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OBJECTIVE: This study aimed to evaluate the effect of resistance exercise on peripheral inflammatory biomarkers in healthy adults. MATERIALS AND METHODS: Four databases, including PubMed, Web of Science, Cochrane Library, and SPORTDiscus, were searched from inception until April 1st, 2022. A meta-analysis was conducted using a random-effects model, followed by sensitivity analysis, subgroup analysis, meta-regression analysis, and publication bias analysis. RESULTS: 15 randomized controlled trials were included in the meta-analysis. The pooled results showed that resistance exercise significantly decreased TNF-α levels (SMD = -0.81, 95% CI: -1.42 to -0.20, p = 0.009) but did not affect IL-6 and CRP levels. Individuals with BMI 18.5-24.9 exhibited significantly decreased IL-6 levels, while moderate strength resistance exercise could significantly decrease TNF-α levels. Finally, age might be a confounding factor influencing the effect of resistance exercise on IL-6. CONCLUSIONS: Resistance exercise could reduce TNF-α levels in healthy adults, and resistance exercise with moderate intensity could reduce TNF-α levels more effectively. [ABSTRACT FROM AUTHOR]

OBJECTIVES: The aim of this study was to investigate the effect of quercetin on P-glycoprotein (P-gp) transport ability in vivo. SUBJECTS/METHODS: Genotype data were available from a total of 165 health volunteers. An open, randomized, two-period crossover clinical trial was performed in eighteen subjects with different MDR1 3435 C/T genotypes. All subjects took 500 mg quercetin or placebo daily from 1st to 13th day or from 43st to 55th day, and 100 mg talinolol was given at the 14th or 56th day. The washout period is 28 days. RESULTS: In this study, we found the values of area under the curve [(AUC).sub.0-48h], [AUC.sub.0-∞] and [C.sub.max] of talinolol in all subjects significantly decreased (6496.6 ± 2389.9 vs 7809.5 [+ or -] 2386.8 ng.h/ml, P = 0.04), (8414.7 ± 344.8 vs 10478.2 ± 4195.4 ng.h/ml, P = 0.03), (412.9 ± 132.6 vs 543.3 ± 97.9 ng.h/ml, P = 0.01) after administration of quercetin, respectively. There were no significant differences in [t.sub.max] and [t.sub.1/2] of talinolol. The results also showed [AUC.sub.0-48 h] (5598.6 ± 2202.1 vs 8229.4 [+ or -] 1491.7 ng.h/ml, P = 0.02) and [AUC.sub.0-∞] (7110.0 ± 3437.0 vs 12681.2 ± 4828.2 ng.h/ml, P = 0.01) of talinolol to be significantly decreased in MDR1 3435 TT individuals administered of quercetin. The [C.sub.max] of talinolol in MDR1 3435 TT (382.4 ± 149.1 vs 584.9 ± 115.2 ng/ml, P = 0.04) and MDR1 3435 CT (383.5 ± 104.9 vs 554.6 ± 80.6 ng/ml, P = 0.01) individuals significantly decreased after the administration of quercetin. CONCLUSIONS: Quercetin significantly induced the activity of P-gp and this induced effect was more obvious in MDR1 3435 TT individuals. European Journal of Clinical Nutrition (2013) 67, 390- 394; doi: 10.1038/ejcn.2013.5; published online 20 February 2013 Keywords: quercetin;talinolol;MDR1;drug transporter; gene polymorphisms; pharmacokinetcs, INTRODUCTION The P-glycoprotein (P-gp) is an ATP-dependent drug efflux transporter encoded by the multi-drug resistance gene (MDR7). (1) It is not only highly expressed in many types of cancer cells, [...]

