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1.
Am J Rhinol Allergy ; 36(4): 412-414, 2022 07.
Artigo em Inglês | MEDLINE | ID: mdl-37802132
3.
World Neurosurg ; 126: e165-e172, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30794981

RESUMO

OBJECTIVE: At our institution, skull base reconstruction using a free mucosal graft from the nasal cavity floor has been the standardized technique after pituitary adenoma resection via transsellar approach. In this study, the expected appearance of the reconstruction on postoperative magnetic resonance imaging (MRI) scans is described and its integrity and impact on the sinonasal cavity are assessed. METHODS: Fifty patients were selected, and their electronic medical records were reviewed for postoperative course, Sino-Nasal Outcome Test-22 (SNOT-22) scores, and nasal endoscopy reports. A total of 116 postoperative MRI scans were available to evaluate 1) the appearance and thickness of the graft, 2) the enhancement of the graft, and 3) the T2 signal in sphenoid sinus as a potential indication for inflammatory disease. RESULTS: There was no significant change in the thickness of the graft over time. Except for the 7 scans that were obtained without intravenous contrast, all scans showed enhancement of the graft. About half of the patients showed persistent T2 hyperintense signal at 12 and 24 months. However, this finding was not clinically significant, because postoperative SNOT-22 scores showed minimal sinonasal impact. CONCLUSIONS: Postoperative MRI surveillance scans showed a stable appearance of the graft that mimics the native mucosa, with enhancement through time, reflecting its robust vascularization and integration to the skull base. Although persistent T2 hyperintense signal was detected in the sphenoid sinus, clinical evidence based on nasal endoscopy reports and SNOT-22 scores indicated minimal sinonasal morbidity.


Assuntos
Endoscopia/métodos , Cavidade Nasal/cirurgia , Mucosa Nasal/transplante , Procedimentos Neurocirúrgicos/métodos , Procedimentos de Cirurgia Plástica/métodos , Base do Crânio/diagnóstico por imagem , Base do Crânio/cirurgia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Base do Crânio/anormalidades , Resultado do Tratamento , Adulto Jovem
4.
Nat Commun ; 3: 616, 2012 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-22233626

RESUMO

Hereditary haemorrhagic telangiectasia (HHT) [corrected] is a vascular dysplasia syndrome caused by mutations in transforming growth factor-ß/bone morphogenetic protein pathway genes, ENG and ACVRL1. HHT [corrected] shows considerable variation in clinical manifestations, suggesting environmental and/or genetic modifier effects. Strain-specific penetrance of the vascular phenotypes of Eng(+/-) and Tgfb1(-/-) mice provides further support for genetic modification of transforming growth factor-ß pathway deficits. We previously identified variant genomic loci, including Tgfbm2, which suppress prenatal vascular lethality of Tgfb1(-/-) mice. Here we show that human polymorphic variants of PTPN14 within the orthologous TGFBM2 locus influence clinical severity of HHT, [corrected] as assessed by development of pulmonary arteriovenous malformation. We also show that PTPN14, ACVRL1 and EFNB2, encoding EphrinB2, show interdependent expression in primary arterial endothelial cells in vitro. This suggests an involvement of PTPN14 in angiogenesis and/or arteriovenous fate, acting via EphrinB2 and ACVRL1/activin receptor-like kinase 1. These findings contribute to a deeper understanding of the molecular pathology of HHT [corrected] in particular and to angiogenesis in general.


Assuntos
Proteínas Tirosina Fosfatases não Receptoras/fisiologia , Telangiectasia Hemorrágica Hereditária/genética , Receptores de Ativinas Tipo I/metabolismo , Receptores de Activinas Tipo II/metabolismo , Animais , Mapeamento Cromossômico , Efrina-B2/metabolismo , Éxons , Feminino , Variação Genética , Haplótipos , Humanos , Masculino , Camundongos , Camundongos Congênicos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Modelos Genéticos , Mutação , Fenótipo , Proteínas Tirosina Fosfatases não Receptoras/genética , Especificidade da Espécie , Fator de Crescimento Transformador beta/metabolismo
5.
J Vasc Surg ; 54(2): 427-32, 432.e1-4, 2011 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-21664093

RESUMO

BACKGROUND: The relationship between lifetime physical activity and the risk of developing peripheral arterial disease (PAD) is not known. METHODS: We studied 1381 patients referred for elective coronary angiography in a point prevalence analysis. PAD was defined as ankle-brachial index (ABI) <0.9 at the time or a history of revascularization of the lower extremities regardless of ABI measure. We used a validated physical activity questionnaire to retrospectively measure each patient's lifetime recreational activity (LRA). Multivariate and logistic regression analyses were used to assess the independent association of LRA to ABI and the presence of PAD. RESULTS: PAD was present in 19% (n = 258) of all subjects. Subjects reporting no regular LRA had greater diastolic blood pressure and were more likely to be female. They had lower average ABI, and a higher proportion had PAD (25.6%). In a regression model, including traditional risk factors and LRA, multivariate analysis showed that age (P < .001), female gender (P < .001), systolic blood pressure (P = .014), fasting glucose (P < .001), serum triglycerides (P = .02), and cumulative pack years (P < .001) were independent negative predictors of ABI, and LRA was a positive predictor of ABI (P < .001). History of sedentary lifestyle independently increased the odds ratio for PAD (odds ratio, 0.46; 95% confidence interval, 1.01-2.10) when assessed by logistic regression. Intriguingly, there is a correlation between physical activity and gender, such that women with low LRA are at greatest risk. CONCLUSION: Recalled LRA is positively correlated to ABI and associated with PAD. Whereas the mechanism for this effect is not clear, LRA may be a useful clinical screening tool for PAD risk, and strategies to increase adult recreational activity may reduce the burden of PAD later in life.


