CO2 浓度升高对两种沈阳城市森林树种光合特性的影响

利用开顶式气室, 研究了CO2浓度升高条件下城市森林主要树种油松(Pinus tabulaefomis)和银杏(Ginkgo biloba)主要光合特性的变化。结果表明, 整个生长季, CO2浓度升高(700 mmol.mol-1)条件下2树种叶片的净光合速率、可溶性糖、淀粉和可溶性蛋白含量均接近或高于相应对照(自然CO2浓度)值, 但不同树种增加的幅度不同; 而2树种的叶绿素含量和Chl a/Chl b值对CO2浓度升高反应不一, 表现为CO2浓度升高条件下油松的叶绿素含量较对照值高, Chl a/Chl b值降低, 银杏的叶绿素含量为前期升高, 后期降低, Chl a/Chl b值变化与之正好相反, 说明城市森林组成树种对CO2浓度升高的响应具有复杂性。CO2浓度升高条件下, 两树种均未发生光合适应现象。     

CO2浓度升高对两种沈阳城市森林树种光合特性的影响

利用开顶式气室,研究了CO2浓度升高条件下城市森林主要树种油松(Pinus tabulaefomis)和银杏(Ginkgo biloba)主要光合特性的变化.结果表明,整个生长季,CO2浓度升高(700μmol·mol-1)条件下2树种叶片的净光合速率、可溶性糖、淀粉和可溶性蛋白含量均接近或高于相应对照(自然CO2浓度)值,但不同树种增加的幅度不同;而2树种的叶绿素含量和Chl a/Chl b值对CO2浓度升高反应不一,表现为CO2浓度升高条件下油松的叶绿素含量较对照值高,Chl a/Chl b值降低,银杏的叶绿素含量为前期升高,后期降低,Chl a/Chl b值变化与之正好相反,说明城市森林组成树种对CO2浓度升高的响应具有复杂性.CO2浓度升高条件下,两树种均未发生光合适应现象.     

CO2浓度升高对毛竹器官矿质离子吸收、运输和分配的影响

为了给大气CO2浓度逐渐升高背景下的毛竹林适应性经营管理提供理论依据,运用开顶式气室(OTCs)模拟大气CO2浓度升高(500、700 μmol/mol)情景,以目前环境背景大气为对照,研究了Na+、Fe2+-Fe3+、Ca2+、Mg2+等矿质离子在毛竹器官中吸收、运输和分配的变化规律.结果显示,除CO2浓度700 μmoL/mol对Ca2+浓度在毛竹器官中大小排序会产生影响外,CO2浓度500、700 μmol/mol并未改变毛竹器官中Na+、Fe2+,Fe3+、Mg2+、Ca2+浓度的大小排序.CO2浓度升高对竹叶Fe2+-Fe3+和竹枝Fe2+-Fe3+、Mg2+浓度无明显影响,但对器官的其它矿质离子浓度会有不同程度的影响,竹叶Ca2+和Mg2+、竹枝Na+和Ca2+、竹秆Na+和Ca2+及Mg2+、竹根Na+和Mg2+浓度明显提高,竹叶Na+、竹秆Fe2+-Fe3+、竹根Fe2+-Fe3+和Ca2+浓度明显降低;随着CO2浓度的升高,竹叶Fe2+-Fe3+/Na+、Mg2+/Na+和Ca2+/Na+,竹枝Ca2+/Mg2+及各器官Mg2+/Fe2+-Fe3+、Ca2+/Fe2+-Fe3+均逐渐增大,而竹枝、竹秆、竹根Fe2+-Fe3+/Na+、Mg2+/Na+、Ca2+/Na+和竹叶、竹秆、竹根Ca2+/Mg2+均逐渐减小;CO2浓度升高后除竹根-竹秆Sca.Na、竹秆-竹枝SMg,Fe和竹枝-竹叶Sca,Mg明显下降外,其余的毛竹器官矿质离子向上运输系数变化平缓或明显提高.研究表明CO2浓度升高增强了毛竹立竹根部积累Na+能力和Fe2+-Fe3+、Ca2+和Mg2+的向上选择性运输能力,提高了光合器官竹叶中矿质养分元素浓度,可维持体内矿质养分元素平衡,有利于提高毛竹对高浓度CO2环境的适应能力.     

