Reduced population size does not affect the mating strategy of a vulnerable and endemic seabird.

Bottleneck episodes may occur in small and isolated animal populations, which may result in decreased genetic diversity and increased inbreeding, but also in mating strategy adjustment. This was evaluated in the vulnerable and socially monogamous Monteiro's Storm-petrel Hydrobates monteiroi, a seabird endemic to the Azores archipelago which has suffered a dramatic population decline since the XVth century. To do this, we conducted a genetic study (18 microsatellite markers) in the population from Praia islet, which has been monitored over 16 years. We found no evidence that a genetic bottleneck was associated with this demographic decline. Monteiro's Storm-petrels paired randomly with respect to genetic relatedness and body measurements. Pair fecundity was unrelated to genetic relatedness between partners. We detected only two cases of extra-pair parentage associated with an extra-pair copulation (out of 71 offspring). Unsuccessful pairs were most likely to divorce the next year, but genetic relatedness between pair mates and pair breeding experience did not influence divorce. Divorce enabled individuals to improve their reproductive performances after re-mating only when the new partner was experienced. Re-pairing with an experienced partner occurred more frequently when divorcees changed nest than when they retained their nest. This study shows that even in strongly reduced populations, genetic diversity can be maintained, inbreeding does not necessarily occur, and random pairing is not risky in terms of pair lifetime reproductive success. Given, however, that we found no clear phenotypic mate choice criteria, the part played by non-morphological traits should be assessed more accurately in order to better understand seabird mating strategies.

Enhanced plasma levels of oxidized low-density lipoprotein increase circulating nuclear factor-kappa B activation in patients with unstable angina.

OBJECTIVES: The purpose of this study was to investigate the effect of circulating levels of oxidized low-density lipoprotein (ox-LDL) on nuclear factor-kappa B (NF-kB) activation in peripheral blood mononuclear cells (PBMC) of patients with unstable angina (UA) or stable angina (SA) and control subjects. BACKGROUND: Nuclear factor-kB might be involved in atherosclerosis, as is suggested by the presence of activated NF-kB in human atherosclerotic lesions. METHODS: Levels of plasma ox-LDL and circulating NF-kB in PBMC (and in separated lymphocytes and monocytes) were measured in 27 control subjects and 29 SA and 27 UA patients. In in vitro studies, the effect of ox-LDL and of the sera derived from a subgroup of UA patients and control subjects on monocytic NF-kB activation was also evaluated. RESULTS: The UA and SA patients had higher levels of circulating ox-LDL and NF-kB in PBMC than control subjects (p < 0.001). The increase in circulating NF-kB was mainly due to the activation of monocytes. In the in vitro studies, ox-LDL dose-dependently increased the activation of NF-kB in monocytes, but not in lymphocytes derived from healthy volunteers. This increase was related to the expression of lectin-like ox-LDL receptor-1 on monocytes. The incubation of monocytes with the sera derived from the UA patients induced a significant increase in NF-kB activation compared with the sera derived from the control subjects. CONCLUSIONS: The data suggest that the activation of NF-kB in monocytes of UA patients is, at least in part, induced by circulating molecules such as ox-LDL, which has been found to be particularly elevated in UA patients.

Plasma levels of oxidized-low-density lipoproteins are higher in patients with unstable angina and correlated with angiographic coronary complex plaques.

OBJECTIVES: To measure circulating levels of oxidized-low-density lipoproteins (ox-LDL) in patients with stable and unstable angina and controls, and to investigate their correlation with the extent of coronary artery disease (CAD) and the presence of complex plaques at coronary angiography. METHODS AND RESULTS: Circulating ox-LDL were assessed, using ELISA, in patients with unstable angina (UA, n=26), stable angina (SA, n=29) and in controls (C, n=27). All patients underwent coronary angiography. The extent of CAD was evaluated using a quantitative score, while the presence of complex, vulnerable plaques was angiographically assessed. Ox-LDL were higher in UA patients than in SA patients and in C subjects, and in SA patients than in C subjects (C, 45.6+/-12.8 U/L; SA, 58.8+/-11.0 U/L; UA, 73.7+/-13.6 U/L; p<0.001). No correlation was found with the extent of atherosclerotic disease in the coronary tree. Patients with angiographic complex lesions showed significantly higher levels of ox-LDL (68.4+/-13.9 U/L versus 55.2+/-16.4 U/L, p<0.001). Multiple regression analysis showed that ox-LDL were independent predictors of the presence of complex plaques (p<0.023). CONCLUSIONS: Ox-LDL levels are higher in unstable patients and correlate with the presence of angiographically documented complex plaques. Ox-LDL might be markers of destabilization of CAD.

The platelet-endothelium interaction mediated by lectin-like oxidized low-density lipoprotein receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells.

