党参多糖对神经干细胞硫代硫酸钠损伤的保护作用

目的研究党参多糖对神经干细胞硫代硫酸钠损伤的保护作用。方法采用离子交换柱层析和凝胶柱层析纯化得到党参多糖；取出大鼠胚胎纹状体进行神经干细胞培养，神经干细胞硫代硫酸钠损伤模型模拟脑梗死中神经元的缺氧性损伤。实验分正常对照组，硫代硫酸钠损伤组和将不同浓度党参多糖加入硫代硫酸钠损伤纽培养液中的试验组。观察硫代硫酸钠损伤后各组神经干细胞死亡率和乳酸脱氢酶漏出率，研究党参多糖对神经干细胞硫代硫酸钠损伤的保护作用。结果加入多糖的实验组神经干细胞损伤有不同程度的减轻。高浓度多糖实验组神经干细胞死亡率和乳酸脱氢酶漏出率较低，与硫代硫酸钠损伤组比较有显著性差异。结论党参多糖对神经干细胞硫代硫酸钠损伤有明显的保护作用。     

Frequency-dependent potentiation of voltage-activated responses only in the intact neurohypophysis of the rat

The loose-patch-clamp technique was used with multiple-pulse protocols to study the frequency dependence of currents from the surface of the intact rat neurohypophysis (NH) and hypothalamus. In the NH, but not in the corresponding supraoptic nucleus of the hypothalamus, an initial, single pulse of 3–8 ms duration (long pulse) potentiated a secondary pulse response starting 20–50 ms after the initial pulse. Potentiation was abolished by 4-aminopyridine (4-AP), but not by tetraethylammonium (TEA) chloride or tetrandrine, indicating the participation of A-type potassium currents. Potentiation was also abolished by CdCl₂, CoCl₂ or 1 µM nicardipine, indicating the participation of calcium currents. The potentiation was reduced significantly in the presence of 4–6 mM extracellular CaCl₂, indicating that the potentiation is not due to calcium influx. An initial train with as few as two pulses, each of 0.3–0.7 ms duration (short pulses) at 64–1,100 Hz also potentiated the secondary short pulse response significantly. We conclude that voltage-gated channels underlie this potentiation, which is due to interstitial calcium and potassium homeostasis changes induced by action potential activity and occurs only in the intact NH. A model is proposed for the participation of calcium and potassium channels in the burst patterning that is optimal for secretion from the NH.     

Erythrocyte membrane acetylcholinesterase, Na+, K+-ATPase and Mg2+-ATPase activities in patients with classical galactosaemia

BACKGROUND: Classical galactosaemia is commonly presented by high blood galactose (Gal) and galactose-1-phosphate (Gal-1-P) levels followed by mental retardation, seizures, etc. dependent on the mutation of the patients. AIM: To evaluate Gal and Gal-1-P in the blood of patients and to correlate their levels with their erythrocyte membrane acetylcholinesterase (AChE), Na+,K+-ATPase and Mg2+-ATPase activities. METHODS: Blood was obtained from nine patients on poor diet (group B) followed by a 30-d strict diet (group A) and controls (group C) in order to evaluate Gal and Gal-1-P in Guthrie cards and to correlate their concentrations with the above enzyme activities, which were measured spectrophotometrically. RESULTS: With the patients on a "loose" diet, AChE, Na+,K+-ATPase and Mg2+-ATPase activities were found to be decreased, as compared with those on strict diet and controls. Significantly (p<0.01) inverse correlation coefficients of the enzyme activities were found with Gal-1-P levels. CONCLUSION: (a) AChE, Na+,K+-ATPase and Mg2+-ATPase activities were determined to be decreased in poorly controlled patients with classical galactosaemia. (b) The enzyme activities were inversely correlated with the Gal-1-P blood levels. (c) Since Na+,K+-ATPase in the erythrocyte membranes is the isomer of Na+,K+-ATPase distributed in many tissues and in the brain, evaluation of the enzyme activity in the erythrocytes could be a useful peripheral marker of Gal-1-P toxicity.     

Expression of calcium transporters in the retina of the tiger salamander (Ambystoma tigrinum)

Changes in intracellular calcium concentration, [Ca2+]i, modulate the flow of visual signals across all stages of processing in the retina, yet the identities of Ca2+ transporters responsible for these changes are still largely unknown. In the current study, the distribution of plasma membrane and intracellular Ca2+ transporters in the retina of tiger salamander, a model system for physiological studies of retinal function, was determined. Plasma membrane calcium ATPases (PMCAs), responsible for high-affinity Ca2+ extrusion, were highly expressed in the salamander retina. PMCA isoforms 1, 2, and 4 were localized to photoreceptors, whereas the inner retina expressed all four isoforms. PMCA3 was expressed in a sparse population of amacrine and ganglion neurons, whereas PMCA2 was expressed in most amacrine and ganglion cells. Na+/Ca2+ exchangers, a high-capacity Ca2+ extrusion system, were expressed in the outer plexiform layer and in a subset of inner nuclear and ganglion layer cells. Intracellular Ca2+ store transporters were also represented prominently. SERCA2a, a splice variant of the sarcoplasmic-endoplasmic Ca2+ ATPase, was found mostly in photoreceptors, whereas SERCA2b was found in the majority of retinal neurons and in glial cells. The predominant endoplasmic reticulum (ER) Ca2+ channels in the salamander retina are represented by the isoform 2 of the IP3 receptor family and the isoform 2 of the ryanodine receptor family. These results indicate that Ca2+ transporters in the salamander retina are expressed in a cell type-specific manner.     

