本刊加入“万方数据——数字化期刊群”的声明

为了实现科技期刊编辑、出版发行工作的电子化,推进科技信息交流的网络化进程,我刊现已入网“万方数据———数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据———数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据———数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。本刊加入“万方数据——数字化期刊群”的声明@本刊编辑部     

本刊加入“万方数据——数字化期刊群”的声明

为了实现期刊编辑、出版工作的网络化,我刊现已入网“万方数据——数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据——数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊或特别声明需另作处理。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据——数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。本刊加入“万方数据——数字化期刊群”的声明@本刊编辑部     

本刊加入“万方数据——数字化期刊群”的声明

为了实现科技期刊编辑、出版发行工作的电子化,推进科技信息交流的网络化进程,我刊现已入网“万方数据———数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据———数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据———数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。本刊加入“万方数据——数字化期刊群”的声明@本刊编辑部     

本刊加入“万方数据——数字化期刊群”的声明

为了实现科技期刊编辑、出版发行工作的电子化,推进科技信息交流的网络化进程,我刊现已入网“万方数据——数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据——数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据——数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。本刊加入“万方数据——数字化期刊群”的声明@本刊编辑部     

本刊加入“万方数据——数字化期刊群”的声明

为了实现科技期刊编辑、出版发行工作的电子化 ,推进科技信息交流的网络化进程 ,我刊现已入网“万方数据———数字化期刊群” ,所以 ,向本刊投稿并录用的稿件文章 ,将一律由编辑部统一纳入“万方数据———数字化期刊群” ,进入因特网提供信息服务。凡有不同意者 ,请另投它刊。本刊所付稿酬包含刊物内容上网服务报酬 ,不再另付。“万方数据———数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作 ,读者可上网查询浏览本刊内容 ,并征订本刊本刊加入“万方数据——数字化期刊群”的声明@本刊编辑部…     

本刊加入《万方数据-数字化期刊群》、《中国学术期刊(光盘版)》等的声明

为了实现科技期刊编辑、出版、发行工作的电子化,推进科技信息交流的网络化进程,我刊已加入《万方数据—数字化期刊群》、《中国学术期刊(光盘版)》、《中文科技期刊数据库》与《中国期刊网》、《首席医学网》。向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入以上网络,进入英特网提供信息服务。凡有不同意者,请声明或另投它刊。本刊所付稿酬已含刊物上网服务报酬,不再另付。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。本刊网址:http://ekyx.chinajournal.net.cn。本刊加入《万方数据—数字化期刊群》、《中…     

本刊加入《万方数据——数字化期刊群》《中国学术期刊（光盘版）》与《中国期刊网》的声明

为了实现科技期刊编辑、出版发行工作的电子化,推进科技信息交流的网络化进程,我刊已加入《万方数据——数字化期刊群》《中国学术期刊(光盘版)》与《中国期刊网》。向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入以上网络,进入英特网提供信息服务。凡有不同意者,请声明或另投它刊。本刊所付稿酬已含刊物上网服务报酬,不再另付。《万方数据——数字化期刊群》是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容(本刊网址:http://ekyx.chinajournal.net.cn),并征订本刊。《儿科药学杂志》编辑部…     

《中国现代应用药学》过刊上网通知

为了适应新时期科技期刊数字化发展的需要，本刊已完成过刊的数字化制作工作。在创刊25周年之际，特在本刊网站www．chinjmap．com推出。各位读者可以通过网络随时随地查阅本刊所有己刊出文献的全文。     

本刊加入“万方数据--数字化期刊群”的声明

为了实现期刊编辑、出版工作的网络化,我刊现已入网“万方数据——数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据——数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊或特别声明需另作处理。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据——数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。     

本刊加入“万方数据——数字化期刊群”的声明

为了实现期刊编辑、出版工作的网络化,我刊现已入网“万方数据——数字化期刊群”,所以,向本刊投稿并录用的稿件文章,将一律由编辑部统一纳入“万方数据——数字化期刊群”,进入因特网提供信息服务。凡有不同意者,请另投它刊或特别声明需另作处理。本刊所付稿酬包含刊物内容上网服务报酬,不再另付。“万方数据——数字化期刊群”是国家“九五”重点科技攻关项目。本刊全文内容按照统一格式制作,读者可上网查询浏览本刊内容,并征订本刊。     

