Sperm Flagellar 1 Binds Actin in Intestinal Epithelial Cells and Contributes to Formation of Filopodia and Lamellipodia.

BACKGROUND & AIMS: Sperm flagellar 1 (also called CLAMP) is a microtubule-associated protein that regulates microtubule dynamics and planar cell polarity in multi-ciliated cells. We investigated the localization and function of sperm flagellar 1, or CLAMP, in human intestinal epithelia cells (IECs). METHODS: We performed studies with SKCO-15 and human intestinal enteroids established from biopsies from different intestinal segments (duodenal, jejunum, ileal, and colon) of a single donor. Enteroids were induced to differentiation after incubation with growth factors. The distribution of endogenous CLAMP in IECs was analyzed by immunofluorescence microscopy using total internal reflection fluorescence-ground state depletion and confocal microscopy. CLAMP localization was followed during the course of intestinal epithelial cell polarization as cells progressed from flat to compact, confluent monolayers. Protein interactions with endogenous CLAMP were determined in SKCO-15 cells using proximity ligation assays and co-immunoprecipitation. CLAMP was knocked down in SKCO-15 monolayers using small hairpin RNAs and cells were analyzed by immunoblot and immunofluorescence microscopy. The impact of CLAMP knock-down in migrating SKCO-15 cells was assessed using scratch-wound assays. RESULTS: CLAMP bound to actin and apical junctional complex proteins but not microtubules in IECs. In silico analysis predicted the calponin-homology domain of CLAMP to contain conserved amino acids required for actin binding. During IEC polarization, CLAMP distribution changed from primarily basal stress fibers and cytoplasm in undifferentiated cells to apical membranes and microvilli in differentiated monolayers. CLAMP accumulated in lamellipodia and filopodia at the leading edge of migrating cells in association with actin. CLAMP knock-down reduced the number of filopodia, perturbed filopodia polarity, and altered the organization of actin filaments within lamellipodia. CONCLUSIONS: CLAMP is an actin-binding protein, rather than a microtubule-binding protein, in IECs. CLAMP distribution changes during intestinal epithelial cell polarization, regulates the formation of filopodia, and appears to assist in the organization of actin bundles within lamellipodia of migrating IECs. Studies are needed to define the CLAMP domains that interact with actin and whether its loss from IECs affects intestinal function.

Enteropathogenic Escherichia coli (EPEC) Recruitment of PAR Polarity Protein Atypical PKCζ to Pedestals and Cell-Cell Contacts Precedes Disruption of Tight Junctions in Intestinal Epithelial Cells.

Enteropathogenic Escherichia coli (EPEC) uses a type three secretion system to inject effector proteins into host intestinal epithelial cells, causing diarrhea. EPEC induces the formation of pedestals underlying attached bacteria, disrupts tight junction (TJ) structure and function, and alters apico-basal polarity by redistributing the polarity proteins Crb3 and Pals1, although the mechanisms are unknown. Here we investigate the temporal relationship of PAR polarity complex and TJ disruption following EPEC infection. EPEC recruits active aPKCζ, a PAR polarity protein, to actin within pedestals and at the plasma membrane prior to disrupting TJ. The EPEC effector EspF binds the endocytic protein sorting nexin 9 (SNX9). This interaction impacts actin pedestal organization, recruitment of active aPKCζ to actin at cell-cell borders, endocytosis of JAM-A S285 and occludin, and TJ barrier function. Collectively, data presented herein support the hypothesis that EPEC-induced perturbation of TJ is a downstream effect of disruption of the PAR complex and that EspF binding to SNX9 contributes to this phenotype. aPKCζ phosphorylates polarity and TJ proteins and participates in actin dynamics. Therefore, the early recruitment of aPKCζ to EPEC pedestals and increased interaction with actin at the membrane may destabilize polarity complexes ultimately resulting in perturbation of TJ.

EPEC NleH1 is significantly more effective in reversing colitis and reducing mortality than NleH2 via differential effects on host signaling pathways.

