调控五配位Al^(3+)含量制备高性能低温Sabatier反应催化剂

为了制备出高性能低温Sabatier反应Ru基催化剂,通过调控Al_(2)O_(3)载体中五配位Al^(3+)的含量(五配位Al^(3+)占Al物种的比例),实现对Ru基活性位点电子性质的调控。在此过程中,利用~(27)Al固体核磁共振(~(27)Al-NMR)检测Al_(2)O_(3)载体中五配位Al^(3+)的含量,借助X射线光电子能谱仪(XPS)和H_2程序升温还原(H_(2)-TPR)考察Ru基活性位点电子性质的调控效果,利用固定床反应器测试催化剂性能。结果表明,Al_(2)O_(3)载体中的五配位Al^(3+)可有效调控Ru基活性位点的电子性质,进而提升低温Sabatier反应Ru基催化剂性能。其中,以五配位Al^(3+)含量约为28.1%的Al_(2)O_(3)载体制备的Ru基催化剂,在低温区(<300℃)的CO_(2)转化率和CH_4选择性均可达90%以上。而且,在100 h的稳定性测试中,催化性能没有明显降低。

接力识别Al^(3+)及F^(-)的偶氮类荧光探针合成与应用

以6-氨基间甲酚和1-萘酚为原料,合成了2-(2-羟基-4-甲基苯偶氮)-1-萘酚(探针NA-M),通过^(1)HNMR、^(13)CNMR、FTIR、HRMS表征了其结构。测试了探针NA-M对Al^(3+)的选择性识别性能及其与Al^(3+)形成的络合物(NA-M+Al^(3+))对F^(-)的选择性识别性能,推测了探针NA-M与Al^(3+)和F^(-)间的作用机制。考察了探针NA-M在实际样品中的应用。结果表明,在pH=7.4、V(甲醇)∶V(N-2-羟乙基哌嗪-N'-2-乙磺酸)=9∶1的溶剂中,探针NA-M与Al^(3+)在590 nm处发生显著的荧光增强作用,并对Al^(3+)的识别表现出高选择性、抗金属离子干扰性和良好的灵敏度(检测限为8.4×10^(-7)mol/L),Al^(3+)与探针NA-M形成了配位比为1∶2的NA-M+Al^(3+);NA-M+Al^(3+)在F^(-)加入后发生显著的荧光猝灭现象,F^(-)可以捕获NA-M+Al^(3+)中的Al^(3+),从而引起荧光变化。NA-M+Al^(3+)对F^(-)的识别也显示出高选择性和良好的抗其他阴离子干扰能力和灵敏度(检测限为9.5×10^(-7)mol/L);在体系pH为5~10时,探针NA-M识别Al^(3+)及F^(-)表现出良好的效果,交替加入Al^(3+)和F^(-)可引起其荧光强度的可逆变化,探针NA-M可以通过荧光信号的“关-开-关”转变,用于接力识别Al^(3+)和F^(-)。在实际样品的检测中,Al^(3+)的回收率在98.8%~107.0%之间,相对标准偏差(RSD)为2.6%~4.3%;F^(-)的回收率为97.8%~101.4%,RSD为1.4%~2.3%。

Modeling time-dependent mechanical behavior of hard rock considering excavation-induced damage and complex 3D stress states

To investigate the long-term stability of deep rocks,a three-dimensional(3D)time-dependent model that accounts for excavation-induced damage and complex stress state is developed.This model comprises three main components:a 3D viscoplastic isotropic constitutive relation that considers excavation damage and complex stress state,a quantitative relationship between critical irreversible deformation and complex stress state,and evolution characteristics of strength parameters.The proposed model is implemented in a self-developed numerical code,i.e.CASRock.The reliability of the model is validated through experiments.It is indicated that the time-dependent fracturing potential index(xTFPI)at a given time during the attenuation creep stage shows a negative correlation with the extent of excavationinduced damage.The time-dependent fracturing process of rock demonstrates a distinct interval effect of the intermediate principal stress,thereby highlighting the 3D stress-dependent characteristic of the model.Finally,the influence of excavation-induced damage and intermediate principal stress on the time-dependent fracturing characteristics of the surrounding rocks around the tunnel is discussed.

