If you reach for water when a muscle cramp strikes, you might want to think again. New research from Edith Cowan University (ECU) has revealed drinking electrolytes instead of pure water can help prevent muscle cramps.
The study, published in the Journal of the International Society of Sports Nutrition, found that people who drank electrolyte enhanced water during and after exercise were less susceptible to muscle cramps than those who drank pure water.
Muscle cramps are a common painful condition affecting many people, including around 39 per cent of marathon runners, 52 per cent of rugby players and 60 per cent of cyclists.
Dilution solution
Lead researcher Professor Ken Nosaka, from ECU’s School of Medical and Health Sciences, said the study builds on the evidence that a lack of electrolytes contributes to muscle cramps, not dehydration.
“Many people think dehydration causes muscle cramps and will drink pure water while exercising to prevent cramping,” he said.

Scientists are learning that a lesser-studied region on the pandemic coronavirus is recognized by COVID-19 infection-fighting antibodies. These antibodies were identified in blood samples from previously infected patients, and were found to potently prevent the virus from infecting cells.
The coronavirus spike protein is the key that unlocks the door to the cell, and antibodies bind to the spike protein to jam this function. Much attention has been given to studying antibodies that target the receptor-binding domain on the coronavirus spike protein. (The receptor-binding domain of the spike is responsible for triggering the merging of the virus with a host cell to achieve a takeover.)
However, some of the recovered patients’ antibodies blocked the coronavirus by binding to a different place on the virus spike — the N-terminal domain. These antibodies were as strong as those that bind to receptor-binding domain, a recent study shows.
Using electron cryo-microscopy (cryoEM) to map where these antibodies bound showed that all the antibodies that prevent infection bind a single place on the N-terminal domain. The research published in Cell demonstrated that these antibodies protected Syrian hamsters from SARS-CoV-2, the coronavirus that causes COVID-19 in people.
Additional recent findings indicate that the virus is slowly defying these antibodies that people are acquiring. The virus is adapting to these antibodies by accumulating mutations that help the virus escape these defenses, becoming so-called variants-of-concern.
Some of these variants, such as those first detected in the United Kingdom and South Africa, contain mutations that appear to make the virus less vulnerable to the neutralizing power of the N-terminal domain antibodies.

People who start eating before 8:30 a.m. had lower blood sugar levels and less insulin resistance, which could reduce the risk of developing type 2 diabetes, according to a study presented virtually at ENDO 2021, the Endocrine Society’s annual meeting.
“We found people who started eating earlier in the day had lower blood sugar levels and less insulin resistance, regardless of whether they restricted their food intake to less than 10 hours a day or their food intake was spread over more than 13 hours daily,” said lead researcher Marriam Ali, M.D., of Northwestern University in Chicago, Ill.
Insulin resistance occurs when the body doesn’t respond as well to the insulin that the pancreas is producing and glucose is less able to enter the cells. People with insulin resistance may be at higher risk of developing type 2 diabetes. Both insulin resistance and high blood sugar levels affect a person’s metabolism, the breaking down of food to its simpler components: proteins, carbohydrates (or sugars), and fats. Metabolic disorders such as diabetes occur when these normal processes become disrupted.
“With a rise in metabolic disorders such as diabetes, we wanted to expand our understanding of nutritional strategies to aid in addressing this growing concern,” Ali said. Previous studies have found that time-restricted eating, which consolidates eating to a shortened timeframe each day, has consistently demonstrated improvement in metabolic health, she noted. Her group wanted to see whether eating earlier in the day affected metabolic measures.
The researchers analyzed data from 10,575 adults who participated in the National Health and Nutrition Examination Survey. They divided participants into three groups depending on total duration of food intake: less than 10 hours, 10-13 hours, and more than 13 hours per day. They then created six subgroups based on eating duration start time (before or after 8:30 a.m.).
They analyzed this data to determine if eating duration and timing were associated with fasting blood sugar levels and estimated insulin resistance. Fasting blood sugar levels did not differ significantly among eating interval groups. Insulin resistance was higher with shorter eating interval duration, but lower across all groups with an eating start time before 8:30 a.m.
“These findings suggest that timing is more strongly associated with metabolic measures than duration, and support early eating strategies,” Ali said.
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A study conducted at Columbia University Mailman School of Public Health reports a high global prevalence of both depression and anxiety during the COVID-19 pandemic and shows how implementation of mitigation strategies including public transportation and school closures, and stay-at-home orders impacted such disorders. The results are published in Psychological Medicine.
