1,4—二取代酰氨基硫脲类化合物(DATCDs)的植物生理效应与应用研究——Ⅴ.DATCD-A对离体黄瓜子叶扩张及核酸代谢的影响

本实验以离体黄瓜子叶为材料,研究了 DATCD—A 对子叶扩张及核酸代谢的影响。结果表明,DATCD—A 可显著地促进离体黄化子叶扩张,使其鲜重明显增加;并且在处理后期逐渐提高子叶干重。在离体子叶扩张变绿的过程中,DATCD—A 促进离体黄化子叶 RNA、DNA 含量和 DNA/RNA 比率明显上升,且 RNA 的增加发生在 DNA 合成增加之前。凝胶电泳证明,RNA 的增加主要是25s 和18s 的 rRNA。     

外阴皮肤营养不良组织中人乳头瘤病毒DNA的检测

采用Southern Blot分子杂交方法检测了9例外阴皮肤营养不良组织中人乳头瘤病毒DNA的存在情况。结果显示8例增生型营养不良组织中,2例HPV-16阳性,1例HPV33阳性,在3例组织中探测到HPV16相关序列,在1例混合型中也检测到HPV16相关序例,HPV DNA的总检出率为77％。结果提示外阴皮肤营养不良的发生可能与HPV感染有关。     

Tissue distribution,metabolism, and elimination of perfluorooctanoic acid in male and female rats

The elimination, tissue distribution, and metabolism of [1-¹⁴C]perfluorooctanoic acid (PFOA) was examined in male and female rats for 28 days after a single ip dose (9.4 μmol/kg, 4 mg/kg). A sex difference in urinary elimination of PFOA-derived ¹⁴C was observed. Female rats eliminated PFOA-derived radioactivity rapidly in the urine with 91% of the dose being excreted in the first 24 hr. In the same period, male rats eliminated only 6% of the administered ¹⁴C in the urine. The sex-related difference in urinary elimination resulted in the observed difference in the whole-body elimination half-life (t_1/2) of PFOA in males (t_1/2 = 15 days) and females (t_1/2 < 1 day). Analysis of PFOA-derived ¹⁴C in tissues showed that the liver and plasma of male rats and the liver, plasma, and kidney of female rats were the primary tissues of distribution. The relatively high concentration of PFOA in the male liver was further examined using an in situ nonrecirculating liver perfusion technique. It was shown that 11% of the PFOA infused was extracted by the liver in a single pass. The ability of the liver to eliminate PFOA into bile was examined in rats whose renal pedicles were ligated to alleviate sex differences in the urinary excretion of PFOA. In a 6-hr period following IP administration of PFOA, there was no apparent difference in biliary excretion, where both males and females eliminated less than 1% of the PFOA dose via this route. We hypothesized that the sex difference in the persistence of PFOA was due to a more rapid formation of a PFOA-containing lipid (i.e., a PFOA-containing mono-, di-, or triacylglycerol, cholesteryl ester, methyl ester, or phospholipid) in the male rat. Also, the increased urinary elimination of PFOA in females may have been due to increased metabolism to a PFOA-glucuronide or sulfate ester. However, no evidence that PFOA is conjugated to form a persistent hybrid lipid was obtained, nor were polar metabolites of PFOA in urine or bile detected. In addition, daily urinary excretion of fluoride in male and female rats before or after PFOA treatment were similar, suggesting that the parent compound is not defluorinated. Thus, the more rapid elimination of PFOA from female rats is not due to formation of a PFOA metabolite.     

Linoleic acid-induced endothelial cell injury: Role of membrane-bound enzyme activities and lipid oxidation

High plasma levels of linoleic acid (18:2) may injure endothelial cells, resulting in decreased barrier function of the vascular endothelium. The effects of linoleic acid on endothelial barrier function (transendothelial movement of albumin), membrane-bound enzyme activities, and possible autooxidation of linoleic acid under experimental conditions were studied. The exposure of endothelial monolayers to 18:2 for 24 hr at 60, 90, and 120 μM. fatty acid concentrations caused a significant increase in transendothelial movement of albumin, with maximum albumin transfer at 90 μM. Fatty acid treatment resulted in the increased appearance of cytosolic lipid droplets. Activities of the membrane-bound enzymes, angiotensin-converting enzyme (ACE), and Ca²⁺-ATPase increased steadily with increasing time of cell exposure to 90 μM 18:2, reaching significance at 24 hr. Treatment of endothelial cultures with up to 120 μM 18:2 did not cause cytotoxicity, as evidenced by a nonsignificant change in cellular release of [₃H]-adenine. Incubation of 18:2-supplemented serum-containing culture media with 1000 μM 18:2 at 37°C for up to 48 hr did not result in formation of autooxidation products. These results suggest that 18:2 itself, and not its oxidation products, plays a major role in disrupting endothelial barrier function.     

