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Biomedical subjects

S Peters

Publications and source records attributed to S Peters.

At least 217 records · Page 12Linked to original sources
PubMed1988

Activated Fc alpha T cells in Crohn's disease are involved in regulation of IgA.

Activated peripheral T cells (APT) of patients with Crohn's disease (CD) have been analysed for the expression of IgA-Fc receptors and for competence of IgA regulation. It was found that within the subset of APT an increased number of cells express binding sites for IgA (IgA-Fc), that was not found in other diseases with elevated numbers of APT. Moreover the number of IgA-Fc receptor expressing T cells was found to be increased in the inflamed mucosa too. Cocultures with autologous B cells revealed that isolated IgA-Fc receptor bearing T cells of patients with CD suppress IgA secretion. These data support the hypothesis that APT are involved in the immunopathogenesis of CD.

Antibodies, Monoclonal↗
PubMed1988

First experiences with resin-bonded bridges and splints--a cross-sectional retrospective study, Part II.

This second report establishes that the success of treatment with resin-bonded bridges was dependent upon many factors. Factors controlled by the clinician, such as case selection and treatment planning greatly influence the clinical success. It was possible to show that framework preparation and the amount of available enamel were significant factors, whereas isolation technique, type of retention mechanism and type of adhesive used were of less importance. Longitudinal studies are needed to confirm these observations. Seventeen clinicians placed 496 resin-bonded bridges and splints with different retention mechanisms and bonding agents. These reconstructions were examined in regard to the failure rate and in regard to reattachment problems. Ninety-seven per cent of the bridges and 90% of the splints were still in place after 1 year. For bridges and splints a 90% success rate was ascertained after 2 years.

Adhesives↗
PubMed1988

Pharmacology of glutamate neurotoxicity in cortical cell culture: attenuation by NMDA antagonists.

The antagonist pharmacology of glutamate neurotoxicity was quantitatively examined in murine cortical cell cultures. Addition of 1-3 mM DL-2-amino-5-phosphonovalerate (APV), or its active isomer D-APV, acutely to the exposure solution selectively blocked the neuroexcitation and neuronal cell selectively blocked the neuroexcitation and neuronal cell loss produced by N-methyl-D-aspartate (NMDA), with relatively little effect on that produced by either kainate or quisqualate. As expected, this selective NMDA receptor blockade only partially reduced the neuroexcitation or acute neuronal swelling produced by the broad-spectrum agonist glutamate; surprisingly, however, this blockade was sufficient to reduce glutamate-induced neuronal cell loss markedly. Lower concentrations of APV or D-APV had much less protective effect, suggesting that the blockade of a large number of NMDA receptors was required to acutely antagonize glutamate neurotoxicity. This requirement may be caused by the amplification of small amounts of acute glutamate-induced injury by subsequent release of endogenous NMDA agonists from injured neurons, as the "late" addition of 10-1000 microM APV or D-APV (after termination of glutamate exposure) also reduced resultant neuronal damage. If APV or D-APV were present both during and after glutamate exposure, a summation dose-protection relationship was obtained, showing substantial protective efficacy at low micromolar antagonist concentrations. Screening of several other excitatory amino acid antagonists confirmed that the ability to antagonize glutamate neurotoxicity might correlate with ability to block NMDA-induced neuroexcitation: The reported NMDA antagonists ketamine and DL-2-amino-7-phosphono-heptanoate, as well as the broad-spectrum antagonist kynurenate, were all found to attenuate glutamate neurotoxicity substantially; whereas gamma-D-glutamylaminomethyl sulfonate and L-glutamate diethyl ester, compounds reported to block predominantly quisqualate or kainate receptors, did not affect glutamate neurotoxicity. The present study suggests that glutamate neurotoxicity may be predominantly mediated by the activation of the NMDA subclass of glutamate receptors--occurring both directly, during exposure to exogenous compound, and indirectly, due to the subsequent release of endogenous NMDA agonists. Given other studies linking NMDA receptors to channels with unusually high calcium permeability, this suggestion is consistent with previous data showing that glutamate neurotoxicity depends heavily on extracellular calcium.

2-Amino-5-phosphonovalerate↗
PubMed1987

Quinolinate is a weak excitant of cortical neurons in cell culture.

Defined concentrations of quinolinate (QUIN) were administered to murine cortical neurons in culture impaled for intracellular recording. In physiological recording medium containing 1 mM Mg, concentrations of QUIN up to 2 mM had minimal effect on membrane potential and input resistance; only at higher concentrations did QUIN produce consistent depolarizations, which were accompanied by apparent increases in membrane resistance. In the absence of Mg, responses to QUIN were larger and were accompanied by decreases in membrane resistance, but QUIN was still a weak neuroexcitant, exhibiting an ED50 of greater than 1 mM. Phthalic, dipicolinic and nicotinic acids, structural analogues of QUIN, were even less potent neuroexcitants. The relationship between QUIN depolarization amplitude and membrane potential was linear in the absence of Mg, but in the presence of 1 mM Mg showed a non-linearity consistent with the voltage-dependent Mg block of N-methyl-D-aspartate (NMDA) receptor-mediated responses described by others. QUIN responses had a marked dependence on the presence of extracellular Na, and an extrapolated reversal potential of +12 mV, consistent with the large involvement of an Na influx. The responses were attenuated by the selective NMDA receptor antagonists, DL-2-amino-5-phosphonovalerate and ketamine, as well as by the broad spectrum antagonist kynurenate, but not by L-glutamate diethylester or gamma-D-glutamylaminomethyl sulfonate, compounds reported to block quisqualate or kainate receptors. The present study is consistent with the suggestion of other workers that QUIN neuroexcitation is mediated in large part by an Na influx through cation permeable NMDA-activated channels, but provides new quantitative data suggesting that the potency of QUIN as a cortical neuroexcitant is low. This low potency may argue against a role for QUIN as a traditional fast excitatory neurotransmitter.

