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  1. Mechanisms of contractile dysfunction in congestiv
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Overuse injuries are common sequelae of exercise and sporting activities in general, and of running in particular. Anatomical Concepts Related to Human Movement. As a result of reading this article, physicians should be able to: 1. Beveled suture Shear force [Squamosal suture] 3. Schematic overview of tissue layer thickness measurements: a original interface tissue area white in a slice, b when a circle as large as the instrument diameter fits within the interface tissue area, it is projected on this area, c the area of the circle is subtracted from total tissue area, d whole interface tissue area is scanned, e remaining interface tissue shown in white Alterations in tendon structure and muscle performance have been suggested as mechanisms driving improvement in pain and function with mid-portion Achilles tendinopathy AT.

Joint contact forces during the impact peak are three to five times smaller than they are during the active force peak, and are therefore within the normal operating ranges for joint function and unlikely to contribute to the development of running injury. The work space created by this configuration is spherical. The majority of class time will be spent reviewing and critically analyzing biomechanics and kinesiology research literature to gain insight into the nature and relevance of research questions being asked and the interpretation Introduction. Review briefly the structure of muscle and the mechanism of skeletal muscle contraction.

External layer is a tough, flexible, fibrous capsule that is continuous with the periosteum of the articulating bones; the capsule functions to help hold the bones of the joint in place. A systemic approach to these often difficult to diagnose problems can lead to the appropriate treatment, and if necessary, the appropriate surgical intervention.

ORPR Chapter 1: Biomechanical Applications to Joint Structure and Function 13 WbLf 40 N Figure Vector representation of the pull of the weight boot on the leg-foot segment weightboot-on-legfoot [WbLf] , with a magnitude proportional to the mass and equivalent to the weight of the apparatus. International Scholarly Research Notices is a peer-reviewed, Open Access journal covering a wide range of subjects in science, technology, and medicine.

To meet the requirements of sports equipment, the materials of choice often consist of a mixture of material types—metals, ceramics, polymers, and composite concepts. In the case of the fully clamped joint, the gradient vectors do not change their length and orientation, allowing for the use of the constant strain assumptions. When used to measure a single-axis joint such as the knee or elbow, or when measuring a single plane of a twin-axis joint, simply connect one channel, the other remains redundant.

The biomechanical integrity of implants comprises the mechanical behavior of implant materials, surface-induced bone micromechanics, and adaptive bone remodeling. Joint cavity is enclosed by a double-layered capsule. For every joint, there is a position called the self-braced closepacked position in which there is a maximum congruence of the articular surfaces and maximum tension Summary Joints in the body are classified on the basis of structure and function.

Bone Joint Surg. Atlas of Orthotics: Biomechanical Principles and Application. Joint reaction forces, torques, speeds, and power consumptions are also checked. The goal of this study was to provide a simplified model for evaluating this insulation system, which included either a single or multilayer composite structure in order to predict optimal performance.

Types of motion in subtalar joint. Thorough explanations of biomechanical concepts are discussed in other works. Biomechanics of hip joint Those results are used in the current paper to represent the connection between the column and the spindle of an idealized column-spindle machine structure. Yoav Morag, Jon A. The application of biomechanics to the musculoskeletal system has led to a better understanding of both joint function and dysfunction, resulting in design improve-ments in devices such as joint arthroplasty systems and orthotic devices.

Follow a program that exercises the shoulders in a balanced way. The purpose of this study was to investigate the biomechanical effect of ITSI and screw fixation of the ankle by finite element FE analysis. J Biomech Eng. Therapy consisted of Maitland's passive accessory mobilization of the dominant hand during 4 sessions over 2 weeks. The Hip Joint and Computational models greatly improve the predictive ability to acquire information about the mechanical mechanisms of the human body's inner structure that may not be easily obtained in experimental studies.

Describe the overall structure of a story, including describing how the beginning introduces the story and the ending concludes the action. Surgical technique. Lumbar spine offers support to the human body structure, and it is involved in almost all the functional body movements. Several different designs of ISPs have been developed in recent years and are currently under clinical evaluation [11,55,56], but their gross biomechanical function in the spine appears to be fairly similar [57].

