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Alterative and plastic insufficiency of cardiomyocytes: isoproterenol-induced damage to myocardium during anthracycline cardiomyopathy.

https://arctichealth.org/en/permalink/ahliterature10133
Source
Bull Exp Biol Med. 2001 Jun;131(6):589-94
Publication Type
Article
Date
Jun-2001
Author
E L Lushnikova
L M Nepomnyashchikh
D E Semenov
Author Affiliation
Department of General Pathology and Pathomorphology, Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. pathol@cyber.nsk.ma.ru
Source
Bull Exp Biol Med. 2001 Jun;131(6):589-94
Date
Jun-2001
Language
English
Publication Type
Article
Keywords
Animals
Antibiotics, Antineoplastic - toxicity
Cardiomyopathies - chemically induced - pathology - physiopathology
Cardiotonic Agents - pharmacology
Cell Death - drug effects
Daunorubicin - toxicity
Isoproterenol - pharmacology
Myocardial Contraction - drug effects
Myocardium - pathology
Rats
Rats, Wistar
Abstract
The development of regenerative and plastic myocardial insufficiency induced by anthracycline antibiotic rubomycin is accompanied by a decrease in cardiomyocyte sensitivity to damage produced by synthetic catecholamine isoproterenol. The incidence and the size of coagulation necrosis foci of cardiomyocytes developed 6 h after isoproterenol injection significantly decreased with increasing in the interval between rubomycin injection and subsequent administration of isoproterenol. In Wistar rats receiving rubomycin 3-5 days prior to isoproterenol and exhibiting signs of regenerative and plastic insufficiency, no cardiomyocyte contracture, intracellular myocytolysis, or lump degradation characteristic of cardiac insufficiency induced by endo- and exogenous catecholamines were found.
PubMed ID
11586415 View in PubMed
Less detail

Anthracycline-induced cardiomyopathy is manifested in decreased protein synthesis, impaired intracellular regeneration, and non-necrotic death of cardiomyocytes.

https://arctichealth.org/en/permalink/ahliterature53866
Source
Bull Exp Biol Med. 2001 May;131(5):505-10
Publication Type
Article
Date
May-2001
Author
D E Semenov
E L Lushnikova
L M Nepomnyashchikh
Author Affiliation
Department of General Pathology and Pathomorphology, Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. pathol@cyber.nsk.ma.ru
Source
Bull Exp Biol Med. 2001 May;131(5):505-10
Date
May-2001
Language
English
Publication Type
Article
Keywords
Animals
Anthracyclines - pharmacology
Antibiotics, Antineoplastic - pharmacology
Apoptosis
Cardiomyopathies - chemically induced - pathology
Cell Death
Cell Nucleolus - drug effects
Cytoplasm - metabolism
Daunorubicin - pharmacology
Heart - drug effects
Male
Myocardium - cytology - pathology - ultrastructure
Myofibrils - drug effects
Necrosis
Rats
Rats, Wistar
Sarcomeres - drug effects
Abstract
The cytostatic anthracycline antibiotic daunomycin hydrochloride led to the development of plastic myocardial insufficiency characterized by impaired intracellular regeneration of cardiomyocytes and progressive involution of cytoplasmic structures. Morphological signs of plastic myocardial insufficiency included fragmentation, annulation, or collapse of nucleoli in cardiomyocyte nuclei, lysis of myofilaments, sarcomeres, or myofibrils, focal degradation of the cytoplasm, and intensive autophagy. Fatal anthracycline-induced cardiac insufficiency was associated with massive cardiomyocyte loss due to their non-necrotic death and elimination. Our findings indicate that anthracycline-induced cardiomyopathy in laboratory animals is a convenient model for studying general mechanisms underlying the pathogenesis of regenerative and plastic cardiac insufficiency in humans.
PubMed ID
11550068 View in PubMed
Less detail

Focal degradation of cytoplasmic organelles in cardiomyocytes during regenerative and plastic myocardial insufficiency.

