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Temsirolimus acts as a mammalian target of rapamycin (mTOR)-dependent autophagic inhibitor. In order to clarify its effects and mechanisms on human salivary adenoid cystic carcinoma (ACC), we examined whether temsirolimus induced autophagy as the mTOR inhibitor in ACC, both in vitro and in vivo. In this study, MTT assay showed that the inhibition effect of temsirolimus assumed an obvious dose-response relationship on ACC-M cells, and the 50% inhibitory concentration (IC(50)) approached 20 μmol/l; numerous autophagosomes were observed by the transmission electron microscopy (TEM) in temsirolimus treatment groups; notably, expression of LC3 and Beclin1 was significantly up-regulated by temsirolimus. More importantly, the xenograft model provided further evidence of temsirolimus-induced autophagy in vivo by inhibiting mTOR activation as well as up-regulation the expression of Beclin1. These results suggest that temsirolimus could act as an mTOR inhibitor to induce autophagy in adenoid cystic carcinoma both in vitro and in vivo.

Ischemia-reperfusion (I/R) injury may influence graft function following transplantation. Ulinastatin, a urinary trypsin inhibitor has been shown to attenuate I/R injury in various organs such as intestine, heart, and kidney in animals. The present experiment was designed to evaluate the effect of pretreatment with ulinastatin on I/R-induced lung injury.After establishing a constant left lung warm ischemia-reperfusion model in rats, 45 animals were randomly divided into three experimental groups: sham group (n = 15), IR group (n = 15), and ulinastatin (5000 U/kg pre-ischemia) + IR group (n = 15). The lung injury was evaluated by tissue myeloperoxidase activity, with simultaneous estimation of the serum concentration of TNFalpha.The ulinastatin-pretreated animals exhibited markedly decreased lung tissue myeloperoxidase activity (P.05). Blood gas analysis demonstrated, that the treated animals had significantly ameliorated pulmonary oxygenation (P.05). The serum concentration of TNF-alpha in the ulinastatin-pretreated group was markedly decreased compared with that of the I/R group (P.05).Ulinastatin attenuated I/R-induced lung injury. This function is partly related to the capacity of the agent to inhibit myeloperoxidase activity in lung tissue and decrease systemic expression to TNF-alpha.

Background Endothelial progenitor cells (EPCs) are involved in endothelium repair of acute lung injury (ALI). Numerous studies have demonstrated that statins can promote EPC function in vitro and in vivo; therefore, the purpose of this study was to determine whether simvastatin enhances the function of EPCs participating in the repair of ALI. Methods BALB/C mice were initially pretreated with simvastatin by intraperitoneal administration 24 h before, and again at the time of, intratracheal instillation of lipopolysaccharide (LPS) and subsequently treated with EPCs by IV transplantation 2 h later. The effects of capillary permeability, endothelium repair, and inflammatory cytokines were measured. Results This study revealed that both simvastatin administration and EPC transplantation can reduce the severity of LPS-induced ALI in mice, and the effect can be further improved by combining the two therapies. Conclusions The administration of simvastatin and EPC transplantation can reduce the severity of LPS-induced ALI in mice, and improvement is moderately enhanced in some respects when EPC transplantation is combined with simvastatin administration. The beneficial role of simvastatin on EPCs may be a component of its pleiotropic effects. Although the exact mechanism remains unknown, the combined administration of simvastatin and EPC transplantation may be a potentially important, cell-based, inflammation-mediated therapy for patients with ALI/ARDS.

