Objective: To compare the intraoperative signal-to-noise ratio (SNR), reproducibility and rapidity of popliteal fossa (PF), optimized P37, standard P37 and P31 potentials. Methods: Raw sweeps and 11 averages doubling ...Objective: To compare the intraoperative signal-to-noise ratio (SNR), reproducibility and rapidity of popliteal fossa (PF), optimized P37, standard P37 and P31 potentials. Methods: Raw sweeps and 11 averages doubling sweep number from 2 to 2048 were compared in 37 patients undergoing scoliosis surgery. Optimized (highest amplitude or SNR) P37 derivations were Cz-CPc (22), CPz-CPc (27), Pz-CPc (7), iCPi-CPc (8), CPi-CPc (1), Cz-Pz (2)orPz-FPz (3), and in two patients with non-decussation, Cz-CPi (1) or CPz-CPi (3). Standard P37 and P31 derivations were CPz-FPz and FPz-C5S. Signal amplitude was measured in 2048 sweep averages; peak noise was measured in raw sweeps and ±averages; SNR was amplitude/noise. Visual superimposability and < 20-30%amplitude variation determined reproducibility. Sweeps to reproducibility determined rapidity. Results: The SNR order was PFoptimized P37 > standard P37 > P31. Mean optimized P37 SNR advantages over the standard P37 and P31 were 2.1:1 and 4.9:1. SNR had powerful non-linear correlations to reproducibility and rapidity. Median sweeps to reproducibility were PF: 2, optimized P37: 128, standard P37: 512 and P31: 1024. EEG noise was greatest in FPz derivations. Burst-suppression increased scalp potential SNR and rapidity. Conclusions: Optimized P37 and PF recordings are most rapidly reproducible due to superior SNRs and are recommended. FPz should be avoided. Burst-suppression may be desirable. Significance: CPz-FPz and FPz-C5S should no longer be standard.展开更多
Objectives:Chemotherapy-induced lung inflammation limits the efficacy of anticancer therapies such as gefitinib in non-small cell lung cancer(NSCLC).Glutamic acid-leucine-arginine positive(ELR+)CXC chemokines and thei...Objectives:Chemotherapy-induced lung inflammation limits the efficacy of anticancer therapies such as gefitinib in non-small cell lung cancer(NSCLC).Glutamic acid-leucine-arginine positive(ELR+)CXC chemokines and their receptors,CXC chemokine receptor 1 and 2(CXCR1 and CXCR2),mediate both inflammatory responses and tumor progression.This study evaluated the effects of CXCR1/2 antagonism by G31P,a CXC motif chemokine ligand 8(CXCL8)-mutated peptide,alone or in combination with gefitinib,on lung cancer growth and chemotherapyinduced pulmonary inflammation.Methods:Human NSCLC cell lines(A549 and H460)were treated with gefitinib and/or G31P.Cell proliferation,apoptosis,and signaling pathways,including protein kinase B(AKT)and extracellular signal-regulated kinase(ERK)phosphorylation,were evaluated by cell counting kit-8(CCK-8)assay,flow cytometry,and Western blotting.An orthotopic lung tumor xenograft model was established in BALB/c nude mice to evaluate tumor growth,metastasis,cytokine expression,and lung histopathology.A bleomycin-induced lung injury model was also used to assess the anti-inflammatory effects of G31P,with or without gefitinib,by quantitative reverse transcription polymerase chain reaction(qRT-PCR)and flowcytometry of inflammatorymarkers.Results:G31P andGefitinib,either alone or combined,inhibited proliferation and migration of A549 and H460 cells in vitro.Combination treatment effectively reducedAKT and ERKphosphorylation in both cell lines.In vivo,G31Pwith gefitinib significantly suppressed tumor growth,metastasis,and increased apoptosis.G31P decreased CXCL1 and CXCL2,and tumor necrosis factoralpha(TNF-α)mRNA levels,lung hydroxyproline content,and myeloperoxidase(MPO)activity in the lungs of mice.In the bleomycin-induced lung injury model,G31P similarly reduced inflammatory responses.Conclusion:CXCR1/2 antagonismby G31P attenuates chemotherapy-induced pulmonary inflammation and enhances the anti-tumor efficacy of gefitinib in NSCLC.These findings support the therapeutic potential of G31P as an adjuvant to epidermal growth factor receptor tyrosine kinase inhibitors(EGFR-TKIs)to improve clinical outcomes by limiting inflammation.展开更多
