Fe3+,Ce3+共掺杂纳米TiO2的制备及其光催化性能

 以溶胶-凝胶法制备Fe³⁺,Ce³⁺共掺杂的纳米TiO₂光催化剂.研究了不同的三价铁、三价铈掺杂量及烧结温度对日光灯照射下TiO₂光催化降解甲基橙性能的影响.结果表明,Fe³⁺,Ce³⁺共掺杂能抑制TiO₂晶粒的生长,并使TiO₂的吸收带边明显红移约100nm;在普通日光灯下,共掺杂样品光催化效果优于单掺样品,Fe³⁺和Ce³⁺共掺杂对提高TiO₂在可见光下的催化活性具有协同效应,最佳掺杂量物质的量比为n(Fe³⁺):n(Ce³⁺):n(TiO₂)=0.005:0.015:1,最佳烧结温度为650℃.     

一种新型发红光材料SrGdGa3O7:Eu 3+及其性质研究

 采用高温固相法合成了发红光的荧光粉SrGdGa₃O₇:Eu³⁺。漫反射光谱和激发光谱中Eu^₃₊的电荷迁移带、Eu³⁺离子f→f跃迁以及Gd³⁺离子^8S_7/2→⁶I_7/2的跃迁相互吻合;监测Eu³⁺离子的特征发射,激发谱中有Gd^3+离子的激发线表明存在Gd³⁺→Eu³⁺的能量传递。发射光谱中以⁵D₀→⁷F₂ 跃迁为主,表明Eu³⁺离子所占据的晶体学格位没有对称中心的Cs格位。根据低温下的发射光谱计算了⁷F₁ 和^7F₂ 能级完全解除简并后的每个分裂能级的位置。Eu³⁺的发射发生明显的温度猝灭现象,同时发射谱线的分辨率也逐渐降低。Eu³⁺离子的⁵D₀→ ⁷F₂ 跃迁在不同温度下的荧光衰减曲线相似;随着温度的升高,荧光发射强度衰减越快,但是仍然处于毫秒数量级;⁵D₀ → ⁷F₂ 跃迁是宇称和自旋禁阻的跃迁,所以荧光衰减时间比较长。     

激光共聚焦扫描显微镜观测自噬小体变化的应用

文章探讨激光共聚焦扫描显微镜技术在检测低氧诱导小鼠心肌细胞损伤自噬小体变化的应用价值.在无菌条件下,取胚胎型小鼠心肌细胞备用.采用低氧环境+缺氧液方法诱导心肌细胞损伤并发生自噬现象作为实验组,正常环境下培养细胞的方法作为对照组.待心肌细胞长到一定程度后,分别利用激光共聚焦扫描显微镜和正置荧光显微镜对免疫荧光染色的自噬小体表达的LC3A/B蛋白情况进行观测并比较2种检测方法的优缺点.结果显示利用低氧环境+缺氧液方法诱导小鼠心肌细胞损伤并自噬小体形成是可行的.与正常对照组比较,低氧缺氧诱导小鼠心肌细胞损伤组(实验组)自噬小体呈高表达状态.与普通型正置荧光显微镜比较,激光共聚焦扫描显微镜成像速度快,一次可以获得多副图像且图像清晰.激光共聚焦扫描显微镜技术具有成像速度快、灵敏度高和精确度高等优点,可以实时、准确观测低氧诱导小鼠心肌细胞损失自噬小体的表达情况,具有重要临床应用价值.     

红树林内源真菌 Fusarium sp#ZZF51吸附Cu2+的研究

 采用生物吸附法去除废水中Cu²⁺,研究了南海红树林内源真菌Fusarium sp#ZZF51吸附Cu²⁺的行为特性、吸附模型及吸附机理。结果表明：受试菌吸附Cu²⁺的吸附平衡时间为90 min,常温常压下吸附最佳pH值为6.5,Cu²⁺初始浓度50 mg/L,吸附时间90 min,此时受试菌对Cu²⁺的吸附率和吸附容量分别为82.14%和20.53 mg/g。Langmuir方程比Freundlich方程能更好地描述该受试菌对Cu²⁺的平衡吸附行为。通过比较受试菌吸附Cu²⁺前后红外光谱图得知,在吸附过程中,羟基和羰基都起着十分重要的作用。     

