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Tuesday, 23 May 2017

Ebola death risen to 4 at Republic of Congo

Medical workers treating a patient suspected of having Ebola in the Democratic Republic of Congo in 2007 (Image: Getty Images)

The overall cases of Ebola rise at Republic of Congo from 29 to 37.

World Health Organization has reported that a forth reported person has possibly died of Ebola in a remote place at northeastern of Republic of Congo.

Since early May 37 cases has been reported with hemorrhagic fever with 2 confirmed Ebola cases,  3 with probable case (including recent death) and 32 are suspected.

Mobile laboratories have been dispatched to monitor around 416 people who are known to be in contact with the sufferers.

Sunday, 21 May 2017

The slow moving Microbes in deep down under the sea

Sea bed (Image: Pixabay)

The seabed is constantly filling with dead plankton, biological life and also brining down the bio-remnants from the shore. This is ultimately packing up all the ingredients that microbes need to sustain happily. But overtime new sources accumulate layer by layer on the previous sediments. So going deep under will unveil the past sources like moving back in time.

Deep down under the compressed time provides the evolutionary biologists huge difficulty to track genetic turn with community shifts in such a stable environment. In such no change in fluid movement can allow microbes to move or give back clues for horizontal gene transfer. Thus only chance that can happen is with any possible evolutionary changes or death. It has opened consequences that microbes still thrive as we go much deep down under the seabeds.

In a recent study that published in Proceedings of the National Academy of Sciences determined how microbial communities in sea behave as they are suffocated with newer biological layers and being captivated without any movement. Dr. Piotr Starnawski from Center for Geomicrobiology, Aarhus University led the study of seven top meters of Aarhus bay sediment. He along with his team collected sediments from different points, counting cells and sequenced full genomes. Using several factors like carbon use, cell count and how much carbon turns into biomass (assumed 8%), team calculated the rate of reproduction. They found that on the surface microbes divide every few months but those which are deep down under much slower which takes decades to divide. The energy starved microbes deep inside needs enough time to accumulate the essential carbon and energy to replicate.
Such lower rates give rare possibility for mutation in their genome and to mark for evolution. 

Researchers on calculation found a  rate of 10-5 of mutation rate per genome per generation of a single bacterial species. This has a frequency of almost 100times slower than the surface microbes. So when this mutation does take place is mostly “synonymous”, i.e. the change in DNA does not change the protein structure and function.

Journal Source:
Starnawski P, Bataillon T, Ettema T, Jochum L, Schreiber L, Chen X et al. Microbial community assembly and evolution in subseafloor sediment. Proceedings of the National Academy of Sciences. 2017;114(11):2940-2945.


Thursday, 4 May 2017

How does the immune system know friend from foe in gut bacteria?

Our guts are home to a complex community of more than 100 trillion microbial cells that play an important role in health and disease. These gut-resident microbes, or gut microbiota - which with their genetic material are known as the gut microbiome - influence metabolism, nutrition, and immune function. Scientists are discovering that disruption in the gut microbiota is linked to obesity, inflammatory bowel disease, and other gastrointestinal disorders. It has also been suggested that obesity’s effect on the gut microbiome may explain its strong link with type 2 diabetes. Others have likened the uniqueness of a person's gut microbiota to that of a "DNA fingerprint," raising potential privacy concerns for participants of human microbiome research projects. The new study concerns of cell called dendritic cells (DCs) that have evolved two distinctive - and what may appear to be opposite - roles in the human body, in that they can both promote and inhibit immune response. DCs help to activate the immune system in response to infection, but they are also involved in actively suppressing it in certain situations. They suppress immunity by triggering induced regulatory T cells (iTregs), a type of cell that controls the development of immune tolerance. As immunity inhibitors in the gut, DCs help to train the immune system to treat gut microbiota as friend rather than foe. They do this by internalizing proteins from the microbiota and migrating to lymph nodes associated with the gut.

