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BackgroundObesity is regarded as a potential risk factor for atopy. The aim of this study was to assess the associations of obesity with atopic dermatitis, rhinitis, asthma and food allergy in Chinese adults.MethodsTwo hundred and sixty six (266) atopic cases in Harbin, China, were identified according to the current Chinese guidelines for the diagnosis of atopic diseases. All cases had a previous diagnosis of atopic disorders (atopic dermatitis, rhinitis, asthma or food allergy) and were positive in one or more allergen specific IgE tests to 16 common allergens in the region. Each case was individually matched to two healthy controls based on their age, sex, and residential regions. All 532 healthy controls were negative in allergen specific IgE tests. The associations of obesity with four atopic disorders were assessed using a conditional logistic regression method.ResultsObesity was significantly associated with the presence of atopic diseases (OR = 3.2, 95% CI: 1.8, 5.7). Males and females had a similar association (OR = 3.1 for males and 3.2 for females). The associations of obesity with atopic dermatitis (OR = 2.7, 95% CI: 1.2, 6.3) and atopic rhinitis (OR = 3.1, 95% CI: 1.1, 8.7) were statistically significant. Although obesity was positively associated with atopic asthma, this association was not statistically significant (OR = 3.4, 95% CI: 0.6, 19.9). The association between obesity and food allergy was weak and not significant (OR = 1.1, 95% CI: 0.4, 3.7).ConclusionsObesity is positively associated with the presence of atopic diseases in Chinese adults. Specifically, obesity is significantly associated with atopic dermatitis and rhinitis. Our findings warrant further investigation on the causal nature between obesity and atopic diseases and the effect of weight reduction on preventing atopic diseases.

Objective. The aim of this study was to explore the clinical efficacy of conventional heparin anticoagulation in combination with apixaban in the treatment of patients with cerebral venous thrombosis (CVT) and its influence on serum D-dimer (D-D) and fibrinogen (FIB). Methods. One hundred and fifty-seven consecutive CVT patients admitted to our hospital from January 1, 2006, to December 31, 2013, were allocated into two groups according to the different treatment methods, of which 95 cases received standard anticoagulation therapy (standard group (SG)) and the remaining 62 cases were given apixaban therapy (research group (RG)). The curative effects and the changes of coagulation function during the treatment, as well as the incidence of adverse reactions, were analyzed in the two groups. The changes of D-D and FIB levels before treatment and at days 1, 4, and 7 posttreatment were detected. Results. In treatment efficacy, RG was superior to SG. No evident difference was observed in the incidence of adverse events or coagulation function between the two groups. At day 1 posttreatment, D-D level was increased largely in both SG and RG, but the increase was much more significant in RG. However, D-D level was decreased gradually with time in both groups, and the reduction was more notable in RG. The FIB level in SG declined gradually with time after treatment and was higher than that in RG at the same time point. In RG, FIB was decreased gradually at day 1 and day 4 posttreatment, and its level at day 7 posttreatment showed no difference compared with that at day 4 posttreatment. Spearman’s analysis identified that the higher the D-D level or the lower the FIB level at day 1 posttreatment was, the better the treatment efficacy was. After seven-day treatment, the lower the level of D-D and FIB was, the better the therapeutic effect was. Logistic analysis indicated that age, time of diagnosis, deep vein thrombosis (DVT), Glasgow Coma Scale (GCS) score, infection, Apixaban, D-D, and FIB all independently affect the treatment effect of patients. Conclusions. The combined use of Apixaban with heparin is high-performing and safe in the treatment of CVT. The changes of D-D and FIB levels during the treatment are strongly linked to the therapeutic effect, which can be used as plausible evaluation indexes for the efficacy of CVT.

Circular RNAs (circRNAs) function as efficient microRNA (miRNA) sponges that regulate gene expression in the pathogenesis of many human malignancies. However, their roles in cervical adenocarcinoma remain largely unknown. In this study, we aimed to seek novel circRNAs that regulate cervical adenocarcinoma carcinogenesis and to explore their regulatory mechanisms as well as clinical significance. We identified that 24 circRNAs were differentially expressed in cervical adenocarcinoma tissues by RNA sequencing. Among them, circEYA1 was the most significantly downregulated circRNA in cervical adenocarcinoma. In cervical adenocarcinoma cells, circEYA1 overexpression led to suppression of cell viability and colony formation, promotion of apoptosis, and a decrease of the xenograft tumor growth. The mechanism underlying these observations is that circEYA1 functioned as a sponge of miR-582-3p and abrogated its suppression of CXCL14 expression. Consistently, miR-582-3p inhibition phenocopied the biological effects of circEYA1 overexpression in cervical adenocarcinoma cells. Moreover, miR-582-3p overexpression reversed the suppressive behaviors of circEYA1 in vitro and in vivo. In addition, the expression, correlation, and clinical diagnostic value of cir-cEYA1/miR-582-3p/CXCL14 were confirmed in 198 clinical cervical tissue samples. In summary, our findings highlight a novel tumor suppressive role of circEYA1 in cervical adenocarcinoma tumorigenesis and may provide a potential diagnostic marker and therapeutic target for patients with cervical adenocarcinoma.

Autophagy is an important self-adaptive mechanism that is involved in inhibiting reactive oxygen species (ROS) in spinal cord neurons. Pterostilbene, a natural plant extract, has been demonstrated to possess antioxidant effects; however, it has not yet been investigated whether pterostilbene could activate autophagy and protect spinal cord neurons from oxidative stress. In the present study, primary spinal cord neurons of Sprague Dawley rats were cultured. Cell counting kit-8 analysis was used to detect cytotoxicity of pterostilbene. Cells were treated with various doses of pterostilbene for 24 and 48 h, respectively, and H2O2 was used to induce ROS production. Western blot analysis was performed to assess the protein expression of microtubule-associated protein 1 light chain 3 (LC3)-II, Beclin-1, p62, p-p70S6K and p-mechanistic target of rapamycin (mTOR). Furthermore, the green fluorescent protein (GFP)-LC3 assay was used to detect the level of autophagy level and activation mechanism. 2′,7′-Dichlorofluorescin diacetate and MitoSOX Red staining were used to detect ROS production, and Terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling assay was used to analyze apoptosis percentage. ATG5 small interfering (si)RNA transfection was used to analyze the involvement of autophagy. A dose-dependent increase in the expression of LC3-II and Beclin-1, as well as the p62 decline, were observed in the pterostilbene-treated neurons; however, p-p70S6K and p-mTOR expression was inhibited by pterostilbene. Pterostilbene increased the expression of LC3-II in H2O2-treated cells, and GFP-LC3 analysis demonstrated an increased number of autophagosomes. Furthermore, pterostilbene significantly inhibited the ROS production and apoptosis induced by H2O2; however, ATG5 siRNA transfection significantly reversed the protection of pterostilbene. These results indicate that pterostilbene may inhibit the ROS production and apoptosis in spinal cord neurons by activating autophagy via the mTOR signaling pathway.