Teletrabajo y la cultura organizacional en los trabajadores del Hospital de la Amistad Perú Corea Santa Rosa II-2, Piura, 2022

El presente trabajo de investigación titulado “Teletrabajo y C. Org. en los Trabajadores del Hospital de la Amistad Perú Corea Santa Rosa II-2 Piura”, tuvo como objetivo principal determinar la relación entre el teletrabajo y la c. org. en los trabajadores del Hospital de la Amistad Perú Corea Santa Rosa II-2 Piura 2022, donde la investigación se realizó bajo el enfoque cuantitativo, nivel correlacional y tipo de investigación aplicada, en ese sentido la población de estudio se conformó por 1049 trabajadores, donde la muestra fueron 170 trabajadores dado que fue un muestreo no probabilístico por formula. En cuanto a los resultados obtenidos en los cuestionarios tuvieron una confiabilidad de 0.959 y 0.968, llegando a concluir que el instrumento es fiable, tras la aplicación de un coeficiente de correlación de Rho de Spearman se obtuvo un valor de r = 0,734 entre las variables de estudio. De acuerdo al Sig. (Bilateral) = 0.01 < 0,05 indicó que se rechazó la hipótesis nula y se aceptó la hipótesis alterna; afirmando que, si existió una correlación altamente positiva considerable entre las variables teletrabajo y c. org., la cual favoreció a los trabajadores del Hospital de la Amistad Perú Corea Santa Rosa II-2 Piura

Atraumatic acromioclavicular joint dislocation: A case report treated with excision of the distal clavicle margin and button slide system with allograft tendon reinforcement at coracoclavicular and acromioclavicular joint

Producción CientíficaAlthough acromioclavicular joint (ACJ) dislocation is a common injury following trauma involving the shoulder, it is rare in the absence of trauma. In this manuscript, we describe a case of ACJ in a 15-year-old girl who presented a painful dislocation with spontaneous shortening of the right acromioclavicular joint that forced her to temporarily abandon her sports career. After failure of conservative physiotherapy treatment, surgical intervention was proposed by performing an arthroscopic-assisted button slide combined with augmented hamstring allograft reconstruction. After the intervention and the subsequent recovery period, the athlete was able to return to her semi-professional training. The follow-up of the patient is 5.5 years post-surgery. The result obtained could help in planning the treatment of future cases

Pharmacological characterization of recombinant human neuronal nicotinic acetylcholine receptors

ABSTRACT Human neuronal nicotinic acetylcholine receptors (nAChRs) h␣2␤2, h␣2␤4, h␣3␤2, h␣3␤4, h␣4␤2, h␣4␤4 and h␣7 were expressed in Xenopus oocytes and tested for their sensitivities to the nicotinic agonists acetylcholine (ACh), nicotine, cytisine (CYT) and 1,1-dimethyl-4-phenylpiperazinium (DMPP) and the nAChR. antagonists mecamylamine (MEC), d-tubocurarine and dihydro-␤-erythroidine. CYT was the least efficacious agonist at hnAChRs containing ␤2 subunits, but it displayed significant activity at h␣2␤4, h␣3␤4, h␣4␤4 and h␣7 nAChRs. ACh was one of the most efficacious agonists at all hnAChRs, except at h␣3␤2, where DMPP was markedly more efficacious than ACh. ACh was among the least potent agonists at all hnAChRs. The rank order of potency displayed by h␣3␤2 and h␣3␤4 nAChRs (DMPPϷCYTϷnicotineϾACh and DMPP Ͼ CYTϷnicotineϾACh, respectively), differs from that reported for their rat homolog

Endogenous cholinergic inputs and local circuit mechanisms govern the phasic mesolimbic dopamine response to nicotine

Nicotine exerts its reinforcing action by stimulating nicotinic acetylcholine receptors (nAChRs) and boosting dopamine (DA) output from the ventral tegmental area (VTA). Recent data have led to a debate about the principal pathway of nicotine action: direct stimulation of the DAergic cells through nAChR activation, or disinhibition mediated through desensitization of nAChRs on GABAergic interneurons. We use a computational model of the VTA circuitry and nAChR function to shed light on this issue. Our model illustrates that the α4β2-containing nAChRs either on DA or GABA cells can mediate the acute effects of nicotine. We account for in vitro as well as in vivo data, and predict the conditions necessary for either direct stimulation or disinhibition to be at the origin of DA activity increases. We propose key experiments to disentangle the contribution of both mechanisms. We show that the rate of endogenous acetylcholine input crucially determines the evoked DA response for both mechanisms. Together our results delineate the mechanisms by which the VTA mediates the acute rewarding properties of nicotine and suggest an acetylcholine dependence hypothesis for nicotine reinforcement.Peer reviewe

Identification of a Negative Allosteric Site on Human α4β2 and α3β4 Neuronal Nicotinic Acetylcholine Receptors