Enteropathogenic Escherichia coli (EPEC) is a foodborne pathogen that uses a type III secretion system to translocate effector molecules into host intestinal epithelial cells (IECs) subverting several host cell processes and signaling cascades. Interestingly, EPEC infection induces only modest intestinal inflammation in the host. The homologous EPEC effector proteins, NleH1 and NleH2, suppress the nuclear factor-κB (NF-κB) pathway and apoptosis in vitro. Increased apoptosis and activation of NF-κB and MAP kinases (MAPK) contribute to the pathogenesis of inflammatory bowel diseases (IBD). The aim of this study was to determine if NleH1 and NleH2 also block MAPK pathways in vitro and in vivo, and to compare the effects of these bacterial proteins on a murine model of colitis. Cultured IECs were infected with various strains of EPEC expressing NleH1 and NleH2, or not, and the activation of ERK1/2 and p38 was determined. In addition, the impact of infection with various strains of EPEC on murine DSS colitis was assessed by change in body weight, colon length, histology, and survival. Activation of apoptosis and MAPK signaling were also evaluated. Our data show that NleH1, but not NleH2, suppresses ERK1/2 and p38 activation in vitro. Interestingly, NleH1 affords significantly greater protection against and hastens recovery from dextran sodium sulfate (DSS)-induced colitis compared to NleH2. Strikingly, colitis-associated mortality was abolished by infection with EPEC strains expressing NleH1. Interestingly, in vivo NleH1 suppresses activation of ERK1/2 and p38 and blocks apoptosis independent of the kinase domain that inhibits NF-κB. In contrast, NleH2 suppresses only caspase-3 and p38, but not ERK1/2. We conclude that NleH1 affords greater protection against and improves recovery from DSS colitis compared to NleH2 due to its ability to suppress ERK1/2 in addition to NF-κB, p38, and apoptosis. These findings warrant further investigation of anti-inflammatory bacterial proteins as novel treatments for IBD.

EPEC effector EspF promotes Crumbs3 endocytosis and disrupts epithelial cell polarity.

Enteropathogenic Escherichia coli (EPEC) uses a type III secretion system to inject effector proteins into host intestinal epithelial cells causing diarrhoea. EPEC infection redistributes basolateral proteins ß1-integrin and Na+ /K+ ATPase to the apical membrane of host cells. The Crumbs (Crb) polarity complex (Crb3/Pals1/Patj) is essential for epithelial cell polarisation and tight junction (TJ) assembly. Here, we demonstrate that EPEC displaces Crb3 and Pals1 from the apical membrane to the cytoplasm of cultured intestinal epithelial cells and colonocytes of infected mice. In vitro studies show that EspF, but not Map, alters Crb3, whereas both effectors modulate Pals1. EspF perturbs polarity formation in cyst morphogenesis assays and induces endocytosis and apical redistribution of Na+ /K+ ATPase. EspF binds to sorting nexin 9 (SNX9) causing membrane remodelling in host cells. Infection with ΔespF/pespFD3, a mutant strain that ablates EspF binding to SNX9, or inhibition of dynamin, attenuates Crb3 endocytosis caused by EPEC. In addition, infection with ΔespF/pespFD3 has no impact on Na+ /K+ ATPase endocytosis. These data support the hypothesis that EPEC perturbs apical-basal polarity in an EspF-dependent manner, which would contribute to EPEC-associated diarrhoea by disruption of TJ and altering the crucial positioning of membrane transporters involved in the absorption of ions and solutes.

ZO proteins redundantly regulate the transcription factor DbpA/ZONAB.

The localization and activities of DbpA/ZONAB and YAP transcription factors are in part regulated by the density-dependent assembly of epithelial junctions. DbpA activity and cell proliferation are inhibited by exogenous overexpression of the tight junction (TJ) protein ZO-1, leading to a model whereby ZO-1 acts by sequestering DbpA at the TJ. However, mammary epithelial cells and mouse tissues knock-out for ZO-1 do not show increased proliferation, as predicted by this model. To address this discrepancy, we examined the localization and activity of DbpA and YAP in Madin-Darby canine kidney cells depleted either of ZO-1, or one of the related proteins ZO-2 and ZO-3 (ZO proteins), or all three together. Depletion of only one ZO protein had no effect on DbpA localization and activity, whereas depletion of ZO-1 and ZO-2, which is associated with reduced ZO-3 expression, resulted in increased DbpA localization in the cytoplasm. Only depletion of ZO-2 reduced the nuclear import of YAP. Mammary epithelial (Eph4) cells KO for ZO-1 showed junctional DbpA, demonstrating that ZO-1 is not required to sequester DbpA at junctions. However, further depletion of ZO-2 in Eph4 ZO-1KO cells, which do not express ZO-3, caused decreased junctional localization and expression of DbpA, which were rescued by the proteasome inhibitor MG132. In vitro binding assays showed that full-length ZO-1 does not interact with DbpA. These results show that ZO-2 is implicated in regulating the nuclear shuttling of YAP, whereas ZO proteins redundantly control the junctional retention and stability of DbpA, without affecting its shuttling to the nucleus.

