紫外线对大豆胚芽化学发光的影响

紫外线对大豆胚芽化学发光的影响范立通（山西大学分子科学研究所,太原０３００６）ＥＦＦＥＣＴＯＦＵＴＲＡＶＩＯＬＥＴＲＡＹＯＮＴＨＥＣＨＥＭＩＬＵＭ－ＩＮＥＳＣＥＮＣＥＯＦＳＯＹＢＥＡＮＥＭＢＲＹＯＮＩＣＳＨＯＯＴ￥Ｆａｎｌｉ－ｔｏｎｇ（Ｉｎｓｔｉｔｕ...     

TWO NEW SPECIES FROM TRICHOSANTHES（CUCURBITACEAE）

ＴＷＯＮＥＷＳＰＥＣＩＥＳＦＲＯＭＴＲＩＣＨＯＳＡＮＴＨＥＳ（ＣＵＣＵＲＢＩＴＡＣＥＡＥ）ＹｕｅｈＣｈｕｎ－ｈｓｉＨｕａｎｇＬｕ－ｑｉＣｈｅｎｇＣｈｉｎｇ－ｙｕｎｇ〔ＡＢＴＲＡＣＴ〕ＴｒｉｃｈｏｓａｎｔｈｅｓｒｅｆｅｒａｃｔａＹｕｅｈｅｔＬ．Ｑ．Ｈ...     

大耳白兔动脉血和脑脊液酸碱电解质值及其相互关系

３０只正常大耳白兔,经股动脉穿刺插管和枕骨下经皮穿刺入枕骨下池,在严格隔绝空气情况下,分别取得动脉血和脑脊液（ＣＳＦ）标本,用ＡＢＬ３型血气分析仪及ＣＮ６４４型生化分析仪检测主要酸碱变量及电解质值。经统计学处理结果表明：ＣＳＦｐＨｅｙ ｋ＾＋、Ｃａ＾２＋、Ｍｇ＾２＋浓度〈动脉血,ＣＳＦＰＣＯ２及ＨＣＯ３＾－、Ｃｌ＾－Ｎａ＾＿、Ｈ＾＋〉动脉血。另外,ＣＳＦＰＨ与ｐＨａ,ＣＳＦＰＣＯ２与ＰａＣＯ２、Ｃ     

金樱子花粉形态及营养成分研究

金樱子花粉形态及营养成分研究刘剑秋,张清其,吴文珊（福建师范大学生物系,福州３５０００７）ＳＴＵＤＩＥＳＯＮＭＯＲＰＨＯＬＯＧＹＡＮＤＮＵＴＲＩＴＩＯＮＣＯＭＰＯＳＩＴＩＯＮＳＯＦＰＯＬＥＮＯＦＲＯＳＡＬＡＥＶＩＧＡＴＡ￥ＬｉｕＪｉａｎｇ－ｑｉｕ;Ｚ...     

缺氧诱导因子1和红细胞生成素3‘—增强子调节内皮细胞？…

目的和方法：将红细胞生成素（ＥＰＯ）３＇－增强子野生片断及点突变片断借脂质体主人脐静脉内皮细胞株ＥＣＶ－３０４,用半定量ＲＴ－ＰＣＲ测定正常秘缺氧诱导因子－１（ＨＩＦ－１）诱导剂氧化钴（ＣｏＣｌ２）作用下培养６ｈ的细胞环氧合酶２（ＣＯＸ－２）和血栓素合酶（ＴＸＳ）的ｍＲＮＡ。结果：ＨＩＦ－１诱导剂ＣｏＣｌ２可放ＣＯＸ－２和ＴＸＳ基因转明显增强２,向细胞导入野生ＥＰＯ３＇增强子片断可阻断ＣｏＣｌ２诱     

