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Aim: To examine the changes in electrolyte concentrations after addition of zeolite-based hemostat QuikClot in blood and the effects of zeolite on blood coagulation in vitro. Methods: Fresh blood was taken from healthy adult volunteers and sheep, and the electrolyte concentrations in blood were measured using a blood electrolyte analyzer. Zeolite Saline Solution (ZSS) was prepared by addition of 2 g zeolite to 0.9% NaCl solution (4, 8, or 16 mL). The electrolytes in ZSS were measured using inductively coupled plasma atomic emission spectroscopy. The prothrombin time (PT) and activated partial thromboplastin time (APTT) of blood were measured using the test tube method. The activated clotting time (ACT) and clotting rate (CR) of blood were measured with Sonoclot Coagulation and Platelet Function Analyzer. Results: Addition of zeolite (50 and 100 mg) in 2 mL human blood significantly increased Ca 2+ concentration, while Na + and K + concentrations were significantly decreased. Addition of zeolite (50 and 100 mg) in 0.9% NaCl solution (2 mL) caused similar changes in Ca 2+ and Na + concentrations. Si 4+ (0.2434 g/L) and Al 3+ (0.2575 g/L) were detected in ZSS (2 g/8 mL). Addition of ZSS in sheep blood shortened APTT in a concentration dependent manner, without changing PT. ZSS or aqueous solution of CaCl 2 that contained Ca 2+ concentration identical to that of ZSS significantly shortened ACT in human blood without significantly changing CR, and the effect of ZSS on ACT was not significantly different from that of CaCl 2 . Conclusion: Zeolite releases Ca 2+ into blood, thus accelerating the intrinsic pathway of blood coagulation and shortening the clot formation time.

Cell death‐inducing DFF45‐like effector (CIDE) family proteins, including cell death‐inducing DFF45‐like effector A (CIDEA), cell death‐inducing DFF45‐like effector B (CIDEB) and cell death‐inducing DFF45‐like effector C (CIDEC) [fat‐specific protein of 27 kDa in rodent (FSP27) in rodents], were originally identified by their sequence homology to the N‐terminal region of DNA fragmentation factor DFF40/45. Recent reports have revealed that CIDE family proteins play important roles in lipid metabolism. Several studies involving knockdown mice revealed that FSP27 is a lipid droplet‐targeting protein that can promote the formation of lipid droplets. However, the detailed roles of human CIDEC in the differentiation of human adipocytes remain unknown. In the present study, we found that the expression of CIDEC increased during the differentiation of fetal adipose tissues, but decreased during the de‐differentiation of adipocytic tumors, suggesting that the expression of CIDEC should be positively correlated with the differentiation of adipocytes. Furthermore, we verified that human CIDEC was localized on the surface of lipid droplets. Using human primary pre‐adipocytes, we confirmed that the expression of CIDEC was elevated during the differentiation of pre‐adipocytes, and knockdown of CIDEC in human primary pre‐adipocytes resulted in differentiation defects. These data demonstrate that CIDEC is essential for the differentiation of adipose tissue. Together with regulating adipocyte lipid metabolism, CIDEC should be a potential target for regulating adipocyte differentiation and reducing fat cell mass.

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RNPT clearly shows beneficial effects in treating the infected soft tissue blast injury in comparison with the gauze dressing therapy in swine.

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Pericytes play a crucial role in the homeostasis and maturation of newly formed vessels, but their precursor and the process of their differentiation remain unclear. In this study, we show that in vivo, pericytes in human granulation tissue taken from burn patients expressed CD13 and collagen I, which are cell markers of peripheral blood fibrocytes (PBFCs). Mouse PBFCs, ex vivo labeled by PKH-26 and administered intravenously back to mice, formed lumens in the granulation tissue and expressed pericyte marker NG2. Furthermore, in cell culture, human PBFCs in co-culture with human umbilical vascular endothelial cells or human dermal microvascular endothelial cells (HDMECs) expressed pericyte markers desmin and myosin heavy chain of smooth muscle cell, and some migrated to the membrane of human umbilical vascular endothelial cells or HDMECs to form PBFC/vascular endothelial cell clusters, or formed round PBFC only clusters with their nuclei aligned along a circle. The formation of PBFC/vascular endothelial cell clusters and round PBFC clusters were inhibited by an antibody against monocyte chemotactic protein-1. PBFCs cultured with homogenate of granulation tissue also expressed desmin and myosin heavy chain of smooth muscle cell. Our findings support that the PBFC is a precursor of pericytes, the differentiation of PBFCs is induced by vascular endothelial cells in a paracrine fashion.