Biomedical subjects
A Taylor
Publications and source records attributed to A Taylor.
Chest wall pain after aortocoronary bypass surgery using internal mammary artery graft: a new pain syndrome?
During an 18-month period 11 patients were seen at the Toronto Western Hospital Pain Clinic 4 months to 5 years after internal mammary artery (IMA) bypass with a specific cluster of chest wall symptoms and signs confined to the site of IMA graft harvesting. Sympathetic ganglia blocks produced dramatic but temporary relief of symptoms in two of the most severely affected patients. In two other patients seen quite early after surgery, use of transcutaneous electrical stimulation produced considerable and permanent decrease of symptoms within 3 weeks. Such a chronic pain syndrome has not been previously reported in the literature. We postulate that IMA bypass surgery may be associated with a specific pain syndrome. This syndrome may arise from injury to the anterior branches of the intercostal nerves at the site of graft harvesting. Possible neurophysiologic mechanisms are discussed.
Effects of chloralose-urethane anesthesia on single-axon reciprocal Ia IPSPs in the cat.
Reciprocal Ia inhibitory postsynaptic potentials (IPSPs) generated by single afferents have been recorded with signal averaging in unanesthetized ischemic-decapitate cats for comparison with measurements previously obtained from preparations anesthetized with a mixture of chloralose and urethane. The results are similar to those which we obtained recently for single-axon recurrent IPSPs. Together, the studies show that chloralose-urethane anesthesia has a depressant effect on two widely studied circuits in the mammalian spinal cord.
Syncope while vomiting during migraine attack.
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Kikuchi's disease simulating acute appendicitis.
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Vitamin D metabolite profiles in moderate renal insufficiency of childhood.
In a prior study, we reported vitamin D metabolite profiles in the plasma of healthy children. In view of these findings, we investigated these same profiles in children with moderate renal insufficiency. Specimens were obtained in both summer and winter in untreated patients, and before and after treatment for up to 1 year, with either 25(OH)D3 or 1,25(OH)2D3. Mean pretreatment 1,25(OH)2D levels were normal. Levels of 25(OH)D3 were also normal and continued to vary with season. Mean pretreatment 24,25(OH)2D3 levels were significantly lower in patients and, interestingly, did not show the normal seasonal variation. Treatment with 25(OH)D3 resulted in consistent and sustained rises in 25(OH)D3 and 24,25(OH)2D3 levels, but no increase in 1,25(OH)2D levels. After 1,25(OH)2D3 treatment, 25(OH)D3 levels were unchanged but still showed seasonal variation in some patients, suggesting a lack of feedback control by 1,25(OH)2D3. Levels of 24,25(OH)2D3 were not significantly different from baseline values. Levels of 1,25(OH)2D increased initially then dropped to pretreatment levels or lower. Normal 1,25(OH)2D levels and reduced 24,25(OH)2D3 levels with the loss of seasonal variation suggests in our patients that the kidney was able to maintain 1,25(OH)2D levels at the expense of 24,25(OH)2D3 levels, presumably to preserve calcium homeostasis.
Intracellular protein degradation in cultured bovine lens epithelial cells.
Although several proteases have been identified in homogenates of cultured epithelial cells of the eye lens and in lens tissues, there is little information regarding intracellular protein degradation in intact lens cells in vitro. Cultured lens cells may be useful in the study of intracellular protein degradation in the lens, a tissue with a wide range of protein half-lives. This is of interest because alterations in protein turnover in the lens have been implicated in cataract formation. This study examines intracellular protein degradation in cultured bovine lens epithelial cells (BLEC). Cell cultures were incubated with radiolabeled leucine to label intracellular proteins. Protein degradation was measured by monitoring the release of trichloroacetic-acid-soluble radioactivity into the culture medium. The average half-life of long-lived proteins (half-life greater than 50 h) was typically about 57 h in serum-supplemented medium. Average rates of degradation of long-lived proteins increased by up to 73% when fetal bovine serum was withdrawn from the culture medium. Serum had no effect on the degradation of short-lived proteins (half-life less than 10 h). Degradation of long-lived proteins in the presence and absence of serum was further studied in cultured BLEC from population doubling level (PDL) 2 to 43. Average half-life of proteins in serum-supplemented medium was 52 to 58 h and did not vary significantly as a function of PDL. Degradation rates in serum-free medium increased approximately twofold up to PDL 7, but returned by PDL 25 to original levels, which were maintained through PDL 43.