肌球蛋白轻链激酶CaM结合位点突变体对肌球蛋白ATP酶活性的影响

目的:探讨肌球蛋白轻链激酶(MLCK)钙调蛋白(CaM)结合位点突变体对肌球蛋白ATP酶活性的影响.方法:构建牛胃重组全长野生型MLCK CaM结合位点突变型蛋白(△CaM/MLCK);孔雀绿方法检测△CaM/MLCK对肌球蛋白的Mg2+-ATP酶活性的影响.结果:在无Ca2+/CaM存在时,随着△△CaM/MLCK浓度的增加,非磷酸化肌球蛋白的Mg2+-ATP酶活性明显增加;而磷酸化肌球蛋白的Mg2+-ATP酶活性明显降低.结论:△CaM/MLCK对肌球蛋白Mg2+-ATP酶活性的影响表明MLCK具有非激酶活性.     

CO2浓度倍增对城市银杏(Ginkgo biloba)叶片膜脂过氧化与抗氧化酶活性的影响

以生长在沈阳市区内的银杏为试材,使用开顶箱模拟法对倍增CO2浓度（700μmolmol-1）和正常空气CO2浓度（≈350μmolmol-1）条件下银杏生长参数,超氧阴离子自由基（O2^-.）产生速率,丙二醛（MDA）含量,抗坏血酸（ASA）含量,超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）及谷胱甘肽还原酶（GR）活性动态变化进行分析,探讨高浓度CO2对银杏膜脂过氧化与抗氧化酶活性的影响。结果表明,在短期（60d）内CO2浓度倍增使银杏细胞内O2^-.产生速率与H2O2含量减少,而ASA含量与SOD、APX、GR活性升高。与对照相比,大多数测定显示出显著差别。但较长期（70d以上）CO2浓度倍增处理则使试验结果发生逆转,活性氧O2-.产生速率略有升高,SOD、APX、GR活性略有下降,ASA含量仍略高于对照（但与对照相比差异并不显著）,长期CO2浓度倍增处理可能使试验结果发生逆转。     

生长前期叶面喷施乙烯利对甘蔗茎细胞几种酶活性的影响

在甘蔗分蘖初期用乙烯利进行叶面喷施处理 ,并在不同的时期分别对蔗茎细胞质和细胞壁的几种代谢关键酶活性进行测定 ,结果表明 :适当浓度的乙烯利处理提高了整个生长期甘蔗茎细胞质的过氧化物酶活性、生长前中期甘蔗茎细胞质和细胞壁的 Ca2 +-ATP酶、细胞质的 Mg2 +-ATP酶活性和生长后期细胞质的多酚氧化酶活性 ,较高浓度的乙烯利处理普遍提高整个生长期甘蔗茎细胞质和细胞壁的 Ca2 +-ATP酶活性、细胞壁的 Mg2 +-ATP酶活性和旺盛生长期间细胞壁的过氧化物酶活性     

CO2浓度升高对凤梨叶片生长和光合特性的影响

研究了CO2浓度升高对开顶式气室中凤梨叶片的生长与光合生理的影响。结果表明:高CO2浓度(1000±100μmolmol-1)下生长的凤梨植株的株高、叶面积、鲜重和干重均高于对照(360±30μmolmol-1),处理90d时分别为对照的120.19%、119.22%、177.91%和161.04%;凤梨叶片的净光合速率也增加了136%-259%,且促进了叶片中可溶性糖和淀粉的积累,但叶绿素含量则下降了33.91%。高CO2浓度处理的凤梨叶片中RuBP羧化酶活性没有明显变化,乙醇酸氧化酶活性则明显下降。     

大气CO2和O3浓度升高对银杏构件生长的影响

采用开顶箱模拟试验,探讨了大气CO2和O3浓度升高对银杏构件生长的影响。结果表明：高浓度O3抑制银杏主枝和侧枝生长（P〈0．01）;高浓度CO2对银杏粗生长影响不显著（P〉0．05）,但在高浓度O3和CO2、O3复合气体条件,银杏粗生长受到严重抑制（P〈0．01）;高浓度CO2可促进银杏叶片面积和干物质的增加,并能提高叶片含水量和抗干旱能力,但在高浓度CO2、O3复合气体条件下,叶片面积增加不显著（P〉0．05）,而干物质增加极显著（P〈0．01）;O3对银杏叶片构件生长有明显抑制作用,叶面积大小和干物质量明显低于对照株（P〈0．05）。     

