Do sensory neurons mediate adaptive cytoprotection of gastric mucosa against bile acid injury?

Pretreatment with the mild irritant 1 mmol acidified taurocholate protects the gastric mucosa from the injury induced by the subsequent application of 5 mmol acidified taurocholate, a phenomenon referred to as "adaptive cytoprotection." How this occurs remains an enigma. The purpose of this study was to investigate the role of sensory neurons and mucus secretion in this phenomenon. Prior to injury with 5 mmol acidified taurocholate (pH 1.2), the stomachs of six groups of rats were subjected to the following protocol. Two groups were topically pretreated with either saline or the mild irritant 1 mmol acidified taurocholate. Two other groups received the topical anesthetic 1% lidocaine prior to pretreatment with either saline or 1 mmol acidified taurocholate. The last two groups got the mucolytic agent 10% N-acetylcysteine (NAC) after pretreatment with either saline or 1 mmol acidified taurocholate. Injury was assessed by measuring net transmucosal ion fluxes, luminal appearance of deoxyribonucleic acid (DNA), and gross and histologic injury. Pretreatment with the mild irritant 1 mmol acidified taurocholate significantly decreased bile acid-induced luminal ion fluxes and DNA accumulation, suggesting mucosal protection (corroborated by gross and histologic injury analysis). This effect was negated by lidocaine but not by NAC. Thus, it appears that sensory neurons, and not increased mucus secretion, play a critical role in adaptive cytoprotection.     

Corticotropin-releasing factor binding sites undergo axonal transport in the rat vagus nerve

Corticotropin-releasing factor (CRF) binding sites were found to be present in the rat vagus nerve and underwent axonal transport. Binding sites accumulated on both sides of ligatures placed on the nerve and at similar rates following ligation of right or left cervical vagal trunks of either male or female rats. CRF binding sites also accumulated proximal and distal to ligatures on subdiaphragmatic vagal trunks. Binding was specific, reversible and inhibited by the CRF receptor antagonist α-helical-CRF(9-41). [(125) l]Tyr(0) -ovine-CRF binding to rat vagus nerve was not guanine nucleotide-sensitive. CRF and cholecystokinin binding sites were transported at a similar rate in the cervical vagus, although turnover of CRF binding sites was more rapid. No differences in CRF binding site transport were observed between Zucker rats of lean or obese genotype.     

Web creep: the role of infection and delayed healing

Summary Twenty-five digital webs from 21 patients, where web creep was noted after division of simple syndactyly were reviewed. In all cases web creep was related to delayed healing and the average time to its appearance was 8 months.     

Nasal symmetry: a 10-year comparison between the Pigott and McComb nasal correction.

The objective assessment of the symmetry of the cleft lip nose has not been properly evaluated. A simple technique using enlarged photographs and area assessment is described. Two different techniques were assessed, the Pigott "alar leapfrog" technique and the McComb alar lift technique. The children were assessed at 10 years of age. The results show no differences in the linear measurements or when the symmetry is assessed in the frontal view. In the worm's eye view, the Pigott correction was shown to produce a more asymmetric nose when compared with the McComb technique. Both corrections produce significant asymmetry when compared with a control group.     

Socioeconomic status and prevalence of allergic rhinitis and atopic eczema symptoms in young adolescents