Acetylcholine-based neurotransmission is regulated by cationic, ligand-gated ion channels called nicotinic acetylcholine receptors (nAChRs). These receptors have been linked to numerous neurological diseases and disorders such as Alzheimer's disease, Parkinson's disease, and nicotine addiction. Recently, a class of compounds has been discovered that antagonize nAChR function in an allosteric fashion. Models of human α4β2 and α3β4 nicotinic acetylcholine receptor (nAChR) extracellular domains have been developed to computationally explore the binding of these compounds, including the dynamics and free energy changes associated with ligand binding. Through a blind docking study to multiple receptor conformations, the models were used to determine a putative binding mode for the negative allosteric modulators. This mode, in close proximity to the agonist binding site, is presented in addition to a hypothetical mode of antagonism that involves obstruction of C loop closure. Molecular dynamics simulations and MM-PBSA free energy of binding calculations were used as computational validation of the predicted binding mode, while functional assays on wild-type and mutated receptors provided experimental support. Based on the proposed binding mode, two residues on the β2 subunit were independently mutated to the corresponding residues found on the β4 subunit. The T58K mutation resulted in an eight-fold decrease in the potency of KAB-18, a compound that exhibits preferential antagonism for human α4β2 over α3β4 nAChRs, while the F118L mutation resulted in a loss of inhibitory activity for KAB-18 at concentrations up to 100 µM. These results demonstrate the selectivity of KAB-18 for human α4β2 nAChRs and validate the methods used for identifying the nAChR modulator binding site. Exploitation of this site may lead to the development of more potent and subtype-selective nAChR antagonists which may be used in the treatment of a number of neurological diseases and disorders

IPF, a vesicular uptake inhibitory protein factor, can reduce the Ca 2+ -dependent, evoked release of glutamate, GABA and serotonin

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66179/1/j.1471-4159.2001.00120.x.pd

Characterizing Ligand-Gated Ion Channel Receptors with Genetically Encoded Ca++ Sensors

We present a cell based system and experimental approach to characterize agonist and antagonist selectivity for ligand-gated ion channels (LGIC) by developing sensor cells stably expressing a Ca2+ permeable LGIC and a genetically encoded Förster (or fluorescence) resonance energy transfer (FRET)-based calcium sensor. In particular, we describe separate lines with human α7 and human α4β2 nicotinic acetylcholine receptors, mouse 5-HT3A serotonin receptors and a chimera of human α7/mouse 5-HT3A receptors. Complete concentration-response curves for agonists and Schild plots of antagonists were generated from these sensors and the results validate known pharmacology of the receptors tested. Concentration-response relations can be generated from either the initial rate or maximal amplitudes of FRET-signal. Although assaying at a medium throughput level, this pharmacological fluorescence detection technique employs a clonal line for stability and has versatility for screening laboratory generated congeners as agonists or antagonists on multiple subtypes of ligand-gated ion channels. The clonal sensor lines are also compatible with in vivo usage to measure indirectly receptor activation by endogenous neurotransmitters

Ubiquitous molecular substrates for associative learning and activity-dependent neuronal facilitation.

Recent evidence suggests that many of the molecular cascades and substrates that contribute to learning-related forms of neuronal plasticity may be conserved across ostensibly disparate model systems. Notably, the facilitation of neuronal excitability and synaptic transmission that contribute to associative learning in Aplysia and Hermissenda, as well as associative LTP in hippocampal CA1 cells, all require (or are enhanced by) the convergence of a transient elevation in intracellular Ca2+ with transmitter binding to metabotropic cell-surface receptors. This temporal convergence of Ca2+ and G-protein-stimulated second-messenger cascades synergistically stimulates several classes of serine/threonine protein kinases, which in turn modulate receptor function or cell excitability through the phosphorylation of ion channels. We present a summary of the biophysical and molecular constituents of neuronal and synaptic facilitation in each of these three model systems. Although specific components of the underlying molecular cascades differ across these three systems, fundamental aspects of these cascades are widely conserved, leading to the conclusion that the conceptual semblance of these superficially disparate systems is far greater than is generally acknowledged. We suggest that the elucidation of mechanistic similarities between different systems will ultimately fulfill the goal of the model systems approach, that is, the description of critical and ubiquitous features of neuronal and synaptic events that contribute to memory induction

P2 receptors are involved in the mediation of motivation-related behavior

The importance of purinergic signaling in the intact mesolimbic–mesocortical circuit of the brain of freely moving rats is reviewed. In the rat, an endogenous ADP/ATPergic tone reinforces the release of dopamine from the axon terminals in the nucleus accumbens as well as from the somatodendritic region of these neurons in the ventral tegmental area, as well as the release of glutamate, probably via P2Y1 receptor stimulation. Similar mechanisms may regulate the release of glutamate in both areas of the brain. Dopamine and glutamate determine in concert the activity of the accumbal GABAergic, medium-size spiny neurons thought to act as an interface between the limbic cortex and the extrapyramidal motor system. These neurons project to the pallidal and mesencephalic areas, thereby mediating the behavioral reaction of the animal in response to a motivation-related stimulus. There is evidence that extracellular ADP/ATP promotes goal-directed behavior, e.g., intention and feeding, via dopamine, probably via P2Y1 receptor stimulation. Accumbal P2 receptor-mediated glutamatergic mechanisms seem to counteract the dopaminergic effects on behavior. Furthermore, adaptive changes of motivation-related behavior, e.g., by chronic succession of starvation and feeding or by repeated amphetamine administration, are accompanied by changes in the expression of the P2Y1 receptor, thought to modulate the sensitivity of the animal to respond to certain stimuli