The role of wild rodents in the transmission of Trypanosoma evansi infection in an endemic area of the Canary Islands (Spain).

Trypanosoma evansi was diagnosed for the first time in camels in the Canary Islands in 1997. Several sanitary measures including treatment of infected animals were taken; however, nowadays a little area is still infected. In order to determine possible reservoirs 138 wild rodents were trapped, 64 of them in the infected farms and the remaining 74 in other areas. The captured species were Rattus rattus (24), Rattus norvegicus (69) and Mus musculus domesticus (45). Serological (CATT/T. evansi), parasitological (micro-Hematocrit Centrifugation technique and stained smears) and molecular (PCR) methods for T. evansi and T. lewisi were used as diagnostic methods. None of the examined rodents was positive for T. evansi; 18, however, showed motile trypanosomes at micro-Hematocrit Centrifugation technique and resulted positive for T. lewisi by PCR. The results would suggest that the studied rodent species would not play a relevant role in the epidemiology of T. evansi infection in Canaries.

Insight into the role of CYBA A640G and C242T gene variants and coronary heart disease risk. A case-control study.

The CYBA gene variants have been inconsistently associated with coronary heart disease (CHD) risk. A case-control study was conducted genotyping 619 subjects to explore the contribution of C242T and A640G to CHD risk in the population. A significant risk was found associated with GG homozygosity (odds ratio (OR) 2.132, 95% confidence interval, 1.113-4.085). The C242T variant was associated with CHD risk in women. Bias due to population stratification was analysed. Phenotype changes linked to these polymorphisms were evaluated. Superoxide measurements revealed higher production as indicated by the presence of the G and T alleles. Differences in mRNA concentration in heterozygous A640G samples were analysed. Higher levels of G allele mRNA compared with A allele mRNA were found. NAD(P)H oxidase p22phox sub-unit expression was evaluated with Western blot. Experiments revealed a gradual relationship in p22phox protein expression according to genotypes of the analysed variants. Those GG TT double homozygous showed increased p22phox protein expressions regarding AA CC double homozygous. This study has demonstrated increased expression and activity of the NAD(P)H system components during atherogenesis and the results could help explain the relevance of the A640G variant as a CHD marker.

Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model.

BACKGROUND: Thiazolidinediones exert anti-inflammatory and anti-oxidative roles and attenuate atherosclerosis by mechanisms partially independent of their metabolizing actions. High doses of angiotensin type 1 receptor (AT1R) blocker losartan (LST) seem to promote fat cell formation by preserving PPARgamma activity. METHODS: C57BL/6J diet-induced atherosclerotic susceptible mice randomly received a normal or a high-fat high-cholesterol (HFHC) diet and were treated with rosiglitazone (RG), LST or a vehicle for 12 weeks. RESULTS: HFHC was associated with increased PPARgamma gene expression without an over regulation of PPARgamma responsive genes, whereas RG and LST treatments were found to maintain PPARgamma activity without resulting in increased PPARgamma gene expression. A better anti-inflammatory and antioxidant profile in mice treated with RG regarding LST was observed in spite of a similar PPARgamma preserved activity. Chromatin immunoprecipitation (ChIP) assays revealed that animals under HFHC diet treated with RG showed a significant nuclear factor erythroid 2-like 2 (Nrf2)-dependent down-regulation of the expression of the CD36 gene. CONCLUSION: The PPARgamma agonist RG exerts antioxidant properties that significantly reduced Nrf-2-dependent CD-36 up-regulation in mice under HFHC diet. Because LST treatment was also associated with a preserved PPARgamma activity, our data suggests that these RG antioxidant effects are partially independent of its PPARgamma metabolizing properties.

[Arterial blood pressure variations: homocysteine and nitric oxide synthase gene polymorphisms (NOS3)]. / Presión arterial, homocisteína y variantes polimórficas del gen de la óxido nítrico sintasa (NOS3).

