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Leadership. Promoting potential.
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Leadership. Unleashing the potential.
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Interactions between inositol tris- and tetrakis-phosphates. Effects on intracellular Ca2+ mobilization in SH-SY5Y cells.
The potential Ca2(+)-releasing activity of the inositol tetrakisphosphates Ins(1,3,4,6)P4 and DL-Ins(1,4,5,6)P4 and the inositol pentakisphosphate Ins(1,3,4,5,6)P5 and their effect on Ins(1,4,5)P3- and DL-Ins (1,3,4,5)P4-mediated Ca2+ release were examined in permeabilized SH-SY5Y human neuroblastoma cells. Neither DL-Ins(1,4,5,6)P4 nor Ins(1,3,4,5,6)P5 exhibit Ca2(+)-releasing activity at concentrations up to 10 microM, but Ins(1,3,4,6)P4 releases Ca2+ dose-dependently, with an EC50 value (conen, giving half-maximal effect) of 5.92 +/- 0.47 microM. Maximal response by this tetrakisphosphate (49 +/- 2.5%) is significantly less than that seen with Ins(1,4,5)P3 (60 +/- 3%) and is achieved at a concentration of 30 microM. In the presence of this concentration of Ins(1,3,4,6)P4 the EC50 value for Ins(1,4,5)P3-mediated Ca2+ release increases from 0.12 +/- 0.02 microM to 2.11 +/- 0.51 microM, providing evidence that this naturally occurring inositol tetrakisphosphate may recognize and exhibit its Ca2(+)-releasing activity via the Ins(1,4,5)P3 receptor. DL-Ins(1,3,4,5)P4, however, at its maximally effective concentration (10 microM) does not significantly affect Ins(1,4,5)P3-mediated Ca2+ release, and therefore appears to mediate its Ca2(+)-mobilizing action through a receptor distinct from that for Ins(1,4,5)P3.
Ice/Water Interface: Zeta Potential, Point of Zero Charge, and Hydrophobicity.
The ice/water interface is a common and important part of many biological, environmental, and technological systems. In contrast to its importance, the system has not been extensively studied and is not well understood. Therefore, in this paper the properties of the H(2)O ice/water and D(2)O ice/water interfaces were investigated. Although the zeta potential vs pH data points were significantly scattered, it was determined that the isoelectric point (iep) of D(2)O ice particles in water at 3.5 degrees C containing 10(-3) M NaCl occurs at about pH 3.0. The negative values of the zeta potential, calculated from the electrophoretic mobility, seem to decrease with decreasing content of NaCl, while the iep shifts to a higher pH. The point of zero charge (pzc) of D(2)O ice and H(2)O ice, determined by changes in pH of 10(-4) M NaCl aqueous solution at 0.5 degrees C after the ice particle addition, was found to be very different from the iep and equal to pH 7.0 +/- 0.5. The shift of the iep with NaCl concentration and the difference in the positions of the iep and pzc on the pH scale point to complex specific adsorption of ions at the interface. Interestingly, similar values of iep and pzc were found for very different systems, such as hydrophilic ice and highly hydrophobic hexadecane droplets in water. A comparison of the zeta potential vs pH curves for hydrophilic ice and hydrophobic materials that do not possess dissociative functional groups at the interface (diamond, air bubbles, bacteria, and hexadecane) indicated that all of them have an iep near pH 3.5. These results indicate that the zeta potential and surface charge data alone cannot be used to delineate the electrochemical properties of a given water/moiety interface because similar electrical properties do not necessary mean a similar structure of the interfacial region. A good example is the aliphatic hydrocarbon/water interface in comparison to the ice/water interface. Although the experiments were carried out with care, both the zeta potential, measured with a precise ZetaPlus meter, and DeltapH values (a measure of surface charge) vs pH were significantly scattered, and the origin of dissemination of the data points was not established. Differently charged ice particles and not fully equilibrium conditions at the ice/water interface may have been responsible for the dissemination of the data. Copyright 1999 Academic Press.
Psyllids as a potential source of heavy metals for predators.
