Recurs multimedia del treball de camp en geologia

El portal Geocamp s'ha creat per aplicar-lo al procés d'aprenentatge de la Geologia al camp, enllaçant conceptes teòrics amb metodologia de treball fora de l'aula o el laboratori. S'adreça a docents i estudiants d'universitat, secundària, batxillerat, formació de professorat o públic en general. Aquest portal conté materials didàctics propis i enllaços amb tot tipus d'informacions relatives al treball de camp en Ciències de la Terra. L'element més innovador rau en la seva utilitat a l'hora de plantejar les activitats de preparació de les excursions. També hi trobem pautes metodològiques per a treballar en els afloraments, idees sobre les activitats de síntesi etc. Geocamp consta de 4 blocs: "Preparem la sortida" (elecció del lloc, transport, predicció meteorològica, material necessari, materials didàctics, enllaços d'interès etc.), "El treball de camp" (pautes d'observació, descripció i interpretació de les roques, recomanacions de seguretat etc.), "Itineraris" (exemples regionals propis o disponibles a la xarxa) i "Després de la sortida" (propostes de realització d'un informe final etc.)

Minimal state models for ionic channels involved in glucagon secretion

Pancreatic alpha cells synthesize and release glucagon. This hormone along with insulin, preserves blood glucose levels within a physiological range. During low glucose levels, alpha cells exhibit electrical activity related to glucagon secretion. In this paper, we introduce minimal state models for those ionic channels involved in this electrical activity in mice alpha cells. For estimation of model parameters, we use Monte Carlo algorithms to fit steadystate channel currents. Then, we simulate dynamic ionic currents following experimental protocols. Our aims are 1) To understand the individual ionic channel functioning and modulation that could affect glucagon secretion, and 2) To simulate ionic currents actually measured in voltage-clamp alpha-cell experiments in mice. Our estimations indicate that alpha cells are highly permeable to sodium and potassium which mainly manage action potentials. We have also found that our estimated N-type calcium channel population and density in alpha cells is in good agreement to those reported for L-type calcium channels in beta cells. This finding is strongly relevant since both, L-type and N-type calcium channels, play a main role in insulin and glucagon secretion, respectively

Facies y paleogeografia de la 'Arenisca de Aren' (Nota preliminar)

Los resultados preliminares de una investigación sedimentológica y estratigráfica han permitido precisar acerca del originario ambiente de sedimentación de la "Arenisca de Aren" y de esbozar un cuadro deposicional de los mismos, mucho más complejo de lo que se había creído precedentemente.After the result of a preliminary sedimentological and stratigraphical investigation it has been possible to remark the depositional conditions of "Arenisca de Aren" and to present their depositional model, more complex than it was belived to be before

Facies y paleogeografia de la 'Arenisca de Aren' (Nota preliminar)

Los resultados preliminares de una investigación sedimentológica y estratigráfica han permitido precisar acerca del originario ambiente de sedimentación de la "Arenisca de Aren" y de esbozar un cuadro deposicional de los mismos, mucho más complejo de lo que se había creído precedentemente.After the result of a preliminary sedimentological and stratigraphical investigation it has been possible to remark the depositional conditions of "Arenisca de Aren" and to present their depositional model, more complex than it was belived to be before

Impaired Ca(2+) signaling in β-cells lacking leptin receptors by Cre-loxP recombination.

Obesity is a major risk factor for diabetes and is typically associated with hyperleptinemia and a state of leptin resistance. The impact of chronically elevated leptin levels on the function of insulin-secreting β-cells has not been elucidated. We previously generated mice lacking leptin signaling in β-cells by using the Cre-loxP strategy and showed that these animals develop increased body weight and adiposity, hyperinsulinemia, impaired glucose-stimulated insulin secretion and insulin resistance. Here, we performed several in vitro studies and observed that β-cells lacking leptin signaling in this model are capable of properly metabolizing glucose, but show impaired intracellular Ca(2+) oscillations and lack of synchrony within the islets in response to glucose, display reduced response to tolbutamide and exhibit morphological abnormalities including increased autophagy. Defects in intracellular Ca(2+) signaling were observed even in neonatal islets, ruling out the possible contribution of obesity to the β-cell irregularities observed in adults. In parallel, we also detected a disrupted intracellular Ca(2+) pattern in response to glucose and tolbutamide in control islets from adult transgenic mice expressing Cre recombinase under the rat insulin promoter, despite these animals being glucose tolerant and secreting normal levels of insulin in response to glucose. This unexpected observation impeded us from discerning the consequences of impaired leptin signaling as opposed to long-term Cre expression in the function of insulin-secreting cells. These findings highlight the need to generate improved Cre-driver mouse models or new tools to induce Cre recombination in β-cells

Transmission electron microscopy reveals autophagy within <i>Lepr^flox/flox RIP-Cre</i> β-cells.

