Strong sesquiterpene emissions from Amazonian soils.

The Amazon rainforest is the world's largest source of reactive volatile isoprenoids to the atmosphere. It is generally assumed that these emissions are products of photosynthetically driven secondary metabolism and released from the rainforest canopy from where they influence the oxidative capacity of the atmosphere. However, recent measurements indicate that further sources of volatiles are present. Here we show that soil microorganisms are a strong, unaccounted source of highly reactive and previously unreported sesquiterpenes (C15H24; SQT). The emission rate and chemical speciation of soil SQTs were determined as a function of soil moisture, oxygen, and rRNA transcript abundance in the laboratory. Based on these results, a model was developed to predict soil-atmosphere SQT fluxes. It was found SQT emissions from a Terra Firme soil in the dry season were in comparable magnitude to current global model canopy emissions, establishing an important ecological connection between soil microbes and atmospherically relevant SQTs.

1,4-Naphthoquinones potently inhibiting P2X7 receptor activity.

P2X7 receptor (P2X7R) is an ATP-gated ion-channel with potential therapeutic applications. In this study, we prepared and searched a series of 1,4-naphthoquinones derivatives to evaluate their antagonistic effect on both human and murine P2X7 receptors. We explored the structure-activity relationship and binding mode of the most active compounds using a molecular modeling approach. Biological analysis of this series (eight analogues and two compounds) revealed significant in vitro inhibition against both human and murine P2X7R. Further characterization revealed that AN-03 and AN-04 had greater potency than BBG and A740003 in inhibiting dye uptake, IL-1ß release, and carrageenan-induced paw edema in vivo. Moreover, we used electrophysiology and molecular docking analysis for characterizing AN-03 and AN-04 action mechanism. These results suggest 1,4-napthoquinones, mainly AN-04, as potential leads to design new P2X7R blockers and anti-inflammatory drugs.

Liver transplantation in a patient with clinical manifestations of cryptogenic cirrhosis: a case report of hepar lobatum as a primary liver condition.

BACKGROUND: This article reports a case of hepar lobatum, a peculiar and rare type of liver deformity, originally described in association with infectious or parasitic diseases and with malignancies. CASE REPORT: We have described a 42-year-old woman with this disorder, which was unrelated to the known conditions and referred for liver transplantation for having clinical manifestations of cirrhosis, portal hypertension, and impaired hepatic function. CONCLUSIONS: The observed histologic pattern suggests that hepar lobatum could be, in some patients, the effect of a primary process of hamartomatous origin involving the organ vascular supply.

Liver failure and the need for transplantation in 6 patients with hepatoportal sclerosis.

Hepatoportal sclerosis (HPS), first reported by Mikkelsen et al in 1965, is a pathologic condition that does not cause cirrhotic portal hypertension. The primary hepatic lesion in HPS is found in portal vein branches with preserved synthetic function. Rarely do patients with HPS need liver transplantation. The aim of this study was to describe the clinical and pathologic features of 6 HPS cases who underwent liver transplantation (OLT). From 2000 to 2008, 6 OLT candidates were diagnosed with HPS: 3 displayed bleeding varices and 4 ascites. Child-Pugh evaluation was class B (n = 4) or C (n = 2). The Model for End-stage Liver Disease scores were 18 (n = 2), 20 (n = 3), and 22 (n = 1). Cirrhosis resulted from presumed diagnoses of alcohol n = (1), autoimmune n = (2) or cryptogenic cirrhosis n = (3). On histologic examination, there was marked phlebosclerosis in all cases, including nonocclusive portal vein thrombosis (n = 3), intense portal fibrosis (n = 1), moderate portal fibrosis (n = 5), and uniform moderate sinusoidal dilatation without megasinusoid formation, but with ductal biliary proliferation and ductal biliary fibrosis in all cases. Cholestasis was observed in 1 and incomplete septal cirrhosis in 4 cases. None of the subjects showed histological features of the presumed underlying liver disease. The overall survival of this group was no different from that of other OLT patients. HPS causing hepatic failure may require liver transplantation. Fhlebosclerosis andportal fibrosis may contribute to the loss of hepatic synthesis leading to the need for hepatic transplant. Significant portal fibrosis and phlebosclerosis can contribute to hepatic parenchymal and posterior synthetic loss.