介孔La_(1-x)Sr_(x)MnO_(3)催化剂的COK-12纳米浇铸法制备

钙钛矿型催化剂在汽车尾气净化方面具有良好的应用潜力。本文以表面活性剂P123为软模板剂,廉价的硅酸钠为硅源,在近中性条件下制备了介孔材料COK-12。并以此为基础,以对二甲苯为扩容剂对COK-12进行改性,得到了大孔径、有序的介孔材料。随后以改性介孔材料为模板剂,采用纳米浇铸法结合溶胶-凝胶法制备了介孔La_(0.8)Sr_(0.2)MnO_(3)催化剂。结果显示,在550℃下合成的催化剂具有较大的比表面积(72.11 m^(2)/g),表面Mn^(4+)/Mn^(3+)和O_(ads)/O_(lat)摩尔比最高。此外,样品的CO催化性能测试转化表明,550℃下合成的样品具有最好的催化活性和优秀的高温稳定性,其特征温度T_(50)和T_(90)分别为180和218℃。

NoV GⅡ.2亚型RT-RPA-CRISPR/Cas12a检测方法的建立

近年来,一种新的诺如病毒GⅡ.2亚型(norovirus GⅡ.2,NoV GⅡ.2)通过牡蛎等生食海鲜感染人群,引发急性胃肠炎,并在全球广泛传播。为实现NoV感染的现场诊断和快速疫情响应,亟需建立快速便捷的NoV GⅡ.2亚型核酸检测方法。本研究通过设计引物、crRNA,经优化反应条件后,建立了NoV GⅡ.2亚型RTRPA-CRISPR/Cas12a检测方法。结果显示:利用引物NoV-GⅡ.2-F1B和NoV-GⅡ.2-R1对NoV GⅡ.2标准RNA进行RT-RPA扩增,结合crRNA1介导的CRISPR/Cas12a报告体系,能在40 min内完成NoV GⅡ.2核酸检测;该方法检测灵敏度为10 copies/μL,且与轮状病毒、腺病毒、星形病毒、人副肠孤病毒、博卡病毒和札如病毒无交叉反应;应用该方法和qRT-PCR法,分别对30份临床模拟样本进行检测,发现总符合率达96.67%。结果表明,本研究建立的NoV GⅡ.2亚型RT-RPA-CRISPR/Cas12a检测方法无需依赖昂贵设备,具有灵敏度高、特异性强、操作便捷快速等特点,为NoV GⅡ.2感染的现场检测和防控提供了新方法。

Engineering of oxygen vacancy and bismuth cluster assisted ultrathin Bi_(12)O_(17)Cl_(2)nanosheets with efficient and selective photoreduction of CO_(2)to CO

The photocatalytic conversion of CO_(2)into solar‐powered fuels is viewed as a forward‐looking strategy to address energy scarcity and global warming.This work demonstrated the selective photoreduction of CO_(2)to CO using ultrathin Bi_(12)O_(17)Cl_(2)nanosheets decorated with hydrothermally synthesized bismuth clusters and oxygen vacancies(OVs).The characterizations revealed that the coexistences of OVs and Bi clusters generated in situ contributed to the high efficiency of CO_(2)–CO conversion(64.3μmol g^(−1)h^(−1))and perfect selectivity.The OVs on the facet(001)of the ultrathin Bi_(12)O_(17)Cl_(2)nanosheets serve as sites for CO_(2)adsorption and activation sites,capturing photoexcited electrons and prolonging light absorption due to defect states.In addition,the Bi‐cluster generated in situ offers the ability to trap holes and the surface plasmonic resonance effect.This study offers great potential for the construction of semiconductor hybrids as multiphotocatalysts,capable of being used for the elimination and conversion of CO_(2)in terms of energy and environment.