Cardiomyopathy with arrhythmias and ectodermal dysplasia: a previously unreported association.
Hidrotic ectodermal dysplasia represents a group of congenital or hereditary disorders that involve ectodermal derivatives. It is characterized by partial or complete alopecia, dystrophic nails, and dental abnormalities. Dilated cardiomyopathy has not previously been reported in association with this illness. We report the cases of three children with fatal dilated cardiomyopathy with associated cardiac arrhythmias and ectodermal dysplasia. Laboratory investigations revealed no specific cause for the cardiomyopathy. It is speculated that this association is not simply coincidental.
Regulation of membrane permeability by vasopressin; activation of the water permeability pathway in toad urinary bladder by N-ethyl-maleimide.
1. Vasopressin induces a rapid increase in water permeability and stimulates net sodium transport in responsive epithelia through the mediation of cAMP. 2. In amphibian urinary bladder, the increase in water permeability is dependent on an intact cytoskeleton and is associated with the exocytotic insertion of tubular vesicles containing particle aggregates (the putative water channels) into the apical membrane of the granular epithelial cells. 3. In the toad bladder, mucosal addition of NEM, 0.1 mM, elicits a slow and irreversible increase in transepithelial water flow, whilst decreasing net sodium transport. 4. The hydrosmotic response to mucosal NEM is inhibited by cellular acidification, by pretreatment with cytoskeleton-disruptive drugs, and by agents that increase cytosolic calcium. 5. Mucosal NEM potentiates the hydrosmotic response to a submaximal, but not a maximal, dose of vasopressin. 6. Mucosal NEM, like vasopressin, induces both vesicle fusion and the appearance of particle aggregates at the granular cell apical surface. 7. NEM, unlike vasopressin, does not increase cellular cAMP content. 8. Mucosal NEM appears to increase transcellular water flow by activating cellular processes normally triggered by vasopressin, at a step beyond cAMP.
Nucleotide sequence and expression of the human skeletal alpha-actin gene: evolution of functional regulatory domains.
Regulation of the actin multigene family involves the recognition of regulatory sequences that specify the tissue type and developmental program of expression for each actin isotype. In order to investigate the underlying regulatory mechanisms, the human skeletal alpha-actin gene and its 5' regulatory region have been cloned and sequenced. This actin gene has seven exons; there is one large intron in the 5' untranslated region which is characteristic of the actins and many muscle-specific genes. The 5' flanking sequences are sufficient to direct tissue-specific and differentiation-regulated expression when transfected into the heterologous rat L8 myogenic cells, indicating a highly conserved regulatory system. The DNA sequence was compared to that of other actin genes, and several regions of sequence similarity were identified, particularly within regions known to be important for gene expression. Most notable among the conserved sequences are the CC(A/T rich)6GG (CArG box) motifs which have demonstrated interactions with trans-acting transcriptional factors. This same motif has been identified in several other genes and in some also serves as a binding site for transcription regulatory factors.
Protease activities in cultured beef lens epithelial cells peak and then decline upon progressive passage.
Beef lens cells in culture are readily obtained and provide many opportunities to study phenomena related to cell differentiation and maturation, environmental stress, disease, and perhaps mechanisms of transformation. Although altered rates of proteolysis are known to accompany these phenomena, the proteolytic activities available in cultured beef lens epithelial cells have not been documented. In this work are documented the specific activities, based on protein and DNA content, of neutral exo- and endopeptidase, cathepsins B- and D-like enzymes and acid phosphatase in lens epithelial cortical and core tissue and in cultured epithelial cells at passages 1-43. Maximal activity of each protease occurs almost routinely at passage 5 or 9, reaching values of approx. 1400-, 0.77-, 4520-nmol min-1 per mg protein for neutral exopeptidase (passage 5), neutral endopeptidase (passage 5) and cathepsin B (passage 5) respectively, and 7.1 micrograms trichloroacetic acid soluble peptide min-1 per mg protein for cathepsin D (passage 15). On a microgram-1 DNA basis, the maximal specific activities for the same enzymes were 48 (passage 5), 0.03 (passage 5), 283 (passage 9), and 0.5 (passage 9) respectively. In subsequent passages, the specific activities declined to values which were similar to or lower than the specific activities observed for these proteases in lens epithelial tissue.
