The psychometric properties of the barriers to insulin treatment questionnaire in Chinese patients with type 2 diabetes mellitus using insulin.

Aim: The objective of this study was to translate the Barriers to Insulin Treatment Questionnaire (BIT) into Chinese and test its psychometric properties in middle-aged and elderly type 2 diabetes mellitus (T2D) patients using insulin in the Han people of urban China. Methods: We established the Barriers to Insulin Treatment Questionnaire in Chinese (BIT-C). We selected 296 patients with T2D for testing BIT-C's the reliability and validity, of which 120 patients were retested four weeks later. Another 200 patients with T2D were selected to perform the confirmatory factor analysis (CFA). Results: The final BIT-C consisted of 11 items (BIT-C-11) and four factors. The explained variances of the BIT-C-11 and its four factors were 90.153%, 51.308%, 18.810%, 10.863%, and 9.173%. CFA validated that the four-factor model fit with the data of the BIT-C-11. Standardized factor loadings ranged between 0.77 and 0.90. The Cronbach's α coefficients of the BIT-C-11 and its four factors were 0.903, 0.952, 0.927, 0.938, and 0.917. Correlation analysis was performed between the BIT-C-11 and General Adherence Scale in Chinese (GAS-C) to calculate the criterion-related validity (r = 0.598, p < 0.001). The correlation coefficient r of the BIT-C-11's test-retest reliability was 0.810 (p < 0.001). Conclusion: The BIT-C-11 has good reliability and validity. It can be used for psychological resistance to insulin therapy studies of middle-aged and elderly patients with T2D using insulin in the Han people of Chinese cities.

Long non-coding RNA (LncRNA) CASC9/microRNA(miR)-590-3p/sine oculis homeobox 1 (SIX1)/NF-κB axis promotes proliferation and migration in breast cancer.

Long non-coding RNA (lncRNA)-microRNA-mRNA signaling axes have recently been shown to have a key role in the development of breast cancer (BC). In this study, we investigated how the cancer susceptibility candidate 9 (CASC9) gene affects the cell growth, invasion, migration, and apoptosis of BC cells. The levels of microRNA-590-3p (miR-590-3p), CASC9, and the sine oculis homeobox 1 (SIX1) gene were determined through qRT-PCR. We conducted cell counting kit-8 (CCK-8) assays to assess cell proliferation, transwell assays to detect cell migration/invasion, and flow cytometry to evaluate cell apoptosis. StarBase v2.0 was used to predict interactions between miR-590-3p and SIX1 or CASC9, and dual-luciferase reporter assays were used to verify these predictions. CASC9 protein was overexpressed in BC cells and tissues, while CASC9 knockdown inhibited BC cell growth, invasion, and migration and promoted apoptosis. Additionally, we verified that CASC9 competes for binding with miR-590-3p. Moreover, SIX1 was determined to be a target of miR-590-3p, and SIX1 expression was inhibited by miR-590-3p overexpression. CASC9 enhanced BC development by downregulating miR-590-3p and upregulating SIX1 during the activation of the NF-κB pathway. These data suggest that the CASC9/miR-590-3p/SIX1/NF-κB axis is involved in breast cancer progression, providing insight into the function of CASC9 in breast cancer development.

Long non-coding RNA CASC9/microRNA-590-3p axis participates in lutein-mediated suppression of breast cancer cell proliferation.

Previous studies have shown that lutein can inhibit the proliferation of breast cancer cells. However, the mechanism of lutein inhibiting the proliferation of breast cancer cells remains unclear. The present study aimed to determine whether the long non-coding RNA (lncRNA) Cancer Susceptibility 9 (CASC9)/microRNA (miR)-590-3p axis participates in the antiproliferative effects of lutein via lncRNA microarray hybridization, reverse transcription-quantitative PCR, dual-luciferase reporter and MTT assays. The results demonstrated that CASC9 was the most significantly downregulated lncRNA in MCF7 cells treated with lutein. miR-590-3p was identified as the target of CASC9. In addition, lutein downregulated CASC9 expression and upregulated miR-590-3p expression in dose- and time-dependent manners, respectively. CASC9 knockdown or overexpression of miR-590-3p inhibited the proliferation of breast cancer cells. Notably, simultaneous transfection with miR-590-3p mimics and CASC9 small interfering RNA increased the potency of lutein in inhibiting the proliferation of breast cancer cells. Taken together, these results suggest that the CASC9/miR-590-3p axis participates in the antiproliferative effects of lutein on breast cancer.

