RESUMO
OBJECTIVE: To investigate clinical effect of sternoclavicular hook plate in treating acute proximal clavicle fracture. METHODS: The clinical of 12 patients with acute unstable proximal clavicle fracture from June 2016 to June 2019 were retrospectively analyzed. There were 8 males and 4 females, aged from 46 to 63 years old. Ten patients caused by car accident and 2 patients caused by high falling. All patients had multiple injuries;the time from injury to surgery ranged from 2 to 14 d. All patients were treated with domestic sternoclavicular joint hook plate. The operative time ranged from 40 to 115 min. The intraoperative bleeding volume ranged from 30 to 110 ml, follow-up time ranged from 10 to 36 months, the fracture healing time ranged from 8 to 18 weeks. At the latest follow-up, the efficacy was evaluated by using shoulder joint function score (Rockwood score). RESULTS: All 12 patients were followed up, with no obvious pain at the latest follow-up. The rockwood scores of the affected shoulder ranged from 13 to 14, and the healthy shoulder ranged from 14 to 15. CONCLUSION: The sternocleidoclavicular joint plate is fixed with preformed plate. The cantilever is designed to retain the motion of the sternoclavicular joint. It's safe and simple, avoid, the injury of important organs during operation, and has a good prognosis. It is an ideal fixation method for the treatment of proximal clavicle fracture.
Assuntos
Fraturas Ósseas , Articulação Esternoclavicular , Masculino , Feminino , Humanos , Pessoa de Meia-Idade , Clavícula/cirurgia , Clavícula/lesões , Articulação Esternoclavicular/cirurgia , Articulação Esternoclavicular/lesões , Estudos Retrospectivos , Fixação Interna de Fraturas/métodos , Resultado do Tratamento , Fraturas Ósseas/cirurgiaRESUMO
Wound healing is related to proliferation, migration, and angiogenesis of keratinocytes. Insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is an important N6-methyladenosine (m6A) reader, which is involved in multiple processes, including wound healing. However, the function and mechanism of IGF2BP2 in keratinocyte processes are largely uncertain. In the present study, expression levels of IGF2BP2 and heparanase (HPSE) were detected by quantitative reverse transcription polymerase chain reaction and western blotting assays. Cell proliferation was investigated by cell counting kit-8 (CCK-8) analysis. Cell migration was determined through wound healing assay. Angiogenesis was measured by tube formation assay and vascular endothelial growth factor (VEGF) level using enzyme linked immunosorbent assay (ELISA). The interaction between IGF2BP2 and HPSE was analyzed by RNA immunoprecipitation, pull-down and luciferase reporter analyses. The results showed that IGF2BP2 expression was enhanced in wound healing. IGF2BP2 downregulation constrained HaCaT cell proliferation, migration, and angiogenesis. IGF2BP2 knockdown decreased HPSE expression. IGF2BP2 could regulate HPSE stability by binding with 3' untranslated region (UTR) of HPSE. HPSE upregulation attenuated silencing IGF2BP2-mediated suppression of proliferation, migration, and angiogenesis. As a conclusion, IGF2BP2 knockdown repressed proliferation, migration, and angiogenesis of HaCaT cells by decreasing HPSE stability.
Assuntos
Movimento Celular , Glucuronidase/metabolismo , Queratinócitos/metabolismo , Queratinócitos/patologia , Neovascularização Patológica/metabolismo , Proteínas de Ligação a RNA/metabolismo , Regiões 3' não Traduzidas/genética , Movimento Celular/genética , Proliferação de Células/genética , Estabilidade Enzimática , Perfilação da Expressão Gênica , Regulação da Expressão Gênica , Técnicas de Silenciamento de Genes , Células HaCaT , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Neovascularização Patológica/genética , Ligação Proteica , Cicatrização/genéticaRESUMO
A key challenge facing drug discovery today is variability of the drug target between species, such as with 12/15-lipoxygenase (12/15-LOX), which contributes to ischemic brain injury, but its human and rodent isozymes have different inhibitor specificities. In the current work, we have utilized a quantitative high-throughput (qHTS) screen to identify compound 1 (ML351), a novel chemotype for 12/15-LOX inhibition that has nanomolar potency (IC50 = 200 nM) against human 12/15-LOX and is protective against oxidative glutamate toxicity in mouse neuronal HT22 cells. In addition, it exhibited greater than 250-fold selectivity versus related LOX isozymes, was a mixed inhibitor, and did not reduce the active-site ferric ion. Lastly, 1 significantly reduced infarct size following permanent focal ischemia in a mouse model of ischemic stroke. As such, this represents the first report of a selective inhibitor of human 12/15-LOX with demonstrated in vivo activity in proof-of-concept mouse models of stroke.
