I appreciate his ability to speak and his ability for the most part to keep politics aside. I do sense that when he gets frustrated or considers something unimportant, he whips out the hammer. His comment of “get an essential job” yesterday is a good example. I see his laundry list of bans to include his response to vaping to be akin to this behaviour. Kinda like I don’t want to deal with it so fuck it and ban it!
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No need to apologize… to me anyway. I understand this virus is very serious but at the same time we need a good chuckle once in awhile to maintain our sanity. Laughter is like medicine to the bones…thanks for making me smile. 
My question is does this virus pass to alien life form and if so, are you worried? 
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I get it. Every living thing is going to have the capacity to breath the virus into their lungs. The next event to watch is can the virus achieve a viral load significant enough and effective enough to make the host ill. It appears with cats that they can develop symptoms. I haven’t followed this too closely but it seems that they are developing mild symptoms. The third event is if the host can shed the virus with a viral load significant enough to cause spread. I can see the medical community being reticent to make claims without concrete proof.
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There is no evidence that a human can pass the virus to an alien…
There is no evidence that a human can’t pass the virus to an alien…
absolutely not worried, lets call it concerned.
#N95forall (even cats and aliens)
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(Science Magazine, April 21, 2020):
“Antibody surveys suggesting vast undercount of coronavirus infections may be unreliable”
… survey results, from Germany, the Netherlands, and several locations in the United States, find that anywhere from 2% to 30% of certain populations have already been infected with the virus. The numbers imply that confirmed COVID-19 cases are an even smaller fraction of the true number of people infected than many had estimated and that the vast majority of infections are mild. But many scientists question the accuracy of the antibody tests and complain that several of the research groups announced their findings in the press rather than in preprints or published papers, where their data could be scrutinized. …
… A German antibody survey was the first out of the gate several weeks ago. At a press conference on 9 April … the study suggested the virus kills only 0.37% of the people infected. (The rate for seasonal influenza is about 0.1%.) The team concluded in a two-page summary that “15% of the population can no longer be infected with SARS-CoV-2, and the process of reaching herd immunity is already underway.” They recommended that politicians start to lift some of the regions’ restrictions. …
… Christian Drosten, a virologist at Charité University Hospital in Berlin, told reporters later that day that no meaningful conclusions could be drawn from the antibody study based on the limited information Streeck presented. Drosten cited uncertainty about what level of antibodies provides protection and noted that the study sampled entire households. That can lead to overestimating infections, because people living together often infect each other. Streeck and his colleagues claimed the commercial antibody test they used has “more than 99% specificity,” but a Danish group found the test produced three false positives in a sample of 82 controls, for a specificity of only 96%. That means that in the Heinsberg sample of 500, the test could have produced more than a dozen false positives out of roughly 70 the team found. …
… A California serology study of 3300 people released last week in a preprint also drew strong criticisms. … Fifty antibody tests were positive - about 1.5%. But after adjusting the statistics to better reflect the county’s demographics, the researchers concluded that between 2.49% and 4.16% of the county’s residents had likely been infected. That suggests, they say, that the real number of infections was as many as 80,000. That’s more than 50 times as many as viral gene tests had confirmed and implies a low fatality rate - a reason to consider whether strict lockdowns are worthwhile, argue Bendavid and co-author John Ioannidis, who studies public health at Stanford. …
… Twitter threads and blog posts outlined a litany of apparent problems with the Santa Clara study. Recruiting through Facebook likely attracted people with COVID-19-like symptoms who wanted to be tested, boosting the apparent positive rate. Because the absolute numbers of positive tests were so small, false positives may have been nearly as common as real infections. The study also had relatively few participants from low-income and minority populations, meaning the statistical adjustments the researchers made could be way off. “I think the authors of the paper owe us all an apology,” wrote Columbia University statistician and political scientist Andrew Gelman in an online commentary. The numbers “were essentially the product of a statistical error.” Bhattacharya says he is preparing an appendix that addresses the criticisms. But, he says, “The argument that the test is not specific enough to detect real positives is deeply flawed.” …
… Another serology study, in the Netherlands, produced a similar figure for antibody prevalence … The results made it clear that the country was not yet near the “herd immunity” that some had hoped for. …
… A small study in the Boston suburb of Chelsea has found the highest prevalence of antibodies so far. … they collected blood samples from 200 passersby on a street corner. … Sixty-three were positive (31.5%). The result carries several large caveats. The team used a test whose maker, BioMedomics, says it has a specificity of only about 90% … pedestrians on a single corner “aren’t a representative sample” of the town, Naranbhai acknowledges. …
… Even if the antibody surveys show a COVID-19 death rate well below 1%, says Michael Osterholm, an infectious disease expert at the University of Minnesota, Twin Cities, control measures will be needed for a long time to avoid overwhelmed hospitals. “The seroprevalence data only confirm the challenge we face. The data [these studies] are generating … is just showing how hard this is.”