斜纹夜蛾幼虫不同组织对Zn2+积累作用的比较研究

 通过在人工饲料中添加不同质量分数的Zn²⁺,研究了植食性昆虫斜纹夜蛾Spodoptera litura Fabricius连续3代幼虫取食含不同质量分数Zn²⁺饲料后,第1和第3代6龄幼虫不同组织对Zn²⁺的积累作用。结果表明,经连续3个世代的胁迫,Zn²⁺在第1、3代斜纹夜蛾6龄幼虫脂肪体、表皮和中肠中的积累量随幼虫饲料中Zn²⁺ 质量分数及胁迫时间的增加而升高;中肠对Zn²⁺的积累作用最强,表皮次之,脂肪体最低。     

白光LED用高亮度橙色高温相Ca3SiO4Cl2:Eu2+荧光粉

 采用高温固相法合成了高亮度橙色高温相Ca_2.99Eu_0.01SiO₄Cl₂荧光粉,进行了发光特性表征并探索了其在LED上的应用。Eu²⁺离子在Ca₃SiO₄Cl₂基质中可被300~450 nm光有效激发发出橙黄光,发射光谱是Eu²⁺离子的特征4f⁶5d¹→4f⁷跃迁发射带。测量得到的Eu²⁺离子的荧光寿命为微秒量级,分别是 τ₁＝1.53 μs和τ₂＝7.29 μs。用该荧光粉制备了395nm近紫外芯片基和460 nm蓝光芯片基发光二极管,并测试了它们的发光性能,表明高温相Ca_2.99Eu_0.01SiO₄Cl₂荧光粉适合于用作白光LED的红黄色组分。     

小鼠T细胞发育相关基因RS21-C6的表达谱及其编码蛋白的细胞内定位

研究了小鼠T细胞发育相关基因RS21-C6的表达谱及其在细胞内的定位.提取小鼠8种组织及处于5个发育阶段的胸腺细胞总RNA,逆转录成cDNA后,利用RS21-C6基因特异性引物,观察了RS21-C6基因的表达;同时构建pEGFP-N3/RS21-C6重组表达载体,在激光共聚焦荧光显微镜下观察了细胞内荧光分布.RT-PCR结果表明RS21-C6基因在所检测的组织和细胞中除骨骼肌和CD4SP胸腺亚群外均有不同程度的表达.激光共聚焦荧光显微镜观察结果表明,RS21-C6-GFP(绿色荧光蛋白)融合蛋白表达在胞浆内,RS21-C6-GFP融合基因的瞬间和稳定表达均获得了相同结果.     

Pr(0.5)Yb(3):ZBLAN双频激发上转换的研究

报道了Pr(0.5)Yb(3):ZBLAN玻璃在960 nm半导体激光和氙灯光双频激发下的激发态吸收上转换现象. 发现上转换发射谱的480.1, 519.0, 601.9和631.8 nm的上转换发光与常规荧光发射谱的荧光吻合得很好, 还发现双频激发下的上转换激发谱有3组明显的谱峰, 它们依次对应于856.0 nm的[¹G₄(Pr³⁺)→¹I₆(Pr³⁺)+¹G₄(Pr³⁺)→³P₁(Pr³⁺)]的上转换激发跃迁, 789.0 nm的¹G₄(Pr³⁺)→³P₂(Pr³⁺)的上转换激发跃迁, 803.7 nm的³H₆(Pr^{3+)→1D₂(Pr3+)的上转换激发跃迁. 1G₄(Pr3+)→1I₆(Pr3+)的上转换过程因其振子强度f=23.040×10-6很大而尤其强, 在上转换激发谱上呈现出了一个强的激发态吸收上转换激发峰. 这导致了Pr(0.5)Yb(3):ZBLAN玻璃在一束激光和一束常规连续光的双频激发下的新颖有趣的激发态上转换发光现象.}     

Y3+掺杂LiV3O8正极材料电化学性能研究

 利用固相合成干冷空气淬火法,合成了一系列Y³⁺掺杂的LiV_3-yY_yO₈ (y=0,0.01,0.03,0.05,0.1,0.2)正极材料.XRD结果表明,Y³⁺掺杂量不同对LiV₃O₈结构的影响不同.适量Y³⁺掺杂能保持LiV₃O₈的原有结构,增大其d₁₀₀值,同时降低材料的结晶度.当Y³⁺掺杂过多时,样品中会产生YVO₄杂相.充放电循环、循环伏安(CV)及交流阻抗(EIS)测试结果表明,Y³⁺掺杂虽然降低了材料的初始容量,但适量的Y³⁺掺杂能稳定材料的循环性能.电池存放实验表明Y³⁺掺杂还能提高电池的存放性能.在高电压下存放15d后,掺杂样的放电容量保持率为94.2%,高于未掺杂样的88.2 %.     

