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From colonized compost headspace, three antennally active volatiles were isolated by gas chromatography coupled with electroantennography and subsequently identified with gas chromatography coupled mass spectrometry as 1-hepten-3-ol, 3-octanone and 1-octen-3-ol. In behavioral assays the addition of said synthetic volatiles to uncolonized compost separately and in combination to mimic colonized compost resulted in avoidance. We thus partially elucidate the role of fungal volatiles in the habitat seeking behavior of Lycoriella ingenua.
It was reported that inhaled corticosteroids (ICS) treatment may affect local immunity and microbial community of the airway. However, whether ICS treatment increases the risk of influenza in patients with asthma remains unclear. This meta-analysis aimed to compare the risk of influenza between ICS and non-ICS treatment in patients with asthma.
PubMed, Embase, Cochrane Library and Clinical Trials.gov were searched from inception until November 2019. Randomized controlled trials (RCTs) were included that compared ICS treatment with non-ICS treatment on the risk of influenza in patients with asthma. Meta-analyses were conducted by the Peto approach and Mantel-Haenszel approach with corresponding 95% CIs.
Nine trials involving 6486 patients were included in this meta-analysis. The risk of influenza was not different between ICS treatment and the control groups (Peto OR 1.01, 95% CI 0.74-1.37, P = 0.95). The results of subgroup analyses based on durations (long-term and short-term treatment), doses (high-, medium- and low-dose treatment) and types (fluticasone and budesonide treatment) of ICS were consistent with the above pooled results. Moreover, subgroup analysis based on patients' age also revealed that use of ICS did not increase the risk of influenza. Results of the two meta-analysis approaches were similar.
Use of ICS does not increase the risk of influenza in patients with asthma. This study adds to safety evidence of ICS as a regular controller treatment for patients with asthma.
Use of ICS does not increase the risk of influenza in patients with asthma. This study adds to safety evidence of ICS as a regular controller treatment for patients with asthma.
To determine whether topical tacrolimus can lessen steroid-induced intraocular pressure (IOP) elevation.
Open cohort post hoc analysis study.
Five hundred eleven patients with vernal keratoconjunctivitis or atopic keratoconjunctivitis (mean age 17.0 ± 9.2years) were studied. All 511 patients were treated with topical tacrolimus with or without topical steroids, and the changes in IOP were measured monthly for 3months. The elevation in IOP induced by use of topical steroids was calculated using mixed linear regression analyses. The relationship between the elevation in IOP within 4weeks and the use or nonuse of tacrolimus reported in published data was analyzed using metaregression analysis to estimate the effects of tacrolimus on the IOP in eyes treated with topical steroids.
The mean topical steroid-induced IOP elevation in tacrolimus-treated eyes was lower, by 5.2mmHg (P = 0.04), than that in earlier published data without tacrolimus as the control. In the tacrolimus-treated eyes, the mean betamethasone-induced IOP elevation was 1.3mmHg without discontinuation of the steroid. Metaregression analysis indicated that glaucoma history and younger age had significant effects on topical steroid-induced IOP elevation, by 4.0mmHg (P = 0.002) and 3.9mmHg (P = 0.01), respectively. In tacrolimus-treated eyes, the most significant effect on the IOP was associated with glaucoma history or medication; however, its effect on the IOP was limited to 1.7mmHg elevation (P = 0.006).
Topical tacrolimus may lessen the steroid-induced elevation in IOP in younger individuals and may be a good adjunctive therapy to avoid IOP elevation in refractory cases.
Topical tacrolimus may lessen the steroid-induced elevation in IOP in younger individuals and may be a good adjunctive therapy to avoid IOP elevation in refractory cases.This study was aimed at evaluating the protective effect of sodium selenite (SS) on DNA integrity, antioxidant/oxidant status, and histological changes on 4-nonylphenol (4-NP)-induced toxicity in liver and kidney tissues of rats. Twenty-four adult male Sprague Dawley rats were divided into 4 groups as control, SS, 4-NP, and SS+4-NP group. Control group was untreated. selleck chemicals The SS group was supplemented with SS (0.5 mg/kg/day) and the 4-NP group was given 4-NP (125 mg/kg/day). The rats in the SS+4-NP group received SS followed by 4-NP 1 h later at the abovementioned doses. The treatments were administered by oral gavage for 48 days. DNA damage was analyzed by comet assay in lymphocytes. Oxidative stress parameters were measured, and histological evaluation was performed in liver and kidney tissues. Results showed that SS administration significantly decreased % Tail DNA and Mean Tail Moment in SS+4-NP group as compared with 4-NP group. Catalase activity in liver was significantly lower in 4-NP group only. SS treatment significantly increased the glutathione level and decreased high malondialdehyde level in tissues of the SS+4-NP group as compared with 4-NP group. Dilation of central vein, ballooning degeneration, vacuolar degeneration, and deterioration in the structure of remark cords in 4-NP-administered were alleviated in rats that received SS supplementation before administration of 4-NP. Moreover, glycogen intensity in hepatocytes and the wall of central vein increased in the SS+4-NP group. In addition, the SS supplementation in the SS+4-NP group decreased glomerular degeneration as well as the width of cavum glomeruli and congestion intensity in the kidney. These results indicate that SS may have a protective effect against 4-NP-induced hepato-nephrotoxicity in rats.
Oncogenic K-Ras mutations in colorectal cancer (CRC) combined with APC mutations worsen CRC prognosis and lower drug effectiveness. Thus, inhibition of both Wnt/β-catenin and Ras-MAPK signaling may be a rational strategy to improve the treatment of this cancer.
To identify a novel compound inhibiting both Wnt/β-catenin and Ras-MAPK signaling in CRC.
We developed a two-part screening system consisting of analysis of TOP flash reporter cells and then potential toxicity effects on primary neural stem cells (NSCs). We then screened 2000 chemical compounds and tested efficacy of candidates against isogenic colon cancer cells harboring wild-type or mutant K-Ras. We employed immunohistochemistry and immunocytochemistry to determine marker signatures associated with development of disease phenotypes.
We identified CPD0857, a compound that inactivates Wnt/β-catenin signaling and promotes ubiquitin-dependent proteasomal degradation of β-catenin and Ras proteins. CPD0857 effectively decreased proliferation and increased apoptosis of CRC cell lines, and overcame resistance of CRC harboring APC and K-Ras mutations to treatment with an EGFR monoclonal antibody (mAb).
My Website: https://www.selleckchem.com/products/TGX-221.html
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