细胞分裂素生物合成基因在调节一组烟草病理相关蛋白基因表达中的作用

对一组病理相关蛋白基因在烟草 ( N icotiana tabacum cv. Wisconsin 38)中的表达情况进行了研究 ,包括 :碱性几丁质酶、β- 1 ,3-葡萄糖苷酶、渗透蛋白及伸展蛋白。RNA杂交实验表明在正常烟草植株中上述 4个基因具有发育和器官专一性的表达。在含有细胞分裂素生物合成基因的转基因烟草丛生芽中 ,这 4个基因的表达受过量合成的内源细胞分裂素和载体效应的共同调节 ,细胞分裂素降低这些基因的表达 ,而载体效应则促进它们的表达。热激处理也明显降低这 4种基因的表达水平。上述结果表明这些病理相关蛋白基因具有复杂的调控系统     

Age-dependent aluminum accumulation in the human aorta and cerebral artery

The purpose of this study was to determine the extent of aluminum (Al) accumulation in the human aorta and cerebral arteries. The Al contents in the aortae and in the cerebral arteries from 23 human subjects was determined by inductively coupled plasma atomic emission spectrophotometry (ICP-AES). The subjects' age range was 45–99-yr-old; 15 of the subjects were males and 8 were females. Al was detected in twelve aortae and in six cerebral arteries, when the entire specimen was analyzed. Two specimens where Al was found in the cerebral arteries contained no Al in the aorta. No relationship to the subject's sex was found. When related to age, two groups were established. Group L (45–75 yr old) and group H (>75 yr old), which exhibited aortal Al concentrations of 33.3 and 72.7%, respectively. When the aortic wall was dissected into the tunica intima, media, and adventitia, Al was found mainly in the tunica media. In the aorta, significant relationships were found between Al and phosphorus (P) levels (r=0.801,p<0.01) and between Al and calcium (Ca) (r=0.661,p<0.05). We have concluded that Al accumulation is age-dependent and that it occurs both in the aorta and in the cerebral artery. In the aorta, accumulation occurs mainly in the tunica media. Both P and Ca appear to enhance aortal Al accumulation.     

The bronchial tree,lobular division,and blood vessels of the lung of the silvered lutong (Presbytis cristata)

The lungs of three silvered lutongs (Presbytis cristata) were examined. The right and left lungs have the dorsal, lateral, ventral, and medial bronchiole systems, which arise from the corresponding sides of both bronchi, respectively. Bronchioles in the dorsal and lateral bronchiole systems are well developed, whereas those in the ventral and medial bronchiole systems are poorly developed and lack some portions. According to the fundamental structure of bronchial ramifications of the mammalian lung (Nakakuki, 1975, 1980), the right lung consists of the upper, middle, lower, and accessory lobes, whereas the left lung consists of a bilobed middle lobe and a lower lobe, in which the right upper lobe is extremely well developed. The right pulmonary artery runs across the ventral side of the right upper lobe bronchiole, and then across the dorsal side of the right middle lobe bronchiole. Initially it runs along the lateral side of the right bronchus and then gradually comes to run along the dorsal side. During its course, it gives off branches which run mainly along the dorsal or lateral side of the bronchiole. The left pulmonary artery runs across the dorsal side of the left middle lobe bronchiole, and then follows the same course as that in the right lower lobe. The pulmonary veins run medially or ventrally to the bronchioles, and finally enter the left atrium as four or five large veins.     

猴B病毒相关抗体及B病毒抗体检测的比较研究

本文比较了用ＨＳＶ－１（ＩＥＡ）和Ｂ病毒（ＩＦＡ）的方法检查猴Ｂ病毒相关抗体和Ｂ病毒抗体的结果：ＩＥＡ检查出的Ｂ病毒相关抗体阴性猴,经ＩＦＡ检查,全部为Ｂ病毒抗体阴性。用ＩＦＡ检查了Ｂ病毒相关抗体阴性的恒河猴,在单笼隔离饲养六个月后,有９８．３％的动物Ｂ病毒相关抗体仍为阴性,表明ＩＲＡ的阴性结果有较好的一致性。本文讨论了建立无Ｂ病毒感染猴群的可行性。     

Properties of the ATP-sensitive K+ current activated by levcromakalim in isolated pulmonary arterial myocytes

