为了探明叶面喷施硒条件土壤施磷对甘薯(Ipomoea batatas(L.)Lam.)硒吸收、分配和转化的影响,于2021和2022年在山东莱阳市开展连续2年的田间试验。采用裂区试验设计,主区纯硒用量分别为0 g hm^(–2)(Se0)和150 g hm^(–2)(Se_(1)),副区P...为了探明叶面喷施硒条件土壤施磷对甘薯(Ipomoea batatas(L.)Lam.)硒吸收、分配和转化的影响,于2021和2022年在山东莱阳市开展连续2年的田间试验。采用裂区试验设计,主区纯硒用量分别为0 g hm^(–2)(Se0)和150 g hm^(–2)(Se_(1)),副区P_(2)O_(5)施用量分别为0 kg hm^(–2)(P_(0))、75 kg hm^(–2)(P_(1))、225 kg hm^(–2)(P_(2)),测定甘薯各器官干物质量、总硒和有机硒含量并计算硒利用率。结果表明,施磷可显著增加甘薯不同器官干物质量,施硒对不同器官干物质量的影响不显著。施磷可显著提高甘薯块根中硒含量和硒累积量,与不施磷(P_(0))相比,施用低磷(P_(1))可使施硒条件下块根硒含量和硒累积量平均增加19.54%和27.74%,施用高磷(P_(2))可使施硒条件下块根硒含量和硒累积量平均增加40.24%和52.64%。施硒条件下施磷还可提高甘薯块根中的硒分配率和硒利用率,施用低磷(P_(1))和施用高磷(P_(2))块根硒分配率较不施磷(P_(0))平均提高7.77和12.46个百分点,硒利用率平均提高1.81和3.36个百分点,施磷对甘薯全株硒利用率影响不显著。施磷提高了甘薯块根中总硒含量的同时,还提高了块根中有机硒含量,但对块根中有机硒占总硒的比例影响不显著。综上所述,富硒甘薯生产中,适量增加施磷量可以提高甘薯不同器官干物质量,增加块根中的总硒和有机硒含量,提高硒利用率,但应避免过量施磷带来的环境风险。展开更多
目的识别癌症患者补充替代疗法特征及对症状群的干预效果,为患者症状群管理提供借鉴和参考。方法采用范围综述的方法,检索PubMed,Cochrane Library,Web of Science,Embase,PsycINFO,CINAHL,中国知网,万方和维普数据库,检索时限为2016年...目的识别癌症患者补充替代疗法特征及对症状群的干预效果,为患者症状群管理提供借鉴和参考。方法采用范围综述的方法,检索PubMed,Cochrane Library,Web of Science,Embase,PsycINFO,CINAHL,中国知网,万方和维普数据库,检索时限为2016年1月至2024年1月。结果纳入20项研究,从癌症研究对象、补充替代疗法干预特征、症状群类型、补充替代疗法效果评价4方面进行概括和总结。乳腺癌、晚期癌症和放化疗癌症患者是症状群管理中常见的研究对象;运动疗法、行为认知干预、中医特色疗法、多学科协作模式及特异性干预方案是症状群管理中常见的补充替代疗法;疲乏、心理、疼痛、消化道症状群是症状群管理中常见的干预类型。结论不同补充替代疗法类型,其干预效果及核心症状群尚存在差异,部分干预方案的效果有待进一步明确;现有补充替代疗法干预方案仍存在许多不足之处,未来研究应关注症状群的前哨和核心症状,基于症状管理理论构建规范化、个性化的症状群干预方案,从而更好地管理癌症患者的症状群。展开更多
目的探讨SMRACAD1对胃癌细胞增殖和侵袭的影响及作用机制。方法对癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库中373个胃癌组织和32个正常组织的SMRACAD1表达进行差异分析及京都基因与基因组百科全书(Kyoto Encyclopedia of Gen...目的探讨SMRACAD1对胃癌细胞增殖和侵袭的影响及作用机制。方法对癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库中373个胃癌组织和32个正常组织的SMRACAD1表达进行差异分析及京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)富集分析,采用蛋白印迹法(Western blot,WB)和实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction,qPCR)检测SMRACAD1在人正常胃黏膜上皮细胞(GES-1)、人胃癌细胞(HGC-27)和人胃腺癌细胞(AGS)的表达。构建AGS细胞下调SMRACAD1表达和空白对照模型,平板克隆和CCK-8实验检测AGS细胞的增殖能力,划痕实验检测迁移能力,Transwell实验检测迁移和侵袭能力。WB检测SMRACAD1下调后对上皮-间充质转化(epithelial-mesenchymal transition,EMT)相关蛋白表达(E-cadherin、N-cadherin、Vimentin、Snail)及PI3K/AKT/mTOR信号通路的影响。结果SMRACAD1在胃癌组织和AGS细胞中高表达。下调SMRACAD1表达抑制了AGS细胞增殖、侵袭和迁移能力(P<0.05),抑制了AGS细胞EMT过程和PI3K/AKT/mTOR信号通路的激活。结论SMARCDA1在胃癌组织和胃癌细胞系中表达上调,通过抑制PI3K/AKT/mTOR信号通路激活下调SMRACAD1表达可抑制胃癌细胞的增殖、侵袭、迁移和EMT。展开更多
