Introduction Urotensin II (UII) is an important vasoactive peptide involved in the pathogenesis of atherosclerosis. Monocytes/macrophages play important roles in every step of atherosclerosis. Although UII has a chemoattractant effect on monocytes, it is unclear whether UII regulates inflammatory responses in macrophages. The present study sought to explore whether UII can promote leukotriene B 4 (LTB 4 ) production by macrophages. Material and methods The mRNA expression level of LTB 4 and 5-lipoxygenase were determined by real-time polymerase chain reaction. The protein level of LTB 4 and 5-lipoxygenase expression was assayed by enzyme-linked immunosorbent assay and Western blot, respectively. Western blot analysis was also employed to determine the phosphorylated forms of Akt. Reactive oxygen species (ROS) level was detected by the fluorescent probe 2′,7′-dichlorofluorescin diacetate and fluorescence intensity was measured with a multiwell fluorescence plate reader. Results Urotensin II promoted LTB 4 release and increased 5-lipoxygenase expression in a concentration- and time-dependent manner in RAW264.7 cells. Leukotriene B4 production and 5-lipoxygenase expression were decreased by blocking the UII receptor (UT) with urantide, eliminating ROS with N-acetylcysteine and diphenyliodonium, and inhibiting Akt phosphorylation with LY294002. UII significantly elevated ROS production, whereas urantide, N-acetylcysteine and diphenyliodonium substantially attenuated this effect. UII also enhanced Akt phosphorylation significantly, and this effect was potently inhibited by urantide, N-acetylcysteine, diphenyliodonium and LY294002. Conclusions Urotensin II may promote 5-lipoxygenase expression and LTB 4 release in RAW264.7 macrophages via UT-ROS-Akt pathways. These results indicate that UII may participate in macrophage activation and suggest a potential new mechanism underlying atherosclerosis.
Slippery scar is one of the most destructive diseases encountered in the cultivation of Auricularia polytricha (hairy wood ear); however, the identity of the pathogenic agent has remained uncertain. This study was designed to identify the causative pathogen of slippery scar in A. polytricha and to investigate the taxonomic classification of the pathogen by morphological observations, in vivo pathogenicity tests, and molecular evidences of ITS and RPB2 sequences. The results showed that the pathogen was a new Scytalidium species, here named Scytalidium auriculariicola. Scytalidium auriculariicola was characterized by its rapid growth rate, the catenate conidia of variable size, and the pale brown to brown chlamydoconidia. Phylogenetic analyses based on internal transcribed spacer regions and RPB2 sequences on the pathogen isolated and related species supported that S. auriculariicola was a true Scytalidium species. It was congeneric with and close to Scytalidium lignicola, the type species of Scytalidium. However, it differed from the latter species in the size of conidia, 33 different nucleotide bases in ITS sequences and 30 different nucleotide bases in RPB2 sequences.
Adventitia is the outer part of the arterial wall where the inflammatory response often occurs. Urotensin II (UII) is a potent vasoconstrictive peptide that also promotes the inflammatory process in patients with cardiovascular disease. Leukotriene C4 (LTC4), a lipid mediator, was recently found to play a role in the inflammatory process in the artery. We hypothesized that the adventitia is one of the resources of LTC4 and that UII may promote LTC4 production through the 5-LO (5-lipoxygenase) pathway in adventitial fibroblasts. Rat adventitial fibroblasts were isolated and incubated in serum-free medium with either UII alone or in combination with inhibitors of p38 MAPK, ERK, and UII receptors. The expression of 5-LO was detected using real-time polymerase chain reaction and Western blot. The translocation and binding activity of nuclear factor (NF)-κB were measured using immunofluorescence and electrophoretic mobility shift assay, respectively. The production of LTC4 was measured by enzyme-linked immunosorbent assay. The results indicated that: (1) adventitial fibroblasts were a source of LTC4 production; (2) UII increased the expression of the 5-LO mRNA and the protein by NF-κB activation through p38 MAPK and ERK pathways; and (3) UII promoted the LTC4 release in fibroblasts through the 5-LO pathway by p38 MAPK and ERK activations. The 5-LO pathway mediates LTC4 production, which may be a new mechanism in the pathogenesis of the vascular adventitial inflammation caused by UII.
Objective Perioperative cardiovascular events constitute the majority of complications in noncardiac surgery. Older and female patients have been less investigated. We aimed to evaluate differences in perioperative cardiovascular outcomes by age and sex. Methods We enrolled 1079 patients (57.5 ± 17.0 years, 42.6% women) undergoing intra-abdominal surgery from July 2007 to June 2008 and compared occurrence of perioperative cardiac events by age (≥65 vs. <65 years) and sex. Multivariable logistic regression was used to investigate associations between age, sex, and outcomes. Results Age ≥65 years was associated with perioperative myocardial infarction (MI) (odds ratio [OR] 2.9, 95% confidence interval [CI]: 1.3–6.6) and total cardiovascular events (OR 2.4, 95% CI: 1.3–4.2). Age ≥65 years was associated with higher perioperative MI risks in men (OR 4.7, 95% CI: 1.3–17.6) than in women (OR 3.1, 95% CI: 1.2–8.3). Advanced age was associated with heart failure in women (OR 13.9, 95% CI: 1.7–110.5). Female sex was a risk factor for heart failure in elderly patients (OR 4.2, 95% CI: 1.1–15.7). Conclusions Advanced age appeared to be associated with increased perioperative cardiac risk but differed by sex. Tailored strategies should be considered with respect to the patient’s sex.
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