Cranial Sutures 1. It is still unclear how lubrication works, but there are many theories, based on man-made ball-bearings. Conditions such as joint malalignment and loss of normal meniscal function lead to focal concentration of compressive loads in the joint, particularly in the setting of obesity.

Mechanisms of contractile dysfunction in congestiv

For reasons arising from the dramatically different length scales associated with those dissipative mechanisms and the length scales characteristic of the overall structure, this physics cannot be captured through direct numerical simulation DNS of the contact mechanics within a structural dynamics analysis. Summary The TMJ literature underlines the importance of biomechanical analysis of the natural joint to better understand the structural and functional aspects; and of the reconstructed joint to assess the implant function and performance. Trigger point dry needling can be used to achieve one of three objectives.

The authors model a computational fluid dynamics CFD -based approach for the leakage flow of brush seals. But they usually sprinkle around words such as stress, strain, load, tension, shear, compression, torsion, etc. Photodynamic devices for replacement of an articular head of a bone are provided. This paper proposes an automatic method to synthesize planar multiple joint kinematic chains. Quay and Domenic A.

If your access is via an institutional subscription, please contact your librarian to request reinstatement. UTS as a function of both carbon composition and processing parameters. Structural Kinesiology. Therefore, the following review was performed to better elucidate their anatomy, function and involvement in pathology. Between the condyle and the articular fossa is a disc made of fibrocartilage that acts as a cushion to absorb stress and allows the This paper proposes a probabilistic approach for the design of elastic elements to be used in structure-controlled variable stiffness actuators VSA for robotic applications.

A 'read' is counted each time someone views a publication summary such as the title, abstract, and list of authors , clicks on a figure, or views or downloads the full-text. Arthropathies are called polyarticular multiarticular when involving many joints and monoarticular when involving only a single joint. In particular, wire bond reliability of the power module related to the thermal fatigue material degradation of aluminum wire is one of the main concerns.

This resource provides students with foundational information and real-world applications of rehabilitative techniques and serves as a referential cornerstone for experienced rehabilitation clinicians. Statistical significance is denoted by asterisks. Form structure follows Function. NOTE: The following references turned up as hits while searching relevant terms according to a search engine, however it was not always possible to verify the validity of each reference. To move the joint through its full range of motion, the FDP with a known moment arm of 1 cm must have an excursion of 1.

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The closed contours indicate the core As a toe extends at the MTP joint, the corresponding metatarsal plantar flexes and bears more weight at the distal condyles. Peripheral sensitization of the nervous system is defined as increased responsiveness and reduced threshold of nociceptors to stimulation of their receptive fields. If joint motion is not free, the involved muscles that move it cannot function and cannot be restored to normal.

J Bone Joint Surg Am. Algebraic equations of this new spherical CV coupling mechanism are derived. Thus, impaired muscle function leads to impaired joint function, and, conversely, impaired joint function leads to impaired muscle function. The joint is lined by wear resistant hyaline cartilage and is bathed by synovial fluid. An adaptive task controller for a physical robot interaction task si validated in the last part of the chapter.

Recognize posterior tibialis tendon dysfunction and begin to include it in differential diagnoses. Angular function in the singular stress field at the vertex in the three-dimensional joint is calculated using an eigenvector determined from the eigenvalue analysis. Biomechanical Evaluation. Joint Biomechanics: Concerns in Resistance Training Shoulders The shoulder is prone to injury during weight training because of its structure and the forces to which it is subjected. Exercise at a controlled speed. Start studying Principles of Orthotic Design.

Examples of an implant used in hip and knee joints are shown in Fig. It is an effective tool to solve ill-posed regression problems by adding extra constraints in the prior distribution under the Bayesian framework. Knowledge of the mechanisms involved in an injury is necessary to evaluate an injury accurately.

Rank is commensurate with experience and qualifications. The proposed facility will allow researchers to understand and characterize structure-property relationships within nanoscience. Gene therapy aims to correct a genetic defect in a given cell type, to restore function, or to provide novel functions. Edgar Lopategui Corsino M. This measurement instrument is a helpful, clinical tool that allows for objective measurements in order to accurately track progress in a rehabilitation program.

