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Biomedical subjects

T D Smith

Publications and source records attributed to T D Smith.

90 records · Page 5Linked to original sources
PubMed1978

Pulsatile cerebral echo in diagnosis of brain death.

Conclusive diagnosis of brain death can be made by the demonstration of prolonged cessation of cerebral blood flow. This report describes a simple method to determine the presence or absence of the blood flow in the brain by recording the pulsatile midline echo on one channel of the electroencephalogram (EEG) or on any four-channel monitoring system in the intensive care unit. A firm transducer holder has been developed to eliminate artifacts caused by transducer motion, The pulsations of the midline echo are assumed to be the result of displacement of the midline structures by the arterial injection of each cardiac systole. Thus, the absence of these midline pulsatile echoes correlates with the absence of cerebral blood flow and, if the absence persists over 30 minutes in the presence of normal blood pressure, then the result is brain death. Twenty-eight cases of clinical brain death with electrocerebral silence of EEG and 18 obtained patients with various types of cerebral pathology were examined by the echo-pulsation technique. Twenty-six of the 28 cases showed no pulsation of the midline echo. The validity of the technique was documented in four cases by four-vessel cerebral angiogram.

Adolescent↗
PubMed1976

A simple kit for the preparation of 99mTc-labeled red blood cells.

A simple kit for the preparation of 99mTc-labeled red blood cells in a closed sterile system is described. Whole blood (3-6 ml) is automatically drawn from the patient into a 10-ml Vacutainer tube, containing a freeze-dried stannous citrate formulation, with heparin as an anticoagulant. The kit provides consistent 97% yields in 20 min with small blood samples. The radionuclide is added at the end of the labeling sequence to minimize operator exposure. Freeze-dried kits have performed well after more than 12 months. Some technetium solutions produced low labeling yields. Experimental evidence suggests that the poor yields were due to carrier 99Tc. This effect may explain low labeling yields obtained with some other radiopharmaceuticals.

Erythrocytes↗
PubMedDate not supplied

Cholinergic binding sites in rat brain: analysis by age and cognitive status.

Age-related alterations in the density of cholinergic receptor binding and reuptake sites were examined in discrete forebrain regions of behaviorally tested rats using quantitative autoradiography. Neurochemical changes associated with chronological age alone were distinguished from memory-dependent alterations by correlating density of binding sites with performance in the Morris water maze task. An initial analysis of tritium quenching indicated no reliable differential quenching in the study population. Modest age-related reductions in selected subtypes of cholinergic binding sites in basal forebrain, basal ganglia, and thalamus were observed. However, these reductions were not correlated with a spatial memory deficit. In contrast, no significant changes in the analysis by chronological age were detected for the density of [3H]hemicholinium binding to high affinity choline uptake sites or [3H]pirenzepine binding to M1 receptors in any brain region but strong correlations were found between behavioral performance of aged rats and density of these sites in dorsal hippocampal subfield CA3 and dentate gyrus. These findings indicate the value of combined neurobiological/behavioral assessment.

Aging↗
PubMedDate not supplied

Chloral hydrate: unusually high concentrations in a fatal overdose.

A case in which chloral hydrate as a pure chemical rather than the prescribed drug caused the death of a 27-year-old white male is presented. Trichloroethanol was quantified in blood and tissues by electron capture gas chromatography. The blood trichloroethanol concentration found in this case (1700 mg/L) was higher than had been previously reported in the literature.

Adult↗
PubMedDate not supplied

Positional changes of the frontoparietal ossification centers in perinatal craniosynostotic rabbits.

