Normal atrial and ventricular myocardial structures

ESC CardioMed ◽  
2018 ◽  
pp. 72-76
Author(s):  
Damián Sánchez-Quintana ◽  
José Angel Cabrera
Keyword(s):  
Extracellular Matrix ◽  
Fibrous Tissue ◽  
Three Dimensional ◽  
Atrial Septum ◽  
Structural Basis ◽  
Ventricular Contraction ◽  
Connective Tissue Matrix ◽  
Heart Functions ◽  
Tissue Matrix ◽  
Shape And Size

The heart functions by means of a three-dimensional arrangement of myofibres supported by an extracellular matrix which plays an important role in maintaining the size and shape of the heart. In both atria, the structure of the walls and the atrial septum confers a three-dimensional arrangement of muscle bundles and myoarchitecture that allows preferential electrical intra- and interatrial conduction which is important for a better understanding of atrial activation and arrhythmias. The myoarchitecture within the ventricular walls has a three-dimensional arrangement of myofibres, within a supporting matrix of fibrous tissue, which changes orientation from being oblique in the subepicardium to circumferential in the middle and to longitudinal in the subendocardium, allowing the chambers to change in shape and size through the cardiac cycle. Within each ventricle, the circumferential portion is the thickest transmurally, with the longitudinal portion the thinnest. The three-dimensional arrangement of the ventricular mesh serves to realign the myocytes during ventricular contraction, accounting for the extent of systolic mural thickening. Abnormal myoarchitecture in combination with alterations in the connective tissue matrix provide the structural basis for abnormalities in myocardial function.

Normal atrial and ventricular myocardial structures

2018 ◽  
Author(s):  
Damián Sánchez-Quintana ◽  
José Angel Cabrera
Keyword(s):  
Cardiac Cycle ◽  
Myocardial Function ◽  
Fibrous Tissue ◽  
Three Dimensional ◽  
Atrial Septum ◽  
Structural Basis ◽  
Connective Tissue Matrix ◽  
Atrial Activation ◽  
Heart Functions ◽  
Tissue Matrix

The heart functions by means of a three-dimensional arrangement of myofibres supported by an extracellular matrix which plays an important role in maintaining the size and shape of the heart. In both atria, the structure of the walls and the atrial septum confers a three-dimensional arrangement of muscle bundles and myoarchitecture that allows preferential electrical intra- and interatrial conduction which is important for a better understanding of atrial activation and arrhythmias. The myoarchitecture within the ventricular walls has a three-dimensional arrangement of myofibres, within a supporting matrix of fibrous tissue, which changes orientation from being oblique in the subepicardium to circumferential in the middle and to longitudinal in the subendocardium, allowing the chambers to change in shape and size through the cardiac cycle. Within each ventricle, the circumferential portion is the thickest transmurally, with the longitudinal portion the thinnest. The three-dimensional arrangement of the ventricular mesh serves to realign the myocytes during ventricular contraction, accounting for the extent of systolic mural thickening. Abnormal myoarchitecture in combination with alterations in the connective tissue matrix provide the structural basis for abnormalities in myocardial function.

Toward a kinetic theory of connective tissue micromechanics

1993 ◽  
Vol 74 (2) ◽  
pp. 665-681 ◽  
Author(s):  
S. M. Mijailovich ◽  
D. Stamenovic ◽  
J. J. Fredberg
Keyword(s):  
Connective Tissue ◽  
Three Dimensional ◽  
Elastic Fibers ◽  
Tissue Elasticity ◽  
Field Equations ◽  
Fiber Network ◽  
Rate Dependent ◽  
Connective Tissue Matrix ◽  
Tissue Matrix ◽  
And Diffusion

The aim of this study is to develop unifying concepts at the microstructural level to account for macroscopic connective tissue dynamics. We establish the hypothesis that rate-dependent and rate-independent dissipative stresses arise in the interaction among fibers in the connective tissue matrix. A quantitative theoretical analysis is specified in terms of geometry and material properties of connective tissue fibers and surrounding constituents. The analysis leads to the notion of slip and diffusion boundary layers, which become unifying concepts in understanding mechanisms that underlie connective tissue elasticity and energy dissipation during various types of loading. The complex three-dimensional fiber network is simplified to the interaction of two ideally elastic fibers that dissipate energy on slipping interface surfaces. The effects of such interactions are assumed to be expressed in the aggregate matrix. Special solutions of the field equations are obtained analytically, whereas the general solution of the model field equations is obtained numerically. The solutions lead to predictions of tissue behavior that are qualitatively, if not quantitatively, consistent with reports of a variety of dynamic moduli, their dependencies on the rate and amplitude of load application, and some features associated with preconditioning.

