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Biomedical subjects

M A Robertson

Publications and source records attributed to M A Robertson.

At least 37 records · Page 2Linked to original sources
PubMed1995

Successful treatment of supraventricular tachycardia-induced cardiomyopathy with amiodarone: case report and review of literature.

Permanent junctional reciprocating tachycardia (PJRT) is a rare cause of supraventricular tachycardia in the pediatric population and is resistant to most pharmacological therapy. A case of supraventricular tachycardia that, on the basis of postnatal electrocardiographic and Holter monitor evidence, was diagnosed as PJRT and presented in utero as an atypical tachycardia with severe tachycardia-induced cardiomyopathy confirmed postnatally is presented. It is the only case of which the authors are aware that was controlled in the neonatal period by amiodarone and that resulted in complete resolution of systolic dysfunction. The literature discussing how tachycardia may induce cardiomyopathy and the use of amiodarone in treatment both pre- and postnatally are reviewed.

Adult↗
PubMed1994

Isosmotic modulation of cell volume and intracellular ion activities during stimulation of single exocrine cells.

Stimulation of salivary secretion is associated with a rise of [Ca2+]i in acinar cells. We examined the osmotic and ionic consequences of activation of Ca(2+)-dependent K+ and Cl- channels, by simultaneous optical determinations of cell volume and [Ca2+]i, [Cl-]i or [Na+]i during muscarinic stimulation of single salivary acinar cells, using a differential interference contrast (DIC)-fluorescence microscope. Carbachol caused a rapid rise of [Ca2+]i, as well as a substantial cell shrinkage. Despite variability in the level and kinetics of the subsequent sustained phase of the [Ca2+]i response, cell volume was correlated with [Ca2+]i in all cases. Elevated [Ca2+]i was both necessary and sufficient to cause these changes in cell volume. The proposition that changes in cell volume reflected changes in cell solute content was confirmed by simultaneously measuring [Cl-]i and cell volume. Simultaneous determinations of cell volume and [Na+]i indicated that the initial cell shrinkage was due entirely to K+ and Cl- efflux. Subsequent to the initial shrinkage, [Na+]i rose to high levels, primarily due to activation of Na+/H+ exchange. Thus, modulation of ion transport activities under isosmotic conditions results in substantial changes in cell solute content and cell volume. Subsequent to the early Ca(2+)-induced changes in these parameters, other transporters become active, but it is unclear what signals their activation. Cell swelling by osmotic dilution of the bath resulted in compensatory cell shrinkage (RVD) which was sensitive to K+ and Cl- gradients. Nevertheless, a rise of [Ca2+]i was not necessary for RVD. Osmotic shrinkage and/or cell acidification were insufficient to activate Na+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1994

Na+ transport pathways in secretory acinar cells: membrane cross talk mediated by [Cl-]i.

Fluid secretion by epithelial cells can be modulated by agents that activate Cl- channels in the apical membrane. To sustain secretion, Cl- influx across the basolateral membrane must also be accelerated. To examine the cellular mechanisms that couple Cl- efflux across the apical membrane to Na(+)-coupled Cl- entry across the basolateral membrane, we employed optical imaging techniques, utilizing single rat salivary acinar cells. Na+ influx was negligible in resting cells but was rapidly increased by carbachol due to activation of a Na(+)-H+ exchanger, a Na(+)-K(+)-2Cl- cotransporter, and, most likely, a nonselective cation channel. Receptor stimulation was not necessary, since elevation of intracellular Ca2+ concentration ([Ca2+]i) by thapsigargin activated the Na+ transporters at equivalent rates. Cell acidification, activation of protein kinase C, cell shrinkage, and other events associated with the rise of [Ca2+]i had little effect on Na+ transport in resting cells. Nevertheless, stimulation of cells in a medium that prevented normal Ca(2+)-induced cell shrinkage prevented activation of all three transport pathways. The block of the activation was not overcome by osmotic shrinkage but was relieved when [Cl-]i was allowed to fall, including conditions in which [Cl-]i fell in the absence of cell shrinkage. Activation of a Na(+)-H+ exchanger, Na(+)-K(+)-2Cl- cotransporter, and nonselective cation channel therefore exhibits a requirement for agonist-induced fall in [Cl-]i. Low [Cl-]i may create a permissive environment for Ca(2+)-dependent activation of multiple Na(+)-transport pathways, providing a mechanism for cross talk that coordinates transport activities of the apical and basolateral membranes in secretory epithelial cells.

