本文采用完全活性空间自洽场(complete active space self-consistent field,CASSCF)和加戴维森校正的多参考组态相互作用(multireference configuration interaction with Davidson correction,MRCI+Q)方法,研究了超氧阴离子(O_(2)^(-)...本文采用完全活性空间自洽场(complete active space self-consistent field,CASSCF)和加戴维森校正的多参考组态相互作用(multireference configuration interaction with Davidson correction,MRCI+Q)方法,研究了超氧阴离子(O_(2)^(-))的低激发电子态及自旋-轨道耦合(spin-orbit coupling,SOC)效应对电子态的影响.使用aug-cc-pV5Z-dk基组,计算了O_(2)^(-)第一和第二解离极限对应的42个Λ-S态的势能曲线(potential energy curves,PECs)以及束缚态的光谱常数.同时考虑SOC效应,计算了这42个Λ-S态分裂形成的84个Ω态的PECs和部分束缚态的光谱常数.其中第一解离极限结果与已有文献高度一致,第二解离极限结果为本文计算提供.这些结果为研究O_(2)^(-)的电子结构和光谱性质提供了重要的理论依据.针对a^(4)Σ_(4)^(-)态的双势阱现象,本文通过比较不同基组下的计算结果,证实了a^(4)Σ_(4)^(-)态的双势阱形成源于与a^(4)Σ_(4)^(-)态的避免交叉影响.此外,研究发现基组大小直接影响a^(4)Σ_(4)^(-)态的首个势阱深度,这进一步表明基组选择对光谱常数计算的精确性至关重要.展开更多
Background:Atherosclerosis(AS)is a chronic progressive inflammatory disease,and plaque stability plays a critical role in preventing acute events.Tanyu Tongzhi formula(TTF),a traditional Chinese medicine,has potential...Background:Atherosclerosis(AS)is a chronic progressive inflammatory disease,and plaque stability plays a critical role in preventing acute events.Tanyu Tongzhi formula(TTF),a traditional Chinese medicine,has potential therapeutic effects on AS.Methods:We used an AS animal model to examine the effects of TTF on atherosclerotic plaque vulnerability and CD40^(+)monocyte differentiation.AS plaque area,collagen content,and lipid area were assessed using histological staining.AS plaque-related biomarkers(monocyte chemoattractant protein 1(MCP-1),monocyte plus macrophage(MOMA-2),von Willebrand factor(vWF),CD31,and alpha-smooth muscle actin(α-SMA))were detected using immunohistochemistry.Inflammatory cytokines were determined using enzyme-linked immunosorbent assay.CD40 mRNA expression was detected by real-time quantitative PCR.CD40^(+)monocyte differentiation was evaluated by flow cytometry analysis in ApoE-/-mice and peripheral blood mononuclear cells(PBMCs).AMPK/NF-κB signaling pathways-related protein expression was investigated through western blotting.Results:TTF treatment reduced AS plaque area,collagen content,and lipid area in AS model mice.Levels of MCP-1,MOMA-2,vWF,and CD31 were decreased,whileα-SMA level was increased by TTF in model mice.TTF reduced inflammatory cytokines levels,including tumor necrosis factor receptor-α(TNF-α),high-sensitivity C-reactive protein(hs-CRP),and interleukin-6(IL-6).TTF inhibited CD40^(+)monocyte differentiation and decreased the number of CD40^(+)/CD40-and Ly6C^(+)/Ly6C-cells and M1/M2 ratio in AS model mice and human PBMCs.Additionally,TTF modulated the AMPK/NF-κB signaling pathway in human PBMCs.Conclusion:TTF attenuates atherosclerotic plaque vulnerability by inhibiting CD40^(+)monocyte differentiation,possibly through the regulation of the AMPK/NF-κB signaling pathway.These findings suggest that TTF could be a potential therapeutic agent for preventing plaque rupture and subsequent cardiovascular events in patients with AS.展开更多
文摘目的探讨增强T2^(*)加权血管成像(enhanced T2 star-weighted angiography,ESWAN)序列中R2^(*)值、相位值、幅度值在T2WI低信号肾脏病变良恶性鉴别诊断中的可行性。材料与方法回顾性收集行ESWAN检查、经病理组织学证实的145例T2WI低信号肾脏病变患者(共145个病灶,恶性病变112个,良性病变33个)的术前MRI图像。在肿瘤最大面积的层面上绘制肿瘤T2WI低信号的感兴趣区。通过Kruskal-Wallis检验、卡方检验对参数进行比较,将有统计学意义的参数进行联合,通过多变量logistic回归建立模型,分析差异有统计学意义的参数,并且绘制其鉴别T2WI低信号肾脏病变良恶性的受试者工作特征(receiver operating characteristic,ROC)曲线,采用DeLong检验评价其诊断效能。结果R2^(*)值和幅度值鉴别T2WI低信号肾脏病变良恶性差异具有统计学意义(P=0.001)。R2^(*)值的ROC曲线下面积(area under the curve,AUC)为0.891[95%置信区间(confidence interval,CI):0.829~0.937,P<0.001],敏感度、特异度分别为97.3%、72.7%;幅度值的AUC为0.869(95%CI:0.803~0.920,P<0.001),敏感度、特异度分别为86.6%、81.8%;相位值的AUC为0.563(95%CI:0.478~0.645,P=0.249),敏感度、特异度分别为67.9%、54.6%;R2^(*)值联合幅度值的AUC为0.886(95%CI:0.823~0.933,P<0.001),敏感度、特异度分别为97.3%、72.7%;R2^(*)值联合病变长径的AUC为0.894(95%CI:0.832~0.939,P<0.001),敏感度、特异度分别为92.0%、81.8%;幅度值联合病变长径的AUC为0.858(95%CI:0.790~0.910,P<0.001),敏感度、特异度分别为75.9%、90.9%。结论R2^(*)值、R2^(*)值联合病变长径、R2^(*)值联合幅度值是鉴别T2WI低信号肾脏病变良恶性的有效方法,R2^(*)值联合病变长径具有更好的诊断性能。
