The pandemic also helped by normalizing remote work.
A new report by Vice.
“That’s the only reason I got my job this year,” one worker referred to only as Ben said of OpenAI’s tool.
Fulltimetraveller/iStock.
Artificial-intelligence tools can enable remote workers to not just more than one job, but to do them with time left to spare. Vice spoke anonymously to various workers holding down two to four full-time jobs with help from these tools and they all were in agreement that it is an ideal way to increase one’s income.
Senescent cells are those that have stopped dividing but haven’t read the “time to die” memo. Instead, they hang around, accumulating in the body and fueling chronic inflammation – sometimes called inflammaging – which in turn, contributes to conditions such cardiovascular diseases, chronic kidney disease, type 2 diabetes, cancer, sarcopenia and degenerative disorders.
Longevity. Technology: In mice, eliminating senescent cells from aging tissues can restore tissue balance and lead to an increased healthy lifespan. Now a team led by investigators at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), has found that the immune response to a virus that is ubiquitously present in human tissues can detect and eliminate senescent cells in the skin [1].
For the study, which is published in Cell, the scientists analyzed young and old human skin samples to learn more about the clearance of senescent cells in human tissue.
Neuroscientists at MIT have discovered a way to potentially reverse neurodegeneration and other issues related to Alzheimer’s disease, according to a news release from the school.
Researchers, experimenting on mice, found that interfering with an enzyme that is typically overactive in the brains of people with Alzheimer’s can reverse the degeneration in the brain.
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The cells in your body are like computer software: they’re “programmed” to carry out specific functions at specific times. If we can better understand this process, we could unlock the ability to reprogram cells ourselves, says computational biologist Sara-Jane Dunn. In a talk from the cutting-edge of science, she explains how her team is studying embryonic stem cells to gain a new understanding of the biological programs that power life — and develop “living software” that could transform medicine, agriculture and energy.
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Researchers have recently made a groundbreaking discovery in the field of kidney disease. They have found a new pathway that could potentially prevent kidney failure in thousands of people. Dr. Carl May and his team at Bristol Medical School, with funding from Kidney Research UK, have discovered a new treatment pathway for non-genetic nephrotic syndrome.
This targets the unknown factor that leads to kidney failure. Nephrotic syndrome is a rare kidney condition that causes protein to leak into the urine, affecting around 10,000 people annually in the UK. The discovery offers hope for patients, especially children, who may develop kidney failure.
Researchers from Bristol Renal have identified a receptor called PAR-1 that works in conjunction with an unknown factor to cause kidney failure in patients with idiopathic nephrotic syndrome (INS). They found that anti-PAR-1 treatments could block the effect of the factor and prevent kidneys from failing, potentially making transplantation a more viable option for more patients.
Reversing schizophrenia with gene therapy year 2023.
Copy-number variations in the ARHGAP10 gene encoding Rho GTPase–activating protein 10 are associated with schizophrenia. Model mice (Arhgap10 S490P/NHEJ mice) that carry “double-hit” mutations in the Arhgap10 gene mimic the schizophrenia in a Japanese patient, exhibiting altered spine density, methamphetamine-induced cognitive dysfunction, and activation of RhoA/Rho-kinase signaling. However, it remains unclear whether the activation of RhoA/Rho-kinase signaling due to schizophrenia-associated Arhgap10 mutations causes the phenotypes of these model mice. Here, we investigated the effects of fasudil, a brain permeable Rho-kinase inhibitor, on altered spine density in the medial prefrontal cortex (mPFC) and on methamphetamine-induced cognitive impairment in a touchscreen‑based visual discrimination task in Arhgap10 S490P/NHEJ mice. Fasudil (20 mg/kg, intraperitoneal) suppressed the increased phosphorylation of myosin phosphatase–targeting subunit 1, a substrate of Rho-kinase, in the striatum and mPFC of Arhgap10 S490P/NHEJ mice. In addition, daily oral administration of fasudil (20 mg/kg/day) for 7 days ameliorated the reduced spine density of layer 2/3 pyramidal neurons in the mPFC. Moreover, fasudil (3–20 mg/kg, intraperitoneal) rescued the methamphetamine (0.3 mg/kg)-induced cognitive impairment of visual discrimination in Arhgap10 S490P/NHEJ mice. Our results suggest that Rho-kinase plays significant roles in the neuropathological changes in spine morphology and in the vulnerability of cognition to methamphetamine in mice with schizophrenia-associated Arhgap10 mutations.
Proteins are involved in every biological process, and use the energy in the body to alter their structure via mechanical movements. They are considered biological ‘nanomachines’ because the smallest structural change in a protein has a significant effect on biological processes. The development of nanomachines that mimic proteins has received much attention to implement movement in the cellular environment. However, there are various mechanisms by which cells attempt to protect themselves from the action of these nanomachines. This limits the realization of any relevant mechanical movement of nanomachines that could be applied for medical purposes.
The research team led by Dr. Youngdo Jeong from the Center for Advanced Biomolecular Recognition at the Korea Institute of Science and Technology (KIST, President Seok-Jin Yoon) has reported the development of a novel biochemical nanomachine that penetrates the cell membrane and kills the cell via the molecular movements of folding and unfolding in specific cellular environments, such as cancer cells, as a result of a collaboration with the teams of Prof. Sang Kyu Kwak from the School of Energy and Chemical Engineering and Prof. Ja-Hyoung Ryu from the Department of Chemistry at the Ulsan National Institute of Science and Technology (UNIST, President Yong Hoon Lee), and Dr. Chaekyu Kim of Fusion Biotechnology, Inc.
The joint research team focused on the hierarchical structure of proteins, in which the axis of the large structure and the mobile units are hierarchically separated. Therefore, only specific parts can move around the axis. Most existing nanomachines have been designed so that the mobile components and axis of the large structure are present on the same layer. Thus, these components undergo simultaneous movement, which complicates the desired control of a specific part.
