Las redes sociales como canales útiles en el acercamiento de jóvenes universitarios de pregrado de Lima al mundo científico : la experiencia en Facebook de “MASATO : más saber para todos”

Cultura científica y comunicación científica son conceptos que guardan relación entre sí. El modo de difundir los contenidos de esta área es determinante para la comprensión, retención y replicación de la información a un público no científico. Por otro lado, los jóvenes estudiantes de Lima Metropolitana tienen participación total en medios sociales, especialmente en Facebook, y crear una fanpage en donde se realiza comunicación científica puede contribuir a generar interés en contenidos de esa índole y crear más cultura científica. Diversas teorías socioculturales de la comunicación comulgan con las características de la Web 2.0 (caracterizada por los softwares sociales) y los internautas jóvenes. Además, las potencialidades de los medios sociales borran la distinción entre espacios de aprendizaje, espacios sociales y de ocio, sugiriendo la utilidad de juntar estos tipos de actividades. Por ello, la comunicación científica debe adaptarse a los cambios en los medios de comunicación y en la forma de interactuar con sus audiencias. Se desarrolla, ejecuta y administra por 2 años una fanpage en Facebook dedicada a la divulgación científica, previo estudio de factibilidad (entrevistas y focus group). En dicho periodo se evalúa su rendimiento en 3 ocasiones y, finalmente, indaga la respuesta y percepción (entrevistas) hacia la fanpage por parte del público objetivo. Se observa que, emplear el entretenimiento, identificar e incluir aspectos científicos en situaciones de la vida cotidiana constituyen los métodos más efectivos para realizar comunicación científica, Así también, las promociones off line son más ventajosas: tanto para conseguir más seguidores como potenciales colaboradores. Se concluye que la comunicación científica fortalece su implementación a través de la Web 2.0, ya que ésta permite saciar necesidades como la comunicación, la socialización y la participación en los intereses compartidos de los internautas. Todo ello propicia una comunicación científica afín a los intereses de los jóvenes universitarios.Scientific culture and scientific communication are concepts related to each other. The way of disseminating the contents of this area is determinant for the understanding, retention and replication of the information to a non-scientific public. On the other hand, Lima Metropolitana university students have full participation in social media, especially in Facebook. Thus, creating a fanpage where run scientific communication can contribute to generate interest in such content and create more scientific culture. Several socio-cultural theories of communication commune with the characteristics of Web 2.0 (characterized by social softwares) and young internet users. In addition, the potentialities of social media erase the distinction between learning spaces, social and leisure spaces, suggesting the usefulness of bringing together these types of activities. For this reason, scientific communication must adapt to the changes in the media and in the way of interacting with its audiences. After a feasibility study (interviews and focus group), it develops, executes and manages for 2 years a fanpage on Facebook dedicated to scientific dissemination. During this period, its performance is evaluated three times and, finally, it investigates the response and perception (interviews) towards the fanpage by the target audience. It is observed that, using entertainment, identifying and including scientific aspects in everyday situations are the most effective methods for scientific communication. Also, offline promotions are more advantageous: both to get more followers and potential collaborators. It is concluded that scientific communication strengthens its implementation through Web 2.0, since it allows satisfying needs such as communication, socialization and participation in the shared interests of Internet users. All this fosters a scientific communication related to the interests of university students.Tesi

Grip strength in mice with joint inflammation: A rheumatology function test sensitive to pain and analgesia

