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1.
Zhongguo Gu Shang ; 33(4): 301-5, 2020 Apr 25.
Artigo em Chinês | MEDLINE | ID: mdl-32351081

RESUMO

OBJECTIVE: To explore the effect of Mimics assisted virtual reduction and personalized additional fixation with proximal femoral nail anti rotation in the treatment of unstable intertrochanteric fracture of lateral wall. METHODS: From January 2015 to June 2018, 11 cases of intertrochanteric fracture with unstable lateral wall injury were analyzed retrospectively, including 3 males and 8 females, aged 64 to 81 years old. There were 3 cases of A3.1, 6 cases of A3.2 and 2 cases of A3.3 according to AO classification. All patients underwent CT scanning, according to the CT scanning data, three-dimensional reconstruction of fracture was performed by Mimics soft. Virtual reduction was performed first, and PFNA was implanted after satisfactory reduction. According to the relationship between the fracture characteristics of the lateral wall and the position of the lag screw tail in the lateral wall, 4 cases were treated with PFNA and titanium cable or steel wire, and 7 cases were treated with PFNA and reconstruction locking plate.The quality of reduction and healing were evaluated by follow up, and Harris score of hip joint was performed in the last reexamination. RESULTS: All patients were followed up for 12 to 18 months. No postoperative infection of incision and loosening of internal fixation occurred. The time of fracture healing was 12 to 20 weeks. At the final follow up, Harris score of hip joint was excellent in 6 cases, good in 3 cases and fair in 2 cases. CONCLUSION: The treatment of intertrochanteric fracture of femur with Mimics assisted virtual reduction and PFNA is helpful to preoperative planning and improve the surgical effect.


Assuntos
Fixação Intramedular de Fraturas , Fraturas do Quadril , Idoso , Idoso de 80 Anos ou mais , Pinos Ortopédicos , Feminino , Fraturas do Quadril/cirurgia , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Software , Resultado do Tratamento
2.
J Neuroinflammation ; 15(1): 347, 2018 Dec 20.
Artigo em Inglês | MEDLINE | ID: mdl-30572907

RESUMO

BACKGROUND: Neuroinflammation is closely associated with functional outcome in subarachnoid hemorrhage (SAH) patients. Our recent study demonstrated that fluoxetine inhibited NLRP3 inflammasome activation and attenuated necrotic cell death in early brain injury after SAH, while the effects and potential mechanisms of fluoxetine on neuroinflammation after SAH have not been well-studied yet. METHODS: One hundred and fifty-three male SD rats were subjected to the endovascular perforation model of SAH. Fluoxetine (10 mg/kg) was administered intravenously at 6 h after SAH induction. TAK-242 (1.5 mg/kg), an exogenous TLR4 antagonist, was injected intraperitoneally 1 h after SAH. SAH grade, neurological scores, brain water content, Evans blue extravasation, immunofluorescence/TUNEL staining, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot were performed. RESULTS: Fluoxetine administration attenuated BBB disruption, brain edema, and improved neurological function after SAH. In addition, fluoxetine alleviated the number of Iba-1-positive microglia/macrophages, neutrophil infiltration, and cell death. Moreover, fluoxetine reduced the levels of pro-inflammatory cytokines, downregulated the expression of TLR4 and MyD88, and promoted the nuclear translocation of NF-κB p65, which were also found in rats with TAK-242 administration. Combined administration of fluoxetine and TAK-242 did not enhance the neuroprotective effects of fluoxetine. CONCLUSION: Fluoxetine attenuated neuroinflammation and improved neurological function in SAH rats. The potential mechanisms involved, at least in part, TLR4/MyD88/NF-κB signaling pathway.


Assuntos
Lesões Encefálicas/tratamento farmacológico , Proteínas de Ligação ao Cálcio/metabolismo , Fluoxetina/uso terapêutico , Proteínas dos Microfilamentos/metabolismo , Fármacos Neuroprotetores/uso terapêutico , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Animais , Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/fisiopatologia , Edema Encefálico/tratamento farmacológico , Edema Encefálico/etiologia , Lesões Encefálicas/etiologia , Lesões Encefálicas/mortalidade , Lesões Encefálicas/patologia , Citocinas/genética , Citocinas/metabolismo , Modelos Animais de Doenças , Regulação da Expressão Gênica/efeitos dos fármacos , Fator Estimulador de Colônias de Granulócitos/metabolismo , Interleucina-3/metabolismo , Masculino , Fator 88 de Diferenciação Mieloide/metabolismo , NF-kappa B/metabolismo , Ratos , Ratos Sprague-Dawley , Proteínas Recombinantes de Fusão/metabolismo , Hemorragia Subaracnóidea/complicações , Hemorragia Subaracnóidea/mortalidade , Sulfonamidas/uso terapêutico
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