Predicting medication nonadherence risk in the Chinese type 2 diabetes mellitus population - establishment of a new risk nomogram model: a retrospective study.

OBJECTIVE: To investigate the risk factors of medication nonadherence in patients with type 2 diabetes mellitus (T2DM) and to establish a risk nomogram model. METHODS: This retrospective study enrolled patients with T2DM, which were divided into two groups based on their scores on the Morisky Medication Adherence scale. Univariate and multivariate logistic regression analyses were used to screen for independent risk factors for medication nonadherence. A risk model was then established using a nomogram. The accuracy of the prediction model was evaluated using centrality measurement index and receiver operating characteristic curves. Internal verification was evaluated using bootstrapping validation. RESULTS: A total of 338 patients with T2DM who included in the analysis. Logistic regression analysis showed that the educational level, monthly per capita income, drug affordability, the number of drugs used, daily doses of drugs and the time spent taking medicine were all independent risk factors for medication nonadherence. Based on these six risk factors, a nomogram model was established to predict the risk of medication nonadherence, which was shown to be very reliable. Bootstrapping validated the nonadherence nomogram model for patients with T2DM. CONCLUSIONS: This nomogram model could be used to evaluate the risks of drug nonadherence in patients with T2DM.

Involvement of miR-199a-3p/DDR1 in vascular endothelial cell senescence in diabetes.

Endothelial cell dysfunction is a prominent feature of diabetic cardiovascular complications, and endothelial cell senescence is considered to be an important contributor to endothelial dysfunction. Discoidin domain receptor 1 (DDR1) has been reported to be involved in atherogenesis and cerebral ischemia/reperfusion injury. In this study, we aimed to explore the role of DDR1 in endothelial cell senescence under diabetic conditions and elucidate the underlying mechanisms. A diabetic rat model was established by a single intraperitoneal injection of streptozocin (STZ) (60 mg/kg), which showed an increase in senescence-associated ß-galactosidase (SA-ß-gal) staining signal of thoracic aortic endothelium, impaired vascular structure and function, accompanied by an up-regulation of DDR1. Next, we verified the role of DDR1 in endothelial senescence and the underlying mechanisms in high glucose-treated human umbilical vein endothelial cells (HUVECs). Consistent with the in vivo findings, high glucose induced endothelial senescence, impaired endothelial function and elevated DDR1 expression, accompanied by the elevation of senescence-related genes p53 and p21 expression, and these effects were reversed by DDR1 siRNA. DDR1 has been documented to be a potential target of miR-199a-3p. Here, we found that miR-199a-3p was down-regulated by high glucose in the aorta tissue and HUVECs, while miR-199a-3p mimic significantly suppressed increased endothelial senescence and elevated DDR1 induced by high glucose. In conclusion, our data demonstrated that miR-199a-3p/DDR1/p53/p21 signaling pathway was involved in endothelial senescence under diabetic conditions, and therapeutic targeting DDR1 would be exploited to inhibit endothelial senescence owing to high glucose exposure.

Asymmetric dimethylarginine: An crucial regulator in tissue fibrosis.

Fibrosis is a reparative process with very few therapeutic options to prevent its progression to organ dysfunction. Chronic fibrotic diseases contribute to an estimated 45% of all death in the industrialized world. Asymmetric dimethylarginine (ADMA), an endothelial nitric oxide synthase inhibitor, plays a crucial role in the pathogenesis of various cardiovascular diseases associated with endothelial dysfunction. Recent reports have focused on ADMA in the pathogenesis of tissue fibrosis. This review discusses the current knowledge about ADMA biology, its association with risk factors of established fibrotic diseases and the potential pathophysiological mechanisms implicating ADMA in the process of tissue fibrosis.

Rapid determination of 1,3-propanediol in fermentation process based on a novel surface-enhanced Raman scattering biosensor.

The production of 1,3-propanediol (1,3-PDO) is an important fermentation process. However, 1,3-PDO could not be distinguished separately and efficiently in fermentations previously because it has a highly similar molecular structure to the feedstock glycerol (GLY) and by-product lactic acid (Lac), which leads to the difficulty of quantification. In this paper, a low-cost and environmentally friendly biosensor based on surface-enhanced Raman scattering (SERS) technique was developed. Using it, the concentration of 1,3-PDO and Lac in a fermentation solution can be determined directly from their respective characteristic peaks in Raman spectroscopy. Moreover, by analyzing the respective contributions of 1,3-PDO, Lac, and GLY to the integrated intensities of the 2920 cm-1 Raman peak common to these three substances, the concentration of GLY could also be quantified. SERS study on various 1,3-PDO:GLY and Lac:GLY molar ratios were conducted to establish the proportional relationships of these compounds by analyzing the relationship between the concentration and the Raman peak intensities. The 1,3-PDO:Lac:GLY with serial concentration gradient was carried out to verify the relationship between the concentration and the Raman peak intensities by the high-performance liquid chromatography (HPLC) with relative deviations <25%. Concentrations of 1,3-PDO and Lac as low as 1 g/L and concentration of GLY as low as 4 g/L were analyzed to determine the limit of detection. Therefore, this new method allows the rapid quantification of 1,3-PDO, Lac and GLY concentrations on a SERS-based biosensor.