Objectives To study the effect of preoperative platelet transfusion for splenectomy and devascularization in the prevention of intraoperative and postoperative bleeding.Methods The 230 patients with cirrhosis and portal hypertension who received splenectomy and periesophagogastric davascularization were divided into strata A,B and C according to the platelet counts.Stratum A patients had a platelet count of less than 30× 10/L,B between 30× 10/L and 50× 109/L,and C more than 50 × 109/L.The patients in each stratum were then randomly divided into a preoperative transfusion group (T group) and a non-transfusion group (NT group).The amounts of intraoperative bleeding,postoperative drainage in 48 hours after operation,rates of postoperative bleeding,and general medical conditions were compared.Results A comparison in stratum A showed lower amounts of intraoperative bleeding and 48 hour postoperative drainage,and a lower rate of bleeding in the T group (P＜0.05).There were no significant differences between the T and the NT groups in strata B and C (P＞0.05).Conclusions For patients with a platelet count lower than 30 × 109/L,preoperative platelet transfusion significantly reduced bleeding suggesting that preoperative platelet transfusion for splenectomy and periesophagogastric devascularization should be a routine.For those patients whose platelet count was above 30 × 109/L,platelet transfusion is not recommended.

Objective To investigate the relationship between the expression of Fas ligand mRNA and the biological behavior and prognosis of colon cancer.Methods The expression of Fas ligand mRNA was examined in 52 cases of colon cancer by in situ hybridization (ISH) technique.Results Fas ligand mRNA expression was found in 30 out of 52 cases of colon cancer (58%). Fas ligand mRNA expression was positive in cancer tissues in 3 out of 12 cases (25%) with pericancer inflammation and in 27 out of 40 cases (68%) with no pericancer inflammation ( P

Objective To investigate the clinical allocation significance of modified early warning score (MEWS) for emergency department patients.Methods MEWS of 1 069 patients in medical emergency department from August 2011 to March 2013 were recorded and analyzed.The admitted differences of MEWS among in intensive care unit(ICU),general wards and emergency transfer observing patients were compared.Results The MEWS of emergency department patients were different.The deaths and ICU patients together as ICU patients,MEWS ≥ 7 scores the proportion of patients admitted to ICU were significantly higher than those of MEWS 3-6 scores and 0-2 scores [37.8％(14/38) vs.2.1％ (6/289) and 0.1％(1/742)](P＜0.01).Conclusion MEWS provides an objective allocation basis for emergency department patients.

Objective To investigate the role of surfactant protein (SP)-A and SP-D in urinary tract infection mouse model,and evaluate the effects of SP-A and SP-D absence on urinary tract infection.Methods SP-A and SP-D double knockout (SP-A/D KO) mice were made.SP-A/D KO and wild-type (WT) C57BL/6 female mice were used for this study.The expression of SP-A and SP-D in kidney was detected by immunohistochemistry (IHC).The levels of p-p38 and p38 protein in kidneys were measured by Western blotting.Uropathogenic Escherichia coli or buffer was delivered into the bladder of female mice.At 24 and 48 h after inoculation,CFU of Escherichia coli in the kidney and urine of the treated and control mice were measured.Histological,cellular and molecular analysis were performed by several methods of H/E staining,IHC and Western blotting.The effects of SP-A and SP-D on bacterial growth were studied in vitro.Results SP-A and SP-D in kidney were located in the proximal tubules and collecting tubules.Compared with WT mice,infected SP-A/D KO mice with UPEC had higher CFU in kidneys and urine at 24 h and 48 h,increased inflammatory cells infiltration in kidneys (P＜0.05).Compared with WT mice,SP-A/D KO mice had higher p38 MAPK phosphorylation levels in kidneys (P ＜ 0.05).Growth of Escherichia coli was greatly inhibited by both SP-A and SP-D (P＜0.05).Conclusions Both SP-A and SP-D are expressed in kidney.SP-A and SP-D can attenuate UTI induced by UPEC which may be through inhibiting bacterial growth and modulating renal inflammation.

Objective To explore whether adiponectin activates AMP-activated protein kinase(AMPK) via LKB1 pathway or not in skeletal muscle and liver tissues.Methods Male Sprague-Dawley rats ( n =28 ) were divided into normal control diet( NC,n =15 ) and high-fat diet( HF,n =13 ) groups.After 16 weeks feeding,fasting blood free fatty acids( FFA ),triglyceride( TG ),total cholesterol( TC ),fasting plasma glucose( FPG ),fasting insulin(FINS),and adiponectin were determined.The protein levels of AMPKα,phosphorylated AMPKα ( p-AMPK ),and LKB1 in the skeletal muscle and liver tissues were analyzed with Western blot.Cultured primary skeletal muscle cells and hepatic cells were incubated with aditonectin and radicicol.The expression of AMPKα,p-AMPKα,and LKB1 inthese cells were analyzed with immunofluorescence method.Results Compared with NC group,body weight,FFA,TG,FPG,and FINS in rats of HF group were significantly higher( all P＜0.05 ) while serum adiponeetin level was lower( P＜0.05 ).The levels of AMPKα phosphorylation and LKB1 expression in the skeletal muscle and liver tissues of HF group were lower than those in NC group. In primary skeletal muscle cells and hepatic cells,adiponectin significantly increased the levels of AMPKα phosphorylation and LKB1 expression ( all P＜ 0.05 ),which were decreased by radicicol ( P＜0.05 ).Conclusion Adiponectin may activate AMPK via LKB1 pathway in skeletal muscle and liver tissues of rats.