Effect of Basal Gastric Acid Secretion on the Pharmacodynamics of Ranitidine

Twelve patients with inactive ulcer disease were administered placebo and ranitidine via bolus and continuous intravenous infusions, at doses ranging from 50 every 8 h, to 12.5 mg/h for 24 h. Gastric acid was collected for 20 min each h for 24 h, and ranitidine serum concentrations were measured ± every 2 h, during each of the six study periods. Cosinor analysis of gastric acid secretion during placebo treatment revealed a significant circadian rhythm in all subjects. Mesor acid output ranged from 1.7 to 11.6 mmol/h (mean 5.6 ± 2.8 mmol/h) and the amplitude ranged from 0.7 to 6.5 mmol/h (mean 2.8 ±1.6 mmol/h). Peak acid output (acrophase) occurred at 10 p.m. ± 3 h. A pharmacodynamic model, relating ranitidine serum concentration to hourly acid secretion, was derived, which incorporated the circadian change in basal acid output. Data for this fractional response model included basal acid secretion-as determined by time of day, measured acid secretion, and associated serum ranitidine concentration. The 50% inhibitory concentration (IC₅₀) for ranitidine ranged from 10-75 ng/ml, with a mean of 44 ng/ml. The variation in IC₅₀ and in basal acid secretion combined to produce a wide variation in the pharmacodynamic response to ranitidine. The model-predicted serum concentrations, required to maintain acid secretion at 0.1 mmol/h, ranged from 250 to 1550 ng/ml, at the time of peak evening acid secretion. Despite a constant degree of acid inhibition by ranitidine during the day, higher serum concentrations are required during times of peak acid output to maintain adequate suppression of hydrogen ion secretion.     

Mg2+ restores membrane potential in rat liver mitochondria deenergized by Ca2+ and phosphate movements

Cellular ornithine biosynthesis could be expected to play a significant role in putrescine formation and hence in growth. Two enzymes are involved in ornithine biosynthesis: arginase and transamidinase. These enzyme activities were studied in two human melanoma cell lines differing in their K_m of diamine oxidase for putrescine and in their tumorigenicity in nude mice. Arginase activity accounts for the majority of ornithine formed in the highly tumorigenic cell line, while the majority of ornithine is derived from transamidinase action in the poorly tumorigenic cell line, with concomitant formation of methyl guanidine, a potent inhibitor of diamine oxidase.     

The old REH theory remains unsatisfactory and the new REH theory is problematical - a reply to holmquist and jukes

Summary In response to criticism of REH theory (Fitch 1980), Holmquist and Jukes (1981) have mostly avoided the criticism or misunderstood it. Since they themselves state in their response that Amino acid sequence data alone cannot be used to estimate total nucleotide substitutions, they agree with the criticism. Most of their paper treats the newer theory (here designated as the REHN theory) which attempts to use the nucleotide sequences encoding proteins to better estimate total nucleotide substitutions (Holmquist and Pearl 1980). Since I made no criticism of REHN theory, their comments are frequently beside the point of my original criticism of REH theory. Nevertheless, it is shown here that REHN theory is also unsatisfactory in that: One, the varions are now more clearly defined but in such a way as to preclude the same codon from suffering a nucleotide substitution in more than one evolutionary interval. Two, the set of codons that accepts silent substitutions is identical to the set that accepts amino acid changing nucleotide substitutions. Three, the uncertainty in the REH estimate is considerable in that alternative excellent fits to the same observatuonal data may give alternative REH values that differ significantly even before stochastic variation and selective bias are considered. Four, the fit of their model to data is an irrelevancy where there are zero degrees of freedom.     