文摘Objective: To compare the intraoperative signal-to-noise ratio (SNR), reproducibility and rapidity of popliteal fossa (PF), optimized P37, standard P37 and P31 potentials. Methods: Raw sweeps and 11 averages doubling sweep number from 2 to 2048 were compared in 37 patients undergoing scoliosis surgery. Optimized (highest amplitude or SNR) P37 derivations were Cz-CPc (22), CPz-CPc (27), Pz-CPc (7), iCPi-CPc (8), CPi-CPc (1), Cz-Pz (2)orPz-FPz (3), and in two patients with non-decussation, Cz-CPi (1) or CPz-CPi (3). Standard P37 and P31 derivations were CPz-FPz and FPz-C5S. Signal amplitude was measured in 2048 sweep averages; peak noise was measured in raw sweeps and ±averages; SNR was amplitude/noise. Visual superimposability and < 20-30%amplitude variation determined reproducibility. Sweeps to reproducibility determined rapidity. Results: The SNR order was PFoptimized P37 > standard P37 > P31. Mean optimized P37 SNR advantages over the standard P37 and P31 were 2.1:1 and 4.9:1. SNR had powerful non-linear correlations to reproducibility and rapidity. Median sweeps to reproducibility were PF: 2, optimized P37: 128, standard P37: 512 and P31: 1024. EEG noise was greatest in FPz derivations. Burst-suppression increased scalp potential SNR and rapidity. Conclusions: Optimized P37 and PF recordings are most rapidly reproducible due to superior SNRs and are recommended. FPz should be avoided. Burst-suppression may be desirable. Significance: CPz-FPz and FPz-C5S should no longer be standard.
基金supported by grants from the National Natural Science Foundation of China,No.U1604174Health Commission of Henan Province-Province and Ministry Co-Construction Project,Nos.20170123,SBGJ202002004Health Commission of Henan Province-Research Innovative Talents Project(51282).
文摘Objectives:Chemotherapy-induced lung inflammation limits the efficacy of anticancer therapies such as gefitinib in non-small cell lung cancer(NSCLC).Glutamic acid-leucine-arginine positive(ELR+)CXC chemokines and their receptors,CXC chemokine receptor 1 and 2(CXCR1 and CXCR2),mediate both inflammatory responses and tumor progression.This study evaluated the effects of CXCR1/2 antagonism by G31P,a CXC motif chemokine ligand 8(CXCL8)-mutated peptide,alone or in combination with gefitinib,on lung cancer growth and chemotherapyinduced pulmonary inflammation.Methods:Human NSCLC cell lines(A549 and H460)were treated with gefitinib and/or G31P.Cell proliferation,apoptosis,and signaling pathways,including protein kinase B(AKT)and extracellular signal-regulated kinase(ERK)phosphorylation,were evaluated by cell counting kit-8(CCK-8)assay,flow cytometry,and Western blotting.An orthotopic lung tumor xenograft model was established in BALB/c nude mice to evaluate tumor growth,metastasis,cytokine expression,and lung histopathology.A bleomycin-induced lung injury model was also used to assess the anti-inflammatory effects of G31P,with or without gefitinib,by quantitative reverse transcription polymerase chain reaction(qRT-PCR)and flowcytometry of inflammatorymarkers.Results:G31P andGefitinib,either alone or combined,inhibited proliferation and migration of A549 and H460 cells in vitro.Combination treatment effectively reducedAKT and ERKphosphorylation in both cell lines.In vivo,G31Pwith gefitinib significantly suppressed tumor growth,metastasis,and increased apoptosis.G31P decreased CXCL1 and CXCL2,and tumor necrosis factoralpha(TNF-α)mRNA levels,lung hydroxyproline content,and myeloperoxidase(MPO)activity in the lungs of mice.In the bleomycin-induced lung injury model,G31P similarly reduced inflammatory responses.Conclusion:CXCR1/2 antagonismby G31P attenuates chemotherapy-induced pulmonary inflammation and enhances the anti-tumor efficacy of gefitinib in NSCLC.These findings support the therapeutic potential of G31P as an adjuvant to epidermal growth factor receptor tyrosine kinase inhibitors(EGFR-TKIs)to improve clinical outcomes by limiting inflammation.
