Comparative epidemiology of heterosexual gonococcal and chlamydial networks: implications for transmission patterns

OBJECTIVE: Networks of sex-partner interaction affect differential risk of acquiring sexually transmitted infections. The authors evaluated sociodemographic and behavioral factors that correlated with membership in networks of gonococcal and chlamydial transmission. METHODS: Face-to-face interviews were conducted with 127 patients with gonorrhea and 184 patients with chlamydia (index cases) and their named sex partners, as well as the partners of infected partners. Detailed information was obtained regarding demographic, behavioral, and sexual-history characteristics of all respondents. RESULTS: Gonococcal-network members differed significantly from chlamydial-network members in a number of demographic variables, including race or ethnicity, education, and unemployment status. Gonococcal-network members were more likely to report past history of crack-cocaine use, sexual assault, and having been in jail. Gonococcal-network members also reported having more sex partners during the past 1 year and 3 months than did chlamydial-network members. Gonococcal and chlamydial mixing matrices demonstrated assortativeness for sex partner selection by race or ethnicity but not by sexual activity level, and no systematic differences between networks were noted. Gonococcal networks were larger than chlamydial networks. CONCLUSIONS: Network analyses of gonococcal and chlamydial infections demonstrated significant differences in sociodemographic and behavioral variables. Further research is required to delineate specific predictors of network membership among persons at risk for sexually transmitted infections.     

Less severe retinopathy of prematurity induced by surfactant replacement therapy

To assess the effect of surfactant replacement therapy (SRT) on the prevalence and severity of retinopathy of prematurity (ROP), we compared data from 160 SRT-treated preterm infants with data from 230 historic controls. The prevalence of ROP was 30.6% in the treatment group and 23.4% in the control group. Severe ROP (stages 3-4) was seen in 6.1% of the infants with ROP in the treatment group and 20.3% of the ROP patients in the control group. Surfactant therapy had no influence on the prevalence of ROP (odds ratio 1.4, 95% confidence interval 0.797-2.459, p = 0.242). However, SRT was associated with a decreased risk for severe ROP, compared to mild ROP (odds ratio 0.226, 95% confidence interval 0.056-0.905, p = 0.036). These data suggest that SRT is associated with a decreased risk for severe ROP.     

Suppression of N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis by dietary feeding of auraptene

The modifying effects of auraptene on N-nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis were investigated in male F344 rats. At 5 weeks of age, all animals, except those with the test chemical alone and control rats, received s.c. injections of NMBA (0.5 mg/kg body weight/injection, three times per week) for 5 weeks. At the end of the study (20 weeks), 75% of the rats treated with NMBA alone had esophageal neoplasms (papillomas). However, the groups who received a dose of 500 ppm auraptene during the initiation phase developed significantly reduced incidence of tumors (39%; P<0.05). Exposure to auraptene (500 ppm) during the post-initiation phase also decreased the frequency of the tumors (29%; P<0.01). The reduction of the incidence of severe dysplasia was obtained when auraptene was administered in the post-initiation phase (P<0.05). Cell proliferation in the esophageal epithelium determined by proliferating cell nuclear antigen (PCNA) was lowered by auraptene (P<0.01). Blood polyamine contents in rats who received NMBA and the test compound were also smaller than those of rats that received the carcinogen (P<0.05). These findings suggest that dietary auraptene is effective in inhibiting the development of esophageal tumors by NMBA when given during the initiation as well as post-initiation phases, and such inhibition is related to suppression of cell proliferation in the esophageal epithelium.     

