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The effect of shortening article publication time on the publication cycle, impact factor, contributions, quality control and sustainable development of medical journals was elaborated with some measures proposed for preventing their negative effect.
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Objective To investigate the origin of α-SMA positive cells in the outflow tract ridge of the embyonic mouse heart and to explore the ultrastructure change of the mesenchymal cells during the ridges fusion. Methods Sections of embryonic day 10(E10d) to E14d mouse embryonic hearts were stained by immunohistochemistry assay with monoclonal antibodies against α-smooth muscle actin (α-SMA), α-sarcomeric actin(α-SCA) and in situ hybridization method with PlexinA2 probe. The outflow tract ridges fusion was observed by transmission electron microscopy at E12.5d. Results From E10d to E11d, PlexinA2 positive cells were seen in the neural tube with mesenchymes around it, the aortic sac and aortic arch. These cells also migrated into the outflow tract ridge along the aortic sac wall and part of them expressed α-SMA. At E12d, PlexinA2 was expressed in the spinal ganglia, the pharyngeal mesenchyme, the aorto-pulmonary septum and the ascending aorta and pulmonary trunk. The septum showed α-SMA strongly positive. But only a few of α-SMA positive cells were observed in the ascending aorta and pulmonary trunk. At E12.5d, two clusters of condensed mesenchymal cells in the outflow tract ridges formed and began to express PlexinA2 weakly and α-SMA strongly. When the ridges began to fuse, the endothelial cells formed a cellular seam, which rapidly broke into pieces and disappeared and were replaced by the sparsed mesenchymal cells containing a few of microfilaments. Two clusters of condensed mesenchymal cells gradully moved to merge. It was noted that some mesenchymal cells contained plenty of microfilament bundles, mitochondria and focal contacts between them. Some mesenchymal cells only had a few of microfilaments and plasma membrane fusion was seen between them. Conclusionα-SMA positive cells in the outflow tract cushion may be derived from cardiac neural crest. The endothelial cells might participate in the fusion of the outflow tract ridges by endothelial-mesenchymal transformation. Mesenchymal cells of the condensed cell mass contain plenty of microfilament bundles and focal contacts or membrane fusion, which contribute to the ridges fusion.
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Objective To investigate the effects of Shenyankangfupian on the expression of macrophage migration inhibitory factors(MIF) in children with henoch-schoenlein purpura nephritis(HSPN).Methods Sixty children with HSPN were divided into two groups randomly.Patients in the control group(n=30) receivded routine therapy for 3 months,and those in the treatment group(n=30) receivded routine therapy plus Shenyankangfupian.Clinical symptoms and the MIF variation were assessed.Results Blcod and protein in urine following Shenyankangfupian therapy were markedly reduced in the treatment group (P＜0.05 ).Compared with the control group (0.68 ± 0.23 ) g/24 h,protein in urine in the treatment group (0.31 ± 0.16 ) g/24 h indicated a statistical significance (P＜0.05 );There is also a statistical difference(P＜0.05) in MIF between the treatment group(2.54 ± 1.06) ng/L and the control group(2.97 ± 1.14) ng/L.Conclusion Shenyankangfupian could markedly relieve symptoms in children with HSPN by mitigating the expression of MIF thus reducing protein in urine.
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Objective To investigate the effects and mechanism of trimetazidine dihydrochloride on children with viral myocarditis(VMC). Methods 102 patients with VMC were randomly divided into two groups:patients in control group(n=44) received routine therapy,and patients in treatment group(n=58) received trimetazidine dihy-drockloride with routine therapy for three months. Serum levels of interleukin-18 (IL-18) and tumor necrosis factor (TNF-α) were measured pre- and post- therapy. Results Compared with control group,the serum levels of IL-18 and TNF-α was decreased following trimetazicline dihydrechlofide therapy(P<0.05). Conclusion Trimetazidine di-hydrochloride could retard progression in VMC patients which was achieved through improving serum levels of IL-18 and TNF-α.