Designing celebrity‐endorsed behavioral interventions in conservation

The use of celebrity endorsement in environmental conservation interventions aiming to influence human behavior has increased in recent decades. Although good practice in designing, implementing, and evaluating behavioral interventions is outlined in recent publications, guidance on developing conservation interventions with celebrity endorsement remains limited. To fill this gap, we devised a guide for decision‐making relating to celebrity‐endorsed behavioral interventions based on the behavioral, project design, and celebrity endorsement literatures. The guide advises conducting research to understand the behavior system in question; defining endorser selection models and celebrities based on the research; developing an endorsement strategy with the appropriate communication channels; testing the celebrity, channels, and strategy with the target audience and making adjustments as needed; and, finally, evaluating the intervention after implementation. We applied this strategy to a case study, the aim of which was to design a celebrity‐endorsed intervention to reduce consumption of wild meat in Ho Chi Minh City, Vietnam. Following our guide, we found that employing evidence‐based decision‐making substantially enhanced our ability to understand the complexity and potential cost associated with using celebrity endorsements in behavioral interventions

High lithium conductivity of miscible poly(ethylene oxide)/methacrylic sulfonamide anionic polyelectrolyte polymer blends

In this work, we develop novel single-ion polymer electrolytes by mixing poly(lithium 1-[3-(methacryloyloxy) propylsulfonyl]-1-(trifluoromethanesulfonyl) imide) (PLiMTFSI) and poly(ethylene oxide) (PEO) with different molecular weights. The impact of PLiMTFSI on the crystallization and conductivity of the blends was explored in detail. When PLiMTFSI (an amorphous polymer) is added to PEO, the crystallization ability of PEO decreases. However, blends with high-molecular weight PEO (1000 kg/mol) experience a lower reduction in crystallinity and melting points. As a result, lower conductivity values were obtained in these blends, which is why most of the study was then focused on blends incorporating a lower-molecular weight PEO (100 kg/mol). We show that the melting point, degree of crystallinity, spherulitic growth, and overall crystallization kinetics decrease in the presence of PLiMTFSI, which are all signs of miscibility. Furthermore, the blends show a single glass transition temperature over the whole composition range. Therefore, our results indicate that PEO and PLiMTFSI are miscible, as corroborated by applying the Nishi-Wang equation and obtaining negative χ12 values (i.e., the Flory-Huggins interaction parameter) for all blends. Our results show that intermediate molecular weight blends (100 kg/mol PEO and 50 kg/mol PLiMTFSI) showed the highest ionic conductivity value. Interestingly, a value of 2.1 × 10-4 S/cm was obtained at 70 °C, which is one of the highest reported so far for a free-standing film of single-ion conducting polymer electrolytes. Finally, employing dielectric spectroscopy, the contribution of ion density and ion mobility to ionic conductivity could be separated. It was found that ion mobility is the parameter that has a greater weight in the conduction process.We wish to thank the Consejo Nacional de Ciencia y Tecnología (the National Council of Science and Technology) (CONACYT), Mexico, for the grant awarded to J.L.O.-M. no. 471837. L.P. has received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement no. 797295. We acknowledge funding from the Basque Government through grant IT1309-19 and IT1175-19. Authors would like to thank IONBIKE-RISE project, and this project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement no. 823989

Propuesta de un plan estratégico de negocios para una agencia de viajes de turismo gay, enfocada al sector ejecutivo.

Tesis (Licenciatura en Turismo), Instituto Politécnico Nacional, EST, 2008, 4 archivo PDF, ( 561 pàginas). tesis.ipn.m

Inhibition of the proteasome preserves Mitofusin-2 and mitochondrial integrity, protecting cardiomyocytes during ischemia-reperfusion injury

Cardiomyocyte loss is the main cause of myocardial dysfunction following an ischemia-reperfusion (IR) injury. Mitochondrial dysfunction and altered mitochondrial network dynamics play central roles in cardiomyocyte death. Proteasome inhibition is cardioprotective in the setting of IR; however, the mechanisms underlying this protection are not well-understood. Several proteins that regulate mitochondrial dynamics and energy metabolism, including Mitofusin-2 (Mfn2), are degraded by the proteasome. The aim of this study was to evaluate whether proteasome inhibition can protect cardiomyocytes from IR damage by maintaining Mfn2 levels and preserving mitochondrial network integrity. Using ex vivo Langendorff-perfused rat hearts and in vitro neonatal rat ventricular myocytes, we showed that the proteasome inhibitor MG132 reduced IR-induced cardiomyocyte death. Moreover, MG132 preserved mitochondrial mass, prevented mitochondrial network fragmentation, and abolished IR-induced reductions in Mfn2 levels in heart tissue and cultured cardiomyocytes. Interestingly, Mfn2 overexpression also prevented cardiomyocyte death. This effect was apparently specific to Mfn2, as overexpression of Miro1, another protein implicated in mitochondrial dynamics, did not confer the same protection. Our results suggest that proteasome inhibition protects cardiomyocytes from IR damage. This effect could be partly mediated by preservation of Mfn2 and therefore mitochondrial integrity.Comisión Nacional de Investigación Científica y Tecnológica (CONICYT, Chile), Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT): 1130407, 1180613, 11170962, 1160704, 1200490, 11181000, 3190546, 3160549. Comisión Nacional de Investigación Científica y Tecnológica (CONICYT), CONICYT FONDAP

Inhibition of chymotrypsin-like activity of the proteasome by ixazomib prevents mitochondrial dysfunction during myocardial ischemia

The heart is critically dependent on mitochondrial respiration for energy supply. Ischemia decreases oxygen availability, with catastrophic consequences for cellular energy systems. After a few minutes of ischemia, the mitochondrial respiratory chain halts, ATP levels drop and ion gradients across cell membranes collapse. Activation of cellular proteases and generation of reactive oxygen species by mitochondria during ischemia alter mitochondrial membrane permeability, causing mitochondrial swelling and fragmentation and eventually cell death. The mitochondria, therefore, are important targets of cardioprotection against ischemic injury. We have previously shown that ixazomib (IXA), a proteasome inhibitor used for treating multiple myeloma, effectively reduced the size of the infarct produced by global ischemia in isolated rat hearts and prevented degradation of the sarcoplasmic reticulum calcium release channel RyR2. The aim of this work was to further characterize the protective effect of IXA by determining its effect on mitochondrial morphology and function after ischemia. We also quantified the effect of IXA on levels of mitofusin-2, a protein involved in maintaining mitochondrial morphology and mitochondria-SR communication. We found that mitochondria were significantly preserved and functional parameters such as oxygen consumption, the ability to generate a membrane potential, and glutathione content were improved in mitochondria isolated from hearts perfused with IXA prior to ischemia. IXA also blocked the release of cytochrome c observed in ischemia and significantly preserved mitofusin-2 integrity. These beneficial effects resulted in a significant decrease in the left ventricular end diastolic pressure upon reperfusion and a smaller infarct in isolated hearts.Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 1110257 1130407 11170962 118061