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In a study published in Environment International researchers at Karolinska Institutet in Sweden show how PFAS industrial chemicals, which are used in many consumer products, pass through the placenta throughout pregnancy to accumulate in fetal tissue. Further research is now needed to ascertain the effect that highly persistent PFAS chemicals have on the fetus.

The PFAS () group comprises thousands of human-made chemicals, which, thanks to their water- and grease-resistant properties, are used in everything from frying pans and food packaging to clothes, cleaning agents and firefighting foams.

“We’ve focused on six of these PFAS substances and found that all appear to the same extent in as in the placenta,” says Richelle Duque Björvang, doctoral student at the Department of Clinical Science, Intervention and Technology, Karolinska Institutet. “So when the baby is born, it already has a build-up of these chemicals in the lungs, liver, brain, and elsewhere in the body.”

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Monitoring their sleeping patterns, researchers identified an increase in the duration and continuity of REM sleep and specific brain oscillations characteristic of REM sleep, whereas ‘deep’ sleep, or non-REM sleep, did not change. The changes in REM sleep were very tightly linked to deficiency in the regulation of the stress hormone corticosterone. Mild stress also caused changes in gene expression in the brain.

The first and most distinct consequence of daily mild stress is an increase in rapid-eye-movement (REM) sleep, a new study in the journal PNAS reports. The research also demonstrated that this increase is associated with genes involved in cell death and survival.

REM sleep, also known as paradoxical sleep, is the sleep state during which we have most of our dreams and is involved in the regulation of emotions and memory consolidation. REM sleep disturbances are common in mood disorders, such as depression. However, little was known about how sleep changes are linked to molecular changes in the brain.

During this 9-week study, conducted by researchers from the Surrey Sleep Research Centre at the University of Surrey in collaboration with Eli Lilly, mice were intermittently exposed to a variety of mild stressors, such as the odour of a predator. Mice exposed to mild stressors developed signs of depression; they were less engaged in self-care activities; were less likely to participate in pleasurable activities such as eating appetising food, and became less social and interested in mice they hadn’t encountered before.

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Food additives known as dietary emulsifiers, commonly found in processed foods to improve texture and extend shelf life, may adversely affect anxiety-related and social behaviors in mice, Georgia State researchers have found.

The scientists also observed sex differences in the mice’s behavioral patterns, suggesting that emulsifiers affect the brain via distinct mechanisms in males and females.

The study, published in Scientific Reports, was led by Geert de Vries, professor of neuroscience and associate vice president for research at Georgia State, and Benoit Chassaing, assistant professor of neuroscience. Andrew T. Gewirtz, professor in the Institute for Biomedical Sciences, also contributed.

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A research team with the participation of the Institute for Integrative Systems Biology (I2SysBio) of the University of Valencia, together with FISABIO and CIBERESP, has carried out the first metatranscriptomic study of the gut microbiota of babies, which has allowed to unveil the metabolism of the intestinal bacterial community during the first year of life, with a level of detail unknown until now.

This work has also involved researchers from the Joint Unit in Genomics and Health of the Foundation for the Promotion of Health and Biomedical Research of the Valencian Community (FISABIO) and the Biomedical Research Consortium in Epidemiology and Public Health Network (CIBERESP), dependent on the Carlos III Health Institute.

The environment is very important in the first years of life, both for the baby and for the bacteria of its gut microbiota. Bacteria and humans coexist in a harmonious symbiosis: people share with them the food they eat, which helps them to metabolise (10% of the energy obtained from food is as a consequence of bacterial action). In addition, bacteria influence the development of the immune and nervous systems.

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Immune cells called macrophages are supposed to serve and protect, but cancer has found ways to put them to sleep. Now researchers at the Abramson Cancer Center of the University of Pennsylvania say they’ve identified how to fuel macrophages with the energy needed to attack and eat cancer cells. It is well established that macrophages can either support cancer cell growth and spread or hinder it. But most tumors also express a signal called CD47, which can lull macrophages into a deep sleep and prevent them from eating. Researchers have found that rewiring macrophage metabolism can overcome this signal and act like an alarm clock to rouse and prepare macrophages to go to work. Their findings were published in Nature Immunology today.

Macrophages are just like T and B cells, but differ in that they can eat cells that are not supposed to be in the body. In fact, they are the most prominent immune cell found in cancer, but unfortunately, most are often convinced to help cancer grow and spread. Cancer cells frequently stop macrophages from attacking them by expressing CD47, a “don’t eat me” signal. Researchers now say that merely blocking inhibitory signals like CD47 is not always sufficient to convince macrophages to attack cancer. Instead, two signals are required. First, they need a signal to activate them—such as a toll-like receptor agonist. After that, a second signal—such as a CD47 inhibitor—can lower the threshold needed to wage battle on the cancer.

“It turns out macrophages need to be primed before they can go to work, which explains why may resist treatment with CD47 inhibitors alone,” said the study’s senior author Gregory L. Beatty, MD, Ph.D., an assistant professor of Hematology-Oncology at Penn’s Perelman School of Medicine. Jason Mingen Liu, an MD and Ph.D. graduate student in Beatty’s lab, is the study’s lead author.

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| Local | http://idahostatejournal.com/ Cutting calories (dieting) and increasing caloric expenditure (exercise) cause your brain to activate neurons that will not allow you to utilize fat or lose weight.

Recently, and at a most appropriate time, another study published in the journal eLife has given explanation as to why your current New Year’s Resolution diet will not work.

Cutting calories (dieting) and increasing caloric expenditure (exercise) cause your brain to activate neurons that will not allow you to utilize fat or lose weight.

Evolutionarily, when our ancestors living in what we now call Pocatello were hard pressed to find food, their brains stopped energy expenditure (using energy to move, be active, play, etc.) to slow them down to keep them alive.

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Hybrid vs Heirloom Vegetables with Levi.

What is the difference between hybrid and heirloom? Are hybrids bad? Are they natural? What is an heirloom? How old is an heirloom? Those questions and more are answered in this episode of Levi Explains.

.99 Heirloom Vegetable Seeds: http: www.migardener.com/store

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