文摘本文采用完全活性空间自洽场(complete active space self-consistent field,CASSCF)和加戴维森校正的多参考组态相互作用(multireference configuration interaction with Davidson correction,MRCI+Q)方法,研究了超氧阴离子(O_(2)^(-))的低激发电子态及自旋-轨道耦合(spin-orbit coupling,SOC)效应对电子态的影响.使用aug-cc-pV5Z-dk基组,计算了O_(2)^(-)第一和第二解离极限对应的42个Λ-S态的势能曲线(potential energy curves,PECs)以及束缚态的光谱常数.同时考虑SOC效应,计算了这42个Λ-S态分裂形成的84个Ω态的PECs和部分束缚态的光谱常数.其中第一解离极限结果与已有文献高度一致,第二解离极限结果为本文计算提供.这些结果为研究O_(2)^(-)的电子结构和光谱性质提供了重要的理论依据.针对a^(4)Σ_(4)^(-)态的双势阱现象,本文通过比较不同基组下的计算结果,证实了a^(4)Σ_(4)^(-)态的双势阱形成源于与a^(4)Σ_(4)^(-)态的避免交叉影响.此外,研究发现基组大小直接影响a^(4)Σ_(4)^(-)态的首个势阱深度,这进一步表明基组选择对光谱常数计算的精确性至关重要.
基金Natural Science Foundation of Zhejiang Province(grant number LY20H290005)Key Research and Development Program of Zhejiang Province(grant number 2020C03119)+2 种基金National Natural Science Foundation of China(grant numbers 81673706,81973579,82174150)Science and Technology Program of Zhejiang Traditional Chinese Medicine(grant number 2018ZY005)TCM science and Technology Foundation Project of Zhejiang Province(grant number 2023ZL411).
文摘Background:Atherosclerosis(AS)is a chronic progressive inflammatory disease,and plaque stability plays a critical role in preventing acute events.Tanyu Tongzhi formula(TTF),a traditional Chinese medicine,has potential therapeutic effects on AS.Methods:We used an AS animal model to examine the effects of TTF on atherosclerotic plaque vulnerability and CD40^(+)monocyte differentiation.AS plaque area,collagen content,and lipid area were assessed using histological staining.AS plaque-related biomarkers(monocyte chemoattractant protein 1(MCP-1),monocyte plus macrophage(MOMA-2),von Willebrand factor(vWF),CD31,and alpha-smooth muscle actin(α-SMA))were detected using immunohistochemistry.Inflammatory cytokines were determined using enzyme-linked immunosorbent assay.CD40 mRNA expression was detected by real-time quantitative PCR.CD40^(+)monocyte differentiation was evaluated by flow cytometry analysis in ApoE-/-mice and peripheral blood mononuclear cells(PBMCs).AMPK/NF-κB signaling pathways-related protein expression was investigated through western blotting.Results:TTF treatment reduced AS plaque area,collagen content,and lipid area in AS model mice.Levels of MCP-1,MOMA-2,vWF,and CD31 were decreased,whileα-SMA level was increased by TTF in model mice.TTF reduced inflammatory cytokines levels,including tumor necrosis factor receptor-α(TNF-α),high-sensitivity C-reactive protein(hs-CRP),and interleukin-6(IL-6).TTF inhibited CD40^(+)monocyte differentiation and decreased the number of CD40^(+)/CD40-and Ly6C^(+)/Ly6C-cells and M1/M2 ratio in AS model mice and human PBMCs.Additionally,TTF modulated the AMPK/NF-κB signaling pathway in human PBMCs.Conclusion:TTF attenuates atherosclerotic plaque vulnerability by inhibiting CD40^(+)monocyte differentiation,possibly through the regulation of the AMPK/NF-κB signaling pathway.These findings suggest that TTF could be a potential therapeutic agent for preventing plaque rupture and subsequent cardiovascular events in patients with AS.
