The medical college admission test as a predictor of grade factors.
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Biomedical subjects
Publications and source records attributed to J V Haley.
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Strains of Neisseria gonorrhoeae requiring arginine, hypoxanthine, and uracil (AHU) may cause disseminated gonococcal infection (DGI). A significant epidemiologic association was noted between the incidence of disseminated gonococcal infection and the presence of gonococci of the AHU auxotype in the community over a nine-year period. Thirty-nine patients with DGI were identified from hospital records of January 1974-December 1982. During this interval, gonococcal isolates from patients in the community were collected at a venereal disease clinic and a hospital emergency room. The incidence of patients hospitalized for DGI dropped significantly after 1978. The year of highest incidence of DGI was 1977, when there were 429 cases of DGI per 100,000 cases of uncomplicated gonorrhea; the incidence of gonococcal isolates of the AHU auxotype in that year was 26.3%. In contrast, this auxotype accounted for only 4.6% of gonococcal isolates in 1980, when the incidence of DGI had decreased to 58 cases per 100,000 cases of uncomplicated gonorrhea. When DGI and gonococci of the AHU auxotype from the community were ranked for incidence by year, a significant correlation between the two was found (P less than .001). Thus the incidence of patients with DGI in the hospital reflected the presence of gonococci of the AHU auxotype in the community.
Urethral gonorrhea is typified by the presence of large numbers of polymorphonuclear leukocytes, which are presumably attracted to the urethra by an as yet uncharacterized chemotaxin. Culture supernatants from three different auxotypes of Neisseria gonorrhoeae, one requiring arginine, hypoxanthine, and uracil (Arg-,Hyx-,Ura-), one requiring proline, arginine (not satisfied by ornithine), and uracil (Pro-,Arg-[Orn*],Ura-), and one requiring proline (Pro-), were tested for their chemotactic activity against leukocytes from men of two racial groups, white and black. These auxotypes were chosen because the Pro- auxotype is isolated more frequently from black patients, and the Arg-,Hyx-,Ura- and the Pro-,Arg-(Orn*),Ura- auxotypes are isolated more frequently from white patients. Chemotaxis was tested in blind-well chambers in the absence of complement; membranes with a pore size of 3 microns were used. The culture supernatants of the Pro- auxotype were the most chemotactic, while those of the Arg-,Hyx-,Ura- were the least chemotactic when analyzed by a three-way analysis of variance: F = 22.83, df = 2.6, P less than .001. There were no differences in migration with respect to the race of the donor. Gonococcal culture supernatants did not require complement for chemotaxis.
The effect of halothane on intracardiac impulse conduction was assessed in dogs before and after pharmacologic vagotomy. Impulse conduction was measured by anesthetic-related changes in the A-H and H-V intervals of the His bundle electrogram. Prior to vagotomy, both "light" and "deep" halothane prolonged the A-H interval significantly. Maximal A-H interval prolongations corresponded to the maximal decrease in heart rate with either dose of anesthetic. Following vagotomy, the A-H prolongation produced by light halothane was abolished and the prolongation produced by the deep level greatly reduced. Neither dose of halothane had a measurable effect on the H-V interval before or after vagotomy. In one animal in which the effects of increasing rates of atrial pacing were measured without the addition of halothane, the A-H interval lengthened with no measurable change in the H-V interval. In two dogs in which the heart rate was held near pre-halothane levels by atrial pacing, the A-H interval was slightly prolonged and the H-V interval unchanged during the administration of deep halothane. These studies indicate that during sinus rhythm: (1) halothane prolongs A-V impulse conduction, (2) that this effect is correlated with a concomitant decrease in heart rate, and (3) that these effects are largely dependent upon intact vagal innervation of the heart. During atrial pacing, A-V conduction is prolonged by increased heart rate or by deep halothane when the heart rate is held constant. Thus, in addition to the known effects of halothane on pacemaker automaticity, concomitant changes in conduction may contribute to the antiarrhythmic action of this anesthetic.
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