Smith, L.; Lambert, M. A.*; Brochu, P.†; Jasmin, G.; Qureshi, I. A.*; Seidman, E. G. Author Information

The oxidative phosphorylation as well as calcium transporting properties of heart mitochondria and calcium transport activities of the fragments of the sarcoplasmic reticulum (microsomes) were studied during the life span of cardiomyopathic hamsters (UM-X7.1). Control healthy hamsters of the same age group were used for comparison. No changes in the oxidative phosphorylation ability of cardiomyopathic mitochondria were seen at early and moderate stages of heart failure; however, at severe stages, mitochondrial respiratory functions, but not the ADP:0 ratio, were impaired. Both creatine phosphate and ATP contents were decreased without any significant changes in the ATPase activities of myofibrils from the failing hearts. Heart mitochondria from cardiomyopathic animals at severe stages of failure exhibited less calcium binding and uptake activities in comparison with the control values whereas no changes in the mitochondrial calcium binding and uptake were seen in cardiomyopathic hamsters which showed no clinical signs of heart failure. Although mitochondrial calcium binding in cardiomyopathic hearts at early and moderate stages of failure was decreased, mitochondrial calcium uptake was not significantly different from the control. Microsomal calcium binding activity, unlike calcium uptake activity, was decreased in the hearts of cardiomyopathic hamsters without any signs of heart failure. Both calcium binding and calcium uptake activities of microsomes from animals with early, moderate and severe heart failure were less in comparison with the control values but were not associated with any changes in the Ca2+-stimulated ATPase activity. These results suggest that changes in the process of mitochondrial energy production and mitochondrial Ca2+-transport may be secondary to other factors whereas alterations in the sarcoplasmic reticular Ca2+-transport may lead to the development of heart failure in the cardiomyopathic hamsters.

The purpose of this study was to identify alterations in specific enzyme and Ca2+ binding activities in cardiac sarcolemmal fractions from UM-X7.1 myopathic Syrian hamsters during the development of cardiomyopathy. Experimental and healthy control animals were examined from 25 to 200 days of age. Sarcolemmal Na+, K+-ATPase activity was depressed in the myopathic hamsters throughout the time course of this study. Sarcolemmal ATP-independent Ca2+ binding was found to be depressed in experimental animals as early as 55 days of age. Ca2+ -stimulated, Mg2+ -dependent ATPase activity was depressed in the experimental animals by 90 days of age and this decrease in enzyme activity was accompanied by a decrease in ATP-dependent Ca2+ binding capacity of the sarcolemmal membranes. Mg2+ -ATPase and Ca2+ -ATPase activities were only affected in the latter stages of the disease (155 to 200 days old). NaF, epinephrine and Gpp(NH)p stimulation of the sarcolemmal adenylate cyclase activity was also observed to be attenuated during the latter stages of the disease. These defects in adenylate cyclase system of the sarcolemmal fraction appeared specific since basal adenylate cyclase activity was not altered at any age studied. The results demonstrate that the earliest lesions in sarcolemmal activity in myopathic hamster heart occur in Na+, K+-ATPase and ATP-independent Ca2+ binding capacity. These defects correspond temporally to the initial stages of cardiac necrotic development in this strain of myopathic hamster.

Terminal motor innervation and the histochemical profile of muscle fibers were investigated, before and after sciatic nerve crushing, in 1- to 150-day-old myopathic hamsters. The observed morphologic abnormalities in terminal motor innervation were of varying degree prior to the nerve injury. These abnormalities were found in close proximity to lesions of the myofibers, and became more pronounced with age and the progression of the disease process. Collateral ramification of healthy axons occurred in hamsters of 120 days of age with reinnervation of damaged muscle fibers. When submitted to sciatic nerve crushing, myopathic hamsters showed an ability to regenerate and reinnervate the subneural apparatuses. The regenerative process in these animals was essentially the same as in normal, sciatic nerve-crushed hamsters. Thus, it was concluded that the morphologic changes in terminal motor innervation were secondary to muscle cell degeneration.

We present the 8th case so far published of generalized giant axonal neuropathy. Many features of the neurological picture of this 8 year 8 month old boy were suggestive of progressive bulbar paralysis of childhood. Muscle and sural nerve biopsies disclosed typical nodular axonal swellings measuring between 10--29 nm. Ultrastructure of the inflated portions of the axon consisted almost exclusively of 10 nm filaments. Normally appearing constituents were found in the non-dilated portions of the axons with this particularity that glycogen and mitochondria were aggregated. Previous clinical and pathological evidence indicates that this rare disorder not only affects the peripheral nerves but also the whole CNS. Our case differs from the others reported in literature by its rapidly deteriorating course and by the prominent involvement of some brain-stem motor functions; we offer the theory that a link might be implicated between this entity and Fazio-Londe disease.

