Objective To summarize our experience of the diagnosis and treatment in patients with abdominal aortic aneurysm(AAA).[WT5”HZ]Methods [WT5”BZ]From 1980 to 1999 sixty five AAA patients were hospitalized with 40 cases of general type, 18 cases of rupture type,4 cases of inflammatory type and 3 cases of infective type. In situ artificial graft transplantation was performed in 62 cases and nonanatomy pathway in 2 cases. The remaining one with inflammatory type was treated by interventionel therapy.[WT5”HZ]Results [WT5”BZ]57 cases were cured and were followed up from 1 to 12 years without complications.Death occurred in 7 cases.[WT5”HZ]Conclusions [WT5”BZ]The abdominal pulsate mass should draw much attention. Ultrasound is the selected examination and DSA, helix CT are accurate image appliance. It can elevate the curative ratio and decrease the mortality through rational operation based on the location, type and individual condition of AAA patients.

Obesity is rapidly becoming a pandemic and is associated with increased carcinogenesis,especially hepatocellular carcinoma (HCC).Adipose tissue has been considered as an endocrine organ because of its capacity to secrete a wide variety of adipokines,such as leptin,adiponectin and resistin.Recently,adipokines have been demonstrated to be associated with many kinds of chronic liver diseases,liver fibrosis and cirrhosis,and carcinogenesis.Direct evidence supporting the inhibitory and/or activating role of adipokines in the process of carcinogenesis and progression of human HCC has been rapidly accumulating. This review aims to provide important insights into the potential mechanisms of adipokines in the development of HCC.Further investigations will shed light on a new therapeutic target in HCC.

Objective To summarize the diagnosis and treatment of 33 cases of Leriche syndrome. Methods A retrospective review of the clinical data of 33 cases of Leriche syndrome was done. Results Claudication and impotence occurred in 79.9% and 70.4% of the cases. Color Doppler ultrasonography, especially combining with CTA or MRA, was helpful for the diagnosis. Aortic angiography or DSA was necessary for the determination of the clinical patterns and selecting the therapeutic methods. Surgical patterns selestion should be considering the patients' general status and conditions of the affected vessels. Surgical treatment was performed on 25 cases, including12 aortoiliac artery bypasses , 6 aortobifemoral artery bypasses , 4 axillo bifemoral artery bypasses, 2 embolectomies by Fogarty tube only and 1 aortal interposition with artificial vessel plus renal artery plasty. Aorta iliac artery bypasses get the best results with 1 year patency rate(100%) in all cases, and 5 year patency rate of 75.0%, which was significantly superior to those axillo bifemoral artery bypass grafts with 5 year patency rate of 37.5%. All the other 8 patients without operation died within 5 months. Conclusions Early diagnosis and comprehensive therapy should be adopted to improve the long term patency rates of grafts transplantation in Leriche syndrome.

ObjectiveTo evaluate the surgical outcomes and prognosis of patients after liver resection for noncolorectal liver metastases.Methods72 patients with liver metastases who underwent liver resection at Tianjin Medical University Cancer Hospital were retrospectively studied.There were 32 males and 42 females,aged between 35～78 years.After liver resection,68 patients had a R0 resection (negative histological margin),and 4 patients had a R1 resection (positive histological margin).The primary tumours were breast,(n =16,22.2 ％),lung (n =14,19.4 ％),gastrointestinal (n=12,16.7％),gynecological (n =8,11.1％),pancreatobiliary (n =8,11.1％),melanoma (n=4,5.6％),sarcoma (n=4,5.6％),and genitourinary (n=2,2.8％).The mean diameter of the main tumour was 4.8 cm (range,1.5- 11.0 cm).The mean number of liver metastases was 1.2 (range,1-5).Liver metastases were synchronous in 6 patients (8.3％) and metachronous in the remaining 66 patients (91.7％).ResultsThe operative mortality was 0％.The mean hospital stay was 14.4 days (range 6-67 days).The median overall survival was 31 months (range,6-127 months).The 1-,3- and 5-year survival rates were 81.9％,37.5％ and 23.6％,respectively.Univariate analysis revealed primary tumour sites (breast vs.others),histological type (adenocarcinoma vs.others),postoperative chemotherapy,number of liver metastases (solitary vs.multiple) and time to liver metastases from diagnosis of primary tumours (≤ 12 months vs.＞ 12 months) were associated with overall survival (all,P＜0.05).In multivariate analysis,factors independently associated with poor survival were nonbreast origin (P =0.012),time to liver metastases from diagnosis of primary tumours ＜12 months (P=0.027) and multiple liver metastases (P=0.008).ConclusionsIn selected patients,liver resection is an effective and safe treatment for noncolorectal liver metastases.The time to liver metastases from diagnosis of primary tumours was independently associated with overall survival.For solitary or liver metastasis of breast origin,surgical resection significantly improved survival.

