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Researchers at Tel Aviv University and the University of Lisbon have jointly identified and synthesized a small molecule that could be a more accessible and effective alternative to an antibody that is successfully used to treat a range of cancers. Behind the groundbreaking development is an international team of researchers led by Prof. Ronit Sachi-Fainaro, Head of the Center for Cancer Biology Research and Head of the Laboratory for Cancer Research and Nanomedicine at the Sackler Faculty of Medicine, Tel Aviv University, and Prof. Helena Florindo and Prof. Rita Guedes from the Research Institute for Medicines at the Faculty of Pharmacy, University of Lisbon. The results of the study were published in the Journal for ImmunoTherapy of Cancer.

“In 2018, the Nobel Prize in Medicine was awarded to James Allison and Tasuku Honjo for their contribution to the study of immunotherapy, the treatment of cancer through activation of the immune system,” says Prof. Satchi-Fainaro, a 2020 Kadar Family Award recipient. “Honjo discovered that called T cells express the protein PD-1 that disables the T-cells’ own activity when it binds to the protein PD-L1 expressed in cancer cells. In fact, the interaction between PD-1 and PD-L1 allows cancer cells to paralyze the T cells, preventing them from attacking the cancer cells. Honjo developed antibodies that neutralize either PD-1 or PD-L1, thereby releasing the T cells to fight cancer effectively.”

The antibodies against PD-1/PD-L1 proteins are already approved for and are considered the great promise in the fight against cancer. This immunotherapy can significantly improve patient outcomes, without the that accompany treatments such as chemotherapy. But the antibodies are expensive to produce, and hence not available to all patients. Moreover, the treatment does not affect all parts of the solid tumors because the antibodies are too large to penetrate and reach less accessible and less exposed areas of the tumor. Now, researchers at Tel Aviv University and the University of Lisbon have used bioinformatic and data analysis tools to find a smaller, smarter alternative to these antibodies.

A fruit fly genome is not a just made up of fruit fly DNA—at least for one fruit fly species. New research from the University of Maryland School of Medicine’s (UMSOM) Institute for Genome Sciences (IGS) shows that one fruit fly species contains whole genomes of a kind of bacteria, making this finding the largest bacteria-to-animal transfer of genetic material ever discovered. The new research also sheds light on how this happens.

The IGS researchers, led by Julie Dunning Hotopp, Ph.D., Professor of Microbiology and Immunology at UMSOM and IGS, used new genetic long-read sequencing technology to show how genes from the bacteria Wolbachia incorporated themselves into the fly genome up to 8,000 years ago.

The researchers say their findings show that unlike Darwin’s finches or Mendel’s peas, isn’t always small, incremental, and predictable.

View insights.


Transfusing young mice with blood from older rodents quickly triggers ageing, suggesting that cellular ageing isn’t just a case of wear and tear.

There is a longstanding hypothesis that surgically connecting an old mouse with a young rodent causes a transfer of blood that de-ages the older animal. While this benefits the older mouse, the effects on the young donor rodent were less clear.

To learn more, Irina Conboy at the University of California, Berkeley, and her colleagues transfused blood between young and old mice. Those aged 3 months got blood from animals that were approaching 2 years old.

Scientists Have Created the World’s First Synthetic Embryo with the beginnings of a Brain: 30 Second video.


For the first time ever #scientists have created a #synthetic #embryo using the #stemcell of mice!

Abstract: Journal Cell.
https://www.cell.com/cell/fulltext/S0092-8674(22)00981&#…-149563237

#brain #animals #biology #heart #science #breakthrough #groundbreaking #discovery #israel #research #amazing #doctor #wow #organ #organtransplant

Bioelectronics are a relatively new scientific field that could one day result in a new class of medicines that would not be pills or injections but miniaturised, implantable devices.

GSK believes that these devices could be programmed to read and correct the electrical signals that pass along the nerves of the body, including irregular or altered impulses that can occur in association with a broad range of diseases. The hope is that through these devices, disorders as diverse as inflammatory bowel disease, arthritis, asthma, hypertension and diabetes could be treated.

In a first-of-its-kind gathering at the New York Academy of Sciences, researchers from some of the world’s leading universities and institutions convened to discuss at the 13th annual Key Symposium the various applications of bioelectronic medicine, the cutting-edge field that uses technology to treat disease and injury. While still in early stages of development, bioelectronic medicine has already been proven in studies and clinical trials to successfully treat conditions including paralysis and rheumatoid arthritis.

This panel, moderated by Miles O’Brien from PBS’ NewsHour, discusses what life will be like when we can fully modulate the nervous system and the impact that would have on disease, drugs, the healthcare industry, personal freedom, and privacy. The panel includes Polina Anikeeva, PhD, from the Massachusetts Institute of Technology, Chad Bouton from The Feinstein Institute for Medical Research at Northwell Health, Peder S. Olofsson, MD, PhD, from the Karolinska Institutet, and Doug Weber, PhD, from the U.S. Defense Advanced Research Projects Administration.

To learn more about this year’s event, visit feinsteininstitute.org/key-symposium

Genetic mutations which cause a debilitating hereditary kidney disease affecting children and young adults have been fixed in patient-derived kidney cells using a potentially game-changing DNA repair-kit. The advance, developed by University of Bristol scientists, is published in Nucleic Acids Research.

In this new study, the international team describe how they created a DNA repair vehicle to genetically fix faulty podocin, a common genetic cause of inheritable Steroid Resistant Nephrotic Syndrome (SRNS).

Podocin is a protein normally located on the surface of specialized and essential for . Faulty podocin, however, remains stuck inside the cell and never makes it to the surface, terminally damaging the podocytes. Since the disease cannot be cured with medications, gene therapy which repairs the causing the faulty podocin offers hope for patients.