Composite beta-AgVO3@V5+1.6V4+0.4O4.8 hydrogels and xerogels for catalytic applications

Comunicación (Poster) en panel del congreso: Designing New Heterogeneous Catalysts, Faraday Discussion, 4–6 April 2016. London, United Kingdom.

Mechanisms Responsible for the Trophic Effect of Beta-Adrenoceptors on the I-to Current Density in Type 1 Diabetic Rat Cardiomyocytes

Background/Aims: In diabetic ventricular myocytes, transient outward potassium current (I-to) amplitude is severely reduced because of the impaired catecholamine release that characterizes diabetic autonomic neuropathy. Sympathetic nervous system exhibits a trophic effect on I-to since incubation of myocytes with noradrenaline restores current amplitude via beta-adrenoceptor (beta AR) stimulation. Here, we investigate the intracellular signalling pathway though which incubation of diabetic cardiomyocytes with the beta AR agonist isoproterenol recovers I-to amplitude to normal values. Methods: Experiments were performed in ventricular myocytes isolated from streptozotocin-diabetic rats. I-to current was recorded by using the patch-clamp technique. Kv4 channel expression was determined by immunofluorescence. Protein-protein interaction was determined by coimmunoprecipitation. Results: Stimulation of beta AR activates first a G alpha s protein, adenylyl cyclase and Protein Kinase A. PKA-phosphorylated receptor then switches to the G alpha i protein. This leads to the activation of the beta AR-Kinase-1 and further receptor phosphorylation and arrestin dependent internalization. The internalized receptor-arrestin complex recruits and activates cSrc and the MAPK cascade, where Ras, c-Raf1 and finally ERK1/2 mediate the increase in Kv4.2 and Kv4.3 protein abundance in the plasma membrane. Conclusion: beta(2)AR stimulation activates a G alpha s and G alpha i protein dependent pathway where the ERK1/2 modulates the Ito current amplitude and the density of the Kv4.2 and Kv4.2 channels in the plasma membrane upon sympathetic stimulation in diabetic heart.

A High Degree of LINE-1 Hypomethylation Is a Unique Feature of Early-Onset Colorectal Cancer

12 p.

Running Pace Decrease during a Marathon Is Positively Related to Blood Markers of Muscle Damage

Background: Completing a marathon is one of the most challenging sports activities, yet the source of running fatigue during this event is not completely understood. The aim of this investigation was to determine the cause(s) of running fatigue during a marathon in warm weather. Methodology/Principal Findings: We recruited 40 amateur runners (34 men and 6 women) for the study. Before the race, body core temperature, body mass, leg muscle power output during a countermovement jump, and blood samples were obtained. During the marathon (27 uC; 27% relative humidity) running fatigue was measured as the pace reduction from the first 5-km to the end of the race. Within 3 min after the marathon, the same pre-exercise variables were obtained. Results: Marathoners reduced their running pace from 3.5 6 0.4 m/s after 5-km to 2.9 6 0.6 m/s at the end of the race (P,0.05), although the running fatigue experienced by the marathoners was uneven. Marathoners with greater running fatigue (. 15% pace reduction) had elevated post-race myoglobin (1318 6 1411 v 623 6 391 mg L21; P,0.05), lactate dehydrogenase (687 6 151 v 583 6 117 U L21; P,0.05), and creatine kinase (564 6 469 v 363 6 158 U L21; P = 0.07) in comparison with marathoners that preserved their running pace reasonably well throughout the race. However, they did not differ in their body mass change (23.1 6 1.0 v 23.0 6 1.0%; P = 0.60) or post-race body temperature (38.7 6 0.7 v 38.9 6 0.9 uC; P = 0.35). Conclusions/Significance: Running pace decline during a marathon was positively related with muscle breakdown blood markers. To elucidate if muscle damage during a marathon is related to mechanistic or metabolic factors requires further investigation.

Development of appropriateness explicit criteria for cataract extraction by phacoemulsification

Background: Consensus development techniques were used in the late 1980s to create explicit criteria for the appropriateness of cataract extraction. We developed a new appropriateness of indications tool for cataract following the RAND method. We tested the validity of our panel results. Methods: Criteria were developed using a modified Delphi panel judgment process. A panel of 12 ophthalmologists was assembled. Ratings were analyzed regarding the level of agreement among panelists. We studied the influence of all variables on the final panel score using linear and logistic regression models. The explicit criteria developed were summarized by classification and regression tree analysis. Results: Of the 765 indications evaluated by the main panel in the second round, 32.9% were found appropriate, 30.1% uncertain, and 37% inappropriate. Agreement was found in 53% of the indications and disagreement in 0.9%. Seven variables were considered to create the indications and divided into three groups: simple cataract, with diabetic retinopathy, or with other ocular pathologies. The preoperative visual acuity in the cataractous eye and visual function were the variables that best explained the panel scoring. The panel results were synthesized and presented in three decision trees. Misclassification error in the decision trees, as compared with the panel original criteria, was 5.3%. Conclusion: The parameters tested showed acceptable validity for an evaluation tool. These results support the use of this indication algorithm as a screening tool for assessing the appropriateness of cataract extraction in field studies and for the development of practice guidelines.