1000 resultados para Vías autónomas
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La crisis financiera y la crisis de la deuda soberana han tenido un gran impacto en el Estado autonómico y han polarizado las posiciones entre los partidarios de una mayor centralización y los que consideran agotado el modelo autonómico y defienden la necesidad de articular nuevas vías para alcanzar y garantizar el nivel de autogobierno. En este análisis se argumenta que a pesar de que la crisis ha tenido un impacto negativo en el debate sobre la viabilidad del Estado autonómico y en la percepción ciudadana sobre el nivel de gasto y de competencias de las Comunidades Autónomas este debate es anterior a la crisis económica. Además la crisis ha tenido un mayor impacto en estados de estructura unitaria o poco descentralizada, y menor en estados de estructura federal, por lo que no parece que exista una relación directa entre descentralización y crisis económica.
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En esta nota se analiza la financiación definitiva de las comunidades autónomas de régimen común en el año 2011 a la luz de la liquidación del sistema correspondiente a dicho ejercicio, que ha sido hecha pública recientemente.
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En este trabajo se construyen series de financiación a competencias homogéneas e igual esfuerzo fiscal para las comunidades autónomas de régimen común durante el período 2002-11, así como series complementarias de financiación por caja y financiación destinada a competencias singulares. También se recopilan otros agregados de interés que pueden servir para relativizar la financiación autonómica, incluyendo la población ajustada regional. Estas series se utilizan en la segunda parte del trabajo para ilustrar algunos rasgos de interés de la evolución de la financiación agregada regional y de la posición relativa de las distintas comunidades autónomas en términos de financiación por unidad de necesidad.
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Melatonin, the pineal hormone produced during the dark phase of the light-dark cycle, modulates neuronal acetylcholine receptors located presynaptically on nerve terminals of the rat vas deferens. Recently we showed the presence of high affinity nicotine-binding sites during the light phase, and low and high affinity binding sites during the dark phase. The appearance of the low affinity binding sites was due to the nocturnal melatonin surge and could be mimicked by exposure to melatonin in vitro. The aim of the present research was to identify the receptor subtypes responsible for the functional response during the light and the dark phase. The rank order of potency of agonists was dimethylphenylpiperazinium (DMPP) = cytisine > nicotine > carbachol and DMPP = nicotine = cytisine > carbachol, during the light and dark phase, respectively, due to an increase in apparent affinity for nicotine. Mecamylamine similarly blocked the DMPP response during the light and the dark phase, while the response to nicotine was more efficiently blocked during the light phase. In contrast, methyllycaconitine inhibited the nicotine-induced response only at 21:00 h. Since a7 nicotinic acetylcholine receptors (nAChRs) have low affinity for nicotine in binding assays, we suggest that a mixed population composed of a3ß4 - plus a7-bearing nAChR subtypes is present at night. This plasticity in receptor subtypes is probably driven by melatonin since nicotine-induced contraction in organs from animals sacrificed at 15:00 h and incubated with melatonin (100 pg/ml, 4 h) is not totally blocked by mecamylamine. Thus melatonin, by acting directly on the short adrenergic neurons that innervate the rat vas deferens, induces the appearance of the low affinity binding site, probably an a7 nAChR subtype.
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Gonadal hormones regulate the expression of alpha1-adrenoceptor subtypes in several tissues. The present study was carried out to determine whether or not cyproterone acetate, an anti-androgenic agent, regulates the alpha1-adrenoceptor subtypes that mediate contractions of the rat vas deferens in response to noradrenaline. The actions of subtype selective alpha1-antagonists were investigated in vas deferens from control and cyproterone acetate-treated rats (10 mg/day, sc, for 7 days). Prazosin (pA2 ~9.5), phentolamine (pA2 ~8.3) and yohimbine (pA2 ~6.7) presented competitive antagonism consistent with activation of alpha1-adrenoceptors in vas deferens from both control and treated rats. The pA2 values estimated for WB 4101 (~9.5), benoxathian (~9.7), 5-methylurapidil (~8.5), indoramin (~8.7) and BMY 7378 (~6.8) indicate that alpha1A-adrenoceptors are involved in the contractions of the vas deferens from control and cyproterone acetate-treated rats. Treatment of the vas deferens from control rats with the alpha1B/alpha1D-adrenoceptor alkylating agent chloroethylclonidine had no effect on noradrenaline contractions, supporting the involvement of the alpha1A-subtype. However, this agent partially inhibited the contractions of vas deferens from cyproterone acetate-treated rats, suggesting involvement of multiple receptor subtypes. To further investigate this, the actions of WB 4101 and chloroethylclonidine were reevaluated in the vas deferens from rats treated with cyproterone acetate for 14 days. In these organs WB 4101 presented complex antagonism characterized by a Schild plot with a slope different from unity (0.65 ± 0.05). After treatment with chloroethylclonidine, the complex antagonism presented by WB 4101 was converted into classical competitive antagonism, consistent with participation of alpha1A-adrenoceptors as well as alpha1B-adrenoceptors. These results suggest that cyproterone acetate induces plasticity in the alpha1-adrenoceptor subtypes involved in the contractions of the vas deferens.
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Ca2+ pumps are important players in smooth muscle contraction. Nevertheless, little information is available about these pumps in the vas deferens. We have determined which subtype of sarco(endo)plasmic reticulum Ca2+-ATPase isoform (SERCA) is expressed in rat vas deferens (RVD) and its modulation by calmodulin (CaM)-dependent mechanisms. The thapsigargin-sensitive Ca2+-ATPase from a membrane fraction containing the highest SERCA levels in the RVD homogenate has the same molecular mass (∼115 kDa) as that of SERCA2 from the rat cerebellum. It has a very high affinity for Ca2+ (Ca0.5 = 780 nM) and a low sensitivity to vanadate (IC50 = 41 µM). These facts indicate that SERCA2 is present in the RVD. Immunoblotting for CaM and Ca2+/calmodulin-dependent protein kinase II (CaMKII) showed the expression of these two regulatory proteins. Ca2+ and CaM increased serine-phosphorylated residues of the 115-kDa protein, indicating the involvement of CaMKII in the regulatory phosphorylation of SERCA2. Phosphorylation is accompanied by an 8-fold increase of thapsigargin-sensitive Ca2+ accumulation in the lumen of vesicles derived from these membranes. These data establish that SERCA2 in the RVD is modulated by Ca2+ and CaM, possibly via CaMKII, in a process that results in stimulation of Ca2+ pumping activity.
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Tesis (Maestría en Enfermería con Especialidad en Salud Comunitaria) U.A.N.L.
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Tesis (Especialista en Cirugía General) U.A.N.L.
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Tesis (Maestría en Ciencias Odontológicas con Especialidad en Ortodoncia) U.A.N.L.
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Tesis (Maestría en Ciencias de Enfermería) UANL, 2009.
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Tesis (Maestría en Ciencias con orientación en Ingeniería Ambiental) UANL, 2014.
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UANL
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UANL
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Tesis (Doctor en Ciencias con Especialidad en Microbiología) UANL, 2013.
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Tesis (Doctor en Ciencias con especialidad en Biología Molecular e Ingeniería Genética) UANL, 2014.