放化疗性口腔黏膜炎动物模型研究进展

由放疗和(或)化疗诱发的口腔黏膜炎症,可能导致患者疼痛、说话吞咽困难、局部和全身感染风险增高,甚至中断抗癌治疗,严重影响患者生活质量。放化疗性口腔黏膜炎的发病机制复杂而且防治较为困难,而动物模型在探究放化疗性口腔黏膜炎的发病机制以及探索更好的防治方法中发挥了重要作用,本文就以现有的放化疗性口腔黏膜炎动物模型的复制及评估方法予以综述。文献复习结果表明,国内外采用小鼠、大鼠、金仓鼠等动物来复制动物模型;放疗诱发的口腔黏膜炎的诱导方法有仅采用X射线设备对动物进行局部单剂量照射或局部分割照射,或照射时辅助使用化疗药物5 氟尿嘧啶或顺铂,也可以采用137铯作为放射源进行局部照射;单纯使用化疗药物5 氟尿嘧啶诱发的口腔黏膜炎一般症状较轻,因此多采用5 氟尿嘧啶联合机械刺激或乙酸进行诱导;评估放化疗性口腔黏膜炎的方法主要为大体样本观察及组织病理学观察。     

Thermal Decomposition Behavior of Prussian Blue in Various Conditions

Prussian blue analogs (PBA) are widely studied for radioactive cesium decontamination. However, there are fewer works related to their post use storage. Considering the oxidative stabilization of the material after the selective uptake of Cs, the thermogravimetric properties in powder and bead form, with various Cs and other alkali metal ions adsorbed, and various heating rates were studied. TG-DTA taken in dry air condition shows an exothermic decomposition at ~270 °C. This temperature varied with the heating rate, mass, and the proportion of adsorbed ions. The best condition for complete oxidation of Prussian blue (PB) is found to be a gradual oxidative decomposition by heating in the temperature range of 200–220 °C until the total mass is decreased by >35%. After this, the temperature could be safely increased to >300 °C for the complete oxidative decomposition of PB that formed iron oxide and salt of the adsorbed Cs. A pilot scale test conducted using the radioactive Cs adsorbed Prussian blue microbeads (PB-b) confirmed that no Cs was released in the effluent air during the process.     

Hyperpolarization-activated ion currents in cultured rat cortical and spinal cord astrocytes

Hyperpolarization-activated currents were recorded from rat brain cortical and spinal cord astrocytes maintained in culture. Spinal cord astrocytes expressed primarily an inward rectifier potassium current characterized by time-dependent inactivation, a strong dependence on extracellular Na⁺ and insensitivity to intracellular GTP-γ-S (0.2 mM). In cortical astrocytes voltage clamp protocols aimed to elicit currents activated at, or negative to cell membrane potentials led to the development of two distinct ion currents. The most prominent current resembled the inward rectifier potassium current. This component was sensitive to blockade by extracellular cesium and was greatly reduced during recordings performed with GTP-γ-S (0.2 Mm) added to the pipette solutions. The remaining current component was similar to the endothelial I_ha current. I_ha conductance was enhanced by extracellular potassium and the current reversal potential behaved as expected for a mixed cation, Na⁺/K⁻ current, I_ha was nearly abolished after removal of extracellular Na⁺. These results are consistent with the expression of a novel mixed cation conductance in glial cells, possibly involved in extracellular potassium buffering. © 1996 Wiley-Liss, Inc.     

Impact of Cesium Concentration on Optoelectronic Properties of Metal Halide Perovskites

Performance of a perovskite solar cell is largely influenced by the optoelectronic properties of metal halide perovskite films. Here we study the influence of cesium concentration on morphology, crystal structure, photoluminescence and optical properties of the triple cation perovskite film. Incorporation of small amount (x = 0.1) of cesium cations into Cs_x(MA_0.17FA_0.83)_1−x Pb(I_0.83Br_0.17)₃ leads to enhanced power conversion efficiency (PCE) of the solar cell resulting mainly from significant rise of the short-current density and the fill factor value. Further increase of Cs concentration (x > 0.1) decreases the film’s phase purity, carrier lifetime and correspondingly reduces PCE of the solar cell. Higher concentration of Cs (x ≥ 0.2) causes phase segregation of the perovskite alongside with formation of Cs-rich regions impeding light absorption.     

氯化铯对小鼠空间学习记忆的影响

目的探讨氯化铯(CsCl)一种非选择性的超极化激活-环核苷酸门控的阳离子通道(HCN通道)阻断剂对小鼠空间学习记忆的影响及其作用的机制。方法在小鼠脑缺血/再灌模型上,连续2wk给予CsCl(200、400mg·kg-1,ig),用Morris水迷宫实验方法检测小鼠空间学习记忆成绩,实验结束后动物处死取脑测定海马组织MDA的含量,SOD、tNOS和iNOS的活性。采用离体海马脑片培养,用高效液相荧光检测方法测定CsCl(0.2,2,20mmol.L-1)对脑片培养液中谷氨酸、甘氨酸和牛磺酸释放的影响。结果与缺血/再灌组相比,CsCl组小鼠的游泳距离延长(P<0.05),海马组织MDA的含量,SOD、tNOS和iNOS的活性无明显改变.在离体海马脑片培养实验,CsCl可剂量依赖性抑制谷氨酸的释放(P<0.05);对其它氨基酸的释放没有影响。结论提示CsCl可损伤小鼠的空间学习记忆,该作用可能与其抑制海马谷氨酸的释放有关。     

Functional role of the potassium-induced stimulation of oxygen uptake in brain slices studied with cesium as a probe