OBJECTIVES: To address the potential role of the endothelial lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the thrombotic system, in this study we first examined whether platelet interaction with LOX-1 generated reactive oxygen species (ROS) and superoxide (O2.-) and then investigated the relationship between the intracellular production of O2.- and the availability of nitric oxide (NO). BACKGROUND: Oxidative inactivation of NO is regarded as an important cause of its decreased biologic activity which may favor platelet-dependent arterial thrombosis. METHODS: Bovine aortic endothelial cells (BAECs) and Chinese hamster ovary-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) were incubated at different times with human platelets. The ROS, O2.-, and NO were measured in cells by flow cytometry. RESULTS: The incubation of BAECs and BLOX-1-CHO cells with human platelets induced a sharp and dose-dependent increase in intracellular concentration of ROS and O2.- (p from <0.01 to <0.001). The increase in intracellular concentration of O2.- was followed by a dose-dependent reduction in basal and bradykinin-induced intracellular NO concentration (p from <0.01 to <0.001). The increase in O2.- and the reduction of NO were inhibited by the presence of vitamin C and anti-LOX-1 monoclonal antibody (p < 0.001). CONCLUSIONS: The results of this study show that one of the pathophysiologic consequences of platelet binding to LOX-1 may be the inactivation of NO through an increased cellular production of O2.-.

Nebivolol and its 4-keto derivative increase nitric oxide in endothelial cells by reducing its oxidative inactivation.

OBJECTIVES: The objective of the present study was to elucidate the vasodilator mechanisms of nebivolol, a high selective beta(1)-receptor antagonist with antioxidant properties. BACKGROUND: Oxidative inactivation of nitric oxide (NO) is regarded as an important cause of its decreased biological activity. METHODS: Oxidative stress was induced through the binding of oxidized (ox)-low-density lipoprotein (LDL) to its specific endothelial receptor, called "lectin-like oxidized LDL receptor-1" (LOX-1), in bovine and human endothelial cells and in Chinese hamster ovary cells stably expressing bovine LOX-1 (BLOX-1-CHO cells). Reactive oxygen species (ROS), superoxide (O(2)(*-)), and NO were measured in cells by flow cytometry. RESULTS: Nebivolol and its 4-keto derivative prevented in a dose-dependent manner the increase of ROS (p < 0.001) and O(2)(*-) (p < 0.001) in bovine aortic endothelial cells (BAECs), human umbilical vein endothelial cells (HUVECs), and BLOX-1-CHO cells stimulated with ox-LDL. Atenolol had no effect. The incubation of HUVECs and BAECs with ox-LDL reduced basal and bradykinin-induced NO and nitrite concentration (p from <0.001 to <0.01). Nebivolol and its 4-keto derivative prevented the reduction of basal and stimulated NO and nitrite concentration (p from <0.001 to <0.01) while atenolol had no effect. The preincubation of BAECs with blocking anti-LOX-1 monoclonal antibody (LOX-1 mAb) significantly counteracted the effect of ox-LDL on stimulated generation of NO (p < 0.001), but the effect was significantly lower than that of nebivolol and its 4-keto derivative alone (p < 0.01). CONCLUSIONS: In conclusion, the findings of the present study indicate that nebivolol increases NO also by decreasing its oxidative inactivation.

Zofenopril inhibits the expression of adhesion molecules on endothelial cells by reducing reactive oxygen species.

Hypertension and coronary artery disease are intimately connected. The migration of circulating monocytes into the subendothelial occurs through the expression of some adhesion molecules on endothelial cells. The nuclear factor (NF)-kappaB, a redox-sensitive element, plays a key role in adhesion molecule gene induction. In this study we have compared the effects of two different angiotensin converting enzyme (ACE) inhibitors, one possessing an active sulfhydryl group (zofenopril) and one lacking this group (enalapril) on the cellular redox state (monitored by measuring intracellular reactive oxygen species and thiol status), expression of adhesion molecules, and activation of NF-kappaB in human umbilical vein endothelial cells (HUVECs). Zofenoprilat, the active form of zofenopril, significantly and dose dependently reduced the intracellular reactive oxygen species (ROS) and superoxide formation induced by oxidized low-density lipoprotein (ox-LDL) (P <.001) and tumor necrosis factor-alpha (TNF-alpha) (P <.001). Enalaprilat, the active form of enalapril, was ineffective. Zofenoprilat but not enalaprilat also decreased the consumption of the intracellular GSH induced by ox-LDL (P <.01) and TNF-alpha (P <.01). Although zofenoprilat significantly and dose dependently reduced the expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin induced by ox-LDL (P <.01) and TNF-alpha (P <.01) on HUVECs, enalaprilat did not. Ox-LDL and TNF-alpha increased the activation of NF-kappaB and the preincubation of HUVECs with zofenoprilat, but not with enalaprilat, dose dependently reduced its activation (P <.001). The conclusion is that the sulfhydryl (SH)-containing ACE inhibitors may be useful in inhibiting foam cell formation and thus slow the development of atherosclerosis.

