The role of stress in the relationships between gender and health‐promoting behaviours

Scand J Caring Sci; 2010; 24; 572–580
The role of stress in the relationships between gender and health‐promoting behaviours Studies have shown that in Western societies, women live longer than men. Among other factors, this has been attributed to health behaviours; men engage in health‐risking behaviours, while women perform health‐promoting behaviours. These tendencies were argued to align with cultural notions of masculinity and femininity. There may be some evidence, however, that men and women engage in different types of health‐promoting behaviours, and stress may play a role in these tendencies. This study attempts to examine the various types of health‐promoting behaviours women engage in and compare them to the tendencies of men. Secondly, it examines the mediating role of stress in the relationships between gender and health‐promoting behaviours. The sample was comprised of 402 young Israeli adults. Half were undergraduate university students majoring in social work. The remaining participants were sampled by ‘snowball sampling’. Participants completed a questionnaire containing 63 closed‐ended questions on various health issues. For the purpose of this study, gender, stress and health‐promoting behaviours measures were used. Data were collected over three academic years by the teacher responsible for the course and were received by the author at the end of the data collection phase. The study was approved by the institution’s internal review board. The results indicate that,‐while women engage in ‘type 2 behaviours’‐ refraining from smoking and drinking, eating breakfast regularly and sleeping 7–8 hours per night‐men engage in ‘type 1 behaviours’‐ physical exercise, refraining from snacking, and maintaining an appropriate body mass. We also found that, to some extent, women refrain from ‘type 1 behaviours’ because of their levels of general stress. Our study suggests that the social construction of masculinity and femininity which undermines individuals’ health needs to be challenged and addressed. In particular, the enduring role of stress in women’s health outcomes should be addressed.     

Spermatic vein ligation in varicocele: prognosis and associated male and female infertility factors

The fertility outcome of 129 spermatic vein ligations with good postoperative anatomic results is analyzed. For each couple, specific attention was also directed to other infertility factors. The study analyzes four groups: group I, 55 patients with varicocele only; group II, 16 patients with varicocele and prostatovesiculitis; group III, 16 patients with varicocele and a severe degree of testicular failure; and group IV, 42 patients with a varicocele only and associated female infertility factors. In each group, the pregnancy rate within 6 to 24 months after the operation was recorded. The control subjects were 36 patients with varicocele only who had declined or postponed intervention for 6 months. The best results were obtained in group I. Sperm motility improved following ligation and was associated with a greater percentage of pregnancies within a shorter period: 51% and 62% within 6 and 12 months, respectively, as compared with the control group (14% within 6 months). The prostatic disease required additional treatment for a longer period, but results similar to those of group I were eventually obtained (50% pregnancy rate). With testicular failure or female infertility factors, the prognosis worsened (31% overall pregnancy rate).     

Proton pump activation in stimulated parietal cells is regulated by gastric acid secretory capacity: a human study

Under normal physiological conditions, gastric acid production is controlled by a negative feedback mechanism. Proton pump inhibitors, such as pantoprazole, inhibit gastric acid secretion by irreversibly binding and inactivating luminally active hydrogen potassium ATPase. Recovery of acid production after treatment with a proton pump inhibitor is driven by new pump synthesis, activation of existing cytoplasmic pumps, or reversal of proton pump inhibition. The authors measured the time course of the inhibition and recovery of acid secretion in healthy volunteers following intravenous administration of pantoprazole to determine the rate of proton pump activation under maximally stimulated conditions. Gastric acid production was measured in 27 Helicobacter pylori negative healthy volunteers (mean age = 31 +/- 7 years; 17 men, 10 women) who received single doses of intravenous pantoprazole (20, 40, 80, or 120 mg) in the presence of a continuous intravenous infusion of 1 ug/kg/h of pentagastrin. From the time profile of acid secretion, the authors described the rate of change of acid output using an irreversible pharmacodynamic response model represented by the equation dR/dt = -k x R x Cpanto + Ln2/PPR x (Ro-R) and correlated the parameter values with demographic factors and gastric acid measurements. Mean stimulated acid output secretion was 21.6 +/- 18.4 mEq/h (range: 1.6-90.5) prior to the administration of pantoprazole and remained steady for 25 hours after placebo administration. Intravenous pantoprazole inhibited acid output in a dose-response fashion, with maximal inhibition (99.9%) occurring after an 80 mg dose. Mean proton pump recovery time was 37.1 +/- 21.0 hours (range: 6.7-75), and recovery was independent of the dose of pantoprazole. There was no association noted between proton pump recovery time and gender, age, race, body weight, or pantoprazole dose. However, there was an inverse correlation between acid output during baseline stimulation and recovery of acid secretion. Mean proton pump recovery time in stimulated normal human volunteers was 37.1 +/- 21.0 hours, with a range of 6.7 to 75 hours. The authors hypothesize that there may be a normal homeostatic mechanism that maintains acid secretory capability within a normal range by altering the rate of proton pump activation dependent on the individual's parietal cell mass. Abnormalities of this process may be responsible for the development of acid peptic disease in susceptible individuals.     