Grip strength deficit is a measure of pain-induced functional disability in rheumatic disease. We tested whether this parameter and tactile allodynia, the standard pain measure in preclinical studies, show parallels in their response to analgesics and basic mechanisms. Mice with periarticular injections of complete Freund's adjuvant (CFA) in the ankles showed periarticular immune infiltration and synovial membrane alterations, together with pronounced grip strength deficits and tactile allodynia measured with von Frey hairs. However, inflammation-induced tactile allodynia lasted longer than grip strength alterations, and therefore did not drive the functional deficits. Oral administration of the opioid drugs oxycodone (1–8 mg/kg) and tramadol (10–80 mg/kg) induced a better recovery of grip strength than acetaminophen (40–320 mg/kg) or the nonsteroidal antiinflammatory drugs ibuprofen (10–80 mg/kg) or celecoxib (40–160 mg/kg); these results are consistent with their analgesic efficacy in humans. Functional impairment was generally a more sensitive indicator of drug-induced analgesia than tactile allodynia, as drug doses that attenuated grip strength deficits showed little or no effect on von Frey thresholds. Finally, ruthenium red (a nonselective TRP antagonist) or the in vivo ablation of TRPV1-expressing neurons with resiniferatoxin abolished tactile allodynia without altering grip strength deficits, indicating that the neurobiology of tactile allodynia and grip strength deficits differ. In conclusion, grip strength deficits are due to a distinct type of pain that reflects an important aspect of the human pain experience, and therefore merits further exploration in preclinical studies to improve the translation of new analgesics from bench to bedside.This study was partially supported by the Spanish Ministry of Economy and Competitiveness (MINECO, grant SAF2013-47481P), the Junta de Andalucía (grant CTS 109), and funding from Esteve and the European Regional Development Fund (FEDER)

Modulation by Sigma-1 Receptor of Morphine Analgesia and Tolerance: Nociceptive Pain, Tactile Allodynia and Grip Strength Deficits During Joint Inflammation

Sigma-1 receptor antagonism increases the effects of morphine on nociceptive pain, even in morphine-tolerant animals. However, it is unknown whether these receptors are able to modulate morphine antinociception and tolerance during inflammatory pain. Here we used a mouse model to test the modulation of morphine effects by the selective sigma-1 antagonist S1RA (MR309), by determining its effect on inflammatory tactile allodynia (von Frey filaments) and on grip strength deficits induced by joint inflammation (a measure of pain-induced functional disability), and compared the results with those for nociceptive heat pain recorded with the unilateral hot plate (55 C) test. The subcutaneous (s.c.) administration of morphine induced antinociceptive effects to heat stimuli, and restored mechanical threshold and grip strength in mice with periarticular inflammation induced by Complete Freund’s Adjuvant. S1RA (80 mg/kg, s.c.) administered alone did not induce any effect on nociceptive heat pain or inflammatory allodynia, but was able to partially reverse grip strength deficits. The association of S1RA with morphine, at doses inducing little or no analgesic-like effects when administered alone, resulted in a marked antinociceptive effect to heat stimuli and complete reversion of inflammatory tactile allodynia. However, S1RA administration did not increase the effect of morphine on grip strength deficits induced by joint inflammation.MT was supported by a postdoctoral grant from the University of Granada.MR-C and IB-C were supported by FPU grants from the Spanish Ministry of Economy and Competitiveness (MINECO). This study was partially supported by the Spanish Ministry of Economy and Competitiveness (Grants SAF2013-47481P and SAF2016-80540-R), the Junta de Andalucía (Grant CTS109), and FEDER funds

Professional development and a discussion of the professional preparation provided by information and library science degree programs in public universities in Madrid, 2000-2005

A study was designed to determine how the degree programs in Information and library science available in 2000-2005 at the public universities of Madrid fit the labour market needs of their students. The methodology used was the development of a questionnaire addressed to graduates. Although the number of surveys completed is not high (118), the authors believe that the results obtained permit a series of conclusions that may be extrapolated to the entire cohort

TARGETING IMMUNE-DRIVEN OPIOID ANALGESIA BY SIGMA-1 RECEPTORS: OPENING THE DOOR TO NOVEL PERSPECTIVES FOR THE ANALGESIC USE OF SIGMA-1 ANTAGONISTS