SR9009联合吲哚丙酸通过核因子κB信号通路减轻C2C12成肌细胞的炎症反应

背景:钟基因Rev-erbα参与调节炎症,但激活Rev-erbα会增加心脑血管疾病风险。为降低相关风险,探索Rev-erbα激动剂SR9009联合其他药物来减轻骨骼肌成肌细胞炎症,奠定治疗炎症相关性骨骼肌萎缩的理论基础。目的:探讨脂多糖刺激C2C12成肌细胞时吲哚丙酸、SR9009与核因子κB信号通路的关系。方法:①1μg/mL脂多糖刺激C2C12成肌细胞,RNA转录组测序结合KEGG通路富集分析信号通路。②CCK-8法检测C2C12成肌细胞活性,筛选吲哚丙酸的最佳给药浓度;然后将细胞分为空白对照组、脂多糖(1μg/mL)组、SR9009(10μmol/L)+脂多糖组、吲哚丙酸(80μmol/L)+脂多糖组、吲哚丙酸+SR9009+脂多糖组,ELISA检测细胞上清液中白细胞介素6水平,RT-qPCR检测白细胞介素6、肿瘤坏死因子α、Toll样受体4、CD14 mRNA表达,Western blot检测NF-κB p65、p-NF-κB p65蛋白表达。③siRNA敲减Rev-erbα,RT-qPCR评估敲减效率,检测白细胞介素6、肿瘤坏死因子αmRNA表达。结果与结论:①与空白对照组比较,脂多糖时间依赖性抑制成肌细胞融合形成肌管,白细胞介素6、肿瘤坏死因子αmRNA表达水平升高,细胞上清液中白细胞介素6水平显著升高;KEGG通路分析支持脂多糖刺激激活核因子κB信号通路。②吲哚丙酸浓度>80μmol/L时抑制C2C12成肌细胞活性;吲哚丙酸和SR9009通过抑制核因子κB信号通路发挥抗炎作用,降低白细胞介素6、肿瘤坏死因子α、Toll样受体4、CD14 mRNA表达水平,p-NF-κB p65/NF-κB p65蛋白表达比值低于脂多糖组。SR9009联合吲哚丙酸显著降低脂多糖诱导的炎症,Toll样受体4、CD14、白细胞介素6和肿瘤坏死因子αmRNA表达水平进一步下调,p-NF-κB p65/NF-κB p65蛋白表达比值显著低于吲哚丙酸+脂多糖组和SR9009+脂多糖组。③Rev-erbα随脂多糖刺激时间依赖性升高;siRNA敲减Rev-erbα效率达58%以上,成功敲减Rev-erbα后添加脂多糖,白细胞介素6和肿瘤坏死因子αmRNA表达较脂多糖组显著上调。④结果说明,Rev-erbα可以作为调节炎症反应的靶点,SR9009靶向激活Rev-erbα联合吲哚丙酸能抑制核因子κB信号通路显著减轻C2C12成肌细胞的炎症反应,联合抗炎效果优于单独干预。

Novel thick-target inverse kinematics method for the astrophysical ^(12)C+^(12)C fusion reaction

The ^(12)C+^(12)C fusion is one of the most important reactions in modern nuclear astrophysics.The trend and magnitude of the reaction rate within the Gamow window strongly influence various astrophysical processes.However,direct measurement of this reaction is extremely difficult,which makes it necessary to develop indirect methods.In this study,the ^(23)Na+p reaction system was used to study the compound nucleus ^(24)Mg.We employed a thick-target inverse kinematics method combined with theγ-charged-particle coincidence technique to measure the proton andα exit channels of ^(24)Mg.Technical details of the ^(23)Na+p thick-target inverse kinematics experiment and analysis are presented herein.

烧结助剂ZnO对Li_(6.5)La_(3)Zr_(1.5)Nb_(0.5)O_(12)固态电解质离子电导率及循环稳定性的影响

采用固相合成法制备Li_(6.5)La_(3)Zr_(1.5)Nb_(0.5)O_(12)(简称LLZNO)固态电解质,分析了质量分数为0.00%~2.00%的ZnO对LLZNO离子电导率和循环稳定性的影响。采用X射线衍射仪、扫描电子显微镜、电化学阻抗谱以及恒流充放电测试,探究了样品的晶体结构、断面形貌、离子电导率及其对锂循环稳定性。结果表明:随着样品中ZnO质量分数的增加,样品烧结气孔数量明显减少,断面形貌平整。当ZnO的质量分数为0.50%时,样品为立方相,室温离子电导率提升了14.63%;在80h(40次)的恒流充放电循环中,电压保持稳定,具有良好的循环性能。

Evaluating serum CXCL12,sCD22,Lp-PLA2 levels and ratios as biomarkers for diagnosis of Alzheimer's disease