Insect movement behavior is highly important in entomological population ecology, behavioral ecology and conservation, and in invasion ecology. In this study, we used an exotic lace bug (Corythucha ciliata) as a model organism to address the hypothesis that an insect species invading a new area has a high host location ability and rapid mobility by which it can be successfully carried to a new habitat. To test this hypothesis, three movement parameters (speed, duration and distance) of C. ciliata were assessed using laboratory and field observations. We found that 5th-instar nymphs of C. ciliata could move as far as 750 cm throughout their lifespan and that they moved an average of 0.038 m/min during the first 15 minutes after release, which was significantly farther than that of other instars. Of the tested nymphs, 21.85% could locate their host trees; of adults released 20 m from hosts, 11% reached the host trees on the first day, with an average flight distance of 22.14 m and a maximum flight distance of 27 m. The results of this study partly explain the mechanism of rapid diffusion. These results are also important for predicting population spread, improving eradication surveys, and managing future introductions of C. ciliata.

Objective: Acute lung injury is a common complication after cardiopulmonary bypass (CPB). Oxidative damage greatly impacts CPB-induced lung ischemic pathogenesis and may represent a target for treatment. We aimed to investigate whether curcumin upregulates heme oxygenase 1 (HO-1) expression and ameliorates lung injury in a rat CPB model. Methods: A total of 80 male Sprague-Dawley rats were divided into 2 sets of 5 groups (n = 8 per group): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 hours prior to CPB. Lung tissue, serum, and bronchoalveolar lavage fluid was harvested 2 or 24 hours postoperatively. In the control group, CPB-induced lung injury was confirmed by histopathologic examination and a significantly increased wet-to-dry lung weight ratio and pulmonary permeability index value was observed ( P < .05 vs sham group). Cardiopulmonary bypass was associated with a marked rise in the level of malondialdehyde and myeloperoxidase and a fall in superoxide dismutase 2 and 24 hours after surgery ( P < .05 vs sham group). Administration of curcumin ameliorated lung damage and reversed the oxidative stress markers in a partially dose-dependent manner ( P < .05 vs vehicle group). Furthermore, HO-1 gene transcription and protein expression were elevated to a greater extent in the lungs after curcumin pretreatment compared with the vehicle pretreatment. Conclusions: Curcumin has the potential to provide protection from CPB-induced lung damage reflected in the expression of oxidative stress markers. The antioxidant effect of curcumin may be partly related to upregulation of HO-1.

Inflammation has been implicated as a contributing factor in the development of abdominal aortic aneurysms (AAA). Quercetin, a natural flavonoid with anti-inflammatory properties, is known for its beneficial effects on vascular disease. In this study, we examined the effects of quercetin to inflammatory cell infiltration, subsequent expression of cytokines and activation of proteases on the expansion of experimental AAA. Aneurysms were induced by abluminal application of calcium chloride in C57/BL6 mice. Quercetin (60 mg/kg) was administered once daily by gavage beginning 2 weeks before AAA induction and continuing for 8 weeks. Mice treated with quercetin exhibited a 32.7% reduction in aortic size compared with vehicle-treated controls. Prevention of AAA was associated with preservation of medial structure, as well as a relative reduction in macrophage and CD3(+) T cell infiltration in aortic tissue, inflammatory cytokines release and nuclear factor κB activation. Quercetin also reduced the expression of matrix metalloproteinase (MMP)-2, MMP-9, cathepsin B, and cathepsin K in aortic tissue. In addition, quercetin treatment increased tissue inhibitors of metalloproteinases (TIMP)-1 gene expression. These data indicate that quercetin may be useful for the prevention and treatment of AAA via blocking the inflammatory response and inhibiting the proteases involved in the pathogenesis of this disease.

