细胞内游离Ca2+在发育中大鼠皮层神经元无镁诱导惊厥性损伤中的作用

目的: 观察细胞内游离Ca2+([Ca2+]i)在培养的不同发育阶段皮层神经元无镁诱导惊厥性损伤中的作用,探讨惊厥性脑损伤年龄依赖性的可能机制.方法:体外培养6 d、17 d的胚胎大鼠皮层神经元用无镁细胞外液处理3 h,或于无镁处理前用NMDA(N-甲基-D-门冬氨酸)受体拮抗剂或Ca2+通道阻滞剂预处理,用MTT代谢率测定的方法检测神经元损伤,以Fluo-3作标记用激光共聚焦显微镜扫描的方法检测[Ca2+]i.结果:体外培养6 d、17 d的神经元单纯无镁组MTT代谢率较同期对照组降低.应用MK-801 10 μmol*L-1、AP-5 50 μmol*L-1、尼莫地平10 μmol*L-1预处理后再给无镁处理,培养6 d、17 d的神经元MTT代谢率均不同程度高于同期单纯无镁组.培养6 d、17 d的神经元相对荧光强度之间差异有显著性,两者与基线荧光强度比较差异亦有显著性.应用上述各种拮抗剂后,[Ca2+]i改变的峰值均明显低于同期单纯无镁组.结论: 在体外不同发育阶段的神经元,短暂无镁处理诱导惊厥样放电所引起的神经元线粒体功能损伤以及[Ca2+]i改变程度不同.这种[Ca2+]i改变的年龄依赖性可能是惊厥导致神经元损伤的年龄依赖性的机制之一.NMDA受体-Ca2+通道激活是导致这种[Ca2+]i改变及神经元损伤的关键环节.     

PLACENTAL CALCIUM PUMP: CLINICAL-BASED EVIDENCE

Placenta can be considered as a pump of calcium necessary for the normal development of the fetus. We believe that the location of this pump is in the placental basement membrane. The calcification of this membrane has been described only in cases of in utero fetal death. In this study we describe for the first time a case of placental calcification in a living fetus. The fetus of a normal 21-year-old pregnant woman showed heart abnormalities but the genetic analysis showed a normal male karyotype. The histology of the placenta demonstrated multiple intravillous linear and granular calcific incrustations The hemtoxylin/eosin stain of the sections revealed basement membrane calcific incrustations and intravillous calcium deposits. We postulate that the fetal circulation in the villi was impaired and the calcium that reached the villi from the mother was deposited at this level.     

预防性应用钙拮抗剂对缺血大鼠心肌细胞和红细胞内钙变化的影响

利用大鼠缺血模型观察预防性应用钙桔抗剂尼莫地平对大鼠缺血心肌和红细胞内钙的影响发现，缺血时大鼠心肌细胞、心肌组织和红细胞内均有钙积聚，红细胞膜钙泵活性下降；缺血前30分钟给予尼莫地平可使红细胞内钙恢复至正常水平，红细胞膜钙泵活性升高；心肌细胞和心肌组织内钙虽较缺血鼠降低，但仍高于对照组。提示：（1）缺血时细胞的钙内流可能是全身性的；（2）预防性应用尼莫地平可阻滞或减轻细胞内钙超载，同时还可保护细胞膜膜泵活性。     

雌激素,胎盘生乳素,钙,磷与妊高征的关系

目的：探讨雌激素，胎盘生乳素，钙在妊高征发病中的作用及其相互关系，方法：采用放射免疫法及离心分析钙试剂，测定了４２例妊高征患者血清雌二醇，胎盘生乳素，钙，磷及尿钙，磷的含量，３４例同期门诊正常孕妇作为对照组，结果：轻度妊高征患者血清雌二醇明显增加（Ｐ〈０．０５）。重度妊高征患者血清胎盘生乳素显著减少（Ｐ〈０．０５），轻，中，重度妊高征患者血钙，尿钙含量显著降低（Ｐ〈０．０５，Ｐ〈０．０１，Ｐ〈０．     

