Gestión del talento humano y calidad de servicio en la Municipalidad Provincial de Bagua

Gestión del talento humano es un problema en las entidades del estado que se manifiesta mediante el inadecuado proceso de reclutamiento, capacitación y evaluación que afecta a la entidad en los servicios que brinda; para el estudio se planteó como objetivo determinar la correlación de la gestión del talento humano en la calidad de servicio. Condición que será solucionado según se implemente los indicadores adecuadamente del reclutamiento, capacitación y evaluación. El estudio es aplicado en modalidad propositiva, se desarrolló bajo un enfoque descriptivo simple con propuesta. La muestra fue 125 entre usuarios y trabajadores, se aplicó la encuesta y un cuestionario por cada variable como instrumentos, la información fue analizada, mediante el estadístico SPSS 26 y la correlación mediante la Rho Spearman (p 0.05). Los resultados dan cuenta del problema existente en la gestión del talento humano y calidad de servicio es deficiente según los promedios de valores asignados, existe brecha del 95.5% reclutamiento, 60% capacitación, 60.6% evaluación, 100% empatía y fiabilidad. Se sustenta el estudio en base a los diversos estudios realizados referentes al tema de investigación, se propone estrategias para mejorar la gestión del talento humano

Manipulating myocyte cell cycle control for cardiac repair

This editorial refers to ‘Cardiomyocyte proliferation and protection against post-myocardial infarction heart failure by cyclin D1 and Skp2 ubiquitin ligase’ by Tamamori-Adachi et al.,11 pp. 181–190, this issu

Ribose Treatment Reduced the Infarct Size and Improved Heart Function after Myocardial Infarction in Rats

Objective: In this study the effect of ribose on heart function and infarct-size was analyzed 6 h after myocardial infarction (MI) in rats. Methods: Continuous i.v.-infusion of NaCl or ribose (200 mg/ kg/h) was started one day prior to induction of MI in female Sprague-Dawley rats which was done by ligation of the left coronary artery. Six hours after MI heart function was measured with 3F tip catheter, cardiac output by thermodilution method. Thereafter the ischemic area was delineated by Evans Blue infusion, and the infarct area was visualized by triphenyltetrazolium chloride staining. The mRNA expression of interleukin (IL)-1β, IL-6, matrixmetalloproteinase (MMP)-8, and -9 was measured by ribonuclease protection assay. Results: Heart function was severely depressed 6 hours after coronary artery occlusion, but recovered significantly under the influence of ribose. Left ventricular (LV) systolic pressure (LVSP) and contractility (LVdP/dtmax) were restored to the normal levels of sham-operated animals, while parameters of LV relaxation (LVdP/dtmin and time constant of relaxation τ) were impaired compared to sham-operated animals, but significantly improved by ribose treatment compared to shamtreated MI-rats. Moreover, the infarct size was significantly smaller in the ribose treated animals despite a comparable ischemic area at risk in all MI-rats. The cytokine mRNA expression after MI was significantly reduced after ribose treatment, while there were no differences regarding MMP expression. Conclusion: MI size was significantly reduced and LV function significantly improved by ribose treatment at 6 h after MI. This seemed to be based on slowing the velocity of the necrotic wave front across the LV wall after MI resulting in smaller infarcts.Fil: González, Germán Esteban. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Rabald, Steffen. University of Leipzig; AlemaniaFil: Briest, Wilfried. University of Leipzig; AlemaniaFil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Seropian, Ignacio Miguel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; ArgentinaFil: Zimmer, Heinz Gerd. University of Leipzig; AlemaniaFil: Deten, Alexander. University of Leipzig; Alemani

Specific Mechanisms underlying Right Heart Failure

AIMS: Research into right ventricular (RV) physiology and identification of pathomechanisms underlying RV failure have been neglected for many years because function of the RV is often considered to be less important for overall hemodynamics and maintenance of blood circulation. In view of this, the present study focuses on identifying specific adaptive mechanisms of the right and left ventricle (LV) during a state of chronic nitric oxide (NO) deficiency, one of the main causes of cardiac failure. NO deficiency was induced in rats by L-NAME feeding over a four weeks period. The cardiac remodeling was then characterized separately for the RV/LV using qRT-PCR, histology, and functional measurements. RESULTS: Only the RV underwent remodeling that corresponded morphologically and functionally with the pattern of dilated cardiomyopathy. Symptoms in the LV were subtle and consisted primarily of moderate hypertrophy. A massive increase in reactive oxygen species (ROS) (+4.5+/-0.8 fold, vs. control) and a higher degree of oxidized tropomyosin (+46+/-4% vs. control) and peroxynitrite (+32+/-2% vs. control) could be identified as the cause of both RV fibrosis and contractile dysfunction. The expression of superoxide dismutase-2 was specifically increased in the LV by 51+/-3% and prevented the ROS increase and the corresponding structural and functional remodeling. INNOVATION: This study identified the inability of the RV to increase its antioxidant capacity as an important risk factor for developing RV failure. CONCLUSION: Unlike the LV, the RV did not display the necessary adaptive mechanisms to cope with increased oxidative stress during a state of chronic NO deficiency

The Inflammatory Response and Cardiac Repair After Myocardial Infarction

One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-α) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction

Post-infarct remodelling: contribution of wound healing and inflammation

In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and function. MI and the consequent loss of myocardium are the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains poor in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to improve healing of the cardiac wound to maintain structure and function of the heart. Healing in the heart occurs in overlapping phases. Herein, we review the inflammatory phase as a trigger of tissue formation

Accumulation of fibronectin in the heart after myocardial infarction: a putative stimulator of adhesion and proliferation of adipose-derived stem cells

