RESUMO
Multidirectionally unstable supracondylar humeral fractures cause severe instability in both flexion and extension movements. The traditional closed reduction often fails to overcome this lack of stability. The aim of this study is to use a closed reduction technique with a transolecranon pin to achieve temporary stability. From 35 pediatric multidirectionally unstable supracondylar humeral fractures hospitalized between March 2012 and March 2018 at our hospital, 23 fractures (65.7%) were treated with closed reduction and percutaneous pinning (CRPP) (group 1) and the remaining twelve fractures (34.3%) were treated utilizing a transolecranon pin joystick technique of CRPP (group 2). Both groups were followed over 16 weeks. The outcomes of our analysis included surgical time, times of fluoroscopy, Baumann angle, postoperative range of motion and complications. The surgical time and times of fluoroscopy were significantly shorter for patients in group 2 when compared with group 1 (P < 0.05). All cases showed restoration of the normal anterior humeral line-capitellar relationship. However, the quality of reduction on the anteroposterior radiographic view was significantly better for patients in group 2 than that of group 1 (P < 0.05). No immediate postoperative complications were observed. The range of motion was similar in both groups during the last follow-up appointment. A transolecranon pin is a safe and effective method for closed reduction of multidirectionally unstable supracondylar humeral fractures in children. The joystick technique can shorten surgical time and improve quality of reduction with no increasing risk of complications. Level of evidence: level III.
Assuntos
Pinos Ortopédicos , Fraturas do Úmero/cirurgia , Olécrano , Pré-Escolar , Feminino , Humanos , Fraturas do Úmero/diagnóstico por imagem , Lactente , Masculino , Duração da Cirurgia , Complicações Pós-Operatórias , Amplitude de Movimento Articular , Estudos Retrospectivos , Resultado do TratamentoRESUMO
BACKGROUND AND AIMS: Atherosclerosis (AS) is the leading cause of cardiovascular diseases. PGC-1α is a key regulator of cellular energy homeostasis, but its role in AS remains debatable. METHODS AND RESULTS: In our study, PGC-1α was shown to be significantly decreased in the media of human atherosclerotic vessels. To explore whether miRNAs might be regulated by PGC-1α in vascular smooth muscle cells (VSMCs), microarray analysis was performed. Microarray and Pearson's correlation analysis showed that PGC-1α and miR-378a were positively correlated in vivo and in vitro. As an upstream co-activator, PGC-1α was found to regulate miR-378a through binding to the transcriptional factor NRF1 in VSMCs. Therefore, the decreased expression of PGC-1α might account for suppression of miR-378a in VSMCs in AS. Furthermore, IGF1 and TLR8, two genes known to be aberrantly up-regulated in atherogenic vessels, were identified as direct targets of miR-378a. In vitro up-regulation of miR-378a markedly inhibited free fatty acid (FFA)-induced VSMC proliferation, migration and inflammation through targeting IGF1 and TLR8. CONCLUSIONS: These findings highlight the protective role of the PGC-1α/NRF1/miR-378a regulatory axis in AS progression and suggest miR-378a as potential therapeutic target for AS treatment.
Assuntos
Aterosclerose/metabolismo , Movimento Celular , Proliferação de Células , Inflamação/metabolismo , MicroRNAs/metabolismo , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Fator 1 Nuclear Respiratório/metabolismo , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo , Aterosclerose/genética , Aterosclerose/patologia , Células Cultivadas , Regulação da Expressão Gênica , Humanos , Inflamação/genética , Inflamação/patologia , Fator de Crescimento Insulin-Like I/genética , Fator de Crescimento Insulin-Like I/metabolismo , MicroRNAs/genética , Músculo Liso Vascular/patologia , Miócitos de Músculo Liso/patologia , Fator 1 Nuclear Respiratório/genética , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética , Transdução de Sinais , Receptor 8 Toll-Like/genética , Receptor 8 Toll-Like/metabolismoRESUMO
The protein tyrosine phosphatase PTP1B, which is encoded by PTPN1, is a ubiquitously expressed nonreceptor protein tyrosine phosphatase. PTP1B has long been known to negatively regulate insulin and leptin receptor signalling. Recently, it was reported to be aberrantly expressed in cancer cells and to function as an important oncogene. In this study, we found that PTP1B protein levels are dramatically increased in breast cancer (BC) tissues and that PTP1B promotes the proliferation, and suppresses the apoptosis, of both HER2-positive and triple-negative BC cell lines. Bioinformatics analysis identified that the miRNA, miR-193a-3p, might potentially target PTP1B. We demonstrate that miR-193a-3p regulates PTP1B in BC cells and that it regulates the proliferation and apoptosis of BC cells by targeting PTP1B, both in vitro and in vivo. In conclusion, this study confirms that PTP1B acts as an oncogene in BC and demonstrates that miR-193a-3p can serve as a tumour suppressor gene in BC by targeting PTP1B.