Breast cancer,a predominant global health issue,requires ongoing exploration of new therapeutic strategies.Palbociclib(PAL),a well-known cyclin-dependent kinase(CDK)inhibitor,plays a critical role in breast cancer tre...Breast cancer,a predominant global health issue,requires ongoing exploration of new therapeutic strategies.Palbociclib(PAL),a well-known cyclin-dependent kinase(CDK)inhibitor,plays a critical role in breast cancer treatment.While its efficacy is recognized,the interplay between PAL and cellular autophagy,particularly in the context of the RAF/MEK/ERK signaling pathway,remains insufficiently explored.This study investigates PAL’s inhibitory effects on breast cancer using both in vitro(MCF7 and MDA-MB-468 cells)and in vivo(tumor-bearing nude mice)models.Aimed at elucidating the impact of PAL on autophagic processes and exploring the potential of combining it with trametinib(TRA),an MEK inhibitor,our research seeks to address the challenge of PAL-induced drug resistance.Ourfindings reveal that PAL significantly decreases the viability of MCF7 and MDA-MB-468 cells and reduces tumor size in mice while showing minimal cytotoxicity in MCF10A cells.However,PAL also induces protective autophagy,potentially leading to drug resistance via the RAF/MEK/ERK pathway activation.Introducing TRA effectively neutralized this autophagy,enhancing PAL’s anti-tumor efficacy.A combination of PAL and TRA synergistically reduced cell viability and proliferation,and in vivo studies showed notable tumor size reduction.In conclusion,the PAL and TRA combination emerges as a promising strategy for overcoming PAL-induced resistance,offering a new horizon in breast cancer treatment.展开更多
文摘为了探明叶面喷施硒条件土壤施磷对甘薯(Ipomoea batatas(L.)Lam.)硒吸收、分配和转化的影响,于2021和2022年在山东莱阳市开展连续2年的田间试验。采用裂区试验设计,主区纯硒用量分别为0 g hm^(–2)(Se0)和150 g hm^(–2)(Se_(1)),副区P_(2)O_(5)施用量分别为0 kg hm^(–2)(P_(0))、75 kg hm^(–2)(P_(1))、225 kg hm^(–2)(P_(2)),测定甘薯各器官干物质量、总硒和有机硒含量并计算硒利用率。结果表明,施磷可显著增加甘薯不同器官干物质量,施硒对不同器官干物质量的影响不显著。施磷可显著提高甘薯块根中硒含量和硒累积量,与不施磷(P_(0))相比,施用低磷(P_(1))可使施硒条件下块根硒含量和硒累积量平均增加19.54%和27.74%,施用高磷(P_(2))可使施硒条件下块根硒含量和硒累积量平均增加40.24%和52.64%。施硒条件下施磷还可提高甘薯块根中的硒分配率和硒利用率,施用低磷(P_(1))和施用高磷(P_(2))块根硒分配率较不施磷(P_(0))平均提高7.77和12.46个百分点,硒利用率平均提高1.81和3.36个百分点,施磷对甘薯全株硒利用率影响不显著。施磷提高了甘薯块根中总硒含量的同时,还提高了块根中有机硒含量,但对块根中有机硒占总硒的比例影响不显著。综上所述,富硒甘薯生产中,适量增加施磷量可以提高甘薯不同器官干物质量,增加块根中的总硒和有机硒含量,提高硒利用率,但应避免过量施磷带来的环境风险。
文摘目的识别癌症患者补充替代疗法特征及对症状群的干预效果,为患者症状群管理提供借鉴和参考。方法采用范围综述的方法,检索PubMed,Cochrane Library,Web of Science,Embase,PsycINFO,CINAHL,中国知网,万方和维普数据库,检索时限为2016年1月至2024年1月。结果纳入20项研究,从癌症研究对象、补充替代疗法干预特征、症状群类型、补充替代疗法效果评价4方面进行概括和总结。乳腺癌、晚期癌症和放化疗癌症患者是症状群管理中常见的研究对象;运动疗法、行为认知干预、中医特色疗法、多学科协作模式及特异性干预方案是症状群管理中常见的补充替代疗法;疲乏、心理、疼痛、消化道症状群是症状群管理中常见的干预类型。结论不同补充替代疗法类型,其干预效果及核心症状群尚存在差异,部分干预方案的效果有待进一步明确;现有补充替代疗法干预方案仍存在许多不足之处,未来研究应关注症状群的前哨和核心症状,基于症状管理理论构建规范化、个性化的症状群干预方案,从而更好地管理癌症患者的症状群。