Immune cells have a known role in pronociception, since they release a myriad of inflammatory algogens which interact with neurons to facilitate pain signaling. However, these cells also produce endogenous opioid peptides with analgesic potential. The sigma-1 receptor is a ligand-operated chaperone that modulates neurotransmission by interacting with multiple protein partners, including the µ-opioid receptor. We recently found that sigma-1 antagonists are able to induce opioid analgesia by enhancing the action of endogenous opioid peptides of immune origin during inflammation. This opioid analgesia is seen only at the inflamed site, where immune cells naturally accumulate. In this article we review the difficulties of targeting the opioid system for selective pain relief, and discuss the dual role of immune cells in pain and analgesia. Our discussion creates perspectives for possible novel therapeutic uses of sigma-1 antagonists as agents able to maximize the analgesic potential of the immune systemUniversity of GranadaMartín Escudero postdoctoral programFPU grants from the Spanish Ministry of Economy and Competitiveness (MINECO)Juan de la Cierva-Incorporación postdoctoral grant from MINECOMINECO [grant number SAF2016-80540-R]Junta de Andalucía (grant CTS109)FEDER fund

Urinary bladder sigma-1 receptors: A new target for cystitis treatment

Supplementary material related to this article can be found, in the online version, at doi:https://doi.org/10.1016/j.phrs.2020.104724.No adequate treatment is available for painful urinary bladder disorders such as interstitial cystitis/bladder pain syndrome, and the identification of new urological therapeutic targets is an unmet need. The sigma-1 receptor (σ1-R) modulates somatic pain, but its role in painful urological disorders is unexplored. The urothelium expresses many receptors typical of primary sensory neurons (e.g. TRPV1, TRPA1 and P2X3) and high levels of σ1- R have been found in these neurons; we therefore hypothesized that σ1-R may also be expressed in the urothelium and may have functional relevance in this tissue. With western blotting and immunohistochemical methods, we detected σ1-R in the urinary bladder in wild-type (WT) but not in σ1-R-knockout (σ1-KO) mice. Interestingly, σ1-R was located in the bladder urothelium not only in mouse, but also in human bladder sections. The severity of histopathological (edema, hemorrhage and urothelial desquamation) and biochemical alterations (enhanced myeloperoxidase activity and phosphorylation of extracellular regulated kinases 1/2 [pERK1/2]) that characterize cyclophosphamide-induced cystitis was lower in σ1-KO than in WT mice. Moreover, cyclophosphamide-induced pain behaviors and referred mechanical hyperalgesia were dose-dependently reduced by σ1-R antagonists (BD-1063, NE-100 and S1RA) in WT but not in σ1-KO mice. In contrast, the analgesic effect of morphine was greater in σ1-KO than in WT mice. Together these findings suggest that σ1-R plays a functional role in the mechanisms underlying cyclophosphamide-induced cystitis, and modulates morphine analgesia against urological pain. Therefore, σ1-R may represent a new drug target for urinary bladder disorders.Spanish Ministry of Economy and Competitiveness (MINECO) SAF2016-80540-REuropean Regional Development Funds (ERDF), Junta de Andalucia grant CTS 109Esteve PharmaceuticalsInnovative Medicines Initiative 2 Joint Undertaking 777500European Union's Horizon 2020 research and innovation programmeEFPI

Proyecto: Botella filtrante de agua

En el presente trabajo de investigación se demostrará el análisis de la viabilidad de un proyecto innovador creado por el equipo de trabajo. El producto innovador elegido para dicha investigación es una botella purificante de agua, que mediante un proceso de tecnología avanzada el agua ingresada de cualquier medio podrá ser filtrada y lista para ser consumida. Este innovador producto posee una tapa con roceador o “spray” del contenido líquido que servirá para momentos de altas temperaturas de hoy en día. Con nuestro producto vamos a revertir la función de un tomatodo simple y con esto la idea de que nuestra botella solo sirve para tomar agua purificada. Sino que tendrá la función adicional del spray y sostenedor de objetos, así como para ser colgado en mochilas y bolsos.En el presente trabajo de investigación se demostrará el análisis de la viabilidad de un proyecto innovador creado por el equipo de trabajo. El producto innovador elegido para dicha investigación es una botella purificante de agua, que mediante un proceso de tecnología avanzada el agua ingresada de cualquier medio podrá ser filtrada y lista para ser consumida. Este innovador producto posee una tapa con roceador o “spray” del contenido líquido que servirá para momentos de altas temperaturas de hoy en día. Con nuestro producto vamos a revertir la función de un tomatodo simple y con esto la idea de que nuestra botella solo sirve para tomar agua purificada. Sino que tendrá la función adicional del spray y sostenedor de objetos, así como para ser colgado en mochilas y bolsos