9—蒽羧酸对豚鼠心室动作电位和L型Ca电流的影响

目的：研究９－蒽羧酶（９－ＡＣ）对豚鼠以肌动作电位（ＡＰ）和Ｌ型Ｃａ电流（Ｌｃａ）的影响。方法：电流钳配合制霉菌素膜等孔方法记录心室肌动作电位,用全细胞式膜片钳（Ｗｈｏｌｅ ｃｅｌｌ ｒｅｃｏｒｄｉｎｇ）技术记录Ｌｃａ。结果：在低ＣＩ＾－状态下,β肾上腺素能受体激动剂异丙肾上腺素（ＩＳＯ）可使动作电位时程（ＡＰＤ）明显延长。９－ＡＣ单独使用时对ＡＰ无作用,但在ＩＳＯ的作用下,蛋白磷酸酶抑制剂９－Ａ     

沙竹中内生固氮菌的分离及鉴定

沙竹中内生固氮菌的分离及鉴定李久蒂孙捷匡柏健陈仲新（中国科学院植物研究所,北京１０００９３）ＩＳＯＬＡＴＩＯＮＡＮＤＣＨＡＲＡＣＴＥＲＩＺＡＴＩＯＮＯＦＥＮＤＯＰＨＹＴＩＣＤＩＡＺＯＴＲＯＰＨＳＩＮＰＳＡＭＭＯＣＨＬＯＡＭＯＮＧＯＬＩＣＡＬｉＪｉｕ－...     

水分胁迫下Ca^2＋,PEG预处理对小麦幼苗保护酶系统活性的影响

水分胁迫下Ｃａ￣（２＋）、ＰＥＧ预处理对小麦幼苗保护酶系统活性的影响洪法水,马成仓,董振吉,周谋文（淮北煤炭师范学院生物系,淮北２３５０００）ＥＦＦＥＣＴＳＯＦＣＡ￣（２＋）．ＰＥＧＰＲＥＴＲＥＡＴＭＥＮＴＯＮＤＥＦＥＮＳＩＶＥＥＮＺＹＭＥＳＡＣＴＩ...     

人粒细胞集落刺激因子（hG—CSF）cDNA3‘—UTR对其表达的影响

利用人粒细胞集落刺激因子（ｈＧ－ＣＳＦ（）ｃＤＮＡ３＇端非翻译区（３＇ＵＴＲ）中存在的ＤｒａＩ酶切位点,通过部分酶切与完全酶切,删除３＇－ＵＴＲ不同长度构建了四种ｈＧ－ＣＳＦ ｃＤＮＡ瞬时重组表达质粒,转染ＣＯＳ－７细胞手,生物活性测定结果提示,ｈＧ－ＣＳＦｃＤＮＡ３＇－ＵＴＲ对其表达起负调控作用,其关键性序列位于紧接终止密码子ＴＧＡ下游的６５ｂｐ范围内,３＇－ＵＴＲ对ｈＧ－ＣＳＦ ｃＤＮＡ表达的     

云南四药门花属—新种

云南四药门花属—新种钱义咏（云南省思茅行署林业局，思茅６６５０００）ＡＮＥＷＳＰＥＣＩＥＳＯＦＴＥＴＲＡＴＨＹＲＩＵＭＦＲＯＭＹＵＮＮＡＮ￥ＱＩＡＮＹｉ－Ｙｏｎｇ（ＳｉｍａｏＡｄｉｍｉｎｉｓｔｒａｔｉｖｅＯｆｆｉｃｅＦｏｒｅｓｔｒｙＢｕｒｅａｕ，Ｙｕ...     

Effect of sotalol on transmembrane ionic currents responsible for repolarization in cardiac ventricular myocytes from rabbit and guinea pig

The effects of sotalol, a β-adrenoceptor blocker and class III antiarrhythmic agent, on transmembrane ionic currents were examined in single rabbit and guinea pig ventricular myocytes using whole-cell voltage-clamp techniques. In neither of these species did 60 μM sotalol appreciably effect the inward rectifier, the transient outward or the inward calcium currents. In addition, sotalol did not elicit a slowly inactivating component of the sodium current as did 1 μg/ml veratrine. In guinea pig ventricular myocytes, sotalol also significantly depressed the outward delayed rectifier current. An outward delayed rectifier current was not observed in rabbit ventricular myocytes examined at room temperature; and, under these conditions sotalol did not lengthen action potential duration. Sotalol induced lengthening of cardiac action potential duration can, therefore, be explained by depression the outward delayed rectifier current.     

