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1.
Psychopathology ; 57(3): 169-181, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-38467115

RESUMEN

INTRODUCTION: The COVID-19 pandemic had significant repercussions for the everyday life and public health of society. Healthcare professionals were particularly vulnerable. Here, we interviewed medical residents about their lived experiences during the pandemic to offer a phenomenological analysis. To this end, we discuss their pandemic experiences considering Jaspers' "limit situation" concept - that is, a radical shift from their everyday experiences, to one causing them to question the basis of their very existence. METHODS: We interviewed 33 medical residents from psychiatry and other specialties from the Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP) who either (a) worked directly with COVID-19 patients or (b) provided psychiatric care to other healthcare professionals. Semi-structured interviews were developed using the Inductive Process to Analyze the Structure of lived Experience (IPSE). RESULTS: The descriptions of the lived experiences of medical residents during the pandemic were organized into four content themes: (a) existential defense, (b) limit situations during the COVID-19 pandemic, (c) changes in lived experience, and (d) new world meanings through lived experience. CONCLUSION: During the COVID-19 pandemic, medical residents experienced what can be thought of as a "limit situation," as they encountered the healthcare delivery challenges coupled with the social isolation imposed by the COVID-19 pandemic. These challenges included fear of infection and potential death, uncertainty about the future, and the emotional overload caused by the sharp increase in patient deaths. That said, after facing such a limit situation, residents reported feeling strengthened by this experience. This is consistent with the notion that when confronted with limit situations, we draw on our resources to overcome adversity and, in turn, reap existential gains. Health care providers might use these experiences to energize their own professional approach.


Asunto(s)
COVID-19 , Internado y Residencia , Médicos , Brasil , COVID-19/psicología , Acontecimientos que Cambian la Vida , Médicos/psicología , Psiquiatría , Entrevistas como Asunto , Existencialismo/psicología , Mecanismos de Defensa , Ansiedad/psicología , Humanos , Masculino , Femenino
2.
Am J Pathol ; 187(5): 1134-1146, 2017 May.
Artículo en Inglés | MEDLINE | ID: mdl-28322201

RESUMEN

Chronic Chagas disease cardiomyopathy, caused by Trypanosoma cruzi infection, is a major cause of heart failure in Latin America. Galectin-3 (Gal-3) has been linked to cardiac remodeling and poor prognosis in heart failure of different etiologies. Herein, we investigated the involvement of Gal-3 in the disease pathogenesis and its role as a target for disease intervention. Gal-3 expression in mouse hearts was evaluated during T. cruzi infection by confocal microscopy and flow cytometry analysis, showing a high expression in macrophages, T cells, and fibroblasts. In vitro studies using Gal-3 knockdown in cardiac fibroblasts demonstrated that Gal-3 regulates cell survival, proliferation, and type I collagen synthesis. In vivo blockade of Gal-3 with N-acetyl-d-lactosamine in T. cruzi-infected mice led to a significant reduction of cardiac fibrosis and inflammation in the heart. Moreover, a modulation in the expression of proinflammatory genes in the heart was observed. Finally, histological analysis in human heart samples obtained from subjects with Chagas disease who underwent heart transplantation showed the expression of Gal-3 in areas of inflammation, similar to the mouse model. Our results indicate that Gal-3 plays a role in the pathogenesis of experimental chronic Chagas disease, favoring inflammation and fibrogenesis. Moreover, by demonstrating Gal-3 expression in human hearts, our finding reinforces that this protein could be a novel target for drug development for Chagas cardiomyopathy.


Asunto(s)
Cardiomiopatía Chagásica/metabolismo , Galectina 3/metabolismo , Miocarditis/metabolismo , Miocardio/patología , Acetilgalactosamina/farmacología , Animales , Proliferación Celular/fisiología , Supervivencia Celular/fisiología , Enfermedad Crónica , Colágeno Tipo I/biosíntesis , Fibrosis/etiología , Fibrosis/metabolismo , Galectina 3/antagonistas & inhibidores , Trasplante de Corazón , Humanos , Macrófagos/metabolismo , Ratones , Ratones Endogámicos C57BL , Miocarditis/etiología , Miocardio/metabolismo , Miofibroblastos/metabolismo , Linfocitos T/metabolismo
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