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  1. Thanks for this info wxray as I was ruminating about this very think(status of the Canes AHL affiliation) over on the Checkers site.
  2. So, now that our affiliation with the Checkers appears to be no more, and for the life if me I can't see giving up the convenience and ease of movement for what I would imagine is all financial, I guess the name of this thread changes to Chicago Wolves? Sure has been quiet on this front? Guess the name Wolves does have an ironic ring to it?
  3. Your citation above rem confirms what I'd thought in reading about the various co-morbidity factors at risk from a SARS-COV-2 infection, in the case of asthmatics, although I guess I (perhaps we) shouldn't rush too quickly to paint that broad picture as Asthma can be multifactorial can it not? Thus there might be some who could be vulnerable (not you I pray). But thanks for that reference rem.
  4. Not doubting that at all bd58, but consider the population mix of those 2 areas. In the center of town puts the arena squarely in the lap of those populating that area, and the NC State campus still. That's very convenient for a "pop in" visit. Where it is now, it takes a bit of a drive sometimes thru horrendous traffic(my son lives in Durham and he'll vouch for that). Also, think of the peoples' habits from that Chapel Hill/Durham side, and aside from the students, many (not all) in those 2 areas seek more sophisticated entertainment. But the argument is moot as I dread a move to put the arena in town, and in my case, if that came about, I'd seriously consider giving up my 20 yr STH account.
  5. "Deterrent to fans" should really read bd58, to most "long term" fans, but more specially, to those coming from outside the Raleigh area which presents the problem of parking. I could see a shift, if the arena relocation occurs, to a more casual fan base which would attract those whom would not have to negotiate for parking, thus would be inclined to "drop in" as an option to a night's entertainment.
  6. Correct Lake, "prevalence" in this case trumps specificity, and further, as prevalence increases, specificity gains much more "positive predictive value", meaning one has more confidence in the accuracy/validity of a positive test. Not to beat a dead horse any further, but this then means that as prevalence goes up, meaning more of the population has been exposed to a disease (as in COVID-19), and has recovered, developing as they do, an antibody to that agent, then one has more confidence that a positive result from the antibody test actually indicates they've been exposed to the virus, or when a vaccine is developed and administered, that they've responded to it by developing the protective antibody. To respond to one other debate, presently, as I'm sure many have discovered, there's debate as to how long this antibody will persist, however there's a well known facet to this debate, and that is even though an antibody appears to fade and eventually becoming "undetectable", we also believe this is a function of the sensitivity of "in vitro" testing (that is in a test tube if you will), and there's a phenomenon referred to as 2nd set reaction, meaning that "in vivo" (that is in the body) something else is felt to be operative. This involves memory stored of the viral antigen (the usual protein component of the virus recognized as foreign), which despite that antibody being sub detectable in vitro, nevertheless in vivo, a challenge by the viral antigen elicits a 2nd set antibody response, that occurs in a shorter period of time, is stronger than the 1st exposure and is longer lasting. We frequently observe this with several vaccines, thus the need for so called "booster" shot.
  7. Sorry for this double, tried to erase this but couldn't?
  8. Much seems related to ACE-2 receptors so widespread in multiple organs, thus the question in my mind rem, is Does asthma increase the presence of the ACE-2 receptor? I suspect not, but frankly do not know? Possibly that could answer your quandary, meaning an asthmatic would not necessarily be at greater risk despite underlying lung disease?
  9. Relative to this wxray, gradually, as more time allows, the FDA is pulling worthless tests operating under the EUA umbrella, and last I'd read, at least 20 have been pulled as less than worthless.
  10. I do too and at 1st sign of recurrence which we all quickly recognize don't we wxray, I keep Zovirax (presently Valacyclovir) in reserve to quickly take. Wipes it out after about 2 doses.
  11. rem, let me address this thought with another fact. We know that with "mutation" of a virus, like we see with influenza, the change frequently favors a more infectious form, as by virtue of that, it "outgrows" if you will, the lesser infectious form. A component of that mutation apparently, which by extension makes it "more infectious" is that its reduction in mortality spares more "targets" if you will in which to continue propagation. Simply put, the higher the virulence, the higher the mortality, the more quickly the virus dies out for lack of "targets". Thus virulence decreases in favor of sparing of "targets"? Weird how nature is, huh?
