Las Telecomunicaciones de Emergencia: desafíos y agenda pendiente en el Perú

Para nadie es un secreto que el territorio del Perú es altamente propenso a situaciones de emergencia, las que pueden ser tanto fenómenos naturales (sismos, inundaciones, huaycos, etc.), así como desastres causados directamente por la acción del hombre (conflictos sociales, atentados terroristas, etc.). Y, si de situaciones de emergencia estamos hablando, necesariamente debemos referirnos al terremoto de Pisco ocurrido el 15 de agosto de 2018, el cual lamentablemente causó graves daños materiales y pérdidas de cientos de vidas humanas. Es así que, luego de tener cierto acercamiento en un trabajo anterior con el tema del terremoto del 15 de agosto, surgieron muchas interrogantes respecto del rol de las telecomunicaciones en las situaciones de emergencia. Como consecuencia de dichas dudas y planteamientos, es que surgió el interés por investigar a más profundidad este tema desde un punto de vista jurídico, considerando también que muy pocos estudios se han realizado desde esa óptica en la doctrina nacional. Es así que, la presente investigación pretende abordar temas referidos a la importancia de los servicios de telecomunicaciones tanto públicos como privados antes, durante y después de un desastre; su regulación actual tanto en el ámbito internacional como nacional; y, sobre todo, plantear los desafíos y metas que significan para el Derecho Administrativo la regulación nacional actual de los servicios de telecomunicaciones en emergencias.Trabajo académic

Evidence for a Deep Pore Activation Gate in Small Conductance Ca2+-activated K+ Channels

Small conductance calcium-gated potassium (SK) channels share an overall topology with voltage-gated potassium (Kv) channels, but are distinct in that they are gated solely by calcium (Ca2+), not voltage. For Kv channels there is strong evidence for an activation gate at the intracellular end of the pore, which was not revealed by substituted cysteine accessibility of the homologous region in SK2 channels. In this study, the divalent ions cadmium (Cd2+) and barium (Ba2+), and 2-aminoethyl methanethiosulfonate (MTSEA) were used to probe three sites in the SK2 channel pore, each intracellular to (on the selectivity filter side of) the region that forms the intracellular activation gate of voltage-gated ion channels. We report that Cd2+ applied to the intracellular side of the membrane can modify a cysteine introduced to a site (V391C) just intracellular to the putative activation gate whether channels are open or closed. Similarly, MTSEA applied to the intracellular side of the membrane can access a cysteine residue (A384C) that, based on homology to potassium (K) channel crystal structures (i.e., the KcsA/MthK model), resides one amino acid intracellular to the glycine gating hinge. Cd2+ and MTSEA modify with similar rates whether the channels are open or closed. In contrast, Ba2+ applied to the intracellular side of the membrane, which is believed to block at the intracellular end of the selectivity filter, blocks open but not closed channels when applied to the cytoplasmic face of rSK2 channels. Moreover, Ba2+ is trapped in SK2 channels when applied to open channels that are subsequently closed. Ba2+ pre-block slows MTSEA modification of A384C in open but not in closed (Ba2+-trapped) channels. The findings suggest that the SK channel activation gate resides deep in the vestibule of the channel, perhaps in the selectivity filter itself

MÉTODO DE MEDICIÓN DE FUERZA EN EL PROCESO PEDAGÓGICO PARA BOXEADORES CUBANOS

Cuban boxing one of the most recognized worldwide, shows little scientific purpose regarding the development of the force of the punch, so you need to know about how hard stick our boxers, and the need to locate each group and each boxer same division on the average force required for its weight attached, thus measuring the force is paramount stuck in the boxing context. At work the models for the analysis and determination of the impact force, with the design of barometric guantilla measurement device impact (GBI) consisting of a pneumatic guantilla, hose flexible plastic and mercury barometer shows .The procedures used in the study allow us to establish as a starting point, a neurological diagnosis in the behavior of the electrical activity of the brain, also diagnose the force of the punch of the boxers and on that basis establish the relationship between the strength of the pasted and type of alteration produced in this way form a force-measuring test, a table of equivalence and impact scale.El boxeo cubano uno de los más reconocidos a nivel mundial, evidencia una escasa intencionalidad científica respecto al diagnóstico de la fuerza de la pegada, por lo que se necesita conocer aproximadamente con que fuerza pegan nuestros boxeadores, y la necesidad de ubicar a cada grupo de división y a cada boxeador mismo sobre la media de fuerza de pegada exigida para su peso, por tanto la medición de la fuerza de pegada es de suma importancia en el contexto boxístico cubano. En el trabajo se muestran los modelos a seguir para el análisis y determinación de la fuerza de impacto, con el diseño del dispositivo guantilla barométrica de medición de impacto (GBI) constituido por una guantilla neumática, la manguera de plástico flexible y el barómetro de mercurio. Los procedimientos utilizados en el estudio permiten establecer como punto de partida, un diagnostico neurológico en el comportamiento de la actividad eléctrica del cerebro, diagnosticar además la fuerza de la pegada de los boxeadores y sobre esa base establecer la relación que existe entre la fuerza de la pegada y el tipo de alteración producida, para de esta forma conformar un test de medición de fuerza, una tabla de equivalencia y una escala de impacto

