant or planning to become pregnant may want to avoid diets that reduce or eliminate carbohydrates, as they could increase the risk of having babies with neural tube birth defects, according to a new study from the University of North Carolina at Chapel Hill.

Women with low carbohydrate intake are 30 percent more likely to have babies with neural tube defects, such as spina bifida-malformations of the spine and spinal cord and anencephaly-absence of major portions of the brain and skull, that can lead to lifelong disability and infant death, when compared with women who do not restrict their carbohydrate intake.

Folic acid is an essential nutrient that minimizes the risk of neural tube defects. Dietary intake of folic acid among women with restricted carbohydrate intake was less than half of other women. The Centers for Disease Control and Prevention recommends that all women who may become pregnant take a daily multivitamin with at least 400 micrograms of folic acid every day before and during pregnancy.

However, because some pregnancies are not planned, many women do not initiate folic acid supplementation until later in pregnancy, after a neural tube defect may have occurred. This makes fortified foods an important source of folic acid for women who may become pregnant.
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Air pollution linked to irregular menstruation

Air breathes in may be causing irregular menstrual cycles. Well documented negative health effects from air pollution exposure include infertility, metabolic syndrome and polycystic ovary syndrome. This study is the first to show that exposure to air pollution among teen girls (ages 14-18) is associated with slightly increased chances of menstrual irregularity and longer time to achieve such regularity in high school and early adulthood.

While air pollution exposures have been linked to cardiovascular and pulmonary disease, this study suggests there may be other systems, such as the reproductive endocrine system, that are affected as well," said corresponding author Shruthi Mahalingaiah, MD, MS, assistant professor of obstetrics and gynecology at Boston University School of Medicine and a physician in obstetrics and gynecology at Boston Medical Center.

The menstrual cycle is responsive to hormonal regulation. Particulate matter air pollution has demonstrated hormonal activity. However, it was not known if air pollution was associated with menstrual cycle regularity, until now. The researchers used health and location data gathered in the Nurses' Health Study 2 plus air pollution exposure metrics from the EPA air quality monitoring system to understand a participants' exposure during a particular time window. They found exposure to air pollution in during high school was correlated with menstrual cycle irregularity.
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Links between high cholesterol diet and colon cancer

New UCLA research could help explain the link between a high-cholesterol diet and an elevated risk for colon cancer. In a study of mice, scientists from the David Geffen School of Medicine at UCLA discovered that boosting the animals' cholesterol levels spurred intestinal stem cells to divide more quickly, enabling tumors to form 100 times faster. The study identifies a molecular pathway that could serve as a new drug target for colon cancer treatment.

Cholesterol influences the growth of stem cells in the intestines, which in turn accelerates the rate of tumor formation. The connection between dietary cholesterol and colon cancer is well established. The scientists increased cholesterol in the intestinal stem cells in some of the mice by introducing more of the substance into their diets.

In others, the researchers altered a gene that regulates phospholipids, the primary type of fat in cell membranes, which spurred the cells into producing more cholesterol on their own. The stem cells ' ability to multiply increased in both groups.

As the animals' cholesterol levels rose, their cells divided more rapidly, causing the tissue lining their guts to expand and their intestines to lengthen. These changes significantly sped up the rate of tumor formation in their colons.
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Repurposed drug effective for Zika virus

In both cell cultures and mouse models, a drug used to treat Hepatitis C effectively protected and rescued neural cells infected by the Zika virus and blocked transmission of the virus to mouse fetuses. Researchers at University of California San Diego School of Medicine, with colleagues in Brazil and elsewhere, say their findings support further investigation of using the repurposed drug as a potential treatment for Zika-infected adults, including pregnant women.

 Zika infection during the first trimester confers the greatest risk of congenital microcephaly. Outbreaks of Zika virus in Brazil in 2015 and 2016 were marked by an increased incidence of newborns with congenital malformations, most notably undersized heads (microcephaly) and significant neurological abnormalities.

