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P Ludwig

Publications and source records attributed to P Ludwig.

At least 19 recordsLinked to original sources
PubMed2006

Structural properties of screened Coulomb balls.

Small three-dimensional strongly coupled charged particles in a spherical confinement potential arrange themselves in a nested shell structure. By means of experiments, computer simulations, and theoretical analysis, the sensitivity of their structural properties to the type of interparticle forces is explored. While the normalized shell radii are found to be independent of shielding, the shell occupation numbers are sensitive to screening and are quantitatively explained by an isotropic Yukawa model.

Journal Article↗
PubMed2005

Structure of spherical three-dimensional Coulomb crystals.

An analysis of the structural properties of three-dimensional Coulomb clusters confined in a spherical parabolic trap is presented. Based on extensive high-accuracy computer simulations the shell configurations and energies for particle numbers in the range 60 < or = N < or = 160 are reported. Further, the intrashell symmetry and the lowest metastable configurations are analyzed for small clusters and a different type of excited state that does not involve a change of shell configuration is identified.

Journal Article↗
PubMed2005

Anaplasma phagocytophilum infection in a dog: identifying the causative agent using PCR.

A diagnosis of Anaplasma phagocytophilum infection was confirmed in a two-year-old male golden retriever displaying few clinical and haematological abnormalities. This was achieved by demonstrating ehrlichial organisms in circulating neutrophils, by indirect immunofluorescence assay using A phagocytophilum as an antigen, and by detecting DNA specific for the 16S rRNA gene of granulocytic Anaplasma by PCR. After treatment with doxycycline for 10 days the dog showed improvement and the laboratory values returned to normal.

Anaplasma phagocytophilum↗
PubMed2001

Primary commissure pioneer neurons in the brain of the grasshopper Schistocerca gregaria: development, ultrastructure, and neuropeptide expression.

The bilaterally paired primary commissure pioneer neurons in the median domain of the grasshopper brain are large, descending interneurons that uniquely express the TERM-1 antigen, even in the adult. After pioneering the primary interhemispheric brain commissure, these neurons extend TERM-1-immunoreactive collaterals into most parts of the brain except the mushroom bodies. In this report, the authors show that the TERM-1 antigen is located in the cell body cytoplasm of these neurons and not on the membranes. Screening with antisera to insect neuropeptides reveals that an antiserum recognizing peptides of the leucokinin family labels the cell body cytoplasm of the primary commissure neurons. Leucokinin-related peptides are known to modulate motility of visceral muscle, play a role in diuresis, and are likely to be neuromodulators in the insect nervous system. The primary commissure neurons differ ultrastructurally from median neurosecretory cells in that their cell body cytoplasm is more extensive, contains high numbers of mitochondria and extensive endoplasmic reticulum, but does not contain neurosecretory granules. In the adult, the cell somata are enveloped by multiple glia membranes and associated trophospongia. According to these ultrastructural characteristics, the primary commissure pioneers are not classical neurosecretory cells.

Animals↗
PubMed2000

Lazarillo expression reveals a subset of neurons contributing to the primary axon scaffold of the embryonic brain of the grasshopper Schistocerca gregaria.

The authors studied the contribution of seven clusters of Lazarillo-expressing cells to the primary axon scaffold of the brain in the grasshopper Schistocerca gregaria from 26% to 43% of embryogenesis. Each cluster, which was numbered according to when Lazarillo expression first appeared, was uniquely identifiable on the basis of its stereotypic position in the brain and the number of Lazarillo-expressing cells it contained. At no time during embryogenesis was Lazarillo expression found in brain neuroblasts: It was found only in progeny. For ease of analysis, axogenesis was followed in a cell cluster that contained only a single Lazarillo-expressing cell (the lateral cell) in the dorsal median domain of the brain midline. Bromodeoxyuridine incorporation revealed the presence of only a single midline precursor cell in this region during embryogenesis. Intracellular injection of Lucifer yellow into the lateral cell at various ages showed that there was no dye coupling to the midline precursor or to the nearby term-1-expressing primary commissure pioneers. The lateral cell is not related lineally to these cells and most likely differentiates directly from the neuroectoderm of the brain midline. Lazarillo expression appears at the onset of axogenesis as the lateral cell projects an axon laterally toward the next Lazarillo-expressing cell cluster. The cells of this target cluster direct axons into separate brain regions, thereby establishing an orthogonally organized scaffold that the lateral cell axon follows as it navigates away from the brain midline. The primary axon scaffold of the brain results from a stepwise interlinking of discrete brain regions, as exemplified by axons from neighboring Lazarillo-expressing cell clusters.

