Fluorescence and reflectance characteristics of manganese deficient soybean leaves: Effects of leaf age and choice of leaflet

Leaf reflectance and fluorescence characteristics of soybean (Glycine max cv Bragg) are influenced strongly by Mn availability. This report evaluates the effects of leaflet choice, leaf age, and leaf nodal position on several spectral characteristics. Leaves were obtained from soybeans grown hydroponically under controlled environmental conditions with wide differences in Mn supply. The ratio of constant yield fluorescence (F_o) to variable yield fluorescence (F_v), the ratios of reflectance at 750 nm to 550 nm and that at 650 nm to 550 nm, the position of the "red edge" near 700 nm, and an index of leaf "yellowness" were measured periodically. Increasing leaf age caused increases in the "red edge" and in both reflectance ratios. Leaf "yellowness" and the fluorescence ratio F_o/F_v decreased with leaf age and increased with leaf nodal position, primarily in Mn deficient leaves. Effects arising from leaf choice were smaller than those caused by Mn deficiency.     

超高浓度培养基条件下酵母细胞生长及酒精生成的准稳态动力学研究

在1．5L搅拌式发酵罐中,使用葡萄糖质量浓度分别为120、200、280g／L的培养基进行酿酒酵母Saccharomyces cerevisiae连续发酵生成酒精的动力学研究。研究发现,当培养基中葡萄糖浓度为200和280g／L时,发酵液中残糖浓度、酒精浓度以及菌体生物量从小幅度波动的准稳态发展到大幅度波动的振荡状态。提出了伴有周期性振荡现象准稳态过程的概念,并针对该过程,建立了兼有底物和产物抑制的酵母细胞生长和产物酒精生成动力学模型。     

Induction of iron(III) and copper(II) reduction in pea (Pisum sativum L.) roots by Fe and Cu status: Does the root-cell plasmalemma Fe(III)-chelate reductase perform a general role in regulating cation uptake?

We investigated the effects of Fe and Cu status of pea (Pisum sativum L.) seedlings on the regulation of the putative root plasma-membrane Fe(III)-chelate reductase that is involved in Fe(III)-chelate reduction and Fe²⁺ absorption in dicotyledons and nongraminaceous monocotyledons. Additionally, we investigated the ability of this reductase system to reduce Cu(II)-chelates as well as Fe(III)-chelates. Pea seedlings were grown in full nutrient solutions under control, -Fe, and -Cu conditions for up to 18 d. Iron(III) and Cu(II) reductase activity was visualized by placing roots in an agarose gel containing either Fe(III)-EDTA and the Fe(II) chelate, Na₂bathophenanthrolinedisulfonic acid (BPDS), for Fe(III) reduction, or CuSO₄, Na₃citrate, and Na₂-2,9-dimethyl-4,7-diphenyl-1, 10-phenanthrolinedisulfonic acid (BCDS) for Cu(II) reduction. Rates of root Fe(III) and Cu(II) reduction were determined via spectrophotometric assay of the Fe(II)-BPDS or the Cu(I)-BCDS chromophore. Reductase activity was induced or stimulated by either Fe deficiency or Cu depletion of the seedlings. Roots from both Fe-deficient and Cu-depleted plants were able to reduce exogenous Cu(II)-chelate as well as Fe(III)-chelate. When this reductase was induced by Fe deficiency, the accumulation of a number of mineral cations (i.e., Cu, Mn, Fe, Mg, and K) in leaves of pea seedlings was significantly increased. We suggest that, in addition to playing a critical role in Fe absorption, this plasma-membrane reductase system also plays a more general role in the regulation of cation absorption by root cells, possibly via the reduction of critical sulfhydryl groups in transport proteins involved in divalent-cation transport (divalent-cation channels?) across the root-cell plasmalemma.     

