Increased serum asprosin is correlated with diabetic nephropathy.

OBJECTIVE: The adipokine asprosin, which was recently discovered, facilitates hepatic glucose production. The aim of this study is to see whether serum asprosin concentrations are linked to diabetic nephropathy (DN). METHODS: We performed this investigation in a group of 212 type 2 diabetes (T2DM) patients. These patients were classified into three subgroups: DN0 group (normal to mildly increased), DN1 group (moderately increased), and DN2 group (severely increased) on the basis of urine albumin-to-creatinine ratio (ACR). RESULTS: When compared to the controls, T2DM patients had higher serum asprosin levels. The DN2 group had significantly higher serum asprosin than the DN0 and DN1 groups. Furthermore, the DN1 group had higher serum asprosin than the DN0 group. Serum asprosin was linked to a higher risk of T2DM and DN in a logistic regression analysis. Serum asprosin was found to be positively related with disease duration, systolic blood pressure, blood urea nitrogen, creatinine, uric acid, ACR, calcium channel blockers, and angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker therapy, but negatively related with glomerular filtration rate, metformin, and acarbose therapy. CONCLUSION: Serum asprosin increase with the progression of DN. Serum asprosin is correlated with renal function and ACR.

Association of serum and aqueous humor myonectin concentrations with diabetic retinopathy.

Myonectin, a newly discovered myokine, enhances fatty acid uptake in cultured adipocytes and hepatocytes and suppresses circulating levels of free fatty acids in mice. This study is performed to evaluate the association between serum and aqueous humor myonectin concentrations with diabetic retinopathy (DR). This study was performed in a population of 228 patients with type 2 diabetes (T2DM) and 72 control subjects. Diabetic patients were then divided into T2DM patients without DR, non-proliferative diabetic retinopathy (NPDR) patients, and proliferative diabetic retinopathy (PDR) patients. Serum and aqueous humor myonectin concentrations were significantly lower in the case group than in the control group. PDR patients showed significantly decreased serum and aqueous humor myonectin concentrations than in the other two T2DM patients. In addition, NPDR patients showed significantly lower serum and aqueous humor myonectin concentrations than T2DM patients without DR. Logistic regression analysis demonstrated that serum and aqueous humor myonectin was correlated with a decreased risk of T2DM and DR. Simple linear regression analysis showed that serum myonectin was negatively correlated with duration of disease, body mass index (BMI), and HbA1c. Duration of disease and BMI were still correlated with the serum myonectin after a multiple linear regression analysis. Aqueous humor myonectin was negatively correlated with duration of disease, systolic blood pressure (SBP), and diastolic blood pressure. Duration of disease and SBP was still correlated with the aqueous humor myonectin after a multiple linear regression analysis. Our investigation indicates an inverse association of serum and aqueous humor myonectin with DR.

Identification of an immune-related long noncoding RNA signature that predicts prognosis in breast cancer patients.

Aim: The purpose of this study was to identify an immune-related long noncoding RNA (lncRNA) signature that predicts the prognosis of breast cancer. Materials & methods: The expression profiles of breast cancer were downloaded from The Cancer Genome Atlas. Cox regression analysis was used to identify an immune-related lncRNA signature. Results: The five immune-related lncRNAs could be used to construct a breast cancer survival prognosis model. The receiver operating characteristic curve evaluation found that the accuracy of the model for predicting the 1-, 3- and 5-year prognosis of breast cancer was 0.688, 0.708 and 0.686. Conclusion: This signature may have an important clinical significance for improving predictive results and guiding the treatment of breast cancer patients.

Application of positive behavior management in patients after breast cancer surgery.

BACKGROUND: As a radical treatment, breast cancer surgery has a positive psychological impact on most patients. However, some patients do not have a clear understanding of the disease, which requires a more scientific and comprehensive consideration during clinical intervention and are based on cognition. The positive behavior management model is based on this kind of background-derived new interventions, which can better serve the clinical rehabilitation process of patients. The positive behavior management model based on cognitive architecture is a new type of intervention derived from this background, which can better serve the clinical rehabilitation process of patients. AIM: To analyze the influence of a positive behavior management model based on cognitive framework on the degree of hope and self-efficacy of patients with breast cancer surgery. METHODS: Eighty-four patients with breast cancer who underwent surgical treatment in our hospital from August 2016 to December 2018 were included in the study. The patients were divided into the experimental group (n = 42) and control group (n = 42) by random number table grouping. The control group received traditional nursing intervention, while the experimental group received a positive behavior management model based on cognitive framework based on the traditional intervention of the control group. General Self-efficacy Scale, Herth Hope Scale, Self-Rating Anxiety Scale, Self-Rating Depression Scale and Cancer Patient Specific Scale were used to evaluate the two groups before and 1 wk after intervention. RESULTS: After the intervention, self-efficacy and hope level of the experimental group were significantly higher than those of the control group (P < 0.05). The Self-Rating Anxiety Scale and Self-Rating Depression Scale scores in the experimental group were significantly lower than those in the control group (P < 0.05). There was no significant difference in the quality of life scores between the two groups before intervention (P > 0.05). The quality of life scores in all aspects in the experimental group after intervention were significantly higher than those in the control group (P < 0.05). CONCLUSION: The positive behavior management model based on cognitive framework applied to patients with breast cancer surgery improved hope for treatment and self-efficacy, reduced negative emotion, and improved quality of life.