Animals↗
PubMed2000

Photoionization of highly charged ions using an ECR ion source and undulator radiation

Photoionization of Xe4+ to Xe7+ ions was studied by combining an electron cyclotron resonance ion source with synchrotron radiation. Multiconfiguration Dirac-Fock calculations were performed to interpret the data. Many autoionization lines were measured and identified, resulting from excitation of a 4d electron into nf and np orbitals followed by Auger decay of the excited states. Continuum photoionization is negligible for the higher members of the isonuclear series.

Journal Article↗
PubMed1999

Neurogenesis in the median domain of the embryonic brain of the grasshopper Schistocerca gregaria.

Embryonic development in the median domain of the brain of the grasshopper Schistocerca gregaria was investigated with immunohistochemical, histological, and intracellular dye injection techniques. The early head midline is divisible into a dorsal median domain and a ventral median domain based on the orientation of cell somata in each region. At 25% of embryogenesis, a single large midline precursor differentiates in the dorsal median domain and produces a lineage of six neuronal progeny before degenerating. No further precursors arise. In addition, the primary commissure pioneers and a pair of lateral neurons differentiate directly from the ectoderm in this region. Lucifer yellow dye injected into the midline precursor stains only this cell and its progeny. Similarly, there is no dye coupling from the primary commissure pioneers to the midline lineage or to neuroblasts of the brain hemispheres. Neurogenesis in the dorsal median domain therefore proceeds separately within each subset of cells, and is not related to development in the brain hemispheres. Beginning at 42% of embryogenesis, the primary commissure pioneers undergo a morphological transformation and concomittantly express the Term-1 antigen. Expression continues throughout embryogenesis and into the adult, where the midline primary commissure pioneer cells are the only ones labeled by Term-1 in the entire brain. The cellular organization of the dorsal median domain therefore remains remarkably conserved throughout embryogenesis, even as the brain undergoes extensive morphological transformation.

Animals↗
PubMed1999

15(S)-hydroxyeicosatetraenoic acid (15-HETE), a product of arachidonic acid peroxidation, is an active component of hemozoin toxicity to monocytes.

Several studies have shown that human and murine hemozoin-fed phagocytes are functionally impaired. Unpurified hemozoin contains unspecifically attached unsaturated fatty acids such as arachidonic and linolenic acids. The presence in unpurified hemozoin of large quantities of ferric heme with small amounts of free iron makes hemozoin a generator of oxidative radicals capable of forming lipoperoxides or other breakdown products from polyunsaturated fatty acids. Here we show that delipidized hemozoin had reduced toxicity to monocytes. Phorbol myristate acetate (PMA)-elicited burst was poorly affected by delipidized hemozoin (ca. 17% and 21% burst inhibition by delipidized hemozoin vs ca. 75% and 65% burst inhibition by native hemozoin at 20 min or 17 h post-phagocytosis, respectively). Analysis of the lipid fraction isolated from native hemozoin by HPLC and chiral-phase HPLC showed equimolar amounts of 15(R)- and 15(S)-HETE (HETE, 15-hydroxy-6,8,11,13-eicosatetraenoic acid), most likely by-products of non-enzymatic peroxidation of arachidonic acid. The biologically active isomer, 15(S)-HETE, the product of 15-lipoxygenase, is a powerful mediator of inflammation and the effector of a large number of bioactions. 15(R,S)-HETE was found in native hemozoin (0.24 millimole/mole hemozoin heme), in supernatants of hemozoin-fed monocytes (87 nMol) and in hemozoin-fed monocytes (9.6 microMol). Approximately 84% of 15-HETE attached to hemozoin was in the esterified form. A large preponderance of esterified over free 15-HETE was also noted in supernatants of hemozoin-fed monocytes and in hemozoin-fed monocytes. In the latter cells, remarkable levels of the substance were attained. A dose-dependent curve of inhibition of PMA-elicited oxidative burst was observed. Assuming homogenuous distribution of 15-HETE in hemozoin-fed monocytes, 15(S)-HETE concentrations measured in hemozoin-fed monocytes (8 muMol) would bring about ca. 85% inhibition of PMA-elicited burst. In conclusion, derivatives of lipoperoxidation of unsaturated fatty acids such as 4-hydroxynonenal, 15-HETE and others now under study, appear to be relevant causes of hemozoin toxicity.

Animals↗
PubMed1996

Regulation of 15-lipoxygenase expression in lung epithelial cells by interleukin-4.

