Search PubMed⌕ Search

Biomedical subjects

D A Wilson

Publications and source records attributed to D A Wilson.

At least 55 records · Page 3Linked to original sources

Pediatric eighth cranial nerve schwannoma without evidence of neurofibromatosis.

Schwannomas of the eighth cranial nerve are rare in children. We report a 4 10/12 - year-old girl with no evidence of neurofibromatosis who presented with facial droop. Radiographic studies revealed a large cerebellopontine angle tumor. At surgery, the tumor was attached to the eighth cranial nerve and histologically was a schwannoma. This is the youngest reported case of unilateral eighth cranial nerve schwannoma in a patient without the stigmata of neurofibromatosis.

Child, Preschool↗

Tyrosine confounds oxidative electrochemical detection of nitric oxide.

We report evidence that a porphyrinic microsensor for detection of nitric oxide (NO) also detects biologically relevant concentrations of tyrosine (Tyr) in dog brain. Tyr is oxidized by this sensor at the same potential as NO, and the sensitivity for NO and Tyr are of the same order of magnitude. The interference from Tyr is of importance because 1) Tyr is abundant and 2) there is a concentration gradient of Tyr across the blood-brain barrier that can lead to unpredictable results if disturbed by ischemia or hypoxia. The knowledge of this interference is important for the interpretation of results obtained with this sensor and for the design of future studies.

Animals↗

Habituation of odor responses in the rat anterior piriform cortex.

Simultaneous recordings of main olfactory bulb (MOB) and anterior piriform cortex (aPCX) neuron responses to repeated and prolonged odor pulses were examined in freely breathing, urethan-anesthetized rats. Comparisons of odor responses were made between multi-unit recordings of MOB activity and single-unit extracellular and intracellular recordings of Layer II/III aPCX neurons. Odor stimuli consisted of either 2-s pulses repeated at 30-s intervals or a single, prolonged 50-s stimulus. Respiration rate was monitored throughout. MOB and aPCX neuron responses to odor were quantified both through firing frequency and through the temporal patterning of firing over the respiratory cycle. The results demonstrate that aPCX neurons habituate significantly more (faster) than MOB neurons with both repeated and prolonged stimulation paradigms. This enhanced habituation is expressed as both a decrease in aPCX firing despite maintained odor-evoked MOB input and as a decrease in aPCX respiratory cycle entrainment despite maintained MOB cyclic input. Intracellular aPCX recordings suggest that several mechanisms may be involved in this experience-induced change in aPCX function, including 1) decreased excitatory driveof aPCX neurons, 2) decreased excitability of aPCX neurons,and/or 3) enhancement in odor-evoked inhibition of aPCX neurons. These studies provide the initial basis for understanding the mechanisms of nonassociative plasticity in olfactory cortex.

Analysis of Variance↗

Synaptic correlates of odor habituation in the rat anterior piriform cortex.

Responses of anterior piriform cortex layer II/III neurons to both odors and electrical stimulation of the lateral olfactory tract (LOT) were measured with intracellular recordings in urethan-anesthetized, freely breathing rats. Odor-evoked, respiration-entrained postsynaptic potentials (PSPs) rapidly habituated during a 50-s odor stimulus, then spontaneously recovered within 2 min of odor termination. Associated with the decrease in odor-evoked PSP amplitude was a decrease in the monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the LOT. The decrement in LOT-evoked EPSPs recovered with a time course similar to the odor response recovery. These results demonstrate that odor habituation is associated with a decrease in afferent synaptic efficacy in the anterior piriform cortex.

Action Potentials↗

Evaluation of mild lameness in horses trotting on a treadmill by clinicians and interns or residents and correlation of their assessments with kinematic gait analysis.

