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Biomedical subjects

E G Olsen

Publications and source records attributed to E G Olsen.

At least 55 records · Page 3Linked to original sources
PubMed1986

Detection of Coxsackie-B-virus-specific RNA sequences in myocardial biopsy samples from patients with myocarditis and dilated cardiomyopathy.

Full-length virus genomic RNA (7.4 kilobases; kb) was isolated from Coxsackie B2 virus purified from infected monkey kidney cells in culture. DNA complementary to 6.3 kb of virus RNA was prepared by reverse transcription and cloned in a plasmid vector. A 1.6 kb Coxsackie-B-virus-specific DNA clone derived from the conserved 3' region of the virus genome was used as a hybridisation probe to test for the presence of virus nucleic acid sequences in myocardial biopsy samples. Positive hybridisation signals, quantified by densitometry, were obtained with 9 of 17 samples from patients with histological evidence of active or healing myocarditis or dilated cardiomyopathy with inflammatory changes. No Coxsackie-B-virus-specific sequences were detected in 4 samples from patients in whom a viral aetiology was unlikely and the histological diagnosis was negative for myocarditis.

Adolescent↗
PubMed1986

Damage of porcine aortic valve tissue caused by the surfactant sodiumdodecylsulphate.

The Hancock T6 treatment uses 1% sodiumdodecylsulphate (SDS) to prevent or delay calcification in porcine aortic or pericardial bioprostheses. In the current study fresh and glutaraldehyde fixed porcine aortic cusps were treated in 1% SDS. The hydrothermal stability, the histological and the electronmicroscopic appearance of the tissue were assessed and compared before and after treatment. The results suggest that the 1% SDS solution destroys the fresh material causing acellularity, extreme fragmentation and swelling of the collagen, together with a significant loss of hydrothermal stability. Glutaraldehyde fixation prior to SDS treatment seems to provide protection against the harmful effects of the 1% SDS, with only one exception on electronmicroscopic examination where foci of collagen degeneration were found.

Animals↗
PubMed1986

Timolol and cornea.

The influence of timolol on the corneal epithelium and endothelium was studied in organ culture. The cell morphology was not influenced by drug concentrations less than or equal to 690 micrograms/ml. Cell death was observed at 6900 micrograms/ml. Endothelial cell proliferation after an experimental injury was slowed down at a drug concentration of 690 micrograms/ml. Injurious effects were not observed at the drug concentrations found in the aqueous humour by use of ophthalmic eye solution in eyes with a normal cornea. However, it may be indicated to use eye drops with reduced concentration of timolol in conditions facilitating the resorbtion of the drug.

Animals↗
PubMed1986

Peripartum heart disease: an endomyocardial biopsy study.

Endomyocardial biopsies were performed in 11 African women in Nairobi who presented with the clinical features of peripartum cardiomyopathy. The samples were studied by light and electron microscopy. In five patients there was evidence of a "healing myocarditis", that is the presence of a mild inflammatory cell infiltration within the myocardium with foci of necrosis and variable amounts of hypertrophy and fibrosis. Of the nine patients who were followed up, three out of four with myocarditis had persistent heart failure and four out of five without myocarditis improved. Peripheral blood T lymphocyte cell subsets were measured in nine patients by means of monoclonal antibodies. A high helper:suppressor T cell ratio was found in three patients. Almost half of this group of patients with peripartum cardiomyopathy had myocarditis in their biopsy specimens. The myocarditis may have been due to an inappropriate immunological reaction in some patients.

Adolescent↗
PubMed1985

The pathogenesis of eosinophilic endomyocardial disease in patients with carcinomas of the lung.

Studies were done on a patient with a carcinoma of the lung induced by hypereosinophilia who was thought to be at risk from developing eosinophilic endomyocardial disease to see whether the development of heart disease could be related to abnormalities in the morphology or kinetics of blood eosinophils. The patient was a 61-year-old man who had a partial resection of a squamous cell bronchial carcinoma of anaplastic large cell type which has spread locally. Seven months later, he developed a blood eosinophil count of 33.9 x 10(9)/1. There were only transient responses to treatment with steroids and tumor irradiation, and he died 15 weeks later. Up to 3 x 10(9)/1 blood eosinophils were degranulated, correlating with serum levels of eosinophil cationic protein. The blood half-life of 111indium-labeled eosinophils was prolonged to 53 h, but their distribution was normal. Although an unsuccessful search was made during life for the development of endomyocardial damage, at postmortem the left ventricle had features of eosinophilic endomyocardial disease in the acute necrotic stage. Among 13 other reported patients with carcinoma of the lung and hypereosinophilia, three also had endomyocardial disease or myocardial lesions. These findings confirm the suggestion that the presence in the blood of greater than 1 x 10(9)/1 degranulated eosinophils can be used to predict the development of eosinophilic endomyocardial disease before it becomes apparent clinically, and they also add weight to the hypothesis that blood eosinophil degranulation causes this complication of hypereosinophilic states.

Blood Proteins↗
PubMed1985

Histopathologic aspects of viral myocarditis and its diagnostic criteria.

