Characterisation and identification of grapevine cultivars (Vitis vinifera L.) from northwestern Spain using microsatellite markers and ampelometric methods

Nine grapevine varieties from northwestern Spain (8 commonly known as types of Caíño and one as Tinta Femia) were characterised by constructing their typical ‘mean leaves’ and by determining their genetic profiles with respect to 6 microsatellite markers. Leaf morphologies were compared and the similarities between the cultivars were determined. Thirty three alleles were detected at the 6 microsatellite loci analysed. The different cultivars were successfully identified by both methods. In combination, the different techniques provide a more complete variety characterisation. Synonymy between these and other Spanish and Portuguese cultivars is discussed.

Pleiotropic alterations in gene expression in Latin American Fasciola hepatica isolates with different susceptibility to drugs

Background: Fasciola hepatica is the main agent of fasciolosis, a zoonotic disease affecting livestock worldwide, and an emerging food-borne disease in humans. Even when effective treatments are available, drugs are costly and can result in tolerance, liver damage and normally they do not prevent reinfection. Drug-resistant strains in livestock have been reported in various countries and, more worryingly, drug resistance in human cases has emerged in South America. The present study aims to characterize the transcriptome of two South American resistant isolates, the Cajamarca isolate from Peru, resistant to both triclabendazole and albendazole (TCBZR/ABZR) and the Rubino isolate from Uruguay, resistant to ABZ (TCBZS/ABZR), and compare them to a sensitive strain (Cenapa, Mexico, TCBZS/ABZS) to reveal putative molecular mechanisms leading to drug resistance. Results: We observed a major reduction in transcription in the Cajamarca TCBZR/ABZR isolate in comparison to the other isolates. While most of the differentially expressed genes are still unannotated, several trends could be detected. Specific reduction in the expression levels of cytoskeleton proteins was consistent with a role of tubulins as putative targets of triclabendazole (TCBZ). A marked reduction of adenylate cyclase might be underlying pleiotropic effects on diverse metabolic pathways of the parasite. Upregulation of GST mu isoforms suggests this detoxifying mechanism as one of the strategies associated with resistance. Conclusions: Our results stress the value of transcriptomic approaches as a means of providing novel insights to advance the understanding of drug mode of action and drug resistance. The results provide evidence for pleiotropic variations in drug-resistant isolates consistent with early observations of TCBZ and ABZ effects and recent proteomic findings

Implementation of Sliding Mode Control in a Semi Bridgeless Boost Converter with Power Factor Correction

ABSTRACT: This paper proposes a new sliding surface for controlling a Semi-Bridgeless Boost Converter (SBBC) which simultaneously includes Power Factor Correction (PFC) and DC bus regulation. The proposed sliding surface is composed of three terms: First, a normalized DC voltage error term for controlling DC bus and rejecting DC voltage disturbances, normalization was performed for increasing system robustness during start-up and large disturbances. Second, an AC current error term for implementing a PFC scheme and guarantying fast current stabilization during disturbances. Third, an integral of AC current error term for increasing the stability of the overall system. Also, an Adaptive Hysteresis Band (AHB) is implemented for keeping constant the switching frequency and reducing the THDi. The proposed sliding surface was validated by means of sliding mode conditions and Lyapunov stability criteria. Simulations for comparing performance were performed between: a cascade PI control, a hybrid PI-Sliding Mode Control (PI-SMC), and Sliding Mode Control (SMC) with the proposed surface; additionally, it is presented an stability analysis for the proposed surface in start-up and under large perturbations. It is also presented experimental results for PI-SMC and SMC implemented in a SBBC prototype. The proposed surface implemented in the SMC presents the best dynamic behavior removing DC over voltages and responding faster under DC voltage changes or DC load current perturbations

Relationship between Serum Concentration of Uric Acid and Insulin Secretion among Adults with Type 2 Diabetes Mellitus

To determine the relationship between serum concentrations of uric acid and insulin secretion with hyperglycaemic clamp technique among adults with type 2 diabetes mellitus (DM2) without hyperuricemia, we carried out a cross-sectional study on 45 patients of both gender. We observed correlation between uric acid with male gender r = 0.710 (P = 0.001). Also correlation between uric acid and total insulin secretion was positive r = 0.295 (P = 0.049). As well as a positive correlation adjusted for body mass index was demonstrated for the first, second, and total phases of insulin secretion, respectively, r = 0.438 (P = 0.022), r = 0.433 (P = 0.022), and r = 0.439 (P = 0.024). Serum concentration of uric acid showed a positive relationship with the total phase of insulin secretion; even in states prior to hyperuricemia, uric acid can play an important role in the function of the beta cell in patients with DM2

Article Ecto-Nucleotide Triphosphate Diphosphohydrolase-2 (NTPDase2) Deletion Increases Acetaminophen-Induced Hepatotoxicity

Ecto-nucleotidase triphosphate diphosphohydrolase-2 (NTPDase2) is an ecto-enzyme that is expressed on portal fibroblasts in the liver that modulates P2 receptor signaling by regulating local concentrations of extracellular ATP and ADP. NTPDase2 has protective properties in liver fibrosis and may impact bile duct epithelial turnover. Here, we study the role of NTPDase2 in acute liver injury using an experimental model of acetaminophen (APAP) intoxication in mice with global deletion of NTPDase2. Acute liver toxicity was caused by administration of acetaminophen in wild type (WT) and NTPDase2-deficient (Entpd2 null) mice. The extent of liver injury was compared by histology and serum alanine transaminase (ALT). Markers of inflammation, regeneration and fibrosis were determined by qPCR). We found that Entpd2 expression is significantly upregulated after acetaminophen-induced hepatotoxicity. Entpd2 null mice showed significantly more necrosis and higher serum ALT compared to WT. Hepatic expression of IL-6 and PDGF-B are higher in Entpd2 null mice. Our data suggest inducible and protective roles of portal fibroblast-expressed NTPDase2 in acute necrotizing liver injury. Further studies should investigate the relevance of these purinergic pathways in hepatic periportal and sinusoidal biology as such advances in understanding might provide possible therapeutic targets

Ecto-Nucleotide Triphosphate Diphosphohydrolase-2 (NTPDase2) Deletion Increases Acetaminophen-Induced Hepatotoxicity

Ecto-nucleotidase triphosphate diphosphohydrolase-2 (NTPDase2) is an ecto-enzyme that is expressed on portal fibroblasts in the liver that modulates P2 receptor signaling by regulating local concentrations of extracellular ATP and ADP. NTPDase2 has protective properties in liver fibrosis and may impact bile duct epithelial turnover. Here, we study the role of NTPDase2 in acute liver injury using an experimental model of acetaminophen (APAP) intoxication in mice with global deletion of NTPDase2. Acute liver toxicity was caused by administration of acetaminophen in wild type (WT) and NTPDase2-deficient (Entpd2 null) mice. The extent of liver injury was compared by histology and serum alanine transaminase (ALT). Markers of inflammation, regeneration and fibrosis were determined by qPCR). We found that Entpd2 expression is significantly upregulated after acetaminophen-induced hepatotoxicity. Entpd2 null mice showed significantly more necrosis and higher serum ALT compared to WT. Hepatic expression of IL-6 and PDGF-B are higher in Entpd2 null mice. Our data suggest inducible and protective roles of portal fibroblast-expressed NTPDase2 in acute necrotizing liver injury. Further studies should investigate the relevance of these purinergic pathways in hepatic periportal and sinusoidal biology as such advances in understanding might provide possible therapeutic targets