Three people regained leg movements after using a new type of treatment, the latest in a suite of results involving electrical stimulation.
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Category: biotech/medical – Page 2300
Neutralising reactive nitrogen species to make immunotherapy more effective.
Researchers at the University of Notre Dame discovered that amino acid nitration can inhibit the activation of T cells employed in immunotherapy against cancer and that suppression of reactive nitrogen species (RNS) responsible for nitration can significantly boost the effectiveness of immunotherapy [1].
Abstract
Potent immunosuppressive mechanisms within the tumor microenvironment contribute to the resistance of aggressive human cancers to immune checkpoint blockade (ICB) therapy. One of the main mechanisms for myeloid-derived suppressor cells (MDSCs) to induce T cell tolerance is through secretion of reactive nitrogen species (RNS), which nitrates tyrosine residues in proteins involved in T cell function. However, so far very few nitrated proteins have been identified. Here, using a transgenic mouse model of prostate cancer and a syngeneic cell line model of lung cancer, we applied a nitroproteomic approach based on chemical derivation of 3-nitrotyrosine and identified that lymphocyte-specific protein tyrosine kinase (LCK), an initiating tyrosine kinase in the T cell receptor signaling cascade, is nitrated at Tyr394 by MDSCs. LCK nitration inhibits T cell activation, leading to reduced interleukin 2 (IL2) production and proliferation.
Research has discovered that inside every cell in the human body is a kill code designed to trigger self-destruction if it senses a cell is turning cancerous. Across two studies the scientists homed in on the code underlying this mechanism and believe it may lead to a new kind of cancer treatment.
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If you haven’t heard, universities around the world are offering their courses online for free (or at least partially free). These courses are collectively called MOOCs or Massive Open Online Courses.
In the past six years or so, over 800 universities have created more than 10,000 of these MOOCs. And I’ve been keeping track of these MOOCs the entire time over at Class Central, ever since they rose to prominence.
In the past four months alone, 190 universities have announced 600 such free online courses. I’ve compiled a list of them and categorized them according to the following subjects: Computer Science, Mathematics, Programming, Data Science, Humanities, Social Sciences, Education & Teaching, Health & Medicine, Business, Personal Development, Engineering, Art & Design, and finally Science.
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I have always said the trick with being diagnosed with cancer is living long enough to see newer and better therapies coming out to help you outlive your own diagnosis:
Scientists at Northwestern University have discovered a “kill code” in every cell of the body that’s triggered by chemotherapy and that causes cancerous cells to self-destruct. What’s more, they’ve learned enough about the code that they’ve figured out how to trigger it without chemo—a finding that they believe could lead to new therapies.
The discovery, reported in the journals Nature Communications and eLife, is a code that’s found in both large and small ribonucleic acids (RNAs). The researchers also have early evidence that the small RNAs, called microRNAs, can be introduced into cells to trigger the kill switch.
“My goal was not to come up with a new artificial toxic substance,” said lead author Marcus Peter, Ph.D., a professor of cancer metabolism at Northwestern’s Feinberg School of Medicine, in a statement. “I wanted to follow nature’s lead. I want to utilize a mechanism that nature developed.”
The October Journal Club will be focusing on a new study in worms where a combination of compounds acted in synergy to almost double lifespan.
SUMMARY There is growing interest in pharmacological interventions directly targeting the aging process. Pharmacological interventions against aging should be efficacious when started in adults and, ideally, repurpose existing drugs. We show that dramatic lifespan extension can be achieved by targeting multiple, evolutionarily conserved aging pathways and mechanisms using drug combinations. Using this approach in C. elegans, we were able to slow aging and significantly extend healthy lifespan. To identify the mechanism of these drug synergies, we applied transcriptomics and lipidomics analysis. We found that drug interactions involved the TGF-b pathway and recruited genes related with IGF signaling. daf-2, daf-7, and sbp-1 interact upstream of changes in lipid metabolism, resulting in increased monounsaturated fatty acid content and this is required for healthy lifespan extension. These data suggest that combinations of drugs targeting distinct subsets of the aging gene regulatory network can be leveraged to cause synergistic lifespan benefits.
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Evidence has been building in recent years that our diet, our habits or traumatic experiences can have consequences for the health of our children — and even our grandchildren. The explanation that has gained most currency for how this occurs is so-called ‘epigenetic inheritance’ — patterns of chemical ‘marks’ on or around our DNA that are hypothesised to be passed down the generations. But new research from the University of Cambridge suggests that this mechanism of non-genetic inheritance is likely to be very rare.
A second study, also from Cambridge, suggests, however, that one way that environmental effects are passed on may in fact be through molecules produced from the DNA known as RNA that are found in a father’s sperm.
The mechanism by which we inherit innate characteristics from our parents is well understood: we inherit half of our genes from our mother and half from our father. However, the mechanism whereby a ‘memory’ of the parent’s environment and behaviour might be passed down through the generations is not understood.
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