Distinct response of experimental neuroblastoma to combination antiangiogenic strategies

Background: The authors have shown previously that experimental neuroblastoma is partially inhibited (48%) by antivascular endothelial growth factor (anti-VEGF) antibody. The topoisomerase-I inhibitor, topotecan, has been shown to have antiangiogenic activity when administered in a low-dose, high-frequency regimen. We hypothesized that combining topotecan with anti-VEGF would suppress neuroblastoma more effectively than either agent alone. Methods: A total of 10⁶ neuroblastoma cells were implanted intrarenally in athymic mice. Animals received vehicle, topotecan, anti-VEGF, or topotecan plus anti-VEGF (n = 9, 20, 20, 20, respectively). All control and half the treated mice were killed at 6 weeks. Remaining (rebound) mice were maintained without treatment for 3 more weeks. Patterns of vasculature and apoptosis were determined immunohistochemically. Results: Tumor weights at 6 weeks were reduced significantly in topotecan-only (0.07g) and combination-treated animals (0.08 g), compared with controls or anti-VEGF[ndash ]treated mice (1.18 g, 0.53 g; P [lt ] .0007, all). At 9 weeks, rebound tumor weights were greatest in anti-VEGF (2.82 g), intermediate in topotecan (1.82 g), and least in combination-treated animals (1.47 g); however, the only significant difference was between anti-VEGF and combination therapy (P = 0.04). All treated tumors were vascularized sparsely in comparison with controls at 6 weeks, but exhibited brisk neoangiogenesis at 9 weeks. Conclusions: Topotecan either with or without anti-VEGF antibody significantly suppresses neuroblastoma xenograft growth in comparison with controls or anti-VEGF antibody alone. Combining topotecan with anti-VEGF antibody significantly inhibited rebound tumor growth in comparison with anti-VEGF antibody alone. Combination therapy may improve durability of antiangiogenic inhibition of neuroblastoma.     

Combination antiangiogenic therapy: increased efficacy in a murine model of Wilms tumor

BACKGROUND/PURPOSE: Antibody to vascular endothelial growth factor (anti-VEGF) suppresses tumor growth and metastasis in experimental Wilms tumor. However, tumor growth accelerates if antibody is withdrawn. As recently shown, low-dose, frequently administered topotecan, a topoisomerase-1 inhibitor, has anti-angiogenic activity. The authors hypothesized that combined topotecan/anti-VEGF therapy would suppress tumor growth and metastasis more durably than either agent alone. METHODS: Xenografts were induced by intrarenal injection of human Wilms tumor cells in athymic mice (n = 59). Mice were divided into control (n = 10), anti-VEGF (n = 16), topotecan (n = 17), and topotecan plus anti-VEGF (n = 16) groups. All control and half the treated mice were killed at week 6. Remaining ("rebound") mice were maintained without treatment until week 8. Tumor vasculature was mapped by fluorescein angiography/PECAM immunostaining. Endothelial apoptosis was assessed by TUNEL assay. RESULTS: 6 weeks: Tumor weights were reduced significantly in treated mice (P <.003 v control). Seven of ten control and 1 of 25 treated mice displayed lung metastases (P <.003). Rebound tumors were largest in topotecan-only, intermediate in antibody-treated, and smallest in combination-treated mice. Immunostaining and angiography results showed sparse vascularity in treated xenografts. Endothelial apoptosis was observed only in treated tumors. CONCLUSION: Combination low-dose topotecan and anti-VEGF antibody therapy is antiangiogenic and suppresses tumor growth and metastasis in experimental Wilms tumor more durably than either agent alone.     

Regulation of proline catabolism by leucyl,phenylalanyl-tRNA-protein transferase.

A mutant of Escherichia coli lacking leucyl,phenylalanyl-tRNA:protein leucyltransferase, EC 2.3.2.6) exhibited several abnormal growth characteristics relative to the wild type or a revertant when grown with glycerol as a carbon source. All three strains were auxotrophic for proline. The mutant required higher levels of this amino acid than did the other strains to attain a normal growth yield and metabolized exogenous [14C]proline more rapidly. The greater rate of proline utilization was associated with a 4-fold increase in specific activity of proline oxidase. When glucose rather than glycerol was employed as a carbon source, proline oxidase activity was reduced by catabolite repression and the growth ccharacteristics of the mutant were similar to those of the parental and revertant strains. These results suggest that the mutant growth phenotype is due to an altered rate of proline catabolism and constitue evidence for regulation of a specific metabolic pathway by leucyl,phenylalanyl-tRNA-protein transferase.     

How long should you wait for a chest radiograph after placing a chest tube on water seal? A prospective study

OBJECTIVE: The purpose of this study was to determine the optimal time interval for identifying a pneumothorax (PTX) on chest radiograph (CXR) after placing a chest tube on water seal. METHODS: One hundred nineteen chest tubes were placed on water seal according to a prospective, observational study protocol. After water seal, both an early (3.1 +/- 2.1 hours) and a late (17.6 +/- 8.0 hours) CXR was obtained. RESULTS: Thirty-one patients had a PTX on follow-up CXRs. There were 22 early and 9 late PTXs identified. Three patients in the early group had a clinically significant PTX or an increase in the size of PTX on follow-up CXR. None of the patients in the late group had a clinically significant PTX (any worsening of their PTX) or required further intervention. CONCLUSION: A normal chest radiograph obtained 3 hours after placing a chest tube on water seal effectively excludes development of a clinically significant pneumothorax.