2-Amino-5-phosphonovalerate↗
PubMed1987

Zinc selectively blocks the action of N-methyl-D-aspartate on cortical neurons.

Large amounts of zinc are present in synaptic vesicles of mammalian central excitatory boutons and may be released during synaptic activity, but the functional significance of the metal for excitatory neurotransmission is currently unknown. Zinc (10 to 1000 micromolar) was found to have little intrinsic membrane effect on cortical neurons, but invariably produced a zinc concentration-dependent, rapid-onset, reversible, and selective attenuation of the membrane responses to N-methyl-D-aspartate, homocysteate, or quinolinate. In contrast, zinc generally potentiated the membrane responses to quisqualate or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and often did not affect the response to kainate. Zinc also attenuated N-methyl-D-aspartate receptor-mediated neurotoxicity but not quisqualate or kainate neurotoxicity. The ability of zinc to specifically modulate postsynaptic neuronal responses to excitatory amino acid transmitters, reducing N-methyl-to-aspartate receptor-mediated excitation while often increasing quisqualate receptor-mediated excitation, is proposed to underlie its normal function at central excitatory synapses and furthermore could be relevant to neuronal cell loss in certain disease states.

Animals↗
PubMed1987

Correlations between song acquisition, song production, and plasma levels of testosterone and estradiol in sparrows.

Male birdsong is a sexually dimorphic behavior characterized by learned dialects. In a combined study of learning in relation to steroid levels in the plasma, changes in estradiol and testosterone levels were correlated with the timing of the sensitive period for song acquisition and with successive stages in song development. Male swamp sparrows were trained with a changing series of live singing tutors from 26 days to 1 year of age. Song acquisition was concentrated between 26 and 47 days of age (57%). By 85 days of age 71% of acquisition was completed; some occurred as late as 300 days. There were two major periods when testosterone levels were elevated. The first, from 30-80 days, encompassed most of the period of song acquisition. The second, from 260 to at least 360 days of age, coincided with song development. Estradiol levels were elevated from 18 to 170 days of age, encompassing almost all of the period of song acquisition. A marked estradiol peak between 40 and 50 days coincided with a trough in testosterone levels and a hiatus in song acquisition. The strong correlation between the second period of elevated testosterone and song motor development suggests a causal connection, with levels peaking in mid-development and declining during mature song production. Estradiol levels were elevated at the start of the study and remained so during early subsong production, from 30 to 165 days. They then fell to baseline, remaining there throughout the resumption of subsong and plastic song production at 250-326 days. Both estradiol and testosterone are candidates for possibly affecting song acquisition.

Aging↗
PubMed1987

Experiences with resin-bonded bridges and splints--a retrospective study.

In a joint evaluation of 496 resin-bonded bridges and splints anchored by various retention principles and composites, the initial experiences of seventeen clinicians were compiled. The main indications for treatment were congenital anodontia and loss of teeth due to caries and trauma. After 3 months, 95% of the bridges were still in place without need of reattachment procedure. After 6 months the figure was 91%, after 1 year 81.5% and after 1 1/2 years 73%. Seventy-five per cent of the loosened bridges were attached successfully a second time. The success rate for splints was significantly lower.

Adolescent↗
PubMed1987

In vivo studies with fibre components.

There are few studies in man examining the in vivo effects of dietary fibre on bile acid metabolism but divergent results have been recorded depending on the amount and type of fibre eaten. Studies in which the fibre components pectin, cellulose, and lignin were fed to normal volunteers for four weeks have been reported. The highly fermentable component pectin is associated with increased secondary bile acid formation in contrast to the partially fermentable component cellulose in which the opposite occurs. Lignin has no effect on bile acid metabolism. No component significantly alters biliary lipids. Since ordinary diets contain a mixture of different fibres the net effect will depend on the relative amounts of each. Significant changes in bile acid metabolism and biliary lipids in the longer term (greater than 4 weeks) however, are not precluded by the results of these short term studies.

Bile Acids and Salts↗
PubMed1987

Dextrorphan and levorphanol selectively block N-methyl-D-aspartate receptor-mediated neurotoxicity on cortical neurons.

Neocortical neurons in cell cultures prepared from fetal mice were impaled for intracellular recording. Dextrorphan (DX), a clinically tested dextrorotatory morphinan lacking opioid action, did not alter neuronal membrane potential or conductance, but produced a selective attenuation of N-methyl-D-aspartate (NMDA) responses; kainate and quisqualate responses were not affected. DX also antagonized morphological and chemical (lactate dehydrogenase efflux) evidence of cortical neuronal cell injury produced by toxic bath exposure to NMDA, quinolinate or glutamate, but did not affect toxic exposure to quisqualate or kainate. This selective antagonism of neurotoxicity was apparent at micromolar concentrations of DX with an ED50 of 13 to 17 microM. A similar, but less potent neuron-protective effect, was seen with the opioid levorotatory enantiomer of DX, levorphanol (ED50, 40 microM). The O-methyl derivative of DX, dextromethorphan, also antagonized NMDA and glutamate neurotoxicity, but with possibly lower efficacy than DX. The higher potency of DX over levorphanol suggests that this novel neuron-protective action is not mediated by classic opiate receptors; it may be mediated at the "sigma opiate"/phencyclidine site. If further studies establish that DX and related compounds retain neuron-protective efficacy in appropriate animal models, the established clinical safety record of DX and dextromethorphan may allow prompt investigation of the NMDA receptor-blockade strategy in certain neurological disease states.

Animals↗