龙葵糖蛋白对MCF -7细胞内[Ca2+]i的影响

研究龙葵糖蛋白对乳腺癌MCF -7细胞内[Ca2+]i的影响.通过MTT法测定龙葵糖蛋白对MCF -7细胞的细胞毒作用;Hoechst33258染色荧光显微镜下观察龙葵糖蛋白作用MCF -7细胞的形态学变化;采用Fluo - 3/AM探针标记,激光共聚焦技术观测龙葵糖蛋白对MCF -7细胞内[Ca2+]i的影响.结果表...     

Na~+、K~+、Ca~(2+)对柞蚕幼虫在体胸神经节自发放电活动的影响

以柞蚕五龄幼虫为材料 ,运用微电极电生理技术 ,以胞外记录的方法 ,记录了柞蚕幼虫在体胸神经节的自发放电活动 .并观察了胞外Na+、K+、Ca2 +的浓度变化对放电活动的影响 .结果表明 ,柞蚕幼虫胸神经节胞外自发放电有 3种形式 ,即慢节律单个放电、簇状放电及连续放电 ,其离子机制可能既有Na+动作电位 ,又有Ca2 +动作电位     

NMDA receptors mediate calcium accumulation in myelin during chemical ischaemia

Central nervous system myelin is a specialized structure produced by oligodendrocytes that ensheaths axons, allowing rapid and efficient saltatory conduction of action potentials. Many disorders promote damage to and eventual loss of the myelin sheath, which often results in significant neurological morbidity. However, little is known about the fundamental mechanisms that initiate myelin damage, with the assumption being that its fate follows that of the parent oligodendrocyte. Here we show that NMDA (N-methyl-d-aspartate) glutamate receptors mediate Ca2+ accumulation in central myelin in response to chemical ischaemia in vitro. Using two-photon microscopy, we imaged fluorescence of the Ca2+ indicator X-rhod-1 loaded into oligodendrocytes and the cytoplasmic compartment of the myelin sheath in adult rat optic nerves. The AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)/kainate receptor antagonist NBQX completely blocked the ischaemic Ca2+ increase in oligodendroglial cell bodies, but only modestly reduced the Ca2+ increase in myelin. In contrast, the Ca2+ increase in myelin was abolished by broad-spectrum NMDA receptor antagonists (MK-801, 7-chlorokynurenic acid, d-AP5), but not by more selective blockers of NR2A and NR2B subunit-containing receptors (NVP-AAM077 and ifenprodil). In vitro ischaemia causes ultrastructural damage to both axon cylinders and myelin. NMDA receptor antagonism greatly reduced the damage to myelin. NR1, NR2 and NR3 subunits were detected in myelin by immunohistochemistry and immunoprecipitation, indicating that all necessary subunits are present for the formation of functional NMDA receptors. Our data show that the mature myelin sheath can respond independently to injurious stimuli. Given that axons are known to release glutamate, our finding that the Ca2+ increase was mediated in large part by activation of myelinic NMDA receptors suggests a new mechanism of axo-myelinic signalling. Such a mechanism may represent a potentially important therapeutic target in disorders in which demyelination is a prominent feature, such as multiple sclerosis, neurotrauma, infections (for example, HIV encephalomyelopathy) and aspects of ischaemic brain injury.     

