Escala de Respuestas Emocionales por Estrés al Traslado en Transporte Público / Scale of Emotional Responses due to Commuting Stress in Public Transport

Resumen El traslado cotidiano entre la casa y el trabajo demanda un importante uso de recursos personales y puede llegar a ser estresante. El objetivo fue construir y evaluar una escala de respuestas emocionales por el estrés en el traslado en transporte público para la Zona Metropolitana del Valle de México de manera exploratoria. Método: Se realizó un estudio cualitativo a través de entrevistas semi estructuradas con el propósito de identificar emociones asociadas a la experiencia de estrés por el traslado para desarrollar los reactivos de acuerdo con el contexto. Posteriormente, dos estudios cuantitativos permitieron evaluar las propiedades psicométricas. Participaron 196 y 298 personas respectivamente. La aplicación de la escala se realizó en línea en septiembre de 2020 y abril de 2021. Resultados: la escala incluyó 26 respuestas emocionales asociadas al estrés. En el Análisis Factorial Exploratorio se redujo a nueve emociones negativas (X2=1183, gl=36, p=.001, KMO=.94, 60% de varianza explicada, Alfa ordinal=.93), corroboradas en el Análisis Factorial Confirmatorio (X2=41.87, gl=26, X2/gl=1.61, p=.025; RMR=.036, SRMR=.036, RMSEA=.045; GFI=.997, CFI=.999, TLI=.998). Conclusión: la propuesta exploratoria de la escala para evaluar las respuestas emocionales por el estrés en el traslado presenta valores adecuados para aplicarse en la Zona Metropolitana del Valle de México.

Abstract The stress in urban settings is related to a greater request for personal resources to face situations of daily life, such as the commuting, since in big cities, people spend a lot of time on it, and sometimes is uncomfortable and annoying, which can cause stress. Commuting stress has been assessed, through commuting daily hassles, commuting stressful features and physiological responses, but it is possible assess it through emotional responses. The aim of this study was to develop and assess an exploratory scale of emotional responses for the study of commuting stress by public transport in an urban area of México that is densely populated. Method, a cross sectional design was used, in which a qualitative exploratory study was carried out through 23 individual semi-structured interviews and two focus group, where it was identified the main emotions experienced during the commuting stress to develop the items in the language of the population. Subsequently, those emotions were compared with emotions proposed in previous studies to complement the scale. Thus, 26 emotions were included to assess the commuting stress through emotional responses. Finally, two quantitative studies were carried out to assess the psychometric properties of the scale, in which 196 and 298 people participated, respectively. The scale was applied online in September 2020 and in April 2021. Results, from the 26 emotional stress responses were reduced to nine negative emotions in an Exploratory Factor Analysis (X2=1183, df=36, p=.001, KMO= .94, 60% variance, Alfa ordinal=.93). This solution was corroborated with a Confirmatory Factor Analysis (X2=41.87, d.f.=26, X2/d.f.=1.61, p=.025; RMR= .036, SRMR=.036, RMSEA=.045; GFI=.997, CFI=.999, TLI=.998). Conserve only nine negative emotions is due to statistical analysis but also because some emotions referred to conditions of physical exhaustion or body energy level. On the other hand, positive emotions were related with pleasant commuting situations, not with the commuting stress experience. Conclusion, the exploratory scale to assess the commuting stress through emotional responses presents acceptable values to be applied in this urban area of Mexico.