“Our research found an elevated global prevalence of these mental health issues during COVID-19 and also revealed there was a wide variance in each at the region- and country-level,” said, João Castaldelli-Maia, MD, PhD, NIDA-INVEST Postdoctoral Fellow in the Department of Epidemiology, and lead author. In particular, Asia (most studies came from China) presented lower levels of both anxiety and depression, compared to the other regions of the world. Closure of public transportation increased levels of anxiety, whether it was two weeks or four weeks past the passage of closure enactment, especially in Europe.”
Using an end date of July 29th, 2020, the researchers analyzed data from Pubmed, MEDLINE, Web of Science, and medRxiv, among other databases, for depression and anxiety prevalence. They also reviewed the Oxford Covid-19 Government Response Tracker for the containment and closure policies indexes; and the Global Burden of Disease Study for previous levels of depression and anxiety. The WHO database which includes COVID literature for studies published by the same date was also used.
In total, 226,638 individuals were assessed within 60 included studies. Global prevalence of both depression and anxiety during the COVID-19 pandemic were 24 percent and 21 percent, respectively. Asia with rates of 18 percent for each, and China especially, had the lowest prevalence of both disorders. Regarding the impact of mitigation strategies on mental health — whether it was public transportation closures, school closings, workplace closures, cancellation of public events, or restrictions on gathering — only public transportation closures increased prevalence of anxiety, especially in Europe.
Castaldelli-Maia and colleagues found a 21 percent global prevalence of anxiety. Asia had lower levels of anxiety (18 percent) compared to other regions of the world (29 percent). In this case, Europe did not differ from Asia and other regions of the world. Again, a subgroup analysis at the country-level showed that China had a lower prevalence of anxiety at 15.5 percent compared to all other countries at 26 percent.
“Our study confirms how critical it is to investigate levels of mental health disorders and the possible impacts of social distancing measures on mental health outcomes, according to Silvia Martins, MD, PhD, associate professor of Epidemiology at Columbia Mailman School, and senior author. “Mental health concerns should not be viewed only as a delayed consequence of the COVID-19 pandemic, but also as a concurrent epidemic.”
Within the subgroup of Asian countries, estimates of depression prevalence ranged from 15 percent to 20 percent. When comparing the prevalence of depression in the pre-and post-COVID-19 eras, the estimates ranging from 1.3-3.4 percent, are demonstrably larger after the initiation of COVID-19.

Our knowledge of Alzheimer’s disease has grown rapidly in the past few decades but it has proven difficult to translate fundamental discoveries about the disease into new treatments. Now researchers at the California National Primate Research Center at the University of California, Davis, have developed a model of the early stages of Alzheimer’s disease in rhesus macaques. The macaque model, published March 18 in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association could allow better testing of new treatments.
The model was developed by Professor John Morrison’s laboratory at the CNPRC, in collaboration with Professor Jeffrey Kordower of Rush University Medical Center and Paramita Chakrabarty, assistant professor at the University of Florida.
Alzheimer’s disease is thought to be caused by misfolding of the tau and amyloid proteins. Misfolded proteins spread through the brain, leading to inflammation and cell death. Tau protein is commonly found in neurons of the brain and central nervous system, but not elsewhere.
Researchers think that decades may elapse between the silent beginnings of the disease and the first signs of cognitive decline. Understanding what happens over these years could be key to preventing or reversing symptoms of Alzheimer’s disease. But it is difficult to study therapeutic strategies without a powerful animal model that resembles the human condition as closely as possible, Morrison said. Much research has focused on transgenic mice that express a human version of amyloid or tau proteins, but these studies have proven difficult to translate into new treatments.
New translational models needed
Humans and monkeys have two forms of the tau protein in their brains, but rodents only have one, said Danielle Beckman, postdoctoral researcher at the CNPRC and first author on the paper.

Low doses of propylparaben — a chemical preservative found in food, drugs and cosmetics — can alter pregnancy-related changes in the breast in ways that may lessen the protection against breast cancer that pregnancy hormones normally convey, according to University of Massachusetts Amherst research.
The findings, published March 16 in the journal Endocrinology, suggest that propylparaben is an endocrine-disrupting chemical that interferes with the actions of hormones, says environmental health scientist Laura Vandenberg, the study’s senior author. Endocrine disruptors can affect organs sensitive to hormones, including the mammary gland in the breast that produces milk.
