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J Stabel

Publications and source records attributed to J Stabel.

At least 19 recordsLinked to original sources
PubMed2006

Heat treatment of bovine colostrum. I: effects of temperature on viscosity and immunoglobulin G level.

The objective of this study was to identify the critical temperature, at or below which heat-treatment of bovine colostrum would produce no significant changes in viscosity, IgG concentration, or Ig activity. Results of preliminary work, using a Rapid Visco Analyzer (RVA) to heat 50-mL aliquots from 6 unique batches of bovine colostrum at 59, 60, 61, 62, and 63 degrees C, suggested that colostrum could be heated to 60 degrees C for up to 120 min without changing viscosity or IgG concentration. This finding was confirmed by heating 50-mL aliquots from 30 unique batches of colostrum in an RVA for 120 min at 60 and 63 degrees C. Heating colostrum to 63 degrees C resulted in an estimated 34% decrease in IgG concentration and 33% increase in viscosity. However, there was no difference in IgG concentration between preheat-treated (73.4 +/- 26.5 mg/mL) and post-heat-treated (74.5 +/- 24.3 mg/mL) samples after heating colostrum to 60 degrees C in an RVA for 120 min. Similarly, viscosity was unaffected after heating colostrum to 60 degrees C in an RVA for 120 min. High quality colostrum (> or =73.0 mg/mL) suffered greater losses of IgG and greater viscosity changes when heated to 63 degrees C than did moderate quality colostrum (<73.0 mg/mL). However, the effects of colostrum quality were minor if high quality colostrum was only heated to 60 degrees C. The results of a bovine viral diarrhea serum neutralization assay suggested that antibody activity was unchanged after heating colostrum to either 60 or 63 degrees C. However, these results were interpreted as being inconclusive due to a high proportion of missing results because of the congealing of many samples after heat treatment. The results of this study indicate that 50-mL volumes of bovine colostrum can be heat treated at 60 degrees C for up to 120 min in an RVA without affecting IgG concentration or viscosity.

Animals↗
PubMed2006

Heat-treatment of bovine colostrum. II: effects of heating duration on pathogen viability and immunoglobulin G.

Batches (30-L) of first-milking bovine colostrum, inoculated with Mycoplasma bovis (10(8) cfu/mL), Listeria monocytogenes (10(6) cfu/mL), Escherichia coli O157:H7 (10(6) cfu/mL), Salmonella enteritidis (10(6) cfu/mL), and Mycobacterium avium subsp. paratuberculosis (Map; 10(3) cfu/mL), were heat-treated at 60 degrees C for 120 min in a commercial on-farm batch pasteurizer system. Duplicate 50-mL subsamples of colostrum were collected at 15-min intervals throughout the heat-treatment process for the purpose of bacterial culture and for measurement of IgG concentration (mg/mL) and antibody activity [log2(bovine viral diarrhea virus type 1 serum neutralization titer)]. Four replicate batches of colostrum were run for each of the 5 pathogens studied. There was no effect of heating moderate- to high-quality colostrum at 60 degrees C for at least 120 min on mean IgG concentration (pre = 60.5 mg/mL; post = 59.1 mg/mL). Similarly, there was no effect of heat-treatment on the mean log2 bovine viral diarrhea virus type 1 serum neutralization titer (pre = 12.3; post = 12.0). Viable M. bovis, L. monocytogenes, E. coli O157:H7, and S. enteritidis added to colostrum could not be detected after the colostrum was heat-treated at 60 degrees C for 30 min. Average bacteria counts showed that Map was not detected when batches were heated at 60 degrees C for 60 min. Although the authors believe that heat-treating colostrum at 60 degrees C for 60 min should be sufficient to eliminate Map from colostrum in most situations, further research is needed to determine whether these findings may be replicated, given that variability was observed in Map culture results.

Animals↗
PubMed2000

Expression and characterization of a recombinant soluble form of bovine tumor necrosis factor receptor type I.