Effects of Taurine–Magnesium Coordination Compound on Ionic Channels in Rat Ventricular Myocytes of Arrhythmia Induced by Ouabain

Taurine-magnesium coordination compound (TMCC) has anti-arrhythmic effects. The aim of the present study was to explore the targets of the anti-arrhythmic effect of TMCC and the electrophysiological effects of TMCC on ouabain-induced arrhythmias in rat ventricular myocytes. Sodium current (I(Na)), L-type calcium current (I(ca, L)), and transient outward potassium current (I(to)) were measured and analyzed using whole-cell patch-clamp recording technique in normal rat cardiac myocytes and rat ventricular myocytes of arrhythmia induced by ouabain. In isolated ventricular myocytes, I(Na) and I(to) were blocked by TMCC (100, 200, 400 μM) in a concentration-dependent manner, and the effects of TMCC (400 μM) were equal to that of amiodarone. However, I (ca, L) was moderately increased by TMCC (400 μM) while significantly decreased by amiodarone. Ouabain (5 μM) significantly decreased sodium, L-type calcium, and transient outward potassium currents. TMCC (100 μM) relieved abnormal sodium currents induced by ouabain through facilitation of steady-state inactivation. TMCC (200 and 400 μM) relieved abnormal L-type calcium currents induced by ouabain through facilitation of steady-state activation and retardation of steady-state inactivation. TMCC failed to further inhibit abnormal transient outward potassium currents induced by ouabain. However, amiodarone inhibited the decreasing sodium, L-type calcium, and transient outward potassium currents further. These data suggest that I(Na), I(ca, L), and I(to) may be the targets of the antiarrhythmic effect of TMCC, which can antagonize ouabain-induced changes of ionic currents in rat ventricular myocytes.     

Channels involved in transient currents unmasked by removal of extracellular calcium in cardiac cells

In cardiac cells that lack macroscopic transient outward K(+) currents (I(to)), the removal of extracellular Ca(2+) can unmask "I(to)-like" currents. With the use of pig ventricular myocytes and the whole cell patch-clamp technique, we examined the possibility that cation efflux via L-type Ca(2+) channels underlies these currents. Removal of extracellular Ca(2+) and extracellular Mg(2+) induced time-independent currents at all potentials and time-dependent currents at potentials greater than -50 mV. Either K(+) or Cs(+) could carry the time-dependent currents, with reversal potential of +8 mV with internal K(+) and +34 mV with Cs(+). Activation and inactivation were voltage dependent [Boltzmann distributions with potential of half-maximal value (V(1/2)) = -24 mV and slope = -9 mV for activation; V(1/2) = -58 mV and slope = 13 mV for inactivation]. The time-dependent currents were resistant to 4-aminopyridine and to DIDS but blocked by nifedipine at high concentrations (IC(50) = 2 microM) as well as by verapamil and diltiazem. They could be increased by BAY K-8644 or by isoproterenol. We conclude that the I(to)-like currents are due to monovalent cation flow through L-type Ca(2+) channels, which in pig myocytes show low sensitivity to nifedipine.     

Changes in ionic currents and beta-adrenergic receptor signaling in hypertrophied myocytes overexpressing G alpha(q)