BACKGROUND Grasping the underlying mechanisms of Alzheimer's disease(AD)is still a work in progress,and existing diagnostic techniques encounter various obstacles.Therefore,the discovery of dependable biomarkers is essential for early detection,tracking the disease's advancement,and steering treatment strategies.AIM To explore the diagnostic potential of serum CXCL12,sCD22,Lp-PLA2,and their ratios in AD,aiming to enhance early detection and inform targeted treatment strategies.METHODS The study was conducted in Dongying people's Hospital from January 2021 to December 2022.Participants included 60 AD patients(AD group)and 60 healthy people(control group).Using a prospective case-control design,the levels of CXCL12,sCD22 and Lp-PLA2 and their ratios were detected by enzyme-linked immunosorbent assay kit in the diagnosis of AD.The differences between the two groups were analyzed by statistical methods,and the corresponding ratio was constructed to improve the specificity and sensitivity of diagnosis.RESULTS Serum CXCL12 levels were higher in the AD group(47.2±8.5 ng/mL)than the control group(32.8±5.7 ng/mL,P<0.001),while sCD22 levels were lower(14.3±2.1 ng/mL vs 18.9±3.4 ng/mL,P<0.01).Lp-PLA2 levels were also higher in the AD group(112.5±20.6 ng/mL vs 89.7±15.2 ng/mL,P<0.05).Significant differences were noted in CXCL12/sCD22(3.3 vs 1.7,P<0.001)and Lp-PLA-2/sCD22 ratios(8.0 vs 5.2,P<0.05)between the groups.Receiver operating characteristic analysis confirmed high sensitivity and specificity of these markers and their ratios in distinguishing AD,with area under the curves ranging from CONCLUSION Serum CXCL12 and Lp-PLA2 levels were significantly increased,while sCD22 were significantly decreased,as well as increases in the ratios of CXCL12/sCD22 and Lp-PLA2/sCD22,are closely related to the onset of AD.These biomarkers and their ratios can be used as potential diagnostic indicators for AD,providing an important clinical reference for early intervention and treatment.

Preparation and magnetic hardening of low Ti content(Sm,Zr)(Fe,Co,Ti)_(12) magnets by rapid solidification non-equilibrium method

The Sm–Zr–Fe–Co–Ti quinary-alloys with ThMn12 structure has attracted wide attention for ultra-high intrinsic magnetic properties,showing potentiality to be developed into rare-earth permanent magnets.The Ti element in alloys is crucial for phase stability and magnetic properties,and lower Ti content can increase intrinsic magnetic properties but reduce phase stability.In this study,the 1:12 single-phase melt-spun ribbons with low Ti content was successfully prepared using a rapid solidification non-equilibrium method for the Sm1.1Zr_(0.2)Fe_(9.2)Co_(2.3)Ti_(0.5) quinary-alloy.However,this non-equilibrium ribbon did not achieve good magnetic hardening due to the uneven microstructure and microstrain.Then,annealing was carried out to eliminate micro-strain and homogenize microstructure,therefore,remanence and coercivity were significantly improved even the precipitation of a small amount of a-Fe phase which were not conducive to coercivity.The remanence of 86.1 emu/g and coercivity of 151 kA/m was achieved when annealing at 850℃ for 45 min.After hot pressing,under the action of high temperature and pressure,a small portion of ThMn12 phases in the magnet decompose into Sm-rich phases and a-Fe,while remanence of 4.02 kGs(1 Gs=10^(-4) T),and coercivity of 1.12 kOe(1 Oe=79.5775 A·m^(-1))were still acquired.Our findings can provide reference for exploring practical permanent magnets made of 1:12 type quinary-alloys.

Phospholipase A2 enzymes PLA2G2A and PLA2G12B as potential diagnostic and prognostic biomarkers in cholangiocarcinoma

BACKGROUND Phospholipase A2(PLA2)enzymes are pivotal in various biological processes,such as lipid mediator production,membrane remodeling,bioenergetics,and maintaining the body surface barrier.Notably,these enzymes play a significant role in the development of diverse tumors.AIM To systematically and comprehensively explore the expression of the PLA2 family genes and their potential implications in cholangiocarcinoma(CCA).METHODS We conducted an analysis of five CCA datasets from The Cancer Genome Atlas and the Gene Expression Omnibus.The study identified differentially expressed genes between tumor tissues and adjacent normal tissues,with a focus on PLA2G2A and PLA2G12B.Gene Set Enrichment Analysis was utilized to pinpoint associated pathways.Moreover,relevant hub genes and microRNAs for PLA2G2A and PLA2G12B were predicted,and their correlation with the prognosis of CCA was evaluated.RESULTS PLA2G2A and PLA2G12B were discerned as differentially expressed in CCA,manifesting significant variations in expression levels in urine and serum between CCA patients and healthy individuals.Elevated expression of PLA2G2A was correlated with poorer overall survival in CCA patients.Additionally,the study delineated pathways and miRNAs associated with these genes.CONCLUSION Our findings suggest that PLA2G2A and PLA2G12B may serve as novel potential diagnostic and prognostic markers for CCA.The increased levels of these genes in biological fluids could be employed as non-invasive markers for CCA,and their expression levels are indicative of prognosis,underscoring their potential utility in clinical settings.

