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5% sevoflurane markedly increased the expressions of NKA, NKB, CGRP, and SP in the trachea of 21-day-old rats and of NKB, CGRP, and SP in the trachea of 14-day-old rats. The expressions of these molecules were antagonized by capsazepine pretreatment. Conversely, inhalation of 2.6% sevoflurane decreased the expressions of NKA and NKB in the trachea of 42-day-old rats. https://www.selleckchem.com/products/chir-99021-ct99021-hcl.html SIGNIFICANCE Sevoflurane did not upregulate the expression of TRPV1 in the airways of late-developing rats. This anesthetic may have a two-way effect on airways, resulting in considerable effects in pediatric clinical anesthesia management. BACKGROUND/OBJECTIVES Nicotinamide N-methyltransferase (NNMT) is a novel regulator of energy homeostasis in adipocytes. NNMT expression in adipose tissue is increased in obesity and diabetes. Knockdown of NNMT prevents mice from developing diet-induced obesity, which is closely linked to insulin resistance. An early sign of systemic insulin resistance is reduced expression of glucose transporter 4 (GLUT4) selectively in adipose tissue. Adipose tissue-specific knockout and overexpression of GLUT4 cause reciprocal changes in NNMT expression. The aim of the current study was to elucidate the mechanism that regulates NNMT expression in adipocytes. METHODS 3T3-L1 adipocytes were cultured in media with varying glucose concentrations or activators and inhibitors of intracellular pathways. NNMT mRNA and protein levels were measured with quantitative polymerase chain reaction and Western blotting. RESULTS Glucose deprivation of 3T3-L1 adipocytes induced a 2-fold increase in NNMT mRNA and protein expression. This effect was mimicked by inhibition of glucose transport with phloretin, and by inhibition of glycolysis with the phosphoglucose isomerase inhibitor 2-deoxyglucose. Conversely, inhibition of the pentose phosphate pathway did not affect NNMT expression. Pharmacological activation of the cellular energy sensor AMP-activated protein kinase (AMPK) and inhibition of the mammalian target of rapamycin (mTOR) pathway caused an increase in NNMT levels that was similar to the effect of glucose deprivation. Activation of mTOR with MHY1485 prevented the effect of glucose deprivation on NNMT expression. Furthermore, upregulation of NNMT levels depended on functional autophagy and protein translation. CONCLUSION Glucose availability regulates NNMT expression via an mTOR-dependent mechanism. AIMS This study aimed to explore the protective effects and possible mechanisms of baicalein on Aβ25-35-induced toxicity. MAIN METHODS Thioflavin-T (Th-T) dye was used to determine the effects of baicalein on Aβ25-35 aggregation in vitro. PC12 cells were stimulated with Aβ25-35, then the effects of baicalein on apoptosis, mitochondrial membrane potential (MMP), adenosine triphosphate (ATP), mitochondrial respiratory complex I, reactive oxygen species (ROS) and nitric oxide (NO) levels were determined. Moreover, LC-MS metabolomics approach was used to detect metabolic changes induced by baicalein in Aβ25-35-injured PC12 cells. KEY FINDINGS The results showed that baicalein could inhibit the aggregation of Aβ25-35 in vitro. Furthermore, pretreatment with baicalein significantly prevented Aβ25-35-induced cell apoptosis, as manifested by increasing the levels of MMP, ATP and mitochondrial respiratory complex I, decreasing the contents of ROS and NO. LC-MS metabolomics revealed that baicalein can regulate 5 metabolites, mainly involving two metabolic pathways, arginine and proline metabolism, nicotinate and nicotinamide metabolism. SIGNIFICANCE Our study revealed that baicalein has a protective effect on Aβ25-35-induced neurotoxicity in PC12 cells, which may be related to inhibition of apoptosis and metabolic disorders. Work-related hand injuries are the primary cause of disability and prolonged time away from work. This prospective cohort study was conducted to determine the predictors of return to work (RTW) after traumatic work-related hand injuries. Our study included 280 patients who were referred to the Plastic and Reconstructive Center for treatment of their occupational hand injuries from July 2017 to February 2018. Several functional questionnaires were completed, and they were followed up at 1, 3 and 8 weeks. Telephone interviews were done 3 months later. Approximately half the subjects had returned to work during the first 3 months after a median time away of 57 days. No relationship was found between age, gender, marital status, hand dominance and RTW time. Nevertheless, there was correlation between RTW time with cigarette smoking, injury severity and disability. Our study findings suggest that injury severity and higher work disability scores are prognostic factors for RTW. Also, smoking was associated with later RTW, which could be the result of poor circulation and delayed healing. Employers should implement injury prevention programs with appropriate rehabilitation that takes into consideration the severity of the hand injury, and health strategies to improve unhealthy lifestyle factors such as smoking. Betulinic acid (BA) is a pentacyclic triterpenoid found in several plant species. Urethane (URE) is a known promutagen. Here, we examine the genotoxicity and mutagenicity of BA alone or in combination with URE using the bone marrow micronucleus assay in mice bone marrow cells and the Somatic Mutation and Recombination Test in Drosophila melanogaster. Findings revealed that BA alone was not genotoxic, but reduced the frequency of micronucleus when compared to the positive control. No significant differences were observed in the cytotoxicity. Biochemical analyzes showed no significant differences for liver (AST and ALT) or renal (creatinine and urea) function parameters, indicating the absence of hepatotoxic and nephrotoxic effects. BA alone did not increase the frequency of mutant spots, but reduced the total frequency of mutant spots when co-administered with URE in both ST and HB crosses. In addition, BA reduced the recombinogenic effect of URE at the highest concentrations of both crosses. In conclusion, under experimental conditions, BA has modulatory effects on the genotoxicity induced by URE in mice, as well as in somatic cells of D. melanogaster. We suggest that the modulatory effects of BA may be mainly due to its antioxidant and apoptotic properties.

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