Motivos de uso y no uso de puentes peatonales en la Ciudad de México: la perspectiva de los peatones / Use and non-use of pedestrian bridges in Mexico City: the pedestrian perspective

OBJETIVO. Analizar los motivos de uso y no uso de puentes peatonales (PP). MATERIAL Y MÉTODOS. Se empleó un diseño transversal, a partir de una muestra de peatones usuarios y no usuarios de PP; se utilizó regresión logística para identificar los factores que influyen en el uso y no uso de PP. RESULTADOS. La prevalencia de no uso fue 50.5 por ciento en 813 peatones entrevistados; la principal razón para usar PP fue "seguridad", del no uso fue "flojera". Hubo diferencias significativas al analizar motivos de no uso de PP en las edades de 19 a 36 años, ajustando por escolaridad y características físicas del PP, con RMa. 1.7 (IC95 por ciento 1.06-2.86) y RMa. 1.9 (IC95 por ciento 1.14-3.33), respectivamente. CONCLUSIONES. Los resultados de este estudio permiten identificar aspectos importantes a considerar desde la perspectiva de los peatones, antes de construir nuevos PP, así como aquéllos que deben mejorarse para incrementar su uso en zonas de alto riesgo de lesiones por atropellamiento.

OBJECTIVE. To analyze the motives for using and not using pedestrian bridges (PB). MATERIAL AND METHODS. A cross-sectional survey was conducted of a sample of pedestrian users and non-users of PB; a logistic regression model was used to analyze the motives for use and non-use. RESULTS. The prevalence of non-use was 50.5 percent of 813 surveyed pedestrians; the principal reason to use a PB was safety, and not to use it was "laziness". There were significant differences when analyzing the reason of non-use in the age groups 19 to 36 years, adjusted for education and physical characteristics of the PB ([aOR=1.7; 95 percent CI=1.06-2.86] and [ORa.1.9; 95 percent CI=1.14-3.33], respectively). CONCLUSIONS. The results of this study allow us to identify important aspects to consider "from the perspective of the pedestrians" when constructing new PB and improving existing PB to increase use in areas with a high risk of pedestrian injuries.