文摘目的探讨SMRACAD1对胃癌细胞增殖和侵袭的影响及作用机制。方法对癌症基因组图谱(The Cancer Genome Atlas,TCGA)数据库中373个胃癌组织和32个正常组织的SMRACAD1表达进行差异分析及京都基因与基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)富集分析,采用蛋白印迹法(Western blot,WB)和实时荧光定量聚合酶链反应(quantitative real-time polymerase chain reaction,qPCR)检测SMRACAD1在人正常胃黏膜上皮细胞(GES-1)、人胃癌细胞(HGC-27)和人胃腺癌细胞(AGS)的表达。构建AGS细胞下调SMRACAD1表达和空白对照模型,平板克隆和CCK-8实验检测AGS细胞的增殖能力,划痕实验检测迁移能力,Transwell实验检测迁移和侵袭能力。WB检测SMRACAD1下调后对上皮-间充质转化(epithelial-mesenchymal transition,EMT)相关蛋白表达(E-cadherin、N-cadherin、Vimentin、Snail)及PI3K/AKT/mTOR信号通路的影响。结果SMRACAD1在胃癌组织和AGS细胞中高表达。下调SMRACAD1表达抑制了AGS细胞增殖、侵袭和迁移能力(P<0.05),抑制了AGS细胞EMT过程和PI3K/AKT/mTOR信号通路的激活。结论SMARCDA1在胃癌组织和胃癌细胞系中表达上调,通过抑制PI3K/AKT/mTOR信号通路激活下调SMRACAD1表达可抑制胃癌细胞的增殖、侵袭、迁移和EMT。
基金supported by the Sichuan Science and Technology Program(Grant Nos.2020YJ0494,24GJHZ0058,21RCYJ0021,and 2022YFS0620)the National Natural Science Foundation of China(Grant No.81903829)+1 种基金the Southwest Medical University Science and Technology Program(Grant Nos.2021ZKZD015,2021ZKZD018,and 2021ZKMS046)the Macao Science and Technology Development Fund of Macao SAR(Project Nos.SKLQRCM(MUST)-2020-2022 and MUST-SKL-2021-005).
文摘Breast cancer,a predominant global health issue,requires ongoing exploration of new therapeutic strategies.Palbociclib(PAL),a well-known cyclin-dependent kinase(CDK)inhibitor,plays a critical role in breast cancer treatment.While its efficacy is recognized,the interplay between PAL and cellular autophagy,particularly in the context of the RAF/MEK/ERK signaling pathway,remains insufficiently explored.This study investigates PAL’s inhibitory effects on breast cancer using both in vitro(MCF7 and MDA-MB-468 cells)and in vivo(tumor-bearing nude mice)models.Aimed at elucidating the impact of PAL on autophagic processes and exploring the potential of combining it with trametinib(TRA),an MEK inhibitor,our research seeks to address the challenge of PAL-induced drug resistance.Ourfindings reveal that PAL significantly decreases the viability of MCF7 and MDA-MB-468 cells and reduces tumor size in mice while showing minimal cytotoxicity in MCF10A cells.However,PAL also induces protective autophagy,potentially leading to drug resistance via the RAF/MEK/ERK pathway activation.Introducing TRA effectively neutralized this autophagy,enhancing PAL’s anti-tumor efficacy.A combination of PAL and TRA synergistically reduced cell viability and proliferation,and in vivo studies showed notable tumor size reduction.In conclusion,the PAL and TRA combination emerges as a promising strategy for overcoming PAL-induced resistance,offering a new horizon in breast cancer treatment.