Environmental factors are known to influence the development of allergic rhinitis and atopic eczema in genetically susceptible individuals. Socioeconomic status (SES) may be an important indicator of risk for these conditions. The International Study of Asthma and Allergies in Childhood (ISAAC) Phase 1 written questionnaire was used to determine the prevalence and severity of allergic rhinoconjunctivitis and atopic eczema symptoms in 4947 pupils aged 13-14 years attending 30 schools in socioeconomically diverse areas of Cape Town. Home addresses were used to stratify participants into five SES bands. Relationships between symptom prevalence and severity, and SES, recent urbanization and upward socioeconomic mobility were examined. Logistic regression was used to generate odds ratios (OR) and 95% confidence intervals (CI) in order to assess overall trends by SES. The prevalences of self-reported allergic rhinitis symptoms and recurrent itchy rash in the past year were 33.2% and 11.9% respectively. Girls had a significantly higher prevalence of all symptoms than boys. The prevalence of allergic rhinitis symptoms increased from lowest to highest SES (overall OR for rhinitis symptoms in past year = 1.16, 95% CI 1.11-1.21). There was no significant trend in reported eczema symptoms by SES other than for the question, 'Have you ever had eczema' (OR = 0.88, 95% CI 0.83-0.93). Longer period of urbanization was weakly associated only with recurrent itchy skin rash (OR = 1.05, 95% CI 1.01-1.09). 'Socially mobile' pupils, i.e. those resident in the lowest SES areas but attending highest SES schools showed significantly higher prevalences of eczema and some rhinitis symptoms than pupils attending lowest SES schools. These findings may reflect differences in reporting related to language, culture and access to medical care rather than real differences in prevalence.     

The effect of leptin on luteinizing hormone release is exerted in the zona incerta and mediated by melanin-concentrating hormone

The adipose hormone, leptin, not only restrains appetite, but also influences energy expenditure. One such influence is to promote sexual maturation and fertility. The neuromodulatory circuits that mediate this effect are not well known but the present study suggests that one mediator could be melanin-concentrating hormone (MCH). We show that the long-form receptor (Ob-Rb) is expressed in the zona incerta of the rat and that administration of leptin (both 0.5 microg and 1.0 microg/side) into this area of ovariectomized, oestrogen-primed rats stimulated the release of luteinizing hormone (LH) within 1 h, the effect enduring for a further 1 h. Injections of leptin into the arcuate nucleus induced a smaller, transient rise in LH while injections into the paraventricular and ventromedial nuclei were without effect. MCH neurones are present in the zona incerta and administration of this hormone into the medial preoptic area (mPOA) stimulates LH release, therefore we investigated the possibility that MCH might mediate this effect of leptin. An injection of MCH antiserum into mPOA prevented the rise in LH normally induced by leptin injected into the zona incerta. In addition, melanocortin receptor antagonists ([D-Arg8]ACTH(4-10) and [Ala6]ACTH(4-10)), previously shown to inhibit the stimulatory effect of MCH on LH release, also inhibited the effect of leptin. We propose that one route by which leptin may promote reproductive activity is by enhancing MCH release from fibres within the mPOA. Speculative mechanisms for the action of MCH include the following possibilities: MCH may be acting on the specific MCH receptor which in turn interacts with a melanocortin or melanocortin-like receptor; MCH may bind directly to one of the melanocortin receptors; or melanocortin antagonists may interact with the MCH receptor.     

Understanding the Chronic Impacts of Oil Refinery Wastewater Requires Consideration of Sediment Contributions to Toxicity

Previous studies at an oil refinery in Saint John, New Brunswick, Canada, found a diminished fish community downstream of the effluent outfall that appeared to be associated with periodic low dissolved oxygen concentrations due to episodic discharges of contaminated transport vessel ballast water. This study was initiated after the ballast water was removed from the effluent to further investigate the potential causes of residual effects in the study stream, Little River. We used field caging of fish, laboratory bioassays, and chemical analysis of effluents and sediments from the field site to determine if the effluent or contaminated sediments were affecting the recovery of the fish community in Little River. The field studies suggested that exposed, caged fish were affected, displaying >40 % increases in liver sizes and increased liver detoxification enzyme activity (cytochrome P450 1A, CYP1A); however, similar responses were absent in laboratory exposures that used effluent only. Adding sediments collected from the vicinity of the refinery’s outfall to the laboratory bioassays reproduced some of the field responses. Chemical analyses showed high concentrations of PAHs in sediments but low concentrations in the effluent, suggesting that the PAHs in the sediment were contributing more to the impacts than the effluent. Application of effects-based monitoring is suggested as beneficial to identify impacts to fisheries where refinery effluents of this type are involved.