Universidad del Desarrollo

About: Universidad del Desarrollo is a education organization based out in Santiago, Chile. It is known for research contribution in the topics: Population & Entrepreneurship. The organization has 2695 authors who have published 3578 publications receiving 52302 citations.

Network Effects of Demographic Transition

Abstract: Traditional human societies use two of biology’s solutions to reduce free-riding: by collaborating with relatives, they rely on the mechanism of kin-selection, and by forming highly clustered social kin-networks, they can efficiently use reputation dynamics. Both of these solutions assume the presence of relatives. This paper shows how social networks change during demographic transition. With falling fertility, there are fewer children that could be relatives to one another. As the missing kin are replaced by non-kin friends, local clustering in the social network drops. This effect is compounded by increasing population size, characteristic of demographic transition. The paper also shows that the speed at which reputation spreads in the network slows down due to both falling fertility and increasing group size. Thus, demographic transition weakens both mechanisms for eliminating free-riders: there are fewer relatives around, and reputation spreads slower. This new link between falling fertility and the altered structure of the social network offers novel interpretations of the origins of legal institutions, the Small World phenomenon, the social impact of urbanisation, and the birds-of-a-feather friendship choice heuristic.

c-Jun N-terminal kinase (JNK)-dependent internalization and Rab5-dependent endocytic sorting mediate long-distance retrograde neuronal death induced by axonal BDNF-p75 signaling

Abstract: During the development of the sympathetic nervous system, signals from tropomyosin-related kinase receptors (Trks) and p75 neurotrophin receptors (p75) compete to regulate survival and connectivity. During this process, nerve growth factor (NGF)- TrkA signaling in axons communicates NGF-mediated trophic responses in signaling endosomes. Whether axonal p75 signaling contributes to neuronal death and how signaling endosomes contribute to p75 signaling has not been established. Using compartmentalized sympathetic neuronal cultures (CSCGs) as a model, we observed that the addition of BDNF to axons increased the transport of p75 and induced death of sympathetic neurons in a dynein-dependent manner. In cell bodies, internalization of p75 required the activity of JNK, a downstream kinase mediating p75 death signaling in neurons. Additionally, the activity of Rab5, the key GTPase regulating early endosomes, was required for p75 death signaling. In axons, JNK and Rab5 were required for retrograde transport and death signaling mediated by axonal BDNF-p75 in CSCGs. JNK was also required for the proper axonal transport of p75-positive endosomes. Thus, our findings provide evidence that the activation of JNK by p75 in cell bodies and axons is required for internalization to a Rab5-positive signaling endosome and the further propagation of p75-dependent neuronal death signals.

Patología obstructiva no maligna de la vía aérea central

Abstract: Resumen Las causas mas frecuentes de patologia obstructiva no maligna de la via aerea central son las estenosis postintubacion y postraqueotomia, seguidas por los cuerpos extranos y la traqueobroncomalacia. Otras causas, como las secundarias a procesos infecciosos y enfermedades sistemicas, son menos frecuentes. A pesar de la existencia de numerosas clasificaciones, todavia no se ha alcanzado consenso sobre la utilizacion de alguna de ellas en concreto. Un mejor conocimiento de su fisiopatologia nos ha permitido aumentar el diagnostico y mejorar su tratamiento; su presentacion clinica inespecifica exige la realizacion de diversos estudios funcionales, radiologicos y fundamentalmente endoscopicos para su correcto diagnostico. El tratamiento debe ser multidiciplinario e individualizado, requiriendo tratamiento quirurgico o endoscopico mediante diferentes tecnicas termoablativas y mecanicas.

p27Kip1 Knockdown Induces Proliferation in the Organ of Corti in Culture after Efficient shRNA Lentiviral Transduction

Abstract: The cells in the organ of Corti do not exhibit spontaneous cell regeneration; hair cells that die after damage are not replaced. Supporting cells can be induced to transdifferentiate into hair cells, but that would deplete their numbers, therefore impairing epithelium physiology. The loss of p27Kip1 function induces proliferation in the organ of Corti, which raises the possibility to integrate it to the strategies to achieve regeneration. Nevertheless, it is not known if the extent of this proliferative potential, as well as its maintenance in postnatal stages, is compatible with providing a basis for eventual therapeutic manipulation. This is due in part to the limited success of approaches to deliver tools to modify gene expression in the auditory epithelium. We tested the hypothesis that the organ of Corti can undergo significant proliferation when efficient manipulation of the expression of regulators of the cell cycle is achieved. Lentiviral vectors were used to transduce all cochlear cell types, with efficiencies around 4 % for hair cells, 43 % in the overall supporting cell population, and 74 % within lesser epithelial ridge (LER) cells. Expression of short hairpin RNA targeting p27Kip1 encoded by the lentiviral vectors led to measurable proliferation in the organ of Corti and increase in LER cells number but not hair cell regeneration. Our results revalidate the use of lentiviral vectors in the study and in the potential therapeutic approaches for inner ear diseases, as well as demonstrate that efficient manipulation of p27Kip1 is sufficient to induce significant proliferation in the postnatal cochlea.