https://arctichealth.org/en/permalink/ahliterature53949
Source
Bull Exp Biol Med. 2000 Dec;130(12):1190-5
Publication Type
Article
Date
Dec-2000
Author
L M Nepomnyashchikh
E L Lushnikova
D E Semenov
Author Affiliation
Laboratory of General Pathological Anatomy, Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk. pathol@cyber.nsk.ma.ru
Source
Bull Exp Biol Med. 2000 Dec;130(12):1190-5
Date
Dec-2000
Language
English
Publication Type
Article
Keywords
Animals
Antibiotics, Antineoplastic - toxicity
Cardiomyopathies - chemically induced - pathology - physiopathology
Daunorubicin - toxicity
Male
Microscopy, Electron
Myocardium - ultrastructure
Necrosis
Organelles - drug effects - ultrastructure
Rats
Rats, Wistar
Abstract
Focal degradation of cardiomyocyte ultrastructures and cytoplasm, their sequestration, and autophagy were found in Wistar rats with daunomycin-induced regenerative and plastic myocardial insufficiency starting from day 1 after cytostatic treatment. These changes were morphologically manifested in the formation of myelin-like structures, autophagosomes, and secondary lysosomes. Sequestration and partial autophagy of the cytoplasm in cardiomyocytes with diminished or blocked protein synthesis reflect cell regression or involution directed to the adjustment of the cytoplasm volume to functional state of the nucleus.
PubMed ID
11276319 View in PubMed
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IMMUNOHISTOCHEMICAL ANALYSIS OF MAMMARY EPITHELIAL CELLS AT TUMORAL GROWTH IN REPUBLIC OF SAKHA (YAKUTIA).

https://arctichealth.org/en/permalink/ahliterature270948
Source
Wiad Lek. 2015;68(4):537-42
Publication Type
Article
Date
2015
Author
M P Kirillina
K S Loskutova
E L Lushnikova
L M Nepomnyaschih
Source
Wiad Lek. 2015;68(4):537-42
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Apoptosis Regulatory Proteins - metabolism
Arctic Regions
Biomarkers, Tumor - metabolism
Breast Neoplasms - diagnosis - metabolism - ultrastructure
Epithelial Cells - metabolism - ultrastructure
Female
Humans
Immunohistochemistry - methods
Middle Aged
Population Groups
Prognosis
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Russia
Abstract
The analysis of results histological examination of surgical material of breast cancer from 294 women with subsequent immunohistochemical determination of estrogen (ER)--and progesterone (PgR)--receptors, proliferative activity (Ki-67), expression of the mutant suppressor gene (p53) and gene-inhibitor apoptosis (bcl-2) was carried out. The obtained data testify that IHC-research of the tumor progression markers is a defining part in the forecast of course, optimization of therapeutic approaches with an individualization of chemo-, hormonal and beam therapy of mammary cancer, the decision of a question of medicamentous and/or surgical shutdown of the ovaries, based on the research results of the biological activity markers of the tumor.
PubMed ID
26887131 View in PubMed
Less detail

Immunohistochemical study of apoptotic marker p53 as a prognostic factor in breast cancer.

https://arctichealth.org/en/permalink/ahliterature264824
Source
Bull Exp Biol Med. 2014 Nov;158(1):84-7
Publication Type
Article
Date
Nov-2014
Author
K S Loskutova
M P Kirillina
E L Lushnikova
L M Nepomnyashchikh
Source
Bull Exp Biol Med. 2014 Nov;158(1):84-7
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Apoptosis
Breast Neoplasms - genetics - metabolism - pathology
Carcinoma, Ductal, Breast - genetics - metabolism - secondary
Female
Humans
Immunohistochemistry
Lymphatic Metastasis
Middle Aged
Mutation
Prognosis
Russia
Tumor Markers, Biological - metabolism
Tumor Suppressor Protein p53 - genetics - metabolism
Abstract
Histological study of breast cancer specimens obtained from 294 female residents in the Republic of Sakha (Yakutia) of different age and ethnic groups and immunohistochemical analysis of protein expression of mutant suppressor gene p53 in tumor cells were performed. A positive correlation was found between expression of mutant gene p53 protein and the degree of malignancy of breast tumors. The indicator should be considered when assessing malignancy potential and risk of breast cancer, because it is important for optimization and individualization of the treatment.
PubMed ID
25403404 View in PubMed
Less detail

