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The aim of this study was to elucidate the impact of a high-fat, high-fructose diet (HFFD; fat, 52%; fructose, 17%), in the presence of a partial (-65%) pancreatectomy )PPx), on the response of the liver and extrahepatic tissues to an orally administered, liquid mixed meal. Adult male dogs were fed either a nonpurified, canine control diet )CTR; fat, 26%; no fructose; n = 5) or a HFFD In = 5) for 8 wk. Diets were provided in a quantity to maintain neutral or positive energy balance in CTR or HFFD, respectively. Dogs underwent a sham operation or PPx at wk 0, portal and hepatic vein catheterization at wk 6, and a mixed meal test at wk 8. Postprandial glucose concentrations were significantly greater in the HFFD group (14.5 ± 2.0 mmol/L) than in the CTR group (9.2 ± 0.5 mmol/L). Impaired glucose tolerance in HFFD was due in part to accelerated gastric emptying and glucose absorption, as indicated by a more rapid rise in arterial plasma acetaminophen and the rate of glucose output by the gut, respectively, in HFFD than in CTR. It was also attributable to lower net hepatic glucose uptake INHGU) in the HFFD group 15.5 ± 3.9 μmol · kg-1 . min-1) compared to the CTR group 126.6 ± 7.0 μmol kg-1 · min-1), resulting in lower hepatic glycogen synthesis IGSYN) in the HFFD group (10.8 ± 5.4 μmol kg-1 · min-1) than in the CTR group (30.4 ± 7.0 μmol · kg-1 - min-1). HFFD also displayed aberrant suppression of Iipolysis by insulin. In conclusion, HFFD feeding accelerates gastric emptying and diminishes NHGU and GSYN, thereby impairing glucose tolerance following a mixed meal challenge. These data reveal a constellation of deleterious metabolic consequences associated with consumption of a HFFD for 8 wk. [ABSTRACT FROM AUTHOR]

Abstract: We examined the role of vagus nerves in the transmission of the portal glucose signal in conscious dogs. At time 0, somatostatin infusion was started along with intraportal insulin and glucagon at 4-fold basal and basal rates, respectively. Glucose was infused via a peripheral vein to create hyperglycemia (≃2 fold basal). At t = 90, hollow coils around the vagus nerves were perfused with −10°C or 37°C solution in the vagally cooled (COOL) and sham-cooled (SHAM) groups, respectively (n = 6 per group). Effectiveness of vagal blockade was demonstrated by increase in heart rate during perfusion in the COOL vs SHAM groups (183 ± 3 vs 102 ± 5 beats per minute, respectively) and by prolapse of the third eyelid in the COOL group. Arterial plasma insulin (22 ± 2 and 24 ± 3 μU/mL) and glucagon (37 ± 5 and 40 ± 4 pg/mL) concentrations did not change significantly between the first experimental period and the coil perfusion period in either the SHAM or COOL group, respectively. The hepatic glucose load throughout the entire experiment was 46 ± 1 and 50 ± 2 mg · kg−1 · min−1 in the SHAM and COOL groups, respectively. Net hepatic glucose uptake (NHGU) did not differ in the SHAM and COOL groups before (2.2 ± 0.5 and 2.9 ± 0.8 mg · kg−1 · min−1, respectively) or during the cooling period (3.0 ± 0.5 and 3.4 ± 0.6 mg · kg−1 · min−1, respectively). Likewise, net hepatic glucose fractional extraction and nonhepatic glucose uptake and clearance were not different between groups during coil perfusion. Interruption of vagal signaling in the presence of hyperinsulinemia and hyperglycemia resulting from peripheral glucose infusion did not affect NHGU, further supporting our previous suggestion that vagal input to the liver is not a primary determinant of NHGU. [Copyright &y& Elsevier]

