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2.
Technol Cancer Res Treat ; 20: 15330338211041472, 2021.
Article in English | MEDLINE | ID: mdl-34569862

ABSTRACT

Aims: This review aims to identify lipid biomarkers of non-small cell lung cancer (NSCLC) in human tissue samples and discuss the roles of lipids in tissue molecular identification, the discovery of potential biomarkers, and surgical margin assessment. Methods: A review of the literature focused on lipid-related research using mass spectrometry (MS) techniques in human NSCLC tissues from January 1, 2015, to November 20, 2020, was conducted. The quality of included studies was assessed using the QUADAS-2 tool. Results: Twelve studies met the inclusion criteria and were included in the review. The risk of bias was unclear in the majority of the studies. The contents of lipids including fatty acids, phosphatidyl choline, phosphatidyl ethanolamine, phosphatidyl inositol, cardiolipin, phosphatidyl serine, phosphatidyl glycerol, ceramide, lysophosphatidylethanolamine, lysophosphatidylcholine, and lysophosphatidylglycerol differed significantly between cancer and healthy tissues. The sensitivity or specificity of the discrimination model was reported in 8 studies, and the sensitivity and specificity varied among the reported methods. The lipid profiles differed between adenocarcinoma and squamous cell carcinoma NSCLC subtypes. Conclusion: In preclinical studies, MS analysis and multiple discrimination models can be combined to distinguish NSCLC tissues from healthy tissues based on lipid profiles, which provides a new opportunity to evaluate the surgical margin and cancer subtype intraoperatively. Future studies should provide guidance for selecting patients and discrimination models to develop an improved method for clinical application.


Subject(s)
Adenocarcinoma/metabolism , Carcinoma, Non-Small-Cell Lung/metabolism , Carcinoma, Squamous Cell/metabolism , Lipid Metabolism , Lung Neoplasms/metabolism , Lung/metabolism , Biomarkers, Tumor/metabolism , Carcinoma, Non-Small-Cell Lung/diagnosis , Carcinoma, Non-Small-Cell Lung/pathology , Carcinoma, Non-Small-Cell Lung/surgery , Humans , Lung Neoplasms/diagnosis , Lung Neoplasms/pathology , Lung Neoplasms/surgery , Margins of Excision , Mass Spectrometry , Neoplasm Staging , Sensitivity and Specificity
3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-610486

ABSTRACT

Objective To investigate the changes of cardiac sinus node connexin 45 (Cx45), connexin 31.9(Cx31.9) of gap junction in rabbits'' sinus bradycardia model caused by dexmedetomidine, and to discuss whether the negative frequency and negative conduction caused by Dexmedetomidine are related to the expression changes of connexin.Methods Forty-eight healthy adult New Zealand rabbits were divided into three groups (n=16).Sinus bradycardia rabbits were prepared by intravenous injecting Dexmedetomidine through ear vein.After rabbits were anesthetized by sodium pentobarbital, basic procedures were quickly completed in order to monitor MAP and ECG.Rabbits in group C were injected with normal saline.Rabbits in group D1 were injected a loading dose of dexmedetomidine 10 μg/kg for 10 min, and then continuously pumped 5 μg·kg-1·h-1 for 50 min.Rabbits in group D2 were pumped a loading dose of dexmedetomidine 60 μg/kg for 10 min, and then continuously pumped 30 μg·kg-1·h-1 for 50 min.After observation hearts were quickly removed and sinus node tissue was dissected.The average optical density of sinus node Cx45, Cx31.9 were detected by immunohistochemistry, and the genes expression were detected by real-time quantitative.Results Cx45 gene expression of group D2 showed remarkable increase than groups C and D1(P<0.05), there were no significant differences between groups D1 and C, Cx45 average optical density change were consistent with the gene expression.Cx31.9 gene expression of group D1 showed a more remarkable increase than group C(P<0.05), there were no significant differences between groups D2 and C,D1 and D2, Cx31.9 average optical density changes were consistent with the gene expression.Conclusion Dexmedetomidine increases the expression of low electrical conductivity Cx45, Cx31.9 of gap junction on rabbits'' sinus node, which is one of the possibly reasons that slow down cardiac conduction velocity in sinus node.

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