A recombinant soluble bovine tumor necrosis factor receptor type I (sboTNF-RI) was expressed in the methylotrophic yeast Pichia pastoris and evaluated for its ability to inhibit bovine tumor necrosis factor alpha (TNF-alpha) cytotoxicity. A cDNA encoding the extracellular domain of bovine TNF-RI was placed under the control of the powerful and tightly regulated alcohol oxidase1 (AOX1) gene promoter of the pPICZa A vector and the resulting construct integrated into the 5' region of the alcohol oxidase genes of GS115 and KM71 strains of Pichia. Soluble bovine TNF-RI was secreted into the medium following induction of the AOX1 gene promoter with methanol, and purified to greater than 95% purity by ion-exchange chromatography. In in vitro assays, the purified recombinant sboTNF-RI will block the cytolytic activity of bovine TNF-alpha on WEHI 164 cells clone 13 by 50% when used at a concentration of 170 microg/ml, and by nearly 90% when used at a concentration of 310 microg/ml. Results of this study suggest that recombinant sboTNF-RI may have therapeutic value as a TNF inhibitor in cattle with coliform mastitis.

Animals↗
PubMed1994

alpha-Aminoadipic acid blocks the Na(+)-dependent glutamate transport into acutely isolated Müller glial cells from guinea pig retina.

The effect of the glial toxin alpha-aminoadipic acid (AAA) upon the Na+/glutamate cotransporter of acutely isolated guinea pig retinal glial cells was studied using the whole-cell voltage-clamp technique. Glutamate evoked an inward current in these cells at negative holding potentials dependent on the presence of extracellular Na+ and intracellular K+. A reversal potential could not be found for the current. L-trans-Pyrrolidine-2.4-dicarboxylic acid (PDC), a blocker of Na(+)-dependent glutamate uptake, diminished the glutamate current also in our cells. Application of L-AAA also generated an inward current at negative holding potentials, without a reversal potential, being suppressed if extracellular Na+ or intracellular K+ was removed. The glutamate uptake blocker, PDC (200 microM), blocked the L-AAA (1 mM) current. Thus, L-AAA proved to be transported by the Na+/glutamate transporter of Müller cells. Hence, glutamate currents were diminished by L-AAA competitively with a Km of 499 microM at a glutamate concentration of 10 microM. The Na+/glutamate uptake was less sensitive to DL- and D-AAA block. It is suggested that the blocking effect of AAA on Na(+)-dependent glutamate uptake into glial cells might be involved in the well known glia toxicity of this compound.

2-Aminoadipic Acid↗
PubMed1994

Strategies for the development of drugs for pharmacoresistant epilepsies.

Presently, most strategies for development of antiepileptic drugs (AEDs) center around seizure models that are known to respond to presently marketed AEDs. These strategies do not take into account that epilepsy can be a progressive disease. Moreover, region-specific aspects of epileptogenesis are rarely considered when new AEDs are developed. Seizures in the temporal lobe are often difficult to treat. Animal studies on various seizure models in the hippocampus and the entorhinal cortex (EC) suggest that these structures do not a priori produce seizures that are difficult to treat. However, seizure-like events in the EC tend to progress to a state of status epilepticus-like activity that cannot be suppressed by presently marketed AEDs. Loss of gamma-aminobutyric acid (GABA)ergic neurotransmission and increased excitatory synaptic coupling seem to cooperate for induction of this state. Epilepsy induced alterations in the interaction between the EC and the hippocampus may lead to alterations that facilitate precipitation of seizures. Because of the recurrent interaction between the hippocampus and the EC, these seizures may reach an intensity that is no longer controllable by presently available AEDs. Ontogenetic alterations of the circuitry between the EC and the hippocampus, seizure-induced stabilization of synaptic connections overexpressed during ontogenesis, seizure-induced lesions and subsequent rearrangements of internal cell properties, and synaptic arrangements and kindling-like alterations of nerve cell and glial behavior may all be involved in the generation of a neuronal aggregate whose balance between inhibitory and excitatory processes becomes readily disturbed. Strategies for the development of AEDs treating such seizures should suppress hyperactivity and prevent progression of epileptogenesis. AEDs directed against seizures may be effective if they can be given in sufficient concentrations to suppress very intense local seizures.