Animals↗
PubMed1994

Membrane crosstalk in secretory epithelial cells mediated by intracellular chloride concentration.

Fluid secretion by epithelial cells is modulated by agents which activate Cl- channels in the apical membrane. To sustain secretion, Cl- influx across the basolateral membrane must also be accelerated. To examine cellular mechanisms which couple Cl- efflux across the apical membrane to Na(+)-coupled Cl- entry across the basolateral membrane, we employed optical imaging techniques utilizing single rat salivary acinar cells. Na+ influx was negligible in resting cells, but was rapidly increased by carbachol due to activation of a Na(+)-H+ exchanger, Na(+)-K(+)-2Cl- cotransporter and likely a non-selective cation channel. Receptor stimulation was not necessary since elevation of [Ca2+]i by thapsigargin activated the Na+ transporters at equivalent rates. Cell acidification, activation of protein kinase C, and cell shrinkage, other events associated with the rise of [Ca2+]i, had little effect on Na+ transport in resting cells. Nevertheless, stimulation of cells in a medium which prevented normal Ca(2+)-induced cell shrinkage prevented activation of all three pathways. The block of the activation was not overcome by osmotic shrinkage, but was relieved when intracellular Cl- concentration ([Cl-]i) was allowed to fall, including conditions in which [Cl-]i fell in the absence of cell shrinkage. Activation of a Na(+)-H+ exchanger, Na(+)-K(+)-2Cl- cotransporter, and non-selective cation channel therefore exhibit a requirement for agonist-induced fall in [Cl-]i. Low [Cl-]i may create a permissive environment for Ca(2+)-dependent activation of multiple Na+ transport pathways, providing for crosstalk which coordinates transport activities of apical and basolateral membranes in secretory epithelial cells.

Animals↗
PubMed1993

Polymerase chain reaction approaches to Culicoides (Diptera: Ceratopogonidae) identification.

Molecular genetic approaches such as polymerase chain amplification (PCR) of target genomic sequences are finding wide application in systematic and taxonomic studies of arthropods. PCR-based techniques that preclude the need for target DNA sequence information of the species of interest facilitate molecular taxonomic studies. Two such techniques, tDNA-PCR (DNA encoding tRNAs is the analyte) and RAPD-PCR (randomly amplified polymorphic DNA) were investigated for their ability to differentiate certain North American Culicoides spp. larvae and adults.

Animals↗
PubMed1991

Right pulmonary artery obstruction after pulmonary artery banding.

Serial assessment of pulmonary artery flow by Doppler echocardiography was carried out in 15 infants after pulmonary artery banding. Three infants were identified as having branch pulmonary artery obstruction based on diastolic pulmonary artery flow. It is concluded that this flow profile may be specific for branch pulmonary artery obstruction after pulmonary artery banding.

Arterial Occlusive Diseases↗
PubMed1989

[Implantation of collagen coated hydroxyapatite particles. A clinical-histological study in humans].

In this study, histologic behaviour of collagen coated hydroxylapatite particles implanted in human periodontal osseous defects has been analyzed. This material was surgically implanted in four patients, and reentry and block biopsies were carried out 4 and 6 months later. The histologic results demonstrate that this material is well tolerated by surrounding tissues, not eliciting an inflammatory reaction. At four months, the hydroxylapatite particles appear encapsulated by a very cellular connective tissue and at 6 months are found in direct contact with osteoid and mature bone. This material acts as a filler material, being fully biocompatible and stimulating an osseoconductive reaction of the adjacent alveolar bone.

Biocompatible Materials↗
PubMed1988

Genotyping and sequence analysis of apolipoprotein E isoforms.

Apolipoprotein E (apoE), a polymorphic plasma protein, is essential for catabolism of lipoproteins by receptor-mediated endocytosis. One of the apoE isoforms (E2) differs in its binding affinity to specific receptors and contributes to variations in lipoprotein metabolism. Diagnosis of apoE isoforms is done by isoelectric focusing, but it is hindered by various degrees of post-translational sialylation of the apoE protein. Electrophoretically silent structural variations may also escape detection by this technique. We describe a method for genotyping apoE based on hybridization of allele-specific oligonucleotides with enzymatically amplified genomic DNA, which permits unambiguous diagnosis of six common apoE phenotypes within 24 h. Among 100 E2 alleles present in 81 unrelated individuals genotyped by this technique, we found two rare structural mutants of apoE in addition to the common E2 form, E2(158Arg----Cys). Automated sequencing of amplified DNA identified the rare mutants as E2(136Arg----Ser) and E2(145Arg----Cys). The genotypic method may complement or even replace isoelectric focusing for routine determination of apoE phenotypes and for identification of rare structural variants.