Neuroprotective effects of Shaoyao Gancao decoction against excitatory damage in PC12 cells based on the Src-NR2-nNOS pathway

Objective:To explore the neuroprotective effects of the Shaoyao Gancao decoction(SGD)against excitatory damage in PC12 cells and the role of the Src-NR2-nNOS pathway mediation by SGD in regulatingγ-aminobutyric acid(GABA)-glutamate(Glu)homeostasis.Methods: N-Methyl-d-aspartic acid(NMDA)was used to establish a PC12 cell excitability injury model.To investigate the neuroprotective effect of SGD,a cell counting kit-8(CCK-8)assay was used to determine PC12 cell viability,Annexin V/Propidium Iodide(Annexin V/PI)double staining was used to determine PC12 cell apoptosis,and Ca^(2+)concentration was observed using laser confocal microscopy.GABA receptor agonists and antagonists were used to analyze the neuroprotective interactions betweenγ-aminobutyric acid(GABA)and NMDA receptors.Additionally,molecular biology techniques were used to determine mRNA and protein expression in the Src-NR2-nNOS pathway.We analyzed the correlations between the regulatory sites of GABA and NMDA interactions,excitatory neurotoxicity,and brain damage at the molecular level.Results: NMDA excitotoxic injury manifested as a significant decrease in cell activity,increased apoptosis and caspase-3 protein expression,and a significant increase in intracellular Ca^(2+)concentration.Administration of SGD,a GABAA receptor agonist(muscimol),or a GABAB receptor agonist(baclofen)decreased intracellular Ca^(2+)concentrations,attenuated apoptosis,and reversed NMDA-induced upregulation of caspase-3,Src,NMDAR2A,NMDAR2B,and nNOS.Unexpectedly,a GABA_(A)receptor antagonist(bicuculline)and a GABA_(B)receptor antagonist(saclofen)failed to significantly increase excitatory neurotoxicity.Conclusions: Taken together,these results not only provide an experimental basis for SGD administration in the clinical treatment of central nervous system injury diseases,but also suggest that the Src-NR2A-nNOS pathway may be a valuable target in excitotoxicity treatment.

Clinical significance of upregulated Rho GTPase activating protein 12 causing resistance to tyrosine kinase inhibitors in hepatocellular carcinoma

BACKGROUND Hepatocellular carcinoma(HCC)is a major health challenge with high incidence and poor survival rates in China.Systemic therapies,particularly tyrosine kinase inhibitors(TKIs),are the first-line treatment for advanced HCC,but resistance is common.The Rho GTPase family member Rho GTPase activating protein 12(ARHGAP12),which regulates cell adhesion and invasion,is a potential therapeutic target for overcoming TKI resistance in HCC.However,no studies on the expression of ARHGAP12 in HCC and its role in resistance to TKIs have been reported.AIM To unveil the expression of ARHGAP12 in HCC,its role in TKI resistance and its potential associated pathways.METHODS This study used single-cell RNA sequencing(scRNA-seq)to evaluate ARHGAP12 mRNA levels and explored its mechanisms through enrichment analysis.CellChat was used to investigate focal adhesion(FA)pathway regulation.We integrated bulk RNA data(RNA-seq and microarray),immunohistochemistry and proteomics to analyze ARHGAP12 mRNA and protein levels,correlating with clinical outcomes.We assessed ARHGAP12 expression in TKI-resistant HCC,integrated conventional HCC to explore its mechanism,identified intersecting FA pathway genes with scRNA-seq data and evaluated its response to TKI and immunotherapy.RESULTS ARHGAP12 mRNA was found to be highly expressed in malignant hepatocytes and to regulate FA.In malignant hepatocytes in high-score FA groups,MDK-[integrin alpha 6(ITGA6)+integrinβ-1(ITGB1)]showed specificity in ligand-receptor interactions.ARHGAP12 mRNA and protein were upregulated in bulk RNA,immunohistochemistry and proteomics,and higher expression was associated with a worse prognosis.ARHGAP12 was also found to be a TKI resistance gene that regulated the FA pathway.ITGB1 was identified as a crossover gene in the FA pathway in both scRNA-seq and bulk RNA.High expression of ARHGAP12 was associated with adverse reactions to sorafenib,cabozantinib and regorafenib,but not to immunotherapy.CONCLUSION ARHGAP12 expression is elevated in HCC and TKI-resistant HCC,and its regulatory role in FA may underlie the TKI-resistant phenotype.