Acute renal injury is one of the most frequent complications after cardiopulmonary bypass (CPB). This study was designed to evaluate the potential protective effect of erythropoietin (EPO) on CPB-induced renal injury in a rat model. Male Sprague-Dawley rats were randomly divided into three groups, sham-operated group (sham), control CPB group (control), erythropoietin CPB group (EPO). Blood samples were collected at the beginning, at the end of CPB, and at 0.5, 1, 2 and 24 h post-operation, and the kidneys were harvested 24 h postoperatively and observed by optical microscopy. Levels of serum creatinine (Cr) and blood urea nitrogen (BUN) were assayed. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6(IL-6) levels in the renal tissues were evaluated by the method of enzyme linked immunosorbent assay (ELISA). Protein and mRNA levels of nuclear factor kappa B p65 (NF-κB p65), intercellular adhesion molecule-1 (ICAM-1) were also determined using western blot and real-time PCR respectively. Serum Cr and BUN levels as well as TNF-α, IL-1β and IL-6 levels in renal tissues in control group were significantly higher than those in the sham group. However, the levels of above biomarkers were markedly decreased in EPO group when comparing with control group. Furthermore, NF-κB p65, ICAM-1 protein and mRNA expression were significantly down-regulated in EPO group comparing with control group. In addition, microscopic examinations revealed that histological injury was alleviated when treated with EPO. The results indicated that EPO potently protected against CPB-induced acute renal injury and inhibited expression of NF-κB p65 and inflammatory response.

In this paper, a new stochastic model based on cellular automata is established to simulate the occurrence and development of Schistosoma japonicum (S. japonicum) infection in an endemic population. We included the process of the pathogen invasion from exposure to worm development and till worm death when the infection is cleared in the model. We further utilized the model to predict the prevalence as the outcomes of the selected chemotherapy carried out in Jiahu village. Comparing model predicted prevalence and intensities with the observed parameters, it is anticipated that our cellular automaton transmission model can serve as a tool for studying schistosomiasis transmission dynamics in endemic areas.

Background Temporarily pulmonary hilum clamping is available for the trauma surgeon to deal with serious pulmonary injuries, but the physiologic influence needs further evaluation. This study was to establish a temporary pulmonary hilum clamping model for thoracic damage-control surgery and determine the safety time latitude of this manipulation. Methods After anesthetized and catheter instrumented, the left pulmonary hilus of pigs were clamped with a urethral catheter after thoracotomy maintained for three different time period, 90 minutes (C90), 120 minutes (C120), and 150 minutes (C150), and then unclamped. Hemodynamic data were recorded and serum samples were collected for d-dimer detection and other hematology analysis, as well as 1 cm3 pulmonary tissue was obtained for histologic study before clamping, at the end of clamping, and at 0.5, 1, 1.5, 2, and 4 hours after unclamping. Results There were 100% of C90, 83.3% of C120, and 33.3% of C150 pigs survived. Animals of C150 group suffered highest blood pressure and heart rate, respiratory index, pulmonary dynamic compliance, and cardiac output. Pulmonary vascular resistance, platelet count, and D-dimer showed minor significant changes between C90 and C120 groups, whereas a marked changes in C150 animals during the study. There were much more serious histologic changes in C150 group compared with C90 and C120 groups. Conclusions We established a pulmonary hilum clamping animal model for pulmonary damage investigation. It was determined that 120 minutes was the longest safety time for hilum clamping without lethal pulmonary injury in porcine.

Statins have been shown to downregulate the systemic inflammatory response after cardiopulmonary bypass. However, the role of statins as anti-inflammatory agents in heart tissue remains unknown. The aim of this study was to test whether statin pretreatment attenuates local inflammatory cytokines production in heart and to explore whether the underlying mechanism involves peroxisome proliferator-activated receptor (PPAR) γ. A rat model of cardiopulmonary bypass was established. The animals were pretreated with simvastatin 5 mg/kg/day or 10 mg/kg/day for 7 days before operation. The serum concentration and myocardial level of tumor necrosis factor (TNF)-α, interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1 was evaluated by enzyme linked immunosorbent assay. The polymorphonuclear neutrophils accumulation in heart tissue was determined by myeloperoxidase activity assay. The activity of nuclear factor (NF)-κB and PPARγ in the heart was determined by electrophoretic mobility shift assay. The myocardial PPARγ expression was also examined by immunohistochemistry. The systemic and local TNF-α, IL-6 and MCP-1 were all significantly elevated after cardiopulmonary bypass. In contrast, simvastatin pretreatment significantly decreases the serum and myocardial expression level of above cytokines, myocardial myeloperoxidase activity and myocardial NF-κB activity. However, there was an evident increase in the activity and expression of PPARγ. In conclusion, simvastatin pretreatment not only attenuates acute systemic and local inflammatory response induced by cardiopulmonary bypass. The anti-inflammatory effect of simvastatin in myocardium may be partly related to the activation of PPARγ and inhibition of NF-κB.