Correlation between PPAR-α methylation level in peripheral blood and inflammatory factors of NAFLD patients with DM.

The correlation between the methylation levels of peroxisome proliferator-activated receptor-α (PPAR-α) in the peripheral blood and the inflammatory factors associated with non-alcoholic fatty liver disease (NAFLD) patients with diabetes mellitus (DM) was investigated. Thirty-two samples of normal liver tissues (group N) and 35 samples of liver tissues from NAFLD patients with DM (group M) were used for the present study. The levels of alanine transaminase (ALT) and aspartate transaminase (AST) were measured using commercially available kits. The accumulation of lipid droplets and glycogen in the two groups was determined through Oil Red O staining and Sudan III staining. mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-lß (IL-1ß) and IL-6 in liver tissues of groups N and M were detected using reverse transcription-polymerase chain reaction (RT-PCR). In addition, western blotting was used to detect the protein expression of PPAR-α in liver tissues of both groups. The Statistical Product and Service Solutions (SPSS) 17.0 statistical software was used to analyze the expression difference of PPAR-α in liver tissues in the groups. The high levels of ALT and AST indicated severe liver injury in group M. Oil Red O staining and Sudan III staining showed a large number of lipid droplets and glycogen accumulation in the liver of group M patients. RT-PCR showed that the expression of inflammatory factors was extremely high and that the inflammatory injury was severe in the liver of group M patients. Western blotting showed that the expression of PPAR-α in group N was significantly higher than that in group M. ANOVA results showed that the expression of PPAR-α in liver tissues of groups N and M patients were statistically significantly different (P<0.01). Therefore, the abnormal expression of PPAR-α is closely associated with the occurrence and development of NAFLD complicated with DM, and that the abnormal expression of PPAR-α is closely related to inflammatory factors. Results from the present study suggest PPAR-α has important value in the study on NAFLD complicated with DM. The expression of PPAR-α can be used as a new basis for the diagnosis and treatment of NAFLD complicated with DM.

MiR-139-5p protect against myocardial ischemia and reperfusion (I/R) injury by targeting autophagy-related 4D and inhibiting AMPK/mTOR/ULK1 pathway.

This study aimed at investigating the effect and underlying mechanism of miR-139-5p in myocardial ischemia and reperfusion (I/R) injury. A hypoxia/ reoxygenation (H/R) model was established in H9c2 cardiomyocytes. The level of miR-139-5p was detected in H/R-treated cardiomyocytes, and subsequently, the level of miR-139-5p or its target gene autophagy-related 4D (ATG4D) was up- or downregulated. Furthermore, the cell viability, apoptosis, and autophagy, as well as the expression levels of the proteins related to adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/uncoordinated 51-like kinase 1 (ULK1) signaling pathway were determined. The MiR-139-5p was downregulated in H/R-treated cardiomyocytes in comparison to the untreated cells (P < 0.05). H/R treatment significantly decreased the cell viability but increased the cell apoptosis ratio, and autophagy-related proteins levels (P < 0.05). The overexpression of MiR-139-5p significantly promoted cell apoptosis and inhibited cell autophagy induced by H/R (P < 0.05); however, the effects of miR-139-5p on cell apoptosis and cell autophagy were inhibited by its target gene ATG4D (P < 0.05). Furthermore, the upregulated miR-139-5p remarkably inhibited the expression of p-AMPK, p-Raptor, and ULK1, but increased that of p-mTOR (P < 0.05) in H/R-treated cardiomyocytes. The MiR-139-5p has the potential of regulating cell apoptosis and cell autophagy by inhibiting AMPK/mTOR/ULK1 signaling pathway and thereby protecting against myocardial I/R injury.