Tension and patch clamp recording techniques were used to investigate the relaxation of rabbit pulmonary artery and the properties of the K⁺ current activated by levcromakalim in isolated myocytes. Under whole-cell voltage clamp, holding at –60 mV in symmetrical 139 mm K⁺, levcromakalim (10 m) induced a noisy inward current of –116 ± 19 pA (n = 13) which developed over 1 to 2 min. This current could be blocked by either glibenclamide (10 m) or phencyclidine (5–50 M) and was unaffected when extracellular Ca²⁺ was removed. Both these drugs inhibited the levcromakalim-induced relaxation of muscle strips precontracted with 20 mm [K⁺] _o . Application of voltage ramps in symmetrical 139 mm K⁺ confirmed that the levcromakalim-induced current was carried by K⁺ ions and was weakly voltage dependent over the potential range from –100 to +40 mV.The unitary current amplitude and density of the channels underlying the levcromakalim-activated whole-cell K⁺ current was estimated from the noise in the current record. We estimate that levcromakalim caused activation of around 300 channels per cell, with a single channel current of 1.1 pA, corresponding to a slope conductance of about 19 pS. Furthermore, cells dialyzed with an ATP-free pipette solution developed a large noisy inward current at –60 mV, which could subsequently be blocked by flash photolysis of caged ATP. Analysis of the noise associated with this current indicated that the single channel amplitude underlying the ATP-blocked current was 1.4 pA, a value similar to that estimated for the levcromakalim-induced current. We conclude that the conductance of this ATP-sensitive channel is likely to be small under physiological conditions and that it is present at low density.We thank SmithKline & Beecham for the gift of levcromakalim, ICI Pharmaceuticals for the gift of charybdotoxin and Prof. D. Colquhoun for the noise analysis programs. We also thank Mr. R. Davey for technical assistance with tension experiments. This work was supported by the British Heart Foundation and the Wellcome Trust. L.H.C. is a Wellcome Research Fellow and P.L. is an intermediate fellow of the BHF.     

Changes in Metabotropic Glutamate Receptor mRNA Levels Following Global Ischemia: Increase of a Putative Presynaptic Subtype (mGluR4) in Highly Vulnerable Rat Brain Areas

Abstract: Metabotropic glutamate receptors mediate their intracellular response by coupling to G proteins and may be divided into three subfamilies: mGluR1 and mGluR5, which stimulate phosphatidylinositol hydrolysis; mGluR2 and mGluR3, which are negatively coupled to cyclic AMP formation; and mGluR4 and mGluR6, which also inhibit forskolin-stimulated cyclic AMP formation. The mGluR4 subtypes may represent l -2-amino-4-phosphonobutyrate-sensitive presynaptic autoreceptors, and two alternatively spliced variants of the mGluR4 coding for two receptors with different C termini have been identified. Using in situ hybridization, we measured the levels of mGluR1–mGluR5 mRNA in regions of the rat brain 24 h after transient global ischemia, a time point when no neuronal damage can yet be observed morphologically. In the hippocampus, the mRNA levels for mGluR1, mGluR2, and mGluR5 were decreased, mGluR3 mRNA levels were unchanged, and the mGluR4 mRNA levels were strongly increased. The strongest increase appeared to be in the mRNA encoding mGluR4b. The mGluR4 mRNA was also increased in the parietal cortex, whereas the ventral posteromedial thalamic nucleus showed a small decrease in its mRNA content. These results suggest that vulnerable neurons react to an increased extracellular glutamate concentration by differential regulation of the mRNA for pre- and postsynaptically located metabotropic glutamate receptors.     

Superoxide dismutase,catalase, and U78517F attenuate neuronal damage in gerbils with repeated brief ischemic insults

