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Scientists have identified a class of drugs that may have potential to treat a rare and deadly form of brain cancer that affects young children.

The research team, led by Ranjit Bindra, MD, PhD, and colleagues at the Yale Cancer Center, also included co-senior authors Charles Brenner, PhD, professor and DEO of biochemistry at the University of Iowa Carver College of Medicine, and Michael E. Berens, PhD, from the Translational Genomics Research Institute in Phoenix.

The findings, published Aug. 22 in Nature Communications, focus on Diffuse Intrinsic Pontine Glioma (DIPG), a rare, incurable cancer that affects the brainstem in children under age 10. Previous work had identified mutations in a gene called PPM1D as a cause of this cancer.

You are what you eat—right down to the microbiome living in your gut. Diet can affect which microbes are in the intestinal tract, and research has shown that harmful gut microbiome changes can lead to illnesses such as heart disease, obesity and cancer. Today, scientists will report the development of molecules that can change, or remodel, unhealthful gut microbiomes in mice into more healthful ones. The research could also someday be applied to other conditions related to diet.

The researchers will present their results at the American Chemical Society (ACS) Fall 2019 National Meeting & Exposition.

“The gut microbiome contains hundreds of different species of bacteria and is where the largest concentration of bacteria living in us resides,” says M. Reza Ghadiri, Ph.D., leader of the study. “If we all ate a healthy diet, exercised and didn’t age, we wouldn’t have problems with our gut microbiome and many diseases. But, that’s not how all people live. Current methods aimed at improving the makeup of gut microbiomes have involved prebiotics, probiotics or drug therapies. Our goal was to take a totally new approach—to remodel the microbiome.”

First it was human embryos. Now scientists are trying to develop another way to modify human DNA that can be passed on to future generations, NPR has learned.

Reproductive biologists at Weill Cornell Medicine in New York City are attempting to use the powerful gene-editing technique called CRISPR to alter genes in human sperm. NPR got exclusive access to watch the controversial experiments underway.

The research is aimed at finding new ways to prevent disorders caused by genetic mutations that are passed down from men — including some forms of male infertility. The team is starting with a gene that can increase the risk for breast, ovarian, prostate and other cancers.

Nearly one in 30 Americans over the age of 40 experience low vision—significant visual impairment that can’t be corrected with glasses, contact lenses, medication or surgery.

In a new study of patients with retinitis pigmentosa, an inherited degenerative eye disease that results in poor vision, Keck School of Medicine of USC researchers found that adapted augmented reality (AR) glasses can improve patients’ mobility by 50% and grasp performance by 70%.

“Current wearable low vision technologies using virtual reality are limited and can be difficult to use or require patients to undergo extensive training,” said Mark Humayun, MD, Ph.D., director of the USC Dr. Allen and Charlotte Ginsburg Institute for Biomedical Therapeutics, codirector of the USC Roski Eye Institute and University Professor of Ophthalmology at the Keck School.

The ability to edit genes in living organisms offers the opportunity to treat a plethora of inherited diseases. However, many types of gene-editing tools are unable to target critical areas of DNA, and creating such a technology has been difficult as living tissue contains diverse types of cells.

Now, Salk Institute researchers have developed a new tool—dubbed SATI—to edit the mouse genome, enabling the team to target a broad range of mutations and cell types. The new genome-editing technology, described in Cell Research on August 23, 2019, could be expanded for use in a broad range of gene mutation conditions such as Huntington’s disease and the rare premature aging syndrome, progeria.

“This study has shown that SATI is a powerful tool for genome editing,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases.”

In new research published in Psychoneuroendocrinology, scientists have shown that loving-kindness meditation has a positive impact at the cellular level. The study examined how different types of meditation influenced telomere length, an indicator of physiological aging.

Telomeres are the end caps of DNA on our chromosomes, which help in DNA replication and get shorter over time.

“Chronological age and biological age are not identical. The former is measured in years, whereas the latter is often indexed by telomere length,” the authors of the new study explained. “Telomeres progressively shorten with cell division (i.e., aging) in general, but may also be replenished, or lengthened, by the enzyme telomerase.”

A South African professor, Mashudu Tshifularo, and his team at the University of Pretoria pioneered the world’s first middle ear transplant using 3D-printed bones. Here is how he carried out the successful surgery.

What should you chose to get the best pain relief? StemCures in Cincinnati.

Science has officially broadened the blood supply:

Access to efficient enzymes that can convert A and B type red blood cells to ‘universal’ donor O would greatly increase the supply of blood for transfusions. Here we report the functional metagenomic screening of the human gut microbiome for enzymes that can remove the cognate A and B type sugar antigens. Among the genes encoded in our library of 19,500 expressed fosmids bearing gut bacterial DNA, we identify an enzyme pair from the obligate anaerobe Flavonifractor plautii that work in concert to efficiently convert the A antigen to the H antigen of O type blood, via a galactosamine intermediate. The X-ray structure of the N-acetylgalactosamine deacetylase reveals the active site and mechanism of the founding member of an esterase family. The galactosaminidase expands activities within the CAZy family GH36. Their ability to completely convert A to O of the same rhesus type at very low enzyme concentrations in whole blood will simplify their incorporation into blood transfusion practice, broadening blood supply.