Regulation of the slow Ca++ channels of myocardial cells

1996 ◽  
pp. 85-98
Author(s):  
N. Sperelakis ◽  
Y. Katsube ◽  
H. Yokoshiki ◽  
H. Sada ◽  
K. Sumii
Keyword(s):  
Myocardial Cells ◽  
Ca Channels

Regulation of the slow Ca++ channels of myocardial cells

1996 ◽  
Vol 163-164 (1) ◽  
pp. 85-98 ◽  
Author(s):  
N. Sperelakis ◽  
Y. Katsube ◽  
H. Yokoshiki ◽  
H. Sada ◽  
K. Sumii
Keyword(s):  
Myocardial Cells ◽  
Ca Channels

The Ultrastructure of Myocardial Cells in Normal and Cardiac Lethal Mutant Mexican Axolotls, (Ambystoma Mexicanum)

1970 ◽  
Vol 28 ◽  
pp. 62-63
Author(s):  
Larry F. Lemanski ◽  
Eldridge M. Bertke ◽  
J. T. Justus
Keyword(s):  
Fine Structure ◽  
Heart Development ◽  
Osmium Tetroxide ◽  
Picric Acid ◽  
Ambystoma Mexicanum ◽  
Recessive Mutation ◽  
Acid Mixture ◽  
Myocardial Cells ◽  
Lethal Mutant ◽  
Mexican Axolotl

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.

Immunocytochemical localization of desmin and vimentin in chick embryonic myocardial cells

1990 ◽  
Vol 48 (3) ◽  
pp. 448-449
Author(s):  
Yukiko Sugi
Keyword(s):  
Sodium Methoxide ◽  
Intermediate Filament Protein ◽  
Chick Embryos ◽  
Immunocytochemical Localization ◽  
Myocardial Cells ◽  
Immunofluorescence Study ◽  
Immunofluorescent Localization ◽  
Rabbit Igg ◽  
Semithin Sections ◽  
Filament Protein

In cultured skeletal muscle cells of chick, one intermediate filament protein, vimentin, is primarily formed and then synthesis of desmin follows. Coexistence of vimentin and desmin has been immunocytochemically confirmed in chick embryonic skeletal musclecells. Immunofluorescent localization of vimentin and desmin has been described in developing myocardial cells of hamster. However, initial localization of desmin and vimentin in early embryonic heart has not been reported in detail. By quick-freeze deep-etch method a loose network of intermediate filaments was revealed to exist surrounding myofibrils. In this report, immunocytochemical localization of desmin and vimentin is visualized in early stages of chick embryonic my ocardium.Chick embryos, Hamburger-Hamilton (H-H) stage 8 to hatch, and 1 day old postnatal chicks were used in this study. For immunofluorescence study, each embryo was fixed with 4% paraformaldehyde and embedded in Epon 812. De-epoxinized with sodium methoxide, semithin sections were stained with primary antibodies (rabbit anti-desmin antibody and anti-vimentin antibody)and secondary antibody (RITC conjugated goat-anti rabbit IgG).

Allogenic biomaterial - an inducer of autologous stem and committed myocardial cells in ischemic damaged myocardium

2019 ◽  
Vol 17 (1) ◽  
pp. 89-94 ◽  
Author(s):  
E. R. Muldashev ◽  
◽  
A. I. Lebedeva ◽  
S. A. Muslimov ◽  
S. V. Popov ◽  
...  
Keyword(s):  
Myocardial Cells

Paracrine Mechanisms Involved in Mesenchymal Stem Cell Differentiation into Cardiomyocytes

2019 ◽  
Vol 14 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Maryam Farzaneh ◽  
Fatemeh Rahimi ◽  
Masoumeh Alishahi ◽  
Seyed E. Khoshnam
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Dysfunction ◽  
Stem Cell Differentiation ◽  
Myocardial Cells ◽  
Coronary Artery Diseases ◽  
Low Cardiac Output ◽  
Mesenchymal Stem Cell Differentiation ◽  
Proliferation And Differentiation ◽  
The World ◽  
Biochemical Analyses

Cardiovascular disease (CVD) is one of the world-wide healthcare problem that involves the heart or blood vessels. CVD includes myocardial infarction and coronary artery diseases (CAD). Dysfunctional myocardial cells are leading causes of low cardiac output or ventricular dysfunction after cardiac arrest and may contribute to the progression of CVD which could not generate new cardiomyocytes in human adult heart. The mesenchymal stem cells (MSCs) which are present in adult marrow can self-renew and have the capacity of differentiation into multiple types of cells including cardiomyocytes. Recent biochemical analyses greatly revealed that several regulators of MSCs, such as HGF, PDGF, Wnt, and Notch-1 signaling pathways have been shown to be involved in the proliferation and differentiation into cardiomyocytes. Preclinical studies are paving the way for further applications of MSCs in the repair of myocardial infarction. In this study, we discuss and summarize the paracrine mechanisms involved in MSCs differentiation into cardiomyocytes.

ALDH2 Expression In Myocardial Cells Is Increased In Response To Hypoxia Followed By Reoxygenation

2014 ◽  
Vol 186 (2) ◽  
pp. 494
Author(s):  
C.T. Holley ◽  
M.E. Lindsey ◽  
E.M. Chappuis ◽  
E.O. McFalls ◽  
R.F. Kelly ◽  
...  
Keyword(s):  
Myocardial Cells

scholarly journals Complement C9 expression is associated with damaged myocardial cells in pediatric sudden death cases of fulminant myocarditis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Akari Takaya Uno ◽  
Masahito Hitosugi ◽  
Mami Nakamura ◽  
Tomoyuki Nakanishi ◽  
Takahiro Mima ◽  
...  
Keyword(s):  
Sudden Death ◽  
Acute Myocarditis ◽  
Lymphocytic Infiltration ◽  
Pericardial Fluid ◽  
Sirtuin 1 ◽  
Fulminant Myocarditis ◽  
Myocardial Cells ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining ◽  
Complement C9

Abstract Background Because disease progression is so fast in sudden death of acute fulminant myocarditis, damage of myocardial cells is not evident in routine hematoxylin and eosin staining. To understand damage to myocardial cells and the mechanism of sudden death, immunohistochemical staining was performed for two forensic autopsy cases. Case presentation The patients were a healthy 5-year-old girl and 8-year-old boy. They suddenly died within 2 days of appearance of flu-like symptoms. An autopsy showed accumulation of yellowish-clear pericardial fluid containing fibrin deposits, fluid blood in the heart, and congestion of visceral organs. Histologically, minor necrosis or degeneration of myocardial cells with mainly lymphocytic infiltration was observed sometimes in tissue sections. Immunohistochemically, positive complement C9 staining and negative sirtuin 1 staining were found. These findings suggested wide damage of myocardial cells, even in regions with no marked changes in myocardial cells with hematoxylin and eosin staining. These areas corresponded to those with strong accumulation of lymphocytes. Conclusions Immunohistochemistry for complement C9 and sirtuin 1 might become a new tool for evaluating damage of myocardial cells of fulminant acute myocarditis.

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