3D DEM simulation of hard rock fracture in deep tunnel excavation induced by changes in principal stress magnitude and orientation

To achieve the loading of the stress path of hard rock,the spherical discrete element model(DEM)and the new flexible membrane technology were utilized to realize the transient loading of three principal stresses with arbitrary magnitudes and orientations.Furthermore,based on the deep tunnel of China Jinping Underground Laboratory II(CJPL-II),the deformation and fracture evolution characteristics of deep hard rock induced by excavation stress path were analyzed,and the mechanisms of transient loading-unloading and stress rotation-induced fractures were revealed from a mesoscopic perspective.The results indicated that the stressestrain curve exhibits different trends and degrees of sudden changes when subjected to transient changes in principal stress,accompanied by sudden changes in strain rate.Stress rotation induces spatially directional deformation,resulting in fractures of different degrees and orientations,and increasing the degree of deformation anisotropy.The correlation between the degree of induced fracture and the unloading magnitude of minimum principal stress,as well as its initial level is significant and positive.The process of mechanical response during transient unloading exhibits clear nonlinearity and directivity.After transient unloading,both the minimum principal stress and minimum principal strain rate decrease sharply and then tend to stabilize.This occurs from the edge to the interior and from the direction of the minimum principal stress to the direction of the maximum principal stress on theε1-ε3 plane.Transient unloading will induce a tensile stress wave.The ability to induce fractures due to changes in principal stress magnitude,orientation and rotation paths gradually increases.The analysis indicates a positive correlation between the abrupt change amplitude of strain rate and the maximum unloading magnitude,which is determined by the magnitude and rotation of principal stress.A high tensile strain rate is more likely to induce fractures under low minimum principal stress.

基于铝离子敏化牡丹提取物(丹皮酚)荧光法定量分析Al^(3+)的研究

饮用水是人体铝元素的主要摄入来源.微量铝离子可对人体健康造成很大危害.WHO(世界卫生组织)规定,饮用水中允许的最高铝离子浓度为200μg/L(7.41μmol/L).因此铝离子的高灵敏检测显得尤为重要.目前常用的铝离子检测方法存在操作麻烦,周期长等缺点,所以构建一种简便、快捷的铝离子检测方法尤为重要.丹皮酚是一种提取自牡丹皮的有机化合物,其与Al^(3+)结合后荧光会数倍增强.基于丹皮酚与铝离子结合产生荧光增强现象,建立了一种检测铝离子的荧光分析方法.此方法只需常温反应5 min,并且检测限为0.5μmol/L(线性范围:0~100μmol/L),构建的检测方法具有快速、低成本、简单、高特异性和高灵敏等优点,有很好的应用前景.

Transcription factor ABF3 modulates salinity stress-enhanced jasmonate signaling in Arabidopsis

Salinity is a severe abiotic stress that affects plant growth and yield.Salinity stress activates jasmonate(JA)signaling in Arabidopsis thaliana,but the underlying molecular mechanism remains to be elucidated.In this study,we confirmed the activation of JA signaling under saline conditions and demonstrated the importance of the CORONATINE INSENSITIVE1(COI1)-mediated JA signaling for this process.Phenotypic analyses reflected the negative regulation of JASMONATE ZIM-DOMAIN(JAZ)repressors during salinity stress-enhanced JA signaling.Mechanistic analyses revealed that JAZ proteins physically interact with ABSCISIC ACID-RESPONSIVE ELEMENT BINDING FACTOR1(ABF1),AREB1/ABF2,ABF3,and AREB2/ABF4,which belong to the basic leucine zipper(bZIP)transcription factor family and respond to salinity stress.Analyses on the ABF3 overexpression plants and ABF mutants indicated the positive role of ABF3 in regulating JA signaling under saline condition.Furthermore,ABF3 overexpression partially recovered the JA-related phenotypes of JAZ1-D3A plants.Moreover,ABF3 was observed to indirectly activate ALLENE OXIDE SYNTHASE(AOS)transcription,but this activation was inhibited by JAZ1.In addition,ABF3 competitively bind to JAZ1,thereby decreasing the interaction between JAZ1 and MYC2,which is the master transcription factor controlling JA signaling.Collectively,our findings have clarified the regulatory effects of ABF3 on JA signaling and provide new insights into how JA signaling is enhanced following an exposure to salinity stress.

