Search

. Purpose: To identify symptoms potentially related to glaucomatous visual field abnormalities (VFAs) in a population-based setting, and to assess the applicability of using these symptoms to identify persons at risk of developing glaucoma. Methods: In this study, 10 214 Japanese male general workers (mean age, 45.3 ± 8.8 years) filled out a self-administered questionnaire and underwent frequency doubling technology (FDT) perimetry testing. The questionnaire inquired about whether the participant was suffering from any of nine symptoms, with scores for each response graded on a four-item Likert scale: 0 (none), 1 (rarely), 2 (sometimes), and 3 (always). Results from the questionnaire were compared among three groups: participants without any VFAs (9767), participants with VFAs as determined by the FDT test (FDT-VFA; 447), and 227 participants (of the 447 FDT-VFA participants) with glaucomatous VFAs who were newly diagnosed by ophthalmologic examinations. Results: The mean summed scores for the total items were significantly (p < 0.01) higher in FDT- and glaucomatous VFA groups than in normal subjects. In particular, responses citing the symptoms 'feeling of something in the front of the eye' and 'feeling of hardness to see in dark places' were significantly (p < 0.05) more frequent in subjects with FDT- and glaucomatous VFAs than among normal participants. However, the respective areas under the receiver operating characteristic curve of summed scores for the nine total items and for the two items which showed significant differences for the glaucoma groups were 0.57 (95% confidence interval = 0.53-0.60) and 0.58 (95% confidence interval = 0.54-0.61). Conclusion: Although the symptoms 'feeling of hardness to see in dark places' and 'feeling of something in the front of the eye' could be associated with glaucomatous VFA in a population-based setting, inquiring about symptoms is of little aid in identifying subjects with glaucomatous VFA as a strategy for public health. [ABSTRACT FROM AUTHOR]

The roles of inducible nitric oxide synthase (iNOS) in the development and healing of gastric ulcers have not been fully characterized. We characterized iNOS expression in experimentally induced ulcers in rat and mouse stomachs and investigated the roles of iNOS using iNOS gene-deficient (iNOS–/–) mice and wildtype mice. Gastric ulcers were induced in rats and mice by the application of acetic acid and cryoinjury, respectively. iNOS expression was detected on days 1–7 and peaked 3 days after ulcer induction in the rat. iNOS-positive cells were distributed mainly among the infiltrating cells and fibroblasts in the ulcer bed. The almost similar courses of healing and iNOS expression were observed in the ulcers of mice. During the course of healing, the iNOS gene status did not affect cell proliferation in the healing zone or vessel formation in the ulcer bed. iNOS deficiency, however, caused larger ulcers and severer inflammation during ulcer healing; the clearance of inflammatory cells in the ulcer bed by apoptosis was also delayed when the ulcer was re-epithelialized in the iNOS-deficient mice. These results indicate that iNOS is expressed in the ulcer bed and that iNOS activity may play beneficial roles in the ulcer repair process, possibly by regulating inflammation. [ABSTRACT FROM AUTHOR]

Abstract Background: Sodium chloride (NaCl) is a strong promoter of gastric cancer. We hypothesized that inducible nitric oxide synthase (iNOS) induced by NaCl may be involved in its promoting effects. We investigated iNOS expression by hypertonic NaCl solutions and its pathophysiological roles in the gastric mucosa of rats and mice. Methods: iNOS mRNA and protein expressions were examined in the rat and mouse gastric mucosa after intragastric administration of NaCl solution by northern blot, reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The effect on luminal pH by iNOS activity was assessed using aminoguanidine, a potent iNOS inhibitor, and iNOS gene deficient (iNOS–/– ) mice. Results: iNOS expression was detected at concentrations higher than 1.7 M, mainly in the cells infiltrating the damaged mucosa of rats. Administration of a higher than 3.4 M NaCl solution elevated luminal pH of the rat stomach remarkably, enabling bacterial overgrowth and dramatically increasing iNOS expression (n = 5 per concentration). Pretreatment with ampicillin (p.o), an antibiotic, attenuated the iNOS expression in duplicate experiments. Co-treatment with aminoguanidine (s.q) accelerated recovery of elevated luminal pH at 8 h and 16 h or 24 h after administration of 3.4 M (n = 8) and 5.2 M NaCl solution (n = 5), respectively. iNOS expression and luminal pH elevation were also observed in mice stomachs after administration of 3.4 M NaCl solution. The elevated luminal pH of iNOS–/– mice stomachs after the administration of NaCl solution was significantly lower at 6 h (n = 7) and at 9 h (n = 11), compared to that of wild type mice (n = 9 and 10, respectively). Conclusions: Hypertonic NaCl solutions induced iNOS expression in the gastric mucosa. iNOS activity prolonged the elevation of the luminal pH, potentially leading to bacterial overgrowth, which in turn enhanced iNOS expression. This vicious cycle might be related to the promoting effect of NaCl. [ABSTRACT FROM AUTHOR]

AbstractMint1 and mint2 were isolated in the course of seeking the protein ligands to munc18–1, a neuronal protein essential for synaptic vesicle exocytosis. The mint family of proteins has been highly conserved in the course of evolution, being retained from C. elegans to mammals. Several lines of biochemical and genetic evidence have suggested that mint1 and LIN-10, its homologue in C. elegans, function at synapses in the brain. Because the precise subcellular location of mint1 is incompletely known, we used immunostaining to examine the distribution of mint1 in the mouse brain including ultrastructural localization in synapses. Strong, finely punctate mint1 immunolabeling was detected throughout the brain, including cerebral cortex, striatum, hippocampus, thalamus, basal ganglia and cerebellum. At the most synapses in the molecular layer, mint1 was particularly abundant at the active zone and to a lesser extent in association with synaptic vesicles in the presynaptic terminals. In contrast, a very few synapses showed mint1 immunoreactivity in the postsynaptic density and there was no synapse double-positive in presynaptic and postsynaptic terminals. Mint1 distribution within presynaptic terminals overlapped that of munc18–1. These localization results are consistent with previously demonstrated biochemical interactions and strongly support functions of mint1 in synaptic vesicle exocytosis and synaptic organization in the central nervous system. [ABSTRACT FROM AUTHOR]