Biomedical subjects
Publications and source records attributed to R Armstrong.
An 18 week abortus had been prenatally diagnosed as a 45,X/46,XY mosaic. The fetus was a phenotypic male with glandular hypospadias, a horseshoe kidney and asymmetric gonadal dysgenesis. This case represents a rare instance of prenatally diagnosed 45,X/46,XY mosaicism with an abnormal phenotype.
Regenerated and remyelinated nerve fibers have shorter internodes and thus more nodes than normal mature fibers. This requires either a decrease in the number of sodium channels per node or an increase in the number of channels per fiber or both. The purpose of this investigation was to determine what happens to sodium channel number, as estimated by 3H-saxitonin (STX) binding, in regenerated fibers and to relate this to nodal number. Five adult cats underwent cryoaxotomy of ventral root levels L5, L6, L7, and S1 on the left side. After regeneration for 16-45 weeks, binding parameters were determined. On the right (control) side, binding was consistent with that in unoperated animals (b = 1.3, Bmax = 10.2 +/- 0.4 fmol/mg wet, Kd = 0.6 +/- 0.1 nM). However, the regenerated nerves showed a 3.5-fold increase in maximal binding (b = 1.3, Bmax = 36.1 +/- 0.5, Kd = 0.45 +/- 0.4). Computer-aided histologic analysis of the regenerated roots revealed a decrease in fiber size; a significant decrease in internodal length for fibers in a given size class; and a 1.35-fold increase in total fibers per root. These factors account for a 2.36-fold increase in nodes per milligram (wet). The number of STX binding sites per regenerated node was calculated to be 1.95 X 10(6) (1.31, 3.07, 95% confidence limits), whereas it was 1.26 X 10(6) (0.78, 2.02) for the control roots. The difference was not significant (p greater than 0.05). It is concluded that, in regeneration, the increase in nodal number is accompanied by an increase in sodium channels, so that the number of channels per node is normal or slightly increased. There is a marked increase in channels per fiber and an even greater increase in channels per anterior horn cell. The implications of these data for nodal reorganization in remyelination are discussed.
Focal demyelination was produced in rat sciatic nerve by unilateral intraneural injection of anti-galactocerebroside serum. A functional lesion was confirmed by the presence of nerve conduction block. Histologically, this corresponded to demyelination of 50-70% of the fibers in nerve cross sections; axonal structures appeared intact. At the time of maximal demyelination (7 d), 35S-methionine or 3H-fucose was injected bilaterally into the spinal cord ventral horn. At later times (5 hr-7 d), the sciatic nerve was removed and radioactivity in successive nerve segments was quantitated. The transport rates (approximately 260 mm/d) and the composition of transported proteins and glycoproteins (separated on 7-15% polyacrylamide gradient gels) were not altered in lesioned nerves relative to contralateral control nerves. Light microscopic autoradiographic analysis revealed a similar localization of axonally transported and deposited glycoproteins in demyelinated and control fibers. Initially (8 hr), the majority of label was over axons. Labeled glycoproteins remaining in the nerve after 1 week were retained mainly in axolemmal regions. We conclude that acute focal primary demyelination does not lead to major alterations in the transport or deposition of newly synthesized macromolecules.
Four patients received Zyderm collagen implant (ZCI) or Zyplast implant (ZI) in preauricular and infraauricular regions of facial skin periodically between one and nine months. Both materials were identified microscopically in the mid- to deep dermis at all points of the study and, in 60% to 70% of the injected sites, some material was also present subdermally. A slow, gradual colonization of ZCI by fibroblasts was noted compared with a delayed intense interaction of these cells with ZI. Also, there was some new collagen deposition associated with remodeling of the ZI, while no demonstrable synthetic activity occurred in relationship to ZCI. The results suggest that ZCI and ZI "migrate" deeper and eventually move into the subcutaneous plane. This movement could explain the loss of correction at six to nine months that is noted when this implant is used for age-related changes.
