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Viruses are masterful invaders. They cannibalize host cells by injecting their genetic material, often making thousands of copies of themselves in a single cell to ensure their replication and survival.

Some RNA insert their genetic material as a single piece, while others chop it up into pieces. The latter are aptly named segmented viruses.

Such segmented RNA viruses—including several that cause human diseases like influenza—have been a longstanding enigma to researchers: How do they accomplish the precise copying and insertion of each segment? How do they ensure that individual segments are all copied by the same enzyme while ensuring that each segment can make different amounts of RNA? Such exquisite regulation is critical to make the correct levels of the viral proteins necessary for successful replication.

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Scientists might have found an early detection method for some forms of dementia, according to new research by the University of Arizona and the University of Toronto’s Baycrest Health Sciences Centre.

According to the study published in the journal Neuropsychologia last month, patients with a rare neurodegenerative disorder called Primary Progressive Aphasia, or PPA, show abnormalities in in areas that look structurally normal on an MRI scan.

“We wanted to study how degeneration affects function of the brain,” said Aneta Kielar, the study’s lead author and assistant professor in the UA Department of Speech, Language and Hearing Sciences.

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Chikungunya virus, once confined to the Eastern Hemisphere, has infected more than 1 million people in the Americas since 2013, when mosquitoes carrying the virus were discovered in the Caribbean. Most people who become infected develop fever and joint pain that last about a week. But in up to half of patients, the virus can cause severe arthritis that persists for months or years. There is no treatment to prevent the short-lived infection from persisting into chronic arthritis.

Now, researchers have uncovered information that could help stop the debilitating condition. A team at Washington University School of Medicine in St. Louis has snapped high-resolution pictures of the virus latched onto a found on the surface of cells in the joints. The protein used in the study was taken from mice, but people have the same protein, and the virus interacts with the mouse and human proteins in virtually identical ways.

The structures, published May 9 in the journal Cell, shows in atomic-level detail how the virus and cell-surface protein fit together – data that promises to accelerate efforts to design drugs and vaccines to prevent or treat arthritis caused by chikungunya or related viruses.

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University of Sydney research provides new evidence that nanoparticles, which are present in many food items, may have a substantial and harmful influence on human health.

The study investigated the health impacts of food additive E171 (titanium dioxide nanoparticles) which is commonly used in high quantities in foods and some medicines as a whitening agent. Found in more than 900 food products such as chewing gum and mayonnaise, E171 is consumed in high proportion everyday by the general population.

Published in Frontiers in Nutrition, the mice study found that consumption of food containing E171 has an impact on the gut microbiota (defined by the trillions of bacteria that inhabit the gut) which could trigger diseases such as inflammatory bowel diseases and colorectal cancer.

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The human body has powerful healing abilities. But treating brain disorders is no easy task, as brain cells—neurons—have limited ability to regenerate. Nonetheless, stem cells are a form of natural backup, a vestige of our days as still-developing embryos.

The difficulty is that with age, neural stem cells ‘fall asleep’ and become harder to wake up when repairs are needed. Despite efforts to harness these cells to treat neurological damage, scientists have until recently been unsuccessful in decoding the underlying ‘sleep’ mechanism.

Now, researchers at Kyoto University studying brain chemistry in mice have revealed the ebb and flow of gene expression that may wake neural stem cells from their slumber. These findings, which may also apply to stem cells elsewhere in the body, were recently published in the journal Genes & Development.

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As cancer cells respond to cues in their microenvironment, they can enter a highly plastic state in which they are susceptible to transdifferentiation into a different type of cell. Researchers at the University of Basel in Switzerland exploited this critical phase, known as an epithelial-mesenchymal transition (EMT), to coax breast cancer cells in mice to turn into harmless fat cells. The proof-of-concept study appears January 14 in the journal Cancer Cell.

“The breast cancer cells that underwent an EMT not only differentiated into fat cells, but also completely stopped proliferating,” says first author Gerhard Christofori, professor of biochemistry at the University of Basel. What’s more, the did not metastasize. “As far as we can tell from long-term culture experiments, the cancer cells-turned-fat cells remain fat cells and do not revert back to breast cancer cells,” he says.

Epithelial cells undergoing EMT regress from terminally differentiated cells to a more immature state reminiscent of stem cells. EMT is essential for embryonic development, during which stem cells differentiate into a variety of cell types throughout the body, and for tissue regeneration such as wound healing. EMT and the inverse process, mesenchymal-epithelial transition (MET), are implicated in cancer’s ability to metastasize.

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We’d like to draw attention to an initiative whose objectives are close to our own: the German Party for Health Research (GPHR, Partei für Gesundheitsforschung in German). Founded in January 2015 by three biochemists and one actor, the GPHR is rather unique in that it is a single-issue party: its only concern is the creation of effective therapies to treat and prevent the pathologies of old age.

Since its creation, the party has participated in five elections; one of its biggest successes was the Berlin state elections in September 2016, where it received 0.5% of the secondary votes despite being still a rather unknown party. Slowly but steadily, the party has enjoyed an increase in voter support over the years, doing even better than the well-known Pirate Party in one election district during the 2017 federal elections. Currently, the party counts over 250 members, a very heterogeneous group of young and old people with different backgrounds.

The GPHR was founded because the founding members, including biochemist Felix Werth, wanted to give people a new way to support research against age-related diseases; not everyone is willing or capable to help the cause in traditional ways, such as by donating money or time to research or advocacy organizations, while a political party offers simpler yet effective ways to help, such as voting for the party, signing for its participation in elections, or even joining for free as a member.

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The human microbiome, the huge collection of microbes that live inside and on our body, profoundly affects human health and disease. The human gut flora in particular, which harbor the densest number of microbes, not only break down nutrients and release molecules important for our survival but are also key players in the development of many diseases including infections, inflammatory bowel diseases, cancer, metabolic diseases, autoimmune diseases, and neuropsychiatric disorders.

Most of what we know about human– interactions is based on correlational studies between disease state and bacterial DNA contained in stool samples using genomic or metagenomic analysis. This is because studying direct interactions between the microbiome and outside the human body represents a formidable challenge, in large part because even commensal bacteria tend to overgrow and kill within a day when grown on culture dishes. Many of the commensal microbes in the intestine are also anaerobic, and so they require very low oxygen conditions to grow which can injure human cells.

A research team at Harvard’s Wyss Institute for Biologically Inspired Engineering led by the Institute’s Founding Director Donald Ingber has developed a solution to this problem using ‘organ-on-a-chip’ (Organ Chip) microfluidic culture technology. His team is now able to culture a stable complex human microbiome in direct contact with a vascularized human intestinal epithelium for at least 5 days in a human Intestine Chip in which an oxygen gradient is established that provides high levels to the endothelium and epithelium while maintaining hypoxic conditions in the intestinal lumen inhabited by the commensal bacteria. Their “anaerobic Intestine Chip” stably maintained a microbial diversity similar to that in human feces over days and a protective physiological barrier that was formed by human intestinal tissue. The study is published in Nature Biomedical Engineering.

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