Pedestrians either get hit in the street or parking lot, or they get pinned against the wall of a garage (where else are the cars?). In the latter case, the crush injury happens irrespective of the presence of the adhesive layer. We should consider edge cases, but this is a bona fide genius idea. Add a dispersive gel layer underneath the adhesive and this might make a real difference.
Disclaimer: I am a trauma surgeon, and do crash reconstruction work on the side.
I still have my original Motorola pager. Whenever they try to give me one of these crappy new pieces of shit, I tell them that I am the doctor they were warned about in their customer service training, and that they should decide how much blood they want to shed. I think that they have actually written it off by now; no one has bugged me about it for a couple of years.
It is highly amusing to me that young doctors who care about having the newest iThing get jealous of my pager.
If this is the new boss, I'm all for it. I care a lot about politics, privacy, and economics. I come to Slashdot for other stuff.
When the human testing starts, should it be old people first? afftected-continent people first? family-receives-high-payment people first?
Real clinical trials do not work like this. If you want to do a real trial, you first have to establish a team and treatment center that can administer your therapy and collect the data you need. You then establish EXCLUSION criteria, i.e., people who will not be included in the trial (usually old people, who have an annoying tendency to die, and children, because sick kids scare the shit out of most doctors). *Everybody* else who comes to the center, who has the disease, gets offered enrollment in the trial. It's up to them if they want to participate.
Anything else will get you laughed at, at the very least.
Okay, I'll feed the AC troll.
I'm not talking about "most rashes"; real physicians have words to describe different kinds of rashes. The word that describes the rash of Ebola is "purpura." The distinguishing feature of this kind of rash is that when you push on it, it doesn't stop looking like a bruise. That is because the blood isn't contained within blood vessels that can be pressurized and allow the blood to be pushed out of the way. Because IT'S A FUCKING BRUISE.
Once blood leaves the vasculature, it is broken down into a couple of proteins. Hemosiderin is taken up by white blood cells. Biliverdin turns your turds brown (eventually). They make your bruises turn "black and blue" and eventually yellow. This takes days and is the reason why purpuric rashes don't fade immediately in response to anything.
You are conflating "hives" and "purpura." Kindly pay tuition if you want to continue.
I don't disagree with the general premise that reducing antibiotic use in livestock would be helpful in reducing the emergence of resistant strains of bacteria. I have to take issue, though, with the assertion that even eliminating entirely their use in the food industry would provide any sort of enduring solution. It would not.
The dirty little secret about antibiotic resistance that no one wants to talk about is this: resistance emerges from repeated use of different antibiotics in the same human, many of whom are not supposed to (according to nature) survive anyway. This group includes critically ill or injured people, cancer patients, patients with chronic organ failure, and most importantly old people. All of these groups have the common characteristic of impairment of immune function.
Antibiotics don't really "cure" infection. They kill enough of the circulating organisms so that the host immune system can take care of the rest. Some very good antibiotics don't kill any bacteria, they just stop replication. So if you actually wanted to create a petri dish for resistant organisms, you would take a host with poor immune system function, infect it, and give antibiotics that kill most of the bacteria and let the rest play on.
In this regard, the best possible "petri dish" is the transplant recipient. In something of a bittersweet triumph for modern medicine, the exact mechanism by which VRSA (vancomycin-resistant Staph aureus) would later emerge was predicted, carried out in the lab in an elegant esperiment which demonstrated the mechanism (plasmid exchange of the VanA resistance gene from VRE into Staph), and later confirmed when the first case emerged, in the Transplant ICU of the University of Pittsburgh Medical Center (ironically where transplants were originally perfected).
Biological systems have tons of complexity so there will be new drug targets in the future, but the obvious ones have been hit by now, so new drugs will be more expensive. The balanced approach would be to reduce antibiotic use on the human end, which inevitably brings up discussion of limits of care and "death panels." It is no accident that these pathogens tend to emerge in the U.S., where such discussion is difficult with our demographics, and where the entire population (doctors included) holds an almost mythical belief in the power of antibiotics. All they do (seriously) is rearrange the population of bacteria that inhabit your body. Sometimes that helps, a lot. We need to be honest about when those times really occur.
tl;dr Stop all the use of these drugs in livestock and you will only change the rate of emergence of resistance, not the fact. This problem is not going to go away.
"Tell the truth and run." -- Yugoslav proverb