🦇 What Does The Bat Say? 🦇

Unlike most sedentary modern humans, one of the natural hosts for the virus, THE BAT, has to “exercise” regularly to find food, which continually provides a powerful adaptive stimulus to MAINTAIN FUNCTIONAL muscle and MITOCHONDRIA. In effect the bat>
is exposed to regular HORMETIC STIMULI, which could provide clues on how to resist this virus...we review the data that might support the idea that MITOCHONDRIAL health, induced by a HEALTHY LIFESTYLE, could be a KEY FACTOR in resisting the virus
The concept of HORMESIS suggests that it is important to constantly stimulate the renewal and maintenance of a LARGE POPULATION of HEALTHY MITOCHONDRIA. It may therefore be possible to learn something from one of the natural hosts of SARSCoV2, BATS. Bats are the only true>
flying mammal and are exceptionally long-lived for their size. This could be because the evolution of flight has required a whole host of adaptations, including MAINTAINING a LARGE POOL of MITOCHONDRIA that produce VERY LITTLE ROS while maintaining a HIGH ATP OUTPUT.>
This appears to have gone hand-in-hand with changes in the immune system to PREVENT EXCESSIVE INFLAMMATORY activation by stressed mitochondria, for instance, by DAMPENING NLRP3 INFLAMMASOME activity. The net result is that many bats can TOLERATE HIGH LEVELS OF VIRUSES, like the>
CORONAviridae family and do show a reduced antibody and inflammatory response, hinting they are USING ANOTHER PART of their IMMUNE SYSTEM to control the virus.
The INFLAMMASOME may thus be important, as its activation can lead to pyroptosis, an inflammatory form of apoptosis>
and can be triggered by excessive mitochondrial stress. It may well be an essential component in “inflammaging”...in some species of bat, mitochondrial health, despite bursts of oxidative stress, is maintained by STRINGENT MITOCHONDRIAL QUALITY CONTROL mechanisms, like mitophagy>
MITOPHAGY...a negative regulator of NLRP3 inflammasome activity, so although mitochondrial damage can activate the inflammasome, it can also activate counter-balancing mitophagy to prevent excessive inflammation...it seems that powered flight has required the CO-EVOLUTION of>
both mitochondria that tightly control ROS, and a co-adapted immune system. Critically, there is evidence that SARSCoV2 inhibits autophagy, suggesting it might also inhibit mitophagy... mitochondrial fusion, as SARSCoV1 may do...mitochondrial fusion can inhibit mitophagy>
and can inhibit cell death and ensure energy production, although prolonged fusion can also initiate cell death in some circumstances This latter point suggests another innate anti-viral mechanism.>
Overall, modulation of the inflammasome could be one element in how the virus could result in an “INFLAMMAGING” PHENOTYPE.
We here consider COVID-19 as a REDOX DISEASE...considering the vulnerability of complex interconnected systems with multiorgan/multilevel interdependencies. Host/viral glycan interactions>
underpin SC2's extraordinary efficiency in gaining cellular access, crossing the epithelial/endothelial barrier to spread along the vascular/lymphatic endothelium and evading antiviral/antioxidant defenses.
An INFLAMMATION-driven “OXIDATIVE STORM” alters the redox landscape>
eliciting epithelial, endothelial, mitochondrial, metabolic, and immune dysfunction and coagulopathy. Concomitantly reduced nitric oxide availability renders the sulfur-based redox circuitry vulnerable to oxidation, eventual catastrophic failure in redox communication/regulation>

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More from @janieyaya

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2 Minutes to Midnight

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you are as IGNORANT as you are CORRUPT.
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🌬️ Windy 🌬️

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If mechanical ventilation is not available or is insufficient, NATURAL VENTILATION through opening windows and doors should be utilized.
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The Sign

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11 Oct
💊 I Want a New Drug 💊

The team investigated more than 400 COVID patients from hospitals across the US who take ASPIRIN unrelated to their COVID disease, and found that the treatment REDUCED THE RISK of several parameters BY ALMOST HALF: reaching mechanical>
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9 Oct
👄 Bad Mouth 👄

Increased COVID severity may be linked to poor oral health status, especially in patients with cardiovascular diseases...study assessed oral health status, severity of COVID symptoms, C-reactive protein (CRP) levels and duration of recovery.>
“Oral tissues could act as a reservoir for SARSCoV2, developing a HIGH VIRAL LOAD IN THE ORAL CAVITY...The study included 86 Egyptian heart disease patients with a confirmed COVID-19 PCR test... researchers from Cairo University assessed oral health and COVID severity.>
An oral health score was used to determine the effect of oral health on COVID. Data on CRP levels and COVID PCR tests were collected via the questionnaire and confirmed via medical records. CRP levels are used to determine when there is inflammation in the body...the correlation>
Read 5 tweets

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