The purpose of this study was to assess the biomechanical properties of epimysium, the collagenous tissue sheath that surrounds muscles in the body. We also compare performance of the controllers in terms of tracking, control effort, and parameter estimation for both nominal and off-nominal model parameters.

Biomechanics is often overwhelming because of its mathematical and engineering emphasis. Functional electrical stimulation has had some success in improving ventilatory function in adult patients with SCI Glenn et al, ; Carter et al, ; Glenn et al, A lap-joint geometry was modeled for unreinforced polyamide PA 6 specimens. This review will describe the state of the art of Normal muscle function depends on normal joint function, and vice versa.

Ward, Samuel R. Applications of the concepts developed include blood-materials compatibility, biomimetic materials, hard and soft tissue-materials interactions, drug delivery, tissue engineering, and biotechnology. Arthritis is the leading cause of disability in people over the age of T-tubule diameters were measured by the full width at half maximum FWHM of the intensity profile across their images.

The size distribution of control t-tubules from 12 control cells and 4 hearts and diseased tubules from 15 cells and 5 hearts are shown in Figure 3D. The mean diameter of WGA labelled t-tubules of diseased cells was 0. Although close to the diffraction limit, these values are larger than reported for rat ventricular myocytes [26] but similar to those reported for rabbit [30].

These data show that diseased myocytes can undergo significant remodelling of t-tubular structure with a loss of radial directed t-tubules and an increase in oblique and longitudinally oriented t-tubules. There appeared to be large regions of the cell without obvious t-tubule labelling but without a suitable lipid marker for fixed tissue it is possible that some t-tubules might not be WGA labelled due to a change in glycosylation and therefore WGA labelling. To examine this possibility, tissue from 3 control and 3 diseased hearts were dual labelled for WGA and various sarcolemmal membrane proteins: dihydropyridine receptors DHPR , sodium calcium exchangers NCX , and caveolin 3 Cav3.

This labelling suggested that the t-system was more extensive than indicated by WGA alone see Figure 4. These thinner tubules formed ring-like structures which would be consistent with these tubules surrounding myofibrils see Figure 5. In diseased myocytes, similar labelling patterns are seen but the organization of the thinner tubules was generally disrupted. Panels are arranged so that the left column corresponds to normal and the right column diseased tissue. In control myocytes C , finer tubules containing only the NCX label can be seen to connect to larger spoke like tubules containing both labels.

Diseased D myocytes have similar labelling pattern but many connections between larger tubules appear broken. E Again, finer tubules labelled with only Cav3 connect larger tubules containing both labels. Diseased myocytes F have similar labelling pattern but with a reduction in fine Cav3 labelling between larger tubules. Images are z projections of 4 slices with z depth of 0. Panels A and B show transverse sections of normal and diseased myocytes respectively, labelled for Cav3 and f -actin.

The contractile machinery is surrounded by Cav3 labelling at this plane which was selected to be centred at the z-line. Gaps in the centre of contractile bundles contain isolated Cav3 labelling small white arrow and inspection of adjacent sections show that this arises from axial tubules that join transverse tubules outside the presented image plane. A connection between adjacent radial t-tubules is indicated by the large arrow. Panels C and D show transverse sections of normal and diseased tissue respectively labelled for RyR and f -actin.

It is apparent that each contractile bundle is surrounded by several RyR clusters. All images are projections of 4 slices with z depth of 0. Since Cav3 provided a reliable marker of surface membrane, we compared the distribution of Cav3 labelling to that of myofibrillar f -actin Figure 5A and 5B. Myofibrils generally followed the spoke-like arrangement of t-tubules so the contractile machinery appeared as flattened wedges or plates in cross section.

In places, Cav3 labeled t-tubules formed anastamoses between the radial t-system spokes large arrow and some isolated Cav3 labeling could be seen surrounded by myofibrils small arrow. Examination of adjacent sections not shown showed that these tubules were axially oriented and joined radial t-tubules at the next z-line. A similar relationship between Cav3 and f- actin was seen in diseased cells Figure 5B but the overall pattern of labelling was more disjointed with the wedge-like pattern of contractile machinery becoming less obvious.

