They were simply the fastest cells that were among those that were raced; many cells from various species of protists, not to mention sperm cells are capable of faster speeds than that.

Just because an immune response in the form of circulating antibodies from B cells is seen does not mean infection and replication will not occur when a person is exposed to HIV; most people with HIV have high levels of HIV antibodies circulating in their blood, but the rate at which the virus mutates, as well as the fact that the epitopes the body naturally develops immune responses to are "hidden" by the way in which the viral capsular proteins are folded means that the antibodies do little if anything to halt infection. Furthermore, the CD4+ T cells which initiate a more effective immune response are one of the two types of cells the virus infects (the others being macrophages). At this point, the article gives no further details or useful specifics. If they had said they had generated a cytotoxic CD8+ cell response, or perhaps an immune response against one of the conserved regions of the gp120 or gp41 viral receptors, then I'd be interested. Till then, I am going to be quite skeptical about this until they have some efficacy data. (I am a medical student with an MS in biomedical science)

When I worked in IT this site was practically my morning reading. Although you may not be posting stories anymore, hopefully you poke around and comment every once in a while, it'll be priceless to see a "You must be new here" comment on something you write. Best of luck in the future.

You mean apart from every Apollo mission that went translunar?

In children, IQ measures mental age/chronological age. It's useful for assessing developmentally delayed or precocious children. In adults...your mileage may vary.

1) This is precisely the "best" possible way to induce antibiotic resistance. You are basically selecting out the bacteria which are able to tolerate low doses of antibiotic, which are then able to outcompete their more susceptible brethren. The result is the "normal" gut flora of these farm animals now has a built in resistance to that particular antibiotic. 2) The gut flora of these animals is excreted in waste. The mechanisms by which super bugs are created is through transmission of plasmids, bacteriophages, and naked DNA uptake, which many species of bacteria are capable of. (For a new fun threat, see http://en.wikipedia.org/wiki/Vancomycin-resistant_enterococcus ) 3) There is no "therapeutic dose" for healthy animals. Antibiotics are given to animals to increase the rate at which they absorb food. The "normal" state of the lamina propria and mucosa of the gut is a constant state of low level inflammation, which serves as a protection from any bugs that manage to work their way out of the lumen of the gut. Antibiotic use lowers the amount of gut flora, likely leading to a reduction in this inflammation that results in greater absorption of food. I am not aware of a conclusive proof of this, but animals raised in sterile conditions and fed sterilized food support this hypothesis in terms of weight gain and histologic appearance of gut tissue. 4) You don't need all bugs to become super bugs. The majority of bacteria can become much more virulent and resistant to antibiotics. It really only takes one or two, and there are nearly innumerable options that live happily as commensals in either our or other species guts. 5) This is true, but it's not really going to cheer up someone whose opportunistic infection is resistant to antibiotics. Anyway, see #3 for a good idea of the mechanism. It's not a chemical reaction, its a physiologic consequence. FWIW, I am a medical student finishing up microbiology.

Possibly, but it seems to me the neurosurgery required to do that might be more difficult than implanting electrodes in the brain. In the arm, there are three main branches of the brachial plexus that travel the length of the arm, the median, ulnar, and radial nerves, and they all contain both motor and sensory fibers. Making all the connections necessary for natural movement and sense would be an incredibly long and tedious surgery for the motor part alone. I'm not even sure how you would manage do to the sensory part under local anesthesia. In the brain on the other hand, the motor and sensory cortex are basically mirror images of each other, somatotopically arranged across the precentral and postcentral gryrii, respectively. With the patient awake, the surgeon can stimulate the proper region of each, and place the electrodes quite precisely on the necessary areas. That's my two cents as a med student.

nt

I never said it was or that I did. All I did was originally point out how fructose was absorbed by the alimentary tract. I probably should have been more specific when I offhandedly remarked that it is metabolized similarly to sugar, regardless of where that metabolism occurs, it follows similar pathways and utilizes similar enzymes to result in identical metabolites. In any case, fructolysis in the liver yields glycolysis intermediates, which in a normal meal from a person not suffering from starvation would then be likely to undergo gluconeogensis and be either stored as glycogen or released into circulation as glucose, or incorporated into fatty acid synthesis.

The point is that glycolysis and fructolysis both yield a relatively insignificant amount of ATP, not enough to provide enough for normal cell function. Their metabolites are basically the same though, and enter the TCA cycle and then undergo electron transport in the mitochondria, in an identical manner, yielding 16 times as much ATP as the original 6 carbon sugar hydrolysis. Their breakdown pathways, while slightly different (and if you want to be REALLY technical, hexokinase CAN phosphorylate fructose in the same way it acts on glucose, and then it does follow the glycolytic pathway, identically from that step forward), are very, very similar, involving many of the same enzymes, as opposed to protein or fatty acid metabolism.

Without going into the specific pathway, I was referring to the fact that its hydrolysis products are easily utilized in either gluconeogenesis or further metabolized and enter the TCA cycle.

I am a (stressed out) med student studying for a GI physiology exam. Sugars must be broken down in the small intestine to monosaccharides to be absorbed, so sucrose becomes glucose and fructose, lactose (if you're not lactose intolerant) breaks down to glucose and galactose. Glucose and galactose are absorbed via co-transport with sodium via transport proteins. This requires a standing Na+ gradient in the cell, maintained by the Na-K pump, which requires the expenditure of energy. Fructose on the other hand enters the cell by simple facilitated diffusion through the GLUT-5 protein, meaning its transport out of the intestinal lumen requires no energy expenditure. Biochemically it it can enter the glycolytic cycle and is rapidly metabolized in much the same way as glucose.

None of those cited criticisms is at all recent. 1975 was 35 years ago. Litigation against D.O.s ended in the 60s.

Wait times vary considerably from practice to practice. Emergency care will usually pre-empt patients coming in for routine visits, just like triage at a hospital will code someone having a myocardial infarct before someone who crushed their hand in a hydraulic press. Please, find me a citation saying 1/2 of all us docs are millionaires. Dermatologists and radiologists are near the top of the pay scale, and their average salary is quite good, when they finish the 4 years of medical school and 3 years of residency where you make less than minimum wage. These are the most competitive specialties to get into, and they in no way constitute anything close to even 10% of doctors, let alone half. But internists, family medicine and pediatrics are at the bottom of the pay scale, making on average about 165,000 a year. Which is nothing to sneeze at, but hardly millionaire status, especially considering the fact that if you only look at the cost of medical education, not undergrad, they are finishing school with an average debt load of about $150,000. Personally, if you are a pediatric neurosurgeon, who has completed 4 years of medical school, followed 5 years of surgery residency, and an additional 2-3 years of fellowship where you make around $50,000 annually and work about 80 hours per week, I don't a salary of upwards of $350,000 a year is out of line. Then again, ask the parents of the kid who had a life threatening brain tumor removed if they feel differently.