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S M Factor

Publications and source records attributed to S M Factor.

At least 145 records · Page 8Linked to original sources
PubMed1981

Hypertensive-diabetic cardiomyopathy in the rat: an experimental model of human disease.

The authors recently described a group of diabetic patients with severe congestive heart failure, hypertension, and minimal coronary artery disease, who had significant myocardial degeneration apparently secondary to the combined effects of high blood pressure and diabetes on the heart. To evaluate the effects of hypertension and diabetes mellitus more fully, the authors studied four groups of rats with either no disease, streptozotocin-induced diabetes mellitus, renovascular hypertension, or a combination of hypertension and diabetes. They employed semiquantitative light microscopy, which revealed significantly greater replacement fibrosis in the hypertensive-diabetic rats when compared with the other three groups. Interstitial fibrosis was increased in the hypertensive-diabetic animals, though it was just below the 5% level of significance when compared with the hypertensives. Further analysis, however, revealed that those hypertensive-diabetic animals with the greatest relative cardiac hypertrophy, as measured by the heart weight/body weight ratio, had significantly increased interstitial fibrosis. Surprisingly, diabetes mellitus alone produced no morphologic light-microscopic alterations; yet 8 weeks of combined hypertension and diabetes mellitus led to myocardial degeneration similar to the human disease. These changes do not appear to be secondary to abnormalities of intramyocardial muscular vessels. Measurement of 3 parameters of vascular disease revealed that hypertensive animals with less myocardial damage had greater vascular changes than the more severely affected hypertensive-diabetics. This study provides evidence that the combination of diabetes mellitus and hypertension produces significantly greater myocardial lesions than either disease alone. The similarity of the lesions with those observed in human patients suggests that the hypertensive-diabetic rat is a useful model for elucidating the pathogenesis of clinical myocardial disease in patients with hypertension and diabetes mellitus.

Animals↗
PubMed1979

End-capillary loops in the heart: an explanation for discrete myocardial infarctions without border zones.

Separate perfusions of canine coronary arteries with colored silicone-rubber compound reveal that in the region where two microcirculations abut, capillaries derived from individual large vessels are discrete, with no interconnections. Terminal homologous capillaries from loops rather than anastomosing with heterologous capillaries. This anatomic arrangement may account for discrete myocardial infarctions without ischemic border zones.

Animals↗
PubMed1979

Mural vegetations at the site of endocardial trauma in infective endocarditis complicating idiopathic hypertrophic subaortic stenosis.

In two patients infective endocarditis developed as the primary manifestation of idiopathic hypertrophic subaortic stenosis. Infected vegetations were present on the mitral and aortic valves. In addition, bacterial vegetations were observed on the septal endocardium at the site of contact between the mitral valve leaflet and the hypertrophic septum. Thus, chronic endocardial trauma, a common finding in idiopathic hypertrophic subaortic stenosis, may provide a fertile nidus for the development of bacterial vegetation.

Aged↗
PubMed1979

Hereditary and acquired cardiomyopathies in experimental animals: mechanical, biochemical, and structural features.

Evidence has been presented regarding alterations of contractile behavior muscle biochemistry, and ulstrastructure during the course of the hereditary hamster cardiomyopathy. Also, preliminary structural and mechanical data were presented on the acquired cardiomyopathy of diabetes mellitus in experimental animals. In the hamster model, contractile performance, measured as isometric tension and rate of tension development, was shown to be depressed throughout the course of the disease, whereas normalized force-velocity relationships returned to normal only during the compensated stages of hypertrophy. Force-frequency relationships were depressed in myopathic muscles, indicating the presence of alterations in the muscle activation system, namely, the biochemical and functional integrity of the sarcoplasmic reticulum. Analysis of the contractile proteins in myopathic muscle has revealed depressions of Ca2+ activity in purified myosin in addition to an independently increased neutral protease activity that results in the specific degradation of LC2 of myosin. Sympathetic time and norepinephrine turnover increase progressively during the course of the disease. These changes are accompanied by decreasing tissue levels of neorepinephrine and increasing levels of dopamine, indicating a shift in the rate-limiting step for norepinephrine synthesis. Alterations were also noted in nuclear protein composition and serotonin levels. Microscopically, the myolytic and calcification changes that characterize the hamster cardiomyopathy have been confirmed. In addition, contraction bands and lysosomal changes have been observed that may relate to cateholamine hypersensitivity. In the experimental model of diabetic cardiomyopathy, a significant alteration in relaxation process was demonstrated despite the fact that peak tension development and its rate of development were unaltered. Also, the length dependence of contractile behavior was altered when compared to that of age-matched controls, indicating a potential loss of contractility reserve. When animals with combined hypertension and diabetes were studied, bothe contraction and relaxation processes were affected to a greater degree.

Actomyosin↗
PubMed1979

Static testicular imaging utilizing 201Tl.

Successful testicular imaging of rat and rabbit testes was achieved utilizing the radiopharmaceutical Thallium-201. These observations indicate the usefulness of Thallium-201 as an agent for testicular imaging and suggest a clinical application in localizing the impalpable testis in humans.

Animals↗
PubMed1978

Coronary intimal sclerosis in Morquio's syndrome.