Climate-related health impact indicators for public health surveillance in a changing climate: a systematic review and local suitability analysis.

Climate change challenges public health. Effective management of climate-related health risks relies on robust public health surveillance (PHS) and population health indicators. Despite existing global and country-specific indicators, their integration into local PHS systems is limited, impacting decision-making. We conducted a systematic review examining population health indicators relevant to climate change impacts and their suitability for national PHS systems. Guided by a registered protocol, we searched multiple databases and included 41 articles. Of these, 35 reported morbidity indicators, and 39 reported mortality indicators. Using Chile as a case study, we identified three sets of indicators for the Chilean PHS. The high-priority set included vector-, food-, and water-borne diseases, as well as temperature-related health outcomes indicators due to their easy integration into existing PHS systems. This review highlights the importance of population health indicators in monitoring climate-related health impacts, emphasising the need for local contextual factors to guide indicator selection. Funding: This research project was partly funded by ANID Chile and University College London. None of these sources had any involvement in the research conceptualisation, design, or interpretation of the results.

Spef1/CLAMP binds microtubules and actin-based structures and regulates cell migration and epithelia cell polarity.

During migration, cells invade, repair, and create barriers leading to the formation of new cellular contacts in target tissues. Cell migration requires many proteins that collectively form the cytoskeleton. The main cytoskeletal elements are actin filaments, microtubules (MTs), and intermediate filaments. These structures work in concert with a large number of accessory proteins that contribute in a variety of ways to regulate filament assembly and turnover, to alter the configuration or arrangement of filaments by bundling or crosslinking, to link the cytoskeleton to other structures in the cell, such as membranes and junctions, and to transport cargo along the filaments. Sperm flagella protein-1 (Spef1), also designated calponin homology and microtubules-associated protein (CLAMP), is a multifunctional protein that interacts with cytoskeletal structures, including MTs, actin filaments, and focal adhesions in epithelia. In this review, we outline Spef1/CLAMP structure and expression in several cellular models. The function of Spef1/CLAMP in flagellar and ciliary motility, MT-binding and stability, regulation of planar cell polarity, and potential contribution to the maintenance of actin-based structures, such as lamellipodia and filopodia during cell migration, are also discussed.

Validity and Reliability of the Richmond Agitation-Sedation Scale in Pediatric Intensive Care Patients: A Multicenter Study.

Background: There is limited data about the psychometric properties of the Richmond Agitation-Sedation Scale (RASS) in children. This study aims to analyze the validity and reliability of the RASS in assessing sedation and agitation in critically ill children. Methods: A multicenter prospective study in children admitted to pediatric intensive care, aged between 1 month and 18 years. Twenty-eight observers from 14 PICUs (pediatric intensive care units) participated. Every observation was assessed by 4 observers: 2 nurses and 2 pediatric intensivists. We analyzed RASS inter-rater reliability, construct validity by comparing RASS to the COMFORT behavior (COMFORT-B) scale and the numeric rating scale (NRS), and by its ability to distinguish between levels of sedation, and responsiveness to changes in sedative dose levels. Results: 139 episodes in 55 patients were analyzed, with a median age 3.6 years (interquartile range 0.7-7.8). Inter-rater reliability was excellent, weighted kappa (κw) 0.946 (95% CI, 0.93-0.96; p < 0.001). RASS correlation with COMFORT-B scale, rho = 0.935 (p < 0.001) and NRS, rho = 0.958 (p < 0.001) was excellent. The RASS scores were significantly different (p < 0.001) for the 3 sedation categories (over-sedation, optimum and under-sedation) of the COMFORT-B scale, with a good agreement between both scales, κw 0.827 (95% CI, 0.789-0.865; p < 0.001), κ 0.762 (95% CI, 0.713-0.811, p < 0.001). A significant change in RASS scores (p < 0.001) was recorded with the variance of sedative doses. Conclusions: The RASS showed good measurement properties in PICU, in terms of inter-rater reliability, construct validity, and responsiveness. These properties, including its ability to categorize the patients into deep sedation, moderate-light sedation, and agitation, makes the RASS a useful instrument for monitoring sedation in PICU.

