La transición educativa hacia el mundo universitario. Historia de un proyecto que toca su fin

La orientación educativa es un tema del que queda mucho por desarrollar aun en el ámbito universitario. Y el punto de partida podríamos ubicarlo en la transición desde la Educación Secundaria. Así lo entiende un grupo de profesionales de la educación de estos dos ámbitos educativos, que hace ocho años se constituyeron en una Red para desarrollar distintos proyectos de investigación sobre esta temática. En este documento nos planteamos hacer un estudio sobre el funcionamiento de esta Red, las aportaciones que ha realizado a la comunidad científica y lo que ha supuesto para sus integrantes la participación en estos proyectos. Para ello analizaremos la metodología de trabajo seguida por la Red, haremos un estudio bibliográfico sobre las publicaciones en las que la Red ha participado con sus aportaciones, investigaremos las aportaciones externas de la Red (Congresos, Programa de Acción Tutorial y Centros de Secundaria) y realizaremos una valoración individual de cada miembro de este proyecto que toca a su fin. Podemos concluir que en estos ocho años hemos introducido un nuevo concepto en el entorno universitario, hemos aportado ideas interesantes para poner en marcha procesos de orientación en estos ámbitos y nos hemos enriquecido personal y profesionalmente

Contractile responses of human thyroid arteries to vasopressin

Aims: In the present study we investigated the intervention of nitric oxide and prostacyclin in the responses to vasopressin of isolated thyroid arteries obtained from multi-organ donors. Main methods: Paired artery rings from glandular branches of the superior thyroid artery, one normal and the other deendothelised, were mounted in organ baths for isometric recording of tension. Concentration-response curves to vasopressin were determined in the absence and in the presence of either the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10−8 M), the nitric oxide synthase inhibitor NG-monomethyl-Larginine (L-NMMA, 10−4 M), or the inhibitor of prostaglandins indomethacin (10−6 M). Key findings: In artery rings under resting tension, vasopressin produced concentration-dependent, endotheliumindependent contractions. The vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP (10−8 M) displaced the control curve to vasopressin 19-fold to the right in a parallelmanner. The contractile response to vasopressinwas unaffected by L-NMMA or by indomethacin. Significance: Vasopressin causes constriction of human thyroid arteries by stimulation of V1 vasopressin receptors located on smooth muscle cells. These effects are not linked to the presence of an intact endothelium or to the release of nitric oxide or prostaglandins. The constriction of thyroid arteries may be particularly relevant in certain pathophysiological circumstances in which vasopressin is released in amounts that could interfere with the blood supply to the thyroid gland

Arginine Vasopressin Enhances Sympathetic Constriction Through the V1 Vasopressin Receptor in Human Saphenous Vein

Background—Arginine vasopressin (AVP) not only acts directly on blood vessels through V1 receptor stimulation but also may modulate adrenergic-mediated responses in animal experiments in vivo and in vitro. The aim of the present study was to investigate whether AVP can contribute to an abnormal adrenergic constrictor response of human saphenous veins. Methods and Results—Saphenous vein rings were obtained from 32 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. AVP (331029 mol/L) enhanced the contractions elicited by electrical field stimulation at 1, 2, and 4 Hz (by 80%, 70%, and 60%, respectively) and produced a leftward shift of the concentration-response curve to norepinephrine (half-maximal effective concentration decreased from 6.8731027 to 1.0431027 mol/L; P,.05). The V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP (1026 mol/L) prevented the potentiation evoked by AVP. The selective V1 receptor agonist [Phe,2 Orn8]-vasotocin (331029 mol/L) induced potentiation of electrical stimulation– evoked responses, which was also inhibited in the presence of the V1 receptor antagonist (1026 mol/L). In contrast, the V2 receptor agonist desmopressin (1029 to 1027 mol/L) did not modify neurogenic responses, and the V2 receptor antagonist [d(CH2)5, D-Ile,2 Ile,4 Arg8]-vasopressin (1028 to 1026 mol/L) did not prevent the potentiation induced by AVP. The dihydropyridine calcium antagonist nifedipine (1026 mol/L) did not affect the potentiating effect of AVP. Conclusions—The results suggest that low concentrations of AVP facilitate sympathetic neurotransmission and potentiate constrictor effects of norepinephrine in human saphenous veins. These effects appear to be mediated by V1 receptor stimulation and are independent of calcium entry through dihydropyridine calcium channels. Thus, AVP may contribute to vascular mechanisms involved in acute ischemic syndromes associated with venous grafts, particularly if the sympathetic nervous system is activated. (Circulation. 1998;97:865-870.)Medina Besso, Pascual, [email protected] ; Acuña Torre, Antonio, [email protected] ; Martinez Leon, Juan Baustista, [email protected] ; Vila Salinas, José M, [email protected] ; Aldasoro Celaya, Martin, [email protected] ; Lluch Lopez, Salvador, [email protected]

Accumulation of symetric dimethylarginine in hepatorenal syndrome.