Suppression of Cs FAD3 in a JA-dependent manner,but not through the SA pathway,impairs drought stress tolerance in tea

The growth and yield of tea plants are seriously limited by drought stress.Fatty acid desaturases(FADs)contribute to the mediation of membrane fluidity in response to different stresses,although the role ofω-3 FAD(Omega-3fatty acid desaturase)-mediated damage induced by drought stress in tea plants is poorly understood.In this study,drought stress significantly promoted the synthesis of C18:3(linolenic acid)and the expression level of CsFAD3.Yeast experiments further demonstrated that CsFAD3 can convert C18:2 to C18:3,and that the 35S:GFP-CsFAD3fusion protein was localized in the endoplasmic reticulum of Nicotiana benthamiana cells.CsFAD3-silenced tea leaves exhibited poor drought tolerance,with a lower F_(v)/F_(m)and a higher malondialdehyde(MDA)content than the control plants.However,transgenic 35S:CsFAD3 Arabidopsis plants showed the opposite phenotypes.In addition,the jasmonic acid(JA)content and the expression levels of CsLOX2,CsLOX4,CsAOS,CsAOC3 and CsOPR2 were significantly reduced in CsFAD3-silenced leaves under drought stress.However,no substantial difference in the salicylic acid(SA)content was detected under normal or drought conditions.An analysis of Atcoi1(JA receptor)or Atnpr1(SA receptor)mutant Arabidopsis plants in 35S:CsFAD3 backgrounds further revealed that knockout of Atcoi1impaired the drought-tolerant phenotypes of CsFAD3 overexpression lines.Therefore,this study demonstrated that CsFAD3 plays a crucial role in drought tolerance by mediating JA pathways.

Celastrol activates caspase-3/GSDME-dependent pyroptosis in tumor cells by inducing endoplasmic reticulum stress Author links open overlay panel

Objective:To investigate the pyroptosis-inducing effects of celastrol on tumor cells and to explore the potential mechanisms involved,specifically focusing on the role of the caspase-3/gasdermin E(GSDME)signaling pathway and the impact of endoplasmic reticulum(ER)stress and autophagy.Methods: Necrostatin-1(Nec-1),lactate dehydrogenase release(LDH)assay,and Hoechst/propidium iodide(PI)double staining were employed to validate the mode of cell death.Western blot was used to detect the cleavage of GSDME and the expression of light chain 3(LC3)and BIP.Results: Celastrol induced cell swelling with large bubbles,which is consistent with the pyroptotic phenotype.Moreover,treatment with celastrol induced GSDME cleavage,indicating the activation of GSDME-mediated pyroptosis.GSDME knockout via CRISPR/Cas9 blocked the pyroptotic morphology of celastrol in HeLa cells.In addition,cleavage of GSDME was attenuated by a specific caspase-3 inhibitor in celastrol-treated cells,suggesting that GSDME activation was induced by caspase-3.Mechanistically,celastrol induced endoplasmic reticulum(ER)stress and autophagy in HeLa cells,and other ER stress inducers produced effects consistent with those of celastrol.Conclusion: These findings suggest that celastrol triggers caspase-3/GSDME-dependent pyroptosis via activation of ER stress,which may shed light on the potential antitumor clinical applications of celastrol.

基于新绿原酸的紫外吸收和电化学双信号响应的Al^(3+)分析新方法研究

目的 利用新绿原酸(NCGA)与Al^(3+)的相互作用,建立一种基于NCGA的紫外吸收和电化学双信号响应的Al^(3+)分析新方法。方法 基于NCGA与单壁碳纳米管(CNTs)之间的π-π堆积作用,构建了NCGA/CNTs/GC电极。利用差分脉冲(DPV)技术和修饰电极在+0.23 V的氧化电流的下降对Al^(3+)进行定量分析。基于NCGA对Al^(3+)在325 nm处的吸收降低同时伴随365 nm新峰生成的紫外光谱响应,并且在277和340 nm处出现等吸收点,利用365 nm和325nm处的吸光度值之比(A_(365)/A_(325))对Al^(3+)进行定量分析。结果 基于NCGA的分析方法对Al^(3+)的紫外吸收在0.1~100μmol·L^(-1)呈现出良好的线性关系,检测限为0.034μmol·L^(-1);基于NCGA的修饰电极对Al^(3+)的电流响应在0.01~0.1,0.1~10和10~100μmol·L^(-1)呈现良好的线性关系,检测限为0.45 nmol·L^(-1)。生理浓度的其他金属离子和生理活性物质对两种信号测定方法均无明显干扰。在NCGA的紫外分析方法和电化学分析方法下,大鼠血清的加标回收率分别为97.4%~101%(n=3)和98.5%~99.4%(n=3)。结论 本方法具有良好的线性、选择性和准确度,并被成功用于大鼠中Al^(3+)的准确定量。该方法有望应用于Al^(3+)相关的生理和病理事件研究。

