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Long noncoding RNA (lncRNA) is emerging as a vital regulator in various tumors. However, the biological function of ZFPM2-antisense RNA 1 (ZFPM2-AS1) in hepatocellular carcinoma (HCC) remains unclear. The present study aims to explore the function and mechanism of ZFPM2-AS1 in hepatocellular carcinoma progression.The ZFPM2-AS1 expression in HCC cells and tissues was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Effects of ZFPM2-AS1 on tumor cell proliferation and invasion were detected by CCK8 assay or EdU assay or matrigel migration assay and Western blot. The Luciferase reporter assay, RNA pulldown assay, qRT-PCR, and Western blot were performed to explore and confirm the interaction between ZFPM2-AS1 and miR-1226-3p and integrin β1 (ITGB1).ZFPM2-AS1 was overexpressed in HCC tissues and cell lines. High levels of ZFPM2-AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. ZFPM2-AS1 knockdown inhibited cell proliferation and invasion. ZFPM2-AS1 could directly bind to and negatively regulate miR-1226-3p expression. Moreover, ITGB1 was identified as a target gene of miR-1226-3p. ITGB1 was found to be directly negatively regulated by miR-1226-3p and indirectly upregulated by ZFPM2-AS1. Rescue assays demonstrated that ZFPM2-AS1 promotes HCC cell proliferation and invasion through modulating miR-1226/ITGB1 axis.ZFPM2-AS1 promotes cell proliferation and migration by regulating miR-1226-3p/ITGB1 axis in HCC.

To detect cell frequency and surface markers of peripheral CD4Forty RA patients meeting the American College of Rheumatology classification criteria for RA and twenty healthy controls (HC) were included. The peripheral blood mononuclear cells and sera were collected. The expressions of CD4+CXCR5The cell surface marker of CXCR5Peripheral Tfh cells and their relevant cytokines are higher in RA patients than healthy controls, indicating Tfh cells may participate in the pathogenesis of RA, therefore, blocking the pathway of Tfh cells may be reasonable cellular targets for therapeutic intervention.

To observe the effectiveness of chlortetracycline (aureomycin) treatment on vulval white lesions and to explore its possible pathogenesis.From January 2001 to April 2011, 194 patients with vulvar non-neoplastic epithelial disorders were divided into three groups according to therapy regimens received, ie, chlortetracycline treatment group (72 cases), chlortetracycline + beclomethasone treatment group (66 cases), and beclomethasone treatment group (56 cases); their local changes of vulvar lesions were observed and efficacy of these treatment profiles was evaluated after one year.Effective rates of chlortetracycline group, chlortetracycline + clobetasol group and clobetasol groups were 86.1% (62/72), 87.9% (58/66), and 62.5% (35/56), respectively. There was a significant difference among these three groups (Hc = 10.7766,p = 0.0046), the curative rate of clobetasol group was markedly lower than that of the former two groups (p = 0.0072 and p = 0.0019), but was not statistical significant (p = 0.6077) when compared between the former groups.The occurrence of vulvar non-neoplastic epithelial disorders may be associated with chlamydia and mycoplasma infection, the chlortetracycline is an effective drug for this illness, the mechanism of which might be related to killing pathogens directly and inhibiting inflammatory mediators.

Traditional percutaneous laser disc decompression (PLDD) eliminates nucleus pulposus in the center of lumbar discs. Targeted PLDD is an alternative technique that involves elimination and decompression of the target area located 5-8 mm in the front of the herniated disc. We aimed to compare the efficacy of targeted PLDD with traditional PLDD in the treatment of lumbar disc herniation and evaluate the usefulness of guidance by puncture-radiating pain on clinical outcomes of PLDD.We treated 61 patients with lumbar disc herniation. Patients were stratified into control group, which included patients who underwent traditional PLDD, and study group in patients underwent targeted PLDD. Clinical outcomes and efficacies were evaluated at different time points using the visual analog scale (VAS) and modified MacNab criteria.Patients in the study group demonstrated significantly greater decreases in the VAS scores compared with those in control group. These differences were observed on Day 3, and 1 and 3 months after the treatment. Further, VAS scores were markedly lower in the patients whose treatment was guided by the puncture-radiating pain. Thus, at 1 month after the operation, 64.1% of those patients showed excellent or good outcomes based on MacNab criteria, which was almost twice the percentage seen in patients who did not experience the puncture-radiating pain (36.4%).Targeted PLDD is an effective, minimally invasive, and safe technique for lumbar disc herniation, and this technique achieves better short-term postsurgical outcomes than traditional PLDD. Puncture-radiating pain is an important prognostic indicator for better short-term responses to the treatment.

Epidemiological studies report an association between exposure to biomass smoke and cardiopulmonary morbidity. The mechanisms for this association are unclear. The aim of the present study was to characterise the acute pulmonary and systemic inflammatory effects of exposure to forest fire smoke. Seasonal forest firefighters (n = 52) were recruited before and/or after a day of fire-fighting. Exposure was assessed by questionnaires and measurement of carbon monoxide levels (used to estimate respirable particulate matter exposure). The pulmonary response was assessed by questionnaires, spirometry and sputum induction. Peripheral blood cell counts and inflammatory cytokines were measured to define the systemic response. Estimated respirable particulate matter exposure was high (peak levels >2 mg x m(-3)) during fire-fighting activities. Respiratory symptoms were reported by 65% of the firefighters. The percentage sputum granulocytes increased significantly from 6.5 to 10.9% following fire-fighting shifts, with concurrent increases in circulating white blood cells (5.55x10(9) to 7.06x10(9) cells x L(-1)) and band cells (0.11x10(9) to 0.16x10(9) cells x L(-1)). Serum interleukin (IL)-6, IL-8 and monocyte chemotactic protein-1 levels significantly increased following fire-fighting. There were no changes in band cells, IL-6, and IL-8 following strenuous physical exertion without fire-fighting. There was a significant association between changes in sputum macrophages containing phagocytosed particles and circulating band cells. In conclusion, acute exposure to air pollution from forest fire smoke elicits inflammation within the lungs, as well as a systemic inflammatory response.