大鼠小肠上皮细胞培养体系的建立及其影响因素的探讨

作者引进并建立了大鼠小肠上皮细胞（ＩＥＣ－６）的培养传代和活性检测的实验方法，且对几种影响因素进行了探讨，实验发现，ＩＥＣ－６在一定密度范围内与＾３Ｈ－ＴｄＲ参入量呈正相关变化；培养７２ｈ以内，参入量随时间延长而增加，＾３Ｈ－ＴｄＲ，５５．５Ｋｂｑ／孔内，计数值与剂量间呈线性关系，胎牛血清浓度以１０％为宜，但不加胰岛素组显著降低，ｐＨ值以７．２６最好，ＩＥＣ－６在４～２６Ｇｙ照射范围内，剂量效应呈     

重组人白细胞介素2对肺癌病人NK细胞的激活作用

利用3H－TdR释放法，以K562细胞为把细胞，检测了19例肺癌病人（鳞癌12例，腺癌7例）NK活性并在体外用重组人白细胞介素2激活，结果发现，肺癌病人NK活性明显低于正常人血活性（p＜0．001），但鳞病与腺癌组NK活性无显著差异（p＞0．05），体外用重组人白细胞介素2激活后，病人NK活性可显著提高（p＜0．001）。提示，肺癌病人NK活性受损，这种缺陷可用白细胞介素2加以改善。     

吗丙嗪和阿霉素合用对肿瘤细胞周期及DNA合成的影响

目的：观察吗丙嗪（Ｐｒｏ）和阿霉素（Ｄｏｘ）合用对肿瘤细胞周期及ＤＮＡ合成的影响，以探讨吗丙嗪增强阿霉素抗肿瘤作用之机制。方法：采用拒染法观察Ｐｒｏ，Ｄｏｘ和Ｐｒｏ＋Ｄｏｘ对小鼠体外艾氏腹水癌细胞（ＥＡＣ）的杀伤作用；采用标记前体物参入法和显微分光光度术观察两药合用对ＥＡＣ细胞周期及ＤＮＡ合成的影响。结果：Ｐｒｏ２１．４６，４２．９２和６４．３８μｍｏｌ·Ｌ－１增强Ｄｏｘ对ＥＡＣ细胞的杀伤作用；Ｐｒｏ（２１４．５９μｍｏｌ·Ｌ－１）和Ｄｏｘ（１８．０２μｍｏｌ·Ｌ－１）合用对ＥＡＣ细胞ＤＮＡ合成有明显的抑制作用；用药后４～８ｈＧ１期细胞增加，ＤＮＡ直方图左移，各用药组细胞分裂指数无明显差异。结论：Ｐｒｏ可增强Ｄｏｘ的抗肿瘤作用，其机理可能与Ｐｒｏ加强Ｄｏｘ对ＤＮＡ合成的抑制及对Ｇ１期细胞累积作用增强有关。     

Biometrical implications of factorial experiments for the study of lymphocyte mitogenic response

Lymphocyte responsiveness to mitogens is affected by a number of experimental variables; the latter may be conveniently studied several at a time, following a factorial design that allows the complete evaluation of the effects of each variable and of their interplays. Statistical interferences may be drawn through an analysis of variance, provided that the data conform to the underlying model, i.e. that the effects are additive and that the errors are normally distributed and homoscedastic.Thymidine incorporation data should first be transformed to log cpm; the effects on the metameter may then be assumed to be additive, and their errors approach normality; the error variances may be affected by the experimental variables involved, so that the homogeneity of the error must be checked before relying on the pooled estimated of the error for parametric tests of significance.The above considerations have been illustrated with factorial experiments on [³H]TdR incoporation by rabbit spleen cells stimulated with varying amounts of PHA-P or PHA-M, under a variety of culture conditions.     

Pyrimidine acyclonucleosides,inhibitors of uridine phosphorylase

A new class of nucleoside analogs, the pyridimine acyclonucleosides, are competitive inhibitors of uridine phosphorylase but have no effect on thymicline phosphorylase, uridine kinase or thymidine kinase. The most potent of the series is acyclothymidine [5-methyl-1-(2′-hydroxyethoxymethyl)uracil] with a K_i value of 3 μM. K_i values of less than 30 μM were estimated for other analogs substituted at the 5-position of the pyrimicline ring. Extracts of xenografts of six human tumors were assayed for tissue levels of uricline phosphorylase and thymicline phosphorylase and for inhibition of 5-fluoro-2′-deoxyuridine (FUdR) phosphorolytic activity by acyclouridine [1-(2′-hydroxyethoxymethyl) uracil]. FUdR cleavage was inhibited most in those tissues in which the ratio of thymidine phosphorylase to uricline phosphorylase was low. Potential usage of these uricline phosphorylase inhibitors with the chemotherapeutic agent FUdR is discussed.     

