With the increasingly deepening research on the molecular regulatory mechanisms during the development and progres-sion of advanced renal cell carcinoma, the targeted therapy directed on the key proteinase/protein in the molecular signaling pathways significantly improves the management outcomes. However, the occurring resistance during therapy with targeted agents leads to de-creasing effects. The mechanisms of action, resistance, and countermeasures of targeted therapy in advanced renal cell carcinoma are simply reviewed.

ObjectiveTo investigate the management of myonephropathic-metabolic syndrome (MNMS) after acute arterial occlusion. Methods17 cases of MNMS caused by acute arterial occlusion were restrospectively reviewed. Results5 cases were cured, 6 cases died of sudden cardiac arrest induced by hyperkalemia, and another 6 cases died of multiple organ dysfunction syndrome (MODS) complicated by acute renal failure. The total mortality rate was 71% and the amputation rate was 41%.ConclusionEarly revascularization should be performed in acute arterial occlusion. In patients with compartment syndrome, fasciotomy should be performed as soon as possible. Early amputation of gangrene limb is very important to prevent MNMS. Early and effective fluid resuscitation and alkalinization is the key point to prevent ARF, early hemodialysis for ARF is very important in treating MNMS.

Objective: To study the influences of Trastuzumab and IL-2 on human epidermal growth factor receptor-2 (HER2), multidrug resistance-associated protein1 (MRP1) of ACHN in vitro . Methods: ACHN cell line of RCC were cultured by cell culture technique. The tetrazolium-based colorimetric assay was used to evaluate the growth inhibitory effects of trastuzumab and IL-2. S-P method was used to determine the expression of HER2, MRP1 of the cells. Results: Trastuzumab showed the inhibitory effects on growth and multi-drug resistance in RCC from 40 ?g/L or 24 h in time-effective and dose-dependent manner. After treatment with Trastuzumab and/or IL-2, the expression of HER2, MRP1 genes of RCC was decreased significantly( P

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.

Objective To investigate the effect of MicroRNA-9 (miR-9) on cell proliferation and collagen synthesis in hepatic stellate cells (HSCs),and to explore the potential mechanism.Methods HSC-T6 cells were cultured and transfected with miR-9 mimics with lipofectamine 2000.After incubation 48 h,the cells were collected and total proteins and RNAs were extracted.The expression of miR-9 was detected by quantitative real time polymerase chain reaction (qRT-PCR).The protein expression of type Ⅰ collagen and type Ⅲ collagen were measured by Western blot.The methyl thiazolyl tetrazolium (MTT) method was used to asses the proliferation of HSC-T6 cells.The expression of transforming growth factor-β1 receptor 2 (TGFBR2) was detected by qRT-PCR and Western blot.Results Compared to the control group,miR-9 expression in HSCs was increased in the miR-9 mimics group (P ＜ 0.05),type Ⅰ and type Ⅲ collagen protein expression was reduced by (44 ± 2) ％ and (50 ± 3) ％ (P ＜ 0.01),respectively.The proliferation activity of HSCs was decreased by (48 ± 4)％ (P ＜ 0.05).The expression of TGFBR2 was inhibited in the miR-9 mimics group.Conclusions Upregulation of miR-9 plays a role on suppressing cell proliferation and collagen synthesis in HSCs.This process might be mediated by downregulation of TGFBR2.

B7-H1, a recently described member of the B7 family of costimulatory molecules, is thought to be involved in tumor immune escape by inducing T-cell apoptosis. In order to investigate the relationship between B7-H1 and immune escape of bladder cancer, B7-H1 expression in 50 cases of bladder cancer was detected by using immunohistochemical method. Survival curves were constructed using the Kaplan-Meier method and independent prognostic factors were evaluated using the Cox regression model. Our results showed that the positive rate of B7-H1 immunostaining in normal bladder tissue and bladder cancer was 0 and 72% respectively. The expression of B7-H1 was strongly associated with the pathological grade, clinical stage and recurrence (P<0.05). The survival rate was significantly lower in patients with B7-H1 positive group than in those with B7-H1 negative group and multi-variable analysis revealed that B7-H1 could be regarded as an independent factor in evaluating the prognosis of bladder cancer. It is concluded that the expression of B7-H1 is strongly associated with neoplastic progression and prognosis of bladder cancer. The manipulation of B7-H1 may become a beneficial target for immunotherapy in human bladder cancer.
Antigens, CD/genetics ; Antigens, CD/*metabolism ; Antigens, CD80/genetics ; Antigens, CD80/*metabolism ; Prognosis ; Tumor Escape/*genetics ; Urinary Bladder Neoplasms/*immunology ; Urinary Bladder Neoplasms/metabolism