Microwave cell death: Immunohistochemical and enzyme histochemical evaluation

In Japan, microwave coagulation therapy (MCT) has been used for the management of primary and metastatic liver cancer. Needle biopsy examination from the lesion has frequently shown the presence of nucleated cancer cells in histopathological examinations, prompting the conclusion that cancer cells are not completely eliminated by microwave therapy, whereas computed tomography and ultrasonography examinations show tumor regression. To determine whether microwave-treated tissue contains functionally viable cells, an examination of the Na+-K+-ATPase protein and its activity using immunohistochemical and enzyme histochemical methods were carried out in microwave-treated rat liver. Four concentric, morphologically identifiable zones around the microwave probe needle appeared 2 days after treatment. Zone A, which was between the innermost spongy zone and the outer necrotic zone, contained only slight morphological alterations in the hepatocytes, which had slightly hyperchromatic nuclei and mildly eosinophilic cytoplasm. The hepatocytes in zone A were found to be positive for the Na+-K+-ATPase antigenicity but negative for enzyme activity, indicating that zone A was undergoing cell death, although morphologically this was not discernible. This type of cell death caused by microwave treatment is morphologically different from previously known types of cell death, either oncosis or apoptosis.     

Erythropoietin improves cardiac contractility in post-hypoxic mice

Mice myocardia, in which plasma erythropoietin (EPO) concentrations were modified in response to different experimental conditions, were studied to evaluate contractility (dF/dt). CF1 mice were randomly separated into four main groups: group I, normocythaemic normoxic; group II-a, normocythaemic intermittently exposed to hypobaria for 72 h; group II-b, normocythaemic intermittently exposed to hypobaria for 3 weeks; group III, hypertransfused polycythaemic exposed to 72 h hypobaria; and group IV, hypertransfused polycythaemic maintained in normobaric air. Plasma EPO, contractile studies and binding assays were performed. The dF/dt was significantly higher in group II-a than in group I and group II-b; but in groups III and IV, the dF/dt was reduced. The toxic action of ouabain was reduced and delayed in its onset, accompanied by increased numbers of 3H-ouabain binding sites in group II-a. Contractility was positively correlated with plasma EPO (pEPO) in the different groups. Treating group I with recombinant human (rHu)-EPO enhanced contractility while treating group II-a with a monoclonal anti-EPO decreased the dF/dt. The inhibition of enzymatic pathway(s) known to participate in the cytokines signal transduction, decreased the basal dF/dt values on atria from group II-a and on group I atria treated with rHu-EPO. The results demonstrated: (1) a cardiac non-haematopoietic effect of EPO; (2) that mice in which the pEPO concentration increased showed improvement in contractility and in the therapeutic action of ouabain; and (3) it is possible that EPO may act as a cardioprotective agent by modulating the cardiac Na+-K+ pump.     

射频联合紫衫醇＋卡铂方案治疗晚期非小细胞肺癌的临床观察

目的：观察多极射频消融（RFA）联合紫衫醇＋卡铂方案（PC）治疗晚期非小细胞肺癌（NSCLC）的临床效果。方法：30例晚期NSCLC（Ⅲ、Ⅳ期）采用RFA联合PC方案治疗,并与28例单纯PC方案化疗进行比较。结果：以疗效、生活质量评分及生存时间等指标评价,RFA联合PC方案治疗组明显优于单纯PC方案化疗组,疗效差异有显著意义,P〈0.01。结论：RFA联合PC方案化疗明显提高晚期NSCLC治疗效果,可作为晚期NSCLC的综合治疗方法。     

原发性高血压肾病患者红细胞ATP酶活性检测的临床意义

目的 探讨原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶活性的改变参与原发性高血压肾病的可能机制。方法 按Reilni制膜法测定32例原发性高血压无肾病和40例原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶含量,并与35名正常健康人作比较。结果 原发性高血压无肾病组和肾病组细胞膜Na^＋、K＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶活性均显著地低于正常人组（P〈0.01）。原发性高血压肾病组与无肾病组亦有显著性差异（P〈0.05）。结论 原发性高血压肾病的发生和发展与细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP的活性有密切的关系。     

熏洗一号方对大鼠失神经支配骨骼肌乙酰胆碱酶与Na^＋-K^＋-ATP酶影响的实验研究

目的：研究中药熏洗一号方对失神经支配骨骼肌乙酰胆碱酶与Na^＋-K^＋-ATP酶的影响。方法：雄性SD大鼠120只，造模成功后随机分为熏洗一号方组、丹参组、模型组和空白对照组，每组各30只。各组实验动物分别在术后7d、14d和21d处死，股直肌肌腹组织块取材，常规HE染色，分别观察失神经支配后骨骼肌结构，乙酰胆碱酯酶活性和骨骼肌匀浆液Na^＋-K^＋-ATP酶改变。结果：1．HE染色：按优劣排列依次为熏洗一号方组、丹参组、模型组。2．乙酰胆碱酯酶活性：随着试验观察时间的推移，熏洗一号方组乙酰胆碱酯酶活性逐渐增强，最后接近正常水平，染色均匀，运动终板结构规则，呈椭圆形或卵圆形花纹状结构，与空白组相比（P〉0．05）；模型组和丹参组乙酰胆碱酯酶活性弱，与空白对照组相比（P〈0．01）。3．骨骼肌匀浆液Na^＋-K^＋-ATP结果：术后7d各组Na^＋-K^＋-ATP酶组间比较没有统计学意义（P〉0．05）。术后14d熏洗一号方组与空白对照组对比（P〈0．05）。术后21d，熏洗一号方组与空白对照组对比（P〈0．01），且熏洗一号方组Na^＋-K^＋-ATP酶含量最高。结论：熏洗一号方能延缓神经肌肉运动终板（Motor endplate，MEP）与效应器的变性，改善失神经支配骨骼肌的营养供应、延缓骨骼肌的萎缩。