A single population of olfactory sensory neurons mediates an innate avoidance behaviour in Drosophila

All animals exhibit innate behaviours in response to specific sensory stimuli that are likely to result from the activation of developmentally programmed neural circuits. Here we observe that Drosophila exhibit robust avoidance to odours released by stressed flies. Gas chromatography and mass spectrometry identifies one component of this 'Drosophila stress odorant (dSO)' as CO2. CO2 elicits avoidance behaviour, at levels as low as 0.1%. We used two-photon imaging with the Ca2+-sensitive fluorescent protein G-CaMP to map the primary sensory neurons governing avoidance to CO2. CO2 activates only a single glomerulus in the antennal lobe, the V glomerulus; moreover, this glomerulus is not activated by any of 26 other odorants tested. Inhibition of synaptic transmission in sensory neurons that innervate the V glomerulus, using a temperature-sensitive Shibire gene (Shi(ts)), blocks the avoidance response to CO2. Inhibition of synaptic release in the vast majority of other olfactory receptor neurons has no effect on this behaviour. These data demonstrate that the activation of a single population of sensory neurons innervating one glomerulus is responsible for an innate avoidance behaviour in Drosophila.     

Calcium transients in astrocyte endfeet cause cerebrovascular constrictions

Cerebral blood flow (CBF) is coupled to neuronal activity and is imaged in vivo to map brain activation. CBF is also modified by afferent projection fibres that release vasoactive neurotransmitters in the perivascular region, principally on the astrocyte endfeet that outline cerebral blood vessels. However, the role of astrocytes in the regulation of cerebrovascular tone remains uncertain. Here we determine the impact of intracellular Ca(2+) concentrations ([Ca(2+)](i)) in astrocytes on the diameter of small arterioles by using two-photon Ca(2+) uncaging to increase [Ca(2+)](i). Vascular constrictions occurred when Ca(2+) waves evoked by uncaging propagated into the astrocyte endfeet and caused large increases in [Ca(2+)](i). The vasoactive neurotransmitter noradrenaline increased [Ca(2+)](i) in the astrocyte endfeet, the peak of which preceded the onset of arteriole constriction. Depressing increases in astrocyte [Ca(2+)](i) with BAPTA inhibited the vascular constrictions in noradrenaline. We find that constrictions induced in the cerebrovasculature by increased [Ca(2+)](i) in astrocyte endfeet are generated through the phospholipase A(2)-arachidonic acid pathway and 20-hydroxyeicosatetraenoic acid production. Vasoconstriction by astrocytes is a previously unknown mechanism for the regulation of CBF.     

双光子共焦荧光显微系统成像分析及实验研究

双光子共焦荧光显微系统可以突破传统光学显微镜的成像分辨率极限,提高厚荧光物三维扫描的横向及轴向分辨力.基于共焦荧光显微原理和菲涅耳衍射公式,分析了反射式双光子共焦荧光显微系统的三维光学传递函数.讨论了在实验条件下,共焦模块参数对双光子共焦荧光读取分辨率的影响.双光子共焦荧光系统采用的共焦小孔半径为3.92 μm时,其层析能力比采用78.4 μm共焦小孔的系统提高了1.56倍.通过已知尺寸荧光物的双光子共焦荧光成像实验,验证了共焦小孔直径与系统横向及轴向分辨率的反比关系.     

Synaptic calcium transients in single spines indicate that NMDA receptors are not saturated.

At excitatory synapses in the central nervous system, the number of glutamate molecules released from a vesicle is much larger than the number of postsynaptic receptors. But does release of a single vesicle normally saturate these receptors? Answering this question is critical to understanding how the amplitude and variability of synaptic transmission are set and regulated. Here we describe the use of two-photon microscopy to image transient increases in Ca2+ concentration mediated by NMDA (N-methyl-D-aspartate) receptors in single dendritic spines of CA1 pyramidal neurons in hippocampal slices. To test for NMDA-receptor saturation, we compared responses to stimulation with single and double pulses. We find that a single release event does not saturate spine NMDA receptors; a second release occurring 10 ms later produces approximately 80% more NMDA-receptor activation. The amplitude of spine NMDA-receptor-mediated [Ca2+] transients (and the synaptic plasticity which depends on this) may thus be sensitive to the number of quanta released by a burst of action potentials and to changes in the concentration profile of glutamate in the synaptic cleft.     

Ca^2＋ is involved in muscarine-acetylcholine-receptor-mediated acetylcholine signal transduction in guard cells of Vicia faba L.