Objective To investigate the role of genistein (Gen) in the expression of connective tissue growth factor (CTGF) induced by parathyroid hormone (PTH) in human renal tubular epithelia cells. Methods Real-time PCR, Western blotting and reporter gene assay were employed to detect the role of Gen in PTH-induced CTGF expression in HK-2 cells. The activity of NF-κB was measured by EMSA to investigate the mechanism by which PTH induced CTGF expression in HK-2 cells. Inhibitors of NF-κB signaling pathway were used to ascertain which signal pathway was involved. Results HK-2 cells had basic amount of CTGF mRNA and protein, which, however, increased significantly after treatment with PTH, and the luciferase activity increased to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h (1.89±0.08 vs 0.99±0.03, P＜0.01). Gen decreased the expressions of CTGF mRNA and protein induced by PTH in dose-dependent manner. The NF-κB of nucleus was inactivation without PTH, while the activity of NF-κB significantly increased after exposed to PTH, with the maximal response of PTH at a concentration of 10-10 mol/L and the best stimulating time at 30 minute. The NF-κB inhibitor PDTC reduced the increase of CTGF transcript levels in response to PTH stimulation. Gen blunted PTH-mediated NF-κB activation. Conclusion Gen inhibits CTGF expression induced by PTH through bloking NF-κB signaling pathway in human renal tubular epithelial cells.

leptin-induced VSMCs proliferation as well as expression of PCNA and OB-R at both mRNA and protein levels. The maximum effect was at 100 μmol/L(P<0.01).

Objective To investigate the effects of allogenic intra-bone marrow bone marrow transplantation (IBM-BMT) on re-establishing hematopoiesis in mice. Methods Bone marrow mononuclear cells (BMNCs) from BALB/ c mice were transplanted into the C57BL/6 mice treated with a lethal dose of ~(60)Coγ-ray radiation through intra-bone marrow injection or intravenous injection. Sixty of the C57BL/6 mice were randomly divided into three groups as higher dose intra-bone marrow injection group (IBM1 group), lower dose intra-bone marrow injection group (IBM2 group) and intravenous injection group (IV group). The nucleated cell numbers of whole bone marrow from the tibia of each recipient mouse were counted respectively at the day 1, day 3, day 6 and day 9 after the transplantation. The donor-derived total nucleated cells and myeloid cells were quantified by flow cytometry. Results At 6th day after transplantation, more total bone marrow nucleated cells, total donor-derived nucleated cells and donor-derived myeloid cells in the tibia of injected side in both IBM1 group and IBM2 group were found than that in IV group (P<0.05 or P<0.01). Conclusion Compared with traditional bone marrow transplantation (IV-BMT),IBM-BMT improves the bone marrow hematopoiesis in the early hematopoietic re-establishing stage in allogenic bone marrow transplantation.

Objective To characterize the expression of surfactant protein A (SP-A) in normal and acute pyelonephritic rat kidneys and to study the correlation of infection and inflammation with SP-A expression. Methods Twenty-one rats were randomly assigned into three groups: control, sham operation and pyelonephritic group. HE staining was used to determine tubulointerstitial inflammation. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to determine the mRNA expression and protein level of SP-A. Immunohistochemical staining was used to label the localization and intensity of SP-A expression in kidney tissue. The correlation between intensity of SP-A expression and interstitial inflammation was also evaluated. Results In pyelonephritic group, tubulointerstitial inflammation was more prominent than that in control and sham groups (54.3?11.5,6.4?1.4, 8.6?1.9,respectively). RT-PCR and Western blotting revealed that SP-A expression was up-regulated in pyelonephritic group (in mRNA level: 2.2+0.58, 0.9?0.25, 1.1? 0.30; in protein level: 0.45?0.09, 0.24?0.05, 0.26?0.05, respectively). Immunohistochemical staining demonstrated that SP-A expression was mainly localized on epithelial cells in outer medullary and collecting tubules in normal group and sham group, but strong staining extended to collecting tubules in pyelonephritic group. The tubulointerstitial inflammation score was positively correlated with the intensity of SP-A expression (r=0.67,P

Objective To investigate the treatment effect of fasudilon inflammatory bowel disease ( IBD) in rats. IBD was induced by using an enema of trinitro-benzene-sulfonic acid ( TNBS ) . Methods A total of 30 female SD rats were randomly divided into normal control group (0. 9% sodium chloride for induction and 0. 9% sodium chloride for treatment), model control group (TNBS for induction and 0. 9% sodium chloride for treatment), and fasudil group (TNBS for induction and fasudil 4. 5 mg·kg-1 for treatment). The disease activity index(DAI) was estimated 14 days later. The MPO activity, TNF-αcontent and IL-1β level in the colon were investigated, while Rho kinase expression was detected by Western blot. The pathological changes were detected by HE staining. Results The DAI of the normal control, model control, and fasudil groups were:(0. 00±0. 00),(7. 76±1. 32),and (3. 20±0. 98), respectively. MPO activity was (59. 32±9. 08),(96. 65±16. 57),and (69. 58±11. 40) U·g-1, respectively. TNF-α was (0. 15±0. 11),(0. 28±0. 22),and (0. 20±0. 62) ng·mL-1, respectively. IL-1β content was (0. 04±0. 01),(0. 08±0. 02),and (0. 06±0. 02) ng·mL-1, respectively. Rho kinase expression was 0. 713± 0. 170,1. 083±0. 210,and 0. 907±0. 260, respectively. Conclusion Fasudil excerts protective effects against IBD in rats by lowering the expression of Rho kinase and attenuating the release of inflammatory mediators, suggesting that Rho kinase could be a new therapeutic target for IBD.