In patients with cirrhosis, nitric oxide (NO), asymmetric dimethylarginine (ADMA), and possibly symmetric dimethylarginine (SDMA) have been linked to the severity of the disease. We investigated whether plasma levels of dimethylarginines and NO are elevated in patients with hepatorenal syndrome (HRS), compared with patients with cirrhosis without renal failure (no- HRS). Plasma levels of NO, ADMA, SDMA, and L-arginine were measured in 11 patients with HRS, seven patients with no-HRS, and six healthy volunteers. SDMA concentration in HRS was higher than in no-HRS and healthy subjects (1.47 6 0.25 vs. 0.38 6 0.06 and 0.29 6 0.04 lM, respectively; P , 0.05). ADMA and NOx concentrations were higher in HRS and no-HRS patients than in healthy subjects (ADMA, 1.20 6 0.26, 1.11 6 0.1, and 0.53 6 0.06 lM, respectively; P , 0.05; NOx, 94 6 9.1, 95.5 6 9.54, and 37.67 6 4.62 lM, respectively; P , 0.05). In patients with HRS there was a positive correlation between serum creatinine and plasma SDMA (r2¼0.765, P , 0.001) but not between serum creatinine and ADMA or NOx. The results suggest that renal dysfunction is a main determinant of elevated SDMA concentration in HRS. Accumulation of ADMA as a result of impaired hepatic removal may be the causative factor initiating renal vasoconstriction and SDMA retention in the kidney. Exp Biol Med 231:7075, 200

Sugammadex, a neuromuscular blockade reversal agent, causes neuronal apoptosis in primary cultures.

Sugammadex, a γ-cyclodextrin that encapsulates selectively steroidal neuromuscular blocking agents, such as rocuronium or vecuronium, has changed the face of clinical neuromuscular pharmacology. Sugammadex allows a rapid reversal of muscle paralysis. Sugammadex appears to be safe and well tolerated. Its blood-brain barrier penetration is poor (< 3% in rats), and thus no relevant central nervous toxicity is expected. However the blood brain barrier permeability can be altered under different conditions (i.e. neurodegenerative diseases, trauma, ischemia, infections, or immature nervous system). Using MTT, confocal microscopy, caspase-3 activity, cholesterol quantification and Western-blot we determine toxicity of Sugammadex in neurons in primary culture. Here we show that clinically relevant sugammadex concentrations cause apoptotic/necrosis neuron death in primary cultures. Studies on the underlying mechanism revealed that sugammadex-induced activation of mitochondria- dependent apoptosis associates with depletion of neuronal cholesterol levels. Furthermore SUG increase CytC, AIF, Smac/Diablo and CASP-3 protein expression in cells in culture. Potential association of SUG-induced alteration in cholesterol homeostasis with oxidative stress and apoptosis activation occurs. Furthermore, resistance/sensitivity to oxidative stress differs between neuronal cell types

Action of low doses of Aspirin in Inflammation and Oxidative Stress induced by aβ1-42 on Astrocytes in primary culture

Aspirin has been used as anti-inflammatory and anti-aggregate for decades but the precise mechanism(s) of action after the presence of the toxic peptide Aβ1-42 in cultured astrocytes remains poorly resolved. Here we use low-doses of aspirin (10-7 M) in astrocytes in primary culture in presence or absence of Aβ1-42 toxic peptide. We noted an increase of cell viability and proliferation with or without Aβ1-42 peptide presence in aspirin treated cells. In addition, a decrease in apoptosis, determined by Caspase 3 activity and the expression of Cyt c and Smac/Diablo, were detected. Also, aspirin diminished necrosis process (LDH levels), pro-inflammatory mediators (IL-β and TNF-α) and NF-ᴋB protein expression, increasing anti-inflammatory PPAR-γ protein expression, preventing Aβ1-42 toxic effects. Aspirin inhibited COX-2 and iNOS without changes in COX-1 expression, increasing anti-oxidant protein (Cu/Zn-SOD and Mn-SOD) expression in presence or absence of Aβ1-42. Taken together, our results show that aspirin, at low doses increases cell viability by decreasing inflammation and oxidative stress, preventing the deleterious effects of the Aβ1-42 peptide on astrocytes in primary culture. The use of low doses of aspirin may be more suitable for Alzheimer's disease

