Biomedical subjects
G E Burch
Publications and source records attributed to G E Burch.
Of recording your own blood pressure.
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Of classification of cardiomyopathies.
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Encephalomyocarditis (EMC) virus infection of the femoral vein of newborn mice.
The EMC virus was found to infect and injure the femoral veins of newborn mice. EMC viral crystals were found in the advential fibroblasts of these veins. In view of the extensive damage observed in the extremely small amount of tissue examined electron microscopically, the extent of the viral phlebitis must have been considerable. The relationship of these findings to the pathogenesis of thrombophlebitis in man provokes interesting speculations.
Of simplyfying classification of WPW syndrome (left, right, and septal types of WPW syndrome).
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Keep legs up.
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Spherical aggregates of coxsackie B4 virus particles in mouse pancreas.
A high titer culture of Coxsackie B4 virus was used to induce pancreatitis in newborn mice. In animals sacrificed 1 or 2 days after intraperitoneal inoculation, we observed cytonecrosis consistent with picornaviral infection as well as necrosis indicative of pancreatitis. In addition, we observed aggregates of particles which seem to be Coxsackie B4 virus particles, some arranged in the typical picornaviral crystalloid lattice formation and others arranged into spherical masses approximately 102 nm in diameter. Depending upon the depth and orientation of section through the spherical aggregates, the particles were arranged into two patterns which were readily distinguishable. When the plane of section was through the center of the sphere, 10 particles circularly arranged around a dense particle core were observed. When the sphere was cut tangentially, the particles were arranged in a zig-zag pattern so that there were two concentric layers of at least 6 particles per layer, with no central core. Both crystalloid and spherical aggregates were observed free within acinocyte cytoplasm, and within autophagic vacuoles, cytosegresomes, and fine granular bodies of acinocytes, and within phagocytic vacuoles of macrophages. We conclude that the spherical aggregates represent a distinct crystalloid form of Coxsackie B4 virus during its replicative cycle, which may eventually develop into the more typical picornaviral crystalloid lattice configuration and that the spherical aggregates are located in foci of viral synthesis. Marked pathogenicity of Coxsackie B4 virus in the newborn mouse pancreas should be considered a factor in the observations noted.
Coxsackie viral infection of human myocardium.
The myocardiu m of a young patient who had clinically established cardiomyopathy and suspected Coxsackie virus B4 infection was studied. Coxsackie B4 viral antigen was found in the ventricular and atrial myocardium by specific immunofluorescent antibody staining. Histologic examination revealed varying degrees of myocardial damage. Interstitial fibrosis and edema, swelling and deterioration of hypertrophic muscle fibers, connective tissue proliferation, stasis of small coronary blood vessels, atrophy of myocardial fibers with pyknosis of nuclei, and lytic deterioration were observed. Electron microscopic examination showed portions of the Z bands to be either widened or displaced into the sarcomere. Adjacent cell membranes in the region of the intercalated disc in the myocardium of both the ventricle and the atrium were separated, forming large gaps. Morphologic changes were most pronounced in the atrium adjacent to the mitral valve, in which the mitochondria were grossly swollen, and large vesicles were present in the sarcoplasm. The pathologic changes found in the myocardium of all chambers of the heart apparently were due to Coxsackie B4 viral infection.
Survival in a coronary care unit.
The mortality among 253 patients with definite, acute myocardial infarction admitted to the coronary care unit (CCU) of the New Orleans VA Hospital during a two-year period is reported. Thirty-one (12.3%) of these patients died in the CCU. Five others died on the medical wards after release from the CCU. A total of 217 patients was discharged in good condition from the hospital after a minimal stay of three to four weeks, resulting in a survival rate of 85.8%.
The coronary arteries in active viral cardiomyopathies.
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Coxsackie B4 virus crystal formation in mouse pancreas.
For the first time, Coxsackie B4 virus crystals are demonstrated in tissues of animals inoculated with the virus. Until this report, Coxsackie B4 virus had never been found to form crystalline aggregates in tissues of any kind. The viral crystals which were located in the pancreas of newborn mice were associated with ultrastructural damage to the pancreas not observed in control animals, thereby indicating that viruses directly invade and damage these tissues. Thus, this virus must be considered among etiologic factors in pancreatic disease.
Use of digitalis and diuretics.
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Ultrastructural myocardial changes produced by viruses.
Some of the ultrastructural pathological alterations in the myocardium produced by viral infections with members of the picornavirus group are described. These alterations varied from mild to severe, with necrosis. In animals infected with Coxsackie B1 virus and EMC virus, readily identifiable viral crystals were frequently found in association with the myocardial lesions by means of electron microscopy. The electron microscope made it possible to study vary early myocardial changes which were not detected with the light microscope. Although the ultrastructural myocardial changes in rheumatic fever have received little attention, the light and electron microscopic findings in the myocardium and valves of the viral-infected animals described here closely resemble those described in man in association with so-called rheumatic heart disease. The type of investigations presented forms a good model for the study of the natural history of ultrastructural pathology produced in all parts of the heart by viruses.
Effects of cerebral angiography, pneumoencephalography, myelography and ventriculography on the electrocardiogram.
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Echocardiographic abnormalities of interventricular septum associated with "absent Q" syndrome.
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