University of Valencia

About: University of Valencia is a education organization based out in Valencia, Spain. It is known for research contribution in the topics: Population & Context (language use). The organization has 27096 authors who have published 65669 publications receiving 1765689 citations. The organization is also known as: Universitat de València & UV.

Multifunctionality in hybrid magnetic materials based on bimetallic oxalate complexes.

Abstract: This tutorial review illustrates the design of multifunctional oxalate-based magnetic materials through the combination of the intrinsic magnetism of the metal–organic framework and the additional properties introduced by several organic/inorganic functional cations.

Intrinsically determined cell death of developing cortical interneurons

Abstract: The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantation suggests that developmental neuronal-cell death is instead intrinsically determined for interneurons, the main inhibitory cells of the cerebral cortex. Cortical inhibitory circuits are formed by γ-aminobutyric acid (GABA)-secreting interneurons, a cell population that originates far from the cerebral cortex in the embryonic ventral forebrain. Given their distant developmental origins, it is intriguing how the number of cortical interneurons is ultimately determined. One possibility, suggested by the neurotrophic hypothesis1,2,3,4,5, is that cortical interneurons are overproduced, and then after their migration into cortex the excess interneurons are eliminated through a competition for extrinsically derived trophic signals. Here we characterize the developmental cell death of mouse cortical interneurons in vivo, in vitro and after transplantation. We found that 40% of developing cortical interneurons were eliminated through Bax (Bcl-2-associated X)-dependent apoptosis during postnatal life. When cultured in vitro or transplanted into the cortex, interneuron precursors died at a cellular age similar to that at which endogenous interneurons died during normal development. Over transplant sizes that varied 200-fold, a constant fraction of the transplanted population underwent cell death. The death of transplanted neurons was not affected by the cell-autonomous disruption of TrkB (tropomyosin kinase receptor B), the main neurotrophin receptor expressed by neurons of the central nervous system6,7,8. Transplantation expanded the cortical interneuron population by up to 35%, but the frequency of inhibitory synaptic events did not scale with the number of transplanted interneurons. Taken together, our findings indicate that interneuron cell death is determined intrinsically, either cell-autonomously or through a population-autonomous competition for survival signals derived from other interneurons.

Relationship between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues

Abstract: Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

Inclusive charged-current neutrino-nucleus reactions

Abstract: We present a model for weak charged-current induced nuclear reactions at energies of interest for current and future neutrino oscillation experiments. This model is a natural extension of the work in Refs. [1,2], where the quasielastic contribution to the inclusive electron and neutrino scattering on nuclei was analyzed. The model is based on a systematic many-body expansion of the gauge boson absorption modes that includes one, two, and even three-body mechanisms, as well as the excitation of $\ensuremath{\Delta}$ isobars. The whole scheme has no free parameters, besides those previously adjusted to the weak pion production off the nucleon cross sections in the deuteron, since all nuclear effects were set up in previous studies of photon, electron, and pion interactions with nuclei. We have discussed at length the recent charged-current quasielastic MiniBooNE cross section data, and showed that two-nucleon knockout mechanisms are essential to describing these measurements.