The potassium-induced stimulation of oxygen consumption in brain slices has a threshold value of 15-20 mM potassium, and it reaches its maximum at 35-50 mM. Although this phenomenon now has been known for almost 50 years, its physiological role remains undetermined. One reason for this may be that the high concentrations of potassium that are required for this response also have many other consequences, e.g., a depolarization of the cells, and that the different effects to some extent may mask each other. For this reason this investigation studied the effects of cesium, which evokes a maximal stimulation of oxygen consumption already at 15 mM. Like potassium, concentrations of cesium that stimulate oxygen consumption also lead to an enhanced swelling. Unlike potassium, the sodium content is affected very little by these concentrations of cesium, whereas cesium and chloride contents are increased. On this basis it is concluded that the cesium-induced stimulation of oxygen uptake is a metabolic manifestation of an active uptake of cesium and chloride, which secondarily leads to an uptake of water, i.e., the cesium-induced swelling. Analogously, it is suggested that the potassium-induced stimulation of oxygen uptake represents an active accumulation of potassium and chloride.     

Spontaneous, Electrically, and Cesium Chloride Induced Arrhythmia and Afterdepolarizations in the Rapidly Paced Dog Heart

JONES, D.L., et al. : Spontaneous, Electrically, and Cesium Chloride Induced Arrhythmia and Afterdepolarizations in the Rapidly Paced Dog Heart. Despite frequent arrhythmia and sudden death in heart failure, attempts to study arrhythmia mechanisms in patients are difficult. The dog heart, paced for several weeks at a fast rate to induce heart failure is prone to arrhythmia. The aim of this study was to determine the activation patterns of spontaneous and electrically induced arrhythmia and the susceptibility of the failing dog heart to arrhythmia and early afterdepolarization (EAD) induced triggered activity elicited by exogenous administration of cesium chloride (CsCl). The hearts of 56 mongrel dogs were paced at 240 beats/min for 3–5 weeks (heart failure group). Twenty‐one similarly operated, but not paced dogs served as the control group. At baseline, all dogs were healthy as assessed electrophysiologically and hemodynamically. Spontaneous (bradycardia, tachycardia, and arrhythmic deaths) and electrically induced arrhythmia was frequent in dogs with heart failure. Also, the minimal dose of CsCl that produced ventricular tachycardia was significantly lower in the heart failure than the control dogs (1.02 ± 0.02 vs 1.21 ± 0.07 mMol/kg, P < 0.05 ). Epicardial mapping during spontaneous and electrically induced arrhythmia in the heart failure dogs showed initiation patterns with focal origin, often from multiple sites. This pattern was consistent with the patterns observed with CsCl induced ventricular tachycardia. In in vitro microelectrode studies, CsCl superfusion (2.5–5 mMol/L ) induced triggered activity due to EADs within 30 minutes, in seven of the eight Purkinje fibers from four heart failure dogs. EADs were also found in ventricular myocytes of papillary muscle from two heart failure dogs. In contrast, 5 mMol/L CsCl induced EADs in only one of eight Purkinje fibers from the hearts of four control dogs and no papillary myocytes even with continuous superfusion for up to 60 minutes (P < 0.01 ). These results demonstrate that pacing induced heart failure in the dog has an increased tendency to develop ventricular tachycardia and triggered activity unmasked by CsCl.     

Cesium-133: a potential reporter of the hepatic uptake of contrast agents.

NMR spectroscopy of intracellularly located (133)Cs has been used to monitor the uptake of Gd-EOB-DTPA by the isolated rat liver. As shown by (31)P spectroscopy, accumulation of (133)Cs ions in hepatocytes does not produce detectable effects on the metabolism. The hepatic internalization of Gd-EOB-DTPA was followed by the paramagnetic relaxation enhancement of the intracellular (133)Cs ions, and confirmed by parallel quantitations of Gd and Cs run by inductively coupled plasma (ICP) analysis of liver samples and aliquots of perfusate. The relaxation data significantly underestimate the Gd content, suggesting a potential compartmentation of Cs(+) and/or the contrast agent. Magn Reson Med 45:711-715, 2001.     

Inwardly rectifying K(+) (Kir) channels antagonize ictal-like epileptiform activity in area CA1 of the rat hippocampus

Reactive glial cells, for example, from patients with temporal lope epilepsy have a reduced density of inward rectifying K(+) (Kir) channels and thus a reduced K(+) buffering capacity. Evidence is accumulating that this downregulation of Kir channels could be implicated in epileptogenesis. In rat hippocampal brain slices, prolonged exposure to the nonselective Kir channel antagonist, Cs(+) (5 mM), gives rise to an epileptiform field potential (Cs-FP) in area CA1 composed of an initial positive (interictal-like) phase followed by a prolonged negative (ictal-like) phase. We have previously shown that the interictal-like phase depends on synaptic activation. The present study extends these findings by showing that the ictal-like phase of the Cs-FP is (i) sensitive to osmotic expansion of the extracellular space, (ii) reversed very quickly during wash out of Cs(+), and (iii) re-established in the presence of Ba(2+) (30-200 microM) or isosmotic low extracellular concentration of Na(+) ([Na(+)](o), 51.25 mM). The interictal-like phase showed less or no sensitivity to these treatments. In the complete absence of Cs(+), the Cs-FP could be fully reconstructed by the combined application of 4-aminopyridine (0.5 mM), an isosmotic high extracellular concentration of K(+) ([K(+)](o), 7 mM), and low [Na(+)](o) (51.25 mM). These results suggest that the interictal-like phase is initiated through synaptic activation and results from an unspecific increase in neuronal excitability, whereas the ictal-like phase is entirely dependent on blockade of Kir channels in CA1. We propose that glial dysfunction-related loss of Kir channels may not alone be sufficient for starting the induction process, but will likely increase the tendency of an epileptogenic process to proceed into seizure activity.