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The real move at play here, by so called AI Ethics clowns, is a complete shut down of Ai, and AI research. That IS their end goal — end game. See if can really turn it off 6 months. ha! Ok, how about 2 more years! etc… etc…

Ya publicly tipped your hand.


An open letter published today calls for “all AI labs to immediately pause for at least 6 months the training of AI systems more powerful than GPT-4.”

This 6-month moratorium would be better than no moratorium. I have respect for everyone who stepped up and signed it. It’s an improvement on the margin.

I refrained from signing because I think the letter is understating the seriousness of the situation and asking for too little to solve it.

Huntington’s disease (HD) is a neurodegenerative disease caused by a CAG repeat expansion in the Huntingtin (HTT) gene. The resulting polyglutamine (polyQ) tract alters the function of the HTT protein. Although HTT is expressed in different tissues, the medium spiny projection neurons (MSNs) in the striatum are particularly vulnerable in HD. Thus, we sought to define the proteome of human HD patient–derived MSNs. We differentiated HD72 induced pluripotent stem cells and isogenic controls into MSNs and carried out quantitative proteomic analysis. Using data-dependent acquisitions with FAIMS for label-free quantification on the Orbitrap Lumos mass spectrometer, we identified 6,323 proteins with at least two unique peptides. Of these, 901 proteins were altered significantly more in the HD72-MSNs than in isogenic controls. Functional enrichment analysis of upregulated proteins demonstrated extracellular matrix and DNA signaling (DNA replication pathway, double-strand break repair, G1/S transition) with the highest significance. Conversely, processes associated with the downregulated proteins included neurogenesis-axogenesis, the brain-derived neurotrophic factor-signaling pathway, Ephrin-A: EphA pathway, regulation of synaptic plasticity, triglyceride homeostasis cholesterol, plasmid lipoprotein particle immune response, interferon-γ signaling, immune system major histocompatibility complex, lipid metabolism and cellular response to stimulus. Moreover, proteins involved in the formation and maintenance of axons, dendrites, and synapses (e.g., Septin protein members) were dysregulated in HD72-MSNs. Importantly, lipid metabolism pathways were altered, and using quantitative image, we found analysis that lipid droplets accumulated in the HD72-MSN, suggesting a deficit in the turnover of lipids possibly through lipophagy. Our proteomics analysis of HD72-MSNs identified relevant pathways that are altered in MSNs and confirm current and new therapeutic targets for HD.

Improving the seasonal influenza vaccine and public health specialists’ ability to predict pandemic potential in new flu strains may be possible, due to new findings from scientists at St. Jude Children’s Research Hospital. The key is the stability of a viral protein that gains entry into human cells. The findings were published today in Science Advances.

“We found that the protein flu viruses use to enter cells, hemagglutinin, needs to be relatively stable and resistant to acid in an effective H3N2 flu vaccine,” said senior and co-corresponding author Charles Russell, Ph.D., St. Jude Department of Infectious Diseases. “We found a mutation in hemagglutinin that makes the grow better in eggs also causes a mismatch in the vaccine. The mutation makes the virus unstable and makes it look less human-like.”

The H3N2 virus is a subtype of Influenza A and is one of the culprits behind the seasonal flu. Many flu vaccines are made by growing the virus in chicken eggs, but the virus can gain mutations during that process. Some of those changes, like the one uncovered by the St. Jude group, make the vaccine less effective in generating the ideal immune response. At the same time, other mutations have more beneficial impacts.

A large case-control study by international researchers at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan has found that people who carry certain genetic risk factors for gastric (stomach) cancer have a much greater risk if they have also been infected by the bacterium Helicobacter pylori. The study, published in The New England Journal of Medicine, could contribute to the development of tailored genomic medicine for treating stomach cancer.

Stomach is the fourth leading cause of cancer death worldwide and has both environmental and . Environmentally, infection by H. pylori increases the risk of . Because the virulence of H. pylori in East Asia is high, the incidence of stomach cancer is higher in countries like Japan. Genetically, while hereditary gene variation is why we have different colored eyes and are unique as individuals, sometimes gene variants are associated with the risk of disease. For example, individuals who carry a certain hereditary pathogenic variant of the CDH1 gene have an increased risk of .

