Platelet-activating factor(PAF) at different concentrations were added to in vitro cultured bovine=pulmonary artery endothelial cells(BPAEC) when lactate dehydrogenase(LDH) release rate, angiotensin converting enzyme(ACE) activity and malondialdehyde (MDA) content were determined. The influences of specific PAF receptor antagonist on PAF effects and the stimulating effect of PAF on leukocyte-endothelial cell adhesion were also observed. The results showed that when PAF were added to BPAECs, there were no significant change in LDH release rate, ACE activities were only slightly increased. No obvious changes in cellbound MDA, but supernatant MDA content was increased in cells treated with high concentration of PAF (10~(-6)). The PAF receptor antagonist, SRI 63-441 made the cell-bound MDA content higher than that of PAF treated cells, whereas the supernatant MDA became lower. PAF may promote endothelial-leukocyte adhesion either through its effects on endothelial cells or on leukocytes, suggesting that PAF has no obvious damaging effect on endothelial cells but may activate endothelial cells thus promoting endothelialleukocyte adhesion.

Objective To evaluate the effect of perioperative intravenous (Ⅳ) iron sucrose therapy on reducing postsurgical blood transfusion rates in elderly patients with hip fractures.Methods From September 2011 to February 2014,200 patients aged≥65 years with hip fractures were enrolled.The iron sucrose group (n=100) received iron sucrose (600 mg,Ⅳ),while the control group (n=100) did not receive iron sucrose.Postsurgical blood transfusion rates,infection rates,mortality and length of hospital stay were evaluated.Results The difference in blood transfusion rates was significant (25.0％ vs.41.0％,P＜0.05),while differences in infection rates,mortality and length of hospital stay were not significant between the two groups.Conclusions Perioperative Ⅳ iron sucrose can reduce blood transfusion requirements in elderly patients with hip fractures.

A bolus injection of endotoxin and platelet activating factor ( PAF ) via external jugular vein in rats resulted in severe pulmonary edema, accompanied by significant increase in extravascular lung water volume, bronchoalveolar lavage fluid ( BALF ) protein concentration, BALF cell counts and polymorphonuclearcyte percentage. PAF receptor antagonist SRI63-441 showed partial protective effects on endotoxin and PAF induced lung edema and BALF cytological changes.

The effects of hydrogen peroxide (H2O2) on endothelial-polymorphonuclear cells (EC-PMN) adhesion and their mechanisms wsre studied in cultured bovine pulmonary artery endothelial monolayers in vitro. H2O2 at various concentrations (10-1, 10-2, 10-3mol/L respectively) stimulated EC dependent PMN adhesion, of which l02mol/L H2O2 was the most potent one, increasing adhesion to 2.3 times that of the control. Pretreatment of PMNs with SRI 63-441, a platelet-activating factor (PAF) receptor antagonist, had no effect on H2O2 induced EC-PMN adhesion. Pretreatment of ECs with SRI 63-441 before H2O2 exposure significantly decreased PMN adherence to ECs. Pretreatment of ECs with phospholipase A2 inhibitor p-bromophenacyl-bromide or cahnodulin antagonist chlorpromazine and aildum ion chelate EGTA obviously decreased H2O2 induced increment of EC-PMN adhesion. These results suggest that H2O2 may activate ECs, causing the inflow of extracellular calcium or the release of calcium from intracellular deposits. Increased intracellular Ca2+ may bind with calmodulin to activate phospholipase A2 thus initiating PAF synthesis and promoting EC-PMN adhesion.

The understanding of anatomical structures and their adjacent relationship is the founda-tion and key to the development of surgical skills and clinical thinking. In clinical teaching for residents and graduate students , we took the advantage of donor operations in organ transplantation and showed abdominal anal operations anatomical features and relationships through different view angles and compre-hensive ways. This new teaching approach was designed in accordance with processes of organ donation, procurement and back-table operation. The main contents included anatomy of abdominal wall layers, rela-tionships among abdominal organs, locations and courses of important structure, as well as medical human-istic education. In the context of organ donation becoming more and more popular and standardized after the cardiac death of Chinese citizens, this teaching approach is worth exploring.

Intravenous administration of E. coli endotoxin (2mg/kg) caused a persistent increase in platelet activating factor (PAF) contents in arterial blood and bronchoalveolar fluid (BALF). Meanwhile phospholipase A2(PLA2) activity in serum and BALF was elevated and mean arterial blood pressure declined. The total cell number, expecially polymorphonuclear leukocytes and lymphocytes, and protein concentration in BALF were markedly increased 6 h after endotoxin injection. Lung index and extravascular lung water content of endotoxin-treated animals were significantly highter than those of controls. Pretreatment with PAF receptor antagonist SRI 63-441 blocked the increase in PLA, activity and attenuated endotoxin-induced hypotension and acute lung injury. The results suggest that PAF mediates endotoxin-induced lung injury, and leukocyte activation by PAF and the subsequent release of oxygen metabolites and lysoenzymes are important intermediate mechanisms leading to high permeability pulmonary edema.