高浓度CO2对红松(Pinus koraiensis)针叶光合生理参数的影响

以开顶箱内经过6个生长季高浓度CO2处理的原位土壤种植的红松幼树为实验对象,研究了500umolmol-1CO2对针叶光合作用及相应光合参数的影响.实地条件下测定了净光合速率(PN)对光合有效辐射(PAR)及胞间CO2浓度(Ci)的响应曲线,根据光合作用的生化模型,推算出了Rubisco活性或数量限制的最大羧化速率(VCmax)和光饱和条件下由RuBP再生能力限制的最大电子传递速率(Jmzx),以及表观量子产量(AQY)和最大净光合速率(Pmzx)等.5001umolmol-1 CO2使红松针叶的VCmzx降低了4%,Jmzx和Jmzx/VCmzx比分别增加了27%和18%,均与对照差异不显著,所以红松针叶经过6个生长季高浓度C02处理仍未发生光合驯化.在各自生长条件下测定的PN-PAR响应曲线表明,500pumolmol-1CO2使Pmzx增加了94%,AQY增加了21%,Pmzx增长高于AQY和Jmzx的增加比例,说明500umolmol-1CO2使红松针叶对光的利用效率增强.500umolmol-1CO2下的最大气孔导度(gcmzx)和最大蒸腾速率(Emzx)与对照比增加了一倍,与Pmzx增加的幅度接近.500ummol mol-1 CO2下和对照条件下的Ci/C2比均随环境CO2浓度(C2)增加呈非线性下降趋势,在较低Ca处(Ca≤200umol mol-1),500umol mol-1CO2使Ci/Ca比下降了l%-7%,较高Ca处(Ca≥300umol mol-1),500umol mol-1CO2使Ci/Ca比增加了5%-20%.CO2浓度变化会改变Ci/Ca比,由于气孔的调节作用,Ci/Ca比最终还是要维持在一恒定范围,且气孔对较低的CO2浓度更敏感.     

不同CO2浓度下长白山3种树木幼苗的光合特性

选取长白山针叶树红松 (Pinuskoraiensis)、长白赤松 (Pinussylvestriformis)和阔叶树水曲柳(Fraxinusmandshurica)幼苗为研究对象 ,以开顶箱的方式控制CO2 浓度为 5 0 0和 70 0 μmol·mol-1,经过 3个生长季CO2 处理后 ,分别测定了 3个树种的 3年生幼苗在高浓度CO2 和大气CO2 浓度下的光合特性 .结果表明 ,前两个生长季高浓度CO2 处理增强了 3个树种幼苗的光合能力 ;不同树种在相同CO2 浓度下 ,最大净光合速率及光响应参数值不同 ;第 3个生长季 ,除 5 0 0 μmol·mol-1CO2 下生长的长白赤松外 ,各树种的幼苗在高浓度CO2 下并未发生“光合驯化”现象 ;最大净光合速率及光响应参数值随CO2 处理时间的延长有不同幅度的增减 ;高浓度CO2 改变了树木幼苗对强光和弱光的利用能力 .     

Neurotropic activity of phenylpyrrolidones-2

Experiments were conducted on mice and rats; a study was made of the pharmacological activity of three isomers of phenyl derivatives of pyrrolidone-2 (P-2). The latter represented a cylic form of gamma-aminobutyric acid (GABA). All the three preparations suppressed the motor activity, decreased the muscle tone and the body temperature, potentiated the action of hexenal, possessed the antispasmodic and hypnotic activity. 4-phenyl-pyrrolidone-2 (phepyron) proved to be most active. In comparing the pharmacological activity of phenyl P-2 derivatives and analogous GABA derivatives the latter were found to possess no antispasmodic or hypnotic activity, and were less toxic. It is supposed that no transformation of phenyl P-2 derivatives into analogous GABA derivatives occurred in the organism.     

Antiangiogenic activity of 2-deoxy-D-glucose

Background

During tumor angiogenesis, endothelial cells (ECs) are engaged in a number of energy consuming biological processes, such as proliferation, migration, and capillary formation. Since glucose uptake and metabolism are increased to meet this energy need, the effects of the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) on in vitro and in vivo angiogenesis were investigated.