AIM: To investigate microvascular injury quantitatively in the small bowel with respect to cardiopulmonary bypass (CPB) and related mechanisms. METHODS: In 10 male SD rats, normothermic CPB was established and continued with a flow rate of 100-150 mL/kg per minute for 60 min, while another 10 sham-operated animals served as controls. An approximate 10-cm loop of the terminal ileum was exteriorized for observation by means of intravital fluorescence microscopy. The small bowel microcirculatory network including arterioles, capillaries, and collecting venules was observed prior to CPB, CPB 30 min, CPB 60 min, post-CPB 60 min and post-CPB 120 min. The intestinal capillary perfusion, microvascular permeability and leukocyte adherence were also measured. RESULTS: The systemic hemodynamics remained stable throughout the experiment in both groups. In CPB animals, significant arteriolar vasoconstriction, blood velocity reduction and functional capillary density diminution were found. As concomitances, exaggerated albumin extravasation and increased leukocyte accumulation were also noted. These changes were more pronounced and there were no signs of restitution at the end of the observation period. CONCLUSION: CPB induces significant microcirculatory injury of the small bowel in rats. The major underlying mechanisms are blood flow redistribution and generalized inflammatory response associated with CPB.

Erythropoietin (Epo) was recently defined as an endogenous agent with more than hematopoietic functions. Previously we explored the potential of this agent to ameliorate lung ischemia-reperfusion (I/R) injury. The present study aims to determine the optimal dose and timing of administration for improving lung injury, and to further investigate the mechanisms by which Epo ameliorates lung I/R injury. The left lungs of Sprague-Dawley rats underwent 90 min ischemia and 120 min reperfusion. Firstly, animals in different groups were intraperitoneally injected with various doses of recombined human erythropoietin (rhEpo) 24 h prior to operation, 2 h prior to operation, or after the onset of reperfusion. Pulmonary myeloperoxidase (MPO) activity and malondialdehyde (MDA) content were evaluated. Treatment with 3 KU/kg rhEpo 2 h prior to operation was optimal for attenuating pulmonary MPO activity and MDA content. With such treatment, ultrastructural changes of pneumocytes were observed, and the pneumocyte apoptosis index was also determined by terminal dUTP nick-end labeling method. The plasma concentrations of tumor necrosis factor (TNF)-alpha and matrix metalloproteinase (MMP)-9 were evaluated by enzyme-linked immunosorbent assay, and pulmonary expression by immunohistochemistry. When pretreated with rhEpo, the pneumocyte ultrastructure was predominantly maintained and the pulmonary apoptosis index was markedly reduced. In comparison with untreated animals, in treated animals the plasma concentrations of TNF-alpha and MMP-9 were significantly decreased, and their expression in lung tissue was markedly reduced as well. The results indicated that Epo potently protected against lung I/R injury by inhibiting systemic and local expression of TNF-alpha and MMP-9.

Background: The objective of this study was to develop a porcine model of mitral valve replacement (MVR) for long-term evaluation of prosthetic heart valves. Methods: Sixteen 25-kg male Bama miniature pigs underwent MVR using St Jude Medical valve (21 mm). Each animal was allocated to an anticoagulation protocol after surgery (group I, s.c. heparin injection and warfarin (n = 8); group II, s.c. low-molecular-weight heparin and warfarin (n = 8)) and was followed for up to 20 weeks. Terminal studies were carried out on all animals having survived for more than 140 days or died. Results: Fourteen animals survived for more than 1 month without signs of heart failure. One of group I animals died from haemorrhagic (haemopericardium) complications on the 9th postoperative day, and another animal of group I died on the 18th postoperative day because of valve thrombosis. Conclusions: Compared with other species, humans and pigs show remarkable anatomical and physiological similarities. This model is promising for long-term preclinical evaluation of prosthetic heart valves and evaluation of postoperative anticoagulant agents.

