The Rhyothemis princeps Brain Externalization Project

MCC950, an NLRP3 inflammasome inhibitor, was shown to reverse symptoms in two Parkinson's disease mouse models and was reported to have no toxicity issues. The only reason given in the following article for not pursuing clinical trials is that it is off-patent: https://www.genengnews.com/news/parkinsons-disease-drug-that-cools-brains-on-fire-could-enter-human-trials-in-2020/   Given its mechanism of action it could be broadly effective against neurodegenerative diseases and even spinal cord injury ( https://www.frontiersin.org/articles/10.3389/fmolb.2020.00037/full ).   Infections due to immunosuppression may be a problem, but there are reasons to think that MCC950 would be safer than immunosuppressive agents currently used to treat inflammatory conditions:   "Thus, specific targeting of NLRP3 will not result in the complete blockade of IL-1β during infection and antimicrobial responses may remain intact. MCC950 may therefore have less immunosuppressive effects when compa

In trying to find information on the effect of radiation on aquaporins, a paper came up on a treatment for radiation-induced salivary hypofunction: Baum, Bruce J., Changyu Zheng, Ana P. Cotrim, Linda McCullagh, Corinne M. Goldsmith, Jaime S. Brahim, Jane C. Atkinson, et al. “Aquaporin-1 Gene Transfer to Correct Radiation-Induced Salivary Hypofunction.” Handbook of Experimental Pharmacology , no. 190 (2009): 403–18. https://doi.org/10.1007/978-3-540-79885-9_20 .           " Indeed, IR leads to a dramatic loss of the fluid secreting salivary acinar cells, resulting in severe glandular hypofunction (a diminished production of saliva) in most patients ( Vissink et al. 2003 ; Nagler and Baum 2003 ). The reason for this damage remains enigmatic, as salivary acinar cells are well differentiated and very slowly dividing, the opposite of the classical target cell for IR sensitivity [emphasis added] . If patients have sufficient functional acinar tissue post-IR, it is possible t

[2020-07-03] Presentation by Ruslan Medzhitov from 2018 titled "Inflammation and Disease Tolerance: Surviving Acute Illness" 1:25 cost of inflammation and cost vs. benefit trade-off 4:01 sickness behaviors, includes loss of appetite - observed in all animals including insects   5:10 Decreased Food Intake After Listeria Infection - disease induced anorexia   6:32 Anorexia Protects Against Listeria Infection (survival rate)   7:43 Glucose is Sufficient for Lethality in Listeria Infection - even at only 2% of normal caloric intake 8:26 2DG (inhibits metabolism of glucose) increased survivorship (100% survival vs. 50% without 2DG)   9:06 Effects of Feeding on Sepsis Survival - sepsis model using lipopolysaccharide (LPS) injection - same results found for feeding, glucose and 2DG experiments   11:10 Effects of Glucose in LPS Sepsis is Independent of Magnitude of Inflammation   11:48 Mechanism for Glucose-mediated Death in Bacterial Inflammation - review of fasting metab

[2020-06-30] Interesting finding reported by Prostiv et al. earlier this year [1] - human body temperature has decreased in the US since the Industrial Revolution. The authors suggest the change is due to a reduction in chronic inflammation: "Although there are many factors that influence resting metabolic rate, change in the population-level of inflammation seems the most plausible explanation for the observed decrease in temperature over time. Economic development, improved standards of living and sanitation, decreased chronic infections from war injuries, improved dental hygiene, the waning of tuberculosis and malaria infections, and the dawn of the antibiotic age together are likely to have decreased chronic inflammation since the 19 th century. ... Reduction in inflammation may also explain the continued drop in temperature observed between the two more modern cohorts: NHANES and STRIDE. Although many chronic infections had been conquered before the NHANES study, s

Creatine can exacerbate airway inflammation and asthma: Effect of Creatine Supplementation on the Airways of Youth Elite Soccer Players [2019] https://pubmed.ncbi.nlm.nih.gov/30913162/ Creatine Activates Airway Epithelium in Asthma [2010] https://pubmed.ncbi.nlm.nih.gov/21072743/ "Inducible nitric oxide synthase (iNOS) is an isoform of NOS, and increases in its expression have been linked to eosinophilic inflammation and airway remodelling in asthma... we found that creatine supplementation was associated with greater epithelial expression of iNOS and NF- κ B in both non-sensitized and sensitized mice (Fig. 3 a, b ), which could be considered a possible mechanism for the Cr-induced asthmatic phenotype." The increase in iNOS may have something to do with creatine's effect on arginine metabolism, though in macrophages, it looks like creatine reduces iNOS (?) : Creatine shapes macrophage polarization by reprogramming L-arginine metabolism [2019] - https://www.jimmunol.or