Nano nickel oxide (NiO), widely used in industry, has recently been discovered to have pulmonary toxicity. However, no subchronic exposure studies about nano NiO-induced pulmonary fibrosis have been reported. The objective of this study was to investigate pulmonary fibrosis induced by nano NiO and its potential mechanism in rats. Male Wistar rats (n = 40, 200-240 g) were randomized into control group, nano NiO groups (0.015, 0.06, and 0.24 mg/kg), and micro NiO group (0.024 mg/kg). All rats were killed to collect lung tissue after intratracheal instillation of NiO particles twice a week for 6 weeks. To identify pulmonary fibrosis, Masson trichrome staining, hydroxyproline content, and collagen protein expression were performed. The results showed widespread lung fibrotic injury in histological examination and increased content of hydroxyproline, collagen types I and III in rat lung tissue exposed to nano NiO. To explore the potential pulmonary fibrosis mechanism, transforming growth factor beta 1 (TGF-β1) content was measured by enzyme-linked immunosorbent assay, and the messenger RNA expression of key indicators was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The TGF-β1 content was increased in nano NiO exposure groups, as well as the upregulated gene expression of TGF-β1, Smad2, Smad4, matrix metalloproteinase, and tissue inhibitor of metalloproteinase. The findings indicated that nano NiO could induce pulmonary fibrosis, which may be related to TGF-β1 activation. [ABSTRACT FROM AUTHOR]

What is known and objective Warfarin is a widely used anticoagulant with a narrow therapeutic index. Polymorphisms in the VKORC1, CYP2C9 and CYP4F2 genes have been verified to correlate with warfarin stable dosage ( WSD). Whether any other genes or variants affect the dosage is unknown. The aim of our study was to investigate the relationship between GGCX, miR-133 variants and the WSD in Han Chinese patients with mechanical heart valve replacement ( MHVR). Methods A total of 231 patients were enrolled in the study. Blood samples were collected for genotyping. The average WSD among subjects with different GGCX or miR-133 genotypes was compared. Regression analyses were performed to test for any association of genetic polymorphisms with WSD. Results and discussion The warfarin dosage in patients with the GGCX rs699664 TT and rs12714145 TT genotypes was 3.77±0.93 (95% CI: 3.35-4.19) mg/d and 3.70±1.00 (95% CI: 3.32-4.09) mg/d, respectively. The GGCX rs699664 and rs12714145 genotypes were significantly associated with WSD ( P<.05). But they were ruled out in the multivariate regression analysis. There were no significant differences in the average warfarin stable dosage between subjects with MIR133B rs142410335 wild-type and variant genotypes ( P>.05). What is new and conclusion The genotypes of GGCX rs699644 and rs12714145 were significantly associated with WSD ( P<.05), but their contributions were not significant after accounting for other factors. MIR133B rs142410335 makes no significant contributions to warfarin stable dosage in Han Chinese patients with MHVR neither in univariate regression nor in multivariate regression analyses. [ABSTRACT FROM AUTHOR]

Aim Several factors have been implicated in the pathogenesis of colorectal cancer ( CRC) associated with ulcerative colitis ( UC). We investigated markers of cancer cell pluripotency, including CD44 and CD166, micro RNA-21 (miR-21) and micro RNA-215 (miR-215), and APC, K-ras and DCC mutations in biopsy specimens from patients with UC to evaluate any correlations with clinical risk factors. Method We observed 18 patients with UC and collected two biopsy specimens from each patient at diagnosis and at a follow-up end-point. We examined the expression of CD44, CD166, miR-21 and miR-215, and APC, K-ras and DCC mutations. We compared these markers at the two time points and assessed their associations with clinical characteristics, including the duration of colitis, histological alterations and the age of the patient at the onset of UC. Results Most (16/18) patients had alleviation of mucosal inflammation or remained stable during follow-up; one patient developed dysplasia and one had severe aggravation of the lesion during follow-up. Enhanced expression of CD44, CD166 and miR-21 with miR-215 was found in the specimens obtained at follow-up, despite alleviation of mucosal lesions. Coherence of cancer stem cell markers and mi RNAs was seen in patients who had significant worsening of inflammation, dysplasia and a long duration of colitis. APC mutation occurred in only one patient; this patient had the longest duration of UC (23 years). Conclusion Enhanced markers of CRC in follow-up colonic mucosal samples support the conclusion that the duration of UC plays the most important role in UC-related carcinogenesis. [ABSTRACT FROM AUTHOR]