A great deal of research has focused on the pathology of Zika infections, including earlier work by the Muotri lab and collaborators that described how the virus is transmitted from mother to fetus by infecting cells that, ironically, will later develop into the brain's first and primary form of defense against invasive pathogens.

In its latest work, however, the Muotri lab sought clinical solutions. The team investigated an antiviral drug called sofosbuvir, approved and marketed under the brand name Sovaldi to treat and cure hepatitis C infections. The drug works by inhibiting replication of the hepatitis C virus; researchers noted that both hepatitis C and Zika belong to the same viral family and bore strong structural similarities that could make sofosbuvir effective against the latter. In addition, it had been reported that sofosbuvir was protective against Zika in different cell types.

In tests using human neural progenitor cells (NPCs)-self-renewing, multipotent cells that generate neurons and other brain cell types-the scientists found that exposure to sofosbuvir not only rescued dying NPCs infected with the Zika virus, but restored gene expression linked to their antiviral response. In subsequent tests using an immunodeficient mouse model infected by Zika, intravenous injections of sofosbuvir significantly reduced viral loads in blood serum compared to a placebo group.

Fetuses of Zika-infected pregnant mice did not show detectable Zika virus amplification in the sofosbuvir-treated group. This shows that the drug was well-tolerated by the Zika-infected pregnant mice and that it was able to arrest Zika replication in vivo and stop transmission from mother to fetus.
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Smoking linked to heart disease and stroke

Smoking just one cigarette a day has a higher risk of developing coronary heart disease and stroke than expected. The researchers say their findings have important consequences for many smokers and health professionals who believe that smoking only a few cigarettes carries little or no harm. They argue that smokers should stop completely instead of cutting down to significantly reduce their risk of heart disease and stroke.

Individual studies have reported that smoking only one to five cigarettes per day is associated with a higher than expected risk of heart disease. To investigate this further, a team of researchers led by Professor Allan Hackshaw at the UCL Cancer Institute at University College London analysed the results of 141 studies and estimated the relative risks for smoking one, five, or 20 cigarettes per day. They found that men who smoked one cigarette per day had 46% of the excess risk of heart disease and 41% of the excess risk of stroke associated with smoking 20 cigarettes per day (much higher than the expected 5%).

For women, those who smoked one cigarette per day had 31% of the excess risk of heart disease and 34% of the excess risk of stroke associated with smoking 20 cigarettes per day. Women's heart disease risk was more than doubled with one cigarette per day, when only studies that controlled for several factors were included in the analysis. Large proportion of the risk of coronary heart disease and stroke comes from smoking only a couple of cigarettes each day.

Cardiovascular disease, not cancer, is the greatest mortality risk for smoking, causing about 48% of smoking-related premature deaths. Any exposure to smoking is too much, there is no safe level of smoking. Smokers should quit instead of cutting down, using appropriate cessation aids if needed, to significantly reduce their risk of stroke and heart disease.
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Air pollution may shorten telomers in babies

A study conducted before and after the 2004 closure of a coal-burning power plant in Tongliang, China, found children born before the closure had shorter telomeres than those conceived and born after the plant stopped polluting the air. Telomeres are specialized sections of DNA that allow chromosomes to be faithfully copied during cell division. However, with each round of cell division, telomeres shorten, resulting in a gradual loss of genomic stability. Shortened telomere length has been linked with cancer and heart disease, cognitive decline, aging, and premature death.

Led by Deliang Tang and Frederica Perera at Columbia University's Mailman School of Public Health, the research team analyzed telomere length in the umbilical cord blood of 255 newborns, about half of whom were born before the plant closure and half conceived and born after. In babies born pre-closure, researchers found higher levels of PAH-DNA cord adducts, a biomarker for exposure to polycyclic aromatic hydrocarbons , a toxic component of air pollution from coal plants.

 Elevated levels of these adducts in cord blood were associated with shorter telomeres-the first time this relationship has been tested as well as with lower levels of brain-derived neurotropic factor (BDNF), a protein involved in neuronal grown. However, telomere length was not associated with developmental score in the subset of 210 children tested at age 2, although the researchers say the finding doesn't rule out telomere length-related neurodevelopmental problems at later ages.

