Objective To determine co-author contribution for a biomedical scientific paper describing collaborative research by an analytical process model.Methods The important features of contribution were identified,categorized and organized into a logical hierarchy consisting of the main dimensions and sub-dimensions.A face-to-face survey was conducted to obtain data about their relative importance from co-authors.Analytical hierarchy process methodology was used to determine the relative important weights from main dimensions and sub-dimensions along with the consistency.Results Among the 5 main dimensions,all authors considered problem statement as the most important with a weight of 0.4355,and considered research design and data analysis taking the 2nd and 3rd positions.Among the 10 sub-dimensions,hypothesis construction,method development,result interpretation,and critical revision of manuscript were considered the most important contributions.Conclusion Analytical hierarchy process effectively supportto establish the co-authors' priorties for a biomedical scientific paper.

Edong Healthcare Group is cited as an example to introduce the founding background, and summarize its successful practices and outcomes in corporate governance, internal operation management mechanism, and optimized resources deployment within the group.Win-win mechanism is proposed as the key to a successful grouping reform, and further experiment with the hierarchical medical system is recommended for deeper reform in building groups of public hospitals.

[ ABSTRACT] Myosin light chain kinase ( MLCK) activates the regulatory light chain of myosin II, and the phos-phorylated myosin light chain leads to actomyosin contractile activity, as well as the cell contraction and increasing intercel-lular gap, which finally results in endothelial barrier dysfunction.MLCK-dependent hyperpermeability occurs in response to multiple cell signaling molecules and signaling pathways, including Ca2+, Src, PKC, NO, cGMP and mitogen activated protein kinases ( MAPK) .In this review, different mechanisms of endothelial hyperpermeability mediated by MLCK are discussed.

Marburg virus (MARV) is a lethal virus that causes fatal hemorrhagic fever.It belongs to the Filoviridae family which also includes Ebola virus.MARV is similar to Ebola virus in structure and infection mechanism.Moreover,the diseases caused by them have similar clinical symptoms.However,researches on MARV are less than those on Ebola virus.In this review,we focus on the viral structure,especially the structure of MARV glycoprotein (GP) which determines its infectivity,functions of MARV GP as well as protective antibodies and vaccines against this protein.

Objective: To explore the effects of hydrogen sulfide (H 2S) on hypoxic pulmonary vascular smooth muscle cell (VSMC) apoptosis in rats. Methods: Twenty four Wistar rats were divided into 3 groups: control group ( n =8), hypoxia group ( n =8), and hypoxia +NaHS group ( n =8). The plasma level of H 2S was determined by methylene blue spectrophotometric method. VSMC apoptosis was measured by terminal deoxynucleotidyl transferase biotin nick end labeling (TUNEL). The protein expressions of Bcl 2, Fas and caspase 3 in pulmonary arteries were detected by immunohistochemical technique. Results: Compared with rats in the control group, the plasma level of H 2S decreased by 36% in rats of hypoxic group . The apoptotic rate per area in VSMCs detected with TUNEL was significantly decreased by 52.9% in rats of hypoxic group . The expressing integral score of Bcl 2 of VSMCs was increased by 123.9%,while Fas protein expression of VSMCs was decreased by 45% and caspase 3 protein expression of VSMCs was not significantly changed in rats of hypoxia group. But compared with rats in the hypoxia group, the plasma level of H 2S increased by 65% in rats of hypoxia+NaHS group. The apoptotic rate in VSMCs of TUNEL was significantly increased by 62.5% in rats of hypoxia+NaHS group. The Bcl 2 protein expression of VSMCs was decreased by 36.4% in rats of hypoxia+NaHS group. The expressing integral scores of Fas and caspase 3 were significantly higher in rats of hypoxia+NaHS group than in those of hypoxia group. Conclusion: Hypoxia decreased the pulmonary artery smooth muscle cell apoptosis. H 2S inhibited Bcl 2 protein expression of VSMCs and activated Fas and caspase-3 protein expressions of VSMCs, and therefore promoted the pulmonary artery smooth muscle cell apoptosis.