Tyrosine Phosphorylation Modulates the Vascular Responses of Mesenteric Arteries from Human Colorectal Tumors

The aim of this study was to analyze whether tyrosine phosphorylation in tumoral arteries may modulate their vascular response. To do this, mesenteric arteries supplying blood flow to colorectal tumors or to normal intestine were obtained during surgery and prepared for isometric tension recording in an organ bath. Increasing tyrosine phosphorylation with the phosphatase inhibitor, sodium orthovanadate produced arterial contraction which was lower in tumoral than in control arteries, whereas it reduced the contraction to noradrenaline in tumoral but not in control arteries and reduced the relaxation to bradykinin in control but not in tumoral arteries. Protein expression of VEGF-A and of the VEGF receptor FLT1 was similar in control and tumoral arteries, but expression of the VEGF receptor KDR was increased in tumoral compared with control arteries. This suggests that tyrosine phosphorylation may produce inhibition of the contraction in tumoral mesenteric arteries, which may increase blood flow to the tumor when tyrosine phosphorylation is increased by stimulation of VEGF receptors

Neuronal effects of Sugammadex in combination with Rocuronium or Vecuronium.

Rocuronium (ROC) and Vecuronium (VEC) are the most currently used steroidal non-depolarizing neuromuscular blocking (MNB) agents. Sugammadex (SUG) rapidly reverses steroidal NMB agents after anaesthesia. The present study was conducted in order to evaluate neuronal effects of SUG alone and in combination with both ROC and VEC. Using MTT, CASP-3 activity and Western-blot we determined the toxicity of SUG, ROC or VEC in neurons in primary culture. SUG induces apoptosis/necrosis in neurons in primary culture and increases cytochrome C (CytC), apoptosis-inducing factor (AIF), Smac/Diablo and Caspase 3 (CASP-3) protein expression. Our results also demonstrated that both ROC and VEC prevent these SUG effects. The protective role of both ROC and VEC could be explained by the fact that SUG encapsulates NMB drugs. In BBB impaired conditions it would be desirable to control SUG doses to prevent the excess of free SUG in plasma that may induce neuronal damage. A balance between SUG, ROC or VEC would be necessary to prevent the risk of cell damag

Cuarta transición educativa: secundaria-universidad. Necesidades y soluciones (II)

La Red de trabajo “Cuarta transición educativa: Secundaria-Universidad. Necesidades y soluciones (II)” es un equipo y un proyecto de trabajo que se encuentra en el segundo año de una planificación inicial de tres ejercicios investigadores, dentro de la Modalidad III del Programa Redes de Investigación en Docencia Universitaria. La temática que desarrollamos gira en torno a la orientación educativa y acción tutorial, y el eje conductor es la transición del alumnado desde la Educación Secundaria hacia la Universidad. En este segundo ejercicio hemos desarrollado un trabajo importante de puesta en práctica de todas aquellas inquietudes suscitadas a lo largo de los ejercicios anteriores del equipo. La visita a los Centros de Secundaria, y el desarrollo de una línea de investigación novedosa surgida, relacionada con los Ciclos Superiores de Formación Profesional, complementan el trabajo básico de la Red en este segunda curso: el estudio de campo del diseño de investigación iniciado el curso anterior. También se introducen acciones formativas en función de las necesidades básicas de la Red. Y la estructura, en cuanto a miembros de la Red, se mantiene casi al completo, ya que tan sólo causa baja una profesora universitaria, manteniéndose el equipo interdisciplinar e internivelar que viene trabajando

PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

Background and aims: Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods: In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results: MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodilation was affected in both arteries in a different way. The aorta from MetS showed vascular dysfunction, including lower response to acetylcholine and sodium nitroprusside, while the renal artery from MetS presented a preserved relaxation to acetylcholine and an increased sensitivity to sodium nitroprusside. We did not find vascular oxidative stress in the aorta from MetS, but we found a significant decrease in PPARγ, phospho-Akt (p-Akt) and phospho-eNOS (p-eNOS) protein expression. On the other hand, we found oxidative stress in the renal artery from MetS, and PPARγ, Akt and p-Akt were overexpressed. No evidence of atherosclerosis was found in arteries from MetS. Conclusions: MetS affects vascular function differently depending on the vessel. In the aorta, it decreases both the vasodilation and the expression of the PPARγ/Akt/eNOS pathway, while in the renal artery, it increases the expression of PPARγ/Akt signalling pathway without decreasing the vasodilation