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A recent study to be presented at the American Heart Association (AHA) Scientific Sessions 2022 revealed unexpected changes in the electrical conduction system of the first genetically-modified porcine-to-human heart xenotransplant.

Xenotransplantation is the procedure of transplantation/implantation into a human of organs from non-human animal sources. The first pig-to-human heart xenograft was transplanted in January 2022 at the University of Maryland. The recipient survived for 61 days after receiving the xenograft. Research efforts have been underway for this xenotransplantation for over three decades.

Harvesting genetically-modified porcine hearts, the genes of which have been altered for safe transplantation into humans, would become a reality if successful. However, xenotransplantation of organs into a human carries several inherent challenges. With these transplant procedures, there is always the risk of graft rejection, infection, and abnormal heart rhythms.

(https://hannalabweb.weizmann.ac.il/) is a Senior Scientist and Professor in the Department of Molecular Genetics at the Weizmann Institute of Science in Israel, where his lab, and the interdisciplinary group of scientists within it, are focused on understanding the complexity of early embryonic stem cell biology and early developmental dynamics, as well as advancing human disease modeling.

More specifically, Dr. Hanna’s lab investigates the detailed process of cellular reprogramming, in which induced pluripotent stem cells are generated from somatic cells, and they investigate how pluripotency is maintained throughout development in mouse and human. In their studies they employ a diverse arsenal of biological experimentation methods, high throughput screening, advanced microscopy and genomic analyses seeking to combine biological experimentation with computational biology, theory and modeling, to elucidate various biological questions.

Continue reading “Dr. Jacob Hanna, MD, Ph.D. — Synthetic Embryo R&D In Regenerative Medicine & Developmental Biology” »

Mount Sinai researchers have cataloged thousands of sites in the brain where RNA is modified throughout the human lifespan in a process known as adenosine-to-inosine (A-to-I) editing, offering important new avenues for understanding the cellular and molecular mechanisms of brain development and how they factor into both health and disease.

In a study published in Cell Reports, the team described how the rate of RNA editing in the brain increases as individuals age, with implications for dissecting the pathology of altered A-to-I editing across a range of neurodevelopmental and aging disorders.

“Our work provides more nuanced and accurate insights into the contribution of RNA modifications by A-to-I editing during human brain development,” says senior author Michael Breen, Ph.D., Assistant Professor of Psychiatry, and Genetics and Genomic Sciences, at the Icahn School of Medicine at Mount Sinai, and a member of the Seaver Center for Autism Research and Treatment.

Researchers from North Carolina State University have developed a new method for determining which genes are relevant to the aging process. The work was done in an animal species widely used as a model for genetic and biological research, but the finding has broader applications for research into the genetics of aging.

“There are a lot of genes out there that we still don’t know what they do, particularly in regard to aging,” says Adriana San Miguel, corresponding author of a paper on the work and an assistant professor of chemical and biomolecular engineering at NC State.

That’s because this field faces a very specific technical challenge: by the time you know whether an organism is going to live for a long time, it’s old and no longer able to reproduce. But the techniques we use to study genes require us to work with animals that are capable of reproducing, so we can study the role of specific genes in subsequent generations.

On the other, because organisms share the same universal code, they’re vulnerable to outside attacks from viruses and other pathogens—and can transfer their new capabilities to natural organisms, even if it kills them.

Why not build a genetic firewall?

A recent study in Science did just that. The team partially reworked the existing genetic code into a “cipher” that normal organisms can’t comprehend. Similarly, the engineered bacteria lost its ability to read the natural genetic code. The tweaks formed a powerful language barrier between the engineered bacteria and natural organisms, isolating each from sharing genetic information with the other.

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Continue reading “Dietary Fiber And SCFAs Are Relatively Higher in Centenarians-A Pathway To Longevity?” »

In a city in Brazil, male mosquitoes were released that expressed a gene that meant their female offspring, which bite and transmit infections, couldn’t survive.

Here is what the ECG reports of the first patient with the pig heart say.

In January this year, the heart of a genetically modified pig was transplanted into a human for the first time. The patient, David Bennett, managed to survive for two months with the pig heart, and this unique organ transplant operation led to various exciting findings and further research work.

One recently published research reveals that the electrical conduction system (network of cells, signals, and nodes in a heart that collectively controls heart functions and heartbeat) of the genetically modified pig heart differs from that of an ordinary pig’s heart.

Continue reading “The patient who got the world’s first pig heart transplant has died after 2 months” »

Summary: A genetic form of frontotemporal dementia is associated with abnormal lipid accumulation in the brain fueled by disrupted cell metabolism. The findings could pave the way for new targeted therapies for FTD.

Source: Harvard.

Dementia encompasses a range of neurodegenerative conditions that lead to memory loss and cognitive deficiencies and affect some 55 million people worldwide. Yet despite its prevalence, there are few effective treatments, in part because scientists still don’t understand how exactly dementia arises on a cellular and molecular level.