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New paper from the lab🎈. Introducing Micro Immune Response On-chip (MIRO), a device that replicates tumors and their microenvironment to better understand responses to immunotherapies (cyan=immune cells, red=cancer, green=CAFs). IBEC

31,351 görüntüleme • 1 yıl önce •via X (Twitter)

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🧪 Back in the 1980s and early '90s, researchers started uncovering something suprising inside the aloe vera plant: a sugar molecule called acemannan. It wasn't just soothing burns or helping skin heal faster, it was communicating with the immune system. In lab tests and hospital settings, doctors noticed that aloe's compounds could help white blood cells "wake up" and respond more efficiently without overstimulation. 🦠One doctor working with HIV patients even saw immune markers improve after giving them the pure aloe extract. But as soon as the research gained traction, the story fizzled out. Funding dried up, pharmaceutical interests shifted focus, and the patents for acemannan extraction quietly got tucked away under corporate control. What had started as a promising immune discovery suddenly and conveniently disappeared. 🔒 Today, aloe is marketed mostly for skin care or digestion, but that's only a fraction of what it can do. Beneath its green skin lies a compound so unique that it was once granted "orphan drug status" by the FDA in 1995 for its role in supporting immune recovery in HIV patients. That should've been front page news but instead it was buried under the noise of pharmaceutical progress. 🌱 Interesting how this humble desert plant was quietly doing what billions of research dollars were still trying to replicate (helping the body remember how to heal itself but safely with no side effects, no contraindications and no toxicity levels.... ⭐️ Today only about 130 patents for proper extraction and stabilization exist, the most recent patent having the highest immune modulating 1,100 fractions in the world. This essentially means ideal compatibility for the body to recognize and use acemannan immediately upon taking. ❔ Think about how disruptive this could be if people actually started understanding how incredibly powerful their immune system was when it's function properly... -laurae_ramos

𝚃𝙷𝙴 𝚆𝙷𝙸𝚃𝙴 𝚁𝙰𝙱𝙱𝙸𝚃

204,218 görüntüleme • 4 ay önce

Neuralink Integration with ANKTIVA for Revolutionary Immunotherapy Elon Musk, a visionary collaboration opportunity by Dr. Sarabi and Grok. Dear Mr Musk: Good morning sir! I would like to bring to your attention the remarkable work of Dr. Patrick Soon-Shiong, who has developed a groundbreaking therapy, Anktiva, capable of supercharging key immune molecules to combat cancer and COVID-19. In a recent discussion with Tucker Carlson, Dr. Soon-Shiong described this advance as akin to the “E=mc²” of medicine—the discovery of “God’s equation,” a biological key that has eluded us for half a century until now. Just as Tesla has revolutionized the automotive and environmental industries, and SpaceX has advanced the expansion of humanity into a multi-planetary species to ensure our long-term survival, Anktiva represents a comparable paradigm shift in medicine, safeguarding human health and endurance. Given your shared commitment to advancing humanity, I respectfully inquire whether you might consider extending your support to Dr. Soon-Shiong in this critical pursuit. Moreover, I propose exploring the integration of Neuralink, employing the stepwise protocol outlined below, in collaboration with Dr. Soon-Shiong. Such a partnership could propel an unprecedented advancement in medicine and the future of humankind. Grok has developed a preliminary conceptual integration of Neuralink to enhance and supercharge IL-15 production 1/7: Identify Target Neural Circuits • Map the hypothalamic paraventricular nucleus (PVN) and dorsal motor nucleus of the vagus • Trace efferent projections from the PVN to the intermediolateral cell column (IML) in the spinal cord. • Identify sympathetic nerve fibers innervating the spleen and lymph nodes. • Map vagus nerve branches terminating in gut-associated lymphoid tissue and the hepatic portal system. 2/7: Implant Neuralink and Integrate with Neural Pathways • Place Neuralink electrodes in the PVN and dorsal motor nucleus of the vagus, using extended threads for subcortical/brainstem access. • Configure for recording/stimulation to modulate autonomic outflow to the IML at thoracic spinal levels. • Establish central control over peripheral pathways (e.g., splenic/vagus nerves) via targeted brain stimulation. 3/7: Develop Stimulation Protocols • Program Neuralink for high-frequency stimulation to the PVN for sympathetic activation. • Apply low-frequency patterned stimulation to the dorsal motor nucleus to engage feedback loops. • Modulate splenic/vagal pathways with phase-locked cycles through central interfaces. 4/7: Initiate Immune Cell Activation • Stimulate pathways to induce IFN-γ and TNF-α release in spleen/lymph nodes. • Trigger IL-15 transcription/translation in dendritic cells, monocytes, and epithelial cells. • Monitor for increased membrane-bound IL-15/IL-15Rα complex formation. 5/7: Enhance Local IL-15 Presentation • Concentrate stimulation at tumor/inflammation sites. • Promote immune cell clustering via chemokine/adhesion molecule induction. • Sustain localized IL-15/IL-15Rα trans-presentation to NK and CD8+ T cells. 6/7: Implement Real-Time Monitoring and Feedback • Record neural/immune biomarkers continuously via Neuralink telemetry. • Adjust stimulation based on IL-15 levels and NK/T cell activity. • Set safety thresholds to avoid excessive immune activation. 7/7: Synchronize with Immunotherapy • Time stimulation with IL-15 superagonists or adoptive therapies. • Evaluate synergies using immune monitoring/imaging. • Optimize based on patient responses. Thank you! #Neuralink #ANKTIVA #Grok #trendingvideo #cancer #medicalnews #health #trendingnow

Dr. Kash Sarabi

16,057 görüntüleme • 1 yıl önce

A single E. coli cell, placed on a dish, will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.

Niko McCarty.

58,047 görüntüleme • 11 ay önce