Episodic ataxia type-1 mutations in the hKv1.1 cytoplasmic pore region alter the gating properties of the channel

Episodic ataxia type-1 is a rare human neurological syndrome which occurs during childhood and persists through the whole life of affected patients. Several heterozygous point mutations have been found in the coding sequence of the voltage-gated potassium channel gene hKv1.1 of different affected families. V408A and E325D mutations are located in the cytoplasmic putative pore region of hKv1.1 channels and profoundly alter their gating properties. V408A channels showed increased kinetic rates of activation, deactivation and C-type inactivation. Expression of E325D channels in Xenopus oocytes led to an ~13-fold current amplitude reduction and to a 52.4 mV positive shift in the voltage dependence of activation. Moreover, the E325D mutation altered the kinetics of activation, deactivation, C-type inactivation and channel open probability. Heteromeric channels composed of two wild-type and two mutated subunits, linked as dimers, showed gating properties intermediate between channels formed from four normal or four mutated subunits. The results demonstrate that the highly conserved residues Val408 and Glu325 play a pivotal role in several gating processes of a human potassium channel, and suggest a pathogenetic mechanism by which the impairment of the delayed-rectifier function of affected neurons is related to the type and number of mutated subunits which make up the hKv1.1 channels.peer-reviewe

Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization

Although action potentials propagate along axons in an all-­or-­none manner, subthreshold membrane potential fluctuations at the soma affect neurotransmitter release from synaptic boutons. An important mechanism underlying analog-­digital modulation is depolarization-­mediated inactivation of presynaptic Kv1-­family potassium channels, leading to action potential broadening and increased calcium influx. Previous studies have relied heavily on recordings from blebs formed after axon transection, which may exaggerate the passive propagation of somatic depolarization. We recorded instead from small boutons supplied by intact axons identified with scanning ion conductance microscopy in primary hippocampal cultures, and asked how distinct potassium channels interact in determining the basal spike width and its modulation by subthreshold somatic depolarization. Pharmacological or genetic deletion of Kv1.1 broadened presynaptic spikes without preventing further prolongation by brief depolarizing somatic prepulses. A heterozygous mouse model of Episodic Ataxia type 1 harboring a dominant Kv1.1 mutation had a similar broadening effect on basal spike shape as deletion of Kv1.1;; however, spike modulation by somatic prepulses was abolished. These results argue that the Kv1.1 subunit is not necessary for subthreshold modulation of spike width. However, a disease-­associated mutant subunit prevents the interplay of analog and digital transmission, possibly by disrupting the normal stoichiometry of presynaptic potassium channels

Activation and desensitization of the olfactory cAMP-gated transduction channel: identification of functional modules

Olfactory receptor neurons respond to odor stimulation with a receptor potential that results from the successive activation of cyclic AMP (cAMP)-gated, Ca2+-permeable channels and Ca2+-activated chloride channels. The cAMP-gated channels open at micromolar concentrations of their ligand and are subject to a Ca2+-dependent feedback inhibition by calmodulin. Attempts to understand the operation of these channels have been hampered by the fact that the channel protein is composed of three different subunits, CNGA2, CNGA4, and CNGB1b. Here, we explore the individual role that each subunit plays in the gating process. Using site-directed mutagenesis and patch clamp analysis, we identify three functional modules that govern channel operation: a module that opens the channel, a module that stabilizes the open state at low cAMP concentrations, and a module that mediates rapid Ca2+-dependent feedback inhibition. Each subunit could be assigned to one of these functions that, together, define the gating logic of the olfactory transduction channel