Water buffalo are less susceptible to Schistosoma japonicum infection than yellow cattle. The factors that affect such differences in susceptibility remain unknown. A Bos taurus genome-wide gene chip was used to analyze gene expression profiles in the peripheral blood of water buffalo and yellow cattle pre- and post-infection with S. japonicum. This study showed that most of the identified differentially expressed genes (DEGs) between water buffalo and yellow cattle pre- and post-infection were involved in immune-related processes, and the expression level of immune genes was lower in water buffalo. The unique DEGs (390) in yellow cattle were mainly associated with inflammation pathways, while the unique DEGs (2,114) in water buffalo were mainly associated with immune-related factors. The 83 common DEGs may be the essential response genes during S. japonicum infection, the highest two gene ontology (GO) functions were associated with the regulation of fibrinolysis. The pathway enrichment analysis showed that the DEGs constituted similar immune-related pathways pre- and post-infection between the two hosts. This first analysis of the transcriptional profiles of natural hosts has enabled us to gain new insights into the mechanisms that govern their susceptibility or resistance to S. japonicum infections.

It has been known that oxidative stress plays an important role in the development of diabetic nephropathy (DN). The antioxidative effects of Astragalus saponin I (AS I) were studied in vitro and in vivo. In the presence of high glucose and H2O2, the total antioxidative capability, catalase, reduced glutathione, and superoxide dismutase level of rat mesangial cells were significantly decreased, and transforming growth factor β1 (TGF-β1) mRNA level, collagen IV, and laminin level were significantly increased. When compared with those in the high glucose group, these 4 indexes of cells incubated in 2.0 and/or 20 µmol/L of AS I were significantly enhanced, and levels of TGF-β1 mRNA, collagen IV and laminin were statistically decreased. By flowcytomery, percentages of S phase of cells incubated in high glucose and H2O2 were lowered, while those in AS I were increased. Furthermore, the physical behaviors of rats treated with 12 mg/kg of AS I restored with vigor and weight gaining, while the level of HbAlC was significantly reduced. Thus, AS I has antioxidative effects and is a potential compound worth further study because it may prevent the development of DN. Keywords:: Astragalus saponin I, diabetic nephropathy, antioxidative, mesangial cell

Brain natriuretic peptide (BNP) has recently been shown to have a cardioprotective effect in animal models of myocardial ischemia-reperfusion (I-R) injury. We hypothesized that exogenous BNP limits myocardial infarction on nitric oxide synthase pathway.A rat model of myocardial I-R injury was established by ligating the left descending coronary artery for 30 min and then reperfusing for 2 h. BNP was injected with different dose 5 min after the ligation and lasting for 145 min. The myocardial infarct size and the area at risk of ischemia were measured by staining with triphenyltetrazolium chloride (TTC) and Evans blue dye. To examine the role of nitric oxide synthase (NOS), expression of eNOS in the left ventricle was analyzed by western blotting. Nomega-nitro-L-arginine methyl ester (L-NAME; 30 ug/kg), or S-methylisothiourea (SMT; 3 ug/kg) was administrated before I-R with or without BNP.The control infarct-to-risk ratio was 45.1+/-1.72% (means+/-SE). BNP infused 5 min after ischemia limited infarct size in a dosage-dependent manner, with maximal protection observed at 0.01 ug/(kg min) (infarct-to-risk: 24.7+/-1.69%, P0.01 vs. control), associated with a 10-fold increase of myocardial endothelial nitric oxide synthase above the control value. Protection afforded by BNP was abolished by L-NAME but not by SMT, suggesting the involvement of putative endothelial but not inducible nitric oxide synthase activation.We conclude that natriuretic peptide/NOS/NO signaling may constitute an important injury-limiting mechanism in myocardium.