The first Canadian child with complete absence of alpha L-fucosidase is described. The neurological course was characterised by rapid deterioration and he died at the earliest age recorded so far. There are only two published reports of autopsies in this condition to which we add another, together with the ultrastructural findings of a liver biopsy.

Cyclic AMP content, adenylate cyclase (EC 4.6.1.1) activity and phosphodiesterase I (EC 3.1.4.1) activity of the hind leg skeletal muscle and cardiac muscle in 60- and 150-day-old normal and myopathic (UM-X7.1) hamsters were examined. In 60-day-old myopathic animals, cardiac cyclic AMP levels were higher and phosphodiesterase I activity was lower, without any changes in the basal adenylate cyclase activity, whereas in 150-day-old myopathic hamsters, cardiac cyclic AMP and basal adenylate cyclase activity were lower, without any changes in the homogenate phosphodiesterase I activity. On the other hand, basal adenylate cyclase and phosphodiesterase I activities in the skeletal muscle homogenate from 60- and 150-day-old myopathic animals were not different from the normal values but the skeletal muscle cyclic AMP levels were significantly less in 60-day-old myopathic hamsters only. The plasma cyclic AMP levels in 60-day-old myopathic hamsters, unlike 150-day-old myopathic animals, were higher than the normal. Although these results reveal differences in myopathic cardiac and skeletal muscles, it is concluded that changes in adenylate cyclase – cyclic AMP system in myopathy are dependent upon the degree of disease.

Cardiomyopathic hamsters (UM-X7.1) show clinical signs of congestive heart failure and an abnormal EKG pattern. The sarcolemmal fraction obtained from the failing hearts at advanced stages of myopathy exhibited no change in the basal adenylate cyclase activity; however, the activity of this enzyme in the presence of catecholamines or NaF was lower in the failing heart sarcolemma than that in the control. The activities of Ca2+-ATPase, Mg2+-ATPase, and Na+-K+-ATPase in the failing heart sarcolemma were also less than the control values. These results suggest an association of membrane defect with heart failure.

Annals of the New York Academy of SciencesVolume 156, Issue 1 p. 333-343 FACTORS INFLUENCING THE PRODUCTION OF CARDIOMYOPATHIES BY METHOXAMINE AND METARAMINOL* G. Jasmin, G. Jasmin Department of Pathology, University of Montreal Montreal, Canada Research associate of the Medical Research Council of Canada.Search for more papers by this author G. Jasmin, G. Jasmin Department of Pathology, University of Montreal Montreal, Canada Research associate of the Medical Research Council of Canada.Search for more papers by this author First published: January 1969 https://doi.org/10.1111/j.1749-6632.1969.tb16738.xCitations: 4 * These investigations were supported by a grant from the Medical Research Council of Canada. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 JASMIN, G. 1956. Etude de l'inflammation anaphylactoïde. Rev. Canad. Biol. 15: 107. 2 JASMIN, G. & P. BOIS. 1959. Influence des libérateurs d'histamine sur la production et la prévention des ulcères gastriques chez le rat. Rev. Canad. Biol. 18: 367. 3 JASMIN, G. & P. BOIS. 1960. Effect of various agents on the development of kidney infarcts in rats treated with serotonin. Lab. Invest. 9: 503. 4 JASMIN, G. & R. GARBAU. 1961. Histopathological study of muscle lesions produced by paraphenylenediamine in rats. Brit. J. Exp. Path. 42: 592. 5 JASMIN, G. & E. BAJUSZ. 1964. Etude pathogénique des lésions cardiaques rénales et musculaires provoquées chez le rat par la méthoxamine et le métaraminol. Rev. Canad. Biol. 23: 67. 6 BAJUSZ, E. & G. JASMIN. 1964. Influence of variations in electrolyte intake upon the development of cardiac necrosis produced by vasopressor amines. Lab. Invest. 13: 757. 7 RONA, G., D. S. KAHN & C. I. CHAPPEL. 1963. Studies on infarct-like myocardial necrosis produced by isoproterenol: A Review. Rev. Canad. Biol. 22: 241. 8 JASMIN, G. 1965. Cardiac, aortic and pulmonary lesions induced by vasopressors. Vasc. Dis. 2: 115. 9 JASMIN, G. 1966. Morphologic effects of vasoactive drugs. Canad. J. Physiol. Pharmacol. 44: 367. 10 SELYE, H. 1961. The Pluricausal Cardiopathies. : 114. Charles C Thomas. Springfield , III . 11 RONA, G., C. I. CHAPPEL, T. BALAZS & R. GAUDRY. 1959. An infarct-like myocardial lesion and other toxic manifestations produced by isoproterenol in the rat. Arch. Path. (Chicago) 67: 443. 12 BAJUSZ, E. & G. JASMIN. 196465. Enzyme histochemistry of some chemically induced cardiac necroses. II. Myocardial lesions induced by methoxamine. Z. Vitamin. Hormon. Fermentforsch. 14: 43. Citing Literature Volume156, Issue1Experimental “Metabolic” Cardiopathes and their Relationship to Hima Heart DiseaseJanuary 1969Pages 333-343 ReferencesRelatedInformation