Alleles↗
PubMed1987

The dysplastic pulmonary valve: echocardiographic features and results of balloon dilatation.

The feasibility of using balloon dilatation to relieve stenosis caused by dysplasia of the pulmonary valve was assessed in seven patients (five female, mean age two years) with angiographically confirmed dysplasia who were identified among 38 patients with pulmonary valve stenosis selected for balloon dilatation over a two year period. The clinical features in three patients were consistent with Noonan's syndrome. In all patients the gradient across the valve was assessed by cross sectional echocardiography and Doppler echocardiography before cardiac catheterisation. Balloon dilatation was performed by conventional techniques. In one patient, who had balloon dilatation in the operating room before surgical valvectomy, the diameter of the valve orifice increased from 3 mm to 10 mm. Inspection showed a tear along the anterior commissure. The mean (SD) pressure gradients between the right ventricle and pulmonary artery before and immediately after dilatation in five patients were not significantly different (58 (28) and 47 (12) mm Hg) respectively. There was no overall significant change in the degree of stenosis when four of these patients were examined by Doppler echocardiography six months after operation (44 (17) mm Hg), although one patient (case 5) did show a significant reduction in gradient. This patient had angiographic and echocardiographic features of dysplasia and commissural fusion. Several echographic features were common to all patients and distinguished them from cases of typical pulmonary valve stenosis. These were: pronounced thickening of leaflets; leaflet immobility in diastole and systole; no dilatation of the sinuses of Valsalva in diastole, and supra-annular narrowing. These poor results of balloon dilatation suggest that commissural fusion is not an important mechanism for causing stenosis in the dysplastic pulmonary valve. When dysplasia of the pulmonary valve is identified clinically and echocardiographically, balloon dilatation is unlikely to improve haemodynamic function; it should be attempted if commissural fusion is present.

Angioplasty, Balloon↗
PubMed1981

Peripheral nerve function in patients with bronchial carcinoma. Comparison with matched controls and effects of treatment.

Clinical examination of 80 patients with bronchial carcinoma showed minor neurological abnormalities but in only a few cases were these considered to be due to neuromyopathy. Spontaneous activity in the EMG was shown in 35%, consistent with a mild degree of partial denervation; when 50 of the patients were matched with 50 controls the patients showed a small but significant impairment of nerve conduction velocity in comparison with the controls. These findings accord with subclinical neuropathy in a high proportion of patients with bronchial carcinoma consistent with primary axonal change. Thirty patients participated in a prospective study of the effects of treatment. Of these nine were reassessed following surgery or radiotherapy. Although there was a trend towards improvement in sensory conduction there was no consistent change in the electromyographic findings.

Bronchial Neoplasms↗
PubMed1978

Specific changes in the oligosaccharide moieties of VSV grown in different lectin-resistnat CHO cells.

The carbohydrate moieties of the G glycoprotein of vesicular stomatitis virus (VSV) grown in three distinct lectin-resistant (LecR) Chinese hamster ovary (CHO) cell lines have been compared by fine structural analysis of radiolabeled glycopeptides. The mutant WgaRIII, selected for resistance to wheat germ agglutinin (WGA), produces VSV containing G glycoprotein specifically lacking in sialic acid. The mutant PhaRI, selected for resistance to phytohemagglutinin (PHA) and previously shown to lack a particular glycoprotein N-acetyl-glucosaminyl-transferase activity, produces VSV containing G glycoprotein specifically lacking terminal N-acetylglucosamine-galactose-sialic acid sequences and possessing an increased number of mannose residues in the "core" region of its carbohydrate moieties. The mutant PhaRIConARII, a "double" mutant selected from PhaRI cells for resistance to concanavalin A (ConA), produces VSV containing G glycoprotein with a further alteration in the mannose residues of the "core" oligosaccharide region. We discuss the relevance of these findings to the mechanisms of glycoprotein biosynthesis in mammalian cells and to the biochemical bases of lectin resistance in CHO cells.

Cell Line↗