The Rhyothemis princeps Brain Externalization Project

Since March, I have been hoping someone would study whether covid-19 patients with type 2 diabetes (T2D) on metformin fare better than those on other types of anti-diabetes medications. Many of the risk factors associated with severe covid-19 (e.g., obesity, diabetes, hypertension, older age) relate to AMPK signalling and metformin, a drug that improves AMPK signalling, has been found to benefit these conditions.  My question has finally been answered  - T2D patients on metformin have a 70% reduced  risk of death as compared with those on other anti-diabetic medications [1,2]. Unfortunately the study did not control for other important factors such as age, degree of blood sugar control, BMI, and time since diagnosis; a future study designed specifically to examine metformin in covid-19 should be conducted that controls for these factors. The study authors discuss the potential role of AMPK signalling in covid-19, delineating a number of possible mechanisms by which it could impact the

"Aquaporin water channels - from transfusion medicine to malaria" by Dr. Peter Agre Sept. 9, 2015 22:22 Rarity of AQP1 null mutants despite apparently limited effect on phenotype - at birth lung goes from being secretory organ to being absorptive, may be a critical point 25:46 AQP4 and blood brain barrier { not mentioned in lecture: Evidence that pericytes regulate aquaporin-4 polarization in mouse cortical astrocytes https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4223569/ }   26:54 AQP4 - accelerated brain damage   27:49 in many cases or stroke the individual succumbs not to the infarct, but to brain edema 30:04 Aquaporins, stress response , decline in function with aging   41:34 AQP7 and AQP9 - Glycerol Metabolism AQP7 - present in fat; water & glycerol permeation; suppressed by insulin; releases glycerol from fat catabolism during starvation AQP9 - present in liver; water, glycerol & urea permeation; facilitates hepatic glycerol uptake for gluconeogen

[2020-07-07] Fadason et al. (2020)           A preprint  by Fadason et al. [1] discusses a mechanism by which SARS-CoV-2 could alter gene expression of ACE2 and associated genes and produce a host environment that favors its replication. In doing so, it looks like the virus not only 'takes out' ACE2 by binding with its catalytic domain (see update below), it may also decrease ACE2 expression. I am not familiar with this type of alteration of chromatin structure and I don't know how long lasting the changes could be. Some epigenetic alterations can be quite long lasting, even multi-generational.         S everal genes in the network that are also affected impact lipid metabolism and gluconeogenesis. Gluconeogenesis can also be a response to hypoxia [2] and is a common feature of the acute phase response in both infection and injury [5].                      The article does not discuss changes in collectrin expression. The collectrin and ACE2 genes are located on the X chro