Experience in a rehabilitation center for mastectomized women at the start of the COVID-19 pandemic.

OBJECTIVE: Describe the experience lived in an interdisciplinary follow-up care center for mastectomized women at a public university in São Paulo during the beginning of the COVID-19 pandemic. METHOD: Experience report on the health care provided in the health center for mastectomized women. RESULTS: The care was provided three times a week by an interdisciplinary health team. The mentioned areas that cover the women care in the center: Physical, Psychological, Social Support and Health Education. CONCLUSIONS: The attention by an interdisciplinary team becomes prevalent in the care of mastectomized women, since cancer and its treatment produce various changes in women's lives in the short and long term, so follow-up and support must be biopsychosocial, covering all areas that may be affected, especially during the pandemic.

Cyclin D1 is transcriptionally down-regulated by ZO-2 via an E box and the transcription factor c-Myc.

Recent reports have indicated the participation of tight junction (TJ) proteins in the regulation of gene expression and cell proliferation. Here, we have studied the role of zona occludens (ZO)-2, a TJ peripheral protein, in the regulation of cyclin D1 transcription. We found that ZO-2 down-regulates cyclin D1 transcription in a dose-dependent manner. To understand how ZO-2 represses cyclin D1 promoter activity, we used deletion analyses and found that ZO-2 negatively regulates cyclin D1 transcription via an E box and that it diminishes cell proliferation. Because ZO-2 does not associate directly with DNA, electrophoretic mobility shift assay and chromatin immunoprecipitation (ChIP) assay were used to identify the transcription factors mediating the ZO-2-repressive effect. c-Myc was found to bind the E box present in the cyclin D1 promoter, and the overexpression of c-Myc augmented the inhibition generated by ZO-2 transfection. The presence of ZO-2 and c-Myc in the same complex was further demonstrated by immunoprecipitation. ChIP and reporter gene assays using histone deacetylases (HDACs) inhibitors demonstrated that HDACs are necessary for ZO-2 repression and that HDAC1 is recruited to the E box. We conclude that ZO-2 down-regulates cyclin D1 transcription by interacting with the c-Myc/E box element and by recruiting HDAC1.

Crosstalk of tight junction components with signaling pathways.

Tight junctions (TJs) regulate the passage of ions and molecules through the paracellular pathway in epithelial and endothelial cells. TJs are highly dynamic structures whose degree of sealing varies according to external stimuli, physiological and pathological conditions. In this review we analyze how the crosstalk of protein kinase C, protein kinase A, myosin light chain kinase, mitogen-activated protein kinases, phosphoinositide 3-kinase and Rho signaling pathways is involved in TJ regulation triggered by diverse stimuli. We also report how the phosphorylation of the main TJ components, claudins, occludin and ZO proteins, impacts epithelial and endothelial cell function.

p53 response to arsenic exposure in epithelial cells: protein kinase B/Akt involvement.

Inorganic arsenic is a major environmental contaminant associated with an increased risk of human skin cancer. Arsenic modulates cellular signaling pathways that affect diverse processes such as cell proliferation, differentiation, and apoptosis, including genotoxic damage. The p53 protein plays a central role in mediating stress and DNA damage responses, leading to either growth arrest or apoptosis. Several signal transduction pathways activated under a plethora of stressing conditions increase p53 protein levels. To further understand the molecular mechanisms involved in the arsenic mode of action, we explored the effects of this metalloid on the activation of the phosphatidyl inositol 3-kinase (PI3K)/Ca2+/diacylglicerol dependent protein kinase/protein kinase B (PKB) signaling cascade and its repercussion in p53 activation in two epithelial cell types: primary normal human keratinocytes cultures (NHK) and the carcinoma-derived C33-A cell line. Although in both cell systems arsenic leads to an increase in p53 and its binding to DNA, the final outcome is different. In NHK, arsenic triggers a sustained activation of the PI3K/PKB/glycogen synthase kinase-3 beta pathway, driving the cell into a cell-differentiated stage in which the proliferation signals are turned down. In sharp contrast, in C33-A cells, arsenic leads to a transient increase in p53 followed by a drastic reduction in its nuclear levels and an increase in cell proliferation. These findings favor the notion that p53-stage and transcriptional abilities are important to understand modifications in the proliferation-differentiation balance, an equilibrium that is severely impaired by arsenic.

