Immorta Bio just doubled the lifespan of mice using a first-in-class senolytic immunotherapy called SenoVax combined with personalized stem cells from their StemCellRevivify platform. In this deep dive, I break down exactly how it works, why it matters, and what it means for the future of human aging.
SenoVax is a vaccine that trains your immune system to hunt down and destroy senescent cells — the \.
This study investigated the associations between neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, and systemic immune-inflammation index with progression of CSVD.
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Cancer development results from the selection of cells with mutation(s) that provide survival and proliferative advantages. Normal barriers to proliferation are overcome as clones adapt to an ever changing hostile microenvironment, where low oxygen tension, low glucose levels, and an acidic extracellular pH (all of which increase genetic instability) are found. The hypoxia inducible factors, HIF-1 and HIF-2, are upregulated in response to these conditions. This could occur by constitutive activation of PI3K signaling or inactivating mutations in, for example, the von Hippel–Lindau tumor suppressor, VHL [35-37], which normally deacetylates HIF-1α, leading to HIF-1α polyubiquitination and proteasomal degradation [38]. HIFs trans activate genes mediating proliferation, angiogenesis, intermediate metabolism (glycolysis) and pH regulation, which promote tumor development [39].
HIF-1α stimulates production of growth factors, such as transforming growth factor β (TGF-β), insulin-like growth factor 2, interleukin-6 (IL-6), interleukin-8, macrophage migration inhibitory factor (MIF), and growth factor receptors, such as the epidermal growth factor receptor (EGFR), resulting in continuous proliferative signaling. In the hypoxic environment, constitutive activation of these signaling pathways (e.g., Ras [1] and PI3K [2]) stabilizes HIF-1 and may result in “oncogene addiction” that persists through the transition from adenoma to carcinoma. In the case of PI3K, constitutive activation may result from the appearance of mutations in tumor suppressor genes (e.g., the phosphatase and tensin homolog [PTEN]), from activating mutations in the PI3K complex itself, or from aberrant signaling in receptor tyrosine kinases [40].
Like the mathematical universe.
This video about mathematical realism will probably not benefit you in any way. Enjoy. 1) What are numbers? 2) Why Hume’s understanding of mathematics is incorrect. 3) Why Plato’s understanding of mathematics is probably incorrect. 4) Why the common sense view of mathematics is probably incorrect. See second video for more.
But what if our biological makeup limits how creative we can be? Maybe the timing of the clock that governs our introspections forces our intuitive periods—or the times of uncertainty—to be too brief. Could we use our quantum technologies to extend the wavelike processing inside our brains? I am here inspired by Aldous Huxley, who suggested in his famous book, The Doors of Perception, that drugs could alter our consciousness, revealing true reality. But rather than using drugs, I envision quantum chips designed to suppress the “noise” that induces introspection, allowing a longer interference period for our intuitive thoughts to develop. This has the potential to be far more potent than what Huxley could ever have imagined.
For my idea to work, we would first have to understand where and how these superpositions are stored and manipulated in the brain. The British physicist Roger Penrose, PhD, has speculated that this occurs within microtubules, which are dynamic, hollow, rod-like components of the eukaryotic cytoskeleton that are responsible for things such as intercellular transport. Despite some circumstantial evidence, we do not have a strong reason to believe that microtubules are capable of quantum interference, but they are certainly worth further investigation. Once we understand how our brain uses quantum effects, we could then design a quantum chip that interfaces with the relevant biological components. Theoretically, the device would be able to upload superposition states to store them for longer periods and shield them from collapse, helping us to enhance our creative wavelike thinking.
One wonders what kind of power would be unleashed by doing this. I imagine the change would not be purely quantitative, so that we merely become faster calculators or quicker problem solvers, although even that would be amazing. Instead, I think the change could be qualitative, expanding our perception into a completely different realm, effectively creating a new species. We might theoretically become more powerful than modern humans, just as we currently are with respect to other apes. Quantum-enhanced humans would see further domains of reality that would otherwise remain hidden forever from us ordinary humans.
Somewhere, out in the cold depths of space, there is a space rock that could destroy a large chunk of life on Earth. Is this fate inevitable? Could we find a way to stop it, or will we eventually suffer the same fate as the dinosaurs? And should this existential threat be keeping you up at night? Here’s what we know.
The asteroid that killed the dinosaurs 66 million years ago was at least 10 kilometres across, big enough to cause megatsunamis, ignite enormous forest fires and darken the skies the world over. Asteroids of that size are estimated to hit Earth about every 60 million years, based on the planet’s crater record. For the next size class down, asteroids about 1 kilometre across, estimates suggest they hit Earth about every million years, and the most recent one was about 900,000 years ago. Those numbers are enough to make you nervous.
But one of the things that sets humanity apart from the dinosaurs is our ability to look out into space and interpret what we see there. Naturally, researchers around the world have used this ability to attempt to learn how many asteroids are out there and what proportion of them are on trajectories that could be dangerous.
Image: angel_nt/Getty Images.
The dinosaurs were wiped out by an asteroid, but does that mean we risk suffering the same fate — and should you be worried about the possibility? Leah Crane sets the matter straight.
By Leah Crane
Lipid metabolism in cancer.
Cancer cells exhibit distinct lipotypes to sustain functional states crucial for tumorigenesis.
Various lipid metabolism components like biosynthesis, uptake, storage, and degradation of lipids contribute to cancer cell fitness.
Cancer cells dynamically transition across lipotypes under microenvironmental stress.
Targeting essential nodes in lipid metabolism may offer novel cancer therapeutics. sciencenewshighlights ScienceMission https://sciencemission.com/cancer-cell-lipotypes
While the initial transformation of cancer cells is driven by genetic alterations, tumor cell behaviors and functional states are dynamically regulated by cell-intrinsic factors including proteins, metabolites and lipids, and extrinsic microenvironmental factors. Emerging multi-omics technologies highlighted that cancer cells exhibit distinct lipidome compositions and employ specific lipid metabolic circuits for chemical conversions – collectively defined as ‘lipotypes’. We review the interplay between cancer lipotypes and cellular states, focusing on interpreting how being at different positions along the spectra of representative lipid metabolic axes influences cancerous traits. We aim to instill a system biology perspective to integrate ‘lipotypes’ into the established ‘genotype–phenotype’ framework in cancer.
JNeurosci: Lu and Matsunami analyzed gene activity to find proteins that help odor-detecting receptors reach the cell surface. They identified three helper genes—Gfy, Clgn, and Syt1—that support receptor function as olfactory cells mature.
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Odor detection in mammals is primarily mediated by odorant receptors (ORs), the largest family of G-protein-coupled receptors, expressed in olfactory sensory neurons (OSNs; [Buck and Axel, 1991][1]). However, most ORs exhibit little or no cell surface expression in nonolfactory cell types ([Lu et al., 2003][2]; [Hague et al., 2004][3]). While the accessory protein RTP1 and RTP2 enhance the expression of certain ORs, we hypothesized that additional proteins coregulated with RTP1 and RTP2 during OSN maturation may further enhance OR cell surface expression ([Saito et al., 2004][4]; [Zhuang and Matsunami, 2007][5]). To test this, we developed a computational pipeline based on publicly available single-cell transcriptomic data to create an interactive tool for exploring gene expression during OSN maturation.