Almost 4 tonnes of CO2 are released during the production process of a single electric car and, in order to break even, the vehicle must be used for at least 8 years to offset the initial emissions by 0.5 tonnes of prevented emissions annually. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fearth.org%2Fenvironmenta...
Out the door, tonnes CO2e https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fearth.org%2Fwp-content%2Fu...
5.6 ICE
6.5 hybrid
8.8 EV
How long will the battery last? If its 7 years, the EV never came out ahead.
This study came up with a lot closer figures, but used 150k KM as a lifetime. ICE should last more than double that.
(tonnes CO2e)
ICE 24
Hybrid 21
Plug in hybrid 19
EV 19
Based upon a 2015 vehicle in use for 150k KM using 10% ethanol blend and 500g/KWH grid electricity. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fweb.archive.org%2Fweb%2F20...
It would be nice to see the full study in the submission. The way they present the percentages makes it sound like an advertisement.
physical exercise increases tolerance to elevated ambient temperature and oxidative stress. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fdoi.org%2F10.1371%2Fjourna...
Or just wait? FTA
the participants demonstrated gradual adaptation to heatwave impacts over the 15-year period
The eco people won't like this but the solution might be to buy an AC and maybe take breaks if working hard to not overheat?
Furthermore, manual workers, rural residents and participants from communities with fewer air conditioners were more susceptible to the health impacts. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fwww.nature.com%2Farticle...
as soon as HmgB1 goes outside the nucleus, it acquires completely different functions, post-translational modifications, and change of its redox state.
High-mobility group box 1 protein (HMGB1) serves as an inflammatory mediator and has been implicated in the pathogenesis of asthma. Extracellular HMGB1 transduces cellular signals through the plasma membrane receptor for advanced glycation end products (RAGE). The HMGB1/RAGE axis has proven to be a pivotal factor in the progression of tumor growth and inflammation. In this study, we sought to determine whether HMGB1 signaling through RAGE occurs in asthma. Conclusion: In conclusion, a part of the HMGB1 contribution to the pathogenesis of asthma was mediated through binding to RAGE.
NETs overproduction promoted glioma cell proliferation, migration, and invasion. Furthermore, HMGB1 was found to bind to RAGE and activate the NF-B signaling pathway in vitro.
Green tea extract to the rescue
experimental evidences indicate that EGCG can induce the aggregation of HMGB1 protein, a late mediator of inflammation, which subsequently stimulates the autophagic degradation and thus provides protection from lethal endotoxemia and sepsis.
Some interesting info.
HMGB1 is an important player in nuclear transactions because it is very abundant (about 1,000,000 molecules) in most mammalian cells, is extremely conserved between species, and Hmgb1 KO mice are not viable. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fwww.cell.com%2Faction%2Fsh...
With 1 million of these HMGB1 per cell, dumping them into the extracellular plasma might cause quite a reaction (binding to RAGE and precipitating neutrophil extracellular traps). Looks like it might be to fight biofilms.
The extracellular innate-immune effector HMGB1 limits pathogenic bacterial biofilm proliferation https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fwww.jci.org%2Farticles%2Fv...
Might be linked to other diseases too, like alzheimers?
RAGE activation induces AB production https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%2Fa...
Digressing, the body does release heat shock proteins in response to heat, maybe too much heat depletes the body of its mechanisms to ameliorate the damage from heat? Or maybe its like how this paper describes a chicken and the egg which came first type dysfunction caused by heat between the mitochondria and lysosomes? Problems with those two systems on an aggregate scale within the body could lead to big problems.
The maintenance of both lysosomal and mitochondrial physiological functions and cellular homeostasis relies on intracellular temperature dynamics (6, 7). Lysosomes are highly dynamic organelles responsible for the turnover of some proteins and lipids through digestive enzymes (8). The enzymatic activities are highly dependent on a healthy pH and temperature environment. During the process of heatstroke, the pH values of lysosomes have been observed to increase, which leads to cell death. A higher or lower temperature may reduce enzymatic activities and further disturb cellular homeostasis (9). Mitochondria are involved in cellular respiration and function as the energy factory (10). During the respiratory activity, mitochondria transform energy from carbohydrates to adenosine triphosphate (ATP), simultaneously releasing heat as a byproduct.
Due to the lack of enabling techniques and tools, the functions of lysosomes and mitochondria have been independently studied in the past, though there must be intense cross-talk between the two organelles (3): Dysfunctional mitochondria lead to the elevation of lysosomal pH (11); and in some lysosomal storage diseases, the defects in the lysosomes also contribute to the dysfunction of mitochondria because the abnormal mitochondria cannot be cleared by lysosomes, leading to pathological signaling https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fpmc.ncbi.nlm.nih.gov%2Fa...