Assuntos
Doença Arterial Periférica/etiologia , Recreação , Comportamento Sedentário , Idoso , Índice Tornozelo-Braço , Biomarcadores/sangue , Glicemia/análise , Pressão Sanguínea , Feminino , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Doença Arterial Periférica/sangue , Doença Arterial Periférica/diagnóstico , Doença Arterial Periférica/epidemiologia , Doença Arterial Periférica/fisiopatologia , Doença Arterial Periférica/cirurgia , Prevalência , Estudos Retrospectivos , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fumar/efeitos adversos , Inquéritos e Questionários , Triglicerídeos/sangue , Estados Unidos , Procedimentos Cirúrgicos Vasculares
6.
Vasc Med ; 15(6): 443-50, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21183651

RESUMO

To determine whether there are sex differences in the prevalence of peripheral artery disease, we performed an observational study of 1014 men and 547 women, aged ≥ 40 years, referred for elective coronary angiography. Women were slightly older, more obese, had higher low-density lipoprotein cholesterol (LDL-C) levels and systolic blood pressure (BP), and were more likely to be African American. Women had higher high-density lipoprotein cholesterol (HDL-C) levels, lower diastolic BP, and were less likely to smoke or to have a history of cardiovascular disease. Women had less prevalent (62% vs 81%) and less severe coronary artery disease (CAD) (p < 0.001 for both) by coronary angiography, but more prevalent peripheral artery disease (PAD) as determined by the ankle-brachial index (ABI) than men (23.6% versus 17.2%). Independent predictors of lower ABI were female sex, black race, older age, tobacco use, CAD, diabetes, and triglyceride level. In a full multivariable logistic regression model, women had a risk-adjusted odds ratio for PAD of 1.78 (95% CI 1.25-2.54) relative to men. Among patients referred for coronary angiography, women have less prevalent and less severe CAD, but more prevalent PAD, a sex difference that is not explained by traditional cardiovascular disease risk factors or CAD severity. Clinical Trial Registration-URL: http://clinicaltrials.gov. Unique identifier: NCT00380185.


Assuntos
Angiografia Coronária , Doença da Artéria Coronariana/diagnóstico por imagem , Doença Arterial Periférica/epidemiologia , Idoso , Índice Tornozelo-Braço , California/epidemiologia , Doença da Artéria Coronariana/epidemiologia , Estudos Transversais , Feminino , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Cidade de Nova Iorque/epidemiologia , Razão de Chances , Doença Arterial Periférica/diagnóstico , Prevalência , Medição de Risco , Fatores de Risco , Índice de Gravidade de Doença , Fatores Sexuais
7.
Proc Natl Acad Sci U S A ; 103(21): 8125-30, 2006 May 23.
Artigo em Inglês | MEDLINE | ID: mdl-16702541

RESUMO

The human TGFB1 gene is polymorphic, and genetic variants are associated with altered cancer risk. However, human genetic association studies have had variable outcomes because TGFbeta1 action is context-dependent. We used the murine skin model of chemical carcinogenesis in genetic linkage analysis of three independent Mus musculus NIH/Ola x (Mus spretus x M. musculus NIH/Ola)F1 backcrosses, to identify a skin tumor susceptibility locus, Skts14, on proximal chromosome 7. Tgfb1 maps at the peak of linkage. The mouse Tgfb1 gene is polymorphic, resulting in cis-regulated differential allelic mRNA expression between M. spretus and M. musculus in F1 mouse skin. This phenomenon is reflected in differential phospho-SMAD2 levels, downstream of TGFbeta signaling, between these two mouse species. In normal F1 mouse skin, the Tgfb1SPR allele is expressed at higher levels than the Tgfb1NIH allele, and this differential is accentuated by phorbol 12-myristate 13-acetate treatment. In benign F1 papillomas, this imbalance is reversed, possibly by selection against expression of a hyperactive Tgfb1SPR allele in TGFbeta growth-responsive tumors. We demonstrate that skin tumor susceptibility is altered by Tgfb1 gene dosage, but that manifestation of Tgfb1-linked skin tumor susceptibility in M. musculus NIH/Ola x (M. spretus x M. musculus NIH/Ola)F1 backcross mice depends on interactions with another unlinked tumor modifying locus, Skts15, that overlaps Tgfbm3 on chromosome 12. These findings illustrate the power of complex genetic interactions in determining disease outcome and have major implications to the assessment of disease risk in individuals harboring variant TGFB1 alleles.


Assuntos
Predisposição Genética para Doença , Neoplasias Cutâneas/etiologia , Neoplasias Cutâneas/genética , Fator de Crescimento Transformador beta/genética , Alelos , Animais , Mapeamento Cromossômico , Cruzamentos Genéticos , Ligação Genética , Variação Genética , Homozigoto , Camundongos , Polimorfismo Genético , Pele/metabolismo
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