Modulation of epithelial cell polarity by bacterial pathogens.

Epithelial cells constitute a physical barrier that aids in protecting the host from microbial pathogens. Polarized epithelial cells contain distinct apical and basolateral membrane domains separated by intercellular junctions, including tight junctions (TJs), which contribute to the maintenance of apical-basal polarity. Polarity complexes also contribute to the establishment of TJ formation. Several pathogens perturb epithelial TJ barrier function and structure in addition to causing a loss of apical-basal polarity. Here, we review the impact of pathogenic bacteria on the disruption of cell-cell junctions and epithelial polarity.

Heparin (GAG-hed) inhibits LCR activity of human papillomavirus type 18 by decreasing AP1 binding.

BACKGROUND: High risk HPVs are causative agents of anogenital cancers. Viral E6 and E7 genes are continuously expressed and are largely responsible for the oncogenic activity of these viruses. Transcription of the E6 and E7 genes is controlled by the viral Long Control Region (LCR), plus several cellular transcription factors including AP1 and the viral protein E2. Within the LCR, the binding and activity of the transcription factor AP1 represents a key regulatory event in maintaining E6/E7 gene expression and uncontrolled cell proliferation. Glycosaminoglycans (GAGs), such as heparin, can inhibit tumour growth; they have also shown antiviral effects and inhibition of AP1 transcriptional activity. The purpose of this study was to test the heparinoid GAG-hed, as a possible antiviral and antitumoral agent in an HPV18 positive HeLa cell line. METHODS: Using in vivo and in vitro approaches we tested GAG-hed effects on HeLa tumour cell growth, cell proliferation and on the expression of HPV18 E6/E7 oncogenes. GAG-hed effects on AP1 binding to HPV18-LCR-DNA were tested by EMSA. RESULTS: We were able to record the antitumoral effect of GAG-hed in vivo by using as a model tumours induced by injection of HeLa cells into athymic female mice. The antiviral effect of GAG-hed resulted in the inhibition of LCR activity and, consequently, the inhibition of E6 and E7 transcription. A specific diminishing of cell proliferation rates was observed in HeLa but not in HPV-free colorectal adenocarcinoma cells. Treated HeLa cells did not undergo apoptosis but the percentage of cells in G2/M phase of the cell cycle was increased. We also detected that GAG-hed prevents the binding of the transcription factor AP1 to the LCR. CONCLUSION: Direct interaction of GAG-hed with the components of the AP1 complex and subsequent interference with its ability to correctly bind specific sites within the viral LCR may contribute to the inhibition of E6/E7 transcription and cell proliferation. Our data suggest that GAG-hed could have antitumoral and antiviral activity mainly by inhibiting AP1 binding to the HPV18-LCR.

Experience in a rehabilitation center for mastectomized women at the start of the COVID-19 pandemic / Experiência em centro de reabilitação de mulheres mastectomizadas no início da pandemia do COVID-19 / Experiencia en centro de rehabilitación de mujeres mastectomizadas al inicio de la pandemia por COVID-19

ABSTRACT Objective Describe the experience lived in an interdisciplinary follow-up care center for mastectomized women at a public university in São Paulo during the beginning of the COVID-19 pandemic Method Experience report on the health care provided in the health center for mastectomized women. Results The care was provided three times a week by an interdisciplinary health team. The mentioned areas that cover the women care in the center: Physical, Psychological, Social Support and Health Education. Conclusions The attention by an interdisciplinary team becomes prevalent in the care of mastectomized women, since cancer and its treatment produce various changes in women's lives in the short and long term, so follow-up and support must be biopsychosocial, covering all areas that may be affected, especially during the pandemic.

