Identification and Validation of Novel Biomarkers Related to the Calcium Metabolism Pathway in Hypertension Patients Based on Comprehensive Bioinformatics Methods

Background: Hypertension is a universal risk factor for cardiovascular diseases and is thus the leading cause of death worldwide. The identification of novel prognostic and pathogenesis biomarkers plays a key role in disease management. Methods: The GSE145854 and GSE164494 datasets were downloaded from the Gene Expression Omnibus (GEO) database and used for screening and validating hypertension signature genes, respectively. Gene Ontology (GO) enrichment analysis was performed on the differentially expressed genes (DEGs) related to calcium ion metabolism in patients with hypertension. The core genes related to immune infiltration were analyzed and screened, and the activity of the signature genes and related pathways was quantified using gene set enrichment analysis (GSEA). The infiltration of immune cells in the blood samples was analyzed, and the DEGs that were abnormally expressed in the clinical blood samples of patients with hypertension were verified via RT-qPCR. Results: A total of 176 DEGs were screened. GO showed that DEGs was involved in the regulation of calcium ion metabolism in biological processes (BP), actin mediated cell contraction, negative regulation of cell movement, and calcium ion transmembrane transport, and in the regulation of protease activity in molecular functions (MF). KEGG analysis revealed that the DEGs were involved mainly in the cGMP-PKG signaling pathway, ubiquitin-protein transferase, tight junction-associated proteins, and the regulation of myocardial cells. MF analysis revealed the immune infiltration function of the cells. RT-qPCR revealed that the expression of Cacna1d, Serpine1, Slc8a3, and Trpc4 was up regulated in hypertension, the expression of Myoz2 and Slc25a23 was down regulated. Conclusion: Cacna1d, Serpine1, Slc8a3, Trpc4, Myoz2 and Slc25a23 may be involved in the regulation of calcium metabolism pathways and play key roles in hypertension. These differentially expressed calcium metabolism-related genes may serve as prognostic markers of hypertension.

Healing time, calcium and phosphorus contents as well as bone metabolism evaluation after Xianling Gubao-assisted surgical treatment of Colles fracture in elderly women

Objective:To study the effect of Xianling Gubao-assisted surgical treatment on postoperative healing, calcium and phosphorus contents as well as bone metabolism in elderly women with Colles fracture.Methods:A total of 96 elderly female patients with Colles fracture treated in our hospital between June 2013 and December 2015 were selected and randomly divided into two groups, the observation group of patients received Xianling Gubao capsule combined with manual reduction and plaster external fixation therapy, and control group of patients only received reduction and external fixation therapy. The fracture healing time was followed up after treatment, and 3 months after treatment, serum was collected to determine the content of calcium-phosphorus metabolism indexes and bone metabolism indexes.Results:The fracture healing time of observation group was significantly shorter than that of control group;1 month and 3 months after treatment, serum Ca, P, ALP, IGF-1, PDGF, BGP and PICP levels of both groups were significantly higher than those before treatment while CTX-1, tPINP and TRACP-5b levels were significantly lower than those before treatment;serum Ca, P, ALP, IGF-1, PDGF, BGP and PICP levels of observation group after treatment were significantly higher than those of control group while CTX-1, tPINP and TRACP-5b levels were significantly lower than those of control group.Conclusion:Adjuvant Xianling Gubao capsule therapy can promote the Colles fracture healing in elderly women, also improve calcium-phosphorus metabolism, promote bone formation and inhibit bone resorption.

MiR-122 in hepatic function and liver diseases

As the most abundant liver-specific microRNA,mi-croRNA-122(miR-122)is involved in various physio-logical processes in hepatic function as well as in liver pathology.There is now compelling evidence that miR-122,as a regulator of gene networks and pathways in hepatocytes,plays a central role in diverse aspects of hepatic function and in the progress of liver diseases.This liver-enriched transcription factors-regulated miRNA promotes differentiation of hepatocytes and regulates lipid metabolism.With regard to liver diseases,miR-122 was shown to stimulate hepatitis C virus(HCV)replication through a unique and unusual interaction with two binding sites in the 5′-UTR of HCV genome to mediate the stability of the viral RNA,whereas inhibit the expression and replication of hepatitis B virus(HBV)by a miR-122-cylin G1/p53-HBV enhancer regulatory pathway.In addition,miR-122 acts as a suppressor of cell prolif-eration and malignant transformation of hepatocytes with remarkable tumor inhibition activity.Notably,a clinical trial targeting miR-122 with the anti-miR-122 oli-gonucleotides miravirsen,the first miRNA targeted drug,has been initiated for treatment of HCV infection.With further understanding of the comprehensive roles of miR-122 in hepatic functions and the mechanisms in-volved in miR-122 down-regulation in chronic hepatitis or hepatocellular carcinoma,miR-122 appears to be a promising candidate for effective therapeutic ap-proaches against tumor and infectious diseases.

Design of tandem genes cluster for isoflavone engineering

In this paper,a universal effective novel method of constructing tandem genes cluster for isoflavone engineering was reported.A tandem genes cluster CHS-CHI-IFS(rIFS)of secondary metabolites of plant isoflavones was constructed by using the chalcone synthase(CHS),chalcone isomerase(CHI),and isoflavone synthase(IFS)(GenBank accession numbers EU526827,EU526829,EU526830)in only one recombination with the pET22b vector.The resulting expression vector pET-rIFS was heterogeneously expressed and co-incubated with barrenwort extractions,and the genistein-like com-ponent was detected.