Abnormal ventilation-perfusion scan due to swallowed DTPA aerosol and a paralyzed hemidiaphragm.
A case of ventilation-perfusion mismatch due to swallowed DTPA aerosol and a paralyzed hemidiaphragm is shown as a potential source of error in the evaluation of pulmonary embolus. This case emphasizes the importance of radiograph correlation in the interpretation of ventilation-perfusion images.
The role of periodontal receptors in the jaw-opening reflex in the cat.
1. In anaesthetized cats, graded electrical stimulation of the inferior alveolar nerve at just above threshold for the largest afferent fibres caused inhibition of jaw-closer motoneurones. Stimulus strength had to be increased to 1.5 times threshold with double shocks to cause reflex contraction of the digastric muscle. 2. Inhibition of jaw-closer muscles and excitation of digastric muscle resulted from transients of force applied to the upper canine tooth. However, the threshold for the digastric response was approximately 11 times higher than that of the periodontal afferent units recorded in the mesencephalic nucleus of the fifth nerve (MesV). Vibration of the upper canine at 50 Hz, with amplitude adequate to excite periodontal afferents, caused no digastric contraction. 3. Stimulation in the caudal part of the MesV so as to excite periodontal afferents caused no digastric reflex, provided that the stimulus did not spread to other parts of the fifth nerve nuclei. 4. It is concluded that under these conditions the low-threshold periodontal mechanoreceptors cause inhibition of jaw-closer muscles, but no significant excitation of jaw-opener muscles. 5. These findings are discussed from the point of view of the control which periodontal mechanoreceptors may exert over the biting force during mastication.
Effect of thromboxane and serotonin receptor antagonists on intracoronary platelet deposition in dogs with experimentally stenosed coronary arteries.
We have reported previously that thromboxane A2 (TXA2) and serotonin (5-HT, 5-hydroxytryptamine) are important mediators of cyclic flow variations (CFVs) in a canine model of coronary artery stenosis and endothelial injury. The present study tested the hypothesis that a TXA2 receptor antagonist is more effective in reducing intracoronary platelet deposition at sites of endothelial injury and severe stenosis than a 5-HT2 receptor antagonist. CFVs developed after placing a plastic constrictor around the left anterior descending coronary artery (LAD) in 51 of 56 dogs. Autologous platelets labeled with 111In were injected in 48 animals. Ten control dogs (group 1A) were killed after CFVs were observed for 1 hour at the nadir of coronary blood flow. Five dogs (group 1B) did not develop CFVs after placement of the constrictor. CFVs were abolished with SQ 28668 (2.75 +/- 0.36 mg/kg, group 2) and SQ 29548 (0.45 +/- 0.1 mg/kg, group 3), two different TXA2 and PGH2 receptor antagonists, in eight of 10 and six of seven dogs, respectively. In eight of 10 dogs (group 4), CFVs were abolished with ketanserin (0.66 +/- 0.12 mg/kg), a 5-HT2 receptor antagonist. In group 2, 3, and 4 dogs, the respective drugs were given so that the minimal dose required to abolished CFVs was administered. In six of six dogs (group 5), a higher dose of ketanserin (i.e., 1.5 mg/kg) was used to abolish CFVs. At death, intracoronary platelet deposition was evaluated by calculating the LAD platelet accumulation ratio (111In activity in the LAD/111In activity in the circumflex coronary artery) in 43 dogs and, in 22 dogs, by microscopic examination of the LAD. A marked LAD platelet accumulation ratio was found in group 1A dogs at the stenotic site and in segments immediately distal to it. The LAD platelet accumulation ratio was significantly reduced by both the low and the high doses of ketanserin compared with group 1A dogs (p less than 0.001). However, the two TXA2 receptor antagonists further reduced the LAD platelet accumulation ratio compared with ketanserin-treated animals (p less than 0.01). Microscopic examination confirmed these findings. We conclude that SQ 28668 and SQ 29548, two different TXA2 receptor antagonists, reduce residual intracoronary platelet deposition associated with CFVs in this canine model more effectively than ketanserin, a 5-HT2 receptor antagonist.
Mechanism of decreased forward stroke volume in children and swine with ventricular septal defect and failure to thrive.