Keratocyte networks visualised in the living cornea using vital dyes

1993 ◽  
Vol 106 (2) ◽  
pp. 685-691 ◽  
Author(s):  
C.A. Poole ◽  
N.H. Brookes ◽  
G.M. Clover
Keyword(s):  
Three Dimensional ◽  
Corneal Stroma ◽  
Molecular Probes ◽  
Dead Cell ◽  
High Concentration ◽  
Vital Dyes ◽  
Dimensional Network ◽  
Cell Processes ◽  
Connective Tissue Matrix ◽  
Tissue Matrix

Fluorescent viability probes have been used to visualise and investigate the viability, morphology and organisation of the keratocyte within the stroma of the intact living cornea. The live cell probe, calcien-AM, in combination with a dead cell probe, ethidium homodimer (Live/Dead Assay, Molecular Probes, U.S.A.) proved superior to earlier generation vital dyes such as fluorescein diacetate or 5,6-carboxyfluorescein diacetate, initially used in combination with ethidium bromide. The ubiquitous distribution of esterase enzymes that cleave calcien-AM within the keratocyte cytoplasm produced a high concentration of fluorescently active calcein throughout the cell, including fine cell processes. Epi-illuminated fluorescence microscopy on transparent corneal dissections subsequently revealed details of keratocyte microanatomy and three-dimensional network organisation in situ. Three morphologically discrete subpopulations of keratocytes were identified: two formed relatively small bands of cells, immediately subjacent to either Bowman's or Descemet's membranes, the third subpopulation constituting the majority of keratocytes typically located within the corneal stroma. The results indicate that calcein-AM is able to penetrate intact living cornea revealing cell viability, and it also has the capacity to ‘trace’ cellular elements and reveal fine structure within a dense connective tissue matrix.

Laminar structure of the heart: ventricular myocyte arrangement and connective tissue architecture in the dog

1995 ◽  
Vol 269 (2) ◽  
pp. H571-H582 ◽  
Author(s):  
I. J. LeGrice ◽  
B. H. Smaill ◽  
L. Z. Chai ◽  
S. G. Edgar ◽  
J. B. Gavin ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Three Dimensional ◽  
Length Distribution ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Tangential Section ◽  
Connective Tissue Matrix ◽  
The Right ◽  
Tissue Matrix ◽  
Number Of Branches

We have studied the three-dimensional arrangement of ventricular muscle cells and the associated extracellular connective tissue matrix in dog hearts. Four hearts were potassium-arrested, excised, and perfusion-fixed at zero transmural pressure. Full-thickness segments were cut from the right and left ventricular walls at a series of precisely located sites. Morphology was visualized macroscopically and with scanning electron microscopy in 1) transmural planes of section and 2) planes tangential to the epicardial surface. The appearance of all specimens was consistent with an ordered laminar arrangement of myocytes with extensive cleavage planes between muscle layers. These planes ran radially from endocardium toward epicardium in transmural section and coincided with the local muscle fiber orientation in tangential section. Stereological techniques were used to quantify aspects of this organization. There was no consistent variation in the cellular organization of muscle layers (48.4 +/- 20.4 microns thick and 4 +/- 2 myocytes across) transmurally or in different ventricular regions (23 sites in 6 segments), but there was significant transmural variation in the coupling between adjacent layers. The number of branches between layers decreased twofold from subepicardium to midwall, whereas the length distribution of perimysial collagen fibers connecting muscle layers was greatest in the midwall. We conclude that ventricular myocardium is not a uniformly branching continuum but a laminar hierarchy in which it is possible to identify three axes of material symmetry at any point.

