Effectiveness of Teaching of Neonatal Resuscitation Programme at a Workshop for a Mixed Population of Medical Personnel

We evaluated the effectiveness of teaching at a neonatal resuscitation programme (NRP) workshop held for 35 medical personnel (including postgraduate trainee doctors, general duty medical officers, nursing officers and probationer nurses) using a one-group pretest-posttest design. None of the participants had any formal exposure to the NRP guidelines. A pre-workshop test of 20 multiple-choice questions was administered to all the participants. At the end of the workshop, the same 20 questions were administered and the two scores compared using t-test for paired data on SPSS statistical software. The mean pre-workshop score was 9.03 (SD 2.66) which improved to a mean of 15.53 (SD 1.93) post-workshop. This improvement was highly significant with p < 0.0001 (two-tailed) and the 95% confidence interval being -7.41 to -5.59. Subgroup analysis revealed that nursing officers and probationer nurses showed highly significant improvement in the post-workshop scores while trainee doctors doing Medicine, Pediatrics and the general duty medical officers showed statistically significant improvement in the post-workshop scores. This study shows that a medical workshop is an effective means of imparting knowledge to a mixed group of medical personnel.Key Words: Evaluation, Neonatal resuscitation, Teaching, Workshop     

Role of kin and nonkin support in the mental health of low-income women

Data from the Worcester Family Research Project were analyzed to determine whether social support processes are altered by poverty and whether kin and nonkin support are differentially related to mental health in low-income mothers. The authors found that conflict with family and friends predicted adverse mental health and more strongly predicted these outcomes than emotional and instrumental support. Moreover, sibling conflict was a stronger predictor of mental health than parent conflict. Finally, only instrumental support from professionals predicted mental health.     

Survival and normal neurological outcome after CPR with periodic Gz acceleration and vasopressin

BACKGROUND: We showed previously that whole body periodic acceleration along the spinal axis (pGz) is a novel method of cardiopulmonary resuscitation (CPR). The ultimate assessment of the value of any CPR technique is the neurological outcome after using such a technique. In this study, we determined the neurological outcome in pigs after prolonged pGz-CPR, with administration of vasopressin immediately prior to defibrillation. Neurological outcome after pGz-CPR was compared to a control group where no intervention occurred for the same time period (C-NoInterv). METHODS AND RESULTS: Ventricular Fibrillation (VFIB) was induced in 12 animals. After a 3 min non-interventional interval, the animals received either pGz-CPR (n=7), or C-NoInterv (n=5) for 15 min. After 18 min of VFIB, a single dose of vasopressin (0.8 U/kg) was administered along with sodium bicarbonate and bretylium, and defibrillation was attempted. All animals in the pGz-CPR group had return of spontaneous circulation (ROSC) and normal neurological assessment at 24 h. Neurologic outcome remained normal at 48 h. In contrast, none of the animals in the C-NoInterv had ROSC. CONCLUSION: Prolonged pGz-CPR, with administration of vasopressin immediately prior to defibrillation results in normal neurological outcomes at 24 h.     

C-reactive protein and risk of cardiovascular disease: Evidence and clinical application

Prospective epidemiologic data consistently show that elevated C-reactive protein (CRP) levels are associated with an increased risk of subsequent cardiovascular events in apparently healthy populations, and accumulating laboratory research is uncovering possible mechanisms by which CRP may influence the development of atherothrombotic disease. CRP is a stronger predictor of cardiovascular disease than is low-density lipoprotein (LDL) cholesterol. CRP adds prognostic information at all levels of the calculated Framingham risk score and at all levels of severity of the metabolic syndrome. Commercially available high-sensitivity assays suitable for use in clinical settings allow for the routine assessment of CRP as a useful adjunct in cardiovascular risk screening. When such assays are used, CRP levels of less than 1, 1 to 3, and greater than 3 mg/L differentiate patients at low, moderate, and high risk, respectively, for future cardiovascular events. Persons with high CRP but normal LDL cholesterol comprise a high-risk group frequently overlooked in clinical practice. Knowledge of their high-risk status may improve these patients’ compliance with recommended lifestyle changes that are likely to improve prognosis. Preliminary data suggest that individuals with elevated CRP but low LDL cholesterol may benefit from pharmacologic interventions, including statin therapy. Large-scale trials are underway to assess the net efficacy and public health impact of this approach to the primary prevention of myocardial infarction and stroke.     

Physiology and pathophysiology of female sexual function and dysfunction

Female sexual dysfunction is age-related, progressive, and highly prevalent, affecting 30%-50% of American women. While there are emotional and relational elements to female sexual function and response, female sexual dysfunction can occur secondary to medical problems and have an organic basis. This paper addresses the anatomy and physiology of normal female sexual function as well as the pathophysiology of female sexual dysfunction. Although the female sexual response is inherently difficult to evaluate in the clinical setting, a variety of instruments have been developed to assess subjective measures of sexual arousal and function. Objective measurements, used in conjunction with the subjective assessment, help diagnose potential physiologic/organic abnormalities. Therapeutic options for the treatment of female sexual dysfunction, including hormonal, and pharmacological, are also addressed.     