Repeated ischemic insults at one hour intervals result in more severe neuronal damage than a single similar duration insult. The mechanism for the more severe damage with repetitive ischemia is not fully understood. We hypothesized that the prolonged reperfusion periods between the relatively short ischemic insults may result in a pronounced generation of oxygen free radicals (OFRs). In this study, we tested the protective effects of superoxide dismutase (SOD) and catalase (alone or in combination), and U78517F in a gerbil model of repetitive ischemia. Three episodes (two min each) of bilateral carotid occlusion were used at one hour intervals to produce repetitive ischemia. Superoxide dismutase and catalase were infused via osmotic pumps into the lateral ventricles. Two doses of U78517F were given three times per animal, one half hour prior to each occlusion. Neuronal damage was assessed 7 days later in several brain regions using the silver staining technique. The Mann-Whitney U test was used for statistical comparison. Superoxide dismutase showed significant protection in the hippocampus (CA4), striatum, thalamus and the medial geniculate nucleus (MGN). Catalase showed significant protection in the striatum, hippocampus, thalamus, and MGN and the substantia nigra reticulata. Combination of the two resulted in additional protection in the cerebral cortex. Compared to the controls, there was little protection with a dose of 3 mg/kg of U78517F. There was significant protection with a dose of 10 mg/kg in the hippocampus (CA4), striatum, thalamus, medial geniculate nucleus and the substantia nigra reticulata. The significant protection noted with SOD, catalase or U78517F with repeated ischemia supports, the hypothesis that OFRs may play a role in neuronal damage in repeated cerebral ischemia.     

Tri-Calciphor (16,16-dimethyl-15-dehydroprostagalndin B1 trimer)-mediated mitochondrial Ca2+ movements: modulation by phosphate

The trimeric derivative of 16,16-dimethyl-15-dehydroprostaglandin B₁ (termed tri-Calciphor), which protects tissues against ischemic damage, induced Ca²⁺ efflux and swelling in mitochondria in the absence of phosphate, Mg²⁺ and ATP. When glutamate/malate rather than succinate was the substrate, higher tri-Calciphor concentrations were required for the ionophoretic activity. Ca²⁺ efflux and mitochondrial swelling induced by tri-Calciphor were completely inhibited by ATP, phopsphate and Mg²⁺ added together, and partially inhibited with phosphate plus either ATP or Mg²⁺. Between 0 and 7 μM added Ca²⁺ and in the presence of phosphate, ATP and Mg²⁺, tri-Calciphor stimulated the uptake of Ca²⁺ by mitochondria and increased the efficiency of buffering of extramitochondrial Ca²⁺. Thus depending on the assay conditions, two different effects involving Ca²⁺ movements and mitochondria are observed with tri-Calciphor.     

用电子自旋共振（ESR）研究肾缺血移植和再灌注过程产生的自由基

在低温（－１００℃）用ＥＳＲ检测和分析了大鼠肾缺血,移植和再灌注过程中出现的ＥＳＲ信号,发现在体（ｉｎｖｉｖｏ）肾缺血１小时再灌注２分钟肾组织除了出现ｇ＝２．００４０的醌类自由基以及ｇ＝１．９３７０和ｇ＝１．９７３０处与过渡金属离子有关的信号外,在低场区又出现一个很明显的信号（ｇ＝２．０８１２）,该信号的位置同及ＬＯＯ．的ｇ     

Casein Kinase II Activity in the Postischemic Rat Brain Increases in Brain Regions Resistant to Ischemia and Decreases in Vulnerable Areas

Abstract: Casein kinase II (CKII) is a protein kinase acting in the intracellular cascade of reactions activated by growth factor receptors, and that has a profound influence on cell proliferation and survival. In this investigation, we studied the changes in the activity and levels of CKII in the rat brain exposed to 10. 15 and 20 min of transient forebrain ischemia followed by variable periods of reperfusion. The cytosolic CKII activity decreased during reperfusion by ∼ 30 and ∼ 50% in the selectively vulnerable areas, striatum and the CA1 region of the hippocampus, respectively. In the resistant CA3 region of hippocampus and neocortex, the activity increased by ∼ 20 and ∼ 60%, respectively. The postischemic changes in CKII activity were dependent on the duration of the ischemic insult. The levels of CKII did not change after ischemia, suggesting that the enzyme is modulated by covalent modification or is interacting with an endogenous inhibitor/activator. Treatment of the cytosolic fraction from cortex of rats exposed to ischemia and 1 h of reperfusion with agarose-bound phosphatase decreased the activity of CKII to control levels, suggesting that CKII activation after ischemia involves a phosphorylation of the enzyme. The correlation between postischemic CKII activity and neuronal survival implies that preservation or activation of CKII activity may be important for neuronal survival after cerebral ischemia.