As they travel to the lymph nodes, the DCs break down the internalized friendly bacteria proteins into smaller pieces that become similar to "identity badges" that they wear on their cell surfaces. These identity badges are displayed with specific binding proteins that iTregs recognize, with the effect that the iTregs do not promote immune responses against proteins wearing the identity badges. Prof. Brocker says: "We believe that these iTregs are specific for the proteins produced by natural gut bacteria." The team explains that the migration to lymph cells by the DCs - particularly those whose cell surfaces display a protein called CD103+ - is an important part of keeping the immune system updated on the composition of the gut microbiota. However, what the researchers wanted to discover was how this tolerance mechanism might be switched off in an emergency. Their investigation led them to another molecule that DCs display on their cell surfaces - known as CD40 - that behaves in a similar way to an alarm button. When activated, CD40 binds to a partner molecule on the surface of another type of T cell called effector T cells, which turns DCs from inhibitors of immune response to promoters.

In tests on mice, the researchers showed that animals whose CD40 signaling was permanently switched on developed severe colitis, but no other symptoms. They found that the affected dendritic cells still migrate to the lymph nodes from the gut lining, but when they get there they commit cell suicide (apoptosis) and thus deny the regulatory T cells the opportunity to sense the identity badges of the microbiota proteins that would normally protect them from immune attack.
This results in a generalized immune response in which T lymphocytes travel to the gut lining and cause inflammation. The team found that giving the mice antibiotics that killed their gut microbiota also reduced the inflammation, and the animals survived. The researchers now want to find out whether particular regulatory T cells are programmed for specific gut bacteria, as this study might suggest.

Written by Catharine Paddock PhD (Used without permission)

Wednesday, 3 May 2017

Depression in Mice Shown to be Reversed by Probiotics

Is it true that you are what you eat? Well, have some bacteria then and get happy. Actually it’s much more complex than that. New research from the University Of Virginia School Of Medicine has shown that depressive symptoms and behaviours in mice were reversed when the mice were given food containing lactobacillus, which is a probiotic bacteria found in yogurt that is made with live cultures. The research was even able to uncover the specific process for how these probiotics impacted mood. Finding a link that makes such a close connection between the gut microbiome and mental health is a major step forward in learning more about depression and how it can be treated.

Depression isn’t just feeling sad for a while, it’s a very real neurobiological illness. Major depressive disorder affects approximately 14.8 million American adults, or about 6.7 percent of the U.S. population age 18 and older, in any given year. As many as one in 33 children and one in eight adolescents have clinical depression. Depression also puts those who suffer with it at a higher risk for heart attacks, even if they have no other cardiovascular risk factors. Since depression can seriously hinder things like a person’s ability to have a rewarding career and a stable family life, research into treatments and causes are crucial.

Lead researcher on the study at UVA, Alban Gaultier, stated, “The big hope for this kind of research is that we won’t need to bother with complex drugs and side-effects when we can just play with the microbiome. It would be magical just to change your diet, to change the bacteria you take, and fix your health – and your mood. It’s a huge problem and the treatments are not very good, because they come with huge side-effects.”

So what exactly is the “gut microbiome?” It’s the living bacteria inside the intestinal tract that is responsible for, among other things, keeping the body in balance. It’s a popular target of researchers looking into all kinds of illnesses. Connecting it to mental illness or other neurological conditions has been difficult however. Since the mouse model is used in research because of its similarity to humans, Galtier’s team looked at mice that were subjected to stress since stress can cause depression. Of course in mice, it was more about observing how they acted and looking for “depressive like behaviors” and “despair behavior” since there is obviously no other way to judge mood in animals.

When the gut microbiome composition was examined in the mice, both before and after a period of stress there was one major change that stood out. The bacteria lactobacillus was reduced in correlation to the onset of depressive behaviors in the mice. When the researchers added lactobacillus cultures back to the food of the depressed mice, the behaviors stopped and they began to behave as they had before the stress was induced.

The research at UVA took it a step further and also investigated how exactly this mechanism of lactobacillus fluctuation worked. Their study revealed that amounts of Lactobacillus in the gut will impact levels of a metabolite in the blood called kynurenine which is known to fuel depression. When lactobacillus went down, kynurenine went up and the despair behaviors of the mice began. The team hopes that they can translate these results in humans. Graduate student Ioana Marin, a researcher on the study said, “There has been some work in humans and quite a bit in animal models talking about how this metabolite, kynurenine, can influence behavior. It’s something produced with inflammation that we know is connected with depression. But the question still remains: How? How does this molecule affect the brain? What are the processes?

Published first in Medical News

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