OBJECTIVE: To estimate sensitivity and accuracy of subjective evaluation of mild lameness in horses during treadmill locomotion and to correlate subjective evaluation with kinematic analysis. ANIMALS: 19 lame and 5 clinically normal horses. PROCEDURE: Lameness was evaluated by subjective score and kinematic analysis before and after palmar digital nerve block (PDNB). Evaluations were made by 6 clinicians and 7 interns or residents. Within- and between-observer agreement analyses (kappa values) were calculated and compared, using a Student's t-test. Pearson's product-moment correlation coefficients were calculated between clinician's change in score and the change in kinematic variables after PDNB. RESULTS: Within-observer agreement was within the range expected for conditions of moderate diagnostic difficulty. Within-observer agreement was higher for clinicians than for interns or residents. Between-observer agreement was acceptable for scores within 1 value of each other. Between-observer agreement of change in lameness score after PDNB was poor. When kinematic variables were ranked with each clinician's subjective change in score, only 2 were among the top 3 for the majority of clinicians. Asymmetry of vertical head movement between contralateral forelimb stance phases and the point of maximum hoof height during swing decreased as lameness subjectively improved. CONCLUSION: Mild lameness may be difficult to evaluate during treadmill locomotion. Although clinicians were more repeatable in their subjective evaluation of lameness than interns or residents, they were not more reliable at detecting the true state of lameness. CLINICAL RELEVANCE: Lack of agreement between clinician scoring of mild lameness emphasizes the need to use more objective measures for quantifying lameness.

Animals↗

Methionine sulfoximine, a glutamine synthetase inhibitor, attenuates increased extracellular potassium activity during acute hyperammonemia.

Hyperammonemia causes glutamine accumulation and astrocyte swelling. Inhibition of glutamine synthesis reduces ammonia-induced edema formation and watery swelling in astrocyte processes. Ordinarily, astrocytes tightly control extracellular K+ activity [K+]e. We tested the hypothesis that acute hyperammonemia interferes with this tight regulation such that [K+]e increases and that inhibition of glutamine synthetase reduces this increase in [K+]e. Ion-sensitive microelectrodes were used to measure [K+]e in parietal cortex continuously over a 6-h period in anesthetized rats. After i.v. sodium acetate infusion in eight control rats, plasma ammonia concentration was 33 +/- 26 mumol/L (+/- SD) and [K+]e remained stable at 4.3 +/- 1.6 mmol/L. During ammonium acetate infusion in nine rats, plasma ammonia increased to 594 +/- 124 mumol/L at 2 h and to 628 +/- 135 mumol/L at 6 h. There was a gradual increase in [K+]e from 3.9 +/- 0.7 to 6.8 +/- 2.7 mmol/L at 2 h and 11.8 +/- 6.7 mmol/L at 6 h. In eight rats, L-methionine-D,L-sulfoximine (150 mg/kg) was infused 3 h before ammonium acetate infusion to inhibit glutamine synthetase. At 2 and 6 h of ammonium acetate infusion, plasma ammonia concentration was 727 +/- 228 and 845 +/- 326 mumol/L, and [K+]e was 4.5 +/- 1.9 and 6.1 +/- 3.8 mmol/L, respectively. The [K+]e value at 6 h was significantly less than that obtained with ammonium acetate infusion alone but was not different from that obtained with sodium acetate infusion. We conclude that acute hyperammonemia impairs astrocytic control of [K+]e and that this impairment is linked to glutamine accumulation rather than ammonium ions per se.

Ammonia↗

Measurement of cerebral blood flow in dogs with near infrared spectroscopy in the reflectance mode is invalid.

Near infrared spectroscopy (NIRS) is used to measure CBF (CBFNIRS) in humans, based on Fick's principle, using oxygen as an intravascular tracer. We compared CBFNIRS with CBF measured by microspheres (CBF mu) and the venous outflow technique (CBFv) in 15 dogs, altering CBF with ventilation-induced changes in PaCO2. Five hundred forty-nine CBFNIRS measurements were attempted using an integration time of 2.5 s on the saturation signal from the tongue. One hundred ninety-eight (36.1%) of the measurements fulfilled predefined criteria. The coefficient of variation (CV) for six measurements under stable conditions was 29.1%. The CBFNIRS measurements correlated best with microsphere-measured blood flows in the cortical gray matter (median 0.43, range 0.16-0.93); the contributions of the skull and dura were variable. The CBFv varied by a médian of 12% (range 0-67%) during the CBFNIRS measurements. The percentage of acceptable CBFNIRS measurements, the CV, and the correlation coefficients of the CBFNIRS were improved by using saturation signal directly from the artery and varying the integration time with an estimate of the minimum transit time. The current method of measuring CBFNIRS in the reflectance mode is in-accurate when compared with other accepted techniques.

