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ObjectiveThis clinical study was designed to evaluate the efficacy and safety of this therapy in the treatment of respiratory and urinary infections caused by ceftriaxone-resistant bacteria in comparison with the effect of cefoperazone/sulbactam on cefoperazone-resistant bacteria.MethodsA total of 285 patients aged from 18 to 65 years old, with a respiratory or urinary tract bacterial infection, were enrolled into this multicentre, open-label, controlled clinical study, and bacteria that were either ceftriaxone-resistant or cefoperazone-resistant were isolated from the patients, whose condition had not improved after three days of treatment with ceftriaxone or cefoperazone. To be selected for the study, bacterial cultures obtained from the patients had to be positive before enrolment, and all of the isolates were required to be β-lactamase-positive. Of these patients, 253 completed the trial, and 263 were enrolled into the intention-to-treat (ITT) analysis. All of the 285 patients were included in the safety analysis.ResultsThe cure and effective rates were 39.55% and 85.07% in the ceftriaxone/sulbactam group and 36.43% and 79.84% in the cefoperazone/sulbactam group; the bacterial eradication rates were 83.58% and 83.72%; and the adverse-event rates were 7.48% and 7.80%, respectively. There were no significant differences between the two groups (p > 0.05).ConclusionCeftriaxone/sulbactam is as effective and well-tolerated as cefoperazone/sulbactam for the treatment of intermediate and severe bacterial infections caused by resistant strains.

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Objective. Free triiodothyronine (FT3) is an independent risk factor for nonalcoholic fatty liver disease (NAFLD) in patients with euthyroid. However, whether FT3 has an independent effect on NAFLD in a population of type 2 diabetes remains unknown. The purpose of this study was to identify the potential role of FT3 in NAFLD with T2DM. Design. A cross-sectional study. Patient. A total of 859 T2DM patients who met the inclusion criteria were included. There were 506 T2DM patients without NAFLD and 353 T2DM patients with NAFLD. Methods. The independent samples t -test or Wilcoxon rank sum test were used for continuous variables of different distribution types, while the chi-square test was used for categorical variables. Pearson correlation analysis and linear regression were used to analyze the correlation between FT3 and clinical measurements and biochemical indicators. Multivariate logistic regression analysis was used to determine independent predictors. Results. Patients with NAFLD had higher BMI, SBP, and DBP, longer duration of T2DM, and higher islet function index, blood glucose index, liver function index, renal function index, blood lipid index, and FT3. We also found that FT3 was affected by other five indicators, including ALT, CR, GGT, TC, and LDL-C only in the NAFLD group but not in the non-NAFLD group. FT3 was significantly associated with NAFLD in T2DM patients, and the prevalence of NAFLD increased gradually from the lowest FT3 tertile to the highest FT3 tertile ( P   for   trend < 0.001 ). Conclusion. FT3 is independently associated with NAFLD in hospitalized T2DM patients after rigorous adjustment for various metabolic parameters.

Lung cancer is a leading cause of cancer-related morbidity and mortality worldwide. Although there are currently various therapeutic strategies including surgery, chemotherapy and radiotherapy, lung cancer still results in high mortality with a 5-year survival rate of less than 20%. The increasing need for new therapeutic targets and diagnostic/prognostic tools for lung cancer has promoted the demand for a better molecular and mechanistic understanding of its pathobiology. microRNA-30a-3p (miR-30a-3p) was recently recognized to be closely involved in the regulation of cancer cell invasion, migration and proliferation. However, the mechanistic role of miR-30a-3p in regulating the biological behavior of lung cancer, especially lung adenocarcinoma (LADC), is unknown. In the present study, we aimed to confirm the downregulation of miR-30a-3p in LADC tissues, and validate its functional impact on the pathogenesis of LADC via its molecular target, canopy fibroblast growth factor signaling regulator 2 (CNPY2), a known oncogene. Our data confirmed that CNPY2 was upregulated in LADC tissues, and the expression level of CNPY2 was correlated with the clinical outcomes of lung cancer patients. miR-30a-3p was confirmed as a key negative regulator of CNPY2 and reduced miR-30a-3p expression resulted in CNPY2 upregulation in LADC tissues. We then validated the functional outcome of miR-30a-3p in cancer pathobiology by the overexpression of miR-30a-3p in the LADC EKVX cell line. miR-30a-3p overexpression inhibited cancer cell proliferation, invasion and migration, by suppressing CNPY2 expression. In addition, miR-30a-3p inhibited epithelial-mesenchymal transition, a key feature of LADC, via CNPY2 suppression. Taken together, these findings suggest that miR-30a-3p exerts a novel inhibitory role in the pathogenesis of LADC via CNPY2 downregulation, and the miR-30a-3p/CNPY2 pathway is a potential therapeutic target for human LADC.