It has been suggested that craniosynostosis is caused by abnormally located ossification centers (i.e., bony tubers) in the developing skull prior to suture formation [Mathijssen et al., 1996, 1997]. The present study was designed to test this hypothesis in a rabbit model of human familial, nonsyndromic coronal suture (CS) synostosis. Calvariae were taken from 99 New Zealand White rabbit perinates (55 normal controls, 15 with delayed-onset CS synostosis, and 29 with bilateral or unilateral CS synostosis), ranging in age from 23 to 34 days postconception (synostosis occurs at approximately 23 days in this model). Frontoparietal, interfrontal, and interparietal ossification center distances were obtained using a Wild microscope with camera lucida attachment and a 2-D computer digitization technique. Linear regression analysis was used to compare age-related changes in the perinatal ossification centers among groups. Results revealed that frontoparietal ossification center regression line slopes had similar start points (24-day intercepts) with significantly (P < 0.05) diverging slopes over time. Normal and delayed-onset ossification center distance increased more rapidly than in synostosed perinates. No significant (P > 0.05) differences were noted in regression line slopes among groups for interparietal or interfrontal ossification center distances. Results demonstrated that, in synostosed perinates, frontoparietal ossification center location was similar to normals around the time of synostosis and became displaced later. These findings suggest that ossification center (i.e., bony tuber) displacement seen in infants with craniosynostosis is probably a secondary and compensatory, postsynostotic change and not a primary causal factor of synostosis in this rabbit model.

Animals↗
PubMedDate not supplied

Craniosynostosis with autosomal dominant transmission in New Zealand white rabbits.

Although great strides have been made recently in determining the etiology of a number of human craniosynostotic syndromes, pathogenic mechanisms for these conditions are still unclear, in part because of the lack of a genetic animal model with primary craniosynostosis. Recently, we developed an inbred colony of rabbits with congenital coronal suture synostosis. The present study describes long term breeding demographics, karyotypes, and pedigree analysis from this colony in an effort to characterize the genotype and mode of inheritance of craniosynostosis for future etiopathogenic studies. Seventy-six consecutive back- and intercrosses resulted in 46 fetal and term litters and produced 135 normal offspring and 163 affected offspring with either partial or complete coronal suture synostosis. Conception rate, litter size, and gestation length were normal, and karyotype analysis revealed no gross chromosomal abnormalities. Pedigree analysis of the segregation rates observed for each rabbit litter suggests that the craniosynostosis seen in this pedigree is inherited in an autosomal dominant fashion with reduced penetrance and variable expression. Results revealed that the mode of inheritance and phenotypic variability noted in this colony closely parallel the human craniosynostotic condition and several possible candidate gene families are discussed. The utility of developing such a congenital animal model is evident and may lead to a better understanding of gene expression, normal suture morphogenesis, and the pathogenesis of craniosynostosis.

Animals↗
PubMedDate not supplied

Postnatal changes in the cranial base in rabbits with congenital coronal suture synostosis.

Cranial base abnormalities are a common correlate of human craniosynostosis, although controversy exists as to whether they are primary malformations or secondary deformities. The current study assesses longitudinal cranial base growth and shape changes in rabbits with congenital coronal suture (CS) synostosis. Data were collected from 96 New Zealand White rabbits: 21 with complete bilateral or unilateral CS synostosis; 33 with partial CS synostosis; and 42 unaffected, "control" litter mates. Serial radiographs were taken at 1.5, 6, 12, and 18 weeks of age. Linear, angular, and shape measurements of the cranial base were compared among the three groups. Results revealed that at 1.5 weeks of age, rabbits with complete synostosis had significantly (P < 0.05) shortened anterior cranial bases, orthocephalic cranial base angeles, and acute, dysmorphic cribriform plate triangular shapes compared to the two other groups. Some significant differences persisted through 18 weeks of age. No significant differences were noted between partially synostosed and normal rabbits at any time period. If partial synostosis represents a continuum of the craniosynostotic phenotype, then the craniosynostosis may be seen as the primary deformity in this model and the cranial base abnormalaties as secondary, deformational changes. However, fetal data are still needed to more clearly delineate the role of the cranial base in this congenital rabbit model. Results reiterate the appropriateness and continued development of these rabbits for modeling cases of familial, human non-syndromic coronal suture synostoses.

Age Factors↗