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About markeb

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    Cool Cruiser

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    Northern Virginia
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    Watches, Pens, Travel
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  1. That's kind of where I'd be as well. It would be a nice theoretical jump from my A6500, but having the A6500... It's something to keep an eye on, though. I'll be curious to hear people's actual low light performance, for instance. The small form factor will probably make it a little awkward for a full size G lens, which I've found with my 90mm macro lens on the A6500 body, but with that purpose built lens, if the IQ is up there, it could be a great camera option.
  2. Not sure if this will work, but it's teater related and timely! 19 years ago (yesterday), the real Nick and Diane of Come from Away fame were actually screeched in... Still one of our favorite plays!
  3. Still digesting this release. Didn't get an email from Sony, but got one from B&H tonight. Apparently roughly the size of the APS-C α cameras, but full frame. And a purpose built normal zoom for a theoretically pocketable camera... FE mount, from a quick read a host of great features, and specifically designed for portability? But compatible with all the great FE G lenses out there! @pierces Thoughts? Not hunting right now, but this is pretty crazy in a lot of ways!
  4. That, and it was the transitional Bond between Dr. No and Goldfinger. You have the opening sequence, a title song, the super villain (and SPECTRE), the amazing scenery in Istanbul, and the ending with the Bond girl. But also 90% of the movie in between is believable. Goldfinger tops most lists, but it makes the jump into action and fantasy, and they kind of never go back. I was just curious. Google turns up a couple of never produced stage ideas for Bond. And actually something called James Bond: The Musical on Strand Way, which is advertised as some sort of parody. Once the movies started, it would have been very difficult to produce a play based on any of Fleming's novels.
  5. I did not. Looks like it's only used in the book. I always found the books somewhat difficult to read... If you're a Diana Rigg fan, you really should watch "In Her Majesty's Secret Service". It's George Lazenby's only appearance as Bond, Telly Savalas is the villain, and Diana Rigg may have been at the top of her game. She'd just finished the Avengers, She was probably 30 when they filmed it, she was arguably one of the most attractive actors out there, and she had the acting ability to carry the role, and a lot of the movie. It is a 1969 Bond movie, so there are crazy parts, but the scenes with Tracy (at least all I can remember) are all great. I may have to see if it's on Netflix or Prime.
  6. Even looking at just Wikipedia is impressive for an amazing career on stage, screen, and television! But my favorite, much though I loved Emma Peel, is Countess Teresa di Vicenzo, otherwise known, for about an hour (maybe 10-15 minutes screen time), as Tracy Bond, the only Bond "girl" to marry James Bond. We have all the time in the world...
  7. You can at least theoretically use mAbs a couple of ways. Using them in high risk settings prior to infection is essentially the same as the old days of using Gamma Globulin as protection against hepatitis A. As long as it's on board and can bind the virus, it will provide some protection. They'll have a limited lifespan in the body, and unlike an active immunization, you won't make more. It's hard to say where that would be most useful; maybe an outbreak in a high risk population, or preprocedure? It's hard to imagine more widespread use. For treatment, the big challenge with most respiratory viruses is by the time you know what you've got, they've done most of their damage, and you're now fighting the body's own immune response. That's why most folks advocate for early use of mAb or convalescent serum, which sounds counterintuitive, and why the concerns that using mAbs later in the disease won't stop the current disease (they'll bind the virus, but the inflammatory response to dead and infected cells is causing the pathology). And I think that's what BP99 is saying. In theory, if there's enough virus (or SPIKE in this case), someone infected with the virus and treated, either before or after infection, with a mAb should mount their own immune response, which would last a lot longer. As with most things with this virus (and immunology!), it's complicated.
  8. NIH isn't a vaccine developer either. It's a basic research institute with a lot of experience, but not in product development. I hadn't thought about it, but it is odd Moderna didn't partner with a company with a track record getting a vaccine through development. In more normal times, I've seen biotechs largely get buzz and get bought out or merge. Going to market is a bit unusual for them. And I agree, pharma can't rush an unproven product; too much on the line for them.
  9. That's what I was thinking. If it's the SPIKE, you're going to see it in all the approaches. If it's the vector, you shouldn't see it in other approaches. And if the subject has titers to dozens of viruses (which they'll now probably check), it'll take a long time. (Or to use a bad analogy, they just spun out in pit row...) Fingers crossed on subunit candidates, but I think they're still running behind on trials. Haven't looked lately.
