窒息新生儿脐血D-二聚体水平和红细胞膜Na~+-K~+-ATP酶活性变化

目的:分析窒息新生儿脐血pH、D-二聚体水平及红细胞膜Na+-K+-ATP酶活性变化。方法 :选择临产过程出现急性胎儿窘迫孕妇40例,其剖宫娩出新生儿以1min Apgar评分确定为正常者20例(窘迫组),出现窒息者20例(窒息组);另选无急性胎儿窘迫、同样剖宫娩出的正常新生儿20例作为对照组。取各组脐动脉血,血气分析仪检测pH值,免疫比浊法检测D-二聚体水平,定磷法检测红细胞膜Na+-K+-ATP酶活性。比较各组上述指标的差异。结果:方差分析显示,各组脐动脉血pH值、D-二聚体水平和红细胞膜Na+-K+-ATP活性差异均有统计学意义(P0.05)。窒息组脐动脉血pH值明显低于对照组和窘迫组(P均0.05),D-二聚体水平显著高于对照组和窘迫组(P均0.05),红细胞膜Na+-K+-ATP酶活性显著低于对照组与窘迫组(P均0.05);窘迫组pH值和红细胞膜Na+-K+-ATP酶活性显著低于对照组(P均0.05)。结论 :窒息新生儿纤溶和红细胞膜泵功能检测结果,可为新生儿窒息治疗措施的选择提供实验依据。     

Effects of Anthopleurin-Q on Concentration in Cultured the Intracellular Free Ca^2＋ Rat Cortical Astrocytes

Objective： To investigate the effect of anthopleurin Q （AP Q） on the intracellular Ca^2＋ concentration （ECa^2＋]i） in cultured cortical astrocytes of rats. Methods： The [Ca^2＋]i was monitored by calcium imaging with Ca^2＋ sensitive fluorescent probe fura 2. Results： A concentration of 300 nmol/L AP-Q increased the [Ca^2＋]i in astrocytes by （136.98%＋35.63%） （n=28）,when compared with the baseline level. Furthermore, the elevation of [Ca2＋]i was prevented by extracellular calcium free solution or when the extraeellular Na^＋ was replaced by NMDG^＋ , and was decreased by Ni^＋ ,a non specific antagonist of Na^＋/Ca^2＋ exchanger. Conclusion： AP-Q induced the intracellular [Ca^2＋]i elevation in cultured rat cortical astrocytes via activating the reverse mode of Na^＋/Ca^2＋ exchanger. AP-Q may be a useful tool to develop experimental model of seizures.     

阻断NHE1抑制人胶质母细胞瘤细胞增殖和侵袭的研究

目的分析Na⁺/H⁺交换蛋白1（NHE1）抑制剂对癌基因BRAF野生型（BRAF^WT）和激活型BRAF^V600E突变的胶质母细胞瘤（GBM）细胞生长和侵袭能力的影响。 方法NHE1抑制剂Cariporide分别处理U251（BRAF^WT）和AM38（BRAF^V600E）GBM细胞系,乙酰甲酯化的2’,7’-双（2-羧乙基）-5（6）-羧荧光素荧光探针处理细胞并采用紫外分光光度计检测细胞在440 nm与490 nm的荧光强度,计算荧光强度比值以反映NHE1的活性,MTT法检测细胞增殖活性,基质胶-Transwell实验检测细胞侵袭能力。 结果AM38细胞的NHE1活性、增殖和侵袭能力均显著高于U251细胞,差异均有统计学意义（P=0.006、0.010、0.047）;Cariporide处理的U251和AM38细胞的NHE1活性、增殖和侵袭能力均显著低于溶剂二甲基亚砜处理的U251和AM38细胞,差异均有统计学意义（U251：P=0.012、0.023、0.044;AM38：P=0.006、0.001、0.038）。 结论采用Cariporide阻断NHE1活性可有效抑制BRAF^WT和BRAF^V600E突变型GBM细胞的增殖和侵袭。     

AMOG/β2 and glioma invasion: does loss of AMOG make tumour cells run amok?

The beta2 subunit of Na,K-ATPase, initially described as adhesion molecule on glia (AMOG), has been shown to mediate neurone-astrocyte adhesion as well as neural cell migration in vitro. We have investigated the expression of AMOG/beta2 in human gliomas and its effect on glioma cell adhesion and migration. Compared to normal astrocytes of human brain, AMOG/beta2 expression levels of neoplastic astrocytes were down-regulated in biopsy specimens and inversely related to the grade of malignancy. One rat and four human glioma cell lines showed complete loss of AMOG. To investigate the function of AMOG/beta2, its expression was re-established by transfecting an expression plasmid into AMOG/beta2-negative C6 rat glioma cells. In vitro assays revealed increased adhesion and decreased migration on matrigel of AMOG/beta2-positive cells as compared to their AMOG/beta2-negative counterparts. We conclude that increasing loss of AMOG/beta2 during malignant progression parallels and may underlie the extensive invasion pattern of malignant gliomas.     