OBJECTIVE Based on the findings that erythropoietin (EPO) has been proved to be a multiple functional cytokine to attenuate ischemia-reperfusion (I/R) injury in various organs such as brain, heart, and kidney in animals, this experiment was designed to evaluate the effect of pretreatment with recombined human erythropoietin (rhEPO) on I/R-induced lung injury. METHODS Left lungs of rats underwent 90 min of ischemia and then were reperfused for up to 2 h. Animals were randomly divided into three experimental groups as sham group, I/R group, and rhEPO + I/R group (a single dose of rhEPO was injected intraperitoneally 3000 U/kg 24 h prior to operation). Lung injury was evaluated according to semi-quantitative analysis of microscopic changes, tissue polymorphonuclear neutrophils (PMNs) accumulation (myeloperoxidase (MPO) activity), and pulmonary microvascular permeability (Evan's blue dying method). Peripheral arterial and venous blood samples were obtained for blood-gas analysis after 5 min occlusion of right lung hilus at the end of reperfusion. The serum concentration of tumor necrosis factor (TNF)-alpha was also measured by the method of enzyme-linked immunosorbent assay. RESULTS Histological injury scoring revealed significantly lessened lung alveolus edema and neutrophils infiltration in the rhEPO pretreated group compared with I/R group (p < 0.05). The rhEPO pretreated animals exhibited markedly decreased lung microvascular permeability (p < 0.05) and myeloperoxidase activity (p < 0.05). Blood-gas analysis demonstrated that the pretreated animals had significantly ameliorated pulmonary oxygenation function (p < 0.05). The serum concentration of tumor necrosis factor-alpha in rhEPO pretreated group was markedly decreased compared with that of I/R group (p < 0.05). CONCLUSIONS Pretreatment with rhEPO appears to attenuate I/R-induced lung injury. This function is partly related with the capacity that rhEPO inhibits the accumulation of polymorphonuclear neutrophils in lung tissue and decreases the systematic expression of tumor necrosis factor-alpha.

To investigate the preventive and protective effects of bendazac lysine (BDL) on experimental early diabetic nephropathy (DN) rats.After an early DN model was induced by streptozotocin, rats were administered BDL at doses of 100, 200, and 400 mg/kg for 8 weeks. Blood glucose, microalbuminuria, kidney index, total antioxidative capacity, laminin, advanced glycation end products (AGE), aldose reductase (AR) activity, and the relative quantity of transforming growth factor beta1 (TGF- beta1) mRNA were measured by different methods. The ultrastructural morphology was observed by transmission electron microscope.The physical behaviors of early DN rats were hypopraxia, cachexia, and polyuria, while those treated with high doses of BDL were vibrant and vigorous. For BDL-treated DN rats, when compared with vehicle-treated DN rats, the blood glucose level and the intensity of oxidative stress were ameliorated. Also, the microalbuminuria level, AGE either in serum or in renal, and AR activity were significantly reduced. Furthermore, the expression of TGF-beta1 mRNA in the kidney cortex was declined and the thickness of glomerular base membrane was decreased significantly. The ultrastructure of glomerulus and mesangial matrix of BDL-treated DN rats were ameliorated.BDL has protective effects on several pharmacological targets in the progress of DN and is a potential drug for the prevention of early DN.