In contrast to Li/Ca and Mg/Ca, Li/Mg is strongly anticorrelated with temperature in aragonites precipitated by the benthic foraminifer Hoeglundina elegans and a wide range of scleractinian coral taxa. We propose a simple conceptual model of biomineralization that explains this pattern and is consistent with available abiotic aragonite partition coefficients. Under this model the organism actively modifies seawater within its calcification pool by raising its [Ca 2+ ], using a pump that strongly discriminates against both Li + and Mg 2+ . Rayleigh fractionation during calcification effectively reverses this process, removing Ca 2+ while leaving most Li + and Mg 2+ behind in the calcifying fluid. The net effect of these two processes is that Li/Mg in the calcifying fluid remains very close to the seawater value, and temperature-dependent abiotic partition coefficients are expressed in the biogenic aragonite Li/Mg ratio. We further show that coral Sr/Ca is consistent with this model if the Ca 2+ pump barely discriminates against Sr 2+ . In H. elegans the covariation of Sr/Ca and Mg/Ca requires either that the pump more strongly discriminates against Sr 2+ , or that cation incorporation is affected by aragonite precipitation rate via the mechanism of surface entrapment. In either case Li/Mg is minimally affected by such ‘vital effects’ which plague other elemental ratio paleotemperature proxies. [ABSTRACT FROM AUTHOR]

Abstract: Background: Hepatitis C virus (HCV) recurrence after living donor liver transplantation (LDLT) represents a challenging issue due to universal viral recurrence and invasion into the graft, although the incidence of histological recurrence, risk factors, and survival rates are still controversial. Patients and Methods: Recurrence of HCV was studied in 38 of 53 adult patients who underwent LDLT. Results: Recipient and graft survivals were 86.6% at the end of the follow-up which was comparable to literature reports for deceased donor liver transplantation (DDLT). Clinical HCV recurrence was observed in 10/38 patients (26.3%). Four patients developed mild fibrosis with a mean fibrosis score of 0.6 and mean grade of histological activity index (HAI) of 7.1. None of the recipients developed allograft cirrhosis during the mean follow-up period of 16 ± 8.18 months (range, 4–35 months). Estimated and actual graft volumes were negatively correlated with the incidence and early clinical HCV recurrence. None of the other risk factors were significantly correlated with clinical HCV recurrence: gender, donor and recipient ages, pretransplantation Child-Pugh or model for end-stage liver disease (MELD) scores, pre- and postoperative viremia, immunosuppressive drugs, pulse steroid therapy, and preoperative anti-HBc status. Conclusions: Postoperative patient and graft survival rates for HCV (genotype 4)-related cirrhosis were more or less comparable to DDLT reported in the literature. Clinical HCV recurrence after LDLT in our study was low. Small graft volume was a significant risk factor for HCV recurrence. A longer follow-up and a larger number of patients are required to clarify these issues. [Copyright &y& Elsevier]

Abstract: Introduction and objectives: Living donor liver transplantation (LDLT) is an alternative source of organs for patients with end-stage liver disease (ESLD) in absence of deceased donor LT. In LDLT the greatest concern is donor safety. Our objective was to evaluate the outcome of donors after right lobe liver donation in a single LT center in Egypt. Patients and methods: Fifty LDL resections were performed from 2001 to 2004. The mean donor age was 29.2 ± 6.4 years. Residual liver volume was 41.1 ± 4.5%. Mean operative time was 560 ± 62.2 minutes; mean ICU stay, less than 24 hours; mean hospital stay, 15.4 ± 7.7 days; and mean follow-up period, 6 months. Results: There was no mortality. The overall complication rate was 68% (34 donors). Major complications included intraoperative bleeding in one, biliary leak in two, and pneumonia in three donors. Minor complications included mild pleural effusion in 13 donors, transient ascites in 10, mild depression in 7, intra-abdominal collections in 3, and wound infections in 1 donor. Residual liver volume did not affect the complication rate. None required reoperation. Return to predonation activity occurred within 6 to 8 weeks. No liver impairment occurred during follow-up. Conclusion: Right lobe adult LDLT is a safe procedure with regard to donor outcome. Major complications occurred in only 10% of our series. [Copyright &y& Elsevier]