Contents of Al, Fe, Zn, Cu, Cd, Mn, Ni, and Hg were determined in 14 species of psyllids and in leaves of their host plants from unpolluted sites (Finland) and industrially polluted sites in Poland. Generally, psyllids accumulated low amounts of metals, but their metal burdens increased with age. Exuvia were important for the elimination of Al, Ni, and Mn, and larval wax for Al, Cu, and Ni. Biomagnification of metals, expressed as the concentration factor (cf) was low (cf: 0.56-1.08) for Mn, Al, and Ni, but high for Cd (cf: 5.86). Trioza chenopodii, Cacopsylla ulmi, and Psylla betulae represented the microconcentrators (cf: 0.9-1.25); the remaining species were the macroconcentrators (cf: 2.0-4.9). In polluted areas Psyllopsis fraxini eliminated large amounts of Al, Fe, Cu, Mn, and Cd with honeydew. This way of metal elimination was of less importance in species from unpolluted sites. Adults of Cacopsylla mali, P. fraxini, P. betulae, and Cacopsylla sorbi fall a prey to ants and may be important in transfer of Zn, Fe, Cu, Cd, and Ni. In comparison with aphids their role in metal transfer is marginal, due to better self-defence mechanisms and higher mobility, which protect them from potential predators and parasites.
A bacterial group II intron-encoded reverse transcriptase localizes to cellular poles.
The Lactococcus lactis Ll.LtrB group II intron encodes a reverse transcriptase (LtrA protein) that binds the intron RNA to promote RNA splicing and intron mobility. Here, we used LtrA-GFP fusions and immunofluorescence microscopy to show that LtrA localizes to cellular poles in Escherichia coli and Lactococcus lactis. This polar localization occurs with or without coexpression of Ll.LtrB intron RNA, is observed over a wide range of cellular growth rates and expression levels, and is independent of replication origin function. The same localization pattern was found for three nonoverlapping LtrA subsegments, possibly reflecting dependence on common redundant signals and/or protein physical properties. When coexpressed in E. coli, LtrA interferes with the polar localization of the Shigella IcsA protein, which mediates polarized actin tail assembly, suggesting competition for a common localization determinant. The polar localization of LtrA could account for the preferential insertion of the Ll.LtrB intron in the origin and terminus regions of the E. coli chromosome, may facilitate access to exposed DNA in these regions, and could potentially link group II intron mobility to the host DNA replication and/or cell division machinery.
Improved analysis of 1H-MR spectra in the presence of mobile lipids.
Focal brain lesions can be associated with proton magnetic resonance spectra (1H-MRS)-detectable mobile lipids, reflecting severe tissue degradation and necrosis. However, advanced fitting procedures, such as the LCModel, fail to adequately fit spectra in the presence of lipid resonances. To overcome this, different approaches to generate lipid model spectra were compared using a phantom, real in vivo data, and simulated data. Twenty-six in vivo short-echo time (TE) 1H-MRS from 21 malignant gliomas, four infections, and one ischemia were analyzed to evaluate the performance of the modified LCModel fit. Adding simulated aliphatic resonances at 1.3 and 0.9 ppm improved the overall fitting quality remarkably and allowed good separation of lactate and alanine. Also, a better differentiation of glioblastomas and anaplastic gliomas was achieved. In conclusion, we propose a simple way to efficiently include lipid resonances in the LCModel, allowing a better fit of in vivo short-TE 1H-MRS, and demonstrate the diagnostic potential of quantitative assessment of mobile lipids in brain tumors.
Oxidative stress and TNF-alpha induce histone acetylation and NF-kappaB/AP-1 activation in alveolar epithelial cells: potential mechanism in gene transcription in lung inflammation.