BACKGROUND: The nitric oxide synthase (NOS3) G894T gene polymorphism seems as a genetic determinant of total homocysteine (tHcy) concentrations through an effect on folate catabolism. We tested for a significant contribution to blood pressure values for the NOS3 G894T and 4a/b gene polymorphisms and whether those changes could explain the modulating effect on tHcy concentrations. PATIENTS AND METHODS: We analyzed 158 healthy men. The NOS3 gene polymorphisms were determined by polymerase chain reaction (PCR) and restriction fragment analysis (G894T) and by PCR (4a/b). Total homocysteine concentrations were evaluated by the fluorescence polarization immunoassay method. RESULTS: In our population we did not obtain a significant contribution of the G894T to blood pressure variations. However, tHcy mean concentration values differed according G894T genotypes (P = 0.01). Interestingly, we did not obtain a significant modulating effect on tHcy concentrations according to 4a/b genotypes although the 4a/b genotype distribution was statistically associated with blood pressure variations. CONCLUSION: Our results showed a modulating effect of the NOS3 4a/b gene variant on tHcy concentrations that is at least partially provoked by discrete blood pressure increments. Nevertheless, our multivariate analysis did not show a statistical significant role for the NOS3 G894T gene polymorphism on tHcy concentrations.

Presión arterial, homocisteína y variantes polimórficas del gen de la óxido nítrico sintasa (NOS3) / Arterial blood pressure variations: homocysteine and nitric oxide synthase gene polymorphisms (NOS3)

Fundamento y objetivo: El polimorfismo G894T en el gen humano NOS3 se ha sugerido como un determinante genético que contribuye a modular las variaciones de las concentraciones de homocisteína (tHcy) a través de un efecto indirecto sobre el catabolismo del folato. Nos planteamos estudiar la contribución de las variantes NOS3 G894T y 4a/b a las variaciones de presión arterial y la contribución de estas variaciones a la modulación de concentraciones de tHcy. Pacientes y métodos: Analizamos 158 hombres sanos. Los genotipos de los polimorfismos NOS3 se determinaron mediante amplificación por reacción en cadena de la polimerasa (PCR) y posterior digestión enzimática (G894T) y por PCR (4a/b). Las concentraciones de tHcy mediante inmunofluorescencia polarizada. Resultados: En nuestra población la variante G894T no parece contribuir de forma significativa a las variaciones de presión arterial, pero obtuvimos una gradación de concentraciones de tHcy en función de los genotipos G894T (P = 0,01). No obtuvimos un efecto modulador significativo sobre los niveles de tHcy para la variante 4a/b, si bien su contribución a la variación de cifras de presión arterial resultó estadísticamente significativa. Conclusiones: Nuestros resultados muestran un efecto modulador de la variante 4a/b en el gen NOS3 sobre la variación de concentraciones de tHcy que se produce, parcialmente y a expensas de incrementos de valores de presión arterial. En análisis multivariante, el papel del polimorfismo G894T del gen NOS3 sobre la modulación de las concentraciones de tHcy, no resultó sin embargo estadísticamente relevante

Background: The nitric oxide synthase (NOS3) G894T gene polymorphism seems as a genetic determinant of total homocysteine (tHcy) concentrations through an effect on folate catabolism. We tested for a significant contribution to blood pressure values for the NOS3 G894T and 4a/b gene polymorphisms and whether those changes could explain the modulating effect on tHcy concentrations. Patients and methods: We analyzed 158 healthy men. The NOS3 gene polymorphisms were determined by polymerase chain reaction (PCR) and restriction fragment analysis (G894T) and by PCR (4a/b). Total homocysteine concentrations were evaluated by the fluorescence polarization immunoassay method. Results: In our population we did not obtain a significant contribution of the G894T to blood pressure variations. However, tHcy mean concentration values differed according G894T genotypes (P = 0.01). Interestingly, we did not obtain a significant modulating effect on tHcy concentrations according to 4a/b genotypes although the 4a/b genotype distribution was statistically associated with blood pressure variations. Conclusion: Our results showed a modulating effect of the NOS3 4a/b gene variant on tHcy concentrations that is at least partially provoked by discrete blood pressure increments. Nevertheless, our multivariate analysis did not show a statistical significant role for the NOS3 G894T gene polymorphism on tHcy concentrations

Estrategia del gen candidato en la hipertensión arterial: Estudios de ligamiento y asociación / Strategy of the candidate gene in arterial hypertension: linkage and association study

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