Transgenic overexpression of G alpha(q) causes cardiac hypertrophy and depressed contractile responses to beta-adrenergic receptor agonists. The electrophysiological basis of the altered myocardial function was examined in left ventricular myocytes isolated from transgenic (G alpha(q)) mice. Action potential duration was significantly prolonged in G alpha(q) compared with nontransgenic (NTG) myocytes. The densities of inward rectifier K(+) currents, transient outward K(+) currents (I(to)), and Na(+)/Ca(2+) exchange currents were reduced in G alpha(q) myocytes. Consistent with functional measurements, Na(+)/Ca(2+) exchanger gene expression was reduced in G alpha(q) hearts. Kinetics or sensitivity of I(to) to 4-aminopyridine was unchanged, but 4-aminopyridine prolonged the action potential more in G alpha(q) myocytes. Isoproterenol increased L-type Ca(2+) currents (I(Ca)) in both groups, with a similar EC(50), but the maximal response in G alpha(q) myocytes was approximately 24% of that in NTG myocytes. In NTG myocytes, the maximal increase of I(Ca) with isoproterenol or forskolin was similar. In G alpha(q) myocytes, forskolin was more effective and enhanced I(Ca) up to approximately 55% of that in NTG myocytes. These results indicate that the changes in ionic currents and multiple defects in the beta-adrenergic receptor/Ca(2+) channel signaling pathway contribute to altered ventricular function in this model of cardiac hypertrophy.     

氧自由基致豚鼠心室肌细胞跨膜电位变化的离子电流基础

目的：旨在提示氧自由基参与缺血／再灌注性心委失常发生的离子电流基础。方法：采用膜片钳全细胞式记录技术,观察Ｈ２Ｏ２（１ｍｍｏｌ／Ｌ）对豚鼠心室肌细胞跨膜电位和相关离子电流的影响。结果：Ｈ２Ｏ２使豚鼠心肌单细胞的静息电位（ＲＰ）降低,动作电位时程（ＡＳＤ）显著缩短,对动作电位幅度（ＡＰＡ）和超射（ＯＳ）及钠电流的峰值（ＩＮａ）均无明显影响;明显抑制内向整流钾电流（ＩＫ１）,尤其在超极化时;增强延迟外     

Presence of a calcium-activated chloride current in mouse ventricular myocytes

The properties of several components of outward K(+) currents, including the pharmacological and kinetics profiles as well as the respective molecular correlates, have been identified in mouse cardiac myocytes. Surprisingly little is known with regard to the Ca(2+)-activated ionic currents. We studied the Ca(2+)-activated transient outward currents in mouse ventricular myocytes. We have identified a 4-aminopyridine (4-AP)- and tetraethyl ammonium-resistant transient outward current that is Ca(2+) dependent. The current is carried by Cl(-) and is critically dependent on Ca(2+) influx via voltage-gated Ca(2+) channels and the sarcoplasmic reticulum Ca(2+) store. The current can be blocked by the anion transport blockers niflumic acid and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. Single channel recordings reveal small conductance channels (approximately 1 pS in 140 mM Cl(-)) that can be blocked by anion transport blockers. Ensemble-averaged current faithfully mirrors the transient kinetics observed at the whole level. Niflumic acid (in the presence of 4-AP) leads to prolongation of the early repolarization. Thus this current may contribute to early repolarization of action potentials in mouse ventricular myocytes.     

RhoA GTPase regulates L-type Ca2+ currents in cardiac myocytes

Regulation of ionic channels plays a pivotal role in controlling cardiac function. Here we show that the Rho family of small G proteins regulates L-type Ca2+ currents in ventricular cardiomyocytes. Ventricular myocytes isolated from transgenic (TG) mice that overexpress the specific GDP dissociation inhibitor Rho GDI-alpha exhibited significantly decreased basal L-type Ca2+ current density (approximately 40%) compared with myocytes from nontransgenic (NTG) mice. The Ca2+ channel agonist BAY K 8644 and the beta-adrenergic agonist isoproterenol increased Ca2+ currents in both NTG and TG myocytes to a similar maximal level, and no changes in mRNA or protein levels were observed in the Ca2+ channel alpha1-subunits. These results suggest that the channel activity but not the expression level was altered in TG myocytes. In addition, the densities of inward rectifier and transient outward K+ currents were unchanged in TG myocytes. The amplitudes and rates of basal twitches and Ca2+ transients were also similar between the two groups. When the protein was delivered directly into adult ventricular myocytes via TAT-mediated protein transduction, Rho GDI-alpha significantly decreased Ca2+ current density, which supports the idea that the defective Ca2+ channel activity in TG myocytes was a primary effect of the transgene. In addition, expression of a dominant-negative RhoA but not a dominant-negative Rac-1 or Cdc42 also significantly decreased Ca2+ current density, which indicates that inhibition of Ca2+ channel activity by overexpression of Rho GDI-alpha is mediated by inhibition of RhoA. This study points to the L-type Ca2+ channel activity as a novel downstream target of the RhoA signaling pathway.     