Also affected is the endoplasmic reticulum and gut bacteria.
Oxidative stress and endoplasmic reticulum stress (ERS) are both potential outcomes of long-term exposure to high temperatures and have been linked to apoptosis, autophagy, and ferroptosis. In addition, HS (heat stress) alters the composition of the gut microbiota accompanied by changed levels of bacterial components and metabolites, rendering the gut more vulnerable to stress-related injury
This is also interesting
Disruption of ribosome assembly results in the accumulation of aggregation-prone ‘orphaned’ ribosomal proteins that are toxic to cells if left unchecked. A study finds that cells store such ribosomal proteins during heat shock to enable a quick recovery of ribosome assembly after the removal of this stress. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fwww.nature.com%2Farticle...
I still use Windows 7 but with a suite like Libreoffice, with how long its been out, how many changes need to be made? The new versions are not all that different from the Staroffice or Openoffice that came before it. At some point is the software "done" ? I'll be honest, I use Windows 7 and I don't update to the newest version of every software that comes along. Too many times a newer version has bugs that an older one doesn't. If one works well, I stay with it. In a bygone era, I would've jumped at updates, but been burned too many times. People that use 7 and 8 will be happy I think as long as they can get older version of Libreoffice. They have low expectations of being taken care of by devs anyways. TBH its surprising anyone still supports windows 7. Basically only enthusiasts use it now.
Digressing, besides the motor and exhaust, many of the parts are the same on an EV and ICE car. Things that need servicing as a vehicle gets older. Brakes, wheel bearings, CV shafts, tie rods, ball joints, shocks, bushings. Teslas are not some super engineered car that somehow managed to overcome these issues. With you not replacing any of those things, they fall to the next owner. When I buy a car, I usually go through and replace all those things, and they need it because owners like you don't fix anything. Under the false impression their favorite car manufacturer is immune from physics and time. I didn't understand this until I was talking to someone, asked why they didn't do xyz, and they said it was because they were selling it in a couple years. That's the mentality of folks like you, just get it to the next owner. If everyone drove their car into the ground, they'd stay on top of the maintenance and wouldn't be unaware of festering problems.
they need to be able to monitor you
Welcome to ~2014. Telemetry, CEIP etc has all been around for 10 years. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fit.slashdot.org%2Fstory%2F...
Mr. MANZULLO. What you see on page 11 is nothing less than staggering. Because you state that the earnings-per-share range, the minimum payout is $3.13, the maximum was $3.23, with a target of $3.18.
And just by happenstance, coincidence, you could almost say on your terms that for Fannie Mae to pay out the maximum amount in annual incentive payment awards in 1998, the earnings per share would have to be $3.23. It is below the $3.13 minimum payouts threshold, no bonus would occur.
And then you state, remarkably, the 1998 earnings-per-share number turned out to be $3.23 and nine mills, a result that Fannie Mae met the EPS maximum payout goal right down to the penny, and that if they had used the correct accounting practices—which you say in your testimony, accounting violations cannot be dismissed as mere differences of interpretation, Fannie Mae understood the rules and simply chose not to follow them, but if Fannie had followed the practices, there would not have been a bonus that year. Is that not correct?
Mr. FALCON. That is right, Congressman.
Mr. MANZULLO. Well, what are you saying here? Are you saying this is coincidence? Or did somebody cook the books to come up with $3.23 and nine mills so they got the maximum payment.
Mr. FALCON. I think what we are saying is, there are very strong appearances that the management did, in this instance, improperly defer $200 million of this $400 million expense to the next year for the purposes of achieving these bonus targets.
Mr. MANZULLO. So the main purpose was so they could get their bonuses. That is what you just said.
Mr. FALCON. Yes, in addition to the appearances of smoothing earnings. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fcommdocs.house.gov%2Fcom...
Later...
Former Fannie Mae chief Franklin Raines and two other top executives have agreed to a $31.4 million settlement with the government announced today over their roles in a 2004 accounting scandal.
Raines, former Fannie chief financial officer Timothy Howard and former controller Leanne Spencer were accused in a civil lawsuit in December 2006 with manipulating earnings over a six-year period at the company, the largest U.S. financer and guarantor of home mortgages. https://ancillary-proxy.atarimworker.io?url=https%3A%2F%2Fwww.seattletimes.com%2Fb...
We're here to give you a computer, not a religion. - attributed to Bob Pariseau, at the introduction of the Amiga