We have studied the expression of the 15-lipoxygenase gene in various permanent mammalian cell lines in response to interleukins-4 and -13, and found that none of the cell lines tested expressed 5-, 12- or 15-lipoxygenase when cultured under standard conditions. However, when the lung carcinoma cell line A549 was maintained in the presence of either interleukin for 24 h or more, we observed a major induction of 15-lipoxygenase, as indicated by quantification of 15-lipoxygenase mRNA, by immunohistochemistry, by immunoblot analysis and by enzyme activity assays. This effect was 15-lipoxygenases-specific, since expression of 5- and 12-lipoxygenases remained undetectable. The time course of interleukin-4 treatment indicated maximal accumulation of both 15-lipoxygenase mRNA and functional protein after 48 h. Binding studies revealed that A549 cells express about 2100 high-affinity interleukin-4 binding sites per cell. The interleukin-4 mutant Y124D, which is capable of binding to the interleukin-4 receptor but is unable to trigger receptor activation, counteracted the effect of the wild-type cytokine. Other cell lines, including several epithelial cells and various monocytic cell lines expressing comparable numbers of interleukin-4 receptors, did not express 15-lipoxygenase when stimulated with interleukin-4. These data indicate that A549 cells selectively express 15-lipoxygenase when stimulated with interleukins-4 and -13. The activation of the interleukin-4/13 receptor(s) appears to be mandatory, but not sufficient, for 15-lipoxygenase gene expression.

Antigens, CD↗
PubMed1996

The suppression of 5-lipoxygenation of arachidonic acid in human polymorphonuclear leucocytes by the 15-lipoxygenase product (15S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid: structure-activity relationship and mechanism of action.

(15S)-Hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) suppresses in ionophore-A23187-stimulated human polymorphonuclear leucocytes (PMN) the conversion of exogenous arachidonic acid into leukotriene B(4) (LTB4) and (5S)-hydroxy-(6E,8Z,11Z,14Z)-eicosatetraenoic acid (5-HETE). However, contrary to earlier suggestions, 15-HETE is not a genuine 5-lipoxygenase inhibitor under these conditions, but rather suppresses the 5-lipoxygenation of arachidonic acid by switching-over of substrate utilization, as judged from a sizeable formation of labelled (5S,15S)-dihydroxy-(6E,8Z,11Z,13E)-eicosatetr aen oic acid (5,15-diHETE) from 15-[1(-14)C]HETE. Identical results were obtained with human recombinant 5-lipoxygenase. In PMN the formation of 5,15-diHETE is strongly stimulated by either hydroperoxypolyenoic fatty acids or arachidonic acid, suggesting a crucial role of the hydroperoxide tone of the cell. A comparison of a selection of hydroxypolyenoic fatty acids with respect to their capability of suppressing 5-lipoxygenation of arachidonic acid revealed that 15-mono-hydroxyeicosanoids throughout exhibit the highest inhibitory potencies, whereas the other HETEs, 5,15-diHETE as well as octadecanoids, are modest or poor inhibitors. The R and S enantiomers of 15-HETE do not differ from each other, excluding a receptor-like binding of the 15-hydroxy group.

Arachidonate 15-Lipoxygenase↗
PubMed1995

In vivo models of cerebral ischemia: effects of parenterally administered NMDA receptor glycine site antagonists.

Both in vitro and in vivo experiments have implicated extracellular glycine in the pathogenesis of ischemic brain damage. Recently, halogenated derivatives of quinoxaline-2,3-dione have been synthesized that possess bioavailability when parenterally administered and minimal psychotomimetic properties. Such compounds have allowed investigation into the efficacy of glycine receptor antagonism as a strategy for protection against cerebral ischemic insults. Rats underwent either 90 min of middle cerebral artery filament occlusion or 10 min of forebrain ischemia with recovery while receiving intraperitoneal injections of either a glycine receptor antagonist (ACEA-1021, ACEA-1031, or ACEA-1011) or vehicle (dimethyl sulfoxide). Both ACEA-1021 and ACEA-1031 reduced cerebral infarct volumes and were associated with a reduced incidence of hemiparesis resulting from MCA occlusion. ACEA-1011, administered in a smaller dose had no effect. In the forebrain ischemia model, glycine receptor antagonism had no effect on delayed neuronal necrosis in the hippocampal CA1 sector, neocortex, or caudoputamen. We conclude that pharmacologic antagonism of glycine at the strychnine-insensitive glycine receptor presents a neuroprotective profile similar to that previously observed for antagonists of glutamate at the N-methyl-D-aspartate complex with a potential for fewer side effects.