The biologic response to injectable, glutaraldehyde cross-linked, fibrillar collagen implants in the rat subcutaneous model was shown to be a function of the concentration of glutaraldehyde used for cross-linking. The collagen was prepared from bovine hide by pepsin solubilization and reconstituted as a fibrillar suspension of 35 mg collagen/mL. Fibrillar collagen implants cross-linked with glutaraldehyde concentrations equal to or less than 0.01% exhibited a response characterized by fibroblast invasion, neovascularization and little, if any, evidence of inflammation. Implants cross-linked with 0.1 and 1.0% glutaraldehyde elicited a foreign body/giant cell reaction and varying degrees of implant erosion. The interaction of human skin fibroblasts with 0.01% glutaraldehyde cross-linked collagen in vitro was found to be dependent on the culture conditions utilized to evaluate the interaction. When the ratio of cell culture media to collagen was 20:1, cell invasion of the cross-linked preparations was observed, whereas, when this ratio was reduced to 1:1, such interactions could not be detected. Noncross-linked preparations were colonized by cells regardless of the experimental conditions used. Studies of implants in both the rat and guinea pig subcutaneous models indicated that glutaraldehyde cross-linking concentrations as low as 0.0075% provided enhanced wet weight recovery (wet weight persistence) and resistance to biologic degradation (collagen persistence) as compared to noncross-linked fibrillar collagen preparations. These cross-linked implants also exhibited a greater degree of fibroblast infiltration and vascularization. Between 30 and 60 days, some degree of calcification developed in both collagen formulations implanted in rats and guinea pigs; however, the reaction occurred with greater frequency and intensity in cross-linked preparations in guinea pigs. Calcification in the guinea pig was followed by the appearance of focal areas of ossification.
Platelet aggregation to collagen in 12 Type 1 (insulin-dependent) diabetic patients with background retinopathy and 12 Type 1 diabetic patients with proliferative retinopathy was compared with an age- and sex-matched control group. An analogue of prostaglandin H2, 11,9 epoxymethano-prostaglandin H2, which directly stimulates thromboxane receptors, and EP 092, which is a competitive thromboxane A2 receptor antagonist, were used to investigate changes at platelet thromboxane receptor level in these groups. The concentration of collagen (EC50) required to give 50% of maximum aggregation did not differ between the two diabetic groups and the control group. However, platelets from the proliferative retinopathy group were significantly more sensitive to the thromboxane mimetic (11,9 epoxymethano-prostaglandin H2) (p less than 0.005) than the background retinopathy and control groups. This change may be a factor in the development of proliferative retinopathy.
This is a report of a premature infant presenting with an esophageal atresia. At surgery it was realized that there was no posterior mediastinum and a single pleural cavity only. Other serious congenital anomalies were present. She died rather suddenly upon cessation of her prostaglandin E 1 at 34 days of life.
Anterograde axonal transport of phospholipids occurs at a rate of several hundred millimeters per day. However, although labeled precursors are incorporated into phospholipids in the neuronal cell bodies within several hours, these newly synthesized phospholipids are committed to transport over a much longer period of time. Thus, maximal accumulation of radioactive lipids in axons and nerve endings does not occur for several days (e.g., 4 to 7 days in rat optic tract and sciatic nerve). We have now investigated the retrograde axonal transport of endogenous phospholipid molecules in sensory neurons of rat sciatic nerve. Labeled phospholipids were delivered to axons and nerve endings of these cells by anterograde axonal transport following injection of [2-3H] glycerol into the L5 dorsal root ganglion. At various times following precursor injection two ligatures, 9 mm apart, were applied to the mid-thigh region of the sciatic nerve. Animals were sacrificed 3 to 48 hr after nerve ligation, nerves were dissected and sectioned into 5-mm segments, and phospholipid radioactivity in each segment was determined. The time-dependent accumulation of labeled phospholipids distal to the distal ligature demonstrated their retrograde axonal transport. The time course of retrograde transport for these phospholipids was more prolonged and peaked several days later than the time course for the anterograde transport phase. Further information regarding the relationship between radioactive phospholipids arriving at the nerve endings by anterograde transport, and their subsequent "turn-around" and retrograde transport back to the nerve cell bodies, was obtained by analyzing the phospholipid class label distribution of both of these transport phases at various times following precursor injection.(ABSTRACT TRUNCATED AT 250 WORDS)
Central venous catheter systems are an important yet little recognised source of serious air embolism. Scrupulous care and vigilant observation of this equipment is necessary to prevent the severe cardio-respiratory and neurological sequelae which may occur. Air embolism following central venous catheterisation is one of the most serious complications of this procedure. We describe an unusual and hitherto unreported mechanism by which air accidentally entered the circulation; fortunately in this case there were no serious sequelae.