“We found that propylparaben disrupts the mammary gland of mice at exposure levels that have previously been considered safe based on results from industry-sponsored studies. We also saw effects of propylparaben after doses many times lower, which are more reflective of human intake,” Vandenberg says. “Although our study did not evaluate breast cancer risk, these changes in the mammary tissue are involved in mitigating cancer risk in women.”
Hormones produced during pregnancy not only allow breast tissue to produce milk for the infant, but also are partly responsible for a reduced risk of breast cancer in women who give birth at a younger age.
The researchers, including co-lead author Joshua Mogus, a Ph.D. student in Vandenberg’s lab, tested whether propylparaben exposure during the vulnerable period of pregnancy and breastfeeding adversely alters the reorganization of the mammary gland. They examined the mothers’ mammary glands five weeks after they exposed the female mice to environmentally doses of propylparaben during pregnancy and breastfeeding.
Compared with pregnant mice that had not received propylparaben, the exposed mice had mammary gland changes not typical of pregnancy, the researchers report. These mice had increased rates of cell proliferation, which Vandenberg says is a possible risk factor for breast cancer. They also had less-dense epithelial structures, fewer immune cell types and thinner periductal collagen, the connective tissue in the mammary gland.
“Some of these changes may be consistent with a loss of the protective effects that are typically associated with pregnancy,” says Mogus, who was chosen to present the research, deemed “particularly newsworthy” by the Endocrine Society, at the international group’s virtual annual meeting, ENDO 2021, beginning March 20.
Mogus says future studies should address whether pregnant females exposed to propylparaben are actually more susceptible to breast cancer. “Because pregnant women are exposed to propylparaben in many personal care products and foods, it is possible that they are at risk,” Mogus says, adding that pregnant and breastfeeding women should try to avoid using products containing propylparaben and other parabens.
“This chemical is so widely used, it may be impossible to avoid entirely,” Mogus adds. “It is critical that relevant public health agencies address endocrine-disrupting chemicals as a matter of policy.”
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Scientists at Sanford Burnham Prebys Medical Discovery Institute demonstrated for the first time that blocking “cell drinking,” or macropinocytosis, in the thick tissue surrounding a pancreatic tumor slowed tumor growth — providing more evidence that macropinocytosis is a driver of pancreatic cancer growth and is an important therapeutic target. The study was published in Cancer Discovery, a journal of the American Association for Cancer Research.
“Now that we know that macropinocytosis is ‘revved up’ in both pancreatic cancer cells and the surrounding fibrotic tissue, blocking the process might provide a ‘double whammy’ to pancreatic tumors,” says Cosimo Commisso, Ph.D., associate professor and co-director of the Cell and Molecular Biology of Cancer Program at Sanford Burnham Prebys and senior author of the study. “Our lab is investigating several drug candidates that inhibit macropinocytosis, and this study provides the rationale that they should be advanced as quickly as possible.”
Pancreatic cancer remains one of the deadliest cancers. Only one in ten people survive longer than five years, according to the American Cancer Society, and its incidence is on the rise. Pancreatic cancer is predicted to become the second-leading cause of cancer-related deaths in the U.S. by 2030.
“If we want to create a world in which all people diagnosed with pancreatic cancer will thrive, we first need to understand the key drivers of tumor growth,” says Lynn Matrisian, Ph.D., chief science officer at the Pancreatic Cancer Action Network (PanCAN), who wasn’t involved in the study. “This study suggests that macropinocytosis is an important target for drug development, and that progressing this novel treatment approach may help more people survive pancreatic cancer.”
Starving the stroma
Pancreatic tumors are surrounded by an unusually thick layer of stroma, or glue-like connective tissue that holds cells together. This stromal barrier makes it difficult for treatments to reach the tumor, and fuels tumor growth by providing the tumor with nutrients. Commisso’s previous research showed that rapidly growing pancreatic tumors obtain nutrients through macropinocytosis, an alternative route that normal cells don’t use — and he wondered if macropinocytosis in the stroma may also fuel tumor growth.
To test this hypothesis, Commisso and his team blocked macropinocytosis in cells that surround and nourish pancreatic tumors, called pancreatic cancer-associated fibroblasts (CAFs), and co-transplanted the modified cells with pancreatic tumor cells into mice. The scientists found that tumor growth slowed in these mice — compared to control groups in which macropinocytosis remained active in the stroma — suggesting that the approach holds promise as a way to treat pancreatic cancer.
“We are excited about this approach because instead of removing the stroma, which can cause the tumor to spread throughout the body, we simply block the process that is driving tumor growth,” says Yijuan Zhang, Ph.D., postdoctoral researcher in the Commisso lab and first author of the study. “We also deciphered the molecular signals that drive macropinocytosis in the stroma, providing new therapeutic avenues for pancreatic cancer researchers to explore.”
