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1.
Heliyon ; 9(12): e22523, 2023 Dec.
Article in English | MEDLINE | ID: mdl-38046149

ABSTRACT

The application of robotic surgery technologies in neurological surgeries resulted in some advantages compared to traditional surgeries, including higher accuracy and dexterity enhancement. Its success in various surgical fields, especially in urology, cardiology, and gynecology surgeries was reported in previous studies, and similar advantages in neurological surgeries are expected. Surgeries in the central nervous system with the pathology of millimeters through small working channels around vital tissue need especially high precision. Applying robotic surgery is therefore an interesting dilemma for these situations. This article reviews various studies published on the application of brain and spine robotic surgery and discusses the current application of robotic technology in neurological cases.

2.
J Assist Reprod Genet ; 38(10): 2631-2639, 2021 Oct.
Article in English | MEDLINE | ID: mdl-33834328

ABSTRACT

OBJECTIVE: To study the correlation between SNPs at phosphatidylinositol-4, 5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) rs9838117 site, erb-b2 receptor tyrosine kinase 2 (ERBB2) rs1058808 site, and their interactions with environmental factors and the epithelial ovarian cancer (EOC) risk. METHODS: Sanger sequencing was used to analyze the genotypes of PIK3CA rs9838117 and ERBB2 rs1058808 site in 587 patients with epithelial ovarian cancer (EOC). Multi-factor dimensionality reduction (MDR) was applied to analyze the interaction between PIK3CA rs9838117 and ERBB2 rs1058808 site and the clinical data. RESULTS: The risk of EOC in T allele carriers at PIK3CA rs9838117 was 1.95 times (95%CI: 1.55-2.46, P<0.01) that of G allele carriers. The risk of EOC in G allele carriers at ERBB2 rs1058808 was as 0.64 times (95%CI: 0.54-0.75, P <0.01) as the risk for C allele carriers. In the interaction model between clinical data, PIK3CA rs9838117 site and ERBB2 rs1058808 SNP site, EOC risk in high-risk combination was 3.10 times (95%CI: 1.49-6.46, P <0.01) that of low-risk combination. CONCLUSION: The SNPs at PIK3CA rs9838117 and ERBB2 rs1058808 loci were associated with the risk of EOC.


Subject(s)
3' Untranslated Regions , Carcinoma, Ovarian Epithelial/pathology , Class I Phosphatidylinositol 3-Kinases/genetics , Gene-Environment Interaction , Ovarian Neoplasms/pathology , Polymorphism, Single Nucleotide , Receptor, ErbB-2/genetics , Adult , Aged , Carcinoma, Ovarian Epithelial/epidemiology , Carcinoma, Ovarian Epithelial/genetics , Carcinoma, Ovarian Epithelial/surgery , Case-Control Studies , Female , Genetic Predisposition to Disease , Humans , Middle Aged , Ovarian Neoplasms/epidemiology , Ovarian Neoplasms/genetics , Ovarian Neoplasms/surgery , Prognosis , Risk Factors
3.
Int J Biochem Cell Biol ; 93: 25-31, 2017 12.
Article in English | MEDLINE | ID: mdl-28851665

ABSTRACT

Aberrant expression of miR-130a is usually found in cancer studies; however, the role of miR-130a has seldom been reported in glioma. We explored miR-130a's function and the underlying mechanism in glioma. It was found that miR-130a expression was significantly down-regulated in glioma tissues and cell lines. Overexpression of miR-130a decreased glioma cell growth and invasion both in vitro and in vivo. We identified the oncogene HMGB2 as a downstream target of miR-130a by using luciferase and western blot assays. Knockdown of HMGB2 mimicked the effect of miR-130a in glioma cells. Taken together, our study demonstrate that miR-130a may function as a tumor suppressor in glioma and suggest that miR-130a is a potential therapeutic target for glioma patients.


Subject(s)
Down-Regulation , Epithelial-Mesenchymal Transition , Gene Expression Regulation, Neoplastic , Genes, Tumor Suppressor , Glioma/metabolism , HMGB2 Protein/metabolism , MicroRNAs/biosynthesis , Neoplasm Proteins/metabolism , RNA, Neoplasm/biosynthesis , Cell Line, Tumor , Glioma/genetics , HMGB2 Protein/genetics , Humans , MicroRNAs/genetics , Neoplasm Proteins/genetics , RNA, Neoplasm/genetics
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