Acetyicholine (ACh) is an important neuro-chemical transmitter in animals; it also exists in plants and plays a significant role in various kinds of physiological functions in plants. ACh has been known to induce the stomatal opening. By monitoring the changes of cytusolic Ca^2 with fluorescent probe Fiuo-3 AM under the confocal microscopy, we found that exogenous ACh increased cytosolic Ca^2 concentration of guard cells of Vicia faba L. Muscarlne, an agonist of muscarine acetyicholine receptor (mAChR), could do so as well. In contrast, atropine, the antagonist of mAChR abolished the ability of ACh to increase Ca^2 in guard cells. This mechanism is similar to mAChR in animals. When EGTA was used to chelate Ca^2 or ruthenium red to block Ca^2 released from vacuole respectively, the results showed that the increased cytosolic Ca^2 mainly come from intracellular Ca^2 store. The evidence supports that Ca^2 is involved in guard-cell response to ACh and that Ca^2 sigual is coupled to mAChRs in ACh signal transduction in guard cells.     

A functional correlate for the dihydropyridine binding site in rat brain

Calcium channels, controlling the influx of extracellular Ca2+ and hence neurotransmitter release, exist in the brain. However, drugs classed as calcium antagonists and which inhibit Ca2+ entry through voltage-activated Ca2+ channels in heart and smooth muscle, seem not to affect any aspect of neuronal function in the brain at pharmacologically relevant concentrations. Yet the dihydropyridine calcium antagonists (for example, nitrendipine) bind stereospecifically with high affinity to a recognition site on brain-cell membranes thought to represent the Ca2+ channel and consequently, the physiological relevance of these sites has been questioned. However, activation of voltage-dependent Ca2+ channels can increase cytoplasmic Ca2+ and neurotransmitter release in neuronal tissue. We show here that Bay K8644, a dihydropyridine Ca2+-channel activator, can augment K+-stimulated release of serotonin from rat frontal cortex slices and that these effects can be antagonized by low concentrations of calcium antagonists. As 3H-dihydropyridine binding to cortical membrane preparations resembles the binding in heart and smooth muscle where there are good functional correlates we conclude that the dihydropyridine binding sites in the brain represent functional Ca2+ channels that can be unmasked under certain circumstances.     

Heterotrimeric G protein participated in modulation of cytoplasmic calcium concentration in pollen cells

Cytoplasmic free calcium concentration([Ca2+]c) in pollen cells of Lilium daviddi is measured with confocal laser scanning microscopy to investigate the effect of heterotrimeric G protein (G protein) on [Ca2+]c and the possible signal transduction pathway of G protein triggering cellular calcium signal. After application, cholera toxin (CTX), an agonist of G protein, triggers a transient increase of [Ca2+]c in pollen cells, and evokes a spatial-temporal characteristic calcium dynamics; while pertussis toxin (PTX), a G protein antagonist, leads to the decrease of [Ca2+]c. Both L-type Ca2+ channel blocker verapamil and inhibitor of IP3 receptor heparin inhibit CTX-induced [Ca2+]c increase. The results show that G protein may play a role in the modulation of [Ca2+]c through enhancing the extracellular Ca2+ influx and releasing of Ca2+ from intracellular stores.     

不同机制参与黄体酮扩张兔血管作用

用离体血管条灌流实验方法 ,观察黄体酮对血管条去甲肾上腺素 (NA) ,Ca Cl2 ,KCl反应的影响 ,并观察给予 L- NNA、甲烯蓝 (MB)、吲哚美辛、普萘洛尔及去除内皮细胞后 ,黄体酮扩张血管作用的变化 .结果发现 :黄体酮 10 -4 mol· L-1及 10 -5mol· L-1分别使 NA和无 Ca2 +高 K+Krebs液中 Ca Cl2 量效曲线明显右移 ,最大反应压低 ,PD2 ′分别为 3.51和 4 .56 .黄体酮 2 .5× 10 -4mol· L-1使无 Ca2 + 液中 NA10 -6mol· L-1收缩血管作用明显减弱 (p <0 .0 0 1) ,但不影响 Ca Cl210 mmol· L-1引起的收缩 .L - NNA,MB及去除内皮可明显减弱黄体酮扩张 KCl 4 0 mmol· L-1的收缩血管作用 ,但吲哚美辛和普萘洛尔无明显影响 .结果表明 :黄体酮可通过受体操纵 Ca2 + 通道抑制 IP3 途径引起的内 Ca2 + 释放 ,也可通过电压依赖式 Ca2 + 通道抑制外 Ca2 + 内流 ,使血管条舒张 ,其作用有内皮依赖性 ,部分与 NO和 c GMP有关