Animals↗
PubMed1995

Temporal thresholds for hyperglycemia-augmented ischemic brain damage in rats.

BACKGROUND AND PURPOSE: Although acute hyperglycemia is known to increase global ischemic brain damage, the duration of ischemia necessary to elicit such an effect is unknown. Accordingly, an experiment was performed to determine the duration of forebrain ischemia at which hyperglycemia becomes a factor in histological and behavioral outcome in rats. METHODS: Fasted rats were anesthetized and prepared for forebrain ischemia. Before ischemia, rats received either intravenous saline (plasma glucose, 112 +/- 18 mg/dL) or glucose (plasma glucose, 343 +/- 50 mg/dL). After 4, 8, 12, or 15 minutes of ischemia (n = 12), recovery was allowed. Rats surviving 7 days underwent evaluation of motor function and then histological analysis of damage in the caudate putamen, hippocampal CA1, and substantia nigra pars reticulata. RESULTS: After 4 minutes of ischemia, damage was present in all structures. Only in the caudate putamen was hyperglycemia associated with worsened damage, but this did not result in seizures or death. After 8 minutes of ischemia, seizures occurred in 33% of hyperglycemic rats, and a hyperglycemic effect on damage in the CA1 and substantia nigra pars reticulata was observed. No seizures or mortality occurred in normoglycemic rats regardless of duration of ischemia. Longer durations of ischemia resulted in an increased incidence of seizures and mortality in hyperglycemic rats only. Among surviving rats, motor function was worsened in hyperglycemic rats after 12 minutes of ischemia. CONCLUSIONS: Hyperglycemia-augmented brain damage is evident after global ischemic insults as brief as 4 minutes and becomes critical to survival after 8 minutes of ischemia.

Animals↗
PubMed1995

Inhibition of eicosanoid formation in human polymorphonuclear leukocytes by high concentrations of magnesium ions.

The cutaneous antiinflammatory action of Dead-Sea brine is thought to be due to magnesium ions. To elucidate their mode of action, we studied the influence of isotonic solutions containing high concentrations of Mg2+ (up to 115mM) on the formation of 5-lipoxygenase-derived eicosanoids in human polymorphonuclear leukocytes. The cells were stimulated by either ionophore A23187 or the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine. We observed a pronounced inhibition of the formation of leukotriene B4 and 5-hydroxyeicosatetraenoic acid from either added [1-14C] or endogenously liberated arachidonic acid. In the latter case, the sum of arachidonic acid and its oxygenation products was also markedly diminished. The inhibitory effects of Mg2+ depended in a reciprocal manner on the concentration of Ca2+ in the incubation medium. An unspecific damage to cells as reason for the inhibitory effects was excluded. Human recombinant 5-lipoxygenase was also inhibited by Mg2+ in the same concentration range (IC50 16 mM). These data suggest that high concentrations of Mg2+ inhibit the eicosanoid metabolism both at the level of the liberation of arachidonic acid and by direct inhibition of the 5-lipoxygenase enzyme.

Arachidonate 5-Lipoxygenase↗
PubMed1993

Enantioselective and nonenantioselective degradation of organic pollutants in the marine ecosystem.

Enantiomeric ratios of 11 chiral environmental pollutants determined in different compartments of the marine ecosystem by chiral capillary gas chromatography and chiral high-performance liquid chromatography allow discrimination between the following processes: enantioselective decomposition of both enantiomers with different velocities by marine microorganisms (alpha-HCH, beta-PCCH, gamma-PCCH); enantioselective decomposition of one enantiomer only by marine microorganisms (DCPP); enantioselective decomposition by enzymatic processes in marine biota (alpha-HCH, beta-PCCH, trans-chlordane, cis-chlordane, octachlordane MC4, octachlordane MC5, octachlordane MC7, oxychlordane, heptachlor epoxide); enantioselective active transport through the "blood-brain barrier" (alpha-HCH); nonenantioselective photochemical degradation (alpha-HCH, beta-PCCH).

Adipose Tissue↗
PubMed1993

Sevoflurane and halothane reduce focal ischemic brain damage in the rat. Possible influence on thermoregulation.