  12. Okay, wxray and others on this issue of antibody "accuracy", soundness or whatever thoughts on this matter, let me 1st apologize for my part in the continued confusion, then retry to give you all a laboratorians' perspective. 1st, let me hasten to explain that the vast majority of the clinicians with whom I deal don't think in these terms, but simply "sensitivity" and "specificity" of a test. While those 2 dynamics are critical for any test, "sensitivity" referring to if a disease is present, no matter at what minimal response a person manifests, you'd want to detect it; while "specificity" refers to the fact that we want the test to be discriminatory enough that it won't cross react with other similar diseases. As one can see with these 2 test characteristics, they are a tradeoff, thus if a test is too sensitive, one loses specificity(increased False Positives), and the opposite if too specific, than one loses sensitivity(increased FALSE NEGATIVE). Be those parameters as they may, the real crux of the issue goes one step further, and its related to PREVALENCE of the disease being tested for by "antibody assessment", thus the higher the prevalence of the disease in question, the more "accurate" the test result(likelihood there is immunity). To give an example of this to clarify, let's use a population of 100,000 for ease of numbers. Then lets say that the prevalence of COVID-19 in this 100K town is 5% (5% of population has the disease), so that means in this town, 5K have/had this disease, survived and thus have protective antibody. By extrapolation, 95K are non-infected, thus no protective antibody. Now lets take a test claimed to be performing (and note, this is the manufacture's claim) at 95% specificity, which is relatively good. Take this 1 step further, multiply the 95K by 95% and you arrive at 4750 who by the very noted performance of the test broadcast by the manufacturer are "falsely positive". Thus, if the prevalence of the disease is low in a population (we used 5%), then the so called "accuracy" (in laboratorian jargon known as Positive Predictive Value) for this theoretical test is 4750/9750(4750 false positive and 5000 true=9750), or only 49% accuracy!!! This is about the equivalence of a coin flip!!! For this reason, this is why some are saying that "just because one tests positive for this protective antibody, that you should be "precautious". So in conclusion, my mistake when I read that an antibody might not be "protective", was to interpret that to mean that someone is questioning the protective ability of a LEGITIMATE antibody (one that is truly an antibody), which I believe it is, rather than the some flawed test result for the reason I've discussed above. Also I note that one of you talks of mutation and possible loss of protection, but as yet, I've not seen this but rather what is referred to as "genetic drift", meaning MINOR CHANGE in genomic makeup. This does not mean enough change to thwart the antibody like occurs with influenza at present. Now, the next question one should ask is, How do we improve on predictive value, and the answer to that is when the prevalence of a disease becomes more widespread in a given community? That is, more people are exposed and survive, a somewhat scary proposition in this very confusing coronavirus scourge. One further comment, recall above that I interjected a comment "manufacturer's claim", and I did so for one purpose. This comment should not be viewed as my trying to impugn any manufacturer's honesty, but rather to emphasize that when all else is said and done, they want to sell a product, thus often times take the most favorable results to broadcast. From my reading, many claims of sensitivity and specificity are not holding up under more intensive investigations? Imagine that? PS- I had not read rem's response above as I took several hours typing, but hope mine further clarifies his from my laboratorian viewpoint.
  13. Legend, I dug this up 3 pages back and am once again bringing it to the forefront because rem so eloquently phrased it with all his many other rems of details. 1st, in response to the statement you attributed to your wife's doctor, I cannot believe any physician would actually say that "there's no proof of immunity" with this virus? Admittedly, as I'm often reminded and have tried to remind many with whom I've personally spoken as well as have posted on here, the word NOVEL was aptly appended to this coronavirus when it was first KNOWN to have emerged. Failure of adequate testing then, and still, has left scientists WORLDWIDE in the dark in critical characterization of this disease, Much of this confusion has to be laid in the lap of the rapidity of dissemination of truths, half truths and frank lies. Added to that, the chameleon known only to well to hockey fans as "statistics", which can be twisted to any shape desired by the investigator, adds numbers that in many circles takes on the status of a god, thus making further "experts", and now one has total chaos with regard to true knowledge. The concept of Scientific Proof so critical to understanding, has been eroded by journalistic license to get one nugget of fact, then embellish it for mass consumption of one's readers. Back to your wife's physician after that "soapbox stand", UNLESS she is anergic (unable to form antibodies to a challenge of a foreign substance), I would be shocked if she contracted this virus and had no subsequent immunity. The use of "convalescent sera" in some of the critical COVID-19 patients, and their eventual salvage says that antibodies are effective, and if so, demonstrates immunity. I suppose one could point to a disease like the common cold sore (a herpes virus), or shingles ( the V-Z virus of chickenpox, another herpesvirus family member), and say that those are examples of immunity failure, but those viruses undergo a dormancy period where the virus "hides out" in nerve cells, thus not exposed to the immune system. But once reactivated, the disease flares, then subsides due to immunity. So, technically is their "proof of immunity", probably not yet because we're still in this virus' infantile stage, but if there is none, then the End Of Times is upon us.
  14. rem, I'm reminded of the saying, as I'm sure you are, "Experts are those from somewhere else".
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