Annals of the New York Academy of SciencesVolume 138, Issue 1 p. 186-198 HISTOCHEMICAL STUDIES ON DENERVATION, CHEMICALLY INDUCED AND HEREDITARY FORMS OF MYOPATHIES* G. Jasmin, G. Jasmin Medical Research Associate of the Medical Research Council of Canada and Department of Pathology, Faculty of Medicine, University of Montreal, Montreal, P.Q. CanadaSearch for more papers by this author G. Jasmin, G. Jasmin Medical Research Associate of the Medical Research Council of Canada and Department of Pathology, Faculty of Medicine, University of Montreal, Montreal, P.Q. CanadaSearch for more papers by this author First published: September 1966 https://doi.org/10.1111/j.1749-6632.1966.tb41165.xCitations: 8 * This work was supported by Grants from the Medical Research Council of Canada and the Muscular Dystrophy Association of Canada. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Jasmin, G. 1965. Comparative enzyme histochemistry of myopathies. Clinical myopathies. Symposium on Muscle Structure and Function, Univ. of Alberta, June 4, 1964.: 569. Pergamon Press, London . Google Scholar 2 Jasmin, G. 1966. Staining methods in muscle research. In Methods and Achievements in Experimental Pathology. E. Bajusz & G. Jasmin, Ed.. S. Karger, Basel and New York. Google Scholar 3 Dubowitz, V. & A. G. E. Pbarse. 1960. Reciprocal relationship of phosphorylase and oxidative enzymes in skeletal muscle. Nature 185; 701. 10.1038/185701a0 CASPubMedWeb of Science®Google Scholar 4 Engel, W. K. 1962. The essentiality of histo- and cytochemical studies of skeletal muscle in the investigations of neuromuscular disease. Neurology 12: 778. 10.1212/WNL.12.11.778 Web of Science®Google Scholar 5 Gendre, H. 1938. Aspects et localisations du glycogène dans le tissu musculaire strié. Bull. Histol. 15: 265. CASGoogle Scholar 6 Jasmin, G. 1965. Histochemical studies of intermyoflbrillar sarcoplasmic granules. Proc. Can. Fed. Biol. Soc. 8th Annual Meeting, June. Univ. of Ottawa, Ottawa . Google Scholar 7 Carmichael, G. G. 1963. A tetrazolium salt reduction method for demonstrating lipo-proteins in tissue sections. J. Histochem. Cytochem. 11: 738. 10.1177/11.6.738 CASWeb of Science®Google Scholar 8 Barka, T. &. P. J. Anderson. 1963. Histochemistry, theory, practice and bibliography. Hoeber Medical Division, Harper & Row Publishers, Inc., New York , N. Y. Google Scholar 9 Jasmin, G. & R. Gareau. 1961. Histopathological study of muscle lesions produced by paraphenylenediamine in rats. Brit. J. Exp. Pathol. 42: 592. CASPubMedWeb of Science®Google Scholar 10 Ernster, L. & R. Luft. 1963. Further studies on a population of human skeletal muscle mitochondria lacking respiratory control. Exp. Cell Res. 32: 26. 10.1016/0014-4827(63)90065-X CASPubMedWeb of Science®Google Scholar 11 Jasmin, G. & E. Bajusz. 1962. Symposium on Skeletal Muscle. Rev. Can. Biol. 21: 193. Google Scholar 12 Feng, T. P., H. W. Jung & W. Y. Wu. 1962. The contrasting trophic changes of the anterior and posterior latissimus dorsi of the chick following denervation. The effect of use and disuse on neuromuscular functions. Proc. of a Symp., E. Gutmann & P. Hnik, Ed.. Czechoslovak Acad. of Sci. : 431. Prague . Google Scholar 13 Takabatake, Y. 1963. A histological study on process during recovery of muscular dystrophy. Shikoku Acta Med. 19: 411. Google Scholar 14 Golarz, M. N., G. H. Bourne & H. D. Richardson. 1961. Histochemical studies on human muscular dystrophy. J. Histochem. Cytochem. 9: 132. 10.1177/9.2.132 CASPubMedWeb of Science®Google Scholar 15 Fennell, R. A. & W. T. West. 1963. Oxidative and hydrolytic enzymes of homozygous dystrophic and heterozygous muscle of the house mouse. J. Histochem. Cytochem. 11: 374. 10.1177/11.3.374 CASWeb of Science®Google Scholar Citing Literature Volume138, Issue1Experimental Primary Myopathies and their Relationship to Human DiseaseSeptember 1966Pages 186-198 ReferencesRelatedInformation