1,6-二磷酸果糖镁对异丙肾上腺素所致大鼠心肌损伤的保护作用

研究1,6-二磷酸果糖镁（FDP-Mg）对异丙肾上腺素（Iso）所致心肌损伤的保护作用. 大鼠sc Iso (8 mg·kg^-1·d^-1, 3 d)造成心肌损伤模型,测定心肌组织和血清肌酸激酶（CK）, 乳酸脱氢酶（LDH）, 超氧化物歧化酶（SOD）活性及丙二醛（MDA）, Mg²⁺, P和K⁺含量. 结果：每天给予Iso的同时给予FDP-Mg（250-1000 mg·kg^-1·d^-1, 3 d）能明显降低血清CK,LDH水平,抑制心肌组织中CK,LDH释放,提高血清和心肌SOD活性,降低MDA水平,提高心肌及血清Mg²⁺和P含量,降低血清K⁺浓度。综合了FDP-Na₂（530 mg·kg^-1·d^-1, 3 d）和硫酸镁（150 mg·kg^-1·d^-1, 3 d）的作用特点。结果表明,FDP-Mg对Iso所致大鼠心肌损伤具有保护作用,与其抗氧化及改善心肌代谢有关.     

三氟拉嗪对大鼠脑突触体内Ca2+水平和Ca2+, Mg2+-ATP酶活性的作用

用Quin 2法测得大鼠脑突触体内静息游离Ca²⁺浓度([Ca²⁺]_i)为85±13 μmol·g^-1 protein. 三氟拉嗪(TFP) 1, 5和10 μmol·L^-1对静息突触体[Ca²⁺]_i无明显影响, 但能以剂量依赖方式增高65 mmol·L^-1 KCl所致突触体[Ca²⁺]_i升高, 从192±58 μmol·g^-1 protein分别达到233±63, 431±99和661±173 μmol·g^-1 protein. TFP 5,10和50 μmol·L^-1分别使突触体Ca²⁺, Mg²⁺-ATP酶活性降低31％, 41％和45％; 使Mg²⁺-ATP#FK酶活性降低30％, 36％和39％, 提示TFP可能是通过抑制钙调素, 进而抑制Ca²⁺, Mg²⁺-ATP酶活性, 使突触体[Ca²⁺]_i升高, 促进神经末梢释放递质.     

Mg2+在药物无菌检查中的应用

目的探讨Mg2＋作为中和剂在无菌检查中的合理应用。方法添加不同浓度Mg2＋,观察对培养基、稀释剂和冲洗液性状、以及对微生物生长的影响。结果以规定验证菌试验,对Mg2＋最敏感验证菌为铜绿假单孢菌。结论 Mg2＋作为中和剂应用于无菌检查,其使用方式、使用量（浓度）应进行考察,选择合理的应用方式。     

家兔主动脉血管平滑肌细胞内钙动员及小檗胺作用的共聚焦研究

观察小檗胺 (Ber) 对高钾除极,Bay K8644,5-羟色胺 (5-HT) 及咖啡因升高细胞内钙水平 (［Ca²⁺］_i) 的影响。以Fluo-3/AM负载家兔培养的主动脉平滑肌细胞 (VSMC),共聚焦显微术测定［Ca²⁺］_i,结果以荧光强度(FI)表示. 结果：(1) 在细胞外钙为1.3 mmol·L^-1时, VSMC胞浆静息FI明显高于核区, 且不受Ber的影响. (2) Ber 10-100 μmol·L^-1预处理可抑制KCl 60 mmol·L^-1或Bay K8644 100 μmol·L^-1升高的［Ca²⁺］_i,抑制5- HT 1 μmol·L^-1升高［Ca²⁺］_i的持续相,但不影响［Ca²⁺］_i的一过性升高。维拉帕米10 μmol·L^-1具有相似作用. (3) 在无钙Hanks液中,Ber预处理对咖啡因100 mmol·L^-1升高的［Ca²⁺］_i无明显抑制作用。结果表明,Ber可阻断外钙内流,但不抑制内钙释放,这可能与Ber阻断电压依赖性钙通道和受体依赖性钙通道的作用有关.     