Animals↗
PubMed1993

Pharmacological and electrographic properties of epileptiform activity induced by elevated K+ and lowered Ca2+ and Mg2+ concentration in rat hippocampal slices.

We studied some of the physiological and pharmacological properties of an in vitro model of epileptic seizures induced by elevation of [K+]0 (to 8 mM and 10 mM) in combination with lowering of [Mg2+]0 (to 1.4 mM and 1.6 mM) and [Ca2+]0 (to 0.7 mM and 1 mM) in rat hippocampal slices. These concentrations correspond to the ionic constitution of the extracellular microenvironment during seizures in vivo. The resulting activity was rather variable in appearance. In area CA3 recurrent discharges were observed which resulted in seizure-like events with either clonic-like or tonic-clonic-like ictaform events in area CA1. With ion-sensitive electrodes, we measured the field potential and the changes in extracellular ion concentrations which accompany this activity. The recurrent discharges in area CA3 were accompanied by small fluctuations in [K+]0 and [Ca2+]0. The grouped clonic-like discharges in area CA1 were associated with moderate increases in [K+]0 and small decreases in [Ca2+]0 in the order of 2 mM and 0.2 mM, respectively. Large, negative field-potential shifts and increases in [K+]0 to 13 mM, as well as decreases in [Ca2+]0 by up to 0.4 mM, accompanied the tonic phase of ictaform events. The ictaform events were not blocked by D-2-aminophosphonovalerate (2-APV) but were sensitive to 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) alone and in combination with 2-APV and ketamine. In order to determine the pharmacological characteristics of the ictaform events we bath-applied most clinically employed anticonvulsants (carbamazepine, phenytoin, valproate, phenobarbital, ethosuximide, trimethadione) and some experimental anticonvulsants (losigamone, vinpocetine, and apovincaminic acid). Carbamazepine, phenytoin, valproate, and phenobarbital were effective at clinically relevant doses. The data suggest that the high-K+ model of epileptiform activity is a good model of focal convulsant activity.

2-Amino-5-phosphonovalerate↗
PubMed1993

Properties of horizontal cells transiently appearing in the rat dentate gyrus during ontogenesis.

In an ontogenetic study, combining morphological analysis and patch clamp recordings, a transiently appearing horizontal cell type was identified in the dentate gyrus. The cells were exclusively located in the outer third of the stratum moleculare. They were present at postnatal day 2 (P2) and could be identified with fluorescent dyes until around P14. The morphology was bipolar, with a putative axonal and a dendritic process stretching out parallel to the pial surface without any preferential direction. Patch clamp studies in the current and voltage clamp mode were performed in hippocampal slices on visually identified horizontal cells, between P4 and P7, which were subsequently stained with lucifer yellow. The cells had a low resting membrane potential, around -55 mV. They were excitable, displaying broad action potentials (duration 3-20 ms) and, unlike mature dentate granule cells, they also expressed a strong delayed inward rectifier with properties reminiscent of the IQ current. Unlike granule cells, no postsynaptic signals could be observed during elevation of [K+]o or electrical stimulation, suggesting that the horizontal cells did not participate in functional hippocampal circuitry. We suggest that these cells represent migrating cells with subsequent differentiation to granule cells or inhibitory interneurons. Alternatively they may be part of the early radial glia or serve as transient target cells for afferent fibres between the entorhinal cortex and the dentate gyrus.

Animals↗
PubMed1992

Alterations in medial perforant path and mossy fiber induced field potentials in amygdala and beta-carboline (FG 7142) kindled rats.

