Lifeboat Foundation

A new study adds to an emerging, radically new picture of how bacterial cells continually repair faulty sections of their DNA.

Published online May 16 in the journal Cell, the report describes the molecular mechanism behind a DNA repair pathway that counters the mistaken inclusion of a certain type of molecular building block, ribonucleotides, into genetic codes. Such mistakes are frequent in code-copying process in bacteria and other organisms. Given that ribonucleotide misincorporation can result in detrimental DNA code changes (mutations) and DNA breaks, all organisms have evolved to have a DNA repair pathway called ribonucleotide excision repair (RER) that quickly fixes such errors.

Last year a team led by Evgeny Nudler, Ph.D., the Julie Wilson Anderson Professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone Health, published two analyses of DNA repair in living E. coli cells. They found that most of the repair of certain types of DNA damage (bulky lesions), such as those caused by UV irradiation, can occur because damaged code sections have first been identified by a protein machine called RNA polymerase. RNA polymerase motors down the DNA chain, reading the code of DNA “letters” as it transcribes instructions into RNA molecules, which then direct protein building.

Like the lymphatic system in the body, the glymphatic system in the brain clears metabolic waste and distributes nutrients and other important compounds. Impairments in this system may contribute to brain diseases, such as neurodegenerative diseases and stroke.

A team of researchers in the McKelvey School of Engineering at Washington University in St. Louis has found a non-invasive and non-pharmaceutical method to influence glymphatic transport using focused ultrasound, opening the opportunity to use the method to further study brain diseases and brain function. Results of the work are published in the Proceedings of the National Academy of Sciences on May 15.

Hong Chen, associate professor of biomedical engineering in McKelvey Engineering and of neurological surgery in the School of Medicine, and her team, including Dezhuang (Summer) Ye, a postdoctoral research associate, and Si (Stacie) Chen, a former postdoctoral research associate, found the first direct evidence that focused ultrasound, combined with circulating microbubbles—a technique they call FUSMB—could mechanically enhance glymphatic transport in the mouse brain.

Scammers are now cloning people’s voices and using it to scam people.

So just hearing them over the phone may not be enough to their identity.

Continue reading “‘Keep them on the phone, keep it on speaker’: Expert on AI phone scam scare | NewsNation Prime” »

Lions mane the mushroom can actually stop alzheimers and dementia by boosting nerve growth 😗😁

Researchers from The University of Queensland have discovered the active compound from an edible mushroom that boosts nerve growth and enhances memory.

Professor Frederic Meunier from the Queensland Brain Institute said the team had identified new active compounds from the mushroom, Hericium erinaceus.

Continue reading “Mushrooms magnify memory” »

Harnessing the power of Artificial Intelligence to help patients keep track of their medicines, glasses, and even their keys.

It is estimated that the number of people with dementia will significantly increase in the coming years, with some estimates projecting numbers to double in the United States by 2050.

One of the ramifications of dementia, amongst many, is the loss of memories, especially episodic memories. These are of a long-term nature and allow us to recall instances ranging from “How was my first day at school” to sensory information such as “What did I see” and “How did it smell.”

Human DNA is easy to find in the environment, with samples of such good quality it can identify individual people. That’s both a boon and a burden for researchers.

A new study out of the University of Florida has found that human DNA samples, some of extremely high quality, are easily found in the environment wherever researchers looked, offering both a bounty for scientific research but also an ethical dillema not easily solved.

Shutter2U/iStock.

Continue reading “Human DNA is surprisingly easy to find in the environment” »

Understanding how major histocompatibility complex class (MHC) molecules and peptides interact within the immune system is crucial for the advancement of biological sciences and medicine. A better understanding of how and when the immune system is activated can lead to treatments in diseases such as cancer or for the development of new vaccines.

MHC-peptide exchange technology attempts to replicate the immune response where peptide exchange occurs on an MHC molecule. The combination of the peptide sequence and the MHC molecule define the strength of the binding affinity resulting in a weak or strong interaction. In order for in vivo T cell epitope to be immunogenic, it must be able to bind a compatible MHC molecule and remain bound for long enough to be presented to and recognized by T cells to elicit an immune response. This shows that a strong binding affinity of MHC/peptide sequence in vitro may indicate potential strong immune interactions of antigen specific T cells in the desired model test sample. Ultimately obtaining this crucial peptide-MHC partnership, where binding affinity is the optimal amount, and the subsequent T cell reaction is sufficient for a therapeutic response, is difficult and cumbersome. There are many different technologies to explore MHC-peptide binding.

Chimeric antigen receptor (CAR) therapies involve the use of engineered receptors capable of redirecting immune cells to recognize and destroy cancer cells expressing a specific antigen. Currently, CAR-T cells, T cells equipped with CAR, dominate the field of CAR therapy. Since 2017, over 700 clinical trials involving CAR-T therapy have been registered and the U.S. Food and Drug Administration (FDA) has approved six CAR-T therapies for the treatment of leukemia, lymphomas, and multiple myeloma (Fig. 1) ^[1]. However, despite its clinical significance, several factors contribute to the limitations of CAR-T therapy. First, as collecting T cells is costly and time-consuming, this may not be feasible for patients already suffering from a compromised immune system. Second, CAR-T therapies mainly focus on treating hematological malignancies, having limited effectiveness in treating solid tumors. Third, CAR-T cells struggle to penetrate the tumor microenvironment (TME), which can hinder their therapeutic function. To overcome these limitations, promising CAR designs have emerged for multi-target CAR-T alongside novel therapies that utilize other immune cell types such as CAR-Natural killer (NK) and CAR-Macrophage (M) cells.

Figure 1. Timeline of CAR-T FDA approvals in the US. B-ALL, B cell acute lymphoblastic leukemia; LBCL, large B cell lymphoma; MCL, mantle cell lymphoma; MM, multiple myeloma; R/R, relapsed/refractorySource: adapted from Maakaron, J, et al. 2022^[1].

Beware, bad guys—your DNA is in the air.