Stem cell therapy is a promising treatment after myocardial infarction (MI). A major problem in stem cell therapy, however, is that only a small proportion of stem cells applied to the heart can survive and differentiate into cardiomyocytes. We hypothesized that fibronectin in the heart after MI might positively affect stem cell adhesion and proliferation at the site of injury. Therefore, we investigated the kinetics of attachment and proliferation of adipose-tissue-derived stem cells (ASC) on fibronectin and analysed the time frame and localization of fibronectin accumulation in the human heart after MI. ASCs were seeded onto fibronectin-coated and uncoated culture wells. The numbers of adhering ASC were quantified after various incubation periods (5-30 min) by using DNA quantification assays. The proliferation of ASC was quantified after culturing ASC for various periods (0-9 days) by using DNA assays. Fibronectin accumulation after MI was quantified by immunohistochemical staining of heart sections from 35 patients, after different infarction periods (0-14 days old). We found that ASC attachment and proliferation on fibronectin-coated culture wells was significantly higher than on uncoated wells. Fibronectin deposition was significantly increased from 12 h to 14 days post-infarction, both in the infarction area and in the border-zone, compared with the uninfarcted heart. Our results suggest that a positive effect of fibronectin on stem cells in the heart can only be achieved when stem cell therapy is applied at least 12 h after MI, when the accumulation of fibronectin occurs in the infarcted heart. © 2008 The Author(s)

Variability of NT-proBNP and Its Relationship with Inflammatory Status in Patients with Stable Essential Hypertension: A 2-Year Follow-Up Study

The variability of NT-proBNP levels has been studied in heart failure, yet no data exist on these changes over time in hypertensive patients. Furthermore, studies on the relationship between natriuretic peptides and inflammatory status are limited.220 clinically and functionally asymptomatic stable patients (age 59 ± 13, 120 male) out of 252 patients with essential hypertension were followed up, and NT-proBNP was measured at baseline, 12 and 24 months. No differences in NT-proBNP were found with respect to the basal stage in the hypertrophic group, but significant changes were found in non-hypertrophic subjects. The reproducibility of NT-proBNP measurements was better in patients with hypertrophy than in the non-hypertrophic group for the three intervals (stage I-basal; stage II-stage I; stage II-basal) with a reference change value of 34%, 35% and 41%, respectively, in the hypertrophic group. A more elevated coefficient of correlation was obtained in the hypertrophic group than in patients without hypertrophy: basal versus stage I (r = 0.79, p < 0.0001 and r = 0.59, p < 0.0001) and stage I versus stage II (r = 0.86, p < 0.0001 and r = 0.56, p < 0.0001). Finally, levels of NT-proBNP significantly correlated with sTNF-R1 (p < 0.0001) and IL-6 (p < 0.01) during follow-up. A multivariate linear regression analysis showed that sTNF-R1 is an independent factor of NT-proBNP.This work shows that there is good stability in NT-proBNP levels in a follow-up study of asymptomatic patients with stable hypertension and left ventricular hypertrophy. As a consequence, assessment of NT-proBNP concentrations may be a useful tool for monitoring the follow-up of hypertensive patients with hypertrophy. Measured variations in peptide levels, exceeding 35% in a 12-month follow-up and 41% in a 24-month follow-up, may indicate an increase in cardiovascular risk, and therefore implies adjustment in the medical treatment. In addition, this study shows a link between neurohormonal and inflammatory activation in these patients

Impact of pulmonary exposure to gold core silver nanoparticles of different size and capping agents on cardiovascular injury

Background:The uses of engineered nanomaterials have expanded in biomedical technology and consumer manufacturing. Furthermore, pulmonary exposure to various engineered nanomaterials has, likewise, demonstrated the ability to exacerbate cardiac ischemia reperfusion (I/R) injury. However, the influence of particle size or capping agent remains unclear. In an effort to address these influences we explored response to 2 different size gold core nanosilver particles (AgNP) with two different capping agents at 2 different time points. We hypothesized that a pulmonary exposure to AgNP induces cardiovascular toxicity influenced by inflammation and vascular dysfunction resulting in expansion of cardiac I/R Injury that is sensitive to particle size and the capping agent. Methods: Male Sprague–Dawley rats were exposed to 200 μg of 20 or 110 nm polyvinylprryolidone (PVP) or citrate capped AgNP. One and 7 days following intratracheal instillation serum was analyzed for concentrations of selected cytokines; cardiac I/R injury and isolated coronary artery and aorta segment were assessed for constrictor responses and endothelial dependent relaxation and endothelial independent nitric oxide dependent relaxation. Results: AgNP instillation resulted in modest increase in selected serum cytokines with elevations in IL-2, IL-18, and IL-6. Instillation resulted in a derangement of vascular responses to constrictors serotonin or phenylephrine, as well as endothelial dependent relaxations with acetylcholine or endothelial independent relaxations by sodium nitroprusside in a capping and size dependent manner. Exposure to both 20 and 110 nm AgNP resulted in exacerbation cardiac I/R injury 1 day following IT instillation independent of capping agent with 20 nm AgNP inducing marginally greater injury. Seven days following IT instillation the expansion of I/R injury persisted but the greatest injury was associated with exposure to 110 nm PVP capped AgNP resulted in nearly a two-fold larger infarct size compared to naïve. Conclusions: Exposure to AgNP may result in vascular dysfunction, a potentially maladaptive sensitization of the immune system to respond to a secondary insult (e.g., cardiac I/R) which may drive expansion of I/R injury at 1 and 7 days following IT instillation where the extent of injury could be correlated with capping agents and AgNP size.This work was supported by the National Institute of Environmental Health Sciences U19ES019525, U01ES020127, U19ES019544 and East Carolina Universit