The Rhyothemis princeps Brain Externalization Project

[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

There's this book I want to get, Hochachka and Somero's Biochemical Adaptation (or the latest edition, which is  by Somero et al.); of course since it is a science book it is ridiculously expensive and there's no ILL in a pandemic. The book has some interesting passages (p. 402) on Na/K ATPase that are visible on Google Books preview. I took a snip since there's no cut and paste: Main points: - futile cycling of ions may play a vital role in thermogenesis - Na/K ATPase may account for 5-10% of BMR - there are differences in Na/K ATPase activity between ectotherms and endotherms - 7x higher activity in mammals - "Correlated with this difference in estimated costs of sodium pump activity were differences in in the rates if passive efflux of K+ and passive influx of Na+ in liver cells. The costs of maintaining transmembrane gradients in concentrations of Na+ and K+ are reflected in differences in sodium pump-dependent oxygen consumption." - the degree of differen

In the post on osteocalcin that I can never quite finish I paraphrased a review on the topic that suggested that undercarboxylated osteocalcin may be one of the anti-aging factors present in 'young blood'.  Heterochronic parabioss experiments - wherein the circulatory systems of an old and a young mouse are joined - have shown rejuvenating effects for the old mouse and some age-promotion in the young. This has lead to speculation that there are youth-promoting factors in the blood of the younger mouse that provide benefit to the older mouse.  However the Conboys and their research team, who pioneered heterochronic parabiosis experiments, have proposed that it is actually dilution of pro-aging factors that provides the age-reversing effects. They recently published an article [Mehdipour et al. 2020] showing dilution of the blood of an old mouse is sufficient for rejuvenation.  From the article: "The above concept fits well with the age-imposed increase in systemic TGF-beta

[2020-06-13] Talk by Kelvin J.A. Davies on Lon protease from 2013(?) 12:56 Degradation of oxidized proteins by proteasome is mostly ATP independent; degradation by Lon is ATP dependent   20:08 the most decreased mRNA in skeletal muscle in mice in aging is Lon 20:36 the main one that comes up is aconitase, but there are many, many others   20:17 Lon inducibility is diminished in senescent cells & they have more carbonylated proteins   22:20 slide - Aging Decreases Lon Induction and Stress Protection 26:28 Lon attaches to mtDNA and allows for biogenesis; under stress it detaches and degrades oxidized proteins and at that point proliferation stops   28:59 Lon is inducible by H2O2, heat stress, starvation, cold stress, mechanical shear stress, peroxynitrite Also, loss of frataxin upregulates Lon and ClpP proteases and results in too much degradation of Fe-S proteins [1]. 1 - Guillon, Blanche, Anne-Laure Bulteau, Marie Wattenhofer-Donzé, Stéphane Schmucker, Bertrand Friguet,

Who knew? Not me, until this morning. The Lung Is a Site of Platelet Biogenesis and a Reservoir for Haematopoietic Progenitors   [2017] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5663284/ "The contribution of the lungs to platelet biogenesis is substantial, accounting for approximately 50% of total platelet production or 10 million platelets per hour." In the lungs. 10 million an hour - holy moly. This is like when I found out about physiological hematopoietic stem cell migration. Or B cells cranking out between ten and a hundred thousand anitbodies per second: https://youtu.be/J9jcnh3E0Fw

Loss of frataxin is lethal in multicellular organisms. Why is frataxin necessary for multicellular life? Use of Game-Theoretical Methods in Biochemistry and Biophysics [2008] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577752/ "Recently, it has been shown experimentally that stimulation of respiration by frataxin in colon cancer cells reduced growth rate [47]. Thus, cancer can be regarded as a regression to selfish behaviour of cells. Healthy higher organisms possess regulation mechanisms to suppress cancer. However, in early evolution of multicellularity, these mechanisms probably did not yet exist." So that's one reason. Could there be some relationship to osmoregulation? 2020-6-10 Osmoregulation implies maintenance of electrochemical gradients, just as multicellularity implies morphogenesis. Then I remembered Dr Michael Levin's talk on bioelectric fields and morphogenesis: Of course, since comments are turned off I can't make my notes in the YT comment