Electron Microscopy and image reconstruction reveal the structural basis for spectrin's elastic properties

1992 ◽  
Vol 50 (1) ◽  
pp. 510-511
Author(s):  
Amy M. McGough ◽  
Robert Josephs
Keyword(s):  
Electron Microscopy ◽  
Elastic Properties ◽  
Conformational Changes ◽  
Quaternary Structure ◽  
Three Dimensional ◽  
Membrane Skeleton ◽  
Projection Algorithm ◽  
Structural Basis ◽  
Iterative Approximation ◽  
Membrane Skeletons

The remarkable deformability of the erythrocyte derives in large part from the elastic properties of spectrin, the major component of the membrane skeleton. It is generally accepted that spectrin's elasticity arises from marked conformational changes which include variations in its overall length (1). In this work the structure of spectrin in partially expanded membrane skeletons was studied by electron microscopy to determine the molecular basis for spectrin's elastic properties. Spectrin molecules were analysed with respect to three features: length, conformation, and quaternary structure. The results of these studies lead to a model of how spectrin mediates the elastic deformation of the erythrocyte.Membrane skeletons were isolated from erythrocyte membrane ghosts, negatively stained, and examined by transmission electron microscopy (2). Particle lengths and end-to-end distances were measured from enlarged prints using the computer program MACMEASURE. Spectrin conformation (straightness) was assessed by calculating the particles’ correlation length by iterative approximation (3). Digitised spectrin images were correlation averaged or Fourier filtered to improve their signal-to-noise ratios. Three-dimensional reconstructions were performed using a suite of programs which were based on the filtered back-projection algorithm and executed on a cluster of Microvax 3200 workstations (4).

Designing TIMP (tissue inhibitor of metalloproteinases) variants that are selective metalloproteinase inhibitors

2003 ◽  
Vol 70 ◽  
pp. 201-212 ◽  
Author(s):  
Hideaki Nagase ◽  
Keith Brew
Keyword(s):  
Three Dimensional ◽  
Therapeutic Interventions ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Structural Basis ◽  
Structural Elements ◽  
Ridge Structure ◽  
Extracellular Matrix Components ◽  
Metalloproteinase Inhibitors ◽  
The Matrix ◽  
A Disintegrin And Metalloproteinase

The tissue inhibitors of metalloproteinases (TIMPs) are endogenous inhibitors of the matrix metalloproteinases (MMPs), enzymes that play central roles in the degradation of extracellular matrix components. The balance between MMPs and TIMPs is important in the maintenance of tissues, and its disruption affects tissue homoeostasis. Four related TIMPs (TIMP-1 to TIMP-4) can each form a complex with MMPs in a 1:1 stoichiometry with high affinity, but their inhibitory activities towards different MMPs are not particularly selective. The three-dimensional structures of TIMP-MMP complexes reveal that TIMPs have an extended ridge structure that slots into the active site of MMPs. Mutation of three separate residues in the ridge, at positions 2, 4 and 68 in the amino acid sequence of the N-terminal inhibitory domain of TIMP-1 (N-TIMP-1), separately and in combination has produced N-TIMP-1 variants with higher binding affinity and specificity for individual MMPs. TIMP-3 is unique in that it inhibits not only MMPs, but also several ADAM (a disintegrin and metalloproteinase) and ADAMTS (ADAM with thrombospondin motifs) metalloproteinases. Inhibition of the latter groups of metalloproteinases, as exemplified with ADAMTS-4 (aggrecanase 1), requires additional structural elements in TIMP-3 that have not yet been identified. Knowledge of the structural basis of the inhibitory action of TIMPs will facilitate the design of selective TIMP variants for investigating the biological roles of specific MMPs and for developing therapeutic interventions for MMP-associated diseases.

Central ossifying fibroma of mandible

2020 ◽  
Vol 13 (12) ◽  
pp. e239286
Author(s):  
Kumar Nilesh ◽  
Prashant Punde ◽  
Nitin Shivajirao Patil ◽  
Amol Gautam
Keyword(s):  
Fibrous Tissue ◽  
Three Dimensional ◽  
Facial Asymmetry ◽  
Ossifying Fibroma ◽  
Mandible Reconstruction ◽  
Three Dimensional Printing ◽  
Osseous Lesion ◽  
Large Size ◽  
Dimensional Printing

Ossifying fibroma (OF) is a rare, benign, fibro-osseous lesion of the jawbone characterised by replacement of the normal bone with fibrous tissue. The fibrous tissue shows varying amount of calcified structures resembling bone and/or cementum. The central variant of OF is rare, and shows predilection for mandible among the jawbone. Although it is classified as fibro-osseous lesion, it clinically behaves as a benign tumour and can grow to large size, causing bony swelling and facial asymmetry. This paper reports a case of large central OF of mandible in a 40-year-old male patient. The lesion was treated by segmental resection of mandible. Reconstruction of the surgical defect was done using avascular fibula bone graft. Role of three-dimensional printing of jaw and its benefits in surgical planning and reconstruction are also highlighted.

