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1.
Aesthet Surg J ; 43(10): NP738-NP747, 2023 09 14.
Artigo em Inglês | MEDLINE | ID: mdl-37350541

RESUMO

Fat grafting can restore facial volume for reconstructive and cosmetic indications. Common practice often involves extracting lipoaspirate from the most abundant anatomic location. However, grafted fat retains the phenotypic characteristics of its original location and can undergo exaggerated hypertrophy with patient weight fluctuations. The aim of this study was to systematically assess the literature to summarize the reported effects of postoperative weight gain on facial hypertrophy in patients after facial fat grafting and to determine potentially avoidable factors. A search through PubMed/MEDLINE was conducted on October 4, 2022, to identify relevant articles with appropriate search terms. No lower date limit was applied and all eligible nonanimal clinical articles in English were included for review. Reports were summarized and presented as descriptive statistics. The search generated 714 articles. After abstract and full-text review of the initial set of articles, 6 were included in our analysis. All articles described poor cosmetic outcomes resulting from nonanatomic hypertrophy of the grafted fat. None of the articles reported a thorough methodology for selecting the donor site to minimize fat hypertrophy with potential future weight fluctuations. Grafted facial fat is susceptible to exaggerated hypertrophy as a result of changes in patient weight. Specifically, harvesting lipoaspirate from maximally abundant areas of the body may increase this risk. Individualizing the area of fat donation may attenuate unwanted fat growth and further contribute to increased patient quality of life.


Assuntos
Tecido Adiposo , Procedimentos de Cirurgia Plástica , Humanos , Tecido Adiposo/transplante , Qualidade de Vida , Procedimentos de Cirurgia Plástica/efeitos adversos , Face/cirurgia , Transplante Autólogo/efeitos adversos
2.
J Immunol ; 205(10): 2883-2892, 2020 11 15.
Artigo em Inglês | MEDLINE | ID: mdl-33077644

RESUMO

CD98, which is required for the rapid proliferation of both normal and cancer cells, and MET, the hepatocyte growth factor receptor, are potential targets for therapeutic antitumor Abs. In this study, we report that the antiproliferative activity of a prototype anti-CD98 Ab, UM7F8, is due to Ab-induced membrane-associated ring CH (MARCH) E3 ubiquitin ligase-mediated ubiquitination and downregulation of cell surface CD98. MARCH1-mediated ubiquitination of CD98 is required for UM7F8's capacity to reduce CD98 surface expression and its capacity to inhibit the proliferation of murine T cells. Similarly, CD98 ubiquitination is required for UM7F8's capacity to block the colony-forming ability of murine leukemia-initiating cells. To test the potential generality of the paradigm that MARCH E3 ligases can mediate the antiproliferative response to antitumor Abs, we examined the potential effects of MARCH proteins on responses to emibetuzumab, an anti-MET Ab currently in clinical trials for various cancers. We report that MET surface expression is reduced by MARCH1, 4, or 8-mediated ubiquitination and that emibetuzumab-induced MET ubiquitination contributes to its capacity to downregulate MET and inhibit human tumor cell proliferation. Thus, MARCH E3 ligases can act as cofactors for antitumor Abs that target cell surface proteins, suggesting that the MARCH protein repertoire of cells is a determinant of their response to such Abs.


Assuntos
Antígenos de Neoplasias/metabolismo , Antineoplásicos Imunológicos/farmacologia , Cadeia Pesada da Proteína-1 Reguladora de Fusão/metabolismo , Neoplasias/tratamento farmacológico , Ubiquitina-Proteína Ligases/metabolismo , Animais , Anticorpos Monoclonais Humanizados/farmacologia , Anticorpos Monoclonais Humanizados/uso terapêutico , Antígenos de Neoplasias/genética , Antígenos de Neoplasias/imunologia , Antineoplásicos Imunológicos/uso terapêutico , Proliferação de Células/efeitos dos fármacos , Cadeia Pesada da Proteína-1 Reguladora de Fusão/antagonistas & inibidores , Cadeia Pesada da Proteína-1 Reguladora de Fusão/genética , Cadeia Pesada da Proteína-1 Reguladora de Fusão/imunologia , Técnicas de Inativação de Genes , Células HeLa , Humanos , Células Jurkat , Camundongos , Camundongos Knockout , Neoplasias/imunologia , Neoplasias/patologia , Proteólise , Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-met/genética , Linfócitos T/efeitos dos fármacos , Linfócitos T/imunologia , Ubiquitina-Proteína Ligases/genética , Ubiquitinação/imunologia
3.
SAGE Open Med Case Rep ; 12: 2050313X241253731, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38764913

RESUMO

Paget-Schroetter syndrome, the venous variant of thoracic outlet syndrome, is an uncommon presentation of deep vein thrombosis. In patients with Paget-Schroetter syndrome, the subclavian vein is compressed within the thoracic outlet as a result of repetitive and vigorous arm motions. Repeated endothelial injury leads to stasis in flow and eventual thrombus formation in the subclavian vein and its tributaries. This report highlights the case of an active and otherwise healthy 46-year-old patient who presented with swelling and pain of his right upper extremity after a run and was found to have multiple, effort-induced thrombi involving the right subclavian, axillary, brachial, and basilic veins. The unusual clinical picture of Paget-Schroetter syndrome and its presentation commonly in the demographic of young, healthy individuals make it a diagnosis likely overlooked and unfamiliar to many in the clinical setting.

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