BACKGROUND: There has been little systematic examination concerning the comparative effects of the anesthetized versus the awake state on outcome from cerebral ischemia. This experiment evaluated infarct volume and neurologic function in rats subjected to temporary focal ischemia while anesthetized with either sevoflurane or halothane. Outcome in these animals was compared to that observed in rats maintained unanesthetized during a similar ischemic insult. METHODS: All rats were anesthetized with halothane and surgically prepared for filament occlusion of the middle cerebral artery. After preparation, one group (Halothane) remained anesthetized with approximately 1.4 MAC halothane. In another group (Sevoflurane), halothane was discontinued and substituted with sevoflurane, which was administered until electroencephalographic burst suppression was evident (approximately 1.4 MAC). The final group (Awake) was allowed to awaken immediately after the onset of ischemia. Middle cerebral artery occlusion persisted for 90 min in all groups. The middle cerebral artery filament then was removed, and a 96-h survival interval was allowed. Neurologic function and infarct volume were determined. Recent evidence indicates that transient mild hyperthermia occurs in awake rats undergoing filament occlusion of the middle cerebral artery. To examine the potential role of mild hyperthermia in this experiment, a second experiment was performed in which rats anesthetized with halothane underwent 90-min focal ischemia, with pericranial temperatures held at either 38.0 degrees C or 39.2 degrees C. RESULTS: Intraischemic mean arterial pressure was 20-25 mmHg lower in the two anesthetized groups compared with awake animals. Despite this finding, cortical infarct volumes (mean +/- SD; Halothane, 17 +/- 32 mm3; Sevoflurane, 36 +/- 57 mm3; Awake, 115 +/- 104 mm3; Sevoflurane, 36 +/- 57 mm3; Awake, 115 +/- 104 mm3) and subcortical infarct volumes (mean +/- SD; Halothane, 39 +/- 57 mm3; Sevoflurane, 50 +/- 29 mm3; Awake, 88 +/- 46 mm3) were reduced in both groups of anesthetized rats. This reduction correlated with improved neurologic function. The rats in whom the pericranial temperature was maintained at 39.2 degrees C had a larger total infarct volume (218 +/- 81 mm3) and increased neurologic deficits when compared to those in whom the pericranial temperature was maintained at 38.0 degrees C (total infarct volume, 75 +/- 77 mm3). CONCLUSIONS: Both halothane and sevoflurane substantially reduced damage in this focal ischemia model when compared to outcome resulting from the same insult induced in awake rats. The reduction in intraischemic mean arterial pressure caused by the anesthetics did not seem contributory to outcome. Brain temperature differences among the groups were not defined. Because small differences in pericranial temperature were shown to have major effects on outcome, further work is required to determine if differences in brain temperature explain the observed protective effects of these anesthetics.

Anesthesia, Inhalation↗
PubMed1992

Loss of cytosolic 15-lipoxygenase activity in A23187-stimulated human leukocytes: involvement of a translocation process?

We focused our study on the subcellular redistribution of 15-lipoxygenase in human leukocytes challenged with A23187 and arachidonic acid (AA). We found that in cytosolic fractions of stimulated cells the 15-lipoxygenase (15-LO) activity, measured as 15-HETE, was 65% less than in controls. However, no activity was found in cell membranes. This effect was complete within 2 min of incubation and was correlated in a dose dependent manner to exogenously added AA. No significant difference in cytosolic distribution of 15-LO activity was observed when cells were stimulated in presence of various concentrations of Ca++. Immunoblot analysis showed that the loss of cytosolic 15-LO activity registered after challenging with A23187 was associated with a concomitant loss of the enzyme content in the cytosol, suggesting the possibility of a translocation process. Neither the 15-LO activity nor the enzyme was, however, found in the cell membrane under our present experimental conditions. But, addition of protease inhibitors showed a slight increase of 15-LO activity in the membrane fraction. Despite the small effect, this may indicate a translocation of 15-LO following challenge of human leukocytes with A23187.

Adult↗
PubMed1992

The HIV-1 surface protein gp120 has no effect on transmembrane signal transduction in T cells.

The ability of HIV-1 envelope glycoprotein gp120 to induce transmembrane signaling processes in human T cells and tumor T-cell lines was investigated. Differently glycosylated gp120 preparations were characterized with respect to their purity, the fraction of native gp120, and the affinity of the gp120-CD4 interaction. These data were used to establish experimental conditions that allow a substantial fraction of the CD4 receptor to be complexed with gp120 in the course of the experiments. The results are in contrast to several previous studies since no effect of gp120 on the intracellular Ca2+ concentration, the metabolism of inositol phosphates and arachidonic acid, protein kinase C translocation, and tyrosine phosphorylation was found. Cross-linking of the gp120:CD4 complex by anti-gp120 antibodies did not elicit additional effects.

Arachidonic Acids↗