Cancer remains to be the second most common cause of death, and its incidence and mortality rates are increasing in China. According to the 2015 National Central Cancer Registry (NCCR) of China, the incidence of bladder cancer and prostate cancer ranked sixth and seventh, respectively, in male cancers. The majority of prostate cancer patients were diagnosed at an advanced stage. Early diagnosis of prostate cancer is the key to improve prostate cancer survival in China. Radical prostatectomy or radical radiotherapy is the main treatment for localized prostate cancer, and a comprehensive therapy based on androgen deprivation therapy is the treatment for advanced disease. The most common histologic types of bladder cancer in China were urothelial carcinoma, followed by adenocarcinoma and squamous carcinoma. The majority of patients were diagnosed using white-light cystoscopy with biopsy. Fluorescence and narrow-band imaging cystoscopy had additional detection rates and are becoming more popular. Following Chinese guidelines, most non-muscle invasive bladder cancer patients were treated with diagnostic transurethral resection and more than half of the muscle invasive bladder cancer patients were treated with radical cystectomy. Due to the increased detection rate of kidney tumors by ultrasound in physical examination, the number of incidentally diagnosed renal cell carcinoma has increased. Localized kidney cancers are more and more often treated by nephron-sparing surgery. Radical nephrectomy is still the main treatment option for patients with locally advanced renal cell carcinoma. Both laparoscopic and robotic-assisted laparoscopic surgeries have been used in big medical centers. Both testicular cancer and penile cancer have lower incidence levels than that in Europe. As we have an enormous population base, the absolute patient number is big. The diagnosis and treatment follows the Chinese guidelines. In China, both medical professionals and public should concern more on the early diagnosis, as there is not enough cancer prevention information available. Urologists should also take a more active role in educating the population.

Aims/hypothesis Although skeletal muscle insulin resistance has been associated with activation of c-Jun N-terminal kinase (JNK), whether increased JNK activity causes insulin resistance in this organ is not clear. In this study we examined the metabolic consequences of isolated JNK phosphorylation in muscle tissue. Methods Plasmids containing genes encoding a wild-type JNK1 (WT-JNK) or a JNK1/JNKK2 fusion protein (rendering JNK constitutively active; CA-Jnk) were electroporated into one tibialis anterior (TA) muscle of C57Bl/6 mice, with the contralateral TA injected with an empty vector (CON) to serve as a within-animal control. Results Overproduction of WT-JNK resulted in a modest (~25%) increase in phosphorylation (Thr183/Tyr185) of JNK, but no differences were observed in Ser307 phosphorylation of insulin receptor substrate 1 (IRS-1) or total IRS-1 protein, nor in insulin-stimulated glucose clearance into the TA muscle when comparing WT-JNK with CON. By contrast, overexpression of CA-Jnk, which markedly increased the phosphorylation of CA-JNK, also increased serine phosphorylation of IRS-1, markedly decreased total IRS-1 protein, and decreased insulin-stimulated phosphorylation of the insulin receptor (Tyr1361) and phosphorylation of Akt at (Ser473 and Thr308) compared with CON. Moreover, overexpression of CA-Jnk decreased insulin-stimulated glucose clearance into the TA muscle compared with CON and these effects were observed without changes in intramuscular lipid species. Conclusions/interpretation Constitutive activation of JNK in skeletal muscle impairs insulin signalling at the level of IRS-1 and Akt, a process which results in the disruption of normal glucose clearance into the muscle.

No abstract

Previous studies indicated that miR-200s participated in IL-6-induced hepatic insulin resistance. However, the role of miR-200s in hepatic lipid accumulation has not been elucidated. Here we found that miR-200b and miR-200c were reduced in the steatotic livers of mice fed a high-fat diet (HFD) and patients with nonalcoholic fatty liver disease. This down-regulation was accompanied by an increase in the expression of lipogenic proteins such as sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FAS). The suppression of miR-200b and miR-200c in Hep1-6 and NCTC1469 hepatocytes enhanced intracellular triglyceride levels, which were associated with increased SREBP-1 and FAS protein levels. In contrast, the over-expression of miR-200b and miR-200c suppressed lipid accumulation and reduced the expression of SREBP1 and FAS in Hep1-6 and NCTC1469 cells transfected with miR-200b or miR-200c mimics. Importantly, the up-regulation of miR-200b and miR-200c could reverse oleic acid/palmitic acid-induced lipid accumulation in hepatocytes. A luciferase reporter assay identified that miR-200b and miR-200c could directly bind the 3′UTR of jun. JUN activated the transcription of srebp1 to increase lipid accumulation. The data also demonstrated that increased miR-200b and miR-200c expression might be associated with sitagliptin-reduced hepatic lipid accumulation in mice fed a HFD. These findings suggest, for the first time, that reduced miR-200b and miR-200c expression contributes to abnormal hepatic lipid accumulation by stimulating JUN expression and activating the transcription of srebp1.