Objective To investigate the repair function of extracorporeal membrane oxygenation (ECMO) in vivo for the liver after cardiac death with warm ischemia injury for 30 min from cardiac death swinc.Method Ten landraces,30 to 40 kg,randomized to experimental group and control group,were used to make 30-min cardiac death models through clamping trachea after deep anesthesia.An intravenous cannula was placed through right iliac arteries and veins,and connected to ECMO extracorporeal circulation pipes in experimental group.The balloon catheter was placed to diaphragm plane through left femoral artery.The ECMO was performed to infuse abdominal organs,and pH and electrolyte were adjusted.The circulation flow rate,intraperitoneal organ perfusion pressure,venous blood gas,electrolyte,transaminase,and bile product,etc.were monitored and recorded.The livers of control group were retrieved after 30-min cardiac arrest and stored in cold UW for 4 h.Pathological tissue was sliced and stained by HE.Result After 30-min cardiac arrest,the liver showed obvious congestion appearance; pathologically,there were hepatic sinus expansion,blood cells clog,and erythrocyte aggregation.Circulating blood gas analysis revealed severe acidosis.After the ECMO recirculation started,circulation flow rate maintained to 1 L/min,the liver gradually restored bright red,pathological biopsy showed that hepatic sinus expansion disappeared,and clogged blood cells dispelled.AST was markedly increased to (226.0 ± 28.0) U/L after 30-min cardiac arrest and reduced to (150.0 ± 30.0) U/L 4 h after the ECMO recirculation.Average bile production was 7.75 ml/h.Conclusion ECMO recirculation in vivo can repair the injured livers from cardiac death donor with 30-min cardiac arrest.

Objective To clone NT-3 gene from normal rat brain and to purify its fusion protein and to prepare specific high titer antibody so that to provide a foundation for further study for peripheral nerve injury.MethodsWe amplified target gene by RT-PCR and cloned it into the vector of pMD-18T,then analyzed its sequence and compared it with the sequence from GenBank.We subcloned it into pRSET-A vector and introduced it into Escherichia coli BL21.The expression was induced by IPTG,and identified by SDS-PAGE.The fusion protein was purified by niccolum purify kit.We immuned rabbits with immunological adjuvant for specificity antibody preparation.Results We got a 777 bp gene segment by RT-PCR.The DNA sequence was identical to rat NT-3 gene sequence in GenBank.It proved that the target gene was correctly inserted into the vector.A new protein band of about 34 ku appeared on SDS-PAGE after induction of IPTG.A specific high titer antibody of 1∶64000 was gained by immunizing rabbits with adjuvant.

Objective To study the cell apoptosis and the dynamic expression and significance of apoptosis-related genes in graft veins. Methods A rat experimental model of autogenous graft vein was established by transplanting the right external jugular vein to infrarenal abdominal aorta in 100 Wistar rats. TUNEL and immunohistochemistry were used to detect the apoptosis, the expression of apoptosis related genes bcl 2 and bax in vascular smooth muscle cells (VSMCs) of graft veins. Results Within the 8 weeks after transplantation, the apoptotic VSMCs in the graft veins were much more than those in the control group with the apoptotic rate reaching the peak〔(28.5?16.6)%〕 on the 2nd week and dropping to (8.1?2.8)% during the 4th to 8th week. There was statistical difference compared to the control group 〔(0.5?0.2)%, P

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