Animals↗

The hypothalamic-pituitary-thyroid axis in major depression.

We investigated the capacity of several thyroid-axis measures to distinguish between depressed and control subjects and determined whether these variables were related to antidepressant treatment response. We studied 105 subjects who fulfilled the DSM-III-R criteria for a current major depressive episode and 41 volunteers with no current mental disorder. The following thyroid-axis variables were measured: difference between T4 levels at 09.00 hours and 13.00 hours; baseline TSH; maximal TSH response to 400 micrograms TRH (delta max TSH); and presence of a blunted delta max TSH. The T4 difference variable alone distinguished between depressed and control subjects. In multivariate analyses, T4 difference and delta max TSH were independently related to antidepressant-treatment outcome, and predicted a modest proportion (14%) of the variance in outcome. The relationship between these two variables and treatment outcome was particularly strong in depressed male subjects who were receiving desipramine, for whom they accounted for 36% of the variance in treatment outcome. The T4 difference variable both distinguished between depressed and control subjects and was related to treatment outcome. Although this finding requires replication, it is consistent with other reports of the usefulness of thyroid-axis indices measured at different times of day in depressed patients.

Adolescent↗

Role of leukocytes in cerebral autoregulation and hyperemia in bacterial meningitis in rabbits.

The effect of leukocytes on regional cerebral blood flow (rCBF) and cerebrovascular autoregulation in experimental meningitis was determined in rabbits. Four groups of animals were studied. Cerebrospinal fluid (CSF) leukocyte migration was prevented in two groups by pretreatment with 1.5 mg/kg of IB4, a monoclonal antibody directed against CD11/18 leukocyte adhesion receptors. Intracisternal inoculation was performed with saline (control and control-IB4 groups) or Haemophilus influenzae type b (Hib and Hib-IB4 groups). Eighteen hours later, rCBF was determined with radiolabeled microspheres. Autoregulation was assessed by graded hemorrhagic hypotension. Compared with untreated meningitis (Hib group), IB4-pretreated meningitis (Hib-IB4 group) was associated with a reduced CSF leukocyte count (1,980 +/- 880 vs. 200 +/- 110 cells/microliter; P < 0.05) and an elevated CSF colony count (2.87 +/- 0.08 vs. 5.63 +/- 0.72 log10colony-forming units/ml; P < 0.05). Compared with control, baseline CBF was elevated in both untreated and IB4-pretreated meningitis (51 +/- 2, 54 +/- 2, 66 +/- 5, and 102 +/- 17 ml.100 g-1.min-1 in control, control-IB4, Hib, and Hib-IB4 groups, respectively). The degree of hyperemia in meningitis was related to the CSF colony count, with a high CBF occurring in animals with high colony counts. During hypotension, CBF remained at or above baseline in the Hib group and both control groups, indicating preservation of cerebrovascular autoregulation in untreated Hib meningitis. In the Hib-IB4 group, the elevated baseline CBF was not maintained during hypotension, falling to 51% of baseline at a cerebral perfusion pressure of 30 mmHg and indicating impairment of cerebrovascular autoregulation. These results suggest that CSF leukocytes are not primarily responsible for the hyperemic response in Hib meningitis. Cerebral hyperemia may be induced either directly by bacterial components or indirectly by components of the inflammatory cascade that precede CSF leukocyte migration.

Animals↗

NO contributes to neurohypophysial but not other regional cerebral fluorocarbon-induced hyperemia in cats.