Regulatory volume increase in rat pancreatic β-cells

 This study investigated regulatory volume increase (RVI) in rat pancreatic β-cells. Volume changes in isolated β-cells were measured by a video-imaging method. Cell shrinkage was induced by exposure to solutions made hypertonic by the addition of 100 mM mannitol. In HEPES-buffered solutions, β-cells exhibited an RVI which was almost completely abolished by 10 μM bumetanide. These data indicate that Na⁺-2Cl^–-K⁺ cotransporters make a major contribution to RVI in β-cells. In HCO₃ ^–-buffered solutions, however, an RVI was observed in the presence of 10 μM bumetanide. This bumetanide-insensitive component of RVI was inhibited by 100 μM amiloride or 100 μM 4,4’-diisothiocyanatostilbene-2,2’-disulphonic acid (DIDS). These data suggest that, in addition to the Na⁺-2Cl^–-K⁺ cotransporter, functionally coupled Na⁺-H⁺ exchangers and Cl^–-HCO₃ ^– exchangers may also contribute to RVI in pancreatic β-cells. Received: 3 July 1997 / Received after revision and accepted: 1 September 1997     

Cardiovascular,hormonal and body fluid changes during prolonged exercise

Summary During prolonged heavy exercise a gradual upward drift in heart rate (HR) is seen after the first 10 min of exercise. This secondary rise might be caused by a reduction in stroke volume due to reduced filling of the heart, which is dependent upon both hemodynamic pressure and blood volume. Swimming and bicycling differ with respect to hydrostatic pressure and to water loss, due to sweating. Five subjects were studied during 90 min of bicycle exercise, and swimming the leg kick of free style. The horizontal position during swimming resulted in a larger cardiac output and stroke volume. After the initial rise in heart rate the secondary rise followed parallel courses in the two situations. The rises were positively related to the measured increments in plasma catecholamine concentrations, which continued to increase as exercise progresssed. The secondary rise in HR could not be explained by changes in plasma volume or in water balance, nor by changes in plasma [K]. The plasma volume decreased 5–6% (225–250 ml) within the first 5 to 10 min of exercise both in bicycling and swimming, but thereafter remained virtually unchanged. The sweat loss during bicycling was four times greater than during swimming; but during swimming the hydrostatic conditions induced a diuresis, so that the total water loss was only 25% less than during bicycling.     

Mapping human brain capillary water lifetime: high‐resolution metabolic neuroimaging

Shutter‐speed analysis of dynamic‐contrast‐agent (CA)‐enhanced normal, multiple sclerosis (MS), and glioblastoma (GBM) human brain data gives the mean capillary water molecule lifetime (τ_b) and blood volume fraction (v_b; capillary density–volume product (ρ^?V)) in a high‐resolution ¹H₂O MRI voxel (40 μL) or ROI. The equilibrium water extravasation rate constant, k_po (τ_b^?1), averages 3.2 and 2.9 s^?1 in resting‐state normal white matter (NWM) and gray matter (NGM), respectively (n = 6). The results (italicized) lead to three major conclusions. (A) k_po differences are dominated by capillary water permeability (P_W^?), not size, differences. NWM and NGM voxel k_po and v_b values are independent. Quantitative analyses of concomitant population‐averaged k_po, v_b variations in normal and normal‐appearing MS brain ROIs confirm P_W^? dominance. (B) P_W^? is dominated (>95%) by a trans(endothelial)cellular pathway, not the P_CA^? paracellular route. In MS lesions and GBM tumors, P_CA^? increases but P_W^? decreases. (C) k_po tracks steady‐state ATP production/consumption flux per capillary. In normal, MS, and GBM brain, regional k_po correlates with literature MRSI ATP (positively) and Na⁺ (negatively) tissue concentrations. This suggests that the P_W^? pathway is metabolically active. Excellent agreement of the relative NGM/NWM k_pov_b product ratio with the literature ³¹PMRSI‐MT CMR_oxphos ratio confirms the flux property. We have previously shown that the cellular water molecule efflux rate constant (k_io) is proportional to plasma membrane P‐type ATPase turnover, likely due to active trans‐membrane water cycling. With synaptic proximities and synergistic metabolic cooperativities, polar brain endothelial, neuroglial, and neuronal cells form “gliovascular units.” We hypothesize that a chain of water cycling processes transmits brain metabolic activity to k_po, letting it report neurogliovascular unit Na⁺,K⁺‐ATPase activity. Cerebral k_po maps represent metabolic (functional) neuroimages. The NGM 2.9 s^?1 k_po means an equilibrium unidirectional water efflux of ~10¹⁵ H₂O molecules s^?1 per capillary (in 1 μL tissue): consistent with the known ATP consumption rate and water co‐transporting membrane symporter stoichiometries. © 2015 The Authors NMR in Biomedicine Published by John Wiley & Sons Ltd.     

Influence of Alloying Element Mg on Na and Sr Modifying Al-7Si Hypoeutectic Alloy

The influence of alloying element Mg on Na and Sr modifying Al-7Si hypoeutectic alloys was investigated. The residual content of Na and the morphology of modified eutectic silicon were characterized. It was found that the alloying element Mg had an enhanced effect on the uptake of sodium in the Al-7Si hypoeutectic alloy modified by the Na-contained modifier. Moreover, the morphology of eutectic silicon of the modified Al-7Si alloys was significantly different from that of Al-7Si-0.4Mg alloys in the present research. When the addition of the modifier is enough, both modifiers could entirely modify the eutectic silicon phase of Al-7Si alloys, while incompletely modified eutectic silicon was observed in both Na-modified and Sr-modified Al-7Si-0.4Mg alloy. It was observed that there was an adhering relationship between the partially modified eutectic silicon with Mg-rich phases. According to the results, it can be proposed that the addition of Mg will affect the solidification behavior of alloys, thereby, leading to the incomplete modification of eutectic silicon phases.