Yesterday I watched two excellent presentations on Freidreich ataxia (still trying to use the proper nomenclature convention) from back in 2011: Notes: 5:44 frataxin is essential for muticellular eukaryotes (but not single celled organisms) frataxin is needed for the production of iron-sulfur clusters (aconitase is an important TCA enzyme that includes an iron-sulfur cluster that is particularly vulnerable to oxidation) 13:07 Indeed! & also part of the urea cycle 18:35 Reduction in frataxin leads to iron accumulation in the mitochondrion   38:26 summary of therapeutic approaches in relation to hypothetical vicious cycle in FA EPO - erythropoietin increases expression of genes related to iron utilization (lactoferrin and Wim Hof method breathing increase EPO) HDAC inhibitors increase expression of frataxin (butyrate / tributyrin are HDACi) pioglitozone increases mitochondrial biogenesis (PQQ & urolithin A do the same) I think neuroinflammation should be included as part

Adaptation to flight has a big impact on antioxidant defenses; recently this paper came up in my feed (thank Google): Adaptation of the master antioxidant response connects metabolism, lifespan and feather development pathways in birds [2020] - https://www.nature.com/articles/s41467-020-16129-4 “ Birds (Aves) display high metabolic rates and oxygen consumption relative to mammals, increasing reactive oxygen species (ROS) formation. Although excess ROS reduces lifespan by causing extensive cellular dysfunction and damage, birds are remarkably long-lived. We address this paradox by identifying the constitutive activation of the NRF2 master antioxidant response in Neoaves (~95% of bird species), providing an adaptive mechanism capable of counterbalancing high ROS levels. We demonstrate that a KEAP1 mutation in the Neoavian ancestor disrupted the repression of NRF2 by KEAP1, leading to constitutive NRF2 activity and decreased oxidative stress in wild Neoaves tissues and cells. O

From a  discussion with OS on MedCram (which had gone way OT from sex differences relating to covid-19 pathology - link to discussion thread ): re: AMPK bat genetics - not much yet, but there's this one Positive Selection of Cereblon Modified Function Including Its E3 Ubiquitin Ligase Activity and Binding Efficiency With AMPK - https://pubmed.ncbi.nlm.nih.gov/30836149/ Note the same modification is present in both bats and rodents. Hamsters do seem to have some protection from oxidative stress, but they are not particularly long-lived as are bats. They are what's termed 'r selected' - with a life history characterized by high reproductive rate and short life-span. Here's an article that points out that oxidative stress defenses may be tissue specific and that hamsters may not have as much protection in the brain: Oxidative Damage Does Not Occur in Striped Hamsters Raising Natural and Experimentally Increased Litter Size - https://www.ncbi.

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

In response to a post by oksana s on MedCram forum re: research she conducted on DKO mct8/oatp (AHDS) mice - females are reportedly androgenized and aggressive and selectively kill their own female pups. OS also noted an increase in sexual behavior just prior to symptom onset in SOD1 KO mice (ALS model) and reported the same in HD model mice. Your mice reminded me of a news article I had read on sexual development & histamine signalling: https://www.sciencedaily.com/releases/2018/08/180814151001.htm I searched and found this, published 2 yrs prior to the above [this site has some malware scripts on it for some reason, though it looks just to be an academic publishing site - I opened it in a container tab so I could read it]: https://clinical-and-molecular-endocrinology.imedpub.com/thyroid-hormone-derivatives-and-brain-histamine-what-should-we-expect.php?aid=17259 Do you think a histamine modulating drug given during pregnancy would normalize sexual behavior in the resulting pu

Aconitase (aconitate hydratase) is a tricarboxylic acid cycle (TCA) enzyme that converts citrate to iso-citrate via cis-aconitate. It has an iron sulfur cluster that interacts directly with substrate and is prone to oxidation by superoxide. Inactivation of aconitase has been  implicated in neurodegenerative diseases [1]. A mutation in ACO2 is associated with Infantile Cerebellar-Retinal Degeneration [2]. from [2] : "The active (4Fe-4S) cluster was shown to be extremely sensitive to superoxide-mediated inactivation 10 and a decrease in AH activity was observed in several neurodegenerative diseases associated with the development of oxidative stress, in particular Friedreich ataxia [MIM 229300 ], Parkinson [MIM 168600 ], and Alzheimer disease [MIM 104300 ], 11 as well as in mice lacking mitochondrial superoxide dismutase. 12 The reduced AH activity in endomyocardial biopsies of individuals with Friedreich ataxia was attributed not only to oxidative stress but also to the im