Genetically Modified Bacteriophages Appear To Fight Off Resistant Bacteria : Shots — Health News Treatment with genetically altered bacteriophages — viruses that attack bacteria — may have halted a patient’s near-fatal infection, hinting at new ways to fight antibiotic-resistant bacteria.
A soft neural implant that can be controlled by a smartphone is capable of drug delivery and optogenetics. The technology could speed up efforts to uncover the causes of neurological and psychological disorders.
The trial is just one of a few underway to test the powerful CRISPR technology around the world. One of the most promising, for example, is studying whether gene editing can treat, and effectively cure, blood disorders such as beta thalassemia and sickle cell anemia.
In beta thalassemia, the hemoglobin part of red blood cells, which is supposed to pick up oxygen from the lungs and distribute it to the cells in the rest of the body, doesn’t work properly. Patients need to be transfused with donors blood regularly, and even with these transfusions, complications can occur if the dose isn’t right and iron levels in the blood cells spike, which can lead to organ damage and even death. In sickle cell disease, a mutation in the gene that makes hemoglobin causes the red blood cells to collapse into a sickle shape, which makes it more difficult for the cells to flow smoothly through the body’s arteries and veins. Blockages caused by the misshapen blood cells can lead to severe pain and strokes.
The biotech company CRISPR Therapeutics, founded by one of the technology’s co-developers, has engineered a solution to treat both conditions that relies on genetic modifications connected to the production of fetal hemoglobin. Normally fetal hemoglobin, which provides the developing fetus with oxygen via the blood while in utero, is shut off about six months after birth, and genes for adult hemoglobin are turned on. While it’s not clear why adult hemoglobin replaces the fetal version, researchers say that they have not seen any significant differences between the two types when it comes to the ability to transport oxygen to the body’s cells. However, since the genes for adult hemoglobin don’t produce healthy red blood cells in people with beta thalassemia and sickle cell disease, one treatment strategy is to introduce genetic changes that turn on fetal hemoglobin again.
I’m excited to share my new 1 hour interview at Singularity University radio with Steven Parton. Also, check out Singularity Hub and the write-up they did of the interview. We talk all things transhumanism, longevity, Cyborgs, and the future:
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A study of 8,000 years of genetics from Spain and Portugal yields a surprisingly complex picture of the inhabitants’ ancestry.
A common concern about life extension is overpopulation, the idea that there are too many people in the world. Are we really headed for a global overpopulation meltdown, as some people believe? The United Nations’ World Population Prospects 2019 report suggests that while the global population will continue to rise for the next few decades, ultimately, that rise will plateau.
First things first: it’s population growth, not overpopulation
Whenever the topic of defeating age-related diseases comes up, there is inevitably someone who will cite overpopulation as an objection to healthy life extension and a reason why we should continue to let people become sick and die of diseases that science may be able to cure in the coming decades.
Two known gene mutations induce pathways that enhance pancreatic cancer’s ability to invade tissues and evade the immune system. Researchers report the molecular details of this process, providing insights into druggable targets for immunotherapies.
Mutations in the genes KRAS and TP53 are closely linked to pancreatic ductal adenocarcinoma, by far the most common type of pancreatic cancer. Pancreatic cancers are often already malignant when diagnosed, making its five-year survival rate extremely low—less than ten percent. So, understanding how it evolves at the molecular level could help anti-cancer drug development.
Hisataka Sabe of Hokkaido University and colleagues in Japan conducted tests in human cancer cells and in mouse models of the disease to investigate the roles of KRAS and TP53 gene mutations in pancreatic ductal adenocarcinoma. The study was published in the journal Proceedings of the National Academy of Sciences (PNAS).
