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2.
Histol Histopathol ; 31(2): 231-7, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26430761

RESUMO

UNLABELLED: The objective of this study was to determine whether gynecological and periodontal clinical parameters and the immunohistochemical expression in placental chorionic villi of the markers cyclooxygenase-2 (COX-2), interleukin (IL)-1ß, vascular endothelial growth factor receptor 1 (VEGFR1), podoplanin, and Heat Shock Protein 70 (HSP70) are associated with preterm birth (PB) and/or low birth weight (LBW) neonates. MATERIAL AND METHODS: An observational case-control study was performed in 130 puerperal women: mothers of PB/LBW neonates (cases, n=65) and mothers of full-term normal-weight neonates (controls, n=65). Data were gathered from all participants on socio-demographic, gynecological, and periodontal variables and on placental immunohistochemical COX-2, IL-1ß, VEGFR1, podoplanin, and HSP70 expression. RESULTS: Among the 42 women with mild/moderate periodontitis or gingivitis, the studied periodontal variables were significantly worse and the placental COX-2 (p=0.043), HSP70 (p=0.001), IL-1ß (p=0.001), VEGFR1 (p=0.032), and podoplanin (p=0.058) expressions were significantly higher in the cases than in the controls. In comparison to the mothers without periodontitis, only COX-2 (p=0.026) and VEGFR1 (p=0.005) expressions were significantly increased in those with the disease. Increased COX-2 values were detected in the women with a history of genitourinary infection (p=0.036), premature rupture of membrane (p=0.012), or drug treatment (p=0.050). CONCLUSIONS: The etiology of preterm birth and/or low birth weight is multifactorial and involves consumption habits, social-health factors, and infectious episodes. These adverse pregnancy outcomes were associated with periodontitis and the increased placental expression of IL-1ß, COX-2, VEGFR1, and HSP70.


Assuntos
Regulação da Expressão Gênica , Recém-Nascido de Baixo Peso , Doenças Periodontais/complicações , Placenta/metabolismo , Nascimento Prematuro , Adulto , Biomarcadores/metabolismo , Estudos de Casos e Controles , Doença Crônica , Ciclo-Oxigenase 2/metabolismo , Feminino , Perfilação da Expressão Gênica , Proteínas de Choque Térmico HSP70/metabolismo , Humanos , Imuno-Histoquímica , Recém-Nascido , Inflamação , Interleucina-1beta/metabolismo , Glicoproteínas de Membrana/metabolismo , Doenças Periodontais/fisiopatologia , Periodontite/metabolismo , Gravidez , Complicações na Gravidez , Resultado da Gravidez , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/metabolismo
3.
PLoS One ; 6(7): e21271, 2011.
Artigo em Inglês | MEDLINE | ID: mdl-21747934

RESUMO

Recent evidence suggests that an initial barrier to the emergence of tumours is a DNA damage response that evokes a counter-response which arrests the growth of, or eliminates, damaged cells. Early precursor lesions express markers of an activated DNA damage response in several types of tumour, with a diminishing response in more advanced cancers. An important marker of DNA damage is ATM which becomes phosphorylated (pATM) upon activation. We have investigated pATM expression patterns in cultured keratinocytes, skin explants and a spectrum of pre-malignant to malignant keratinocyte skin lesions by immunohistochemistry. We found that pATM was mainly localised to the Golgi apparatus, which contrasts with its nuclear localisation in other tissues. Upon UV irradiation there is transient formation of pATM in nuclear foci, consistent with recruitment to the sites of DNA damage. By immunohistochemistry we show pATM expression in precancerous keratinocyte lesions is greater and predominantly nuclear when compared to the invasive lesions where pATM is weaker and predominantly cytoplasmic. Our results are consistent with the hypothesis that the DNA damage response acts as a barrier to cutaneous tumour formation, but also suggests that ATM expression in skin is different compared to other tissues. This may be a consequence of the constant exposure of skin to UVR, and has implications for skin carcinogenesis.


Assuntos
Carcinoma de Células Escamosas/genética , Proteínas de Ciclo Celular/metabolismo , Dano ao DNA , Proteínas de Ligação a DNA/metabolismo , Regulação Neoplásica da Expressão Gênica , Queratinócitos/metabolismo , Fosfoproteínas/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Neoplasias Cutâneas/genética , Proteínas Supressoras de Tumor/metabolismo , Proteínas Mutadas de Ataxia Telangiectasia , Carcinoma in Situ/genética , Carcinoma in Situ/metabolismo , Carcinoma in Situ/patologia , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/patologia , Linhagem Celular Tumoral , Núcleo Celular/genética , Núcleo Celular/metabolismo , Núcleo Celular/efeitos da radiação , Progressão da Doença , Regulação Neoplásica da Expressão Gênica/efeitos da radiação , Complexo de Golgi/genética , Complexo de Golgi/metabolismo , Complexo de Golgi/efeitos da radiação , Humanos , Queratinócitos/citologia , Queratinócitos/patologia , Queratinócitos/efeitos da radiação , Ceratose Actínica/metabolismo , Invasividade Neoplásica , Neoplasias Cutâneas/metabolismo , Neoplasias Cutâneas/patologia , Fatores de Tempo , Raios Ultravioleta/efeitos adversos
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