毒蕈碱引起大鼠星状神经节细胞除极化及抑制钙依赖性后超极化电位

应用细胞内生物电记录技术，观察毒蕈碱对大鼠星状神经节细胞的影响．毒蕈碱５～１０μｍｏｌ·Ｌ－１可使部分非爆发式发放（ｐｈａｓｉｃ）细胞和部分爆发式发放（ｔｏｎｉｃ）细胞发生膜除极反应．这种除极反应在低钙高镁溶液中或在含河豚毒素（０．１μｍｏｌ·Ｌ－１）的溶液中仍然存在．毒蕈碱引起除极反应时常伴膜电阻的增加．当膜电位增大时，除极反应幅度减小．毒蕈碱引起除极反应的同时，可见细胞钙依赖性后超极化电位减小．此外，当对神经节灌流毒蕈碱时，向非爆发式发放细胞输入去极化电流，常见此类细胞出现爆发式发放．结果表明，毒蕈碱对星状神经节细胞的多种作用可能是其使细胞膜钾电导降低所致．     

氯丙烯引起的神经电生理及细胞内Na+, K+, Ca2+等离子含量的改变

为探讨氯丙烯的周围神经损伤机制, 用荧光分子探针, 电子探针X线微区分析和电生理学方法研究了氯丙烯引起的鸡胚神经细胞和大鼠坐骨神经纤维轴浆内的Na⁺, Ca²⁺离子和Na, K, Ca, Mg, Cl, P元素含量和神经细胞静息膜电位(RMP), 大鼠坐骨神经复合动作电位(CAP)及小鼠肋间神经束膜内动作电位(APIPS)的改变. 结果显示, 随着氯丙烯剂量的增加, 鸡胚脑神经细胞[Ca²⁺]_i明显增加, [Na⁺]_i在高剂量时亦增加; 大鼠坐骨神经轴浆内Ca增加, K减少, Na增加不如Ca明显; RMP减小; 大鼠坐骨神经CAP的峰值明显下降, 时程稍延长; 小鼠肋间神经APIPS的K⁺电压波形消失. 表明氯丙烯引起的RMP, CAP及APIPS的改变, 均与细胞和轴浆内的Na⁺, Ca²⁺离子和Na, K, Ca, Mg, Cl, P元素的改变有关. 提示中毒患者出现运动和感觉障碍可能与轴浆内外Na⁺, K⁺浓度差减小造成神经兴奋与传导降低和Ca²⁺进入轴浆过多导致神经纤维变性有关.     

Interactions of magnesium and verapamil on tone and contractility of vascular smooth muscle

Previous studies on isolated blood vessels indicate that (1) withdrawal of magnesium ([Mg²⁺]₀) induces calcium-dependent contractile responses, and (2) [Mg²⁺]₀ and verapamil (VE) inhibit calcium influx across the cell membrane. The present study, using isolated rat aortic strips and portal veins, was designed to assess the interactions of [Mg²⁺]₀ and VE on increases in active tension and contractility induced by withdrawal of [Mg²⁺]₀. [Mg²⁺]₀ was found to: (1) enhance VE-induced inhibition of portal vein amplitude, and (2) antagonize VE-induced enhanced frequency of spontaneous phasic contractions in portal veins. Both [Mg²⁺]₀ and VE could prevent and reverse the increases in active tension developed in aortic smooth muscle upon removal of [Mg²⁺]₀. [Mg²⁺]₀ markedly potentiated the inhibitory effect of verapamil on calcium-induced contractions of K⁺-depolarized aorta but not in K⁺-depolarized portal vein. This synergistic effect in aorta could be due to the influence of Mg and VE at the membrane and/or the influence of Mg at intracellular sites resulting in decreased levels of functional (activator) cytoplasmic Ca²⁺. On the other hand, the lack of synergism in portal vein could indicate that both of these agents might be inactivating the same membrane channels involved in calcium influx.     

Alleviation effects of magnesium on copper toxicity and accumulation in grapevine roots evaluated with biotic ligand models

Copper toxicity and accumulation in plants are affected by physicochemical characteristics of soil solutions such as the concentrations of coexistent cations (e.g., Ca²⁺, Mg²⁺, K⁺, Na⁺, and H⁺). The biotic ligand model (BLM) approach has been proposed to predict metal phyto-toxicity and -accumulation by taking into account the effects of coexistent cations, given the assumption of the partition equilibrium of metal ions between soil solution and solid phase. The alleviation effects of Mg on Cu toxicity and accumulation in grapevine roots were the main concerns in this study and were investigated by using a hydroponic experiment of grapevine cuttings. The BLM approach, which incorporated competition of Mg²⁺ with Cu²⁺ to occupy the biotic ligands on root surfaces, was developed to predict Cu rhizotoxicity and accumulation by grapevine roots. In the results, the effective activity of Cu, {Cu ²⁺}, resulting in a 50 % reduction of root elongation (EA ₅₀), linearly increased with increments of Mg activity, {Mg ²⁺}. In addition, the Cu concentration in root, Cu _root , was retarded by an increase of {Mg ²⁺}. The linear model was significantly fitted to the relationship between {Cu ²⁺}/Cu _root and {Mg ²⁺}. According to the concept of BLM, the present results revealed that the amelioration effects of Mg on Cu toxicity and accumulation in roots could arise from competition between Mg²⁺ and Cu²⁺ on the binding sites (i.e., the biotic ligands). Then, the developed Cu-BLMs incorporating the Mg²⁺ competition effectiveness were validated provide accurate predictions of Cu toxicity and accumulation in grapevine roots. To our knowledge this is the first report of the successful development of BLMs for a woody plant. This BLM approach shows promise of being widely applicable for various terrestrial plants.     