The objectives of this study were 1) to provide more accurate estimates of the relationship between Schistosoma japonicum infection and both protein energy malnutrition (PEM) and anemia through better adjustment for potential confounders such as socioeconomic status (SES) and geo-helminth infections and 2) to assess the role of occult blood loss in mediating S. japonicum-associated anemia. We examined cross-sectionally 729 individuals (86.7% S. japonicum-infected and 13.3% S. japonicum-uninfected) aged 7-30 years in Leyte, The Philippines. The main outcome measures were height-for-age Z-score (HAZ), body-mass-index Z-score (BMIZ), triceps skinfold Z-score, hemoglobin, and fecal occult blood loss. Multivariate models were created to assess the relationship between S. japonicum infection and nutritional status after adjusting for age, gender, other helminths, and SES. After controlling for confounders, intensity of S. japonicum infection was inversely related to hemoglobin in all age groups (P0.0001) and HAZ among children/= 12 years (P = 0.03), but not to BMIZ (P = 0.52) or triceps skinfold Z-score (P = 0.11). Individuals with high-intensity S. japonicum infection were 3.5 times more likely to have occult blood in the stool. Adjustment for occult blood did not attenuate the relationship between S. japonicum and hemoglobin, suggesting other mechanisms are involved. Adjustment for SES allows more accurate assessment of the relationship between S. japonicum and both PEM and anemia. Exploration of the mechanisms of S. japonicum-associated anemia suggests that processes other than extracorporeal blood loss, such as anemia or inflammation, may be involved.

Diabetic nephropathy (DN) has become the leading cause of end stage failure, but no renoprotective treatment has been very available for use in DN. Astragalus saponin I (AS I), a component extracted from Astragalus membranaceus BUNGE, was studied in experimental DN induced by administration of streptozotocin in male rats. The early DN rats were treated with 3 doses of AS I for 8 weeks to analyze its efficacy with different parameters. By comparison with vehicle-treated DN rats, the renal hypertrophy, the oxidative stress intensity, and the blood glucose level of DN rats were ameliorated by AS I. Also, the microalbuminuria level, advanced glycated end-products either in serum or in kidney cortex, and the aldose reductase activity were significantly reduced. Furthermore, the expression of transforming growth factor β1 mRNA in kidney cortex by RT-PCR analysis was markedly declined. Both the relative grade of mesangium hyperplasia by microscopical observation and the thickness of glomerular base membrane by electron microscope measurement were decreased significantly. Therefore, the results suggest that AS I has therapeutic effects on several pharmacological targets in the progress of DN and is a potential drug for prevention of early stage DN. Keywords:: Astragalus membranaceus, Astragalus saponin I, diabetic nephropathy

Background To summarize the diagnostic and therapeutic experiences on the patients who suffered abdominal complications after cardiovascular surgery with cardiopulmonary bypass(CPB). Methods A total of 2349 consecutive patients submitted to cardiovascular surgery with CPB in our hospital from Jan 2004 to Dec 2010 were involved. The clinical data of any abdominal complication, including its incidence, characters, relative risks, diagnostic measures, medical or surgical management and mortality, was retrospectively analyzed. Results Of all the patients, 33(1.4%) developed abdominal complications postoperatively, including 11(33.3%) cases of paralytic ileus, 9(27.3%) of gastrointestinal haemorrhage, 2(6.1%) of gastroduodenal ulcer perforation, 2(6.1%) of acute calculus cholecystitis, 3(9.1%) of acute acalculus cholecystitis, 4(12.1%) of hepatic dysfunction and 2(6.1%) of ischemia bowel diseases. Of the 33 patients, 26 (78.8%) accepted medical treatment and 7 (21.2%) underwent subsequent surgical intervention. There were 5(15.2%) deaths in this series, which was significantly higher than the overall mortality (2.7%). Positive history of peptic ulcer, advanced ages, bad heart function, preoperative IABP support, prolonged CPB time, low cardiac output and prolonged mechanical ventilation are the risk factors of abdominal complications. Conclusions Abdominal complications after cardiovascular surgery with CPB have a low incidence but a higher mortality. Early detection and prompt appropriate intervention are essential for the outcome of the patients.