Methodology/Principal Findings

In cell culture, 2-DG inhibited EC growth, induced cytotoxicity, blocked migration, and inhibited actively forming but not established endothelial capillaries. Surprisingly, 2-DG was a better inhibitor of these EC properties than two more efficacious glycolytic inhibitors, 2-fluorodeoxy-D-glucose and oxamate. As an alternative to a glycolytic inhibitory mechanism, we considered 2-DG''s ability to interfere with endothelial N-linked glycosylation. 2-DG''s effects were reversed by mannose, an N-linked glycosylation precursor, and at relevant concentrations 2-DG also inhibited synthesis of the lipid linked oligosaccharide (LLO) N-glycosylation donor in a mannose-reversible manner. Inhibition of LLO synthesis activated the unfolded protein response (UPR), which resulted in induction of GADD153/CHOP and EC apoptosis (TUNEL assay). Thus, 2-DG''s effects on ECs appeared primarily due to inhibition of LLOs synthesis, not glycolysis. 2-DG was then evaluated in two mouse models, inhibiting angiogenesis in both the matrigel plug assay and the LH_BETAT_AG transgenic retinoblastoma model.

Conclusions/Significance

In conclusion, 2-DG inhibits endothelial cell angiogenesis in vitro and in vivo, at concentrations below those affecting tumor cells directly, most likely by interfering with N-linked glycosylation rather than glycolysis. Our data underscore the importance of glucose metabolism on neovascularization, and demonstrate a novel approach for anti-angiogenic strategies.     

Bcl-2 expression suppresses mismatch repair activity through inhibition of E2F transcriptional activity

Bcl-2 stimulates mutagenesis after the exposure of cells to DNA-damaging agents. However, the biological mechanisms of Bcl-2-mediated mutagenesis have remained largely obscure. Here we demonstrate that the Bcl-2-mediated suppression of hMSH2 expression results in a reduced cellular capacity to repair mismatches. The pathway linking Bcl-2 expression to the suppression of mismatch repair (MMR) activity involves the hypophosphorylation of pRb, and then the enhancement of the E2F-pRb complex. This is followed by a decrease in hMSH2 expression. MMR has a key role in protection against deleterious mutation accumulation and in maintaining genomic stability. Therefore, the decreased MMR activity by Bcl-2 may be an underlying mechanism for Bcl-2-promoted oncogenesis.     

Antiproteinase activity of alpha 2-macroglobulin

Blood serum separation by the method of gel filtration on Sephadex G-200 with the subsequent immunochemical determination of the quantitative content of basic proteolysis inhibitors permitted isolating the alpha 2-macroglobulin fraction while alpha 1-antitrypsin and alpha 1-antichymotrypsin separation was a failure. The immunochemical analysis of the antienzymic activity of the isolated inhibitors showed that 32.3 +/- 3.5% of the introduced kallikrein, 18.7 +/- 0.6% of trypsin and 14.4 +/- 4.1% of chymotrypsin were bound in the zone of alpha 2-macroglobulin. The rest of antienzymic activity was localized in the zone of alpha 1-antitrypsin and alpha 1-antichymotrypsin. After a preliminary saturation of blood serum with trypsin in the amount equivalent to its antitryptic capacity (200 micrograms/ml) the ability of alpha 2-macroglobulin to bind kallikrein and chymotrypsin lowers considerably (by 69 and 72%, respectively). In the zone of alpha 1-antitrypsin and alpha 1-antichymotrypsin a decrease in the ability to bind kallikrein and chymotrypsin amounted to 44 and 12% respectively. Thus, alpha 2-macroglobulin being bound with trypsin looses considerably its ability to bind other enzymes.     

Antimicrobial activity of substituted 2-trifluoromethyl- and 2-pentafluoroethylbenzimidazoles

Antibacterial and antifungal activity of 2-trifluoromethyl- and 2-pentafluoroethylbenzimidazoles, including a number of newly obtained derivatives, were examined by diffusion method (inhibition area diameter in solid agar medium) and minimum inhibitory concentration (MIC, in liquid and agar medium). Some of the derivatives tested affected fungal colony morphology and exerted genotoxic effects in bacteria. Of the tested compounds, 5,6-dichlorosubstituted derivatives appeared the most active against the majority of microorganisms used.     

Cytokine-inducing activity of family 2 cystatins

Cystatins are physiological cysteine proteinase inhibitors. Here we report a novel function for some family 2 cystatins that is not related to these activities. The release of interleukin-6 (IL-6) and interleukin-8 (IL-8) by the gingival fibroblasts and that of IL-6 by murine splenocytes were measured using ELISA systems specific for these cytokine molecules. Family 2 cystatins, including cystatins C, SA1, SA2, S, and egg white cystatin, upregulated the IL-6 production by two-lasts at physiological concentrations. After complete saturation with papain, those family 2 cystatins still upregulated IL-6 production, suggesting that the papain-inhibitory site was not involved in the cytokine-inducing activity.