Morphological characteristics of myocardial remodeling during compensatory hypertrophy in aging Wistar rats.

https://arctichealth.org/en/permalink/ahliterature53689
Source
Bull Exp Biol Med. 2001 Dec;132(6):1201-6
Publication Type
Article
Date
Dec-2001
Author
E L Lushnikova
L M Nepomnyashchikh
M G Klinnikova
Author Affiliation
Laboratory of Cytology and Cellular Biology, Institute of Regional Pathology and Pathomorphology, Siberian Division of Russian Academy of Medical Sciences, Novosibirsk.
Source
Bull Exp Biol Med. 2001 Dec;132(6):1201-6
Date
Dec-2001
Language
English
Publication Type
Article
Keywords
Aging
Animals
Calcium - metabolism
Heart - physiology
Heart Ventricles - pathology
Hypertrophy
Hypertrophy, Left Ventricular
Microscopy, Electron
Myocardium - cytology - pathology
Rats
Rats, Wistar
Time Factors
Abstract
Remodeling of the myocardium in Wistar rats during aging is characterized by cardiomyocyte hypertrophy and increase of their total volume in the left ventricle; the total volume of the connective tissue also increases without marked changes in cardiomyocyte count and total volume of blood capillaries. The number of cardiomyocytes with contracture injuries of different severity in the myocardium of aging animals increases against the background of hemodynamic disorders. At the cellular level, compensatory hypertrophy of cardiomyocytes during aging is characterized by a pronounced increase in the myofibril bulk paralleled by relative deficiency of the mitochondria and pronounced deficiency of agranular sarcoplasmic reticulum and T system, involved in the regulation of intracellular Ca2+.
PubMed ID
12152886 View in PubMed
Less detail

Morphological Evaluation of Oxidative Phosphorylation System in Myocardial Infarction under Conditions of Modified Vascular Endothelial Growth Factor Concentration.

https://arctichealth.org/en/permalink/ahliterature264990
Source
Bull Exp Biol Med. 2015 Jul 25;
Publication Type
Article
Date
Jul-25-2015
Author
M G Shurygin
I A Shurygina
O V Kanya
N N Dremina
E L Lushnikova
R D Nepomnyashchikh
Source
Bull Exp Biol Med. 2015 Jul 25;
Date
Jul-25-2015
Language
English
Publication Type
Article
Abstract
The relationship between vascular endothelium growth factor (VEGF) and cardiomyocyte oxidative phosphorylation level in experimental myocardial infarction, caused by diathermocoagulation of the periconical ventricular artery, was studied by immunofluorescent microscopy. Staining showed uneven distribution of cytochrome c in the mitochondria in the focus of myocardial infarction 2 h after the operation. After 24 h uneven staining of cardiomyocytes was found in the peri-infarction zone and no staining in the zone of myocardial infarction. This indicated a significant decrease in the level of redox enzymes. This picture persisted till day 14. Intraventricular injection of VEGF to animals led to a significant increase of the immunohistochemical reaction intensity, which reached the peak by day 7. The distribution of immunohistochemical reaction products under conditions of VEGF blocking was about the same as in spontaneous postinfarction reparative restitution. Our data indicated that increase of VEGF concentration in the myocardium maintained and stimulated oxidative phosphorylation in cardiomyocytes during the postinfarction period.
PubMed ID
26205728 View in PubMed
Less detail

Morphological manifestations of heart remodeling in anthracycline-induced dilated cardiomyopathy.