Background: To evaluate the in vitro dose delivery characteristics of approved asthma and chronic obstructive pulmonary disease (COPD) therapies delivered via the ELLIPTA® dry powder inhaler across inhalation endpoints representative of the target patient population, using the Electronic Lung (eLung™) to replicate inhaler-specific patient inhalation profiles that were previously recorded in vivo.Methods: Selected profiles, representative of the range of inhalation endpoints achieved by patients with all severities of asthma and COPD, were replicated using the eLung breathing simulator in conjunction with an oropharyngeal cast. A Next Generation Impactor was coupled to the eLung to determine the aerodynamic particle size distribution of the ex-throat dose (ETD) of asthma and COPD therapies delivered via the ELLIPTA inhaler. Delivered dose (DD), ETD, and fine particle dose (FPD; defined as a mass of active substance less than 5 μm) were determined for fluticasone furoate (FF)/vilanterol (VI) 100/25 μg and 200/25 μg (asthma and COPD), umeclidinium (UMEC)/VI 62.5/25 μg (COPD only), FF 100 μg and 200μg monotherapy (asthma only), and UMEC 62.5 μg monotherapy (COPD only).Results: Inhalation profiles replicated by eLung covered a wide range of peak inspiratory flow rates (41.6–136.9 L/min), pressure drops (1.2–13.8 kPa), and inhaled volumes through the inhaler (0.7–4.2L). DD was consistent across the range of patient representative inhalation parameters for all components (FF, VI, and UMEC) of each therapy assessed; although ETD and FPD were also generally consistent, some small variation was observed. Dose delivery was consistent for each of the components, whether delivered as mono- or combination therapy.Conclusions: The in vitro performance of the ELLIPTA inhaler has been demonstrated for the delivery of FF/VI, UMEC/VI, FF monotherapy, and UMEC monotherapy. Across a range of inspiratory profiles, DD was consistent, while ETD and FPD showed little flow dependency.

Recently, it is implicated that aberrant expression of microRNAs (miRs) is associated with insulin resistance. However, the role of miR‐17 family in hepatic insulin resistance and its underlying mechanisms remain unknown. In this study, we provided mechanistic insight into the effects of miR‐20a‐5p, a member of miR‐17 family, on the regulation of AKT/GSK pathway and glycogenesis in hepatocytes. MiR‐20a‐5p was down‐regulated in the liver of db/db mice, and NCTC1469 cells and Hep1‐6 cells treated with high glucose, accompanied by reduced glycogen content and impaired insulin signalling. Notably, inhibition of miR‐20a‐5p significantly reduced glycogen synthesis and AKT/GSK activation, whereas overexpression of miR‐20a‐5p led to elevated glycogenesis and activated AKT/GSK signalling pathway. In addition, miR‐20a‐5p mimic could reverse high glucose‐induced impaired glycogenesis and AKT/GSK activation in NCTC1469 and Hep1‐6 cells. P63 was identified as a target of miR‐20a‐5p by bioinformatics analysis and luciferase reporter assay. Knockdown of p63 in the NCTC1469 cells and the Hep1‐6 cells by transfecting with siRNA targeting p63 could increase glycogen content and reverse miR‐20a‐5p inhibition‐induced reduced glycogenesis and activation of AKT and GSK, suggesting that p63 participated in miR‐20a‐5p‐mediated glycogenesis in hepatocytes. Moreover, our results indicate that p63 might directly bind to p53, thereby regulating PTEN expression and in turn participating in glycogenesis. In conclusion, we found novel evidence suggesting that as a member of miR‐17 family, miR‐20a‐5p contributes to hepatic glycogen synthesis through targeting p63 to regulate p53 and PTEN expression.

BackgroundHyponatremia (serum sodium concentration < 135 mmol/L) is the most common electrolyte abnormality and is a predictor of the mortality of hospitalized patients in Western countries. However, hyponatremia data are lacking in Asian countries. Here we evaluate the epidemiology and mortality of hyponatremia in general medical hospitalized patients in China.MethodsThis is a cohort study of 154,378 adults who were hospitalized between 2008 and 2012 at a teaching hospital in Beijing. We identified hospital patients with hyponatremia and calculated the prevalence and in-hospital mortality of hyponatremia. We also conducted a comprehensive retrospective review of the medical records of patients who had severe hyponatremia (serum sodium <120 mmol/L) during hospitalization in 2012.ResultsThe overall prevalence of hyponatremia at some point during hospitalization was 17.5% (26,990 patients), but only 0.26% (394 patients) of cases were identified with the diagnostic code of hyponatremia. Hyponatremia was more common in patients with infectious disease, cancer, or cardiovascular disease as the primary reason for hospitalization based on discharge diagnosis, with prevalences of 33.0, 25.9 and 24.9%, respectively. The in-hospital mortality was 0.48% amongst patients without hyponatremia compared to 3.57 and 20.23% in patients with serum sodium levels of 130–134 and <120 mmol/L, resulting in multivariable adjusted odds ratios (ORs) of 4.8 (95% CI 4.3–5.4) and 32.9 (95% CI 25.2–42.3), respectively. The mortality risk increased with increasing severity of hyponatremia in all diagnostic groups. After the multivariate adjustment, only the Charlson Comorbidity Index and age were independently associated with death risk (OR 1.36, 95% CI 1.14–1.64 and OR 1.04, 95% CI 1.00–1.09, respectively) in the patients with severe hyponatremia.ConclusionsHyponatremia is highly prevalent among Chinese hospitalized patients and is associated with increased in-hospital mortality risk. Physicians should raise awareness to improve the prognosis of hyponatremia.Electronic supplementary materialThe online version of this article (10.1186/s12882-017-0744-x) contains supplementary material, which is available to authorized users.

This study revealed that the unmarried female migrant was one of the most vulnerable groups concerning SRH. In some policy reforms, appropriate and cost-effective SRH services should be provided for these migrants.