Navegando por Palavras-chave "Sex Hormones"

Agora exibindo 1 - 2 de 2
  • Imagem de Miniatura
    Item
    Acesso aberto (Open Access)
    Ação da terapia hormonal na Esclerose Lateral Amiotrófica: revisão sistemática
    (Universidade Federal de São Paulo (UNIFESP), 2019-12-18) Vasconcelos, Katia De [UNIFESP]; Simoes, Manuel De Jesus [UNIFESP]; Oliveira, Acary Souza Bulle [UNIFESP]; Fuchs, Luiz Fernando Portugal [UNIFESP]; Girão, Manoel João Batista Castello [UNIFESP]; http://lattes.cnpq.br/3911841387107665; http://lattes.cnpq.br/0822381310382371; http://lattes.cnpq.br/0973903299568770; http://lattes.cnpq.br/5987164343458678; Universidade Federal de São Paulo (UNIFESP)
    Amyotrophic Lateral Sclerosis (ALS), a fatal disease characterized by muscle and fasciculations weakness and atrophy and decreased reflexes due to upper and lower motor neurons death. It can be present in both sexes (55-65 years), but with predominance in males. However, in female patients, ALS presents its first symptoms when they are already postmenopausal, when then the incidence ratio of the disease is practically equal between the sexes. Which leads to a probable involvement of sex hormones in the development and protection against ALS. The aim of this systematic review, which used the PRISMA consensus and NOS (New Casttle-Ottawa Scale) score, was to evaluate the evidence of the action of hormone therapy in women with ALS. The Medline and Cochrane databases were accessed from March 2019 to June 2019, and only full text articles in Spanish, English and Portuguese languages were included. Only four articles matched our inclusion criteria. Postmenopausal women who used exogenous estrogen did not have the same protective factor as women still under the action of endogenous estrogen in the same age group. There was also no increase in survival of these women.
  • Nenhuma Miniatura disponível
    Item
    Somente Metadadados
    Efeito dos hormônios sexuais no receptor B2 de Cininas
    (Universidade Federal de São Paulo (UNIFESP), 2021) Arata, Julia Galanakis [UNIFESP]; Pesquero, Joao Bosco [UNIFESP]; Universidade Federal de São Paulo
    Hereditary angioedema (HAE) is a rare genetic autosomal dominant disease characterized by attacks of cutaneous and submucosal swelling, which causes weakness and pain to patients and can be life threatening when affecting the upper airways. Edema formation results from vasodilation and vascular permeability increase, in most cases, by the excessive release of bradykinin (BK), due to a disorder in the plasma kallikrein-kinin system. The frequency, severity, and triggers of attacks vary among patients with the disease. In female patients, the action of estrogen (menstruation, pregnancy, and exogenous administration) is reported as an aggravating stimulus for the angioedema attacks. In the present work, we aimed to investigate mechanisms in the kallikrein-kinin system which could be linked to the phenotype difference between women and men with HAE, through in vitro Ca2+ intracellular mobilization assays in endothelial cells transfected with the kinin B2 receptor (B2R), to verify whether the interaction of B2R and its agonist (BK) is influenced by estradiol, testosterone, and attenuated androgens. In our cellular assays, there was no significant effect of these hormones in the intracellular Ca+2 release due to B2R activation by BK that could indicate a possible direct or indirect allosteric regulation by these hormones over the receptor. Estradiol was able to decrease the activity of recombinant angiotensin converting enzyme (ACE) expressed in endothelial cells, although the difference was not significant. These data indicate a possible influence of estrogen on ACE activity, which could reduce BK degradation, and increase AEH severity.