Oxidants and inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha) activate nuclear factor kappa B (NF-kappaB) and activator protein-1 (AP-1) transcription factors, and enhance the expression of both pro-inflammatory and protective antioxidant genes. Remodelling of chromatin within the nucleus, controlled by the degree of acetylation/deacetylation of histone residues on the histone core around which DNA is coiled, is important in allowing access for transcription factor DNA binding and hence gene transcription. Unwinding of DNA is important in allowing access for transcription factor DNA binding and hence gene transcription. Nuclear histone acetylation is a reversible process, and is regulated by a group of acetyltransferases (HATs) which promote acetylation, and deacetylases (HDACs) which promote deacetylation. The aim of this study was to determine whether oxidative stress and the pro-inflammatory mediator, TNF-alpha, altered histone acetylation/deacetylation and the activation of NF-kappaB and AP-1, leading to the release ofthe pro-inflammatory cytokine IL-8 in human alveolar epithelial cells (A549). Hydrogen peroxide (H2O2) (100 microM) and TNF-alpha (10 ng/ml) imposed oxidative stress in A549 cells as shown by depletion of the antioxidant reduced glutathione (GSH) concomitant with increased levels of oxidised glutathione (GSSG). Treatment of A549 cells with H2O2, TNF-alpha and the HDAC inhibitor, trichostatin A, TSA (100 ng/ml) significantly increased acetylation of histone proteins shown by immunostaining of cells and increased HAT activity, compared to the untreated cells. H2O2, and TNF-a, and TSA all increased NF-kappaB and AP-1 DNA binding to their consensus sites assessed by the electrophoretic mobility shift assay. TSA treatment potentiated the increased AP-1 and NF-KB binding, produced by H2O2 or TNF-alpha treatments in A549 cells. Both H2O2 and TNF-alpha significantly increased IL-8 release, which was further enhanced by pre-treatment of A549 cells with TSA compared to the individual treatments. This study shows that the oxidant H2O2 and the pro-inflammatory mediator, TNF-a induce histone acetylation which is associated with decreased GSH levels and increased AP-1 and NF-kappaB activation leading to enhanced proinflammatory IL-8 release in alveolar epithelial cells. This indicates a mechanism for the pro-inflammatory effects of oxidative stress.
Influence of the ionic composition of fluid medium on red cell aggregation.
The effects of ionic strength and cationic valency of the fluid medium on the surface potential and dextran-induced aggregation of red blood cells (RBC's) were investigated. The zeta potential was calculated from cell mobility in a microelectrophoresis apparatus; the degree of aggregation of normal and neuraminidase-treated RBC's in dextrans (Dx 40 and Dx 80) was quantified by microscopic observation, measurement of erythrocyte sedimentation rate, and determination of low-shear viscosity. A decrease in ionic strength caused a reduction in aggregation of normal RBC's in dextrans, but had no effect on the aggregation of neuraminidase-treated RBC's. These findings reflect an increase in electrostatic repulsive force between normal RBC's by the reduction in ionic strength due to (a) a decrease in the screening of surface charge by counter-ions and (b) an increase in the thickness of the electric double layer. Divalent cations (Ca(++), Mg(++), and Ba(++)) increased aggregation of normal RBC's in dextrans, but had no effect on the aggregation of neuraminidase-treated RBC's. These effects of the divalent cations are attributable to a decrease in surface potential of normal RBC's and a shrinkage of the electric double layer. It is concluded that the surface charge of RBC's plays a significant role in cell-to-cell interactions.
Effects of 2-nicotinamidoethyl nitrate on smooth muscle cells and on adrenergic transmission in the guinea-pig and porcine mesenteric arteries.
