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941.
NO3-胁迫及恢复对黄瓜幼苗叶片叶绿素荧光参数及ATPase活性的影响 总被引:6,自引:2,他引:4
通过水培试验,探讨了不同NO3-浓度胁迫及恢复对黄瓜幼苗叶片叶绿素含量、叶绿素荧光参数及ATPase活性的影响.结果表明,胁迫7 d后,高浓度NO3-(168 mmol·L-1)可极显著提高叶绿素a、叶绿素b、总叶绿素和类胡萝卜素含量,极显著提高初始荧光(Fo)、Mg ATPase和Ca-ATPase活性,而PSⅡ原初光能转化效率(Fv/Fm)、PSⅡ潜在活性(Fv/Fo)和PSⅡ光合电子传递量子效率(ΦPSⅡ),却随NO3-浓度的增加而降低.恢复7 d后,所有处理叶绿素和类胡萝卜素含量均低于对照;初始荧光基本都恢复至对照水平;PSⅡ原初光能转化效率和PSⅡ光合电子传递量子效率在NO3-浓度低于126 mmol·L-1时,基本恢复至对照水平,而高于这一水平时,仍显著低于对照;PSⅡ潜在活性在NO3-浓度为42和126 mmol·L-1的处理基本达对照水平,其它处理仍极显著低于对照;Mg-ATPase和Ca-ATPase活性均出现先降低后升高的变化趋势. 相似文献
942.
一类潜伏期和染病期均传染且具非线性传染率的流行病模型 总被引:1,自引:1,他引:0
研究了一类潜伏期和染病期都传染的具非线性传染率的SEIS流行病模型,确定了各类平衡点存在的条件阈值,讨论了各平衡点的稳定性,揭示了潜伏期传染和染病期传染对流行病发展趋势的共同影响. 相似文献
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945.
Ju Yuan Bao-Zeng Xu Shu-Tao Qi Jing-Shan Tong Liang Wei Mo Li Ying-Chun Ouyang Yi Hou Heide Schatten Qing-Yuan Sun 《PloS one》2010,5(6)
MAPK-activated protein kinase 2 (MK2), a direct substrate of p38 MAPK, plays key roles in multiple physiological functions in mitosis. Here, we show for the first time the unique distribution pattern of MK2 in meiosis. Phospho-MK2 was localized on bipolar spindle minus ends and along the interstitial axes of homologous chromosomes extending over centromere regions and arm regions at metaphase of first meiosis (MI stage) in mouse oocytes. At metaphase of second meiosis (MII stage), p-MK2 was localized on the bipolar spindle minus ends and at the inner centromere region of sister chromatids as dots. Knockdown or inhibition of MK2 resulted in spindle defects. Spindles were surrounded by irregular nondisjunction chromosomes, which were arranged in an amphitelic or syntelic/monotelic manner, or chromosomes detached from the spindles. Kinetochore–microtubule attachments were impaired in MK2-deficient oocytes because spindle microtubules became unstable in response to cold treatment. In addition, homologous chromosome segregation and meiosis progression were inhibited in these oocytes. Our data suggest that MK2 may be essential for functional meiotic bipolar spindle formation, chromosome segregation and proper kinetochore–microtubule attachments. 相似文献
946.
Tong Wang Yaguang Si Orian S. Shirihai Huiqing Si Vera Schultz Richard F. Corkey Liping Hu Jude T. Deeney Wen Guo Barbara E. Corkey 《Obesity (Silver Spring, Md.)》2010,18(8):1493-1502
It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more burning. To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat‐fed mice. Maximum O2 consumption, in vitro, was determined with a chemical uncoupler of oxidative phosphorylation (carbonylcyanide p‐trifluoromethoxyphenylhydrazone (FCCP)). The adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio was measured by luminescence. Mitochondria were localized by confocal microscopy with MitoTracker Green and their membrane potential (ΔψM) measured using tetramethylrhodamine ethyl ester perchlorate (TMRE). The effect of N‐acetylcysteine (NAC) on respiration and body composition in vivo was assessed in mice. Addition of FCCP collapsed ΔψM and decreased the ATP/ADP ratio. However, we demonstrated the same rate of adipocyte O2 consumption in the absence or presence of fuels and FCCP. Respiration was only stimulated when reactive oxygen species (ROS) were scavenged by pyruvate or NAC: other fuels or fuel combinations had little effect. Importantly, the ROS scavenging role of pyruvate was not affected by rotenone, an inhibitor of mitochondrial complex I. In addition, mice that consumed NAC exhibited increased O2 consumption and decreased body fat in vivo. These studies suggest for the first time that adipocyte O2 consumption may be inhibited by ROS, because pyruvate and NAC stimulated respiration. ROS inhibition of O2 consumption may explain the difficulty to identify effective strategies to increase fat burning in adipocytes. Stimulating fuel oxidation in adipocytes by decreasing ROS may provide a novel means to shift the balance from fuel storage to fuel burning. 相似文献
947.
