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Objective: The G‐allele of the ‐1019C/G (rs6295) promoter polymorphism of the serotonin receptor 1A (HTR1A) gene has been implicated in anxiety; however, the underlying neurophysiological processes are still not fully understood. Recent evidence indicates that low parasympathetic (vagal) tone is predictive of anxiety. We thus conducted a structural equation model (SEM) to examine whether the HTR1A rs6295 variant can affect anxiety by altering parasympathetic nervous activity. Method: A sample of 1141 drug‐free healthy Han Chinese was recruited for HTR1A genotyping. Autonomic nervous function was assessed by short‐term spectral analysis of heart rate variability (HRV). Anxiety and stress levels were evaluated by the Beck Anxiety Inventory (BAI) and the Perceived Stress Scale (PSS) respectively. Results: The number of the HTR1A G allele was inversely correlated with high‐frequency power (HF), a parasympathetic index of HRV. The HF index was negatively associated with BAI scores. Furthermore, the good‐fitting SEM, adjusting for confounding variables (e.g., age and PSS levels), revealed a significant pathway linking rs6295 variant to BAI scores via HF index modulation. Conclusion: These results are the first to show that HTR1A ‐1019C/G polymorphism influences anxiety levels by modulating parasympathetic tone, providing a neurophysiological insight into the role of HTR1A in human anxiety. [ABSTRACT FROM AUTHOR]

Objectives. To study the effect of hyperbaric oxygen therapy in alleviating acute lung injury induced by lipopolysaccharide (LPS) in rats. Design and interventions. The rats received an intraperitoneal injection of LPS (15 mg/kg). Animals were either breathing air at 1 ATA or subjected to hyperbaric oxygen (HBO2) therapy. The HBO2 therapy was carried out in a hyperbaric chamber at a pressure of 3 ATA for 90 min. In another two groups, LPS-treated rats also received intraperitoneal injection of Nω-nitro-L-arginine (LNAME, 25 mg/kg) or L-N6-(iminoethyl)lysine (LNIL, 10 ml/kg). Another two groups of LPS-treated rats were subjected to HBO2 exposure after the injection of L-NAME or L-NIL. Measurements and main results. The bronchoalveolar lavage (BAL) was done into the left lung at 7.5 h after intraperitoneal injection of LPS. Parts of the right lung were excised for myeloperoxidase measurement, whereas the rest was collected for wet/dry ratio determination. LPS significantly increased the nitrite/nitrate (NOx-) concentration (34.4±15.7 vs 4.5±3.1 µM), LDH activity (66±17 vs 46±15 mAbs/min), and protein concentration (373±119 vs 180±90 mg/l) in the BAL fluid. Treatment with HBO2 immediately after the injection of LPS enhanced the increase of NOx- production, but reduced the LDH and protein in BAL fluid to the control levels. Pretreatment with either L-NAME or L-NIL abolished the increase of NOx- in the BAL fluid and further elevated the LDH level and protein concentration. Conclusion. Our results suggested that HBO2 alleviates the LPS-induced acute lung injury, which may be related to the enhancement of nitric oxide production. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the medical research paper "Mechanisms Underlying d-Amphetamine-Induced Dopamine Terminal Toxicity in the Striatum of Rats." This paper is to be discussed in the Seventeenth Biennial Meeting of the International Society for Neurochemistry (ISN) and the Thirteenth General Meeting of the European Society for Neurochemistry (ESN) to be held at Berlin, Germany from August 8-14, 1999.

The article presents an abstract of the study "The Nucleus Tractus Solitarii of Rats Is Activated by Systemic Administration of Lipopolysaccharide." The study will be presented at a joint meeting of the International Society for Neurochemistry and the European Society for Neurochemistry which will be organized in Berlin, Germany between August 8 to 14, 1999.