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991.
L Liu J Liu WT Wong XY Tian CW Lau YX Wang G Xu Y Pu Z Zhu A Xu KS Lam ZY Chen CF Ng X Yao Y Huang 《Hypertension》2012,60(3):833-841
Sitagliptin, a selective dipeptidyl peptidase 4 inhibitor, inhibits the inactivation and degradation of glucagon like peptide 1 (GLP-1), which is used for the treatment of type 2 diabetes mellitus. However, little is known about the role of GLP-1 in hypertension. This study investigated whether the activation of GLP-1 signaling protects endothelial function in hypertension. Two-week sitagliptin treatment (10 mg/kg per day, oral gavage) improved endothelium-dependent relaxation in renal arteries, restored renal blood flow, and reduced systolic blood pressure in spontaneously hypertensive rats. In vivo sitagliptin treatment elevated GLP-1 and GLP-1 receptor expressions, increased cAMP level, and subsequently activated protein kinase A, liver kinase B1, AMP-activated protein kinase-α and endothelial NO synthase in spontaneously hypertensive rat renal arteries. Inhibition of GLP-1 receptor, adenylyl cyclase, protein kinase A, AMP-activated protein kinase-α, or NO synthase reversed the protective effects of sitagliptin. We also demonstrate that GLP-1 receptor agonist exendin 4 in vitro treatment had similar vasoprotective effects in spontaneously hypertensive rat renal arteries and increased NO production in spontaneously hypertensive rat aortic endothelial cells. Studies using transient expressions of wild-type and dominant-negative AMP-activated protein kinase-α2 support the critical role of AMP-activated protein kinase-α in mediating the effect of GLP-1 in endothelial cells. Ex vivo exendin 4 treatment also improved endothelial function of renal arteries from hypertensive patients. Our results elucidate that upregulation of GLP-1 and related agents improve endothelial function in hypertension by restoring NO bioavailability, suggesting that GLP-1 signaling could be a therapeutic target in hypertension-related vascular events. 相似文献
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In the present era laparoscopic cholecystectomy (LC) has become the gold standard treatment of choice for gallstone disease. This technique has made a new revolution in minimal invasive surgery, but also the spectrum of complications has changed. In this paper we shared our personal experience of LC in 400 hundred cases from January 2007 to December 2010, its complications and prevention. According to our experience the complications were liver bed injury (n=32, 8%), spilled gall stones (n=29, 7.25%), port site infection (n=11, 2.75%), vascular injury (n=18, 4.5%), conversion to open surgery (n=16, 4%), biliary leak (n=10, 2.5%), bowel injury (n=3, 0.75%), CBD stricture (n=4, 1%) and umbilical port hernia (n=2, 0.5%). Before the procedure, patient consent and awareness to all possible complications which may occur intra-operatively is very important. A good surgical team and experience in this procedure seems to prevent hazardous complications. 相似文献
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Avella DM Li G Schell TD Liu D Zhang SS Lou X Berg A Kimchi ET Tagaram HR Yang Q Shereef S Garcia LS Kester M Isom HC Rountree CB Staveley-O'Carroll KF 《Hepatology (Baltimore, Md.)》2012,55(1):141-152
The high rate of mortality and frequent incidence of recurrence associated with hepatocellular carcinoma (HCC) reveal the need for new therapeutic approaches. In this study we evaluated the efficacy of a novel chemoimmunotherapeutic strategy to control HCC and investigated the underlying mechanism that increased the antitumor immune response. We developed a novel orthotopic mouse model of HCC through seeding of tumorigenic hepatocytes from SV40 T antigen (Tag) transgenic MTD2 mice into the livers of syngeneic C57BL/6 mice. These MTD2-derived hepatocytes form Tag-expressing HCC tumors specifically within the liver. This approach provides a platform to test therapeutic strategies and antigen-specific immune-directed therapy in an immunocompetent murine model. Using this model we tested the efficacy of a combination of oral sunitinib, a small molecule multitargeted receptor tyrosine kinase (RTK) inhibitor, and adoptive transfer of tumor antigen-specific CD8(+) T cells to eliminate HCC. Sunitinib treatment alone promoted a transient reduction in tumor size. Sunitinib treatment combined with adoptive transfer of tumor antigen-specific CD8(+) T cells led to elimination of established tumors without recurrence. In vitro studies revealed that HCC growth was inhibited through suppression of STAT3 signaling. In addition, sunitinib treatment of tumor-bearing mice was associated with suppression of STAT3 and a block in T-cell tolerance. CONCLUSION: These findings indicate that sunitinib inhibits HCC tumor growth directly through the STAT3 pathway and prevents tumor antigen-specific CD8(+) T-cell tolerance, thus defining a synergistic chemoimmunotherapeutic approach for HCC. 相似文献
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Jain P Javdan M Feger FK Chiu PY Sison C Damle RN Bhuiya TA Sen F Abruzzo LV Burger JA Rosenwald A Allen SL Kolitz JE Rai KR Chiorazzi N Sherry B 《Haematologica》2012,97(4):599-607