In clinical practice,regional portal hypertension is infrequent,but it is the only type which could be cured of portal hypertension.Pancreatic diseases are the chief pathogeny of regional portal hypertension,and the obstruction of spleen vein is the basic reason.The common clinical manifestation is isolatism varicose veins of pylorus.The golden standard of its iconography diagnosis is DSA,and the treatment should follow the individual principle.The splenectomy is the basic measure for them who have UGIB or hypersplenism.This is a review about recent advance in regional portal hypertension of etiology and classification,pathology and physiology,clinical manifestation,diagnosis,radiographic examination,cure,and so on.

Cancer cachexia patients have severely metabolic disorders. The release of tumor specific cachectic factors and increased synthesis of cytokines will lead to reinforced catabolism、decreased anabolism and increased energy expenditure of the patients. Progressive depletion of host reserves of adipose tissue and protein will lead to decreasing organs function ,and ultimately the failure of the patients.By increasing understanding of the mechanisms involved in cancer cachexia process,the application of mechanism based anticachectic agents will make great improvements in the therapy of cancer cachexia.

Objective: To investigate the effect of Bortezomib (an inhibitor of proteasome) on IL-6 synthesis and cachexia in colon 26 tumor bearing mice. Methods: Murine colon 26 adenocarcinoma cells were inoculated subcutaneously in male BALB/c mice to induce cachexia. Saline and three doses of Bortezomib (0.1, 0.5 and 1.0 mg/kg) were given intraperitoneally on day 6, 9, 12 and 15 after tumor inoculation and mice were sacrificed on day 16. Body weight, food intake and tumor volume were monitored daily. Serum levels of IL-6 and IL-10, tumor tissue levels of IL-6 and activity of NF-κB in tumor tissues were investigated in all animals. Results: By day 16, saline treated tumor-bearing mice showed significant body weight and carcass weight changes (P<0.01), gastrocnemius muscle wasting and epididymal fat depletion (P<0.01). Furthermore, Tumor-bearing caused a significant increase of IL-6 and IL-10 (P<0.01) in serum and IL-6 in tumor tissues. Administration of Bortezomib attenuated the wasting of carcass weight, gastrocnemius muscle and epididymal fat. Bortezomib dose dependently inhibited the NF-κB activation and IL-6 synthesis of the tumor cells, and the maximal inhibition was observed at the dose of 1.0 mg/kg (P<0.01). Bortezomib 0.5 mg/kg significantly inhibited the increase of serum IL-6 (P<0.01). Bortezomib showed significant anti-tumor effect, and tumor growth was significantly inhibited by Bortezomib with 0.5 and 1.0 mg/kg (P<0.01). Conclusion: Bortezomib can inhibit NF-κB activation, tissue wasting and cancer cachexia.

Objective To evaluated the safety and complications of endovasdcular stenting for symptomatic carotid stenosis with surgical high risk.Methods A series of 11 vessels in 9 patients at surgical high risk were treated by endovascular stenting. The complications during the procedures and postoperative periods were analyzed within one to five months. Results All of the operations were successfully performed without any serious complications. During the follow up period (averaging 6 months), there were no complications of TIAs, stokes and restenoses.Conclusions The study suggests that endovascular stenting may be safe and effective for patients at surgical high risk, but further more study is needed.

Objective:Study on the possibility that human follicular dendritic cells(FDC) can increase HIV infection and to investigate the related mechanisms.Methods:Human FDC was isolated from tonsils and cultured with infected heterogenous pheripheral lymphocytes or cultured with infected hemogenous tonsilar T lymphocytes.HIV P24 antigen,HIV 1 env DNA and HIV 1 nef RNA were determined respectively with ELISA method,PCR or RT PCR method.Results:FDCs were cultured with infected heterogenous lymphocytes,the P24 antigen is 6 7 times higher than the control group(P

Objective To investigate the change of CD8+T lymphocyte non-cytotoxic antivirus response(CNAR)in slow progressors infected by HIV.Methods Applying with density gradient and immunomagnetic beads methods to purify the CD4+T lymphocyte from the healthy person and CD8+T lymphocyte from HIV-infected individuals.The CD4+T cell was infected by HIV(SF-33)virus and cocuhured with CD8+T cell.The culture supernatant was collected and the p24 value was detected by ELISA method.Results Our study showed that the CNAR function decreased by turns of slow progressors(SP),typical progressors(TP),health control group and AIDS group.There was significant difference between groups(P<0.01).We found a significant positive correlation between the CIM+T cell ture count and the CNAR function.The virus load didn't statistically correlate with the CNAR function.Conclusion The CNAR function possibly protected the HIV-infected individuals from progression.

At present,intranasal delivery has entered clinical trial stage.In recent years,how to imroving the efficiency of intranasal delivery has been extensively investigated.This article briefly reviews some factors that impact the targeting of intranasal delivery and the drug concentration in the central nervous system.

MicroRNAs (miRNAs) are endogenous non-coding RNAs composed of 18-25 nucleotides,and they may play a role in gene regulation through completely or partially binding to target gene mRNA complementary sequences and make it degrade or prevent its translation.miRNAs play important roles in the onset and pathophysiological processes of ischemic stroke.This article reviews the roles of miRNAs in the etiology of ischemic stroke and pathophysiological mechanisms after stroke,and the potential application of miRNAs is prospected.

Objective:To better understand the changes of the NKT like cells after HIV infection and HAART treatment.Methods: Peripheral blood from HIV-infected individuals, HAART-treatment AIDS patients and healthy controls were collected, the expression of CD57 and the proliferation ability of NKT like cells before and after HAART were analyzed by flow cytometry.Results:We found that the percentage of NKT like cells before HAART was significantly lower than the healthy controls ( P<0.01 ) , and recovered after HAART treatment ( P<0.05 );the aging of NKT like cells was significantly higher before HAART compared with health individuals (P<0.01),and recovered after HAART treatment(P<0.05)the proliferation was significantly lower in vitro before HAART compared with healthy controls,and partial recovered after HAART.Conclusion: After HAART treatment,the number of NKT like cells,CD57 expression and the proliferation ability of HIV infected patients were restored.

Objective:To study the changes of the NKT like cells after HIV infected. Methods:We collected peripheral blood from 47 untreated HIV infected individuals and 31 healthy controls,and analyzed the expression of Annexin-V,Ki-67,HLA-DR and other surface molecules in NKT like cells by flow cytometry. Results:The NKT like cell percentage of untreated HIV infected group was (3. 03±1. 61)%,the NKT like cell percentage of normal control group was (8. 30±7. 42)%,the percentage of NKT like cells in HIV infected individuals was significantly lower than the healthy controls ( P<0. 05 );the NKT like cell HLA-DR expression of untreated HIV infected group and normal control group were (5. 40±4. 10)% and (0. 89±0. 83)%,the NKT like cell Annexin-V expression of untreated HIV infected group and normal control group were (30. 21±13. 15)% and (5. 40±8. 05)% ,and the activation and apoptosis of NKT like cells was significantly higher after HIV infection compared with health individuals (P<0. 001,P<0. 01),the degree of activation was negatively correlated with CD4 count (r=-0. 885 7,P<0. 05);and the NKT like cell Ki-67 expression of untreated HIV infected group and normal control group were (11. 15±4. 76)% and (27. 63±18. 31)%,the proliferation ability was significantly lower after HIV infection compared with healthy controls(P<0. 05). Conclusion:HIV infection can significantly reduce the number of NKT like cells and its ability to proliferate,and increase its ability to activation and apoptosis.