甘南黄河流域4种典型林分土壤C、N、P化学计量特征

土壤碳（C）、氮（N）、磷（P）是参与植物光合作用和影响生态系统初级生产力的主要元素。甘南高原是黄河流域重要的生态屏障,为了解该区不同林分土壤养分状况的差异,选取该区4种典型林分：云杉林、华北落叶松林、巴山冷杉林以及岷江冷杉糙皮桦混交林为研究对象,研究土壤C、N、P化学计量特征。结果表明：（1）岷江冷杉及糙皮桦混交林土壤C、N含量最高,云杉林土壤N、P含量最低。不同林分间P含量差异显著（P<0.05）,不同土层间C、N含量差异均显著（P<0.05）。（2）云杉林土壤C ： N值显著高于其他林分,岷江冷杉及糙皮桦混交林土壤N ： P及C ： P高于其他林分。（3）海拔、土壤pH、容重与土壤含水量是影响土壤养分的重要因素。土壤C含量与N、P含量均显著相关（P<0.05）。总体来说,不同林分土壤化学计量特征具有显著差异,混交林土壤养分状况较纯林好,未来森林管理和植被建设中,可以通过选择合适的树种和提高树种多样性有效改善森林土壤质量。     

Antigen receptor-induced signal transduction imbalances associated with the negative selection of immature B cells

Signals transduced through the B cell Ag receptor (BCR) drive B cell development. However, BCR-induced responses are developmentally regulated; immature B cells are tolerized following antigenic exposure while mature B cells are triggered to proliferate and differentiate. This differential responsiveness allows for the negative selection of self-reactive immature B cells while simultaneously allowing for clonal expansion of mature B cells in response to foreign Ags. Intrinsic differences in BCR-induced signal transduction at various stages of development may account for this functional dichotomy. We had previously demonstrated that the BCR-induced proliferation of mature B cells is accompanied by an increase in intracellular calcium levels and polyphosphoinositide bis phosphate (PIP2) hydrolysis. In contrast, immature B cells that undergo BCR-induced apoptosis increase intracellular calcium in the relative absence of PIP2 hydrolysis. Since PIP2 hydrolysis leads to the generation of diacylglycerol, a cofactor for protein kinase C (PKC) activation, these data suggested that an "imbalance" in BCR-induced signal transduction resulting from a relative inability to activate PKC may play a role in the susceptibility of immature B cells to BCR-induced apoptosis. In support of this hypothesis, we demonstrate that PKC activation can rescue immature B cells from BCR-induced apoptosis. Furthermore, the susceptibility of immature B cells to BCR-induced apoptosis is recapitulated in mature B cells that are either PKC depleted or are stimulated in the presence of PKC inhibitors, suggesting that an uncoupling of PKC activation from BCR-induced signaling is responsible for the apoptotic response of immature B cells.     

Inhibition of fructose-1,6-bisphosphatase by a new class of allosteric effectors

A highly constrained pseudo-tetrapeptide (OC252-324) further defines a new allosteric binding site located near the center of fructose-1,6-bisphosphatase. In a crystal structure, pairs of inhibitory molecules bind to opposite faces of the enzyme tetramer. Each ligand molecule is in contact with three of four subunits of the tetramer, hydrogen bonding with the side chain of Asp187 and the backbone carbonyl of residue 71, and electrostatically interacting with the backbone carbonyl of residue 51. The ligated complex adopts a quaternary structure between the canonical R- and T-states of fructose-1,6-bisphosphatase, and yet a dynamic loop essential for catalysis (residues 52-72) is in a conformation identical to that of the T-state enzyme. Inhibition by the pseudo-tetrapeptide is cooperative (Hill coefficient of 2), synergistic with both AMP and fructose 2,6-bisphosphate, noncompetitive with respect to Mg2+, and uncompetitive with respect to fructose 1,6-bisphosphate. The ligand dramatically lowers the concentration at which substrate inhibition dominates the kinetics of fructose-1,6-bisphosphatase. Elevated substrate concentrations employed in kinetic screens may have facilitated the discovery of this uncompetitive inhibitor. Moreover, the inhibitor could mimic an unknown natural effector of fructose-1,6-bisphosphatase, as it interacts strongly with a conserved residue of undetermined functional significance.     

