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1.
Eur J Med Res ; 28(1): 494, 2023 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-37941083

RESUMO

The treatment of lumbar spinal synovial cysts (LSCs) which are relatively rare but can cause neurogenic dysfunction and intractable pain has been a controversial topic for many years. Surgical excision of LSCs is the standard treatment for patients in whom conservative treatment options fail. This meta-analysis was undertaken to compare clinical outcomes between minimally invasive approaches using tubular retractors (microscopic vs. endoscopic) and traditional percutaneous approaches for LSCs. Studies reporting surgical management of LSCs were searched in the Cochrane Library, PubMed and Web of Science database. This meta-analysis was reported following the PRISMA Statement, registered in Prospero (CRD42021288992). A total of 1833 patients were included from both the related relevant studies (41 studies, n = 1831) and the present series (n = 2). Meta-analysis of minimally invasive tubular approaches revealed no statistically significant difference in pain improvement, dural tear, residual cyst, recurrence and operation time between minimal groups with traditional groups (p > 0.05). Minimal groups had better Functional improvement of 100% (95% CI 1.00-1.00; p < 0.001, I2 = 75.3%) and less reoperation rates of 0% (95% CI - 0.00-0.00; p = 0.007, I2 = 47.1%). Postoperative length of hospital stay and intraoperative bleeding in minimal groups were also less than traditional groups (p < 0.05). Subgroup analysis revealed endoscopic groups had less operation time (p = 0.004), and there was no significant difference in the rest. For patients with LSCs but without obvious clinical and imaging evidence of vertebral instability, even when preoperative stable grade 1 spondylolisthesis is present, minimally invasive tubular approaches without fusion may provide the best outcome in surgical management.


Assuntos
Fusão Vertebral , Espondilolistese , Cisto Sinovial , Humanos , Resultado do Tratamento , Vértebras Lombares/cirurgia , Procedimentos Cirúrgicos Minimamente Invasivos/métodos , Espondilolistese/cirurgia , Cisto Sinovial/cirurgia , Fusão Vertebral/métodos
2.
CNS Neurosci Ther ; 29(12): 4124-4138, 2023 12.
Artigo em Inglês | MEDLINE | ID: mdl-37408388

RESUMO

AIMS: Previous studies have indicated that IFI30 plays a protective role in human cancers. However, its potential roles in regulating glioma development are not fully understood. METHODS: Public datasets, immunohistochemistry, and western blotting (WB) were used to evaluate the expression of IFI30 in glioma. The potential functions and mechanisms of IFI30 were examined by public dataset analysis; quantitative real-time PCR; WB; limiting dilution analysis; xenograft tumor assays; CCK-8, colony formation, wound healing, and transwell assays; and immunofluorescence microscopy and flow cytometry. RESULTS: IFI30 was significantly upregulated in glioma tissues and cell lines compared with corresponding controls, and the expression level of IFI30 was positively associated with tumor grade. Functionally, both in vivo and in vitro evidence showed that IFI30 regulated the migration and invasion of glioma cells. Mechanistically, we found that IFI30 dramatically promoted the epithelial-mesenchymal transition (EMT)-like process by activating the EGFR/AKT/GSK3ß/ß-catenin pathway. In addition, IFI30 regulated the chemoresistance of glioma cells to temozolomide directly via the expression of the transcription factor Slug, a key regulator of the EMT-like process. CONCLUSION: The present study suggests that IFI30 is a regulator of the EMT-like phenotype and acts not only as a prognostic marker but also as a potential therapeutic target for temozolomide-resistant glioma.


Assuntos
Glioma , beta Catenina , Humanos , beta Catenina/genética , beta Catenina/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Interferon gama/metabolismo , Transição Epitelial-Mesenquimal , Temozolomida/farmacologia , Temozolomida/uso terapêutico , Glicogênio Sintase Quinase 3 beta , Resistencia a Medicamentos Antineoplásicos , Linhagem Celular Tumoral , Movimento Celular , Glioma/genética , Fenótipo , Receptores ErbB/metabolismo , Proliferação de Células , Regulação Neoplásica da Expressão Gênica
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