Correlations between proton-efflux patterns and growth patterns during geotropism and phototropism in maize and sunflower

By placing seedlings of sunflower (Helianthus annuus L.) or maize (Zea mays L.) on agar plates containing a pH indicator dye it is possible to observe surface pH patterns along the growing seedling by observing color changes of the indicator dye. Using this method we find that in geotropically stimulated sunflower hypocotyls or maize coleoptiles there is enhanced proton efflux on the lower surface of the organ prior to the initiation of curvature. As curvature develops the pattern of differential acid efflux becomes more intense. A similar phenomenon is observed when these organs are exposed to unilateral illumination, i.e. enhanced acid efflux occurs on the dark side of the organ prior to the initiation of phototropic curvature and the pattern of differential acid efflux intensifies as phototropic curvature develops. These observations indicate that differential acid efflux occurs in response to tropistic stimuli and that the acid efflux pattern may mediate the development of tropistic curvatures.     

Studies of vegetative compatibility-incompatibility in higher plants

Summary In order to elucidate the events that lead to cellular autolysis, and thus better understand the mechanism of cellular incompatibility betweenSedum telephoides andSolanum pennellii stems, we have followed the appearance and fate of the hydrolytic enzyme acid phosphatase in both the compatibleSedum autograft and the incompatibleSedum/Solanum heterograft. Acid phosphatase was localized by a modified Gomori-type reaction. Following an initial association with the endoplasmic reticulum and dictyosomes by 6–10 hours after grafting, acid phosphatase activity in the compatibleSedum autograft was associated primarily with the plasmalemma, tonoplast, and vacuole. This strict compartmentation in membranes or organelles and absence of enzyme from the cytosol was maintained throughout the development of the compatible autograft inSedum. Although acid phosphatase activity in the incompatible heterograft betweenSedum andSolanum was initially similar to the compatible autograft inSedum, a marked difference in enzyme localization occurred in the two graft partners over time.Solanum cells accumulated increased amounts of acid phosphatase, but the enzyme remained sequestered in the plasmalemma, tonoplast, and vacuole. In comparableSedum cells, however, there was a dramatic increase in acid phosphatase activity in the cytosol, often without any prior compartmentation within the vacuole. This high activity of acid phosphatase in theSedum cytosol was correlated with cellular autolysis, death, and eventual cell collapse to form the characteristic necrotic layer that insulates the stock from the scion. These results suggest that the lethal cellular senescence associated withSedum cells of the incompatible heterograft is correlated with a cytoplasmic release of acid phosphatase. A similar release of the enzyme does not occur in theSolanum stock or in the compatibleSedum autograft. Thus, while acid phosphatase synthesis and/or activation is induced in both the compatible and incompatible grafts, incompatibility betweenSedum andSolanum involves a failure ofSedum cells to isolate hydrolytic enzymes from the cytosol, which subsequently leads to cellular necrosis.Supported in part by grants from the Academic Senate of UCLA, Sigma Xi, the American Philosophical Society, and the URC of Baylor University.     

Evolutionary analysis ofα andβ hemoglobin genes by reh theory under the assumption of the equiprobability of genetic events

Summary It is shown how REH theory in conjunction with mRNA or gene sequence data can be used to obtain estimates of the fixation intensity, the number of varions, and the total mutations fixed between homologous pairs of nucleic acids. These estimates are more accurate than those that can be derived from amino acid sequence data. The method is illustrated for and hemoglobin genes and these improved estimates are compared with those made from the amino acid sequences for which those genes code. Significant differences are found between the estimates made by these two methods. For the hemoglobin gene sequences examined here, the fixation intensity is some-what less than the protein data had suggested, and the number of rations is considerably greater. Depending on the gene sequences examined, between 62 and 83% of the codons appear able to fix mutations during the divergences considered. This reflects the constraints of natural selection on acceptable mutations. The total number of base replacements separating the genes for human, mouse, and rabbit hemoglobin varies from 61 to 105 depending on the pair examined. Rabbit and hemoglobin are separated by at least 290 fixed mutations. For such distantly related sequences estimates made from protein and mRNA data differ less, reflecting the higher quality of information from the many observed changes in primary structure. The effects of nonrandom gene structure on these evolutionary estimates and the fact that various genetic events are not equiprobable are discussed.