Individual's telomere length at birth is known to influence their risk for disease later during adulthood, high levels of air pollution in Tongliang prompted the government to shut down the local coal-burning power plant to improve community health. This action, announced in advance, provided a unique opportunity to compare data on ambient PAH levels, biomarkers, and health outcomes in two successive cohorts of children, with and without prenatal exposure to emissions from the coal-fired power plant.

In previously published research on these cohorts, the authors reported newborns born after the plant closure had lower levels of PAH-DNA adducts, lower rates of various health outcomes, and increased levels of BDNF. The new study adds to the evidence that closing this coal-burning power plant was beneficial to the health and future well-being of newborns there, reducing exposure to air pollution is recommended for pregnant women and infants.
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Links between fetal movements and musculoskeletal malformation

A team of researchers with Imperial College London and Great Ormond Street Hospital, both in the U.K., has found that monitoring fetal movements in pregnant women can help in detecting fetal musculoskeletal malformations.

A kicking baby is one of the milestones of a healthy pregnancy, but as the researchers note, few investigations have been conducted into what actually occurs in the womb as the fetus grows and begins moving around.

Researchers analyzed MRI scans from patients which allowed them to create models of fetal movement. The models produced animated representations of a fetus inside the uterus as it stretched, kicked and moved in other ways, allowing the team to track how much force the fetus was exerting on its environment.

They found that a fetus is able to exert up to 4 kilograms of force against the walls of the uterus at around 30 weeks, the peak time for fetal activity. After that, fetal force was reduced as the fetus found itself with less room to maneuver due to its increasing size.

The team also found that kicking was a form of exercise, helping the growing fetus develop proper muscle and bone structures. They also found that even after the fetus had reduced room for movement, fetal kicking was still important because the stress helped leg and arm joints to develop properly.

The researchers report that fetal movement is critical for normal development of bones and joints. These last findings proved to be particularly useful, the team notes, because a lack of movement, whether kicking or otherwise, could predict musculoskeletal malformations after birth.
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Changes in mother's bacteria causes premature birth

A study of hundreds of women, carried out at Imperial College London, found that subtle changes to the bacteria present in the vagina were strongly associated with the mother's waters breaking early and preterm birth-the baby being born before 37 weeks. According to the researchers, the findings show that a shift away from the usual healthy balance of vaginal bacteria was associated with waters breaking early, and could have an impact on the health of mother and baby, including increasing the risk of sepsis for newborns.

During pregnancy babies are protected inside the amniotic sac, with the surrounding membrane rupturing as part of the normal birthing process when the mother's 'waters break' as a precursor to labour. However, when this occurs before 37 weeks, termed premature rupture of membrane (PPROM), the baby is likely to be born prematurely. After the membranes rupture, the baby remains without the protective membrane and is at increased risk of infection - as the vaginal bacteria spread upwards to the placenta and uterus. In order to reduce this risk, the women whose waters have broken early are given intravenous antibiotics.

Researchers from the Institute of Reproductive and Developmental Biology (IRDB) at Imperial looked at the impact of premature rupturing of the membrane and antibiotic treatment on the vaginal microbiota, taking swabs from the vaginas of pregnant women at different points during their pregnancy and analysing them to reveal the types of bacteria present, their proportions and any changes.

Samples were collected from a prospective group of 250 pregnant women with and without risk factors for giving birth prematurely - such as having a history of preterm birth or miscarriage - of which 27 did in fact have a premature birth. They also collected samples from a second, smaller group of 87 women who presented to hospital with premature membrane rupture.

Previous research has shown that over the course of pregnancy the bacteria that colonise the vagina become less diverse and are dominated chiefly by Lactobacillus species, the same type of bacteria found elsewhere in the body including the gut and mouth. Analysis of the team's samples revealed that premature membrane rupture was associated with a shift in microbiota, with a drop in Lactobacillus and an increase in other types of bacteria, including potentially harmful bugs such as Staphylococcus and Streptococcus.

