Andy Blidy

A couple of California stem cells supporters..... Colby Leis my grandson making a statement YESon14.com with Grandpa

🚨 New research is challenging decades of thinking on a rare, devastating brain disease. NBIA (Neurodegeneration with Brain Iron Accumulation) shows striking iron buildup on MRI scans. But emerging evidence suggests the iron may not be the primary cause — it could be a downstream effect. The real drivers are deeper. And the new research might be relevant for Parkinson's too. Thread 🧵

Scalability looks completely different for an autologous dendritic-cell platform. A standard vaccine is usually an industrial product that can take years to develop, validate, manufacture, fill, finish, distribute, and deploy at population scale. But an autologous dendritic-cell product is not really a “vaccine” in the strict industrial sense. It is the patient’s own immune cells, collected, programmed with the relevant antigen curriculum, polarized into a Type 1 instructional state, functionally tested, and returned to the same patient. In a closed bioreactor model, that immune education process can potentially be completed in about six days. So the bottleneck shifts from mass-producing millions of identical vaccine doses to deploying local manufacturing nodes that rapidly educate each patient’s own immune system. Traditional vaccines deliver information and depend on the body to interpret it correctly. An autologous dendritic-cell platform delivers the interpreter itself.

Dark times ahead at the FDA statnews.com/2026/05/21/fda… My new @statnews column. Why this may be the end of the FDA as an agency as we knew it #stemcells

@PrimeMedicine 12/#StemCells in #allogeneic transplants derived from a healthy donor & not form the #patient himself while in #autologous cell therapies the cells are taken from the same person receiving the transplant - the patient is in fact his own donor

IL-11 inhibition may reduce fibrosis, but the trade-off matters. IL-12 is the master licensing signal for protective immunity. It tells the immune system when antigen recognition should become Type 1 execution: CD4 help, CD8 killing, NK activation, IFN-γ reinforcement, and memory. IL-11 pushes the opposite direction. The literature shows IL-11 suppresses IL-12 production in activated macrophages and monocytes, inhibits NF-κB signaling needed for IL-12p35 and IL-12p40 transcription, drives Th2 polarization, reduces IFN-γ, promotes MDSC biology through STAT3, and suppresses CD4-mediated antitumor immunity. So the question is not simply, “Does IL-11 inhibition reduce fibrosis?” The deeper question is: What happens to long-term immune defense if you suppress a pathway that intersects the IL-12 licensing circuit? Fibrosis is dangerous. But so is losing the Type 1 immune instruction required to control intracellular pathogens, viruses, senescent cells, and cancer. My concern is that anti-aging biology keeps treating inflammation like volume control. Turn it down and lifespan improves. But the immune system is not a volume knob. It is a decision system. IL-12 is not just “inflammation.” It is the licensing signal that determines whether immune recognition becomes protective execution. That distinction matters.

@BBCNews You have $NWBO #AdventBioservices in your backyard that can easily engineer a safe solution.

🚨 Just dropped: Scientists may have found a master switch of human aging ... blocking one protein (IL-11) extended lifespan by +25% in mammals. Now in human Phase II trials. Google’s Calico just invested $596M. Full visual thread with mechanism, data & charts here 📷#Longevity #AntiAging #IL11”

@BNOFeed 🎙️

@CBSNews 👇🏻

@FCDOGovUK @UKinDRC Maybe you should talk to @MHRAgovuk and get this treatment approved for #glioblastoma is taking over 27+ months for them to make a decision so we can also tackle #Ebola. In the meantime, $NWBO #AdventBioservices could definitely use the funding.

@DrIanWeissman Check this article out Dr Weissman.

@DailyMail They should be rerouted to a different type of DC ➡️ #DCVax for #Ebola

The World Health Organization declared the Ebola outbreak in the DRC and Uganda a Public Health Emergency of International Concern on May 17 trib.al/4E3Z20y 🔗

@SkyNews @grok explain what I mean in simple terms.

@SkyNews Has anyone even looked into this yet? Seriously!? There is a solution that can be safely engineered before things get out of hand. $NWBO #AdventBioservices.

@cnni This looks like a job for $NWBO #AdventBioservices.

Spot on ... this is exactly the pressure point we need to keep pushing. You’re right that we’re still flying partially blind without denser, longitudinal biomarkers. Plasma panels, methylation clocks, p16, T-cell subsets, and wearables (HRV, CGM, sleep architecture) are all valuable ... but we need the next generation that can actually read the compartment-specific signals that matter most in aging tissues. That’s why I’m hammering the precision-medicine angle so hard in these threads. Therapies like the IL-11 antibody are powerful, but they’ll only reach their full potential when we can biomarker-stratify patients before treatment and monitor response in real time. The field is finally waking up to this. The next decade of geroscience wins will go to the trials that solve the biomarker problem first. Appreciate you expanding on it

Most people don’t die from “old age”. They die when their heart, lungs, kidneys, or liver slowly scar and fail. Fibrosis contributes to ~35% of all deaths. This IL-11 antibody powerfully reduced fibrosis in multiple organs — and added 25% lifespan in mice. Now in human trials. Full thread with the data 👇

Interesting angle. I appreciate the focus on dendritic-cell integrity and IL-12 signaling — optimizing the immune “instruction” environment (sleep, exercise, circadian rhythm, metabolic health) is foundational. The IL-11 antibody, however, is a precise monoclonal that blocks a downstream pro-fibrotic cytokine driving organ scarring (the actual cause of most age-related deaths). No data yet shows that enhancing IL-12/SIRT1 pathways replicates the 22–25 % lifespan extension or multi-organ fibrosis reversal seen in the Nature 2024 study. Precision medicine means we can (and should) do both: fix the environment and target the specific drivers when the biology demands it. No one-size-fits-all.

@Neuroscope_mp Have you looked into your body’s own ability to create its own IL-12 immune response. a.co/d/0fRshZl5