G2 phase cell cycle disturbance as a manifestation of genetic cell damage

The predominant cell cycle change induced by X-rays and clastogens in peripheral blood mononuclear cells is the accumulation of cells in the G2 phase of the cell cycle. We show that this accumulation consists of cells that are either delayed or arrested within the G2 phase. Since both X-rays and DNA crosslinking chemicals are known to damage DNA, the G2 phase inhibition caused by these agents is thought to be one of the primary manifestations of (unrepaired) DNA damage. This interpretation is supported by two additional findings. (1) Older individuals have elevated baseline levels of mononuclear blood cells that are delayed and/or arrested in the G2 phase of the cell cycle. This coincides with the increased chromosomal breakage rates reported for older individuals. (2) Irrespective of their age, individuals with inherited genetic instability syndromes (such as Fanconi anemia and Bloom syndrome) exhibit elevated G2 phase cell fractions. We show that the method used to detect such induced or spontaneous cell cycle changes, viz. BrdU-Hoechst flow cytometry, is a rapid and highly sensitive technique for the assessment of genetic cell damage.Dedicated to Professor Ulrich Wolf on the occasion of his 60th birthday     

大鼠胰腺γ-氨基丁酸免疫组织化学定位

本文用ABC—GDN免疫组织化学方法,研究了γ-氨基丁酸(Gamma—Aminobutyric Acid,GABA)在大鼠胰腺的定位和分布,并用相邻切片法,观察它与胰岛素的共存关系。结果发现GABA免疫反应阳性细胞主要分布于胰腺内分泌部(胰岛)。在外分泌部亦有少许分布。大部分胰岛细胞呈GABA免疫反应阳性,集中位于胰岛的中央部。相邻连续切片免疫染色证实GABA与胰岛素共存于胰岛B细胞中。外分泌部胰腺GABA免疫反应阳性细胞,呈零散分布于腺泡和导管上皮间。本文为进一步探讨GABA在胰腺的生理作用提供了形态学依据。     

Ce~（3＋）与G－肌动蛋白结合引起的构象变化及对聚合的影响

用Ａｅｄａｎｓ标记肌动蛋白单体Ｇ－Ａｃｔｉｎ上Ｃｙｓ３７４残基作为探针,研究了稀土离子Ｃｅ~（３＋）与Ｇ－Ａｃｔｉｎ的结合及引起的微构象变化。Ｃｅ~（３＋）在低浓度（Ｃｅ~（３＋）／Ａｃｔｉｎ摩尔比＜１）和Ｃａ~（２＋）竞争Ｇ－Ａｃｔｉｎ上二价离子的高亲合位点。Ｃｅ~（３＋）取代Ｃａ~（２＋）引起Ａｅｄａｎｓ荧光强度增强与Ｍｇ~（２＋）取代Ｃａ~（２＋）的结果相同。Ｃｅ~（３＋）／Ａｃｔｉｎ＞ｌ则导致Ａｅｄａｎｓ荧光强度下降。说明Ｃｅ~（３＋）在高低两种浓度条件下结合的位点及对Ｃｖｓ３７４的微构象的影响不同。时间分辩测得的Ａｅｄａｎｓ荧光寿命也支持这一结论。ＣＤ谱结果表明Ｃｅ~（３＋）／Ａｃｔｉｎ＜０．４,Ａｃｔｉｎ的二级结构增加,大于０．４又导致其失去。Ｃｅ~（３＋）－Ａｃｔｉｎ在有／无游离ＡＴＰ时用聚合液诱导的聚合结果表明,无游离ＡＴＰ时,极低浓度Ｃｅ~（３＋）促进聚合,高浓度虽有促进但有所减弱;有游离ＡＴＰ时,Ｃｅ~（３＋）／Ａｃｔｉｎ在实验范围内促进聚合。     

The use of percoll gradients, elutriator rotor elution, and mithramycin staining for the isolation and identification of intraerythrocytic stages of plasmodium berghei

Intraerythrocytic parasites of Plasmodium vinckei and Plasmodium berghei were separated according to their developmental stages using discontinuous Percoll gradients. Contaminating nucleated blood cells such as leukocytes were removed by elutriation centrifugation. The stages were unequivocally identified in smears using a newly developed DNA-specific staining procedure with mithramycin and fluorescence microscopy. This stain can also be used to detect parasites in human blood of very low parasitemias. The combination of methods described has many possible applications in immunologic and biochemical parasite research.     

Metabolism of prostaglandins in spontaneously hypertensive rats: NAD"-dependent 15-hydroxyprostaglandin dehydrogenase activity is decreased in kidney and increased in lung.

Renal, pulmonary and gastric NAD⁺-dependent 15-hydroxyprostaglandin dehydrogenase activities were determined in both spontaneously hypertensive and normotensive rats at 6 and 12 weeks of age. Renal enzyme activity in hypertensive rats was only 30–40% of that present in normotensive controls at both ages. In contract, pulmonary enzyme activity in hypertensive animals was twice as active as that in normal controls. There was no significant difference in gastric enzyme activity. NAD⁺-dependent 9-hydroxyprostaglandin dehydrogenase activity, the enzyme responsible for the conversion of vasoinactive PGF metabolites to PGE metabolites, also failed to show any difference in two types of rat kidneys. The results indicate that, in hypertension, prostaglandin inactivation is impaired in kidney but is facilitated in lung.     

Effect of alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor of ornithine decarboxylase, on polyamine levels in rat tissues.

α-Difluoromethylornithine (RMI 71.782), an enzyme-activated irreversible inhibitor of ornithine decarboxylase (E.C. 4.1.1.17) $\text{in vitro}$, causes a rapid, long-lasting, dose-dependent decrease of ornithine decarboxylase activity in prostate and, to a lesser extent, in thymus and testis of rats when injected intraperitoneally. Repeated doses (100 mg/kg or 1 g/kg) of α-difluoromethylornithine given to rats for two weeks markedly decreased polyamine concentrations in several rat tissues and selectively slowed down growth of ventral prostate and of thymus.