Vitamin B12 deficiency in dialysis patients:risk factors,diagnosis,complications,and treatment:A comprehensive review

Vitamin B12 deficiency is a significant concern among patients with end-stage renal disease undergoing dialysis.However,there hasn’t been extensive research conducted on this particular patient group.The reported incidence rates vary widely,ranging from 20%to 90%,reflecting the complexity of its diagnosis.Dialysis patients often face multiple nutritional deficiencies,including a lack of essential vitamins,due to factors such as dietary restrictions,impaired absorption,and nutrient loss during dialysis.Diagnosing vitamin B12 deficiency in these patients is challenging,and addressing it is crucial to prevent complications and improve their overall quality of life.This review paper delves into the available body of evidence on vitamin B12 deficiency in dialysis patients,examining the contributing risk factors,diagnostic challenges,potential complications,and available treatment options.It provides a well-rounded perspective on the topic,making it a valuable resource for researchers,healthcare practitioners,and policymakers interested in addressing the nutritional needs of dialysis patients.

SnO_2-Cu_2O/CNTs复合催化剂的制备及对FOX-12热分解的催化性能

以氯化铜、四氯化锡和碳纳米管为原料,采用浸渍法和液相化学沉积法相结合制得SnO2-Cu2O/CNTs复合催化剂,采用XRD、SEM、TEM、EDS等对催化剂进行表征,并用DSC研究催化剂对FOX-12热分解特性的影响。结果表明,纳米金属氧化物以5-10 nm的球形颗粒形态附着在碳纳米管表面,分散较均匀。催化剂使N-脒基脲二硝酰胺盐（FOX-12）的分解峰温降低,放热量增加,表面活化能降低,表现出良好的催化效果。当FOX-12与催化剂质量比5∶1混合时,FOX-12的分解峰温降低18.08℃,放热量增加148 J/g。

Br2-MnO2法合成12-溴脱氢松香酸及其甲酯

分别以Br2-冰醋酸、溴代丁二酰亚胺（NBS）和Br2-MnO2三种方法合成12-溴脱氢松香酸和12-溴脱氢松香酸甲酯，并对反应的动力学和不同体系的反应用时、产率、选择性以及合成成本等进行探究。研究表明：Br2-MnO2新方法反应条件温和，操作简单，反应用时短（2h），成本低，选择性好，产率较高（49％～66．7％），合成效率高，适合进一步工业化。

The in vitro Anti Hptocarcinoma Effects of Human Interleukin-12 from Transgenic Potato

[Objective]The aim was to examine the anti heptocarcinoma effects of human interleukin-12（hIL-12） from transgenic potatoes.[Method]Human heptocarcinoma cell line HepG22.2.15 was cocultured with human peripherial blood monocyte（PBMC）.Human IL-12 extracted from its transgenic patatoes was introduced to this coculture system.MTT method and laser confocal microscope were then employed to evaluate its survival rates and morphological changes of HepG22.2.15 cell line.[Result]The HepG22.2.15 survival rate of the plant produced hIL-12 treated group was significantly lower than that of the wild type control,while similar to that of commercial purified recombinant hIL-12 group.As indicated by AnnexinV/PI double staining laser confocal microscope,cocultured heptocarcinoma cells showed the typical early and final phase apoptotic morphological characteristics 48 hours after 2 × 10-4 mg/L potato secreted hIL-12 treatment.[Conclusion] These results demonstrated that Heptocarcinoma HepG22.2.15 cell growth could be actively inhibited by the transgenic potato expressed hIL-12 in vitro.

NO_2^-在维生素B_(12)修饰电极上催化氧化

研究维生素 B12 (VB12 )修饰电极的制备 ,考察其对 NO-2 及共存离子的作用情况 ,对催化作用机理做初步探讨 .VB12 修饰电极在 0 .1mol.L-1KCl底液中对 NO-2 有良好的电化学催化作用和选择性 ,其催化电流在 NO-2 浓度为 0 .10～ 2 .0 0 mol.L-1范围内呈线性关系 ,NO-2 的浓度低至 0 .0 1mol.L-1仍可定量测定 .天然水中常见的离子不干扰测定 ,应用于雨水和湖水中 NO-2 的测定 ,回收率为 10 1%～ 10 3%.