The team also analysed samples from the small group of women with premature rupture before and after the preventative antibiotic treatment - oral erythromycin, four times a day for 10 days. Swabs were taken before treatment and then at 48 hours, one week and two weeks. For those women whose microbial makeup was dominated by Lactobacillus before the treatment, the antibiotics resulted in a decline in Lactobacillus and a greater diversity of bugs. However, in those women with reduced Lactobacillus to begin with, the treatment was beneficial in some, reducing the amount of potentially harmful bacteria as well.

The study also revealed associations between specific vaginal bacteria and newborns who developed sepsis following delivery. While the mothers of healthy babies were dominated by Lactobacillus, samples from the mothers of newborns with sepsis revealed a greater diversity of bacteria, including the presence of Streptococcus and E. coli.
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Social and emotional behaviours improve learning

Students with well-developed and adaptive social and emotional behaviours are most likely to excel in school, according to UNSW researchers in educational psychology. The two-part study of 153,437 NSW kindergarten students shows that adaptive social and emotional behaviours in kindergarten correspond with better results in school years later.

The UNSW researchers, in partnership with the University of Sydney, assessed children on their cooperative, socially responsible, helpful, anxious, and aggressive-disruptive behaviours in kindergarten. These ratings were then used to identify social and emotional behavioural profiles to understand how students tend to fare on the five behaviours.

Children in profiles that were higher in cooperative, socially responsible, and helpful behaviours in kindergarten were more likely to achieve better results in grades 3 and 5. Children in profiles with higher levels of aggressive-disruptive behaviours-such as physical violence, excluding other children, or temper tantrums-tended to receive lower results.

Children who were in profiles higher in anxious behaviours had less obvious outcomes, but often achieved slightly lower school results, possibly because they tended to also exhibit lower helpful and cooperative behaviours. This may have been due to anxiety making socialisation with other students more difficult.

Children's social and emotional behaviours in the early years were powerful predictors of later outcomes, making it essential to teach social and emotional skills and behaviours from an early age.
Five major social and emotional skills that were important precursors to adaptive social and emotional behaviours: self-awareness, which refers to a person's ability to be aware of and understand their emotions, values, strengths, and weaknesses (such as being able to identify feelings of frustration or anger when they occur)

Self-management, which refers to the ability to control or adjust emotions and behaviour as needed in different situations. Social awareness, which refers the ability to take other people's perspective and feel empathy (such as being able to consider how a situation may be perceived by others) relationship skills, which entail the capacity to listen effectively, communicate clearly, cooperate with others, and offer help as needed (such as being able to work well in a group) responsible decision-making, which refers to the capacity to make choices in diverse settings that are respectful and constructive (such as understanding that actions appropriate at home may be different from those appropriate at school).

Social and emotional skills helped children and adolescents form and maintain positive relationships at school and beyond, behave in ways that allowed them to get on well with others, and perform well academically. These skills are fundamental to the way we interact and our capacity to respond to  what life throws our way.
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Links between flu and heart attack

Chances of a heart attack are increased during the first seven days after detection of laboratory-confirmed influenza infection, according to a new study by researchers at the Institute for Clinical Evaluative Sciences (ICES) and Public Health Ontario (PHO). Researchers found a significant association between acute respiratory infections, particularly influenza, and acute myocardial infarction.

The risk may be higher for older adults, patients with influenza B infections, and patients experiencing their first heart attack. The researchers also found elevated risk - albeit not as high as for influenza - with infection from other respiratory viruses. Influenza vaccination reduces cardiovascular events and mortality, support international guidelines that advocate for influenza immunization in those at high risk of a heart attack.

The researchers examined adult cases of laboratory-confirmed influenza infection from 2009 to 2014 and identified 332 patients who were hospitalized for a heart attack within one year of a laboratory-confirmed influenza diagnosis. People at risk of heart disease should take precautions to prevent respiratory infections, and especially influenza, through measures including vaccinations and handwashing.
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