Vías de neuroinmunomodulación. Primera parte

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Summary: Inflammation is a normal response caused by physical stress like infection, injury and trauma; and processive or psychological stress like in psychiatric diseases such as major depression, schizophrenia and posttraumatic stress. The host responds with a complex series of immune, endocrine and nervous reactions to face the stressful stimuli named neuroendocrine immune interaction. These interactions help us to maintain the homeostasis under stressful stimuli. Stress is a physicochemical or emotional process that induces tension. This process promotes the release of proinflammatory cytokines, hormones such as the corticotrophin-release hormone (CRH) and cortisol, and a wide number of neurotransmitters that are together responsible for some behavioral alterations. Both systemic and psychological stress elicits an equivalent response in an organism. Particularly, the onset of inflammation is characterized by release of pro-inflammatory mediators including tumor necrosis factor (TNF)-α, interleukin (IL)-1, adhesion molecules, vasoactive mediators, and reactive oxygen species. The early release of pro-inflammatory cytokines by a widely variety of immune and no-immune cells has a pivotal role in triggering the local inflammatory response. Apart from their involvement in local inflammation, TNF-α and IL-1β are signal molecules for activation of brain derived neuroendocrine and immunomodulatory responses. Excessive production of cytokines, such as TNF-α and IL-1β however can be more injurious than the inciting event, initiating diffuse coagulation, tissue injury, hypotension, and death. The inflammatory response is balanced by anti-inflammatory molecules like the cytokines IL-10 and IL-4, soluble TNF receptors, IL-1 receptor antagonists, and transforming growth factor (TGF)-β. Neuroendocrine pathways, such as the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic division of the Autonomic Nervous System (SNS) control the inflammation process by triggering anti-inflammatory balancing mechanisms. The brain can monitor immune status and sense peripheral inflammation through two main pathways: neural and humoral. The neural mechanism relies upon activation of vagus nerve afferent sensory fibers that signal the brain that inflammation is occurring. Stressful stimuli activate vagal afferents either directly by cytokines released from dendritic cells, macrophages, and other vagal-associated immune cells, or indirectly through the chemoreceptive cells located in vagal paraganglia. The transmission of cytokine signals to the brain through the vagal sensory neurons depends upon the magnitude of the stressful challenge. Subdiaphragmatic vagotomy inhibits the stimulation of the HPA axis and noradrenaline (NA) release in hypothalamic nuclei in response to intraperitoneal administration of endotoxin or IL-1β. Intravenous endotoxin administration induces expression of the neural activation marker c-Fos in the brainstem medulla, regardless of the integrity of the vagus nerve. Vagotomy fails to suppress high dose endotoxininduced. IL-1β immunoreactivity in the brain and increases blood corticosterone levels. It is likely that the vagal afferent neural pathway plays a dominant role in mild to moderate peripheral inflammatory responses, whereas acute, robust inflammatory responses signal the brain primarily via humoral mechanisms. By other hand, humoral pathway are supported by a large body of evidence, especially in cases of systemic immune challenge; circulatory cytokines like IL-1 β and TNF-α can cross the blood-brain barrier and enter cerebrospinal fluid and the interstitial fluid spaces of the brain and spinal cord by a saturable carrier mediated mechanism that may function only at very high plasma cytokine concentrations. Cytokines also can bind to receptors at the surface of the endothelium of the brain capillaries and can enhance the synthesis and release of soluble mediators such as prostaglandins and nitric oxide, which diffuse into the brain parenchyma and modulate the activity of specific groups of neurons. It has been suggested that prostaglandins mediate fever and HPA axis activation. Cytokine-to-brain communication also may occur via circumventricular organs that lack normal blood-brain barrier function. Among the circumventricular organs, the AP (area postrema) appears to represent the best candidate for such a transduction site. The AP is located in the floor of the caudal fourth ventricle and dendrites of neurons in the NTS (nucleus tractus solitarius) and DMN (dorsal motor nucleus) penetrate both the AP and floor of the fourth ventricle. The close proximity of AP to NTS and RVM (rostral ventrolateral medulla) and the existing neural connections provide a way of signaling the SNS and HPA axis. Cytokine-induced production of prostaglandins within the AP, NTS, and RVM may activate the catecholamine projections to the PVN, resulting in subsequent HPA axis activation. This is one possible interaction between the neural and humoral mechanisms of immune to brain communication through which the brain mediates anti-inflammatory responses. Apart from their function in signaling the brain for immunomodulatory responses, cytokines play a multifunctional role in brain injury and neurodegenerative diseases. Restoration of homeostasis as a logical resolution of inflammation does not always occur. For instance, a lack of adequate inflammatory responses may result in increased susceptibility to infections or cancer. On the other hand, excessive responses are associated with autoimmune diseases, diabetes, sepsis, psychiatric diseases with an important inflammatory response like major depression or schizophrenia and other debilitating conditions. When control of local inflammatory responses is lost, pro-inflammatory mediators can spill into the circulation, resulting in systemic inflammation that may progress to shock, multiple organ failure, and death. A recent discovery, showed that a novel neuroimmunomodulatory pathway that interface the brain and the immune system, referred as to the autonomic cholinergic anti-inflammatory pathway, mediate inhibitory responses during inflammation possibly by recruiting central mechanisms that modulate systemic or peripheral inflammatory responses. Still unclear, this neural circuit has been implicated in promoting sort of psychotherapeutical activities such as hypnosis, meditation, prayer, biofeedback, including acupuncture, but this mechanims still remain elusive. The sympathetic and parasympathetic parts of the Autonomic Nervous System rarely operate alone; autonomic responses represent the interplay of both parts. A link between the parasympathetic part of the Autonomic Nervous System and immunoregulatory processes was suggested, when alleviation of T-lymphocyte cytotoxicity by muscarinic cholinergic stimulation was described. Communication between the immune, nervous, and endocrine systems is essential for host defense and involves a variety of mediators including cytokines, neurotransmitters, hormones, and humoral factors. The influence of the brain on immune function and the mechanisms involved in these interactions have been elucidated over the past 3 decades, however, two important questions arise when describing the brain-derived immunomodulation: How is the specific brain initially signaled by cytokines to trigger corresponding neural and neuroendocrine responses?; and: How is immunomodulation achieved through these mechanisms? This review outlines brain-related control mechanisms of immune function in the regulation of inflammation.