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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]

Background: Portal endotoxaemia has been speculated to be crucially involved in the pathogenesis of chronic hepatic inflammation, which is highly associated with the development of type 2 diabetes mellitus. This study tests whether portal endotoxaemia is a pathogenic link between chronic subacute hepatic inflammation and pancreatic beta-cell dysfunction., Materials and Methods: Rats were randomly assigned into two groups: rats with intraportal saline or low-dose lipopolysaccharide (LPS) infusion for 4 weeks. Pathological changes in the liver were evaluated via histological and biochemical examination. Pancreatic insulin secretion was evaluated by in vivo hyperglycaemic clamp study., Results: White blood cell count was significantly increased after intraportal LPS infusion for 4 weeks. Plasma amylase and chemoluminescence counts indicating superoxide levels were significantly increased after LPS treatments for 2 and 4 weeks. Intraportal low-dose LPS infusion significantly increased tumour necrosis factor-alpha and interleukin-6 contents in liver and pancreas. Circulating C-reactive protein, thiobarbituric acid reactive substances (TBARS) and endotoxin levels were not different among groups. The first- and second-phase insulin secretions in hyperglycaemic clamp were significantly decreased in LPS-treated rats. The histopathological scores, de novo production of reactive oxygen substrate and TBARS contents in the liver and pancreas were significantly increased in LPS-infused rats. Leucocyte infiltration was clearly visible in pancreatic islets of LPS-treated rats., Conclusions: The present study demonstrated that mild portal endotoxaemia caused subacute hepatic inflammation and impaired pancreatic insulin secretion, implicating that portal endotoxaemia is a potential risk factor to link chronic subacute hepatic inflammation and pancreatic beta-cell dysfunction.

The origin and course of the cystic artery related to the Calot triangle were studied in 72 autopsies. The cystic artery arises from many possible origins; the right hepatic artery is the most common origin (76.6%). The Calot triangle (hepatocystic triangle), which is an important imaginary referent area for biliary surgery, is bounded by the common hepatic duct (CHD), the cystic duct, and the cystic artery. Of all the cystic arteries, 86.1% coursed through the Calot triangle, and 100% of the cystic arteries originating from the right hepatic artery coursed through the Calot triangle. However, only 54% of the cystic arteries that originated from the left, bifurcation, proper, and common hepatic arteries ran through the triangle. None of the cystic arteries that originated from the gastroduodenal, celiac, superior mesentery, or superior pancreaticoduodenal arteries passed through the triangle. Furthermore, 72.7% of the cystic arteries that originated from the right hepatic artery ran beneath the CHD as they entered the Calot triangle; the others ran anterior to the CHD. Of the cystic arteries that arose from locations other than the right hepatic artery, 29.4% ran posterior to the CHD, and 11.8% ran anterior to the CHD. The current study provides detailed information about anatomic variance in Chinese adults that may help avoid injury during open or laparoscopic cholecystectomies.

The superficial temporal artery is important in head and neck surgery. Ethnologic variation may affect surgical procedure. In this study, we evaluated the variations of the artery in Chinese adults. We measured its bifurcating location, the diameter of its vessels, and its relationship to nearby structures. A total of 26 cadavers with 52 superficial temporal arteries were examined in 3 consecutive years. The superficial temporal artery ran 1.14 cm anteriorly to the bony external auditory canal. The average diameters of the superficial temporal artery, frontal branch, and parietal branch were 2.14, 1.61, and 1.68 mm, respectively. In 45 of 52 cases (86.5 percent), bifurcation of the artery occurred well above the zygomatic arch. The present study thus demonstrated that the superficial temporal artery in the Chinese adult differs from that in the Caucasian and has provided a detailed anatomic distribution analysis of the superficial temporal artery in Chinese adults, which should benefit the clinician in dealing with operation procedures related to this artery.

The calcitonin receptor is known to couple to Gs and Gq, activating adenylyl cyclase and phospholipase C, respectively. The observation of pertussis-toxin-sensitive responses to calcitonin suggests that the receptor is capable of coupling to Gi/o as well. However, the calcitonin-dependent activation of adenylyl cyclase in HEK-293 cells that stably express the cloned rabbit calcitonin receptor, as in many other cells that express calcitonin receptors, shows little pertussis toxin sensitivity. Calcitonin treatment of these cells stimulates protein kinase C, which is reported to antagonize the receptor-dependent activation of Gi. The possibility that protein kinase C could be antagonizing Galphai-adenylyl cyclase coupling was tested by examining the effects of protein kinase C inhibitors (chelerythrine chloride and sphingosine) or of chronic treatment with phorbol ester to deplete protein kinase C. All three treatments led to a reduction of calcitonin-induced adenylyl cyclase activity that was reversed by pertussis toxin. Inhibiting or depleting protein kinase C had no effect on the activation of adenylyl cyclase by cholera toxin, indicating that Gs and adenylyl cyclase were not affected by these treatments. Calcitonin treatment of HEK-293 cells, that stably express a myc-tagged rabbit calcitonin receptor, induced the formation of complexes of the receptor and Galphai subunits, confirming that the calcitonin receptor interacts with Gi. Thus, the calcitonin receptor can couple to Gi, but the inhibition of adenylyl cyclase by Galphai is negatively regulated by protein kinase C.

Calcitonin (CT) is a peptide hormone that is secreted by the parafollicular cells of the thyroid in response to elevated serum calcium levels. It acts to reduce serum calcium by inhibiting bone resorption and promoting renal calcium excretion. In addition to this hypocalcemie effect, calcitonin modulates the renal transport of water and several ions other than calcium and acts on the central nervous system to induce analgesia, anorexia, and gastric secretion. The CT receptor, a member of a newly described family of serpentine G protein-coupled receptors, has recently been shown to couple to multiple trimeric G proteins, thereby activating several signaling proteins, including protein kinase C, cAMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase. In kidney proximal tubule cells (LLC-PK1), the CT-activated signaling mechanisms vary in a cell cycle-dependent manner, with the receptor coupling through a G(s) protein during G(2) phase and through a G(i) protein and possibly a G(q) protein during S phase. These signaling mechanisms differentially modulate the activities of Na(+)/K(+)-ATPase and the apical Na(+)/H(+) exchanger, effector molecules that play important roles in transepithelial Na(+) transport. Cloning of CT receptors has revealed the presence of alternatively spliced cassettes, resulting in the expression of different isoforms of the receptor. The availability of these recombinant CT receptors has allowed preliminary characterization of the effects of changes in the receptor's structure on its ligand binding and signal transduction properties. Thus, the cellular and molecular biology of CT is complex, with several structurally related peptide ligands and multiple isoforms of the CT receptor that can independently activate diverse signaling pathways. As the recent exciting results in this field are extended, we can expect rapid progress in understanding the molecular basis of the diverse effects of CT and, possibly, of the CT-related peptides CGRP and amylin.