The morphologic criteria in diagnosing myocarditis are detailed. In fulminant cases, apart from the inflammatory infiltrate which often consists of chronic inflammatory cells, necrosis is found, frequently in the form of myocytolysis. Two groups of patients are analyzed. The first consisted of 214 cases who were clinically suspected of suffering from myocarditis. In 50% of these cases, the clinical suspicion was confirmed by morphologic examination of tissue obtained by endomyocardial biopsy. The other group of patients were suspected of having dilated cardiomyopathy and consisted of 1200 patients; in 300 of these patients, myocarditis was diagnosed morphologically by biopsy. Following sequential biopsies monitoring the response to treatment with corticosteroids and immunosuppressive agents, a classification into active, ongoing, resolving (healing), or resolved (healed) forms has been advanced. The different stages depend on the severity of the inflammatory infiltrate, the site of the inflammatory cells, the presence or absence of necrosis of adjacent myocardial fibers, and the degree of fibrosis. It has been emphasized that clear concepts and a uniform approach are essential in diagnosing myocarditis, not only to achieve precise diagnosis, accurately monitoring the response to therapy, but also in helping to establish the pathogenetic pathways for certain forms of cardiomyopathy.

Acute Disease↗
PubMed1985

An endocrine experimental model for myofibrillar disarray as found in hypertrophic cardiomyopathy.

The various etiologic suggestions for hypertrophic cardiomyopathy in man have been reviewed and experimental studies for endogenous pathways have been investigated experimentally. Intramuscular administration of triac to adult rats resulted in severe myocardial hypertrophy but no disarray. When studying the effect of triac on the myocardium of developing rats profound changes of disarray as well as hypertrophy were produced, mimicking the ultrastructural changes of hypertrophic cardiomyopathy in man. By using a variety of compounds with beta-adrenergic blocking action or predominantly membrane stabilizing properties or agonist action together with triac, the site where triac exerts its effect has been shown to be the cell membranes. A mechanism for production of cellular disarray has been delineated. Extrapolating to man, these experiments lend support to the suggestion that an endogenous hormonal mechanism may be operative in some patients with hypertrophic cardiomyopathy.

Adrenergic beta-Antagonists↗
PubMed1985

Influence of colchicine on the healing of corneal endothelium.

The healing of a corneal endothelial defect involves cell division and cell migration. Microtubuli form the spindle-fibers and parts of the cytoskeleton, and may therefore play a role in these cellular processes. In the present study colchicine is used in tissue culture to inhibit the assembly of microtubuli. Colchicine causes not only an arresting effect on cell division in the metaphase, but also an inhibitory effect on the cell migration. This latter effect is demonstrated by the radially directed, spindle-shaped cells seen in the repair zone of the control corneas being replaced by flat rounded cells. In this respect, in the presence of colchicine, the corneal endothelial cells behave like fibroblasts and not like epithelial cells.

Animals↗
PubMed1985

Experimental epithelial ingrowth. Epithelial/endothelial interaction through a corneal perforation, studied in organ culture.

The interaction of confronting corneal epithelium and endothelium has been studied by cultivation of corneas with open perforating wounds. In some experiments, the epithelium and the endothelium were initially damaged adjacent to the perforation, and the repair capacity was reduced by adding steroids or colchicine to the culture medium. The specimens were examined by scanning electron microscopy. The epithelium covered the stromal walls of the open perforation within 3 days. In most experiments, the epithelium and the endothelium met at the cut edge of Descemet's membrane, and this appeared to be a stable situation. However, if the endothelium was damaged and had reduced repair capacity, the epithelium invaded Descemet's membrane. The clinical implication is that the risk of epithelial ingrowth is present in eyes with a pathological endothelium.

Animals↗
PubMed1985

Aspects of the surface morphology of the corneal endothelium. An experimental study.

The influence on the surface of the corneal endothelial cells of 1) storage temperature of the enucleated eye, 2) epithelial abrasio, and 3) endothelial linear abrasio, has been examined. The surface structure may change rapidly following these procedures. The treatment of the cornea before fixation for electron microscopy should be standardized and as short as possible.

Animals↗
PubMed1985

The role of microfilaments in the healing of the corneal endothelium.

Actin microfilaments are presumed to play a role in cell locomotion. The function of these filaments may be selectively suppressed by cytochalasin. A dose-dependent delay of the repair of a corneal endothelial defect by the application of cytochalasin in tissue culture has been observed by SEM. This observation confirms that the actin microfilaments are important for the endothelial repair.

Animals↗
PubMed1985

The corneal endothelial cell interface.

The apical edges of corneal endothelial cells have been separated along lines forming a crisscross pattern, by the help of a special method of preparation. The visualization by SEM of the lateral faces of the cells is thereby made possible. The separation leads to the formation of thin strands spanning the gap between the apical edges of adjoining cells. They are formed by stretching of the normal apical flaps. This stretching demonstrates that the main intercellular adherence is located at the tips of the apical flaps. The basal edges of the endothelial cells can be inspected, and it can be seen that the basal face of the cells has and irregular form. Threadlike processes extend from the basal cell edges. They ascend in the intercellular space and make contact with the lateral face of the neighbouring cell at varying levels. These processes are presumed to mediate intercellular transfer.

Animals↗
PubMed1985

Prevalence of overt dilated cardiomyopathy in two regions of England.

The prevalence of dilated cardiomyopathy was assessed in two regions in England from 420 replies to 771 questionnaires sent to general practitioners. Overall point prevalence was 8.317 per 100 000 population in areas covering a total sample of 913 836 inhabitants. There was a statistically significant regional variation between East Anglia (Norfolk, Suffolk, and Cambridgeshire) and Essex, Hertfordshire, and Bedfordshire. Though the natural history of dilated cardiomyopathy remains to be defined, this study has provided an assessment of point prevalence of overt cases of this condition.

Cardiomyopathy, Dilated↗