We established a method to study vascular permeability in vitro on perfused endothelial cell monolayer cultured on micropore filter membrane. It can be used to determine filtration coefficient (Kf) and osmotic reflection coefficient (?) to proteins. Hanks balanced salt solution (HBSS) or 5 g/L albumin in HBSS was used to perfuse confluent endothelial monolayer. Control Kf values were 10.1 ?0.75 and 3.6?0.75?l . min-1 . cm-2 . kPa-1 (n = 3, x?sx) respectively for HBSS and albumin HBSS perfusion, suggesting that albumin may decrease endothelial monolayer permeability to water and small molecules. After exposure of endothelial monolayer to 10-8 mol/L platelet-activating factor (PAF) for 30 min, Kf values increased to 193.1% and 133.3% respectively for HBSS and albumin HBSS perfusion. Protein clearance rate (?l. min-1 . cm-2:) and osmotic reflection coefficient of control endothelial monolayer were 8.0?3.22 and 0. 37?0.09 respectively. In PAF treated endothelial monolayer,they were 12.2 ? 2.95ul min-1 cm 2 and 0.18?0.06, revealing increased permeability to albumin. Computer-assisted image processing demonstrated that PAF treatment decreased cell area while increased cell form factor and intercellular space. The results sug-gest that endothelial cells retracted, rounded and it may be an important mechanism in PAF-induced increased vascular permeability.

Objective To evaluate the protective effect of hydrogen-rich saline on renal ischemia/reperfusion (I/R) in mice. Methods Thirty C57BL/6 mice were randomly divided into 3 groups: sham-operated (SO) group, I/R group (mice were injected with 5 ml/kg saline by tail vein just before ischemia induction) and hydrogen-rich saline group (mice were injected with 5 ml/kg hydrogen-rich saline). At the 6th h after reperfusion, the sera and renal samples subject to IR injury were collected. The Scr and BUN levels in serum were determined and renal histological changes were also examined. The apoptosis of renal tubular epithelial cells was measured by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay. Malondialdehyde (MDA) contents in renal samples were measured using specific kits. The infiltration of F4/80 positive macrophages and neutrophils was assayed by using immunohistochemistry. The mRNA expression of TNF-α, IL-6, IL-1β and IL-17 was detected by using real time reverse transcription PCR. Results As compared with LR group, at the 6th h following reperfusion the levels of Scr and BUN were significantly reduced (P<0.05), histological changes obviously alleviated (P<0.01), apoptosis of renal tubular epithelial cells and MDA contents was decreased (P<0.05) in hydrogen-rich saline group. Moreover, the infiltration of macrophages and neutrophils, and the mRNA expression of TNF-α, IL-6, IL-1β and IL-17 in renal tissue in hydrogen-rich saline group were also declined as compared with IR group (P<0.05). Conclusion Hydrogen-rich saline can ameliorate renal IR injury to some extent, which is associated with inhibition of inflammatory response induced by reperfusion.

Objective To study lymph node micrometastasis in N0 colorectal cancer patients and its clinical significance. Methods In this study, 548 lymph nodes obtained from 62 cases of No colorectal cancer undergoing curative operation were examined by fluorescent quantity polymerase chain reaction assay for the expression of cytokeratin 20 (CK20) mRNA. Results Micrometastasis was detected in 55 lymph nodes (10.0% ) of 24 cases (39%). According to lymph node anatomical locations, micrometastasis was identified in 15. 8%, 5.0% and 3.3% lymph nodes in group Ⅰ ,Ⅱ and Ⅲ (grouped by the distance from the tumor), respectively. Micrometastasis was correlated with invasion depth of primary tumor, but was notrelated to gender, age, tumor size, tumor site and differentiation. Conclusions The expression of CK20mRNA in lymph nodes in patients with No coloreetal cancer could be used to improve the accuracy of clinical staging, and provide information for rational adjuvant therapy.

Objective: To explore the apoptosis-inducing effect of salvianolate on hepatoma SMMC-7721 cells and the underlying mechanism. Methods: SMMC-7721 cells were co-cultured in vitro with different concentrations (0.5, 1, 2 mg/ml) of salvianolate for 24 h. The apoptotic SMMC-7721 cells were examined by flow cytometry, and the changes of mitochondrial transmembrane potential were examined by mitochondrial transmembrane potential JC-1 kit. The activities of caspase-8, caspase-9, and caspase-3 were detected by spectrophotometry in the hepatoma SMMC-7721 cells after co-cultured with 1 mg/ml salvianolate. The changes of apoptotic SMMC-7721 cells induced by salvianolate in the presence or absence of caspase-9 inhibitor or caspase-3 inhibitor were measured by flow cytometry. The expressions of pro-apoptotic protein Bax and anti-apoptotic protein Bcl-2 were detected by Western blotting analysis. Results: Salvianolate significantly induced apoptosis of hepatoma SMMC-7721 cells (P<0.05), and the decline of mitochondrial membrane potential increased with the increase of salvianolate concentration (P<0.05). The activities of caspase-9 and caspase-3, but not caspase-8, were increased in hepatoma cells after treatment with 1 mg/ml salvianolate for 24 h (P<0.05). The apoptosis-inducing effect of salvianolate was significantly decreased in the presence of caspase-9 or caspase-3 inhibitors (P<0.05). Western blotting results showed that salvianolate increased pro-apoptotic protein Bax expression and decreased anti-apoptotic protein Bcl-2 expression. Conclusion: Salvianolate can induce the apoptosis of human hepatoma SMMC-7721 cells in a dose-dependent manner, which is probably mediated by mitochondrial apoptosis pathway.