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Patent ductus arteriosus is the third most common congenital heart disease and resulted from the persistence of ductal patency after birth. Ductus arteriosus closure involves functional and structural remodeling, controlled by many factors. The changes in plasma protein levels associated with PDA closure are not known. Here we for the first time demonstrate six key differential plasma proteins in human patent ductus arteriosus patients using proteomic technology and present a model to illustrate the constriction and closure of ductus arteriosus. Differentially expressed proteins were analyzed by using isobaric tags for relative and absolute quantification and validated by enzyme‐linked immunosorbent assay in new samples. The proteomic data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the data set identifier PXD008568. We found 74 upregulated and 98 downregulated proteins in the plasma of patients with PDA. Five decreased proteins (platelet factor 4, fibrinogen, von Willebrand factor, collagen, and mannose binding lectin‐associated serine protease‐2) and one increased protein (fibronectin) may increase the risk of patent ductus arteriosus. Those proteins are closely related to platelet activation and coagulation cascades, complement mannan‐binding‐lectin, and other systemic signaling pathways. Our findings for the first time indicate that the differential proteins involved in different pathways may play key roles in the nonclosure of the ductus arteriosus in humans and may be developed as biomarkers for diagnosis. All those findings may be served as the basis of understanding the etiology and pathogenesis of patent ductus arteriosus. Ductus arteriosus closure involves functional and structural remodeling, controlled by many factors and we for the first time demonstrate six key differential plasma proteins in human patent ductus arteriosus patients using proteomic technology and present a model to illustrate the constriction and closure of ductus arteriosus. Those proteins are closely related to platelet activation and coagulation cascades, complement mannan‐binding‐lectin, and other systemic signaling pathways. Our findings for the first time indicate that the differential proteins involved in different pathways may play key roles in the nonclosure of the ductus arteriosus in humans and may be developed as biomarkers for diagnosis. All those findings may be served as the basis of understanding the etiology and pathogenesis of patent ductus arteriosus. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate the role of insulin-like growth factor binding protein-related protein 1 ( IGFBP-r P1) in the development of hepatic fibrogenesis in experimental disease models and human liver samples. Methods Cellular distribution patterns of IGFBP-r P1 were assessed by immunohistochemistry in fibrotic and cirrhotic human liver specimens. Gene silencing of IGFBP-r P1 was performed on cultured hepatic stellate cells ( HSCs) by small interfering RNA (si RNA), and the silencing effect was determined by quantitative real-time polymerase chain reaction ( PCR) and Western blot. We also determined the effects of si RNA-mediated gene silencing of IGFBP-r P1 on the production of extracellular matrix ( ECM) components by Western blot. The expression of ECM components and transforming growth factor ( TGF)-β1 was studied by immunohistochemistry and Western blot in C57BL/6 wild-type mice treated with recombinant IGFBP-r P1 (r IGFBP-r P1). Results Expression of IGFBP-r P1 was significantly elevated in fibrotic and cirrhotic human liver specimens, and this increase was positively correlated with the number of collagen fibers observed. si RNA-mediated gene silencing of IGFBP-r P1 resulted in significantly decreased levels of collagen I and fibronectin in HSCs. Moreover, IGFBP-rP1 overexpression significantly increased the production of collagen, fibronectin and TGF-β1 in r IGFBP-r P1-treated mice. Conclusions IGFBP-r P1 contributes to the development of liver fibrosis and may be a novel molecule involved in the progression of hepatic fibrogenesis. [ABSTRACT FROM AUTHOR]

The asymmetric reduction of benzoxazines with trichlorosilane gives the corresponding products (II) with mostly moderate enantioselectivity. [ABSTRACT FROM AUTHOR]

The title compound, [CuCl(C12H8N2)2][SbF6], was synthesized as green block-shaped crystals by the hydro­thermal method. The crystal structure consists of discrete [CuCl(phen)2]+ (phen is 1,10-phenanthroline) and [SbF6]− ions. The Cu atom is coordinated by four N atoms of two 1,10-phenanthroline ligands and by a Cl atom, with a slightly distorted trigonal–bipyramidal stereochemistry. [ABSTRACT FROM AUTHOR]

We have modified the mitral repair technique in infants and small children by using autologous pericardial strips to treat mitral regurgitation resulting from a dilated mitral annulus. Our results demonstrate that this technique maintains stability and flexibility of the mitral annulus and decreases the risk of mitral stenosis., (© 2016 Wiley Periodicals, Inc.)

In the title coordination polymer, [Na(C(4)H(2)N(3)O(4))(H(2)O)(2)](n), the Na(I) atom is six-coordinated by one O atom and one N atom from a 2H-1,2,3-triazole-4-carb-oxy-5-carboxyl-ate ligand and four O atoms from four water mol-ecules, forming a distorted octa-hedal geometry. The Na(I) atoms are bridged by water mol-ecules into a chain structure along [100]. Inter-molecular N-H⋯O, O-H⋯N and O-H⋯O hydrogen bonds connect the chains. An intra-molecular O-H⋯O hydrogen bond between the carboxyl-ate groups is observed.