基于罗丹明B类荧光探针的设计以及对Al^(3+)检测

印染废水中过高浓度的Al^(3+)不仅会破坏生态环境,而且还将危害人类健康。因此,对印染废水中Al^(3+)浓度的精准检测具有十分重要的研究意义。本文以罗丹明B、乙二胺和4-甲酰基-3-羟基苯甲酸为原料,合成了新型荧光探针RhB-AC,并利用高分辨质谱(HRMS)及核磁共振氢谱(1H NMR)对探针RhB-AC的分子结构进行了表征。探针RhB-AC在水中,由于光诱导的电子转移(Photoinduced electron transfer,PET)效应,其荧光发生猝灭。当与Al^(3+)作用后,PET效应被抑制,探针表现出很强的青绿色荧光。另外,该探针对Al^(3+)检测的速度快(3秒以内)、选择性好、灵敏度高(检测限为16 nM)。最后,该探针还能快速、定量检测实际印染废水中的Al^(3+)浓度。

Exosomes derived from microglia overexpressing miR-124-3p alleviate neuronal endoplasmic reticulum stress damage after repetitive mild traumatic brain injury

We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repetitive mild traumatic brain injury remains unclear.In this study,we first used an HT22 scratch injury model to mimic traumatic brain injury,then co-cultured the HT22 cells with BV2 microglia expressing high levels of miR-124-3p.We found that exosomes containing high levels of miR-124-3p attenuated apoptosis and endoplasmic reticulum stress.Furthermore,luciferase reporter assay analysis confirmed that miR-124-3p bound specifically to the endoplasmic reticulum stress-related protein IRE1α,while an IRE1αfunctional salvage experiment confirmed that miR-124-3p targeted IRE1αand reduced its expression,thereby inhibiting endoplasmic reticulum stress in injured neurons.Finally,we delivered microglia-derived exosomes containing miR-124-3p intranasally to a mouse model of repetitive mild traumatic brain injury and found that endoplasmic reticulum stress and apoptosis levels in hippocampal neurons were significantly reduced.These findings suggest that,after repetitive mild traumatic brain injury,miR-124-3 can be transferred from microglia-derived exosomes to injured neurons,where it exerts a neuroprotective effect by inhibiting endoplasmic reticulum stress.Therefore,microglia-derived exosomes containing miR-124-3p may represent a novel therapeutic strategy for repetitive mild traumatic brain injury.

Tranylcypromine upregulates Sestrin 2 expression to ameliorate NLRP3-related noise-induced hearing loss

Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction.However,there are currently no effective pharmacological interventions for patients with noise-induced hearing loss.Here,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory mechanisms.We established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 hours.We found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with tranylcypromine.The noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with saline.These findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell loss.Additionally,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy pathway.Tranylcypromine treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)production.In conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing function.These findings suggest that inhibiting lysine-specific demethylase 1 is a potential therapeutic strategy for preventing hair cell loss and noise-induced hearing loss.

PI3K/AKT signaling and neuroprotection in ischemic stroke:molecular mechanisms and therapeutic perspectives

