Comparing to vehicle (distilled water, DW), caffeine decreased cardiac index, increased systemic vascular resistance, reduced portal pressure, superior mesenteric artery (SMA) flow, mesenteric vascular density, portosystemic shunting, intrahepatic angiogenesis, and fibrosis without affecting liver and renal biochemistry. The beneficial effects were reversed by selective adenosine selleck screening library A1 agonist N6-cyclopentyladenosine (CPA) or A2A agonist GCS21680. Both prophylactic and therapeutic caffeine treatment decreased portal resistance and portal pressure in thioacetamide (TAA, 200mg/kg, thrice weekly for 8 weeks)-induced cirrhotic rats. Caffeine down-regulated

endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), phospho-VEGFR2 and VX 770 phospho-Akt mesenteric protein expressions. Caffeine adversely affected viability of hepatic stellate and sinusoidal endothelial cells, which was reversed by CPA and GCS21680. On the other hand, caffeine did not modify the vascular response to vasoconstrictors

in splanchnic, hepatic and collateral vascular beds. Conclusions: Caffeine decreased portal pressure, ameliorated hyperdynamic circulation, portosystemic shunting, mesenteric angiogenesis, hepatic angiogenesis and fibrosis in cirrhotic rats. Caffeine may be a feasible candidate to ameliorate portal hypertension-related complications in cirrhosis. This article is protected by copyright. All rights reserved. “
“This chapter contains sections titled: Introduction What is the evidence for the role of H. pylori in peptic ulcer disease? Association of H. pylori with ulcer disease (strength, consistency and specificity) Temporal relationship Biological gradient Effects of interventions: outcomes following H. pylori eradication Coherence of the data with earlier epidemiological information Treatment of duodenal ulcer Treatment of gastric ulcer

H. pylori eradication therapy Summary References “
“Hepatocellular carcinoma (HCC) is the sixth-most common malignancy diagnosed worldwide.[1] Late-stage presentation, comorbidities, and limited donor availability enables only 10% of patients to receive curative therapies. Hence, there exists a critical need for novel treatments addressing HCC at all this website stages. During the last decade, several transarterial locoregional therapies have been developed. One of these, yttrium-90 (90Y) radioembolization, has matured into a recognized treatment option, with a demonstration of a clear palliative role by inducing necrosis and delaying progression.[2-8] This overview will describe the biological rationale for 90Y, highlight seminal data, propose research questions, and discuss the future role of 90Y in HCC. HCC is a tumor that arises almost exclusively in cirrhosis caused by viruses, alcohol, or non-alcohol-related steatohepatitis, insulin-resistant metabolism, autoimmunity, and others. Therefore, survival of HCC patients is related to the tumor and underlying liver condition.