重型肝炎并发自发性细菌性腹膜炎患者血清及腹水中NO、TNF-α、IL-6、IL-12水平变化及意义

为探讨一氧化氮 (NO)、肿瘤坏死因子 - α(TNF- α)、白细胞介素 - 6 (IL- 6 )、白细胞介素 - 12 (IL- 12 )在重型肝炎 (SH)并发自发性细菌性腹膜炎 (SBP)患者血清和腹水中的水平及其临床意义 ,分别采用 Griess比色法及放射免疫法 (RIA)检测了 45例 SH并发腹水患者血清及腹水中 NO、TNF- α、IL- 6和 IL- 12含量 ,其中腹水感染组 30例、腹水非感染组 15例 ,结果显示 SH并发 SBP血清和腹水 NO、 TNF- α、 IL- 6和 IL- 12水平均明显高于腹水非感染组 (P<0 .0 5 ) ,其升高水平与血清总胆红素 (SB)、凝血酶原时间 (PT)呈正相关 ,与血清胆固醇呈负相关 (P<0 .0 1)。感染控制后血清和腹水 NO、 TNF- α、 IL- 6、IL- 12水平均明显下降 (P<0 。0 5 ) ,但仅能降至非感染组水平。表明 :NO、 TNF-α、IL- 6和 IL- 12参与 SH及 SBP形成腹水的发生、发展过程 ,其联合检测对 SH并发 SBP的早期诊断。

F-12/碳纤维层间混杂NOL环复合材料研究

本文以ＮＯＬ 环研究了Ｆ－ １２／ 碳纤维混杂复合材料的拉伸性能和剪切性能。试验结果表明，拉伸强度表现出混杂负效应，而剪切强度表现出混杂正效应，两种强度的混杂效应都随混杂比的增大而降低。纤维混杂可以改变材料的破坏模式。

Carnosine对Aβ_(25-35)诱发PC12细胞损伤的神经保护作用

目的 研究 Carnosine对 β淀粉样蛋白片段 (Aβ2 5- 3 5)诱发 PC1 2细胞损伤的神经保护作用。方法 将培养的 PC1 2细胞分为三组 :正常对照组、损伤组和保护组。损伤组用 Aβ2 5- 3 5处理细胞 ,保护组在用 Aβ2 5- 3 5处理前 30 min加入 Carnosine。使用细胞形态学方法、LDH法、MTT法观察 Carnosine的神经保护作用。结果 通过形态学方法 ,保护组细胞数显著比损伤组多 ,受损变圆的细胞数较少。保护组 LDH活性显著少于损伤组(P<0 .0 1 ) ;MTT显著高于损伤组 (P<0 .0 1 )。结论 Carnosine对 Aβ2 5- 3 5诱发 PC1 2细胞损伤有显著的保护作用。

NO在IL-12诱导抗伯氏疟原虫感染免疫效应中的作用

目的 探讨NO在IL 12诱导抗伯氏疟原虫 (P .b)感染免疫效应中的作用。 方法 每只BALB/c小鼠接种 5× 10 5个感染P .b的RBC ,分组后分别给予 5mg/dNO合成酶选择性抑制aminoguanidine、0 .0 3 μg/dIL 12和aminoguani dine联合IL 12处理。观察各组小鼠原虫血症变化及生存时间。感染第 5d收集小鼠血清进行NO水平测定。 结果 aminoguanidine联合IL 12处理组小鼠的原虫血症水平与单独IL 12组差异不明显 ,却使小鼠生存率显著降低 ;IL 12联合aminoguanidine处理组较单独aminoguanidine及感染对照组原虫血症达峰值的时间显著推迟 ,小鼠存活时间明显延长。IL 12处理小鼠血清NO水平显著上升 ;给予aminoguanidine后的小鼠血清NO含量较低 ,与感染对照组水平接近。 结论 aminoguanidine能有效的抑制IL 12诱导的NO的产生 ,显著降低IL 12处理小鼠生存率 ,但对原虫血症水平无明显影响。因此 ,IL 12抗P .b感染的免疫保护作用部分依赖NO介导 ,且NO的作用可能并非是NO对疟原虫的直接杀伤。