P elements, a class of mobile genetic elements that cause hybrid dysgenesis in Drosophila melanogaster, have thus far been shown to occur only in this species. Using whole genome blot analysis, we present evidence which indicates that sequences homologous to D. melanogaster P elements also occur in Drosophila paulistorum, a distant relative. D. paulistorum is considered a species complex, consisting of six known incipient species or semispecies. All six semispecies possess P element homologous sequences. We further show that there is conservation of restriction enzyme recognition sites between the D. melanogaster and D. paulistorum P element sequences. The presence of P elements in these two species may clarify the roles of recent invasion and rapid loss in the temporal distribution of P elements in Drosophila.
Eleven of 90 hybridomas that secreted neutralizing antibodies to various types of poliovirus, were cloned and their monoclonal antibodies tested for the intratypic differentiation of poliovirus isolates. All monoclonal antibodies (MAs) prepared with three types of Sabin vaccine viruses were specific with their homologous viruses but only one of three Saukett MAs was found suitable for intratypic serodifferentiation. A total of 112 poliovirus strains isolated from specimens of human or sewage origin in Canada from 1962 to 1981 were tested with these MAs. Approximately 90% of the virus isolates tested confirmed the findings previously obtained in the antigenic marker assays. Either pools or panels of individual MAs are suitable for the characterization of poliovirus isolates. Preliminary results of experiments conducted with pools of MAs and with single MAs added in various sequences, demonstrated that the location of the virus epitopes played an important role in the neutralization process.
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In this report we present 21 instances in which live rubella virus was isolated from synovial fluid obtained from 6 cases of inflammatory oligoarthritis or polyarthritis over a period of 2 years in the absence of firm clinical evidence of rubella. In 3 cases (cases 1, 2, 6,) a persistent oligoarthritis predominantly affecting the knee joints occurred in 2 adult women and one man, lasting to date 27, 29, and 18 months respectively, and in one of these cases virions were found in cells of the synovial membrane. In case 3 a boy of 9 presented with an illness indistinguishable from the systemic variety of juvenile chronic arthritis (Still's disease). In case 4 a young man with persistent monoarthritis was found to have ankylosing spondylitis, and in case 5 a progressive erosive polyarthritis developed 5 years after an attack of rubella complicated by rubella arthritis. The virus was identified by a variety of virological techniques and infection confirmed by immunofluorescence and (in one case) electron microscopy.
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Male and female patients suffering from rheumatoid arthritis with normal renal function or with renal impairment were treated in hospital with 300 mg of fenbufen 8 hourly for fourteen days. Concentrations of fenbufen and its principal metabolites were measured by high pressure liquid chromatography on days 0, 7, 10 and 14 and also four days after discontinuation of the drug. Renal impairment does not produce cumulation of either fenbufen or its major metabolites in the plasma. The metabolite profile of the drug was similar to that observed in patients with normal renal function.
A cytopathic agent indistinguishable from rubella virus was isolated from the synovial fluid of five patients (two male and three female). In two patients isolations were made on two separate occasions, and in two others on five separate occasions. The patients ranged in age from 9-58 years, and they presented with a variety of clinical syndromes. In particular, none had clinical features suggestive of recent rubella infection; but most cases had very high serum rubella haemagglutination inhibition titres. The identity of the cytopathic agent was shown by a variety of virological techniques to be rubella virus.