Antioxidant activity of different dihydropyridines.

Lacidipine, a dihydropyridine-based calcium antagonist (DHP), has already been demonstrated to possess antioxidant activity and to reduce the intracellular production of reactive oxygen species (ROS). To verify if this effect is a peculiarity of this molecule, or belongs to other DHPs, the activity of lacidipine was compared with those of amlodipine, lercanidipine, nimodipine, and nifedipine. The DHPs were incorporated in bovine aortic endothelial cells (BAECs). Cu(2+)-oxidized LDL (ox-LDL, 5 microM) was incubated with BAECs for 5 min. 2',7'-Dichlorofluorescein (DCF) as expression of intracellular ROS production was measured by flow cytometry. Ox-LDL induced a strong increase in intracellular ROS formation (p<0.001) that was significantly reduced only with lacidipine and lercanidipine (p from <0.05 to <0.01); the effect of lacidipine, however, resulted in being much more evident than lercanidipine (p<0.01); amlodipine, nimodopine, and nifedipine had no effect on ROS formation. The lowest IC50s, i.e. the concentrations determining the 50% reduction of ROS, were obtained with lacidipine (p<0.01). The inhibitory effect of lacidipine on ox-LDL-induced ROS production in endothelial cells is a peculiarity of this molecule through its antioxidant activity.

Cisticercosis cerebral. Elevación de la inmunoglobulina G y su correlación clínica / Cerebral cysticercosis: the clinical correlation of immunoglobulin G levels

La cisticercosis cerebral es una enfermedad pleomórfica y heterogénea. El diagnóstico se realiza mediante métodos de imagen y por estudios inmunológicos. La severidad de la reacción inflamatoria se mide a través de los estudios en LCR. Realizamos un estudio prospectivo en 44 pacientes con cisticercosis cerebral, con la finalidad de evaluar la elevación de la inmunoglobulina G en el LCR. Los pacientes con cisticercosis mixta, parenquimatosa y subaracnoidea (Grupo III) tuvieron un promedio mayor de inmunoglobulina G, que aquellas con cisticercosis parenquimatosa (Grupo II) o con calcificaciones (Grupo I) (p< 0.001). Pensamos que la IgG puede ser un parámetro clínico) más para valorar el curso de la enfermedad.

Cuantificación de halotano y enfluorano por cromatografía en fase gaseosa en los quirófanos de ún hospital pediátrico / Quantification of halothane and enfluorane by gas chromatography in the operating roon of a pediatric hospital

Se cuantificaron Halotano y Enfluorano en el aire ambiente de los quirófanos de un hospital pediátrico, cuyas anestesias son administradas con circuito Bain principalmente. El muestreo se realizó utilizando tubos Vacutainer al vacío de 10 ml., los que se mantuvieron abiertos durante 10 segundos en la atmósfera quirúrgica, analizando posteriormente las muestras así colectadas en un cromátografo de gases con detector de ionización de flama. Los resultados muestran que las concentraciones de Halotano y Enfluorano rebasan sus niveles máximos permisibles y la contaminación ambiental persiste aún después de 24 horas de no administrar anestesias en los quirófanos muestreados, persistiendo aparentemente el Enfluorano en mayor concentración

Efectos adversos de la inhalación subanestésica / Adverse effects of the subanesthetic inhalatión

La exposición a contaminantes químicos ambientales como los anestésicos, pueden constituir un riesgo para salud de población expuesta a ellos, que es importante evaluar y prevenir. Entre los riesgos potenciales de las substancias químicas se encuentran la producción de daño genético, capaz de traducirse en diversas manifestaciones clínicas como: cáncer, envejecimiento prematuro, esterilidad, anomalias congénitas y muerte embrionaria, fetal o perinatal. Además del peligro de mutaciones que pueden ser transmitidas a las generaciones futuras a través de portadores clínicamente sanos

Importancia de la vigilancia y certificación de la calidad sanitaria del agua

Analiza la importancia de la vigilancia y certificación de la calidad del agua para uso y consumo humano, así como de los programas de saneamiento básico y ambiental en el control de las enfermedades transmisibles. Cita los índices de morbilidad y mortalidad para el caso de México. Identifica responsabilidades de diferentes agentes institucionales involucrados en el Sistema de Vigilancia y Certificación de la Calidad del Agua de Uso y Consumo Humano, en México. Incluye estrategias para alcanzar los objetivos que se plantean en el mencionado sistema