It has been reported that the PI3K/AKT signaling pathway plays a key role in the pathogenesis of ischemic stroke.As a result,the development of drugs targeting the PI3K/AKT signaling pathway has attracted increasing attention from researchers.This article reviews the pathological mechanisms and advancements in research related to the signaling pathways in ischemic stroke,with a focus on the PI3K/AKT signaling pathway.The key findings include the following:(1)The complex pathological mechanisms of ischemic stroke can be categorized into five major types:excitatory amino acid toxicity,Ca^(2+)overload,inflammatory response,oxidative stress,and apoptosis.(2)The PI3K/AKT-mediated signaling pathway is closely associated with the occurrence and progression of ischemic stroke,which primarily involves the NF-κB,NRF2,BCL-2,mTOR,and endothelial NOS signaling pathways.(3)Natural products,including flavonoids,quinones,alkaloids,phenylpropanoids,phenols,terpenoids,and iridoids,show great potential as candidate substances for the development of innovative anti-stroke medications.(4)Recently,novel therapeutic techniques,such as electroacupuncture and mesenchymal stem cell therapy,have demonstrated the potential to improve stroke outcomes by activating the PI3K/AKT signaling pathway,providing new possibilities for the treatment and rehabilitation of patients with ischemic stroke.Future investigations should focus on the direct regulatory mechanisms of drugs targeting the PI3K/AKT signaling pathway and their clinical translation to develop innovative treatment strategies for ischemic stroke.

水稻幼苗耐Al^(3+)胁迫的QTL定位分析

用珍汕97B/密阳46构建RIL群体及其遗传图谱,对其种子采用纸培法育苗和培养,并设2个Al3+浓度(20 mg/L和30 mg/L)胁迫处理,以处理20 d后的幼苗相对根长(%)和相对苗高(%)为耐Al3+胁迫指标,用于QTL定位分析。结果表明,以相对根长为指标,检测到2个耐Al3+胁迫的主效应QTL,即qRAC(r)2和qRAC(r)11,其中qRAC(r)2在2个胁迫处理下均被检测到,有效基因来自于珍汕97B,贡献率较大(12.92%和16.15%),表现出较强的耐Al3+胁迫功能。以相对苗高为指标,还检测到qRAC(s)11-2(20 mg/L Al3+)和qRAC(s)11-1(30 mg/L Al3+)2个主效应QTL,它们均位于第11染色体。耐Al3+胁迫的QTL上位性分析还表明,总的QTL上位性互作效应比主效应QTL的作用更大,且显示出相当的复杂性,在不同胁迫浓度下,基因间可以通过不同的互作方式,表现出对高Al3+胁迫的耐性。以相对根长为指标,检测到8对上位性互作,涉及1、23、、5、6、10等6条染色体的15个QTL位点;以相对苗高为指标,共检测到6对上位性互作,涉及第1、2、3、5、6、7、89、、12等9条染色体;且几乎所有互作均发生在背景因子的QTL位点间。

模拟酸雨对赤红壤磷素及Ca^(2+)、Al^(3+)、Fe^(2+)淋失特征的影响

本研究通过室内土柱试验,研究了不同强度和持续时间的模拟酸雨淋溶下赤红壤磷素淋失量及部分阳离子(Ca2+、Al3+、Fe2+)的释放程度和特征。结果表明,经pH 2.0、pH 3.0、pH 4.0、pH 5.0模拟酸雨持续淋溶34 d后,淋溶液pH值变化并不明显(P>0.05),而对Ca2+、Fe2+的溶出有显著的促进作用,Ca2+、Al3+、Fe2+溶出量均随pH值的降低而升高,Al3+和Fe2+淋失量在pH 2.0时均有骤增现象。随淋溶时间的增加,土壤可溶态磷的淋失量表现为先增加后逐渐降低;随着pH值的降低,土壤磷淋失总量也表现为先增加后降低,pH>4.0的酸雨有助于促进土壤磷的释放,pH<4.0时土壤磷的淋失减少。相关分析发现淋溶液中磷淋失总量与Al3+和Fe2+溶出量均呈显著负相关(r1=-0.6531,r2=-0.5107),和Ca2+总溶出量相关关系不显著(r3=-0.1287),表明高强度酸雨降低了土壤磷淋失量,这可能与酸雨导致活性铁、铝的大量释放,增加了磷的活性吸附点位,因而增加了对磷酸根离子配位吸附与固定有关。