Promising drug targets identified
Based on their ongoing macropinocytosis research, the scientists have identified many druggable targets that may inhibit the process. Bolstered by this study’s findings, they will continue to investigate the promise of drug candidates that inhibit macropinocytosis as potential pancreatic cancer treatments.
“We already knew that macropinocytosis was a very important growth driver for pancreatic cancer, as well as lung, prostate, bladder and colon tumors,” says Commisso. “This study further spurs our efforts to advance a drug that targets macropinocytosis, which may be the breakthrough we need to finally put an end to many deadly and devastating cancers.”

The triggers and causes of a severe scarring disease of the lungs — idiopathic pulmonary fibrosis, or IPF — remain unclear.
Now research published in Science Translational Medicine shows how cadmium and carbon black can trigger lung macrophages to produce a modified protein, citrullinated vimentin, or cit vim, which leads to lung fibrosis. Researchers from the University of Alabama at Birmingham and three other American universities also describe a sequence of mechanistic steps in lung macrophages and lung fibroblasts that leads to the lung scarring.
One of the enzymes involved in these steps — peptidylarginine deiminase 2, or PAD2 — may be a promising target to attenuate cadmium/carbon black-induced fibrosis, they say. The researchers also report a potential disease model for lung fibrosis and IPF — the use of cadmium chloride to induce interstitial fibrosis in mice.
The study, led by Veena Antony, M.D., included patients with IPF, tissue experiments and mouse models. Antony is the Endowed Professor of Environmental Medicine in the UAB Department of Medicine, and she directs the UAB Superfund Research Program.
“Altogether, these studies support a role for cit-vim as a damage-associated molecular pattern molecule, or DAMP, that is generated by lung macrophages in response to environmental cadmium/carbon black exposure,” Antony said. Cadmium is a toxic heavy metal recognized as a cause of lung fibrosis. Cadmium can adsorb onto carbon black particles. In the lung, such particles are ingested by macrophages, the sentinel host defense cells of the mammalian lung. Up to two-thirds of IPF patients have a history of smoking, and cigarette smoke contains both cadmium and carbon black. Air pollution from biomass fuels and coal furnaces is also a source of the two pollutants.
Data from human subjects
The researchers evaluated cadmium and cit-vim accumulation in tissue, using lung biopsies from 25 subjects with IPF — eight never-smokers and 17 smokers — and 14 controls — eight never-smokers and six smokers.

Does the incidence of parental burnout depend on a country’s culture? This question was at the heart of the first international study on the subject for which hundreds of scientists in 42 countries mobilised. In other words, the global scientific community is worried about family stress-induced parental burnout. A high level of stress in the family can lead to parental exhaustion. Such suffering has serious consequences for both parents and children.
‘We worked in close collaboration with scientists from all the cultures involved,’ UCLouvain researchers and study initiators and coordinators Isabelle Roskam and Moïra Mikolajczak explained in a statement. ‘They were the only ones capable of collecting data in their countries, guaranteeing their validity and interpreting them correctly. Such exceptional collaboration deserves to be highlighted.’
The study’s findings are categorical: rich, individualistic Western countries, which on average have few children, are the most affected by the phenomenon. Culture, rather than socio-economic and demographic differences between countries, plays a predominant role in parental burnout. ‘Prevalence varies greatly from one culture and country to another,’ Prof. Roskam explains. ‘We could have hypothesised that it would be the same everywhere but that the reasons for exhaustion would be different.’ This is not the case.
Published in Affective Science, the study shows that the values of individualism in Western countries can subject parents to higher levels of stress. The results force us to question ourselves in a context where the mantra of “every one for oneself” is spreading all over the world.
‘Our individualistic countries cultivate a cult of performance and perfectionism,’ says Prof. Roskam, a parental burnout specialist. ‘Parenthood in these countries is a very solitary activity, unlike in African countries, for example, where the entire village is involved in raising children.’ These poorer countries, which often have many children, are more collectivist. This dimension seems to protect against parental burnout. In addition, Western individualism is exacerbated by the current health crisis: families find themselves isolated and cut off from their social relations.
What measures can be taken to prevent stress in parenting? ‘The first would be to revive in our cultures the dimension of sharing and mutual aid among parents within a community,’ Prof. Roskam says. ‘And abandon the cult of the perfect parent and gain some perspective on all the parenting advice out there in order to choose what works for you.’
