RESUMO
La voz es un elemento particular de los primeros años de vida en el sujeto debido a que es una de las formas de manifestar su necesidad, un deseo, u otro, por lo cual se adopta como una herramienta que se vincula a los procesos anímicos; puede ser una forma de ver síntomas o malestares que el paciente no quiere ni confesarse, ni confesar en una consulta. Objetivo: Comprender la manifestación del malestar a través de la voz del sujeto y la forma subjetiva del saber hacer con el conflicto, que apertura la importancia de la voz en el proceso psicoterapéutico. Materiales y métodos: Se enmarcó en un paradigma fenomenológico, es una investigación de campo con enfoque cualitativo mediante un estudio de caso. Resultados: A partir de este estudio se pudo determinar que el malestar incide en la voz del sujeto cuando no puede ser expresado con anterioridad, por tanto, la voz es una forma de expresión inconsciente que en ocasiones no es percibida por el sujeto que manifiesta un malestar. Conclusiones: El fenómeno de la voz está presente en los sujetos que formaron parte de esta investigación, pero cada uno de ellos lo formula de manera distinta, haciendo del malestar un saber hacer individual; por medio de la voz se manifiestan los silencios, el grito, el llanto y variadas formas orales que indican que hay asuntos pendientes, reflejando el conflicto que tiene el individuo con lo que está refiriendo, así deja huellas fonéticas en todo lo que nos relata(AU)
The voice is a particular element of the first years of life in the subject due to which is one of the ways to express their need, a desire, or another, for which it is adopted as a tool that is linked to psychic processes; it may be a way of seeing symptoms or discomforts that the patient does not want to confess or confess in a consultation. Objective:Understand the manifestation of discomfort through the voice of the subject and the subjective form of knowing how to deal with conflict, which opens up the importance of the voice in the psychotherapeutic process. Materials and methods:It was framed in a phenomenological paradigm, it is an investigation of field with a qualitative approach through a case study. Results:From this study it was possible to determine that discomfort affects the voice of the subject when it cannot be expressed with previously, therefore, the voice is a form of unconscious expression that sometimes is not perceived by the subject who manifests discomfort. Conclusions:The phenomenon of the voice is present in the subjects who were part of this investigation, but each one of them formulates it in a different way, making discomfort an individual know-how; through the voice silences, screaming, crying and various oral forms that indicate thatthere are issues pending, reflecting the conflict that the individual has with what he is referring to, thus leaving traces phonetics in everything he tells us(AU)
Assuntos
Regressão Psicológica , Comportamento e Mecanismos Comportamentais , Consultórios Médicos , Afeto , Ajustamento Emocional , Psicologia Clínica , Sinais e Sintomas , Voz , FonéticaRESUMO
Hypothyroxinemia (Hpx) is a thyroid hormone deficiency (THD) condition highly frequent during pregnancy, which although asymptomatic for the mother, it can impair the cognitive function of the offspring. Previous studies have shown that maternal hypothyroidism increases the severity of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model for multiple sclerosis (MS). Here, we analyzed the immune response after EAE induction in the adult offspring gestated in Hpx. Mice gestated in Hpx showed an early appearance of EAE symptoms and the increase of all parameters of the disease such as: the pathological score, spinal cord demyelination, and immune cell infiltration in comparison to the adult offspring gestated in euthyroidism. Isolated CD4+CD25+ T cells from spleen of the offspring gestated in Hpx that suffer EAE showed reduced capacity to suppress proliferation of effector T cells (TEff) after being stimulated with anti-CD3 and anti-CD28 antibodies. Moreover, adoptive transfer experiments of CD4+CD25+ T cells from the offspring gestated in Hpx suffering EAE to mice that were induced with EAE showed that the receptor mice suffer more intense EAE pathological score. Even though, no significant differences were detected in the frequency of Treg cells and IL-10 content in the blood, spleen, and brain between mice gestated in Hpx or euthyroidism, T cells CD4+CD25+ from spleen have reduced capacity to differentiate in vitro to Treg and to produce IL-10. Thus, our data support the notion that maternal Hpx can imprint the immune response of the offspring suffering EAE probably due to a reduced capacity to trigger suppression. Such "imprints" on the immune system could contribute to explaining as to why adult offspring gestated in Hpx suffer earlier and more intense EAE.