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(Forbes, April 23, 2020):
“13.9% Of New Yorkers Positive For Coronavirus Antibodies - Not Enough To Foster Herd Immunity”
Herd immunity happens when over 60% of the population develops immunity -antibodies - to a disease, a phenomenon that usually occurs when a population is vaccinated against a virus.
Here’s another “theory” to ponder…
I spoke to a friend last night, from Spain, who mentioned reading a study that stated higher incidences of severe cases/death from Covid-19 for those who got a flu shot. Less mortality rates in those who didn’t and areas of the world less likely to receive one.
She never mentioned the source and I haven’t found anything online alluding to this. I’m assuming those entering a hospital for treatment are asked during screening if they had a flu shot. If someone has compiled such a list I’d like to see it.
Most articles I’ve read encourage getting one to possibly lessen symptoms but according to said study, is making the outcome of Covid-19 patients worse. We all know in USA that our news is sometimes skewed and filtered and so I’m wondering if any of this might ring true?
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Mew, you are wise to want to see reports, sources, and methods surrounding such an averment.
In cases of a recently received influenza inoculation, or a concurrent (perhaps Influenza) virus (or bacterial, fungal, or parasitic related) infection causing immune-system “busyness” (and thus perhaps, strained immune-resources/efficacy), such speculations (might) have some understandable bases.
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This report quoted below appears to be about a man with concurrent Influenza - and COVID-19 as well that was (thought to be apparently) harder to clinically diagnose (with testing regimens used) as a result
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Yeah that… 
Makes sense and I will try to get study source from my friend next time we speak. Still curious to see those numbers.
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However, “that” (post-inoculation) immune-system “busy” period (of developing immunity against target Influenza strains) seems to be (thought) to only last ~2 weeks ? Imagine how much “busier” one’s immune-system might (comparatively) be if it were instead a live Infuenza infection that one’s system were to grapple with (within a similar 2-week time period - or later, following an Influenza inoculation). As well, each years (3 or 4 variant selected) Influenza strains will differ - making upcoming Influenza inoculation brews not necessarily representative of previously studied Influenza inoculation brews. 
Indeed, it is (in my personal experience) quite true that (particularly marginal due to age/disease-states, and already “busied”) immune-systems can be “compromised”. Few objective “transferrables”, though.
Hmmm… kind of a damned if you do and damned if you don’t scenario perhaps.
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Yes - something perhaps like “varying degrees of challenges”, without easily demarcated “certainties”. (Perhaps) the primary “constants” remain: death; taxes; dentists; ER bills; demagogues; and parasites.
And as well, widespread pervasiveness of ClickBait Acres in our Crave New World readily engenders:
Source: https://en.wikipedia.org/wiki/List_of_fallacies
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With a high prevalence of “glycemic” related conditions in many populaces, this info may be of interest:
(The Lancet, April 23, 2020):
“Practical recommendations for the management of diabetes in patients with COVID-19”
(Science Alert, April 23, 2020):
“Scientists May Have Found The Human Cell Types Most Vulnerable to The New Coronavirus”
In a huge, multi-institutional effort involving dozens of scientists, researchers combed through multiple RNA-sequencing datasets, compiling information for thousands of different kinds of cells in humans, non-human primates, and mice. In particular, the team were looking for gene expression patterns for hundreds of cell types in the lungs, nasal passages, and intestine - areas of the body that we know can harbour SARS-CoV-2.
“Because we have this incredible repository of information, we were able to begin to look at what would be likely target cells for infection,” says chemical physicist Alex Shalek from MIT. “Even though these datasets weren’t designed specifically to study [SARS-CoV-2], it’s hopefully given us a jump start on identifying some of the things that might be relevant there.”
Ultimately, the analysis revealed that only a small minority of human respiratory and intestinal cells have genes that express both ACE2 and TMPRSS2. Amongst the ones that do, three main cell types were identified: lung cells called type II pneumocytes (which help maintain air sacs, known as alveoli); intestinal cells called enterocytes, which help the body absorb nutrients; and goblet cells in the nasal passage, which secrete mucus. …
… Among the new results, the team also made a puzzling discovery. A family of immune proteins called interferons, which usually help the body to fight off infections, turns out to stimulate the ACE2 gene that produces the ACE2 protein.
Just why that is remains unknown, but it means that one of our body’s natural defence mechanisms against pathogens, in this instance, could actually end up promoting SARS-CoV-2, by up-regulating production of the receptor the virus uses to cling on to cells. If so, it could be an example of a sneaky evolutionary adaptation, although the researchers say there’s a lot more work to be done to figure out what’s going on here.
