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  • 1965-1969  (8)
  • 1
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 160 (1968), S. 759-771 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Mice of the RF and C57 black strains, fed an adequate diet, were donors and recipients of subcutaneous tissue implants. Abundant ceroid formed in implants of liver, heart, and adrenal. The pigment developed concurrently with degenerative changes in hepatocytes and myocardial fibers. Ceroid was intracellular in implants of adrenal gland and limited to cortical cells. Skeletal muscle and multilocular fat cells were next most productive sources of ceroid. Unilocular fat cells produced only traces. Isogeneic and allogeneic implants of corresponding tissues revealed comparable amounts of ceroid after two weeks of transplantation. Formation of pigment was correlated with the type of tissue transplanted rather than to specific host-graft responses.Implants of liver tissue were an ideal model for studying genesis of ceroid pigment. Granules of ceroid appeared first at the periphery of the implant in tissue adjacent to obviously degenerating cells of the graft. These small granules of pigment were then engulfed by macrophages. In most instances liposis preceded formation of ceroid. The presence of large amounts of lipid in the tissue at time of implantation did not augment ceroid formation. Hyper- and hypovitaminosis E, choline deficiency (to produce fatty livers), hyperestrogenism, and the administration of immunosuppressive drugs to recipients failed to influence appreciably the production of ceroid. In livers and other tissues containing little fat a relatively rapid post-implantation liposis preceded ceroid formation.
    Additional Material: 3 Tab.
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  • 2
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Mice were given a single injection of cortisone acetate and killed from one to seven days later. Arterial lesions occurred first and were predominantly located in the right ventricle. Hyalin was present in media of these coronary arteries within 24 hours following administration of cortisone. Exudative and proliferative changes in the arterial walls and perivascular spaces followed medial hyalinization. The highest incidence of arterial lesions (90%) was attained on the third day following cortisone injection and then decreased slightly (57%) by the seventh day. Myocardial necrosis was observed first in mice killed 48 hours after receiving cortisone and the incidence did not change significantly thereafter.
    Additional Material: 1 Tab.
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  • 3
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Mice received cortisone alone or concurrently with injections of estrone or diethylstilbestrol.Cortisone alone produced a high incidence of myocardial necrosis and abscesses in hearts, livers, lungs and kidneys. Staining and culture methods showed bacteria in these abscesses. The same technics failed to show infections in the mice receiving estrogen. Unrelated to other lesions the ventricular myocardium and walls of coronary arteries often contained accumulations of fat. Following concurrent injections of cortisone and an estrogen (estrone or diethylstilbestrol) the incidence of medial hyalinization of coronary arteries was 90%-98%. Edema, hemorrhage and hyalinization were observed in the aorta. In the cortisone plus estrogen groups such mural lesions of vessels developed in the absence of bacterial infection as studied by the above methods. The same was true when such infections were prevented by penicillin. The incidence of inflammatory lesions was less in mice receiving both cortisone and estrogen than in the cortisone (alone) group. Frequency of cortisone-induced myocardial necrosis and accumulation of myocardial fat were not altered by the estrogens.
    Additional Material: 2 Tab.
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 161 (1968), S. 23-35 
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Mice (Taconic Swiss) were fed a high-fat (28% lard), low-protein (8% casein), lipotropic-deficient diet for 1-90 days. For 21 days parenchymal liposis was greatest in peripheral and outer middle zones of the lobule. During 21-90 days fat increased in central and middle zones and decreased in peripheral zones.Ceroid pigment developed in Kupffer cells within 12 days. During 31-45 days Kupffer cells coalesced and formed large ceroid globules which increased in size and number during the 46-90 day period. A reticular fibrosis surrounded the masses of ceroid.As early as seven days stromal distortion consisting chiefly of compression of reticulum by fat laden hepatocytes was prominent in peripheral lobular zones. Sinusoids were also obstructed and dilated by this process. Some became non-functional and were transformed to fibrous cords. With progressive liposis (after 30 days) irregular stromal changes developed in all zones of lobules.
    Additional Material: 1 Tab.