Thanks to the study consortium’s collective dynamics, their work opens up many avenues for future intercultural investigations. Until now, all studies on parental burnout focused on personal factors. However, parents affected by this syndrome exercise their parenting in a particular cultural context. It is important to take this into account when treating symptoms.
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To observe how a tiny ball of identical cells on its way to becoming a mammalian embryo first attaches to an awaiting uterine wall and then develops into nervous system, heart, stomach and limbs: This has been a highly-sought grail in the field of embryonic development for nearly 100 years. Prof. Jacob Hanna of the Weizmann Institute of Science and his group have now accomplished this feat. The method they created for growing mouse embryos outside the womb during the initial stages after embryo implantation will give researchers an unprecedented tool for understanding the development program encoded in the genes, and it may provide detailed insight into birth and developmental defects as well as those involved in embryo implantation. The results of this research were published in Nature.
Hanna, who is in the Institute’s Molecular Genetics Department, explains that much of what is known about mammalian embryonic development today comes either from observing the process in non-mammals like frogs or fish that lay transparent eggs, or by obtaining static images from dissected mouse embryos and adding them together. The idea of growing early embryos outside the uterus has been around since before the 1930s, he adds, but experiments based on these proposals had limited success and the embryos tended to be abnormal.
Hanna’s team decided to renew that effort in order to advance the research in his lab, which focuses on the way the development program is enacted in embryonic stem cells. Over seven years, through trial and error, fine-tuning and double-checking, his team came up with a two-step process in which they were able to grow normally developing mouse embryos outside the uterus for six days — around a third of their 20-day gestation — by which time the embryos already had a well-defined body plan and visible organs. “To us, that is the most mysterious and the most interesting part of embryonic development, and we can now observe it and experiment with it in amazing detail,” say Hanna.
The research was led by Alejandro Aguilera-Castrejon, Dr. Bernardo Oldak, the late Dr. Rada Massarwa and Dr. Noa Novershtern in Hanna’s lab and Dr. Itay Maza, a former student of Hanna’s now in the Rambam Health Care Campus of the Technion — Israel Institute of Technology.
For the first step, which lasted around two days, the researchers started with several-day old mouse embryos — right after they would have implanted in the uterus. At this stage the embryos were balls consisting of 250 identical stem cells. These were placed on a special growth medium in a laboratory dish and the team got the balls to attach to this medium as they would to the uterine wall. With this step, they succeeded in duplicating the first stage of embryonic development, in which the embryo doubles and triples in size, as it differentiates into three layers: inner, middle and outer.
Beyond two days, as the embryos entered the next developmental stage — the formation of organs from each of the layers — they needed additional conditions. For this second step, the scientists placed the embryos in a nutrient solution in tiny beakers, setting the beakers on rollers that kept the solutions in motion and continually mixed. That mixing seems to have helped keep the embryos, which were growing without maternal blood flow to the placenta, bathed in the nutrients. In addition to carefully regulating the nutrients in the beakers, the team learned in further experiments to closely control the gases, oxygen and carbon dioxide — not just the amounts, but the gas pressure as well.
To check whether the developmental processes they were observing throughout the two steps were normal, the team conducted careful comparisons with embryos removed from pregnant mice in the relevant time period, showing that both the separation into layers and the organ formation were all but identical in the two groups. In subsequent experiments, they inserted into the embryos genes that labeled the growing organs in fluorescent colors. The success of this attempt suggested that further experiments with this system involving various genetic and other manipulations should produce reliable results. “We think you can inject genes or other elements into the cells, alter the conditions or infect the embryo with a virus, and the system we demonstrated will give you results consistent with development inside a mouse uterus,” says Hanna.
“If you give an embryo the right conditions, its genetic code will function like a pre-set line of dominos, arranged to fall one after the other,” he adds. “Our aim was to recreate those conditions, and now we can watch, in real time, as each domino hits the next one in line.” Among other things, explains Hanna, the method will lower the cost and speed up the process of research in the field of developmental biology, as well as reducing the need for lab animals.
In fact, the next step in Hanna’s lab will be to see if they can skip the step of removing embryos from pregnant mice. He and his team intend to try to create artificial embryos made from stem cells for use in this research. Among other things, they hope to put their new method to work to answer such questions as why so many pregnancies fail to implant, why the window for implantation is so short, how stem cells gradually lose their “stemness” as differentiation progresses and what conditions in gestation may later lead to developmental disorders.
Video: https://www.youtube.com/watch?v=tNb2npuiF3Q