BackgroundMicroRNA (miRNA) is a small, non-coding RNA molecule which plays a role in the carcinogenesis and progression of cancers. Abnormal expression of miRNA in plasma has been found in some patients with malignant tumors.Material/MethodsThis study was conducted to investigate the expression of miRNA-30a in plasma of patients with non-small cell lung cancer (NSCLC). The plasma miRNA-30a in 87 patients with NSCLC, 20 patients with benign lung diseases, and 76 healthy subjects were measured by real-time PCR. The diagnostic value of miRNA-30a in NSCLC was evaluated via the ROC curve method.ResultsPlasma miRNA-30a level was significantly higher in the NSCLC group compared with benign control and healthy control groups (P<0.01). No statistically significant difference was found in the expression level of miRNA-30a among various clinical pathologic features in NSCLC. ROC curve analysis showed that the specificity and sensitivity cut-off points were at 61.0% and 84.3% for NSCLC. The specificity and sensitivity values were 54.9% and 94.4%, respectively, in the analysis based on in-patients only.ConclusionsAll these results suggest that plasma miRNA-30a measurement may be a novel and noninvasive method for NSCLC preliminary screening and differential diagnosis.

Foxa2 is a member of the Forkhead family of nuclear transcription factors that is highly expressed in respiratory epithelial cells of the developing and mature lung. Foxa2 is required for normal airway epithelial differentiation, and its deletion causes goblet-cell metaplasia and Th2-mediated pulmonary inflammation during postnatal development. Foxa2 expression is inhibited during aeroallergen sensitization and after stimulation with Th2 cytokines, when its loss is associated with goblet-cell metaplasia. Mechanisms by which Foxa2 controls airway epithelial differentiation and Th2 immunity are incompletely known. During the first 2 weeks after birth, the loss of Foxa2 increases the production of leukotrienes (LTs) and Th2 cytokines in the lungs of Foxa2 gene-targeted mice. Foxa2 expression inhibited 15-lipoxygenase (Alox15) and increased Alox5 transcription, each encoding key lipoxygenases associated with asthma. The inhibition of the cysteinyl LT (CysLT) signaling pathway by montelukast inhibited IL-4, IL-5, eotaxin-2, and regulated upon activation normal T cell expressed and presumably secreted expression in the developing lungs of Foxa2 gene-targeted mice. Montelukast inhibited the expression of genes regulating mucus metaplasia, including Spdef, Muc5ac, Foxa3, and Arg2. Foxa2 plays a cell-autonomous role in the respiratory epithelium, and is required for the suppression of Th2 immunity and mucus metaplasia in the developing lung in a process determined in part by its regulation of the CysLT pathway.

Purpose To investigate the association between urinary complement proteins and renal outcome in biopsy-proven diabetic nephropathy (DN). Methods Untargeted proteomic and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional analyses and targeted proteomic analysis using parallel reaction-monitoring (PRM)-mass spectrometry was performed to determine the abundance of urinary complement proteins in healthy controls, type 2 diabetes mellitus (T2DM) patients, and patients with T2DM and biopsy-proven DN. The abundance of each urinary complement protein was individually included in Cox proportional hazards models for predicting progression to end-stage renal disease (ESRD). Results Untargeted proteomic and functional analysis using the KEGG showed that differentially expressed urinary proteins were primarily associated with the complement and coagulation cascades. Subsequent urinary complement proteins quantification using PRM showed that urinary abundances of C3, C9, and complement factor H (CFAH) correlated negatively with annual estimated glomerular filtration rate (eGFR) decline, while urinary abundances of C5, decay-accelerating factor (DAF), and CD59 correlated positively with annual rate of eGFR decline. Furthermore, higher urinary abundance of CFAH and lower urinary abundance of DAF were independently associated with greater risk of progression to ESRD. Urinary abundance of CFAH and DAF had a larger area under the curve (AUC) than that of eGFR, proteinuria, or any pathological parameter. Moreover, the model that included CFAH or DAF had a larger AUC than that with only clinical or pathological parameters. Conclusion Urinary abundance of complement proteins was significantly associated with ESRD in patients with T2DM and biopsy-proven DN, indicating that therapeutically targeting the complement pathway may alleviate progression of DN.

