Project description:Interventions: Experiment Group A:use the ultrasonic surgical systems (Ezisurg Medical Co., Ltd.) in the colorectal surgery;Experiment Group B:use the reusable shear for ultrasonic surgical system (Ezisurg Medical Co., Ltd.) in the colorectal surgery;Control Group:use the Harmonic Ace+7, 5mm Diameter Shears with Advanced Hemostasis (Ethicon Endo-Surgery,LLC) in the colorectal surgery
Primary outcome(s): overall good performance rate
Study Design: Parallel
Project description:As cardiac regeneration requires new coronary vessels, exploring the underlying mechanisms behind revascularization will facilitate the development of regenerative therapies for heart failure. Although multiple tissues and chemokines likely orchestrate coronary formation, the interaction between coronary growth and guidance cues remains unclear. Here, by applying single-cell RNA-sequencing (scRNA-seq) analysis, we examined gene expression in zebrafish epicardial cells during coronary vascularization and identified hapln1a-expressing epicardial cells enriched with vascular-regulating genes. Fluorescence reporter assays indicated hapln1a+ cells not only envelop coronary vessels, but also form cellular shear structures in ahead of coronary tips. Live imaging analyses demonstrated coronary growth along the pre-formed shears, with depletion of hapln1a+ cells blocking this growth. Further, we found hapln1a+ cells also pre-lead coronary tips in the regenerating area and hapln1a+ cell loss inhibits coronary revascularization. To characterize the molecular nature of hapln1a+ cells during coronary growth, we profiled hapln1a+ cells in juvenile and regenerating hearts and detected expression of the cell adhesion and migration regulator serpine1 in hapln1a+ cells adjacent to coronary tips. Pharmacological inhibition of serpine1 function blocked coronary vascularization and revascularization. Altogether, our studies reveal that hapln1a+ cells are required for coronary production during heart morphogenesis and regeneration, by establishing a microenvironment to facilitate guided coronary growth.
Project description:As cardiac regeneration requires new coronary vessels, exploring the underlying mechanisms behind revascularization will facilitate the development of regenerative therapies for heart failure. Although multiple tissues and chemokines likely orchestrate coronary formation, the interaction between coronary growth and guidance cues remains unclear. Here, by applying single-cell RNA-sequencing (scRNA-seq) analysis, we examined gene expression in zebrafish epicardial cells during coronary vascularization and identified hapln1a-expressing epicardial cells enriched with vascular-regulating genes. Fluorescence reporter assays indicated hapln1a+ cells not only envelop coronary vessels, but also form cellular shear structures in ahead of coronary tips. Live imaging analyses demonstrated coronary growth along the pre-formed shears, with depletion of hapln1a+ cells blocking this growth. Further, we found hapln1a+ cells also pre-lead coronary tips in the regenerating area and hapln1a+ cell loss inhibits coronary revascularization. To characterize the molecular nature of hapln1a+ cells during coronary growth, we profiled hapln1a+ cells in juvenile and regenerating hearts and detected expression of the cell adhesion and migration regulator serpine1 in hapln1a+ cells adjacent to coronary tips. Pharmacological inhibition of serpine1 function blocked coronary vascularization and revascularization. Altogether, our studies reveal that hapln1a+ cells are required for coronary production during heart morphogenesis and regeneration, by establishing a microenvironment to facilitate guided coronary growth.
Project description:As cardiac regeneration requires new coronary vessels, exploring the underlying mechanisms behind revascularization will facilitate the development of regenerative therapies for heart failure. Although multiple tissues and chemokines likely orchestrate coronary formation, the interaction between coronary growth and guidance cues remains unclear. Here, by applying single-cell RNA-sequencing (scRNA-seq) analysis, we examined gene expression in zebrafish epicardial cells during coronary vascularization and identified hapln1a-expressing epicardial cells enriched with vascular-regulating genes. Fluorescence reporter assays indicated hapln1a+ cells not only envelop coronary vessels, but also form cellular shear structures in ahead of coronary tips. Live imaging analyses demonstrated coronary growth along the pre-formed shears, with depletion of hapln1a+ cells blocking this growth. Further, we found hapln1a+ cells also pre-lead coronary tips in the regenerating area and hapln1a+ cell loss inhibits coronary revascularization. To characterize the molecular nature of hapln1a+ cells during coronary growth, we profiled hapln1a+ cells in juvenile and regenerating hearts and detected expression of the cell adhesion and migration regulator serpine1 in hapln1a+ cells adjacent to coronary tips. Pharmacological inhibition of serpine1 function blocked coronary vascularization and revascularization. Altogether, our studies reveal that hapln1a+ cells are required for coronary production during heart morphogenesis and regeneration, by establishing a microenvironment to facilitate guided coronary growth.
Project description:Bacteria in nature are widely exposed to differential fluid shears which are often a trigger for phenotypic switches. The latter mediates transcriptional and translation remodeling of cellular metabolism impacting among others virulence, antimicrobial resistance and stress resistance. In this study, we evaluated the role of fluid shear on phenotypic switch in an acute hepatopancreatic necrosis disease (AHPND)-causing Vibrio parahaemolyticus M0904 strain under both in vitro and in vivo conditions. The results showed that V. parahaemolyticus M0904 grown at lower shaking speed (110 min-1 constant agitation, M0904/110), causing low fluid shear, develop cellular aggregates or floccules. These cells increased levan production (as verified by concanavalin binding) and developed differentially stained colonies on Congo Red agar plates and resistance to antibiotics. In addition, the phenotypic switch causes a major shift in the protein secretome. At 120 min-1 (M0904/120), PirA/B toxins are mainly produced, while at 110 min-1 PirA/B toxin production is stopped and an alkaline phosphatase PhoX becomes the dominant protein in the protein secretome. These observations are matched with a very strong reduction in virulence of M0904/110 towards two crustacean larvae, namely Artemia and Macrobrachium. Taken together, our study provides substantial evidence for the existence of two phenotypic forms in AHPND Vibrio parahaemolyticus strains displaying differential phenotypes that could be of interest in understanding the epidemiology of AHPND under aquaculture conditions. It might provide the basis for AHPND control by steering phenotypes.