The large increase in cerebral blood flow (CBF) after fluorocarbon (FC)-exchange transfusion is thought to be caused by low oxygen content, decreased viscosity, or direct vasodilatory effect of the FC perfusate. The aim of this study was to determine whether nitric oxide (NO)-mediated vasorelaxation is increased in FC-perfused hemoglobin (Hb)-free cats because NO is not scavenged by Hb. We measured regional CBF with radiolabeled microspheres in three groups of anesthetized mechanically ventilated cats. The first group [FC + N(omega)-nitro-L-arginine methyl ester (L-NAME), n = 7] underwent a complete FC-exchange transfusion with FC-43 and subsequent nitric oxide synthase (NOS) inhibition with L-NAME (10 mg/kg i.v.) followed by L-arginine (100 mg/kg i.v.). A second group (FC + saline; n = 6) underwent an identical protocol, but NOS was not antagonized (saline i.v.). In a third group (blood + L-NAME; n = 7), cats were not FC exchanged but NOS was inhibited. In a separate cohort of four FC-perfused cats, NOS activity in brain tissue samples was reduced to 26% of control after NOS inhibition. FC-exchange transfusion nearly doubled hemispheric blood flow in both FC-exchanged groups, whereas it was constant in the blood + L-NAME group. These increases in regional CBF (hemispheres, brain stem, cerebellum, thalamus, and white matter) were not reversed by inhibition of NOS, except in the neurohypophysis, where L-NAME reduced blood flow to levels comparable to values in the blood + L-NAME group. In summary, increases in regional CBF after total FC-exchange transfusion are not caused by a lack of NO scavenging, with the exception of neurohypophysis. These findings suggest an increased vasorelaxation in neurohypophysis of FC-perfused and Hb-free cats caused by unscavenged NO, but this mechanism does not play a major role in FC-related CBF increases in the rest of the cerebral circulation.

Animals↗

Binaral interactions in the rat piriform cortex.

Single-unit recordings were made from layer II/III anterior piriform cortex (aPCX) neurons in adult Wistar rats to examine odor response patterns to unilaterally and bilaterally delivered stimuli. Isoamyl acetate odor stimulation was presented either unilaterally through tubes inserted into the external nares, or bilaterally during unilateral olfactory bulb lidocaine infusions. Olfactory bulb multiunit or slow-wave activity was recorded simultaneously bilaterally to monitor selectivity of unilateral odor stimulation. The results demonstrate that 1) commissural input to aPCX neurons is sufficient to drive odor responses, and 2) aPCX neurons can be classified on the basis of spatial receptive field type. These receptive fields include cells that respond 1) selectively to ipsilateral stimulation, 2) selectively to contralateral stimulation, 3) to either ipsilateral or contralateral stimulation, and 4) selectively to bilateral stimulation. The potential functions of binaral convergence in the piriform cortex are discussed, and may include enhancement of perceived odor intensity and bilateral access to olfactory memory.

Anesthetics, Local↗

Effects of anesthesia of the palmar digital nerves on kinematic gait analysis in horses with and without navicular disease.

OBJECTIVE: To determine the effect of local anesthesia of the palmar digital nerves on forelimb kinematics in Quarter Horses with and without navicular disease. ANIMALS: 12 adult Quarter Horses; 5 clinically normal (sound) and 7 with navicular disease. PROCEDURE: Kinematic measurements were made on adult horses trotting on a treadmill, before and after palmar digital nerve block (PDNB). Twenty-three displacement, joint angle, and temporal gait measurements of the right forelimb and head were made for 5 strides in each horse. Initial (before local anesthesia) right forelimb measurements were obtained after a left forelimb PDNB. Kinematic measurements were compared before and after PDNB of the right forelimb by multiple ANOVA with an alpha = 0.05, adjusted for posthoc comparisons by Bonferroni correction. RESULTS: In sound horses, the only significant change in kinematic measurements after PDNB nerve block was in the maximum extension of the metacarpophalangeal joint at mid-stance, which was decreased by an angle of 2 degrees. In horses with navicular disease, mean maximum extension of the metacarpophalangeal joint during stance phase and maximum flexion of the carpal joint during swing phase were significantly increased after PDNB. Also, total stance phase, cranial stance phase, and break-over durations were significantly shorter. In horses with navicular disease, differences between minimum head heights during stance phase of each forelimb and total vertical head excursion during a complete stride were significantly smaller after PDNB. CONCLUSION: Several kinematic measurements of gait can be used to determine improvement of lameness in horses with navicular disease after PDNB block while trotting on a treadmill.

Analysis of Variance↗

NMDA-receptor modulation of lateral inhibition and c-fos expression in olfactory bulb.