Children with ventricular septal defect (VSD) often demonstrate failure to thrive (FTT). Such patients usually have reduced systemic cardiac output which has been postulated as a cause for their growth retardation. This study was conducted to ascertain the mechanism of the reduced cardiac output in children with VSD and FTT and also in a porcine model of VSD. Forward stroke volume was reduced in VSD-FTT children, 31 +/- 8 ml/m2, compared to normal children, 49 +/- 15 ml/m2 (P less than 0.05), but was not reduced in children with VSD and normal growth and development (41 +/- 16 ml/m2). Forward stroke volume was also reduced in swine with VSD compared to controls. Contractility assessed by mean velocity of circumferential shortening (Vcf) corrected for afterload was similar in normals and VSD-FTT children. Contractile performance was also similar in normal and VSD swine. Afterload assessed as systolic stress was similar in FTT-VSD children and normal subjects. Preload assessed as end-diastolic stress was increased in the VSD-FTT group. End-diastolic volume was not larger in the VSD-FTT group. We conclude that the reduced stroke volume seen in VSD-FTT children and VSD-swine was not due to reduced contractility, increased afterload or reduced preload. The reduced stroke volume may have been due to failure of end-diastolic volume to increase adequately.
Serum dihydrotachysterol levels and biological action in normal man.
Dihydrotachysterol (DHT2) has been a safe and effective treatment for hypocalcemic disorders for many years, but few assays for quantitation of DHT2 have been developed. Thus little is known about its pharmacokinetics. The 2-fold purpose of this study was 1) to develop a practical method for quantitating DHT2 after oral dosing in normal subjects, and 2) to assess changes in serum DHT2 levels and calcium and phosphorus metabolism after DHT2 administration for 8 days. Peak serum DHT2 levels in six normal subjects, assayed by high performance liquid chromatography were achieved 4 h after administration of 0.4-0.8 mg DHT2; at 24 h, levels had declined by 70% whether DHT2 had been given for 1 or 8 days. These data indicate that a standard approach is needed to interpret the results of serum DHT2 measurements in treated patients. Interfering substances were detected in lipemic serum. The major biological effects of DHT2 administration were hypercalciuria in two subjects and a fall in serum 1,25-dihydroxyvitamin D[1,25-(OH)2D] levels, including free levels when measured, in all subjects. Possible explanations for this fall in serum 1,25-(OH)2D levels include decreased 1,25-(OH)2D production because of competition for the 1 alpha-hydroxylase enzyme by a metabolite(s) of DHT or increased metabolic clearance of 1,25-(OH)2D.
Reduced and total ascorbate in guinea pig eye tissues in response to dietary intake.
Guinea pigs were fed 5 different levels of dietary ascorbate representing a 65-fold range (0.8-52 mg animal-1 day-1). After two months on the diets, levels of reduced and total ascorbate were determined in aqueous humor, vitreous humor, lens and plasma. At low-dietary levels, proportionally higher levels of ascorbate are found in the lens than in other eye tissues. Tissue ascorbate levels began to plateau at dietary intake of approximately 11 mg animal-1 day-1. This is the amount suggested for optimal health, but it is ten times the level needed to prevent scurvy. Over 75% of the eye tissue ascorbate is in the reduced form in animals fed diets which provided 11 mg ascorbate. However, there was less than 50% reduced ascorbate in the eye tissues of the animals fed about 1mg ascorbate per day.
Properties of the ubiquitin conjugation system from bovine eye lens.
A post-translational protein modification system involving the polypeptide ubiquitin results in ubiquitin-protein conjugates of various functions. A ubiquitin-conjugating enzyme system was isolated from the epithelial tissue of bovine eye lens by DEAE-Sepharose and Bio-Gel A-1.5m column chromatography. The lens system shows similar enzymatic properties to the one from rabbit reticulocytes: requirement for ATP and sensitivity to thiol reagents. Two sets of prominent ubiquitin conjugates were formed with endogenous ubiquitin-acceptor proteins from fractions of the Bio-Gel column: a pair of ubiquitin conjugates of approximately 130 kDa and others with very high molecular mass. Extreme specificity is indicated by the ability of the lens system to catalyze conjugation of ubiquitin to the few endogenous acceptor proteins, or to histone H2B, but not to lysozyme, S-carboxymethylated bovine serum albumin, or native or heat-denatured lens alpha crystallin.