We tested in rat hippocampal slices whether kindling causes sprouting of mossy fibers thereby augmenting excitatory coupling and epileptogenicity. Field potentials (fp's) evoked by orthodromic stimulation of the medial perforant path (MPP) and antidromic stimulation of mossy fibers in slices from control, amygdala kindled (AK) and beta-carboline (FG 7142) kindled rats were recorded in the dentate gyrus granule cell layer. Orthodromic paired pulse inhibition was increased in both groups of kindled animals. In contrast, neither in normal medium nor under additional application of the GABAA receptor antagonist bicuculline nor in Mg(2+)-free artificial cerebrospinal fluid (ACSF) there was evidence for an excitatory field EPSP component upon stimulation of mossy fibers in any of the investigated groups. The results indicate that functional mossy fiber sprouting does not occur as an obligatory step in the induction of kindling epilepsy.

Amygdala↗
PubMed1992

Young CA1 pyramidal cells of rats, but not dentate gyrus granule cells, express a delayed inward rectifying current with properties of IQ.

In hippocampal CA1 pyramidal cells (CA1PC) and dentate gyrus granule cells (DGGC) we compared the expression of currents which could cause differences in discharge behaviour. Negative current injections cause a uniform hyperpolarization in DGGC whereas in CA1PC the initial hyperpolarization is followed by a repolarization towards resting membrane potential. The underlying inward current can be classified as IQ. It is sensitive to CsCl, activated at -80 mV, and it has a mean amplitude of -109.8 pA and a mean activation time constant of 187 ms with voltage jumps from -40 to -120 mV. We conclude that some of the differences in response properties of DGGC and CA1PC upon repetitive stimulation can be attributed to differences in the expression of IQ.

Animals↗
PubMed1992

Pharmacological properties of excitatory amino acid induced changes in extracellular calcium concentration in rat hippocampal slices.

We have studied extracellular ionic changes induced by iontophoretic application of excitatory amino acids in rat hippocampal slices. In contrast to kinetics of changes in [Ca2+]o, kinetics of changes in [K+]o, [Na+]o, [Cl-]o as well as in extracellular space size were comparable for different glutamate receptor agonists. Thus, alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA), quisqualate (quis), and kainate caused reductions in [Ca2+]o followed by an increase of [Ca2+]o above baseline, whereas glutamate, aspartate, N-methyl-D-aspartate (NMDA), and DL-homocysteic acid caused only reductions in [Ca2+]o. After blocking the NMDA receptors with ketamine and 2-amino-5- phosphonovaleric acid (2-APV), glutamate-induced decreases in [Ca2+]o were followed by an overshoot. Reduction of the transmembrane Na+ gradient by lowering [Na+]o, blocking of the Na(+)-K+ ATPase by lowering [K+]o, and application of ouabain blocked the overshoots after quis application, whereas vanadate, a blocker of the Ca(2+)-Mg2+ ATPase, had no effects. Lithium enhanced the reductions in [Ca2+]o and blocked the overshoots. Amiloride also reduced the overshoots. All organic Ca2+ entry blockers diminished reductions of [Ca2+]o but increased the overshoots. Inorganic Ca2+ antagonists had variable effects. Ni2+ had similar effects as the organic Ca2+ entry blockers while Cd2+ reduced both the [Ca2+]o decreases as well as the subsequent overshoots. Co2+ had initially a similar action as Ni2+. With prolonged application, [Ca2+]o decreases became augmented and, during wash, overshoots could no longer be elicited. We suggest that the overshoots in [Ca2+]o are due to a combined effect of extracellular space shrinkage and activation of the Na+/Ca2+ exchangers. This would imply that NMDA receptor activation blocks extrusion of Ca2+ from the cells. We tested the hypothesis that quis-induced intracellular Ca2+ release and extrusion of Ca2+ from the cells contributed to the overshoots. Dantrolene was without effect on the quis-induced signals, while ryanodine reduced the overshoots. Caffeine on the other hand diminished the [Ca2+]o decreases with no effects on the overshoots. To test for possible second messenger routes by which NMDA receptor activation might slow Ca2+ extrusion from cells, we investigated the effects of arachidonic acid and N-monomethyl-D- arginine on the quis-induced signals. While these agents reduced decreases in [Ca2+]o, they had no clear effects on the overshoots. Thus a possible route by which NMDA receptor activation may affect Ca2+ extrusion from cells has still to be elucidated.