The clinical heterogeneity of coenzyme Q10 deficiency results from genotypic differences in the Coq9 gene

Primary coenzyme Q10 (CoQ10) deficiency is due to mutations in genes involved in CoQ biosynthesis. The disease has been associated with five major phenotypes, but a genotype–phenotype correlation is unclear. Here, we compare two mouse models with a genetic modification in Coq9 gene (Coq9Q95X and Coq9R239X), and their responses to 2,4‐dihydroxybenzoic acid (2,4‐diHB). Coq9R239X mice manifest severe widespread CoQ deficiency associated with fatal encephalomyopathy and respond to 2,4‐diHB increasing CoQ levels. In contrast, Coq9Q95X mice exhibit mild CoQ deficiency manifesting with reduction in CI+III activity and mitochondrial respiration in skeletal muscle, and late‐onset mild mitochondrial myopathy, which does not respond to 2,4‐diHB. We show that these differences are due to the levels of COQ biosynthetic proteins, suggesting that the presence of a truncated version of COQ9 protein in Coq9R239X mice destabilizes the CoQ multiprotein complex. Our study points out the importance of the multiprotein complex for CoQ biosynthesis in mammals, which may provide new insights to understand the genotype–phenotype heterogeneity associated with human CoQ deficiency and may have a potential impact on the treatment of this mitochondrial disorder.This work was supported by grants from the Marie Curie International Reintegration Grant Programme (COQMITMEL-266691 to LCL) within the Seventh European Community Framework Programme, from Ministerio de Economía y Competitividad, Spain (SAF2009-08315 and SAF2013-47761-R to LCL), from the Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía (P10-CTS-6133 to LCL), and from the ‘CEIBioTic’ (20F12/1 to LCL). MLS is a predoctral fellow from the Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía. LCL is supported by the ‘Ramón y Cajal’ National Programme, Ministerio de Economía y Competitividad, Spain (RYC-2011-07643). MAT is supported by a predoctoral grant from the University of Granada. EJC is supported by the Research Program of the University of Granada. CMQ is supported by NICHD Grants 5K23 HDO65871-05 and P01 HD080642-01, and by a MDA grant. The proteomic analysis was performed in the CSIC/UAB Proteomics Facility of IIBB-CSIC that belongs to ProteoRed, PRB2-ISCIII, supported by Grant PT13/0001

The homozygous R504C mutation in MTO1 gene is responsible for ONCE syndrome

We report clinical and biochemical finding from three unrelated patients presenting ONCE (Optic Neuropathy, Cardiomyopathy and Encephalopathy with lactic acidosis and combined oxidative phosphorylation deficiency) syndrome. Whole-exome sequencing (WES) of the three patients and the healthy sister of one of them was used to identify the carry gene. Clinical and biochemical findings were used to filter variants, and molecular, in silico and genetic studies were performed to characterize the candidate variants. Mitochondrial DNA (mtDNA) defects involving mutations, deletions or depletion were discarded, whereas WES uncovered a double homozygous mutation in the MTO1 gene (NM_001123226:c.1510C>T, p.R504C, and c.1669G>A, p.V557M) in two of the patients and the homozygous mutation p.R504C in the other. Therefore, our data confirm p.R504C as pathogenic mutation responsible of ONCE syndrome, and p.V557M as a rare polymorphic variant.post-print712 K