Researchers from the University of Luxembourg and the German Cancer Research Center have rejuvenated stem cells in the brains of old mice. The rejuvenated stem cells appear to improve regeneration in areas of damaged or diseased brain tissue.
A new way to model stem cells
A new study that was published in the journal Cell sheds light on why many stem cell populations in aged brains stop dividing and enter a dormant state known as quiescence. Quiescent stem cells have ceased to divide, so they no longer support the tissues of which they are part and play no role in regenerating damaged tissue by supplying fresh cells to replace losses. As we age, an increasing number of stem cells, not just in the brain, enter this quiescent state and impair our ability to heal injury and recover from diseases.
The biggest source of variability in the microbiome is the person-to-person variability. It’s a problem if you’re looking for causality. That’s a red flag word for us – causality – meaning something about the bacterial community causes some disease. You actually don’t know whether it’s the bacteria or whether the bacteria are a sign of something that happened before. It’s very much individualized, so everybody’s history matters.
We are all teeming with bacteria that help us digest food or fight disease, but two people might play host to a very different array of bacteria due to diet, where they live, hobbies or even medical histories.
As a result, scientists have struggled to understand which bacteria are linked to disease and which protect against it. Studies comparing people’s bacterial companions – known as the microbiome – to explore what that variation means might disagree because they analyzed different groups or didn’t sample enough people.
Statistics Professor Susan Holmes thinks one way of teasing out which differences are relevant to disease and which are just differences between people could come down to statistics and repeating studies.
NEW YORK (AP) — Did you hear what happened when Bill Gates walked into a bar? Everybody there immediately became millionaires — on average.
That joke about a very rich man is an old one among statisticians. So why did Peter Smibert use it to explain a revolution in biology?
Because it shows averages can be misleading. And Smibert, of the New York Genome Center, says that includes when scientists are trying to understand the basic unit of life, the cell.
Infections with BMMF („Bovine Milk and Meat Factors ) in humans provide a clue, why the consumption of cow milk and meat correlates with colon and breast cancers.
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Division episomal‐persistent DNA in cancer‐ and chronic diseases, deutsches krebsforschungszentrum, heidelberg, germany.
Correspondence to: Harald zur Hausen, Deutsches Krebsforschungszentrum, Heidelberg, Germany, E‐mail:
In the past few decades, a lethal disease has decimated populations of frogs and other amphibians worldwide, even driving some species to extinction. Yet other amphibians resisted the epidemic. Based on previous research, scientists at the INDICASAT AIP, Smithsonian and collaborating institutions knew that skin bacteria could be protecting the animals by producing fungi-fighting compounds. However, this time they decided to explore these as potential novel antifungal sources for the benefit of humans and amphibians.
“Amphibians inhabit humid places favoring the growth of fungi, coexisting with these and other microorganisms in their environment, some of which can be pathogenic,” said Smithsonian scientist Roberto Ibáñez, one of the authors of the study published in Scientific Reports. “As a result of evolution, amphibians are expected to possess chemical compounds that can inhibit the growth of pathogenic bacteria and fungi.”
The team first travelled to the Chiriquí highlands in Panama, where the chytrid fungus, responsible for the disease chytridiomycosis, has severely affected amphibian populations. They collected samples from seven frog species to find out what kind of skin bacteria they harbored.
Posted in biotech/medical, neuroscience
Metastasis is the leading cause of death from cancer, occurring when cancer cells separate from the original tumor to proliferate elsewhere. These new cancer cells travel through the bloodstream or lymphatic system. Since these bodily systems are thoroughly connected, cancer can spread to a variety of locations. Breast cancer, for example, “tends to spread to the bones, liver, lungs, chest wall, and brain.”
Cancer cell plasticity — an ability that allows cancer cells to shift physiological characteristics dramatically — fosters metastasis and is responsible for cancer’s resistance to treatments. To combat its resistance, researchers at the University of Basel in Switzerland decided to turn cancer’s cellular plasticity against itself. They used Rosiglitazone, an anti-diabetic drug, along with MEK inhibitors in mice implanted with breast cancer cells. Their aim was to alter the cancer cells.
The drug combination hijacked the breast cancer cells during epithelial-mesenchymal transition (EMT), a process by which the cells undergo biochemical changes. EMT plays a role in many bodily functions, such as tissue repair. In unaltered cancer cells, EMT allows them to migrate away from the original tumor while maintaining their oncogenic properties.