Amino Acids↗
PubMed1992

The dentate gyrus as a regulated gate for the propagation of epileptiform activity.

Properties of the interaction between the entorhinal cortex (EC) and the dentate gyrus were studied in a combined EC hippocampal slice preparation in which most of the fiber connectivity within this structure is intact. Epileptiform activity was induced by lowering extracellular Mg2+ concentration. This caused short recurrent discharges in the hippocampus while seizure-like events (SLE) slowly spread from the site of initiation to neighboring areas. At the end of a SLE, the EC, the subiculum and the neocortical area Te2 discharged in synchrony. This activity could develop into a state of recurrent tonic discharges highly synchronized between the different areas. These discharges were insensitive to treatment with currently available antiepileptic drugs. Although the SLE increased neuronal firing and extracellular potassium concentration in the dentate gyrus, this activity had only moderate effects on the activity generated in areas CA3 and CA1. Removing GABAergic inhibition with baclofen and bicuculline caused the spread of SLE from the EC to the dentate gyrus. Slow inhibitory postsynaptic potentials and intrinsic properties of dentate gyrus granule cells appear to underlie the filtering function of the dentate gyrus.

Afferent Pathways↗
PubMed1990

Prolonged electrophysiological maturation of transplanted hippocampal neurons.

The CA1 region of the rat hippocampal formation was lesioned by transient forebrain ischemia and subsequently repopulated with dispersed fetal hippocampal neurons. Using the hippocampal slice preparation, 7-12 months post-transplantation, intracellular recordings were made during synaptic activation and extracellular calcium measurements were made during iontophoretic application of excitatory amino acids. The data indicate that the developmental period of the transplanted neurons is prolonged with respect to N-methyl-D-aspartate (NMDA) receptor-mediated responses and may be involved in maintaining calcium dependent developmental processes such as fiber outgrowth.

Animals↗
PubMed1990

Laminar profiles of N-methyl-D-aspartate- and quisqualate-induced [Na+]o changes in rat hippocampus.

Since plastic changes in neuronal tissue are often associated with changes in responses to excitatory amino acids (EAA), a method is required which permits mapping of functional EAA receptor sites. In this study the measurement of extracellular sodium concentration changes [( Na+]o) induced by iontophoretic application of N-methyl-D-aspartate (NMDA) and quisqualate (Quis) is used as a tool to estimate the density of functional NMDA- and Quis-receptor sites in area CA1 and dentate gyrus of rat hippocampus. Largest decreases of [Na+]o induced by NMDA were found in basal and apical dendritic fields of area CA1 and in stratum moleculare of dentate gyrus at a distance of 50-100 microns from stratum granulare. Peak decreases in [Na+]o induced by Quis occurred at similar positions. Bath application of tetrodotoxin (TTX) suppressed that part of the extracellular Na+ loss mediated by Na+ fluxes through voltage activated Na+ channels. However, the laminar profiles of Quis- and NMDA-induced [Na+]o changes were not affected by TTX. Thus, EAA induced decreases in [Na+]o can be used to detect changes in receptor density and in receptor functionality of hippocampus which had undergone plastic changes.

Animals↗
PubMed1990

Effects of lowering [Na+]o and [K+]o and of ouabain on quisqualate-induced ionic changes in area CA1 of rat hippocampal slices.

Changes in extracellular ([Na+]o) and calcium ([Ca2+]o) concentration evoked by quisqualate (Quis), applied iontophoretically, were measured in rat hippocampal slices. Following an initial decrease in [Ca2+]o, Quis causes a post-application overshoot, which may reflect Ca2+ extrusion from cells by the Na+/Ca2+ exchanger. To test this hypothesis, the effects of directly and indirectly reduced transmembrane Na+ gradients on these Quis-induced Ca2+ overshoots were investigated. In all cases the post-application overshoots were reduced. This suggests that the Na+/Ca2+ exchanger is involved in the production of these Quis-induced Ca2+ overshoots which may have important implications for understanding how various types of glutamate receptors differ in their capability to trigger Ca2(+)-activated processes.

Animals↗