Induction of in Vivo Ectopic Hematopoiesis by a Three-Dimensional Structured Extracellular Matrix Derived from Decellularized Cancellous Bone

2019 ◽  
Vol 5 (11) ◽  
pp. 5669-5680 ◽  
Author(s):  
Naoko Nakamura ◽  
Tsuyoshi Kimura ◽  
Kwangwoo Nam ◽  
Toshiya Fujisato ◽  
Hiroo Iwata ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cancellous Bone ◽  
Three Dimensional

scholarly journals Rely on Each Other: DNA Binding Cooperativity Shapes p53 Functions in Tumor Suppression and Cancer Therapy

Cancers ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2422
Author(s):  
Oleg Timofeev ◽  
Thorsten Stiewe
Keyword(s):  
Cancer Therapy ◽  
Dna Binding ◽  
Cell Fate ◽  
Tumor Suppression ◽  
Quaternary Structure ◽  
Three Dimensional ◽  
Structural Basis ◽  
Sequence Specificity ◽  
Cell Fate Decisions ◽  
Cancer Mutations

p53 is a tumor suppressor that is mutated in half of all cancers. The high clinical relevance has made p53 a model transcription factor for delineating general mechanisms of transcriptional regulation. p53 forms tetramers that bind DNA in a highly cooperative manner. The DNA binding cooperativity of p53 has been studied by structural and molecular biologists as well as clinical oncologists. These experiments have revealed the structural basis for cooperative DNA binding and its impact on sequence specificity and target gene spectrum. Cooperativity was found to be critical for the control of p53-mediated cell fate decisions and tumor suppression. Importantly, an estimated number of 34,000 cancer patients per year world-wide have mutations of the amino acids mediating cooperativity, and knock-in mouse models have confirmed such mutations to be tumorigenic. While p53 cancer mutations are classically subdivided into “contact” and “structural” mutations, “cooperativity” mutations form a mechanistically distinct third class that affect the quaternary structure but leave DNA contacting residues and the three-dimensional folding of the DNA-binding domain intact. In this review we discuss the concept of DNA binding cooperativity and highlight the unique nature of cooperativity mutations and their clinical implications for cancer therapy.

scholarly journals Artificial Tumor Microenvironments in Neuroblastoma

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1629
Author(s):  
Colin H. Quinn ◽  
Andee M. Beierle ◽  
Elizabeth A. Beierle
Keyword(s):  
Extracellular Matrix ◽  
Three Dimensional ◽  
Therapeutic Interventions ◽  
3D Bioprinting ◽  
Culture Studies ◽  
In Vivo Models ◽  
Novel Treatments ◽  
Tumor Microenvironments ◽  
Novel Approach

In the quest to advance neuroblastoma therapeutics, there is a need to have a deeper understanding of the tumor microenvironment (TME). From extracellular matrix proteins to tumor associated macrophages, the TME is a robust and diverse network functioning in symbiosis with the solid tumor. Herein, we review the major components of the TME including the extracellular matrix, cytokines, immune cells, and vasculature that support a more aggressive neuroblastoma phenotype and encumber current therapeutic interventions. Contemporary treatments for neuroblastoma are the result of traditional two-dimensional culture studies and in vivo models that have been translated to clinical trials. These pre-clinical studies are costly, time consuming, and neglect the study of cofounding factors such as the contributions of the TME. Three-dimensional (3D) bioprinting has become a novel approach to studying adult cancers and is just now incorporating portions of the TME and advancing to study pediatric solid. We review the methods of 3D bioprinting, how researchers have included TME pieces into the prints, and highlight present studies using neuroblastoma. Ultimately, incorporating the elements of the TME that affect neuroblastoma responses to therapy will improve the development of innovative and novel treatments. The use of 3D bioprinting to achieve this aim will prove useful in developing optimal therapies for children with neuroblastoma.

Sign in / Sign up

Export Citation Format

Share Document