The Rhyothemis princeps Brain Externalization Project

Fucoidan is a sulfated polysaccharide found in brown seaweed that varies in molecular weight and composition. Wakame ( Undaria pinnatifida ) is a brown seaweed commonly consumed in Japan and is a main ingredient in miso soup and is also served as a salad.  Recently it as been reported that fucoidan can inhibit SARS-CoV-2 replication in vitro: https://www.nature.com/articles/s41421-020-00192-8 Of course it remains to be demonstrated in humans, but it's a start.  ~ Wakame fucoidan could be useful for Covid-19 since it inhibits thrombosis without increasing bleeding time: https://pubmed.ncbi.nlm.nih.gov/22084059/ The  Min et al. (2011) study also found in comparison to wakame fucoidan, fucoidan from bladder wrack inhibited thrombus formation, but bleeding time was prolonged (but not as much as for heparin).  An important caveat when considering the therapeutic potential of seaweed/fucoidan is that there are differences in biological activities in fucoidans from different species as we

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

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

The Biochemical Society posted a recording of a fascinating webinar titled ACE2: Friend or Foe. I have indexed the third portion, a talk by Prof Michael Bader on the non-enzymatic functions of ACE2. I hope to index the other portions soon. Highlights:  - ACE2 enzymatic function is not affected by SARS-CoV-2 binding. Dr Roger Seheult, a pulmonologist, and others have proposed what I thought to be a quite plausible hypothesis that loss of ACE2 function due to SARS-CoV-2 binding results in high levels of oxidative stress which in turn causes hypercoagulability and attendant pathologies. Loss of ACE2 activity may be occurring due to reduced ACE2 transcription, however [ see previous post on this ]. - Vascular pericytes are potential targets of infection (very interesting, IMHO) - AT2 pneumocytes are targets of infection in lung tissue - loss of ACE2 results in reduced tryptophan uptake due to loss of amino acid transport function > reduction in serotonin production > loss of exercis

[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