The Psychometric Properties of General Adherence Scale in Chinese (GAS-C) in Patients with Type 2 Diabetes Using Insulin.

PURPOSE: Translate General Adherence Scale (GAS) into Chinese and test its psychometric properties in middle-aged and elderly type 2 diabetes (T2D) patients using insulin in the Han people of urban China. SUBJECTS AND METHODS: We translated the GAS into Chinese and established General Adherence Scale in Chinese (GAS-C). 136 T2D subjects were selected for testing GAS-C's reliability and validity, of which 100 study subjects were retested with GAS-C two weeks later. The other 200 T2D subjects were selected for performing Confirmatory Factor Analysis(CFA). The ceiling effect and floor effect of GAS-C data were checked. RESULTS: No data was lost in our research. In exploratory factor analysis(EFA), the Kaiser-Meyer-Olkin measure of sampling adequacy (KMO) =0.899, Bartlett's Test's χ2=611.821 (df=10 p<0.001). The communalities of the items were between 0.740 and 0.862; The values of Measure of Sampling Adequacy (MSA) were between 0.883 and 0.945. All five items entered the factor analysis process. A common factor was extracted, and it could explain 81.403% of the total variance. CFA validated the.one-factor model was good fits with the data of GAS-C (Ratio of Chi-square to Degrees of Freedom (CMIN/DF)=2.032, Goodness of Fit Index (GFI) =0.981, Comparative Fit Index (CFI) =0.996, Tucker-Lewis Index (TLI) =0.992, Root Mean Square Residual (RMR) =0.011, Root Mean Square Error of Approximation (RMSEA) =0.072). Correlation analysis was performed between GAS-C and MMAS-8 to calculate the criterion-related validity (r=0.542 p<0.001). The internal consistency reliability α=0.942, Intraclass Correlation Coefficient (ICC)= 0.941 (95% CI 0.924-0.955). The correlation coefficient r of the test-retest reliability was 0.772 (p<0.001). Spearman-Brown coefficient of split-half was 0.939. There was no floor effect and ceiling effect on the data. CONCLUSION: GAS-C has good reliability and validity. It can be used for general adherence studies of middle-aged and elderly type 2 diabetic patients using insulin in the Han people of Chinese cities.

Dendrobium candidum protects against diabetic kidney lesions through regulating vascular endothelial growth factor, Glucose Transporter 1, and connective tissue growth factor expression in rats.

Diabetes mellitus (DM) remains a great health problem with approximate 30% of patients with DM eventually suffering from diabetic nephropathy. The search for exogenous protective factors has recently received wide attention. The current study aimed to investigate the protective effects of Dendrobium candidum (DC) on kidneys in diabetic rats. Initially, streptozotocin-induced diabetic rats were established and randomly divided into the model group, DC group (0.2, 0.4, and 0.8 g/kg) and irbesartan group (17.5 mg/kg). The biochemical indexes, pathological changes, and the expressions of vascular endothelial growth factor (VEGF), GLUT-1, and CTGF were examined. It was found that as compared with the model group, the kidney index, serum creatine, blood urea nitrogen, 24-hour urine protein, and VEGF of DC treatment groups were significantly decreased, and pathological changes in kidney were improved in the DC groups and irbesartan group ( P < 0.05 for each parameter). The protein and messenger RNA levels of GLUT-1 and CTGF in treatment groups were significantly lower than those in rats' renal cortex without treatment. Our data suggest that DC may protect the kidneys of diabetic rats via regulating expression of VEGF, GLUT-1, and CTGF.

NrF2/ARE and NF-κB pathway regulation may be the mechanism for lutein inhibition of human breast cancer cell.

AIM: Though lutein can inhibit cancer cell proliferation via alleviating oxidative injury, the molecular mechanisms of lutein involvement in the NrF2/antioxidant response element (ARE) and NF-κB pathways remain poorly understood. MATERIALS & METHODS: MTT, flow cytometry, quantitative real-time PCR (qRT-PCR) and western blot assays were performed. RESULTS: After treatment with lutein, breast cancer cell proliferation was significantly decreased in a dose-dependent manner. Lutein induced nuclear translocation and protein expression of NrF2, improved the expression of cellular antioxidant enzymes and attenuated reactive oxygen species levels. Moreover, lutein treatment decreased NF-κB signaling pathway related NF-κB p65 protein expression. CONCLUSION: The effect of lutein antiproliferation was mediated by activation of the NrF2/ARE pathway, and blocking of the NF-κB signaling pathway.