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1.
Orthop Surg ; 11(3): 348-355, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31197911

RESUMO

Developmental dysplasia of the hip (DDH) is accompanied by morphological alterations on both the acetabular and the femoral side. Total hip arthroplasty (THA) provides effective treatment in cases of neglected DDH but requires elaborate preoperative planning. To determine the morphological changes resulting from the dysplasia, the anatomic acetabular position, the height of the femur head dislocation, the height of the femur head dislocation, and the combined anteversion must all be established. In addition, a vital and complicated process of strategizing leg length balance must be conducted in cases of severe DDH. Each type of leg length discrepancy (LLD), including bony and functional and anatomical LLD, should be evaluated in the context of the presence or absence of a fixed pelvic tilt. Moreover, with severe unilateral dislocated hips, a more inferior change in the original rotational center of the hip must be accounted for. Due to these multiple morphological changes, the accurate size of the prosthesis and the cup position are difficult to predict. In comparison with other methods, CT scan-based 3-dimensional templating provides the best accuracy. Despite the presence of anatomic alterations, various types of acetabular and femoral prostheses have been developed to treat hip dysplasia. Both cemented and cementless cups are used in DDH cases. In DDH accompanied by insufficient acetabular bone stock, a cemented cup combined with bone graft provides a reliable treatment. Monoblock stems can be used when the combined anteversion is less than 55°, and a modular stem system when this parameter is greater than 55°. Customized stems can be designed for DDH coupled with severe proximal femoral distortion. A ceramic-on-ceramic bearing is considered optimal for young DDH patients.

2.
Mol Pharmacol ; 63(5): 1002-11, 2003 May.
Artigo em Inglês | MEDLINE | ID: mdl-12695528

RESUMO

Endothelin-1 (ET-1) has been implicated in fibroblast proliferation. However, the mechanism involving ET-1 is not clear. The present study was performed to examine the role of endogenous ET-1 in ET-1-stimulated fibroblast proliferation and to investigate the regulatory mechanism of ET-1-induced ET-1 gene expression in cardiac fibroblasts. Both ET(A) receptor antagonist [(hexahydro-1H-azepinyl)carbonyl-Leu-D-Trp-D-OH (BQ485)] and endothelin-converting enzyme inhibitor (phosphoramidon) inhibited the increased DNA synthesis caused by ET-1. ET-1 gene was induced by ET-1, as revealed with Northern blotting and ET-1 promoter activity assay. ET-1 increased intracellular reactive oxygen species (ROS), which were significantly inhibited by BQ485 and antioxidants. Antioxidants suppressed ET-1 gene expression and DNA synthesis stimulated by ET-1. ET-1 activated mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase, which were significantly inhibited by antioxidants. Only ERK inhibitor U0126 could inhibit ET-1-induced transcription of the ET-1 gene. Cotransfection of dominant-negative mutant of Ras, Raf, and MEK1 decreased the ET-1-induced increase in ET-1 transcription, suggesting that the Ras-Raf-ERK pathway is required for ET-1 action. Truncation and mutational analysis of the ET-1 gene promoter showed that the activator protein-1 (AP-1) binding site was an important cis-element in ET-1-induced ET-1 gene expression. Antioxidants attenuated the ET-1-stimulated AP-1 binding activity. Our data suggest that ROS were involved in ET-1-induced fibroblast proliferation and mediated ET-1-induced activation of ERK pathways, which culminated in ET-1 gene expression.


Assuntos
Endotelina-1/genética , Fibroblastos/fisiologia , Expressão Gênica/fisiologia , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Animais , Animais Recém-Nascidos , Divisão Celular , DNA/biossíntese , Humanos , Miocárdio/citologia , Oxirredução , Ratos , Receptor de Endotelina A , Receptores de Endotelina/metabolismo , Transcrição Genética
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