RESUMO Objetivo Descrever a experiência vivida em um centro de acompanhamento interdisciplinar de mulheres mastectomizadas de uma universidade pública de São Paulo durante o início da pandemia COVID-19. Método Relato de experiência sobre cuidados de saúde prestados no centro de saúde para mulheres mastectomizadas. Resultados Os atendimentos foram realizados três vezes por semana por uma equipe interdisciplinar de saúde. São mencionadas as áreas que abrangem o atendimento à mulher no centro: Acompanhamento físico, psicológico, social e Educação em saúde. Conclusão A atenção por uma equipe interdisciplinar torna-se predominante no cuidado de mulheres mastectomizadas, pois o câncer e seu tratamento produzem diversas mudanças na vida das mulheres, a curto e longo prazo. Portanto o acompanhamento deve ser biopsicossocial, cobrindo todas as áreas que podem ser afetadas, especialmente durante a pandemia.

RESUMEN Objetivo Describir la experiencia vivida en un centro de atención interdisciplinaria de seguimiento a mujeres mastectomizadas de una universidad pública de Sao Paulo durante el inicio de la pandemia de COVID-19. Método Relato de experiencia sobre las atenciones de salud brindadas en el centro de salud para mujeres mastectomizadas. Resultados Las atenciones fueron realizadas tres veces por semana por un equipo interdisciplinario de salud. Se mencionan las áreas que abarcan la atención de las mujeres en el centro: Acompañamiento físico, Psicológico, Social y la Educación en Salud. Conclusión La atención por un equipo interdisciplinario se torna imperante en el cuidado de mujeres mastectomizadas, ya que el cáncer y su tratamiento producen diversos cambios en la vida de la mujer, a corto y largo plazo, por lo que el seguimiento y acompañamiento debe ser biopsicosocial, abarcando todas las áreas que pueden verse afectadas, especialmente durante la pandemia.

MgcRacGAP interacts with cingulin and paracingulin to regulate Rac1 activation and development of the tight junction barrier during epithelial junction assembly.

The regulation of Rho-family GTPases is crucial to direct the formation of cell-cell junctions and tissue barriers. Cingulin (CGN) and paracingulin (CGNL1) control RhoA activation in epithelial cells by interacting with RhoA guanidine exchange factors. CGNL1 depletion also inhibits Rac1 activation during junction assembly. Here we show that, unexpectedly, Madin-Darby canine kidney epithelial cells depleted of both CGN and CGNL1 (double-KD cells) display normal Rac1 activation and tight junction (TJ) formation, despite decreased junctional recruitment of the Rac1 activator Tiam1. The expression of the Rac1 inhibitor MgcRacGAP is decreased in double-KD cells, and the barrier development and Rac1 activation phenotypes are rescued by exogenous expression of MgcRacGAP. MgcRacGAP colocalizes with CGN and CGNL1 at TJs and forms a complex and interacts directly in vitro with CGN and CGNL1. Depletion of either CGN or CGNL1 in epithelial cells results in decreased junctional localization of MgcRacGAP but not of ECT2, a centralspindlin-interacting Rho GEF. These results provide new insight into coordination of Rho-family GTPase activities at junctions, since apical accumulation of CGN and CGNL1 at TJs during junction maturation provides a mechanism to spatially restrict down-regulation of Rac1 activation through the recruitment of MgcRacGAP.

Burnout y factores predictores en profesionales de Enfermería chilenos a un año de pandemia por COVID-19 / Burnout and predicting factors in Chilean nursing professional after one year of COVID-19 pandemic