金刚大化学成分的研究

从百部科黄精叶钩吻属植物金刚大(Croomia japonica Miq)的根部分得五个成分,分别为粉蕊黄杨胺A(pachysamine A,Ⅰ)、金刚大啶(croomionidine,Ⅱ)、金刚大碱(croomme,Ⅲ)、脱氢金刚大碱(didehydrocroomine,Ⅳ)和β-谷甾醇。应用波谱(IP,MS,¹HNMR和¹³CNMR等)分析、理化数据测定和化学转化,确定丁它们的结构,其中金刚大啶为新甾体生物碱。     

Neural pathways mediating the inhibition of shivering by nonthermal afferent impulses from ischemic limbs

Hind-limb tourniquet ischemia in the rat inhibits thermoregulatory shivering, lowering the ambient temperature at which it commences. This effect was prevented by the injection of 0.5% bupivacaine into the nerve trunks of the hind limbs and around the base of the thighs before the application of the tourniquets and also by lesions in the ventrolateral part of the spinal cord. The effect was also prevented by infiltrating the tissues distal to the tourniquets with 0.5% bupivacaine 15 min after their application. This was not effective if delayed until 105 min after application. We conclude that the afferent impulses that produce this effect ascend in the same part of the spinal cord as those concerned in neuroendocrine responses to trauma. Other effects of tourniquets on the responses to lowering the ambient temperature, i.e., the reduction in slope of the regression line realting the intensity of shivering to ambient temperature and the reduction in the increase in colon temperature, were not corrected by any of these procedures.     

Effects of bradykinin and indomethacin on cyclic GMP and cyclic AMP in lung slices

Bradykinin, 1-100 mug/ml, produced a rapid rise in the concentration of 3':5'-guanosine monophosphate (cyclic GMP) and 3':5'-adenosine monophosphate (cyclic AMP) in slices of guinea pig lung. Concentrations of both nucleotides reached a maximum in about 2 min, then declined to a basal levels in 6-12 min. The transient nature of the effect was presumbaly due to the rapid destruction of bradykinin as evidenced by (1) reaccumulation of nucleotides when bradykinin was added a second time, and (2) potentiation of the bradykinin effects by pyroGlu-Lys-Trp-Ala-Pro, a peptide that inhibits inactivation of bradykinin by kininase. It has been reported elsewhere that histamine, prostaglandins E(1) and E(2), and beta-adrenergic stimulation can cause accumulation of cyclic AMP in lung slices without affecting cyclic GMP concentration, whereas acetylcholine increases the concentrations of both cyclic GMP and cyclic AMP. Thus it was possible that the effects of bradykinin were indirect, i.e., secondary to release of one or more of these compounds. Promethazine (an antihistamine), propranolol (a beta-adrenergic blocking agent) and atropine (an anticholinergic agent) did not alter basal cyclic nucleotide concentrations or the effects of bradykinin. Two inhibitors of prostaglandin synthesis, indomethacin and aspirin, which alone were without effect, in the presence of bradykinin completely prevented the rise in cyclic AMP but did not interfere with cyclic GMP accumulation. Similarly, the effect of acetylcholine on cyclic AMP was abolished by indomethacin while that on cyclic GMP was unaltered. We suggest that in lung and probably in other tissues, bradykinin, acetylcholine, and perhaps other stimuli enhance the synthesis and release of prostaglandins as one of the consequences of their effects on cyclic GMP metabolism.     

Suppression of premature ventricular contractions by acebutolol.

The antiarrhythmic action of the beta-blocking drug, acebutolol, was evaluated in patients with frequent premature ventricular contractions (PVCs). In the 12 hours following administration of a single 300 mg oral dose, 8 of 10 patients showed a greater than 50% reduction in PVC frequency, and statistical analysis indicated that PVC reduction persisted for 10 hours after the single dose. Analysis of plasma concentrations of acebutolol and an acetyl metabolite indicated that after single oral doses of plasma concentrations of the metabolite exceed those of unchanged acebutolol. When patients were studied during periods of 300 mg doses every 8 hours, eight of 11 showed a 70% reduction in PVC frequency, and analysis showed that the therapeutic effect was present throughout the 24-hour monitoring period. Acebutolol slowed the heart rate and prolonged the PR interval without affecting the QT interval. Significant clinical or laboratory toxicity was not encountered. In the small group studied, acebutolol was found to be safe and effective for short-term administration to patients with frequent PVCs and possessed a relatively long duration of antiarrhythmic action.