In the present investigation the structural proteins associated with MAC-1 bacteriophage have been characterized using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE);tandem mass spectrometry of p...In the present investigation the structural proteins associated with MAC-1 bacteriophage have been characterized using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE);tandem mass spectrometry of protein bands from SDS-PAGE gel;from the open reading frames (ORFs) deduced from MAC-1 genome sequence and amino acid sequence homology searches from the Uniprot database (up000002418). Results have led to the identification of at least three structural proteins associated with MAC-1 phage genome. They are: capsid protein (~55,000-daltons);spike protein (~22,000-daltons) and a low molecular weight DNA binding protein (~4000-dal- tons). In addition, two other minor proteins were tentatively identified as replicative and scaffold proteins based on two to three unique peptides from mass spectrometry data. However, other proteins coded (ORFs) by phage genome remain to be identified.展开更多
AIM： To investigate the role of intercellular adhesion molecule-1 （ICAM-1） and its counter receptors LFA-1 and Mac-1 in acute pancreatitis （AP）. METHODS： SD rats were allocated to AP group and control group rand...AIM： To investigate the role of intercellular adhesion molecule-1 （ICAM-1） and its counter receptors LFA-1 and Mac-1 in acute pancreatitis （AP）. METHODS： SD rats were allocated to AP group and control group randomly （25 rats each）. AP was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct. The rats were sacrificed at 1, 3, 6, 12 and 24 h after induction of pancreatitis. Five rats were sacrificed at one time point in the two groups before the blood and specimens from pancreas and lung were obtained. Serum amylase and ascitic fluid were measured at each time point. Expression of ICAM-1 at different time points was assessed by immunohistochemistry in pancreas and lung, and the expression of LAF-1 and Mac-1 on neutrophils at different time points was detected by flow cytometer. RESULTS： Induction of AP was confirmed by the serum levels of amylase and histological studies. The expression of ICAM-1 in pancreas increased significantly than that in the control group at all time points （P 〈 0.05 orP 〈 0.01）, as well as the expression in lung except at 1 h. The expression of LFA-1 and Mac-1 on neutrophil in blood increased significantly in AP group than that in control group at several time points （P 〈 0.05 or P 〈 0.01）. The amount of ascitic fluid and serum amylase level of AP group increased significantly than that of control group at all time points （P 〈 0.05 or P 〈 0.01）. Parallel to these results, a significant neutrophil infiltration was found in pancreas and lung tissues of AP group rats. CONCLUSION： Our findings suggest the important role for ICAM-1, LFA-1 and Mac-1 in mediating the development of AP from a local disease to a systemic illness. Upregulation of ICAM-1, LFA-1, Mac-1 and subsequent leukocyte infiltration appear to be significant events of pancreatic and pulmonary injuries in AP.展开更多
文摘In the present investigation the structural proteins associated with MAC-1 bacteriophage have been characterized using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE);tandem mass spectrometry of protein bands from SDS-PAGE gel;from the open reading frames (ORFs) deduced from MAC-1 genome sequence and amino acid sequence homology searches from the Uniprot database (up000002418). Results have led to the identification of at least three structural proteins associated with MAC-1 phage genome. They are: capsid protein (~55,000-daltons);spike protein (~22,000-daltons) and a low molecular weight DNA binding protein (~4000-dal- tons). In addition, two other minor proteins were tentatively identified as replicative and scaffold proteins based on two to three unique peptides from mass spectrometry data. However, other proteins coded (ORFs) by phage genome remain to be identified.
文摘AIM： To investigate the role of intercellular adhesion molecule-1 （ICAM-1） and its counter receptors LFA-1 and Mac-1 in acute pancreatitis （AP）. METHODS： SD rats were allocated to AP group and control group randomly （25 rats each）. AP was induced by infusion of 5% chenodeoxycholic acid into the pancreatic duct, followed by ligation of pancreatic duct. The rats were sacrificed at 1, 3, 6, 12 and 24 h after induction of pancreatitis. Five rats were sacrificed at one time point in the two groups before the blood and specimens from pancreas and lung were obtained. Serum amylase and ascitic fluid were measured at each time point. Expression of ICAM-1 at different time points was assessed by immunohistochemistry in pancreas and lung, and the expression of LAF-1 and Mac-1 on neutrophils at different time points was detected by flow cytometer. RESULTS： Induction of AP was confirmed by the serum levels of amylase and histological studies. The expression of ICAM-1 in pancreas increased significantly than that in the control group at all time points （P 〈 0.05 orP 〈 0.01）, as well as the expression in lung except at 1 h. The expression of LFA-1 and Mac-1 on neutrophil in blood increased significantly in AP group than that in control group at several time points （P 〈 0.05 or P 〈 0.01）. The amount of ascitic fluid and serum amylase level of AP group increased significantly than that of control group at all time points （P 〈 0.05 or P 〈 0.01）. Parallel to these results, a significant neutrophil infiltration was found in pancreas and lung tissues of AP group rats. CONCLUSION： Our findings suggest the important role for ICAM-1, LFA-1 and Mac-1 in mediating the development of AP from a local disease to a systemic illness. Upregulation of ICAM-1, LFA-1, Mac-1 and subsequent leukocyte infiltration appear to be significant events of pancreatic and pulmonary injuries in AP.