心衰患儿红细胞内外钙离子浓度的变化及临床意义 心衰患儿红细胞内外钙离子浓度的变化及临床意义

目的：为了深讨心肌细胞内钙离子浓度的变化与心力衰竭发生的关系。方法：原子吸收分光技术测定红细胞内外Ca2+含量。我们对住院的56例心力衰竭患儿进行了红细胞内及血浆钙离子浓度的测定，并与30例正常小儿对照。结果：心衰患儿红细胞内Ca2+浓度明显升高，血浆Ca2+浓度降低，与对照组相比有非常显著性差异（P＜0．001）。其升高程度与心衰呈正相关（r=0．63，P＜0．01），即心衰越重，心功能越差，红细胞内Ca2+浓度升高亦越明显。而当心衰纠正，心功能恢复后，红细胞内Ca2+浓度则明显下降，血浆Ca2+浓度也恢复正常。而不同病因所致的心衰，其间红细胞内Ca2+浓度升高程度无明显差异。结论：提示钙离子参与了心力衰竭的发生与发展。     

人血清中IgE含量随年龄增长的改变及临床意义

IgE是反应素型抗体,血清中浓度很低,在体内与嗜碱细胞或肥大细胞表面的IgE受结合.对不同年龄组正常人进行血清IgE检查,发现随年龄增加,IgE含量有增高趋势,并且随年龄增高亦有过敏性疾病多发的趋势.吸烟数量过多、时间长亦可使IgE增高.     

微量元素锌在佝偻病治疗中的效果观察

目的 :探讨补充锌 +维生素D +钙剂治疗佝偻病的效果。方法 :随机分为 3组 ,每组各 5 3例。对照组给予常规治疗 (即维生素D +钙剂 ) ,治疗 1组先给予锌治疗 1个月后 +常规治疗 ,治疗 2组同时给予锌 +常规治疗。 3个月为 1疗程。治疗前后检测血清微量元素及骨碱性磷酸酶 (BALP)等项目。结果 :治疗 1、2组疗效好于对照组 ,差异非常显著 (P <0 0 1) ;治疗1组疗效好于治疗 2组 ,差异有显著性 (P <0 0 5 )。结论 :治疗大多数伴低锌的佝偻病先补锌 1个月 ,再加常规治疗 ,疗效更佳。     

Effect of different phospholipid-cholesterol membrane compositions on liposome-mediated formation of calcium phosphates

Summary The present report compares the effects of different membrane phospholipid (PL)-cholesterol compositions on the kinetics of liposome-mediated formation of calcium phosphates from metastable solutions (2.25 mM CaCl₂; 1.5 mM KH₂PO₄) at 22°C, pH 7.4 and 240 mOsm. In most experiments, the liposomes were composed of 7:2:X mixtures of phosphatidylcholine (PC), neutral or acidic phospholipids, and cholesterol (Chol, X=0, 10, 35, or 50 mol%). The neutral phospholipids (NPL) examined, in addition to PC, were phosphatidylethanolamine (PE) and sphingomyelin (Sph), and the acidic phospholipids (APL) examined were dicetylphosphate (DCP), dioleolylphosphatidylglycerol (DOPG), dioleolylphosphatidic acid (DOPA), phosphatidylserine (PS) and phosphatidylinositol (PI). The 7:2:X liposomes did not initiate mineralization in metastable external solutions per se or, with the exception of DOPA, show extensive Ca-PL binding. However, solution Ca²⁺ losses due to precipitation occurred when the liposomes were encapsulated with 50 mM KH₂PO₄ and made permeable to external Ca²⁺ with X-537A. The extent of these Ca²⁺ losses was sensitive to both the phospholipid and Chol makeup of the membrane. Moderate-to-extensive intraliposomal precipitation occurred in all 7PC:2APL and 7PC:2NPL liposomes containing 0 or 10 mol% Chol. In contrast, at 50 mol% Chol, mineralization inside all liposomes was negligible. The only significant discriminating effect on internal mineralization among the different phospholipids was observed at 35 mol% Chol, where mineral accumulations ranged from negligible to moderate. At 0 or 10 mol% Chol, extraliposomal precipitation was extensive in all but DOPA- and PS-containing liposomes. However, onece intraliposomal yields declined at the higher Chol levels, external mineralization was either delayed or totally blocked in all liposome preparations. Other experiments showed that Sph substituted for PC in 7NPL:2DCP:1Chol liposomes totally blocked both intra- and extraliposomal precipitaiton. PE substituted in this manner, however, blocked only extraliposomal precipitation. The results of this study suggest that interference of the membrane transport processes controlling intraliposomal precipitation [15] by high (50 mol%) Chol levels is not significantly compromised by the specific APL or NPL incorporated in the membrane. Similarly, the data suggest that Chol does not directly affect the specfic interactions of the different membrane APLs with the mineral phase. On the other hand, the substitution of other NPLs for PC can affect the role of APLs such as DCP in liposome-mediated mineralization.