Olfactory bulb primary output neurons, mitral/tufted cells, are glutamatergic and excite inhibitory interneurons, granule cells, by activation of both alpha-amino-3-hydroxy-5-methyl-ioxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) glutamate receptors. The data presented here demonstrate that the NMDA antagonists MK-801 and CGP39551, but not ketamine, significantly enhanced expression of c-fos mRNA by mitral cells as measured by in situ hybridization. All three antagonists significantly reduced mitral/tufted cell excitation of granule cells as measured with extracellular field potentials following antidromic stimulation of the lateral olfactory tract (LOT). In turn, the NMDA antagonists significantly reduced granule cell mediated feedback inhibition of mitral/tufted cells, as measured with field potential recordings of paired-pulse LOT stimulation, suppression of mitral/tufted cell single-unit spontaneous activity following LOT stimulation, and intracellularly recorded IPSP amplitude in mitral/tufted cells following LOT stimulation. While there was not a perfect correlation between the effects of the NMDA antagonists on c-fos mRNA expression and on inhibition, the results suggest that disinhibition of mitral/tufted cells accounts for the observed enhancement in c-fos mRNA expression induced by NMDA receptor antagonists.

2-Amino-5-phosphonovalerate↗

Mycobacterium gordonae in fiberoptic bronchoscopes.

BACKGROUND: Failure of high-level disinfection of bronchoscopes has caused several outbreaks of nosocomial infection or pseudoinfection involving mycobacteria. METHODS: Inocula (10(5) colony-forming units/ml and 10(8) colony-forming units/ml) of a clinical Mycobacterium gordonae isolate were used to contaminate bronchoscopes. Glutaraldehyde, iodophor, and peracetic acid disinfectants were evaluated in manual and automated disinfection procedures after 10- to 20-minute exposures at 20 degrees and > or = 25 degrees C. RESULTS: Four of five manual disinfectant procedures failed to eliminate experimental M. gordonae infection after 10-minute exposure at 20 degrees C. All five manual procedures tested at 20 degrees C were effective after 20-minute exposure to the five disinfectants (two 2% alkaline glutaraldehyde preparations, 3.2% alkaline glutaraldehyde, 75 ppm iodophor, and 0.5% glutaraldehyde-0.03% phenolic). Three of four manual (one 2% glutaraldehyde, 3.2% glutaraldehyde, and 0.5% glutaraldehyde-0.03% phenolic) and three automated (one 2% glutaraldehyde, 0.5% glutaraldehyde-0.03% phenolic, and 0.2% peracetic acid) disinfectant procedures eliminated contamination after a 10- to 12-minute exposure at > or = 25 degrees C. Effective total cycle times for the three automated procedures ranged from 20 to 45 minutes. CONCLUSIONS: Previously Environmental Protection Agency-approved tuberculocidal agents may be ineffective against M. gordonae when used according to label claims under normal clinical conditions. A minimum 20-minute exposure time at 20 degrees C is necessary for manual disinfection methods. Higher temperatures may improve disinfectant efficacy. Newer automatic disinfection machines may be as effective as traditional manual methods and also may reduce hazards to employees.

Bronchoscopes↗

Early locus coeruleus lesions increase the density of beta-adrenergic receptors in the main olfactory bulb of rats.

Norepinephrine is supplied to both deep and superficial layers of the olfactory bulb through dense projections from the locus coeruleus. Beta-adrenergic receptors are located in nearly all bulb laminae, with high-density foci of beta-1 and beta-2-adrenoceptors present in the glomerular layer. Early olfactory experiences that increase norepinephrine levels in the bulb also decrease the density of beta-1- and beta-2-adrenoceptors, as well as the number of high-density glomerular foci of beta-2-receptors. Changes in bulb norepinephrine levels, therefore, may affect the density of beta-adrenoceptors in the bulb. In the current study, we test this hypothesis by performing unilateral lesions of the locus coeruleus with 6-hydroxydopamine on postnatal day 4, and examining the density of beta-1- and beta-2-adrenergic receptors in the main olfactory bulb of the rat using 125I-labeled iodopindolol receptor autoradiography on postnatal day 19. Locus coeruleus destruction resulted in a statistically significant increase in the density of adrenergic receptors in the ipsilateral bulb compared to the contralateral bulb. Both beta-1- and beta-2-adrenoceptor subtypes increased in density with this manipulation, although the number of glomerular layer high-density beta-2 foci was not significantly different between the two bulbs. These results are consistent with the hypothesis that changes in olfactory bulb norepinephrine can regulate the density of beta-adrenergic receptors in the bulb.

Animals↗