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Actually, we're doing a pretty good job here. This discussion will be (missing or poorly implemented) feature incomplete, but the acrid flavor of a Lotus Notes installation will be readily apparently.
See above, see below.
The failed Notes experiments can always be revisited by dropping some bad LSD. Or, in the case of John McAffee, some bath salts.
Slashdot, and in fact the Internet as a whole, has neither the time nor storage to do that subject justice.
The Spanish Inquisition.
(Notes is about as painful.)
Is this a screenplay? CIS:Tennessee?
Well, that definition would also apply to your classical 'antibiotic'. It appears from the Wikipedia site that Triclosan is not a generic antimicrobial in that it won't affect viruses, protozoa or Scientologists.
At in-use concentrations, triclosan acts as a biocide, with multiple cytoplasmic and membrane targets.[16] At lower concentrations, however, triclosan appears bacteriostatic and is seen to target bacteria mainly by inhibiting fatty acid synthesis. Triclosan binds to bacterial enoyl-acyl carrier protein reductase enzyme (ENR), which is encoded by the gene FabI. This binding increases the enzyme's affinity for nicotinamide adenine dinucleotide (NAD+). This results in the formation of a stable ternary complex of ENR-NAD+-triclosan, which is unable to participate in fatty acid synthesis. Fatty acids are necessary for reproducing and building cell membranes. Humans do not have an ENR enzyme, and thus are not affected. Some bacterial species can develop low-level resistance to triclosan at its lower bacteriostatic concentrations because of FabI mutations, which results in a decrease of triclosan's effect on ENR-NAD+ binding, as shown in Escherichia coli and Staphylococcus aureus.[17][18] Another way for these bacteria to gain low-level resistance to triclosan is to overexpress FabI.[19] Some bacteria have innate resistance to triclosan at low, bacteriostatic levels, such as Pseudomonas aeruginosa, which possesses multi-drug efflux pumps that "pump" triclosan out of the cell.[20] Other bacteria, such as some of the Bacillus genus, have alternative FabI genes (FabK) to which triclosan does not bind and hence are less susceptible.
No, you're thinking that because of their personalities.
(Iodine has been deprecated for most things. It's not terribly effective.)
How do they get that stuff through the Internet?
Page Clicks.
Now, was that hard?
I feel happy!
I think I'll go for a walk!
Read the "Scientific Weather Discussion" in Weather Underground forecasts. More often than not, they find that the ECMWF forecast fits the data better. Been that way for years.
Give Libertarians an inch
you have proof the DNA of the disease is the same then as now?
That's a possibility. Virulence factors can change over time. It's been hypothesized that the near complete absence of Rheumatic Fever might be due to less virulent streptococcal A bacteria. Or it might be due to increased treatment, better nutrition, sunspots or something else. It's hard to prove.
FTFA
As much pertussis as we're seeing now, we're still seeing in most places pretty good control in the very young," who are at the highest risk of dying form pertussis, Halperin says. "We're seeing lapsed immunity in school-age kids and we have to solve that. But those kids aren't dying."
Can be interpreted as either the bacterium is the same and the host defenses are better in younger children due to a less effective (but still reasonably useful) vaccine or it could be that current Pertussis strains are not as virulent, especially in infants, but still contagious. Should be possible to determine this by looking at older frozen samples of Pertussis, which I assume are available (but don't really know).
Add a couple of nine volt batteries, a wire and yes, I'm shocked as well.
Except in fantasy land it wasn't mandatory. Here in reality
Diplomacy is the art of letting the other party have things your way. -- Daniele Vare