Muscle membranes of the porcine but not guinea-pig mesenteric artery wee hyperpolarized by applications of over 10(-6) M 2-nicotinamidoethyl nitrate (SG 75; 2-NN) dose-dependently from -53 to -72 mV, due to an increase in the ionic conductance of the membrane. In the porcine mesenteric artery but not guinea-pig, 2-NN suppressed the K-induced contraction in concentrations below 20 mM [K]0. The suppression of the K-induced contraction depended on the degree of hyperpolarization and the level of the resting membrane potential. The norepinephrine-induced contraction was suppressed by 2-NN with hyperpolarization of the membrane in the porcine mesenteric artery, but with no change in the membrane potential in the guinea-pig mesenteric artery, presumably due to suppression of the Ca-mobilization in the cell. The excitatory junction potential (ejp) could be recorded by perivascular nerve stimulation in both mesenteric arteries. Whether or not the membrane was hyperpolarized, 2-NN increased the amplitude of ejp in both tissues and increased the appearances of miniature ejp in the guinea-pig mesenteric artery. Nitroglycerin did not modify the membrane potential, the amplitude of ejp, electrical threshold and spike superimposed on the ejp, while sodium nitroprusside suppressed the amplitude of ejp, the facilitation process produced by repetitive stimulation and the spike superimposed on the ejp. Specific features of 2-NN actions on the muscle cell and adrenergic transmission of the mesenteric arteries in both species were discussed in relation to vasodilating actions, species differences and also in relation to other nitrite compounds.
Membrane depolarization in NRK fibroblasts by bradykinin is mediated by a calcium-dependent chloride conductance.
The effects of the phosphoinositide-mobilizing agonist bradykinin (BK) on membrane potential and intracellular calcium in monolayers of normal rat kidney (NRK) fibroblasts were investigated. BK induced a rapid transient depolarization in these cells, which was mimicked by other phosphoinositide-mobilizing factors such as prostaglandin F2alpha (PGF2alpha), lysophosphatidic acid (LPA), platelet-derived growth factor (PDGF-BB), and serum. Depolarization by BK was independent of extracellular Ca2+ or Na+. It was shown using extracellular Cl- substitutions that the depolarization was caused by an increased Cl- conductance. Depolarization was inhibited by 5-nitro-2-3-phenylpropyl(amino)benzoic acid (NPPB), niflumic acid, and flufenamic acid, inhibitors of calcium-dependent chloride channels. The depolarization provoked by BK could be mimicked by raising intracellular calcium with ionomycin or thapsigargin and could be blocked with geneticin, a blocker of phospholipase C. When intracellular calcium was buffered by loading the cells with 1,2-bis(2-aminophenoxy)ethane-NNN'N'-tetra-acetic acid (BAPTA), depolarization was prevented. We conclude that in NRK fibroblasts extracellular stimuli that increase intracellular calcium, depolarize the cells via the activation of a calcium-dependent chloride conductance. In addition to an increase in intracellular calcium, depolarization may be an important effector pathway in response to extracellular stimuli in fibroblasts. It is hypothesized that, in electrically coupled cells such as NRK fibroblasts, intercellular transmission of these depolarizations may represent a mechanism to coordinate uniform multicellular responses to Ca2+-mobilizing agonists.
Use of mobile phones in the behavioral treatment of driving phobias.
Results of two case studies are presented to illustrate the use of mobile phones with in vivo exposure treatment of refractory driving phobias. Number of miles driven and subjective ratings of anxiety were recorded during a baseline phase and 8 weeks of treatment involving a total of 24 driving practices. One subject's use of a mobile phone increased the number of miles driven alone, but the second subject made little progress and regressed following removal of the phone. These two cases and our experience with other patients suggest that mobile phones can benefit many individuals whose therapeutic progress is impeded by a fear of driving alone, but that phones are counterproductive for certain patients. The potential benefits and disadvantages of using mobile phones are discussed.
Electrokinetic transport in nanochannels. 1. Theory.
Electrokinetic transport in fluidic channels facilitates control and separation of ionic species. In nanometer-scale electrokinetic systems, the electric double layer thickness is comparable to characteristic channel dimensions, and this results in nonuniform velocity profiles and strong electric fields transverse to the flow. In such channels, streamwise and transverse electromigration fluxes contribute to the separation and dispersion of analyte ions. In this paper, we report on analytical and numerical models for nanochannel electrophoretic transport and separation of neutral and charged analytes. We present continuum-based theoretical studies in nanoscale channels with characteristic depths on the order of the Debye length. Our model yields analytical expressions for electroosmotic flow, species transport velocity, streamwise-transverse concentration field distribution, and ratio of apparent electrophoretic mobility for a nanochannel to (standard) ion mobility. The model demonstrates that the effective mobility governing electrophoretic transport of charged species in nanochannels depends not only on electrolyte mobility values but also on zeta potential, ion valence, and background electrolyte concentration. We also present a method we term electrokinetic separation by ion valence (EKSIV) whereby both ion valence and ion mobility may be determined independently from a comparison of micro- and nanoscale transport measurements. In the second of this two-paper series, we present experimental validation of our models.