Objetivo: analizar la asociación de variables sociodemográficas y laborales, estado de salud, inteligencia emocional, apoyo social percibido y espiritualidad en el desarrollo del burnout en profesionales de Enfermería a un año del comienzo de la pandemia COVID-19 en Chile.Método: se llevó a cabo un estudio descriptivo transversal (julio-octubre 2021). La población de estudio fueron enfermeras, que hubieran trabajado durante la pandemia en cualquier centro de atención sanitaria en Chile, atendiendo a pacientes al menos durante tres meses. Se aplicó un cuestionario online que incluía perfil enfermera, Maslach Burnout Inventory, Cuestionario Nórdico Estandarizado, Trait-Meta Mood Scale-24, Escala Multidimensional de Apoyo Social Percibido e Índice Breve de Religiosidad y Espiritualidad. Se llevó a cabo análisis descriptivo, correlaciones y regresión lineal.Resultados: participaron 192 profesionales, 181 (94,3%) eran mujeres. La edad media (DE) fue de 30,8 (6,81) años. La antigüedad laboral media (DE) fue de 5,6 (5,98) años. El 64,1% de las enfermeras presentó burnout. Se evidenció relación inversa y moderada entre las dimensiones de burnout e inteligencia emocional (directas, para el caso de realización personal). Se observó relación directa y moderada entre la realización personal y el apoyo social de amigos. También hubo relación indirecta y cercana a moderada entre cansancio emocional y espiritualidad. En los modelos predictivos, el dolor físico y la inteligencia emocional se asociaron con burnout.Conclusiones: más de la mitad de los profesionales de Enfermería de la muestra presentó burnout, siendo sus principales predictores el dolor físico y la inteligencia emocional.(AU)

Objective: to analyse the impact of sociodemographic and occupational variables, health status, emotional intelligence, perceived social support and spirituality, upon the development of burnout in Nursing professionals at one year after the start of the COVID-19 pandemic in Chile.Methods: a descriptive cross-sectional study was conducted (July to October 2021). The study population were nurses who had worked during the pandemic at any healthcare centre in Chile, seeing patients during at least three months. An online questionnaire was applied, including the nurse profile, the Maslach Burnout Inventory, the Standardized Nordic questionnaire, the Trait-Meta Mood Scale-24, the Multidimensional Scale of Perceived Social Support, and the Brief Spirituality/Religiousness Index. Descriptive analysis, correlations and linear regression were conducted.Results: the study included 192 professionals, 181 (94,3%) were female. Their mean age (SD) was 30.8 (6.81) years. Their mean seniority (SD) was 5.6 (5.98) years. Of these nurses, 64.1% presented burnout. A reverse and moderate relationship was observed between the burnout and emotional intelligence dimensions (direct in the case of personal fulfilment). A direct and moderate relationship was observed between personal fulfilment and social support by friends. There was also an indirect and close to moderate relationship between emotional exhaustion and spirituality. In the predictive models, physical pain and emotional intelligence were associated with burnout.Conclusions: more than half of Nursing professionals presented burnout, and its main predictors were physical pain and emotional intelligence.(AU)

The control of gene expression and cell proliferation by the epithelial apical junctional complex.

The AJC (apical junctional complex) of vertebrate epithelial cells orchestrates cell-cell adhesion and tissue barrier function. In addition, it plays a pivotal role in signalling. Several protein components of the AJC, e.g. the cytoplasmic proteins ß-catenin, p120-catenin and ZO (Zonula Occludens)-2, can shuttle to the nucleus, where they interact with transcription factors to regulate gene expression and cell proliferation. Other junctional proteins, e.g. angiomotin, α-catenin and cingulin, are believed to act by sequestering either transcription factors, such as YAP (Yes-associated protein), or regulators of small GTPases, such as GEF (guanine-nucleotide-exchange factor)-H1, at junctions. The signalling activities of AJC proteins are triggered by different extracellular and intracellular cues, including cell density, and physiological or pathological activation of developmentally regulated pathways, such as the Wnt pathway. The interplay between junctional protein complexes, the actin cytoskeleton and signalling pathways is of crucial importance in the regulation of gene expression and cell proliferation.

[Some ethical dilemmas in the medical praxis]. / Algunos dilemas éticos en la práctica médica.

We reviewed from a bioethical perspective and attempting prevention of potential conflicts derived communication failure during medical practice, palliative treatments and dignified death in the institutional practice as well as general practice; most of conflicts related to patient-doctor relationship could de prevented. We propose an attitude and aptitude plus in deep knowledge of patient, family, friends and legal representatives in terms fully honest communication to prevent most of conflicts and avoid its consequences against doctors and other health workers. Prevention is better and it depends of knowledge of norms, laws, general beliefs and common sense in this country and maybe others.