“This isn’t the only example of that,” Ordovas-Montanes explains. “There are other examples of coronaviruses and other viruses that actually target interferon-stimulated genes as ways of getting into cells. In a way, it’s the most reliable response of the host.”
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Original Research Paper:
“SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells
and is detected in specific cell subsets across tissues”
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(STAT, April 23, 2020):
[British Medical Journal (BMJ), April 22, 2020]:
Editorial: “Remdesivir in covid-19”
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(STAT, April 23, 2020):
(AJEM, April 14, 2020):
“Cardiovascular complications in COVID-19”
Myocardial injury and myocarditis.
Prior viral illnesses, including Middle East respiratory syndrome coronavirus (MERS-CoV), have been associated with myocardial injury and myocarditis with troponin elevation, thought to be due to increased cardiac physiologic stress, hypoxia, or direct myocardial injury. One of the first reports of myocardial injury associated with SARSCoV-2 was a study of 41 patients diagnosed with COVID-19 in Wuhan, China, wherein 5 patients (12%) had a high-sensitivity troponin I above the threshold of 28 pg/mL. Subsequent studies have found that myocardial injury with an elevated troponin level may occur in 7-17% of patients hospitalized with COVID-19 and 22-31% of those admitted to the intensive care unit (ICU). Myocarditis has also been identified with high viral loads and mononuclear infiltrates identified on autopsy of some patients with COVID-19. In fact, one study suggested that up to 7% of COVID-19 related deaths were due to myocarditis. Acute myocarditis presents across a variable range of clinical severity and is a significant diagnostic challenge in the COVID-19 era. Patients with COVID-19 can present with chest pain, dyspnea, dysrhythmia, and acute left ventricular dysfunction. In patients with myocarditis and myocardial injury, serum troponin values will be abnormal. The electrocardiogram (ECG) can demonstrate a range of findings, in some cases mimicking acute coronary syndrome (ACS).
The ECG abnormalities result from myocardial inflammation and include non-specific ST segment-T wave abnormalities, T wave inversion, and PR segment and ST segment deviations (depression and elevation). Echocardiography and consultation with cardiology, if either are available, is encouraged, as differentiating myocarditis and ACS is difficult. Echocardiographic evaluation is more likely to demonstrate a focal wall motion abnormality with active, significant ACS while severe forms of COVID-19-related myocarditis will show either no wall motion defects or global wall motion dysfunction. ECG and echocardiographic abnormalities in the setting of COVID-19 are markers of illness severity and are correlated with worse outcomes. Moreover, troponin elevations in patients with COVID-19 infection have been directly associated with an increased risk of adverse outcome in those patients with severe infection, including mortality.
Acute myocardial infarction.
Severe systemic inflammation increases the risk of atherosclerotic plaque disruption and AMI.
Acute heart failure and cardiomyopathy.
Acute heart failure can be the primary presenting manifestation of COVID-19 infection. One study found that acute heart failure may be present in 23% of patients in their initial presentation for COVID-19, with cardiomyopathy occurring in 33% of patients. Another study found that heart failure was present in 24% of patients and was associated with an increased risk of mortality.
Dysrhythmias.
Palpitations may be a presenting symptom in over 7% of patients with COVID-19. A range of dysrhythmias have been encountered in patients with COVID-19 infection.
Venous thromboembolic event.
Patients with COVID-19 are also at an increased risk of VTEs. Systemic inflammation, abnormal coagulation status, multiorgan dysfunction, and critical illness are all potential contributing factors to the increased risk of VTE.
Medication interactions.
Many of the newly studied medications interact extensively with other cardiovascular drugs, including antihypertensives, antiarrhythmics, anticoagulants, antiplatelets, and statins. Current medications under study include antivirals (e.g., remdesivir, ribavirin, lopinavir/ritonavir, favipiravir), antimalarials (e.g., chloroquine, hydroxychloroquine), azithromycin, corticosteroids, and biologics (tocilizumab).
Somehow, the idea of “viruses in space” is more interesting than “viruses that have cohabited with life-forms all along” (perhaps preceding bacterial forms, in some viewpoints). Yet, by not conforming to our standard definitions of what constitutes a life-form, such remarkable little buggers (having seeming evolutionary “intentions”, and ingenious and robust adaptive-ity to their biochemical circumstances), might be termed “closest” to what one might call “terrestrial aliens” (through our own prisms, anyway). Despite our tendencies to “anthropomorphize”, we are (to all such microbes) “just another substrate”.
Looks like we’ll have to keep a close eye on Georgia.
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