Aminoglycoside-Induced Functional and Biochemical Defects in the Renal Cortex

Aminoglycoside-Induced Functional and Biochemical Defects inthe Renal Cortex. Kaloyanides, G. J. (1984). Fundam. Appl. Toxicol.A, 930–943. The first site of aminoglycoside-cell interactionoccurs at the plasma membrane of renal proximal tubular cellswhich have been shown to selectively transport and accumulatethese drugs Depression of apical membrane transport of organicbase, low-molecular-weight protein, and glucose, together withloss of brush border membrane enzymes and phospholipids in theurine which, results in altered phospholipid composition ofthis membrane, occurs early in the course of aminoglycosideadministration. Less well appreciated are the alterations whichoccur at the basolateral membrane. These include decreased transportof organic bases, Ca²⁺, Na²⁺, and K⁺ increased organic acidtransport; decreased activity of Na⁺-K⁺ ATPase and adenylatecyclase; decreased calcium content; and altered phospholipidcomposition. Many of these changes are evident within 90 minof a single injection of drug. Lysosomal dysfunction is manifestedby the accumulation of phospholipids in the form of myeloidbodies consequent to the inhibition of lysosomal phospholipasesby aminoglycosides. Labilization of lysosomes in vivo has beenpostulated to be a mechanism of cell injury. Mitochondria dysfunctionattributed to aminoglycosides includes impaired respiration,inhibition of Mg²⁺ binding, inhibition of Ca²⁺ uptake, increasedpermeability to monovalent cations, decreased ammoniagenesis,and decreased gluconeogenesis. However, it remains unclear howthe drug gains access to mitochondria in vivo in order to initiatethe functional derangements. It is evident that aminoglycosidescause multiple metabolic derangements at multiple sites withinrenal proximal tubular cells. At present the available evidencedoes not identify which, if any, of these drug effects is responsiblefor initiating the injury cascade. The strong possibility existsthat aminoglycoside nephrotoxicity reflects the net impact ofmultiple minor metabolic derangements which individually areof little significance but when added together seriously compromisethe cell's ability to maintain its structural and functionalintegrity.     

Nifedipine does not alter the increased cystolic free magnesium during inhibition of mitochondrial function in isolated cardiac myocytes

• 1.1. The objectives of this investigation were to determine the effect of inhibition of mitochondrial function on intracellular free Mg concentration, [Mg²⁺]_i, in the heart and to determine whether the calcium channel antagonist nifedipine would alter the response.
• 2.2. Cardiac myocytes were prepared as primary cultures from 7-day-old chick embryonic hearts. [Mg²⁺]_i was determined in single ventricular cells with mag-fura-2.
• 3.3. Inhibition of mitochondrial function with carbonyl cyanide m-chlorophenylhydrozone (CCCP, 3 μM, plus amobarbital, 3 mM, produced a cessation of cardiac contractile frequency that was reversible. This was associated with an increase in [Mg²⁺]_i from 0.48 to 0.98 mM which returned to near basal levels with removal of the drugs. [Ca²⁺]_i oscillations with cell contraction were diminished in the presence of CCCP plus amobarbital and returned to normal following their removal.
• 4.4. In contrast, CCCP plus iodoacetate led to increased [Mg²⁺]_i beyond 2 mM which was associated with elevated [Ca²⁺]_i and cell death.
• 5.5. Nifedipine did not alter the cardiac contractile response to CCCP plus amobarbital. The increment in [Mg²⁺]_i produced by CCCP plus amobarbital was not altered by nifedipine. These data suggest that [Mg²⁺]_i is regulated by mitochondrial metabolism and nifedipine does not alter the increase in [Mg²⁺]_i produced by inhibition of mitochondrial function suggesting increments in [Mg²⁺]_i were from internal sources. Nifedipine may not interfere with the potentially beneficial actions of increased [Mg²⁺]_i.