Objective To investigate the expression of extracellular signal regulated kinase (ERK) and p38 mitogen activated protein kinase (p38 MAPK) in autogenous vein grafts during vascular remodeling.Methods An autogenous vein graft model was established by transplanting the right jugular vein to infrarenal abdominal aorta in 80 Wistar rats. Vein graft samples were harvested 6 hours, 24 hours, 3 days, 7 days, 2 weeks, 4 weeks, 6 weeks and 8 weeks after surgery. Gene expression of ERK and p38 MAPK was measured by reverse transcription PCR. Western blot was used to detect the expression of protein products and phosphorylation protein products of ERK and p38 MAPK. Apoptosis of vascular smooth muscle cells (VSMCs) was determined by TUNEL. Proliferating cell nuclear antigen(PCNA) of VSMCs also was studied.Results The expression of ERK 1 mRNA and p38 MAPK mRNA increased considerably after surgery. ERK 1 mRNA reached the peak on the 7th day 〔(33.2?14.2)%, P

ObjectiveTo investigate the mechanism on endothelial dysfunction of spontaneous hypertensive rats (SHR).MethodsThe animals were divided into two groups: SHRs (n=8) and Wistar-Kyoto (WKY) rats (n=7) all aged 17 months. Blood pressure was measured by the tail-cuff method. NO3- concentration in serum was assayed by activated cadmium reduction method; endothelin (ET) and cGMP levels were assayed by RIA.ResultsCompared with WKY rats, blood NO3- concentration, ET level and vascular cGMP level of SHRs were all reduced significantly (P<0.01); vascular ET level was only uplifted slightly with no significant difference (P>0.05).ConclusionIt indicates that the vascular endothelial dysfunction in SHR is induced possibly by a diminished synthesis or release of NO, not by changes of ET level.

Objective To evaluate expression of inducible nitric oxide synthase (iNOS) in human abdominal aortic aneurysm (AAA) and to identify its initiation in the oxidative vascular injury. Methods This study included 22 AAA patients and 10 cadaveric normal abdominal aorta. In situ hybridization and immunofluorenscent staining were used to localize iNOS messenger RNA (mRNA) and protein. Double staining with a combination of in situ hybridization and immunofluorenscent staining was used to simultaneously demonstrate iNOS mRNA expression and its cellular localization. The presence of end-product of oxidative injury induced by iNOS was indirectly assessed with immunofluorenscent staining by anti-nitrotyrosine antibody, its cellular localization were assessed by double immunofluorenscent staining. Results In situ hybridization and immunohistochemistry confirmed the presence of iNOS in media and adventitia of AAA in all 22 patients. Specific cell markers identified iNOS mRNA-positive cells were T and B lymphocytes, macrophages, and smooth muscle cells. Positive immunostaining for nitrotyrosine was present in macrophages and smooth muscle cells. Normal abdominal aorta demonstrated virtually no iNOS or nitrotyrosine expression. Conclusion Stimulated expression of iNOS is associated with degeneration of AAA in human beings leading to oxidative tissue and cellular injury in AAA.

Objective To sum up our experience in the diagnosis and management of acute superior mesenteric venous thrombosis (SMVT). Methods We retrospectively reviewed 41 patients treated for acute SMVT admitted in our hospital from Jan 1978 to Aug 2003. Before 1995 (group Ⅰ), a surgery was preformed in patients with suspected acute SMVT. Since Jan 1995 (Group Ⅱ), aggressive medical therapy was immediately delivered, and the patients were subjected to laparatomy with suspected peritonity. Results There were 13 cases in group Ⅰ, and 28 in group Ⅱ. Mortality in group Ⅰ was 38.5%, and that in group Ⅱ was 10.7% (P