Following ligature of the main coronary veins in the rat, necrotic foci occur in the subepicardial muscle layers and massive calcification begins in the affected areas. This type of myocardial calcification—unlike the onset of necrosis—was significantly enhanced by parathyroidectomy. On the other hand, this enhancement was prevented by simultaneous thyroidectomy and could not be effected by replacement therapy with thyroxine. The alterations in the serum concentrations of calcium and inorganic phosphorus did not serve to explain the great difference in degree of myocardial calcification seen between the parathyroidectomized and thyroparathyroidectomized rats. It is postulated that some thyroid principle, apparently other than thyroxine, may be responsible for promoting the entry of various ions (such as calcium and phosphorus) into the degenerating tissue and thus may be a more important factor in the pathologic process than are variations in the levels of serum electrolytes.

Research Articles| October 24 2008 Studies on Factors that Selectively Influence Calcification in the Myocardium Subject Area: Cardiovascular System E. Bajusz; E. Bajusz From the Department of Pathology, University of Montreal, Montreal (Canada) Search for other works by this author on: This Site PubMed Google Scholar G. Jasmin G. Jasmin From the Department of Pathology, University of Montreal, Montreal (Canada) Search for other works by this author on: This Site PubMed Google Scholar Cardiologia (1963) 43 (2): 104–114. https://doi.org/10.1159/000167757 Article history Published Online: October 24 2008 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation E. Bajusz, G. Jasmin; Studies on Factors that Selectively Influence Calcification in the Myocardium. Cardiologia 1 February 1963; 43 (2): 104–114. https://doi.org/10.1159/000167757 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsCardiologia Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1963Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.

Journal Article ON THE MECHANISM OF THE ANTI-INFLAMMATORY EFFECT OF ALDACTONE®, AN ANTIMINERALOCORTICOID STEROID SPIRONOLACTONE These studies were supported by the Medical Research Council of Canada and the Canadian Arthritis and Rheumatism Society. Get access E Bajusz, E Bajusz Département d'Anatomie pathologique, Université de Montréal, Montréal, Canada Search for other works by this author on: Oxford Academic Google Scholar G Jasmin G Jasmin Département d'Anatomie pathologique, Université de Montréal, Montréal, Canada Search for other works by this author on: Oxford Academic Google Scholar Acta Endocrinologica (Norway), Volume 40, Issue 3_Supplement, Aug 1962, Page S104, https://doi.org/10.1530/acta.0.040S104 Published: 01 August 1962

2-Methyl-9-fluorocortisol was injected into intact rats in the absence of NaCl dietary supplements during 8 months. All animals became hypertensive and developed myocarditis, nephrosclerosis, and periarteritis nodosa. There were marked cardiac hypertrophy and arteriolosclerosis of the coronary arteries. Evaluation of the basic and maximum work capacity of the heart revealed that the myocardium was functionally equivalent in the control and treated animals. Consequently, sensitization by the intake of large amounts of NaCl is not indispensable for the production of hypertension and cardiovascular lesions with 2-methyl-9-fluorocortisol. In addition, as revealed by the cardiac function tests used, there is no strict parallelism between histologic and functional impairment of the heart.