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Category: biotech/medical – Page 1,793

Plague is an age-old disease that can still be deadly today, but now researchers are developing new vaccines that could potentially protect against plague infection, early research in animals suggests.

In a new study, researchers tested three vaccines that were designed to protect people against infection from the bacteria that cause plague, known as Yersinia pestis. To create the vaccines, the researchers modified several genes of the bacteria so that they couldn’t cause disease, but would likely trigger an immune response in an animal. Specifically, the vaccines were designed to protect people against the bacteria that cause pneumonic plague, the most serious form of plague and the only type that spreads through airborne transmission.

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Here, we discover prototypical pacemaker neurons in the ancient cnidarian Hydra and provide evidence for a direct interaction of these neurons with the commensal microbiota. We uncover a remarkable gene-expression program conservation between the Hydra pacemaker neurons and pacemaker cells in Caenorhabditis elegans and the mammalian gut. We suggest that prototypical pacemaker cells emerged as neurons using components of innate immunity to interact with the microbial environment and ion channels to generate rhythmic contractions. The communication of pacemaker neurons with the microbiota represents a mechanistic link between the gut microbiota and gut motility. Our discoveries improve the understanding of the archetypical properties of the enteric nervous systems, which are perturbed in human dysmotility-related conditions.

Pacemaker neurons exert control over neuronal circuit function by their intrinsic ability to generate rhythmic bursts of action potential. Recent work has identified rhythmic gut contractions in human, mice, and hydra to be dependent on both neurons and the resident microbiota. However, little is known about the evolutionary origin of these neurons and their interaction with microbes. In this study, we identified and functionally characterized prototypical ANO/SCN/TRPM ion channel-expressing pacemaker cells in the basal metazoan Hydra by using a combination of single-cell transcriptomics, immunochemistry, and functional experiments. Unexpectedly, these prototypical pacemaker neurons express a rich set of immune-related genes mediating their interaction with the microbial environment.

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CRISPR-guided DNA cytosine and adenine base editors are widely used for many applications1,2,3,4 but primarily create DNA base transitions (that is, pyrimidine-to-pyrimidine or purine-to-purine). Here we describe the engineering of two base editor architectures that can efficiently induce targeted C-to-G base transversions, with reduced levels of unwanted C-to-W (W = A or T) and indel mutations. One of these C-to-G base editors (CGBE1), consists of an RNA-guided Cas9 nickase, an Escherichia coli –derived uracil DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidine deaminase variant (R33A) previously shown to have reduced off-target RNA and DNA editing activities5,6. We show that CGBE1 can efficiently induce C-to-G edits, particularly in AT-rich sequence contexts in human cells. We also removed the eUNG domain to yield miniCGBE1, which reduced indel frequencies but only modestly decreased editing efficiency. CGBE1 and miniCGBE1 enable C-to-G edits and will serve as a basis for optimizing C-to-G base editors for research and therapeutic applications.

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An international team of scientists has collated all known bacterial genomes from the human gut microbiome into a single large database, allowing researchers to explore the links between bacterial genes and proteins, and their effects on human health.

This project was led by EMBL’s European Bioinformatics Institute (EMBL-EBI) and included collaborators from the Wellcome Sanger Institute, the University of Trento, the Gladstone Institutes, and the US Department of Energy Joint Genome Institute. Their work has been published in Nature Biotechnology.

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AstraZeneca shares fell on Monday even after the publication of positive results from a trial of its experimental COVID-19 vaccine developed in partnership with Oxford University.

The study, published in The Lancet on Monday, said healthy volunteers who received the experimental vaccine, called AZD1222, showed immune responses.

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Last week, The Daily Telegraph reported that blood samples of volunteers in the trial showed both antibodies and T cells.

AstraZeneca said in June that it would supply up to 2 billion doses of the vaccine worldwide.

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Circa 2016

In a world first, Australian scientists have figured out how to reprogram adult bone or fat cells to form stem cells that could potentially regenerate any damaged tissue in the body.

The researchers were inspired by the way salamanders are able to replace lost limbs, and developed a technique that gives adult cells the ability to lose their adult characteristics, multiply and regenerate multiple cell types — what is known as multipotency. That means the new stem cells can hypothetically repair any injury in the body, from severed spinal cords to joint and muscle degeneration. And it’s a pretty big deal, because there are currently no adult stem cells that naturally regenerate multiple tissue types.

“This technique is a significant advance on many of the current unproven stem cell therapies, which have shown little or no objective evidence they contribute directly to new tissue formation,” said lead researcher John Pimanda from the University of New South Wales, Faculty of Medicine (UNSW Medicine). “We are currently assessing whether adult human fat cells reprogrammed into [induced multipotent stem cells (iMS cells)] can safely repair damaged tissue in mice, with human trials expected to begin in late 2017.”

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Kansas State University physicists have taken extremely fast snapshots of light-induced molecular ring-opening reactions—similar to those that help a human body produce vitamin D from sunlight. The research is published in Nature Chemistry.

“Think of this as stop-motion like a cartoon,” said Daniel Rolles, associate professor of physics and the study’s principal investigator. “For each molecule, you start the reaction with a laser pulse, take snapshots of what it looks like as time passes and then put them together. This creates a ‘molecular movie’ that shows how the electronic structure of the molecule changes as a function of how much time passes between when we start and when we stop.”

Shashank Pathak, doctoral student and lead author on the paper, said the idea was to study the dynamics of how a ring opens in a molecule on the time scale of femtosecond, which is one quadrillionth of a second. The researchers use a to visualize how these reactions happen by recording electron energy spectra as the atoms in the molecule move apart.

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Researchers at Tel Aviv University, led by Prof. Yaniv Assaf of the School of Neurobiology, Biochemistry and Biophysics and the Sagol School of Neuroscience and Prof. Yossi Yovel of the School of Zoology, the Sagol School of Neuroscience, and the Steinhardt Museum of Natural History, conducted a first-of-its-kind study designed to investigate brain connectivity in 130 mammalian species. The intriguing results, contradicting widespread conjectures, revealed that brain connectivity levels are equal in all mammals, including humans.

“We discovered that —namely the efficiency of information transfer through the —does not depend on either the size or structure of any specific ,” says Prof. Assaf. “In other words, the brains of all mammals, from tiny mice through humans to large bulls and dolphins, exhibit equal connectivity, and information travels with the same efficiency within them. We also found that the brain preserves this balance via a special compensation mechanism: when connectivity between the hemispheres is high, connectivity within each hemisphere is relatively low, and vice versa.”

Participants included researchers from the Kimron Veterinary Institute in Beit Dagan, the School of Computer Science at TAU and the Technion’s Faculty of Medicine. The paper was published in Nature Neuroscience on June 8.

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