Objective To investigate the expression and relationship of early growth response gene-1((Egr-1)),platelet-derived growth factor-B(PDGF-B) and tranforming growth factor(TGF-?_1) in autogenous vein graft in rats,and the role in vein graft intimal hyperplasia(IH).Methods Autogenous vein graft model was(established) in 90 wistar rats.The vein graft samples were harvested at 1,2,6,24 hours,and 3,7,14,28,42 days after surgery.Normal vein was used as control group.Egr-1、PDGF-B,TGF-?_1 mRNA was measured by reverse transcription-PCR and in situ hybridization.Western blotting and immunohistochemistry were used to detect the protein expression of Egr-1,PDGF-B and TGF-?_1. Results Expression of Egr-1,PDGF-B,TGF-?_1 mRNA and protein was not detected in normal vein.In grafting vein,expression level of Egr1mRNA reached a peak at 28days,and the positive rate of Egr-1mRNA was 45%?6%;(PDGF-BmRNA) reached a peak at 14days(48%?6%);a peak of TGF-?_1mRNA was 46%?9% reached at 7days;Egr-1 protein expression reached a peak at 28days, and the positive rate of Egr-1 protein was 40%?9%.PDGF-B protein reached a peak at 28days(45%?4%),TGF-?_1 protein reached a peak at 14days(41%?7%).Conclusions Intimal hyperplasia of vein graft is closely associated withexpression of Egr-1、PDGF-B and TGF-?_1;the activation and expression of PDGF-B and TGF-?_1 may be(modulated) by Egr-1,and they may contribute to increase expression of Egr-1 by feedback.

Objective To investigate the effect of selenium on proliferation and apoptosis of chondrocytes of articular cartilage cultured in vitro in Kaschin-Beck disease(KBD) patients and normal person, to explore the role of selenium in control of KBD, and to provide evidence for selenium's effect on the growth of normal cartilage cells. Methods The articular cartilage samples of grade Ⅱ and Ⅲ KBD patients were selected according to the national "Clinical Diagnosis of KBD" (GB 16003-1995). Chondrocytes of 5 KBD and 5 non-endemic normal accidentswere separated and cultured in vitro. KBD group and control group were given different doses of selenium (0,0.0125,0.0250,0.0500,0.1000,0.2500,0.5000,1.0000 mg/L, respectively). Methyl thiazolyl tetrazolium (MTT),flow cytometric analysis, and immunocytochemical staining were used to observe the effect of selenium on cell growth and apoptosis in KBD and normal persons. Results MTT results showed that the cell proliferation rate in each dosage group of the control group at the 6th day(0.086 ± 0.025,0.077 ± 0.012,0.073 ± 0.027,0.071 ± 0.017,0.058 ± 0.028,0.052 ± 0.028 and 0.046 ± 0.037) was significantly lower than that of 0 mg/L group(0.138 ± 0.026,all P ＜ 0.05);the average cell proliferation rate was negative( - 0.001 ± 0.001, - 0.003 ± 0.000, - 0.003 ± 0.001and - 0.004 ± 0.001 ) in 0.1000 - 1.0000 mg/L dose group, which was significantly lower than that of the 0 mg/L group(0.025 ± 0.003, all P ＜ 0.05);compared with 0 mg/L group(0. 115 ± 0.011), the KBD 0.2500 mg/L dose group promoted cell proliferation(0.128 ± 0.037, P ＜ 0.05), the KBD 1.0000 mg/L dose group inhibited cell growth (0.071 ± 0.019, P ＜ 0.05). The apoptotic rate of 0.0500 - 1.0000 mg/L dose control group [ (18.88 ± 0.02)%,(17.58 ± 0.01)%, (17.09 ± 0.04)%, (56.00 ± 0.02)%, (57.85 ± 0.03)% ] were higher than that of the 0 mg/L group[(13.51 ± 0.01)%, all P ＜ 0.05];compared with 0 mg/L group[(25.84 ± 0.02)%], the apoptotic rate in KBD 0.0250 - 0.2500 mg/L dose group [ ( 13.69 ± 0.02) %, ( 15.96 ± 0.03 ) %, ( 16.68 ± 0.03 ) %, ( 16.67 ± 0.02) % ]were lower, and the apoptotic rate in 0.5000, 1.0000 mg/L dose group [ (59.58 ± 0.03)%, (73.48 ± 0.04)% ] were significantly higher(all P ＜ 0.05). The Fas expression in KBD 0.0500 - 0.2500 mg/L dose groups[ (41.2 ± 1.5)%,(40.3 ± 2.0)%, (50.2 ± 2.5)%] were lower than those of the same dose control group with selenium intervention [(52.4 ± 1.0)%, (67.2 ± 4.0)%, (75.1 ± 5.0)%, all P ＜ 0.05], the caspase-3 expression in KBD 0.0500,0.1000 mg/L dose groups[ (40.8 ± 1.1 )%, (45.1 ± 2.1 )%] were lower than those of the same dose control group with selenium intervention[ (68.0 ± 3.0)%, (70.6 ± 3.5)%, all P ＜ 0.05 ]. Conclusions Appropriate dose of selenium supplementation (0.1000 - 0.2500 mg/L) could promote the growth of KBD chondrocyte, decrease cell apoptosis,but have a damage when the dose of selenium ＞ 0.5000 mg/L;doses of selenium that could promote the growth of KBD chondrocyte does not mean to promote the growth of normal cartilage cells in vivo.