大豆根缘细胞对Al^(3+)毒害的响应

【目的】研究大豆根缘细胞发育的生物学特性和对Al3+毒害的响应,为提高大豆的耐铝性提供理论依据。【方法】以浙春3号和辽鲜3号为材料,采用悬空气培法,研究大豆根缘细胞产生的数目、活性随根长的变化及Al3+毒胁迫下根缘细胞形成和释放的难易程度。【结果】大豆根冠周围新形成的根缘细胞呈圆形,随着生长逐渐发育成椭圆形或矩形或长条形。当根长为15～25 mm时,根缘细胞数目达最大值,浙春3号约3 000个,辽鲜3号约3 800个。去根缘细胞的大豆分别用100、200、300、400μmol.L-1 Al3+溶液喷洒根尖,根缘细胞的数目和活性明显低于0μmol.L-1Al3+溶液喷洒的处理,且Al3+浓度越高,根缘细胞数目和活性下降幅度越大。200μmol.L-1 Al3+、300μmol.L-1 Al3+处理4 h,两个大豆品种的PME活性明显升高,400μmol.L-1Al3+处理后PME活性均有明显下降。这说明高浓度Al3+不利于根缘细胞的形成和释放,降低细胞活性和PME活性,辽鲜3号的根缘细胞对Al3+胁迫反应更为敏感。【结论】Al3+毒害时,维持较高根缘细胞的数目、活性及PME活性是抗性品种耐铝毒的重要途径。

新型Al^(3+)掺杂硅胶吸附材料的制备与性能

将陶瓷纤维纸经水玻璃、铝盐溶液等浸渍及调节溶液 pH值 ,得到了新型高吸附性能Al3+ 掺杂硅胶吸附材料 .探讨了浸渍条件对材料吸附性能和表面结构的影响 .反应的优化条件为 :水玻璃含量 2 6 .7% (质量分数 ,下同 ) ,铝盐含量 10 % ,浸渍时间 12 0min ,反应温度 6 0℃ ,溶液 pH值 1.8.得到的Al3+ 掺杂硅胶能较好地分布在陶瓷纤维表面及其孔隙中 ,在多孔掺杂硅胶中 ,起吸附作用的主要为中孔 .由于铝替代硅进入硅胶网络(Al3+ 掺杂 ) ,材料的吸附性能、耐热性能及机械强度等均优于同等条件下反应生成的硅胶 .

Al^(3+)对荞麦离体根边缘细胞的作用

以悬空气培法获得荞麦根边缘细胞,并收集、研究了边缘细胞的生物学活性和脱离根冠后对A l3+毒害的响应过程.结果表明,荞麦根边缘细胞绝大多数呈细杆状,少数呈弯曲的长条型.根长为25 mm左右时,边缘细胞的生物学活性最大,为(94±1)%.A l3+对离体边缘细胞有明显的毒害作用,用A l3+浓度为50μmol/L的溶液处理1~6 h就出现细胞死亡症状,在6 h之后毒害作用最大.系列浓度A l3+(0,12.5,25,50,100,200μmol/L,Ca2+浓度为0.1 mmol/L)处理12 h后,A l3+浓度为12.5μmol/L时处理就足以使离体边缘细胞大量死亡,这说明极其微量的A l3+浓度就可以显著影响离体根边缘细胞活性,也表明离体边缘细胞对A l3+的作用较为敏感,边缘细胞对铝毒响应的滞后性是细胞自身抗铝毒的一种生理反应.

偏最小二乘分光光度法同时测定Fe^(3+)和Al^(3+)

以铬天青S(CAS)为显色剂,溴化十六烷基三甲胺(CTMAB)作为增溶增敏剂及丙酮作为稳定剂,采用偏最小二乘(PLS)分光光度法对Fe3+ 和Al3+ 同时测定。综合考虑光源稳定性,双组分吸光度加和性及线性等因素,选取6 10～6 70nm范围内7个波长以供多波长数据采集。作为比较,在后续数据分析中分别采用了CPA矩阵法和偏最小二乘法(PLS) ,结果表明后者具有明显的优势。

Al^(3+)、F^-掺杂LiMn_2O_4的高温电化学性能

采用固相法合成制得正极材料尖晶石型LiMn2O4及LiAl0 1Mn1 9O3 9F0 1固溶体,XRD显示了其具有良好的尖晶石结构。通过恒电流充放电、循环伏安等测试对样品的电化学性能进行对比研究,用SEM观察了它们之间的形貌差别。结果表明:与LiMn2O4相比,LiAl0 1Mn1 9O3 9F0 1具有良好的高温(55℃)循环性能,Al3+、F-的掺杂大大地提高了材料的稳定性,实验电池循环实验15次后容量仍能保持在110mAh/g左右。