  10. Vector related? It's an incompetent virus, but... The numbers sound miniscule, but they're less than miniscule in the general population. I think you've posted over and over that one of the purposes of a large scale Phase III is to identify safety concerns. And there are no approved human vaccines using an adenovirus vector. Burden of proof is and should be very high. If they don't get more cases, and show good protection, I'll be cautiously optimistic. But if this is the diagnosis, and they potentially have 2 cases in less than 30K where 5 cases in a million is expected, forget about speed; accuracy just became really important! (One nice thing about living close to the Beltway is that the WP and the local affiliates have NIAID on speed dial; one of the local anchors sees Dr. F in her neighborhood regularly. I think his response was cautious concern, but we need data...)
  11. Yes to all. But it will take time, and due diligence, to figure out what happened and why. Won't stop them gathering data on already enrolled and vaccinated participants, (and I would think it would be unethical not to collect data on them) and could have absolutely nothing to do with the vaccine, but if they stop new vaccinations and have a biologically plausible side effect (and having now announced the hold, they're almost stuck saying what it was, which I haven't seen anywhere), the pace goes back to some version of normal for awhile...
  12. You ask people to not alter their routine, although some will. Fortunately, you don't know if you got the vaccine or the placebo, so the exposure probability (and viral load from exposure) should be roughly the same between the vaccinated group and the control group. The size of the trial is to give you statistical power to see a difference. Not easy, but it's how these things are normally done. Depending on the trial, there are multiple endpoints which make subtle differences potentially even more subtle. I'd have to look again; I assume most of the trials are checking titres at some point after the initial vaccine or initial series. But other endpoints are going to be whether or not there's actual disease, whether or not you recover the virus on nasal swab, hospitalization comparison between the groups, and I guess somewhat obviously, mortality.
  13. Yes. I've already said that. Those were the studies that appeared to show cardiotoxicity. The dataset could not be verified, and the studies were withdrawn. The original results were more than a little surprising, and I'm much less surprised they couldn't be verified. I'm not a physician. Pre-hospital intervention has not even been shown to be necessary. Ideally, you'd intervene with something with more antiviral activity than HCQ or doxy or azithromycin, but by the time you actually have a diagnosis, given the asymptomatic period, it's unclear how effective any antiviral would be; once you damage enough cells, it's about the inflammatory response. The first 2-3 links on your web page went to 404 file not found when you tried to go to the primary source. One study is a very good safety study on HCQ in RA and I believe SLE. Not surprising results. No, it's shown mixed results at best that have been interpreted by those with an agenda as extremely promising. I actually tried to follow the studies out of curiosity and gave up when the references went nowhere, the, doi numbers went nowhere, and in at least one case, even the primary author went nowhere. Case series with no control group are interesting at best. If they show promise, they tend to trigger actual controlled studies. The NIH multi-center study was randomized and placebo controlled. It found no benefit in hospitalized patients. That was in June. There are currently 250 clinical trials listed globally using HCQ. Many are actually placebo controlled. A few are looking at HCQ versus one or more broad-spectrum antivirals. Only a small handful have completed, and without looking at all 250 (probably less than 25 completed), I may have found one that has gone to publication, but its results are still under review.. A number have been suspended, terminated, or withdrawn for various reasons, including a drop of cases in the study area. Many of those studies with some actual scientific rigor are looking at the pre-hospital setting, but most of them won't finish for months, and won't go to publication for some time after that.
  14. It's been a couple of weeks since I looked, but all of the vaccines in US trials if memory serves were looking at two doses, either 0-14 or 0-30 (days). I think AZ may have had an arm looking at only one dose, but they have something like 30 (exaggeration) arms in their clinical trial! Yellow fever vaccine was always notorious. It was in the battery of required vaccines in the Army in the '80s...
  15. It's really not as simple as total doses. It's going to be paired doses (same vaccine for the same person). And there's a very real possibility that different vaccines will have different efficacies in different people. We just don't know. If you have 50M doses of vaccine A, 50M of vaccine B, and 50M of vaccine C, and each require a two-dose series, you can vaccinate at most 75M people, and at least initially, someone who receives a first dose of vaccine A will need their second dose to also be vaccine A, not B or C; there won't be data on mixing and matching. And efficacy is TBD, and whether antibody response is actually the governing factor is also TBD. It's just what people understand.
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