兔心室肌细胞电生理异质性研究--缺血对动作电位和钾流的影响

实验用全细胞膜片箝技术,观察正常及缺血条件下,兔心内膜下心室肌细胞与心外膜下心室肌细胞的动作电位和稳态外向钾流及其变化。结果显示：（１）正常条件下,心外膜下心室肌细胞与心内膜下心室肌细胞动作电位形态有差异,心外膜下心室肌细胞动作电位时程（ＡＰＤ）较短,复极１期后有明显的初迹,动作电位形态是“锋和圆顶”,而心内膜下心室肌细胞ＡＰＤ较长,并且没有上述动作电位形态特征。这两类细胞静息电位无差异。（２）在     

Direct Comparison of NPPB and DPC as Probes of CFTR Expressed in Xenopus Oocytes

Blockers of CFTR with well-characterized kinetics and mechanism of action will be useful as probes of pore structure. We have studied the mechanism of block of CFTR by the arylaminobenzoates NPPB and DPC. Block of macroscopic currents by NPPB and DPC exhibited similar voltage-dependence, suggestive of an overlapping binding region. Kinetic analysis of single-channel currents in the presence of NPPB indicate drug-induced closed time constants averaging 2.2 msec at −100 mV. The affinity for NPPB calculated from single-channel block, K _D = 35 μm, exceeds that for other arylaminobenzoates studied thus far. These drugs do not affect the rate of activation of wild-type (WT) channels expressed in oocytes, consistent with a simple mechanism of block by pore occlusion, and appear to have a single binding site in the pore. Block by NPPB and DPC were affected by pore-domain mutations in different ways. In contrast to its effects on block by DPC, mutation T1134F-CFTR decreased the affinity and reduced the voltage-dependence for block by NPPB. We also show that the alteration of macroscopic block by NPPB and DPC upon changes in bath pH is due to both direct effects (i.e., alteration of voltage-dependence) and indirect effects (alteration of cytoplasmic drug loading). These results indicate that both NPPB and DPC block CFTR by entering the pore from the cytoplasmic side and that the structural requirements for binding are not the same, although the binding regions within the pore are similar. The two drugs may be useful as probes for overlapping regions in the pore. Received: 14 October 1999/Revised: 18 January 2000     

DITPA restores the repolarizing potassium currents Itof and Iss in cardiac ventricular myocytes of diabetic rats

Diabetes Mellitus (DM) can produce an increase in the cardiac action potential duration and QT interval that can be associated with sudden death. These cardiac effects are due to a region-specific decrease in repolarizing outward K(+) currents. Some authors have suggested that the proarrhythmic effects of diabetes can be due to diabetes-induced hypothyroidism. Thus, we have examined the effect of the thyroid hormone analog diiodothyropropionic acid (DITPA) on calcium-independent outward potassium currents in ventricular myocytes from diabetic rats. Sustained (I(ss)) and fast transient outward (I(tof)) K(+) currents were recorded using the whole-cell configuration of the patch-clamp technique. Myocytes were enzymatically isolated from the free wall of the right ventricle, and the epicardial and endocardial layers of the left ventricle of healthy, diabetic and DITPA-treated diabetic rats. Circulating thyroid hormones were measured by electrochemiluminescence. DITPA-treatment of diabetic rats restored I(tof) and I(ss) current densities in cardiac myocytes from the three regions studied, but did not alter current densities in myocytes of control rats. T(3) and T(4) levels were reduced by diabetes, and DITPA-treatment increased circulating T(3) levels. T(3)-treatment of diabetic rats also restored current densities to control values. However, direct incubation of diabetic myocytes with DITPA did not restore current densities. In summary, DITPA-treatment of diabetic rats restored the potassium current (I(tof) and I(ss)) densities in myocytes from all ventricular regions.