Mitral valve, coronary arteries, cartilage, and liver were studied by light and electron microscopy in a 15 year old boy with Morquio's syndrome, a genetic mucopolysaccharidosis, in which a deficiency of lysosomal hexosamine sulfatase is associated with accumulations of keratan sulfate in various organs. Coronary artery intimal sclerosis was a prominent feature of this disorder. Ultrastructural examination revealed numerous intimal smooth muscle cells containing storage vacuoles consistent with lysosomes. This was associated with marked interstitial deposition of collagen, elastin, and basement membrane material. Recent studies of human and experimental atherosclerosis have demonstrated the accumulation of cholesterol within vascular smooth muscle cell lysosomes. Intralysosomal accumulation of substrates other than cholesterol is also associated with vascular intimal sclerosis in genetic lysosomal disorders such as Fabry's disease and Hurler's syndrome. Lysosomal storage of undegraded substrate may be an important pathogenetic mechanism in the development of sclerotic vascular lesions.

Adolescent↗
PubMed1978

Endocardial fibroelastosis: myocardial and vascular alterations associated with viral-like nuclear particles.

Although clinical, immunologic, and experimental evidence exists implicating in utero viral infection of the myocardium in the development of primary endocardial fibroelastosis, the infectious etiology of this condition remains somewhat controversial. To date, specific features of viral myocarditis and morphological demonstration of viral particles have not been described in EFE. The present case is the first in which extensive light microscopic and ultrastructural analysis of the myocardium revealed abnormalities consistent with a primary viral myocarditis associated with typical EFE. These alterations consisted of chronic myocardial inflammation, extensive interstitial fibrosis, severe degenerative changes in myocardial cells, and a marked proliferation of endothelial cells in large nad small intramyocardial vessels leading to vascular occlusions. In support of the infectious etiology of this disease, similar features were noted in skeletal muscle. Most interestingly, viral-like particles were observed in many myocardial and endothelial nuclei. Although we are not absolutely certain of the viral nature of these particles, their appearance suggests viral assoicated material. We propose that the presence of these particles in this case in association with the other morphological alterations in support for the viral etiology of EFE. The prominent vascular occlusion observed in the myocardium may be an important clue to the pathogenesis of fibroelastosis as either a primary or secondary disease.

Cell Nucleus↗
PubMed1978

The histiocytic origin of the multinucleated giant cells in myeloma kidney.

A recent case of myeloma kidney disease was studied to determine the cellular origin of the syncytial multinucleated giant cell. Light, immunofluorescence, and electron microscopy of the giant cells revealed features characteristic of histiocytes. This finding contradicts the generally accepted conclusion that the giant cell represents a syncytial mass of degenerating or reactive tubular epithelial cells. We conclude that the giant cells arise in the interstitial tissues, migrate through breaks in the tubular basement membrane, and engulf and surround intratubular protein casts.

Aged↗
PubMed1978

The histologic border zone of acute myocardial infarction--islands or peninsulas?

Observation of isolated islands of apparently surviving myocardium within areas of necrotic tissue at the edge of myocardial infarctions has been interpreted by some as histologic evidence of a unique "border zone" region. Serial section reconstruction of transmural canine myocardial infarctions was performed in this study to establish whether these islands were truly isolated or were continuous peninsulas of tissue separated by the plane of section. Three-dimensional analysis of the infarcts revealed no true islands but instead demonstrated a region composed of highly complex interdigitating peninsulas. We conclude that there is an extremely irregular but sharp boundary demarcating normal and infarcted myocardium with no intermediate zone. This observation is discussed in relation to recent data, based on coronary blood flow and creatine phosphokinase analysis, which also demonstrates a sharp boundary between the normal and infarct zones.

Animals↗
PubMed1977

Carcinoma of the breast with multinucleated reactive stromal giant cells. A light and electron microscopic study of two cases.

Two unusual carcinomas of the breast are described, containing nests of infiltrating neoplasm situated within stromal lacunar spaces, and surrounded by numerous benign appearing multinucleated giant cells. Within the stroma, there was extensive hemorrhage, hemosiderin pigment deposition, and large numbers of mononucleated inflammatory cells. The morphology of both tumors resembled the giant cell tumor of bone. Although a similar giant cell reaction has recently been described in association with a uterine leiomyosarcoma, we are aware of only two other examples of this entity in the breast, both reported over 40 years ago in the French literature. This is the first report in which electron microscopy confirmed the benign histiocytic nature of the giant cells. These cells had many of the ultrastructural features of multinucleated giant cells described in tissue culture, skeletal osteoclastomas, and foreign body granulomas. We propose that the giant cells arise from fusion of mononucleated stromal cells, and most likely are reactive histiocytic elements which are in some way related to the tumor cell nests. Further studies of these unusual neoplasms are needed to determine if the giant cell reaction in any way affects the prognosis of the patient.

Adult↗
PubMed1977

Intralysosomal lipid in long-term maintenance transplant atherosclerosis.

Intralysosomal accumulation of lipid has been implicated as an important mechanism in the pathogenesis of atherosclerosis. Although atherosclerosis develops frequently in organ transplants maintained on a long-term basis, to our knowledge no studies to date have demonstrated the intracellular localization of the lipid in this setting. Light and electron microscopic study of a renal artery branch from a transplanted kidney maintained for 3 1/2 years demonstrates that the lipid is sequestered within intimal smooth muscle cell lysosomes. The features of the atherosclerotic plaque in long-term transplantation appear to be identical to spontaneous lesions or those induced experimentally.

Arteriosclerosis↗