环孢霉素A对体外培养人视网膜色素上皮细胞的抑制

为寻找抑制玻璃体内细胞增生的有效药物,用³H-胸腺嗜啶核苷(²H—TdR)掺入及液体闪烁技术,观察了环孢霉素A(CsA)(0.125"μg/ml~4.0μg/ml)对体外培养的加或不加巨噬细胞培养调理液(MCM)的人视网膜色素上皮(RPE)细胞增生的影响。CsA在0.125μg/ml时细胞的抑制率为-3.8%~4.1%(P>0.05);在0.25μg/ml～4.0μg/ml时为8.4%~95.1%(P<0.05),且呈剂量依赖性(r＝0.9413)(P<0.001),ID₅₀为1.49μg/ml。加MCM组细胞增殖较对照组明显（3d,26%;5d,34%;P<0.05),CsA对细胞增殖抑制率较对照组有提高(1.0%～13.9%)．表明CsA对体外培养的人RPE细胞有明显的抑制作用． （中华眼底病杂志,1995,11：22-24）     

Effects of 8-azaadenosine and formycin on cell lethality and the synthesis and methylation of nucleic acids in human colon carcinoma cells in culture

The cytocidal and biochemical effects of formycin and 8-azaadenosine in the presence and absence of the adenosine deaminase inhibitor, 2′-deoxycoformycin, were studied in human colon carcinoma (HT-29) cells in culture. Logarithmically growing cells were unaffected by 24-hr exposure to either 10^?6M formycin or 8-azaadenosine, but 1 to 1.4 log reductions in colony formation were produced by 10^?5M of each analog. In the presence of 10^?6M 2′-deoxycoformycin, a 3- and 30-fold potentiation of the cytocidal activity of 8-azaadenosine and formycin, respectively, was produced. Inhibition of DNA synthesis but not RNA synthesis by 8-azaadenosine paralleled its cytocidal activity; however, neither variable correlated closely with the cytotoxic effects of formycin. In addition, the methylation of nuclear RNA was unaffected by both drugs while the methylation of 5-methyl-deoxycytidine in DNA was inhibited to a lesser extent than DNA synthesis. Measurements of the incorporation of [³H]formycin and [³H]8-azaadenosine into nuclear RNA and DNA in the presence and absence of 2′-deoxycorformycin indicated that formycin substitution in RNA and DNA was enhanced 10- and 20-fold, respectively, while [³H]8-azaadenosine incorporation into both nucleic acids was increased 6- to 7-fold. These results suggest that the incorporation of formycin into nucleic acids, particularly DNA, correlates closely with its lethal effect on cell viability. On the other hand, the cytocidal activity of 8-azaadenosine more clearly parallels its inhibitory effect on DNA synthesis rather than its substitution into nucleic acids.     

Barbiturate inhibition of growth and of synthesis of deoxyribonucleic acid, ribonucleic acid and protein in cultured mammalian cells

Pentobarbital (PB) inhibited growth and the synthesis of nucleic acids and protein in murine, mastocytoma cells (P815Y) grown in culture. The inhibition increased with an increase in the concentration of drug and was also time-dependent with a high level of drug. For example, 0.5 mM PB (id₅₀) reduced both the rate of division of the cells and the synthesis of DNA, RNA and protein by about one-half, compared with the control, over a 12-hr period. In contrast, treatment with a 2-fold higher concentration of PB (1 mM; id₁₀₀) blocked both cell division and the synthesis of protein promptly. It also reduced the synthesis of DNA and RNA by about one-half, compared with the control, during the first 4 hr of treatment. After this time, however, the synthesis of both DNA and RNA stopped abruptly. It is concluded that the inhibition of DNA synthesis caused by barbiturate in the latter case may have been secondary to the inhibition of protein synthesis. Transfer of the inhibited (1 mM PB; 12 hr) cells to drugfree medium caused the synthesis of protein and RNA to begin without apparent delay. In contrast, the synthesis of DNA proceeded slowly for about 8 hr; then the amount of DNA increased parasynchronously. Cell division, which also proceeded slowly during the first 10 hr, occurred as a parasynchronous wave some 2 hr after DNA synthesis began. The inhibitory effects of PB were also studied in murine, lymphoblastic cells (L5178Y) synchronized by sequential treatment with thymidine (5 hr) and deoxycytidine plus Colcemid (5 hr). When the mitotically inhibited cells were transferred to normal medium containing PB (1.5 mM; id₁₀₀), slightly more than one-half of the cells failed to complete mitosis and the synthesis of DNA, RNA and protein was blocked by the drug. The synthesis of DNA, RNA and protein was also blocked by PB addition in the middle of the S-phase. Its addition at the onset of the second wave of mitosis prevented mitosis as before and blocked the initiation of DNA synthesis.     

当归提取液对培养的兔主动脉平滑肌细胞增殖的影响

通过培养的兔主动脉平滑肌细胞（ＳＭＣ）氚胸腺嘧啶核苷掺入量和培养液中超氧化物歧化酶（ＳＯＤ）、脂质过氧化物（ＬＰＯ）、前列环素（ＰＧＩ２）及环磷酸腺苷ｃＡＭＰ含量的测定，观察了当归提取液对ＳＭＣ增殖的影响。结果表明：当归提取液有抑制ＳＭＣ增殖的作用，其作用呈剂量依赖关系。当归提取液可能通过增加ＳＯＤ活性，降低ＬＰＯ水平，升高ＰＧＩ２、ｃＡＭＰ水平（Ｐ均＜０．０５），从而抑制ＳＭＣ增殖     

肝细胞再生因子的分离及促肝细胞增殖作用

目的研究肝细胞再生因子对肝细胞增殖的影响。方法利用分子筛层析、高效液相离子交换层析和毛细管电泳从人胎肝中分离肝细胞再生因子,采用［３Ｈ］ ＴｄＲ参入法观察其对肝源性细胞的增殖作用。结果肝细胞再生因子显著促进［３Ｈ］ ＴｄＲ的参入。结论采用本方法提纯的肝细胞再生因子能有效地促进肝源性细胞增殖。