Localization of SPARC in developing,mature, and chronically injured human allograft kidneys

BACKGROUND: The matricellular protein SPARC (secreted protein acidic and rich in cysteine) is expressed during development, tissue remodeling and repair. It functions as an endogenous inhibitor of cell proliferation, regulates angiogenesis, regulates cell adhesion to extracellular matrix, binds cytokines such as platelet derived growth factor and stimulates transforming growth factor-beta (TGF-beta) production. This study describes the expression of SPARC during human renal development, in normal kidneys and during renal allograft rejection. METHODS: A total of 60 renal specimens, including normal areas from tumor nephrectomies (N = 24), fetal kidneys (N = 27) and explanted renal allografts (N = 9), were included in the study. SPARC protein was localized by immunohistochemistry using two different antibodies. On consecutive sections SPARC mRNA was detected by in situ hybridization. RESULTS: In the normal adult kidney SPARC protein was expressed by visceral and parietal epithelial cells, collecting duct epithelium (CD), urothelium, smooth muscle cells of muscular arteries and focally in interstitial cells. During renal development immature glomeruli demonstrated a polarized SPARC expression in visceral epithelial cells at their surface abutting the capillary basement membranes. In the fully differentiated glomeruli the expression pattern mirrored that of the adult kidney. Furthermore, SPARC was abundantly expressed by derivatives of the ureteric bud, and smooth muscle cells of arterial walls. During chronic allograft rejection SPARC is expressed in neointimal arterial smooth muscle cells, infiltrating inflammatory cells as well as by interstitial myofibroblasts in areas of interstitial fibrosis. SPARC mRNA synthesis detected by in situ hybridization mirrored these protein expression patterns. CONCLUSION: These studies co-localize SPARC to several sites of renal injury previously shown to be sites of PDGF B-chain expression and/or activity. We speculate that SPARC could function as an accessory molecule in chronic PDGF-mediated sclerosing interstitial and vascular injury. SPARC localization to glomerular epithelial cells corresponds to similar findings in rodents, and may reflect its role in cell adhesion and /or regulation of cell shape.     

Socioeconomic status and mortality among the elderly: findings from four US communities

The effect of socioeconomic status (SES) on mortality was examined in the community-dwelling elderly. Data were obtained from four population-based studies that enrolled elderly residents of four US communities (East Boston, Massachusetts; New Haven, Connecticut; east-central Iowa; and the Piedmont region of North Carolina) and followed them for 9 years, starting in 1982 or 1986. Higher SES, whether measured by education, by household income, or by occupational prestige, was generally associated with lower mortality. However, the pattern of findings varied by gender and by community. For men, all three SES indicators were associated with mortality in the majority of cohorts. For women, this was true only for income. SES-mortality associations were attenuated but not eliminated after adjustment for behavior and health status. SES-mortality associations were stronger in New Haven and North Carolina than in East Boston and Iowa. The latter communities are more homogeneous with respect to ethnicity, urbanization, and occupational history than the former. Future research should investigate the relative validity of traditional SES measures for men and women and develop more balanced assessment methods. These findings also suggest that it is important to consider not only individual characteristics but also community attributes that mediate or modify the pathways through which socioeconomic conditions may influence health.     

Short-term carcinogenicity testing of a potent murine intestinal mutagen, 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP), in Apc1638N transgenic mice

Transgenic Apc1638N mice, heterozygous for a targeted frameshift mutation at codon 1638 of the endogenous adenomatous polyposis coli (APC) gene, are predisposed to develop multiple adenomas and adenocarcinomas along the intestinal tract and to a number of extra- intestinal lesions including, among others, mammary tumors. We have studied these mice in a short-term carcinogenicity test with 2-amino-1- methyl-6-phenylimidazo(4,5-b)pyridine (PhIP), a potent murine small intestinal mutagen and lymphomagen. Upon dietary administration of 0.03% PhIP in a short-term (6 months) study, a significantly increased number of small intestinal tumors as well as an increased number of aberrant crypt foci (ACF) were observed in male Apc+/Apc1638N mice compared with untreated transgenic mice. No differences in intestinal and mammary tumor multiplicity were observed between treated and control Apc+/Apc1638N females.      

Effects of long term dietary phenethyl isothiocyanate on the microsomal metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and 4- (methylnitrosamino)-1-(3-pyridyl)-1-butanol in F344 rats

Phenethyl isothiocyanate (PEITC), a cruciferous vegetable component, inhibits lung tumor induction by the tobacco specific nitrosamine, 4- (methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). To gain insight into the mechanism of PEITC lung tumor inhibition, we examined, in male F344 rats, the effects of dietary PEITC (3 micromol/g NIH-07 diet) in combination with NNK treatment (1.76 mg/kg, s.c., three times a week) for 4, 12 and 20 weeks on liver and lung microsomal metabolism of NNK and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), a major metabolite of NNK and also a lung carcinogen. This was compared with rats fed NIH-07 diet, without PEITC, and treated with NNK alone or saline. The protocol was identical to that employed for inhibition of lung tumorigenesis by PEITC. We observed decreased rates of alpha- hydroxylation of NNK and NNAL in lung microsomes of 4-, 12- and 20-week PEITC + NNK treated rats compared with those treated with NNK or saline. NNK treatment alone also decreased lung alpha-methylene hydroxylation of NNK. Long-term NNK + PEITC administration did not significantly affect liver oxidative metabolism of NNK or NNAL, and did not affect the rate of glucuronidation of NNAL in liver microsomes when compared with rats treated with NNK or saline. Thus, PEITC selectively inhibited lung metabolic activation of NNK and NNAL. These results support the hypothesis that PEITC inhibits NNK-induced lung tumors by inhibiting metabolic activation of NNK in the lung. This study also demonstrated that PEITC inhibits lung alpha-hydroxylation of NNAL; this may play a role in PEITC inhibition of lung tumorigenesis by NNK.