Fluid shear stress inhibits TNF-alpha-induced apoptosis in osteoblasts: a role for fluid shear stress-induced activation of PI3-kinase and inhibition of caspase-3

In bone, a large proportion of osteoblasts, the cells responsible for deposition of new bone, normally undergo programmed cell death (apoptosis). Because mechanical loading of bone increases the rate of new bone formation, we hypothesized that mechanical stimulation of osteoblasts might increase their survival. To test this hypothesis, we investigated the effects of fluid shear stress (FSS) on osteoblast apoptosis using three osteoblast cell types: primary rat calvarial osteoblasts (RCOB), MC3T3-E1 osteoblastic cells, and UMR106 osteosarcoma cells. Cells were treated with TNF-alpha in the presence of cyclohexamide (CHX) to rapidly induce apoptosis. Osteoblasts showed significant signs of apoptosis within 4-6 h of exposure to TNF-alpha and CHX, and application of FSS (12 dyne/cm(2)) significantly attenuated this TNF-alpha-induced apoptosis. FSS activated PI3-kinase signaling, induced phosphorylation of Akt, and inhibited TNF-alpha-induced activation of caspase-3. Inhibition of PI3-kinase, using LY294002, blocked the ability of FSS to rescue osteoblasts from TNF-alpha-induced apoptosis and blocked FSS-induced inhibition of caspase-3 activation in osteoblasts treated with TNF-alpha. LY294002 did not, however, prevent FSS-induced phosphorylation of Akt suggesting that activation of Akt alone is not sufficient to rescue cells from apoptosis. This result also suggests that FSS can activate Akt via a PI3-kinase-independent pathway. These studies demonstrate for the first time that application of FSS to osteoblasts in vitro results in inhibition of TNF-alpha-induced apoptosis through a mechanism involving activation of PI3-kinase signaling and inhibition of caspases. FSS-induced activation of PI3-kinase may promote cell survival through a mechanism that is distinct from the Akt-mediated survival pathway.     

Transport interactions between cadmium and zinc in roots of bread and durum wheat seedlings

Field studies have shown that the addition of Zn to Cd-containing soils can help reduce accumulation of Cd in crop plants. To understand the mechanisms involved, this study used ¹⁰⁹Cd and ⁶⁵Zn to examine the transport interactions of Zn and Cd at the root cell plasma membrane of bread wheat ( Triticum aestivum L.) and durum wheat ( Triticum turgidum L. var. durum ). Results showed that Cd²⁺ uptake was inhibited by Zn²⁺ and Zn²⁺ uptake was inhibited by Cd²⁺. Concentration-dependent uptake of both Cd²⁺ and Zn²⁺ consisted of a combination of linear binding by cell walls and saturable, Michaelis-Menten influx across the plasma membrane. Saturable influx data from experiments with and without 10 µm concentrations of the corresponding inhibiting ion were converted to double reciprocal plots. The results revealed a competitive interaction between Cd²⁺ and Zn²⁺, confirming that Cd²⁺ and Zn²⁺ share a common transport system at the root cell plasma membrane in both bread and durum wheat. The study suggests that breeding or agronomic strategies that aim to decrease Cd uptake or increase Zn uptake must take into account the potential accompanying change in transport of the competing ion.     

Regulation of PGE(2) and PGI(2) release from human umbilical vein endothelial cells by actin cytoskeleton

Disruption of microfilaments in human umbilical vein endothelialcells (HUVEC) with cytochalasin D (cytD) or latrunculin A (latA)resulted in a 3.3- to 5.7-fold increase in total synthesis ofprostaglandin E₂ (PGE₂) and a 3.4- to 6.5-foldincrease in prostacyclin (PGI₂) compared with controlcells. Disruption of the microtubule network with nocodazole orcolchicine increased synthesis of PGE₂ 1.7- to 1.9-fold andPGI₂ 1.9- to 2.0-fold compared with control cells.Interestingly, however, increased release of PGE₂ andPGI₂ from HUVEC into the media occurred only when microfilaments were disrupted. CytD treatment resulted in 6.7-fold morePGE₂ and 3.8-fold more PGI₂ released from HUVECcompared with control cells; latA treatment resulted in 17.7-fold more PGE₂ and 11.2-fold more PGI₂ released comparedwith control cells. Both increased synthesis and release ofprostaglandins in response to all drug treatments were completelyinhibited by NS-398, a specific inhibitor of cyclooxygenase-2 (COX-2).Disruption of either microfilaments using cytD or latA or ofmicrotubules using nocodazole or colchicine resulted in a significantincrease in COX-2 protein levels, suggesting that the increasedsynthesis of prostaglandins in response to drug treatments may resultfrom increased activity of COX-2. These results, together with studies demonstrating a vasoprotective role for prostaglandins, suggest thatthe cytoskeleton plays an important role in maintenance of endothelialbarrier function by regulating prostaglandin synthesis and release from HUVEC.