Assuntos
Encefalomielite Autoimune Experimental/etiologia , Encefalomielite Autoimune Experimental/metabolismo , Hipotireoidismo/complicações , Exposição Materna/efeitos adversos , Complicações na Gravidez , Efeitos Tardios da Exposição Pré-Natal , Transferência Adotiva , Animais , Biomarcadores , Diferenciação Celular , Citocinas/metabolismo , Encefalomielite Autoimune Experimental/patologia , Encefalomielite Autoimune Experimental/terapia , Feminino , Hipotireoidismo/sangue , Hipotireoidismo/etiologia , Imunofenotipagem , Ativação Linfocitária , Contagem de Linfócitos , Metimazol/administração & dosagem , Metimazol/efeitos adversos , Camundongos , Proteína Básica da Mielina/metabolismo , Fenótipo , Gravidez , Subpopulações de Linfócitos T/imunologia , Subpopulações de Linfócitos T/metabolismo , Tireotropina/sangue , Tiroxina/sangueRESUMO
Hypothyroxinemia (Hpx) is a highly frequent condition characterized by low thyroxine (T4) and normal 3,3',5'-triiodothyronine (T3) and thyroid stimulating hormone (TSH) levels in the blood. Gestational Hpx is closely related to cognitive impairment in the human offspring. In animal models gestational Hpx causes impairment at glutamatergic synapsis, spatial learning, and the susceptibility to suffer strong autoimmune diseases like experimental autoimmune encephalomyelitis (EAE). However, the mechanisms underlying these phenotypes are unknown. On the other hand, it has been shown that astrocytes and microglia affect the outcome of EAE. In fact, the activation of astrocytes and microglia in the central nervous system (CNS) contributes to EAE progression. Thus, in this work, the reactivity of astrocytes and microglia from rats gestated in Hpx was evaluated aiming to understand whether these cells are targets of gestational Hpx. Interestingly, microglia derived from the offspring gestated in Hpx were less reactive compared to microglia derived from offspring gestated in euthyroidism. Instead, astrocytes derived from the offspring gestated in Hpx were significantly more reactive than the astrocytes from the offspring gestated in euthyroidism. This work contributes with novel information regarding the effects of gestational Hpx over astrocytes and microglia in the offspring. It suggests that astrocyte could react strongly to an inflammatory insult inducing neuronal death in the CNS.
Assuntos
Astrócitos/patologia , Inflamação/sangue , Inflamação/patologia , Microglia/patologia , Tiroxina/sangue , Animais , Apoptose/efeitos dos fármacos , Astrócitos/efeitos dos fármacos , Astrócitos/metabolismo , Células Cultivadas , Quimiocina CXCL2/metabolismo , Feminino , Proteína Glial Fibrilar Ácida/metabolismo , Interleucina-1beta/metabolismo , Masculino , Microglia/efeitos dos fármacos , Microglia/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Gravidez , Ratos Sprague-Dawley , Inibidor Tecidual de Metaloproteinase-1/metabolismo , Fator de Necrose Tumoral alfa/farmacologiaRESUMO
BACKGROUND: Maternal thyroid hormones play a fundamental role in appropriate fetal development during gestation. Offspring that have been gestated under maternal hypothyroidism suffer cognitive impairment. Thyroid hormone deficiency during gestation can significantly impact the central nervous system by altering the migration, differentiation, and function of neurons, oligodendrocytes, and astrocytes. Given that gestational hypothyroidism alters the immune cell ratio in offspring, it is possible that this condition could result in higher sensitivity for the development of autoimmune diseases. METHODS: Adult mice gestated under hypothyroidism were induced with experimental autoimmune encephalomyelitis (EAE). Twenty-one days after EAE induction, the disease score, myelin content, immune cell infiltration, and oligodendrocyte death were evaluated. RESULTS: We observed that mice gestated under hypothyroidism showed higher EAE scores after disease induction during adulthood compared to mice gestated in euthyroidism. In addition, spinal cord sections of mice gestated under hypothyroidism that suffered EAE in adulthood showed higher demyelination, CD4(+) and CD8(+) infiltration, and increased oligodendrocyte death. CONCLUSIONS: These results show for the first time that a deficiency in maternal thyroid hormones during gestation can influence the outcome of a central nervous system inflammatory disease, such as EAE, in their offspring. These data strongly support evaluating thyroid hormones in pregnant women and treating hypothyroidism during pregnancy to prevent increased susceptibility to inflammatory diseases in the central nervous system of offspring.