Introduction We aimed to confirm the association between some single nucleotide polymorphisms (SNPs) and metabolic dysfunction‐associated fatty liver disease (MAFLD) in western China. Methods A total of 286 cases and 250 healthy controls were enrolled in our study. All samples were genotyped for patatin‐like phospholipase domain containing 3 ( PNPLA3 ) rs738409, transmembrane 6 superfamily member 2 ( TM6SF2 ) rs58542926, membrane‐bound O‐acyltransferase domain containing 7 ( MBOAT7 ) rs641738, glucokinase regulator ( GCKR ) rs1260326 and rs780094, and GATA zinc finger domain containing 2A ( GATAD2A ) rs4808199. Using logistic regression analysis, we evaluated the association between MAFLD and each SNP under different models. Multiple linear regression was used to find the association between SNPs and laboratory characteristics. Multifactor dimensionality reduction was applied to test SNP–SNP interactions. Results The recessive model and additive model of PNPLA3 rs738409 variant were related to MAFLD (odds ratio [OR] = 1.791 and 1.377, respectively, p = 0.038 and 0.027, respectively). However, after Benjamini‐Hochberg adjustment for multiple tests, all associations were no longer statistically significant. PNPLA3 rs738409 correlated with AST levels. GCKR rs780094 and rs1260326 negatively correlated with serum glucose but positively correlated with triglycerides in MAFLD. Based on MDR analysis, the best single‐locus and multilocus models for MAFLD risk were rs738409 and six‐locus models, respectively. Conclusions In the Han population in western China, no association was found between these SNPs and the risk of MAFLD. PNPLA3 rs738409 was associated with aspartate aminotransferase levels in MAFLD patients. GCKR variants were associated with increased triglyceride levels and reduced serum fasting glucose in patients with MAFLD.

Background As one of the challenges of aging, older adults with disabilities are often overlooked in remote areas of many developing countries, including southwest China. Similar populations would undoubtedly benefit from a representative, high-quality survey of large samples, which would also enrich global disability data. This study aims to assess the prevalence of disability and associated factors among urban and rural older adults in a typical representative region. Method A large-scale baseline survey was conducted between March and September 2020 using face-to-face interviews with a multistage stratified random sample of 16,536 participants aged ≥ 60 years. Disability was assessed using the BI scale, with a score of 100 representing normal status, 65–95 as mild disability, 45–60 as moderate disability, and 0–40 as severe disability. The prevalence of disability was estimated by demographics and health characteristics, and their associations were explored by robust Poisson regression analysis. Results The prevalence of disability among older adults was 19.4%, and the prevalence of mild, moderate, and severe disability was 16.8%, 1.5%, and 1.1%, respectively. All variables, including older age, residence in a rural area, higher number of hospitalizations, comorbidities, poor self-rated health, falls, cognitive impairment, mental impairment, and alienation from friends and relatives, were shown to be associated with a higher adjusted prevalence of disability. Only formal education can reduce the risk of disability. Conclusion The prevalence of disability among older adults is high in both urban and rural settings in southwest China, and a number of important factors associated with disability have been identified. In addition to increased attention to the health status of older adults, further research on scientific management and effective disability interventions is needed.

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Background: Hyperuricemia is involved in the risk of chronic kidney disease (CKD). However, whether urate-lowering therapy (ULT) can influence the progression of kidney function in patients with asymptomatic hyperuricemia is still controversial. We conducted a systematic review and meta-analysis to evaluate the effect of ULT on the progression of kidney function in asymptomatic hyperuricemia patients.Methods: The MEDLINE, EMBASE and Cochrane databases were searched without language, national or ethnic restrictions for randomized controlled trials published prior to November 30, 2020, that compared ULT with controlled therapy in patients with asymptomatic hyperuricemia.Results: Eleven studies were included for qualitative synthesis. ULT did not ameliorate eGFR slopes (WMD 0.36 ml/min/1.73 m2 per year, 95% CI: −0.31, 1.04), or lead to reductions in kidney events (RR 1.26; 95% CI: 0.80, 2.00) or all-cause mortality (RR 1.00; 95% CI: 0.65, 1.55), although ULT resulted in a decrease in serum uric acid levels (WMD −2.73 mg/dl; 95% CI: −3.18, −2.28) and lowered the incidence of gout episodes (0.9 vs 2.7%, RR 0.38; 95% CI: 0.17, 0.86).Conclusion: In patients with asymptomatic hyperuricemia, ULT did not decay the progression of kidney function. Long-term and larger sample studies are needed to verify the results.Systematic Review Registration: [www.crd.york.ac.uk/PROSPERO/#recordDetails], identifier [CRD42020204482].

MicroRNA-10b may promote proliferation and invasion of 95-C cells by down regulating the expression of KLF4 protein.