Testing for the presence of pathogenic variants is now one of several measures being taken for cancer prevention, surveillance, and treatment selection. However, because large-scale, case-control studies are lacking, and because those that exist have not assessed how the risk for stomach cancer changes when pathogenic variants interact with like H. pylori, it remains unclear what actual clinical measures can be taken. To address this issue, researchers therefore evaluated the risk of gastric cancer in a large case-control study of Japanese people, considering whether they were carriers of pathogenic variants and whether they had been infected by H. pylori.

Superconductors make highly efficient electronics, but the ultralow temperatures and ultrahigh pressures required to make them work are costly and difficult to implement. Room-temperature superconductors promise to change that.

The recent announcement by researchers at the University of Rochester of a new material that is a superconductor at room temperature, albeit at high pressure, is an exciting development – if proved. If the material or one like it works reliably and can be economically mass-produced, it could revolutionize electronics.

Room-temperature superconducting materials would lead to many new possibilities for practical applications, including ultraefficient electricity grids, ultrafast and energy-efficient computer chips, and ultrapowerful magnets that can be used to levitate trains and control fusion reactors.

Jennifer Garrison is an assistant professor at the Buck Institute for Research on Aging and also holds appointments in the Department of Cellular and Molecular Pharmacology at University of California, San Francisco (UCSF) and the Davis School of Gerontology at the University of Southern California.

Over 321 books from 170 plus interviews over 5 years.

Over 321 books from 170 interviews over 5 years for autodidacts

Jennifer Garrison Links.
https://www.buckinstitute.org/lab/garrison-lab/
https://www.linkedin.com/in/drjennifergarrison.
https://twitter.com/jenngarrison?lang=en.

PODCAST INFO:
The Learning With Lowell show is a series for the everyday mammal. In this show we’ll learn about leadership, science, and people building their change into the world. The goal is to dig deeply into people who most of us wouldn’t normally ever get to hear. The Host of the show – Lowell Thompson-is a lifelong autodidact, serial problem solver, and founder of startups.

LINKS
Spotify: https://open.spotify.com/show/66eFLHQclKe5p3bMXsCTRH
RSS: https://www.learningwithlowell.com/feed/podcast/
Youtube: https://www.youtube.com/channel/UCzri06unR-lMXbl6sqWP_-Q
Youtube clips: https://www.youtube.com/channel/UC-B5x371AzTGgK-_q3U_KfA
Website: https://www.learningwithlowell.com/
Shownotes/ Timestamps.
00:00 Introducing Jennifer Garrison.
01:20 Broken Science funding.
10:00 Progress and accountability.
12:10 Why don’t we have the Garrison system.
20:48 Cost to run a lab & cost of university and support systems.
25:18 Neuro peptides and aging.
30:40 Complexity of neuropeptides.
33:12 How do neuropeptides know where to go.
37:20 Human vs animal neuropeptide differences and divergences.
44:42 Reproductive system.
46:20 Regenerating reproductive systems and aging.
48:55 Women reproductive health support.
51:35 Women and diverse population in clinical trials.
53:54 The first domino.
58:15 Why you should care about women’s health even if not a women.
01:00:23 Turning Menopause on and off.
01:04:45 Causes of aging.
01:06:00 2023 projects and thoughts.
01:08:40 What help she needs to accelerate the future at buck.
01:13:30 OBGYN issues and problems women have.
01:20:10 Resources for women and doctors.
01:26:58 Books.
01:29:50 LzzyHalesLegs listener q for identifying opportunities to work on.

Social links.

Altered dystrophin expression was found in some tumors and recent studies identified a developmental onset of Duchenne muscular dystrophy (DMD). Given that embryogenesis and carcinogenesis share many mechanisms, we analyzed a broad spectrum of tumors to establish whether dystrophin alteration evokes related outcomes. Transcriptomic, proteomic, and mutation datasets from fifty tumor tissues and matching controls (10,894 samples) and 140 corresponding tumor cell lines were analyzed. Interestingly, dystrophin transcripts and protein expression were found widespread across healthy tissues and at housekeeping gene levels. In 80% of tumors, DMD expression was reduced due to transcriptional downregulation and not somatic mutations. The full-length transcript encoding Dp427 was decreased in 68% of tumors, while Dp71 variants showed variability of expression.