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  • 5
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: In DBA mice, 12-16 months of age, receiving an adequate commercial diet the incidence of ventricular myocardial necrosis and calcification was 48% and that of pericardial calcification was 12%. Atrial thrombosis did not occur. Young adult mice of the same strain were fed a high-fat (28% lard), low-protein (8% casein) diet, with and without lipotropic supplement of betaine, for 48 weeks. The incidence of ventricular myocardial necrosis and calcification increased significantly over the spontaneous level with the greatest frequency (95%) occurring in the betaine-supplemented group. Pericardial calcification also increased with the highest incidence (100%) in the non-supplemented animals. Dietary induced atrial thrombosis reached lethal dimensions (80%) for most animals in the betaine-supplemented group within 12 weeks. The non-supplemented animals had less atrial thrombosis (50%) and greater longevity. Frequency and types of lesions observed were similar to those which occur in other strains of mice fed the same diet. The genetic susceptibility to spontaneous cardiac lesions did not appear to predispose the DBA mice to a greater sensitivity to dietary induced lesions, but may have contributed to the calcification which characterized the lesions. Dietary betaine seemed to influence significantly the production of a higher incidence of cardiac damage.
    Additional Material: 1 Tab.
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  • 6
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 123 (1968), S. 429-439 
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Daily subcutaneous injections of cortisone acetate (0.5, 1.5 or 2.5 mg) were given to three groups of mice for seven consecutive days. Daily systolic blood pressures of the anesthetized mice were obtained by adapting the method of Friedman and Freed ('49). The maximal arterial pressure increase for the 0.5, 1.5 and 2.5 mg groups was 22%, 31% and 41% respectively. This supports the conclusion that cortisone produces hypertension in mice when administered in large doses. Mural hyalinization, vacuolization and cellular proliferation of coronary arteries were greatest in the 0.5 mg group. The highest incidence of myocardial necrosis, 56%, was in the group receiving 2.5 mg of cortisone daily. The frequency and severity of myocardial and renal cortical necrosis were directly related to the size of the cortisone dose. Adrenal medullary vacuolization and lipid infiltration of the liver were common in all experimental groups.
    Additional Material: 4 Ill.
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  • 7
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Nine edible oils or fats (hydrogenated coconut, cod liver, Wesson, linseed, olive, butter, lard, corn and cocoa-butter) were fed for 50-90 days to study the relation of saturation, chain length and essential fatty acid content to production of cardiovascular lesions. The specific oil or fat (selected for ranges in the above variables) was used as the dietary lipid in a high-fat (28%), low-protein (8%), hypolipotropic diet. Half of the animals received identical diets containing choline chloride (2 gm/100 gm of diet) as a lipotropic supplement.Atrial mural thrombosis and ventricular myocardial necrosis and calcification developed in all dietary groups. Atrial thrombosis was the most frequent lesion. The greatest incidence of atrial thrombosis occurred in mice fed the choline-deficient, butter-containing diet (92%) and the lowest incidence with the supplemented cod liver oil diet (20%). The diet containing unsupplemented hydrogenated coconut oil produced the greatest incidence of ventricular necrosis (79%) and that with choline-supplemented cocoa-butter the lowest (8%). Ventricular calcification was most extensive within the unsupplemented cod liver oil group (83%), most limited in the supplemented lard group (5%). In general, choline-supplemented diets produced a lower incidence of cardiac damage. Little correlation existed between the composition and characteristics of specific fats and their activity in producing the specific cardiac lesions observed here.
    Additional Material: 2 Tab.
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  • 8
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 118 (1966), S. 391-409 
    ISSN: 0002-9106
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Mice of the highly inbred C strain were used. Of these 146 were fed a completely adequate diet. These were 10-66 weeks old when killed. Beginning at 3-4 months of age 45 mice were fed a diet high in fat (40% lard), low in protein (8% casein) and deficient in lipotropic substances for 4-66 weeks.Livers were not fatty in mice fed the adequate diet. Hepatic fibrosis developing within 24 weeks of age, and increasing with age, was observed in more than 60% of these control mice. Fibrosis was usually subcapsular, but in some instances was perivenous or intralobular. Reticular fibers were the chief component.In those fed the atypical diet the livers were fatty in all mice killed during the 4-66 weeks of the study. At approximately 20 weeks liposis declined from the large amounts present earlier (4-18 weeks). Until 52 weeks most of the lipid was located in fatty cysts. Subsequently the livers became excessively fatty. Parenchymal necrosis was limited to three mice. Parenchymal hyperplasia was lacking.In the dietary group of mice there were three patterns of hepatic fibrosis. Subcapsular fibrosis developed within a month and was the most common type. Another type consisted of fibrous septa extending chiefly from central veins. Linkage of septa produced pseudolobulation or pseudoencapsulation of areas of parenchyma. The least common type was an intralobular fibrosis which was unrelated to the capsule or to veins. All three types consisted initially of reticular fibers. Collagen was present in subcapsular and perivenous fibrosis within 16 weeks and in the intralobular type by 52 weeks.
    Additional Material: 3 Tab.
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