https://arctichealth.org/en/permalink/ahliterature53104
Source
Bull Exp Biol Med. 2004 Dec;138(6):607-12
Publication Type
Article
Date
Dec-2004
Author
E L Lushnikova
M G Klinnikova
O P Molodykh
L M Nepomnyashchikh
Author Affiliation
Department of Cell Biology and Morphology, Institute of Regional Pathology and Pathomorphology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk. pathol@soramn.ru
Source
Bull Exp Biol Med. 2004 Dec;138(6):607-12
Date
Dec-2004
Language
English
Publication Type
Article
Keywords
Animals
Anthracyclines - toxicity
Cardiomyopathy, Dilated - chemically induced
Heart - drug effects
Myocardium - pathology
Rats
Abstract
The morphogenesis of anthracycline-induced dilated cardiomyopathy was studied after single sublethal dose of doxorubicin. Cardiomyocyte depopulation (up to 27%) and decrease in their regeneratory plastic reactions were the main mechanisms of cardiac failure development after anthracycline (doxorubicin) treatment, determining the type of heart remodeling by the dilatation variant. Cardiomyocyte elimination and atrophy during the development of anthracycline-induced regeneratory plastic cardiac insufficiency were paralleled by hypertrophy of remaining cardiomyocytes and diffuse and small focal sclerosis of the myocardium, which could be regarded as a correlated compensatory reaction of the connective tissue to the decrease in the number of muscle fibers.
PubMed ID
16134825 View in PubMed
Less detail

Morphometric analysis of the lymph system in rat heart during myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature53637
Source
Bull Exp Biol Med. 2002 Aug;134(2):203-5
Publication Type
Article
Date
Aug-2002
Author
V V Stolyarov
E L Lushnikova
V P Zuevskii
A F Usynin
Author Affiliation
Department of Pathology and Pathomorphology, Institute of Regional Pathology and Pathomorphology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk.
Source
Bull Exp Biol Med. 2002 Aug;134(2):203-5
Date
Aug-2002
Language
English
Publication Type
Article
Keywords
Animals
Lymphatic System - pathology
Male
Myocardial Infarction - pathology
Myocardium - pathology
Rats
Abstract
Simulation of myocardial infarction in random-bred rats showed that lymph vessels play the leading role in the drainage of the myocardium during the acute period of ischemic damage and compensate for the developing insufficiency of interstitial drainage at the expense of venous component of the coronary bed. A pronounced enlargement of the lymph collectors and I, II, and order III vessels in the left and right ventricles of the heart was detected.
PubMed ID
12459851 View in PubMed
Less detail

Parenchyma-stroma relationships in the myocardium: alterative insufficiency of cardiomyocytes and morphogenesis of focal cardiosclerosis.

https://arctichealth.org/en/permalink/ahliterature53638
Source
Bull Exp Biol Med. 2002 Aug;134(2):191-7
Publication Type
Article
Date
Aug-2002
Author
L M Nepomnyashchikh
E L Lushnikova
D E Semenov
V V Stolyarov
Author Affiliation
Department of General Pathology and Pathomorphology, Institute of Regional Pathology and Pathomorphology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk.
Source
Bull Exp Biol Med. 2002 Aug;134(2):191-7
Date
Aug-2002
Language
English
Publication Type
Article
Keywords
Animals
Myocardial Infarction - etiology - pathology
Myocardium - pathology
Rats
Rats, Wistar
Stromal Cells - pathology
Abstract
Remodeling of the myocardium during focal metabolic damages to cardiomyocytes is determined by contracture injuries to myofibrils, their lump degradation, and development of coagulation necrosis. Reactive changes in the stroma develop over the first hours and manifest in acute hemodynamic disturbances followed by proliferation of connective tissue cells. The immature granulation tissue is formed at the site of myocardial damages. Later this tissue is replaced by the mature connective tissue with the formation of small scars. It should be emphasized that sclerotic changes during remodeling of the myocardium after focal metabolic damages are reversible.
PubMed ID
12459849 View in PubMed
Less detail

19 records – page 1 of 2.