No abstract

The aim of the study was to evaluate the clinical efficacy of glucagon-like peptide-1 (GLP-1) analogues in children of pre-diabetes to delay or reverse the development of pre-diabetes into the state of diabetes by early intervention. Prospective and randomized controlled clinical trials were performed in 42 cases of newly diagnosed pre-diabetes in children. The sample size was randomly divided into the two groups. The first group included 21 subjects comprising the lifestyle intervention group, i.e., control group, and the second group included 21 subjects comprising the lifestyle intervention+GLP-1 analogues liraglutide group, i.e., observation group. Interventions carried out lasted 3 months. A review of intervention was carried out at 1 month and after 3 months. Medical examinations were carried out at the the time following diagnosis with pre-diabetes and after the intervention of 3 months. The medical test examinations included the fasting blood glucose (FPG), 2-hour postprandial blood glucose (2hPG), detection of glycated hemoglobin A1c (HbA1C), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), body mass index (BMI), insulin resistance (IR) and the islet cell functions. After 1 month of intervention, the observation group exhibited a better control on FPG and 2hPG compared with the control group (P<0.05). After 3 months of the intervention, FPG and 2hPG levels of the observation group were significantly lower than those of the control group (P<0.01). The levels of HbA1C, TC, TG, LDL-C, HDL-C, and BMI of the observation group were statistically better controlled, when compared with the control group after the intervention of 3 months. The IR index of the observation group was significantly decreased compared to that of the control group (P<0.05) and the islet function index of the β-cell of the observation group showed statistically higher values than that of the control group (P<0.05). In conclusion, GLP-1 analogues are a better regulator of blood sugar levels, effectively improve lipid profile, body mass, IR and islet β-cell function. Furthermore, GLP-1 analogues opens up a new way to intervene pre-diabetes in children.

No abstract

No abstract

The REGγ-proteasome serves as a short-cut for the destruction of certain intact mammalian proteins in the absence of ubiquitin-and ATP. The biological roles of the proteasome activator REGγ are not completely understood. Here we demonstrate that REGγ controls degradation of protein kinase A catalytic subunit-α (PKAca) both in primary human umbilical vein endothelial cells (HUVECs) and mouse embryonic fibroblast cells (MEFs). Accumulation of PKAca in REGγ-deficient HUVECs or MEFs results in phosphorylation and nuclear exclusion of the transcription factor FoxO1, indicating that REGγ is involved in preserving FoxO1 transcriptional activity. Consequently, VEGF-induced expression of the FoxO1 responsive genes, VCAM-1 and E-Selectin, was tightly controlled by REGγ in a PKA dependent manner. Functionally, REGγ is crucial for the migration of HUVECs. REGγ−/− mice display compromised VEGF-instigated neovascularization in cornea and aortic ring models. Implanted matrigel plugs containing VEGF in REGγ−/− mice induced fewer capillaries than in REGγ+/+ littermates. Taken together, our study identifies REGγ as a novel angiogenic factor that plays an important role in VEGF-induced expression of VCAM-1 and E-Selectin by antagonizing PKA signaling. Identification of the REGγ–PKA–FoxO1 pathway in endothelial cells (ECs) provides another potential target for therapeutic intervention in vascular diseases.

Cloud detection for ground-based sky images has attracted much attention in cloud-related fields. In this paper, we proposed a cloud detection algorithm that reduced the sunlight interference in the image. The solar location method was introduced to track the sun in the image used for feature calculation, which was suitable for the case where the camera could not be calibrated. Following this, the adjustable red green difference (ARGD) feature using red and green channels was proposed. The red weight in the feature was determined by the layering region division, which classified the degree of sunlight interference in the image, and the sky state, which discriminated whether there was sunlight interference in the image. Finally, a fixed zero threshold was applied to feature images in order to obtain the cloud detection results. Experimental results showed that the proposed algorithm performs better than the other algorithms and can effectively reduce the sunlight interference.

Background LncRNA H19 expression is down-regulated in patients with asthma. The hyperplasia of airway smooth muscle cells (ASMCs) promotes the development of airway remodeling in asthma. Therefore, we attempted to evaluate the regulatory function of H19 in the proliferation and migration of ASMCs. Methods The expressions of H19 and miR-21 were detected using qRT-PCR. PDGF-BB-induced abnormal proliferation and migration of ASMCs was used as the airway remodeling model in vitro. The expressions of H19 and miR-21 were modified by transfection with pcDNA3.1-H19 and miR-21 mimic, respectively. CCK-8 assay, flow cytometry-based cell cycle analysis was conducted to examine the proliferation ability of ASMCs. The migration ability was measured by transwell assay. Dual-luciferase reporter system was carried out to find the potential relationship between miR-21 and H19 or PTEN. Western blot was conducted to detect the expressions of PCNA, MMP-9, α-SMA, PTEN, and the phosphorylation level of Akt. Results LncRNA-H19 expression was decreased and microRNA-21 expression was increased in serum samples of children with asthma and PDGF-BB-stimulated ASMCs. Overexpression of H19 reduced the proliferation and migration ability of ASMCs with PDGF-BB treatment and these changes were reversed by miR-21 mimic. H19 promoted the protein level of PTEN via sponging miR-21. Overexpression of H19 suppressed miR-21-induced phosphorylation of Akt, and the suppression effect of H19 on phosphorylation of Akt was significantly reduced after transfecting shPTEN in ASMCs. Conclusion In this study, overexpression of H19 suppressed the proliferation and migration of ASMCs induced by PDGF-BB via miR-21/PTEN/Akt axis, which could be a potential biomarker and target for treating hyperplasia of airway smooth muscle cells.

No abstract