<p>Pancreas sections from <i>Lepr^flox/flox</i> (A) and <i>Lepr^flox/flox RIP-Cre</i> (B and D) mice were analyzed by transmission electron microscopy (magnification 9300X and 11000X) and quantified (C). Multigranular bodies were numerous in <i>Lepr^flox/flox RIP-Cre</i> β-cells compared to <i>Lepr^flox/flox</i> β-cells (white squares). Events of macroautophagy (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071075#pone-0071075-g004" target="_blank">Figure 4D</a>, upper inset) and microautophagy (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071075#pone-0071075-g004" target="_blank">Figure 4D</a>, bottom inset) were captured in <i>Lepr^flox/flox RIP-Cre</i> β-cells. Scale bar = 2 µm (A and B) and 0.5 µm (D). Micrographs are representative of 3 pancreata analyzed per group. Data are expressed as mean ± SEM. Statistical analysis was performed using Student t test, ** p<0.01.</p

Decreased amplitude in intracellular Ca²⁺ responses to tolbutamide in <i>Lepr^flox/flox RIP-Cre</i> adult islets.

<p>A: Representative recordings from a control <i>Lepr^flox/flox</i> islet (solid line) and a <i>Lepr^flox/flox RIP-Cre</i> islet (dotted line) in response to tolbutamide. B: Graph plotting ΔFmax-Fmin of each peak in response to tolbutamide in the population of islets that showed two peaks. Data are expressed as mean ± SEM. Statistical analysis was performed using Student t test, *** p<0.0001. Responses are representative of 22 islets from 4 mice per group.</p

<i>Lepr^flox/flox RIP-Cre</i> pancreatic β-cells display impaired intracellular Ca²⁺ oscillations in response to glucose.

<p>A: [Ca²⁺]_i recordings of a <i>Lepr^flox/flox</i> islet (left panel) and <i>Lepr^flox/flox RIP-Cre</i> islet (right panel) in response to increasing glucose (G) concentrations and potassium chloride (KCl) from adult mice. B and C: Representative [Ca²⁺]_i recordings showing three different regions per islet of a <i>Lepr^flox/flox</i> islet (left panel) and a <i>Lepr^flox/flox RIP-Cre</i> islet (right panel) from adult (B) and neonatal (C) mice. Graphs are representative of 17–20 islets from 3 neonatal mice per group, and 37–38 islets from 3–4 adult mice per group.</p

Similar glucose metabolic rates in islets from <i>Lepr^flox/flox</i> and <i>Lepr^flox/flox RIP-Cre</i> adult mice.

<p>A: Two [NAD(P)H]_i representative recordings of a <i>Lepr^flox/flox</i> islet (solid line) and a <i>Lepr^flox/flox RIP-Cre</i> islet (dotted line) in response to glucose (G) and sodium azide (NaN₃). B: Graph plotting percentage of AUC/min in response to different glucose concentrations and normalized to the maximum reduction level obtained with 3 mM NaN₃. Data are expressed as mean ± SEM. Statistical analysis was performed using Student t test. Graphs are representative of 32–34 islets from 3 mice per group.</p

<i>Lepr^+/+ RIP-Cre</i> mice present impaired β-cell Ca²⁺ signaling in response to glucose and tolbutamide.

<p>A: Representative [Ca²⁺]_i recordings of a <i>Lepr^+/+</i> islet (left panel) and <i>Lepr^+/+ RIP-Cre</i> islet (right panel) in response to increasing glucose (G) concentrations and potassium chloride (KCl) from 5–6 week old mice. B: Representative [Ca²⁺]_i recordings of a <i>Lepr^+/+</i> islet (solid line) and <i>Lepr^+/+ RIP-Cre</i> islet (dotted line) in response to tolbutamide. C: Graph plotting the AUC of the Ca²⁺ transients during the stimulation with tolbutamide. Data are expressed as mean ± SEM. Statistical analysis was performed using Student t test. *** p<0.0001. Graphs are representative of 18–20 islets from 3 mice per group (in response to glucose) and 16–27 islets from 2–3 mice per group (in response to tolbutamide).</p