Background
The putative promoter of the holocarboxylase synthetase (HLCS) gene on chromosome 21 is hypermethylated in placental tissues and could be detected as a fetal-specific DNA marker in maternal plasma. Detection of fetal trisomy 21 (T21) has been demonstrated by an epigenetic-genetic chromosome dosage approach where the amount of hypermethylated HLCS in maternal plasma is normalized using a fetal genetic marker on the Y chromosome as a chromosome dosage reference marker. We explore if this method can be applied on both male and female fetuses with the use of a paternally-inherited fetal single nucleotide polymorphism (SNP) allele on a reference chromosome for chromosome dosage normalization.Methodology
We quantified hypermethylated HLCS molecules using methylation-sensitive restriction endonuclease digestion followed by real-time or digital PCR analyses. For chromosome dosage analysis, we compared the amount of digestion-resistant HLCS to that of a SNP allele (rs6636, a C/G SNP) that the fetus has inherited from the father but absent in the pregnant mother.Principal Findings
Using a fetal-specific SNP allele on a reference chromosome, we analyzed 20 euploid and nine T21 placental tissue samples. All samples with the fetal-specific C allele were correctly classified. One sample from each of the euploid and T21 groups were misclassified when the fetal-specific G allele was used as the reference marker. We then analyzed 33 euploid and 14 T21 maternal plasma samples. All but one sample from each of the euploid and T21 groups were correctly classified using the fetal-specific C allele, while correct classification was achieved for all samples using the fetal-specific G allele as the reference marker.Conclusions
As a proof-of-concept study, we have demonstrated that the epigenetic-genetic chromosome dosage approach can be applied to the prenatal diagnosis of trisomy 21 for both male and female fetuses. 相似文献948.
949.
Gosai SJ Kwak JH Luke CJ Long OS King DE Kovatch KJ Johnston PA Shun TY Lazo JS Perlmutter DH Silverman GA Pak SC 《PloS one》2010,5(11):e15460
The development of preclinical models amenable to live animal bioactive compound screening is an attractive approach to discovering effective pharmacological therapies for disorders caused by misfolded and aggregation-prone proteins. In general, however, live animal drug screening is labor and resource intensive, and has been hampered by the lack of robust assay designs and high throughput work-flows. Based on their small size, tissue transparency and ease of cultivation, the use of C. elegans should obviate many of the technical impediments associated with live animal drug screening. Moreover, their genetic tractability and accomplished record for providing insights into the molecular and cellular basis of human disease, should make C. elegans an ideal model system for in vivo drug discovery campaigns. The goal of this study was to determine whether C. elegans could be adapted to high-throughput and high-content drug screening strategies analogous to those developed for cell-based systems. Using transgenic animals expressing fluorescently-tagged proteins, we first developed a high-quality, high-throughput work-flow utilizing an automated fluorescence microscopy platform with integrated image acquisition and data analysis modules to qualitatively assess different biological processes including, growth, tissue development, cell viability and autophagy. We next adapted this technology to conduct a small molecule screen and identified compounds that altered the intracellular accumulation of the human aggregation prone mutant that causes liver disease in α1-antitrypsin deficiency. This study provides powerful validation for advancement in preclinical drug discovery campaigns by screening live C. elegans modeling α1-antitrypsin deficiency and other complex disease phenotypes on high-content imaging platforms. 相似文献
950.
Siu-Kin Ng Wing-Sze Lo Frank W. Pun Cunyou Zhao Zhiliang Yu Jianhuan Chen Ka-Lok Tong Zhiwen Xu Shui-Ying Tsang Qiang Yang Weichuan Yu Vishwajit Nimgaonkar Gerald St?ber Mutsuo Harano Hong Xue 《PloS one》2010,5(3)