Immature monocytes from G-CSF-mobilized peripheral blood stem cell collections carry surface-bound IL-10 and have the potential to modulate alloreactivity.
Production of the anti-inflammatory cytokine IL-10 by monocytes has been implicated as a probable negative regulator of graft-versus-host disease (GvHD) in patients undergoing allogeneic stem cell transplants (SCT). Monocytes from G-CSF-mobilized peripheral blood stem cell (gmPBSC) collections have been reported to produce more IL-10 than unmobilized monocytes in response to proinflammatory factors such as LPS. Why this should occur is unclear. In this study, monocyte phenotype and IL-10 localization and release were investigated in PB mononuclear cells (MNC) from 27 healthy donors mobilized for allogeneic SCT and from 13 patients with hematological malignancies mobilized for autologous SCT. All isolates contained elevated total percentages of monocytes in comparison with unmobilized PB, a high proportion of which displayed an immature phenotype. Stimulation of gmPB MNC with an inflammatory stimulus [fixed Staphylococcus aureus cells (SAC)] induced rapid up-regulation of CD14, indicating conversion to mature status. Localization studies indicated that IL-10 was predominantly present, bound on the surface of CD64(+)/CD14(low/neg) immature monocytes. Inflammatory stimuli (LPS, polyinosinic:polycytidylic acid, or SAC) induced release of variable quantities of IL-10 from the cell surface. MNC, separated into surface IL-10-positive or -negative fractions, differed in their ability to stimulate alloreactivity in MLR, and IL-10(+) MNC induced significantly lower levels of proliferation than IL-10(-) MNC. Thus, the subset of immature monocytes carrying surface-bound IL-10 in gmPB has the potential to modulate alloreactivity and GvHD after allogeneic SCT through cell-to-cell contact and released IL-10.
Methodological issues related to studies of lead mobilization during menopause.
While there has been a substantial decline in lead exposure in the United States during the past two decades, mobilization of existing lead stored in bone potentially represents an important endogenous source of exposure for menopausal women. It has been hypothesized that lead may be mobilized from skeletal stores during conditions of high bone turnover, such as during menopause. However, such mobilization has not been documented in prospective studies. This discussion is focussed on some of the methodological difficulties to be anticipated in longitudinal studies of lead mobilization specific to menopause and the issues that need to be taken into account when evaluating the results of such studies. To evaluate whether lead mobilization occurs during menopause, a prospective repeated measures design is needed using X-ray fluorescence analysis of lead in bone and serial measurements of blood lead. Potential confounders and effect modifiers also need to be taken into account in the statistical analysis.
Sister cities and easy passage: HIV, mobility and economies of desire in a Thai/Lao border zone.
It is recognised that people movement can increase potential risk of HIV transmission. In recent years, mobile populations moving across national borders have become a focus for HIV/AIDS prevention campaigns. These programs generally target border "hot zones" that produce high levels of HIV vulnerability due to the degree of mobility and the risk behaviours fostered by these marginal environments. However, high degrees of movement and social exploitation need not be the only criteria for borders to exacerbate HIV vulnerability. The types of social interactions promoted by mobility take many forms. In this paper we consider a border zone between Thailand and Laos to show that the links between movement and HIV vulnerability are not confined to stereotypical instances of coercion and exploitation. Rather we demonstrate that HIV risk in this area is a product of both a sense of community and a sense of difference that together foster a range of interactions based on mobility back and forth across the border. As HIV/AIDS prevention programs increasingly control forms of sexual interaction, the border provides a practical and symbolic opportunity to establish new forms of sexual relationship falling outside these constraints. This tendency to move outside bounds is not limited to border areas but has implications for prevention programs everywhere.