This labelling showed that each myofilament bundle was surrounded by several RyR clusters and there was no obvious change in the labelling between control and diseased cells beyond a subtle reorganization of the myofibrils. To assess the volume of the cell occupied by contractile apparatus, a binary mask of f- actin labelling was created and expressed as percentage of total area. In control, there were approximately 0.

This visual observation was supported by colocalisation analysis by Pearson's and Mander's coefficients in 3D which showed a significant reduction in DHPR colocalization Table 1. The white line indicates the position of intensity readings along a WGA labelled t-tubule label not shown for clarity. Both labels were non-uniform, and a density plot Figure 6F shows that local concentrations of DHPR were not perfectly aligned with the RyR clusters although considerable overlap between both labels was present.

Given the smaller fraction of membrane area occupied by jSR e.


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This report presents a detailed analysis of the architecture of cellular structures critical to excitation-contraction coupling in normal and failing human myocardium. Quantitative analysis of WGA labelled t-tubules in ventricular myocytes demonstrated major alterations in the tubular network in diseased cells compared to normal cardiac myocytes. Although some changes in the pattern of WGA labelling have been previously noted [21] these changes have not been quantified.

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Disruption of t-tubule architecture in diseased cells was associated with a small loss of RyR clusters and reduced colocalization between RyRs and DHPRs. This indicates remodelling of the t-tubular network in the failing human heart may contribute to calcium handling abnormalities seen in heart failure and underpins many functional studies in animal models. Two previous studies that have examined the t-system in human cardiac myocytes, although not at the level of detail shown here.

One of the papers described major changes [24] while no major changes were found in a second study [25] Our results show that major changes in the structure of t-tubules can occur in human heart failure, in general agreement with conclusions from animal models of heart failure. However, it is important to note that there is a greater variation in t-tubule pathology seen in human myocytes see Figure 2 than the generally simpler loss of t-tubules described for animal models.

We suspect that the high degree of t-tubule morphology shown here may reflect the long er duration of the disease process in humans. Our results also largely agree with previous immunohistochemical examination of cytoskeletal proteins [22] , [23] , [32] , [33] , [34].

We have found that quite normal t-tubular structure can be found adjacent to severely disrupted t-tubules. This indicates that the t-system in humans is more extensive than might be deduced from WGA labelling alone. This is a noticeable difference between human and animal cells, as, for example there is a high degree of overlap between Cav3 and WGA labeling in rat myocytes [35]. Although the cause and role of the changes in glycocalyx as reported here within t-tubules is unclear, it is possible that the expansion of the glycocalyx drives the remodelling of parts of the t-tubule network.

It is also possible that some hypertrophic signals, which lead to the expansion of cytoskeletal proteins [36] in heart failure, also drive t-system remodelling. In contrast to our results, Kaprielian et al. However, we suggest that their different conclusion may have arisen from the dilation of t-tubules in disease reported here which would have made them more obvious. In connection with this point, Figure 8D in their paper showed a dilated non-radial t-tubule in EM similar to the observations reported here.

It should also be noted that, even in normal tissue, the general architecture of the human t-system is different i. In addition to a marked reorganisation of the t-system within the failing human heart, we found a small reduction in the number of RyR clusters per unit myofibril area and a decrease in colocalization between DHPRs and RyRs. The importance of the local geometric arrangement of DHPRs and RyRs has been highlighted in modelling studies where EC coupling gain is diminished with small distortions in junctional geometry [12].


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Our results support this idea, although the level of colocalization observed between DHPR and RyR clusters in control human ventricular myocytes suggests that DHPRs are not almost exclusively restricted to the couplon as has been suggested to be the case in rat [38]. That such a change was not observed in transverse section may be explained by the poorer axial resolution of the microscope and the change in t-tubule orientation towards a axial direction.

Even if the couplons themselves did not move away from z-lines, the presence of non junctional DHPRs in displaced t-tubules would still lead to a reduction in colocalisation. In a rat model of heart failure, Song et. However, it should also be noted that the spatial reorganization of the t-tubule network in human heart failure that we report here is quite different to the loss of transverse tubules and an increase axial tubules reported for the SHR model [14].

We suggest that future study of the mechanisms underlying the control of t-tubule remodelling may lead to new directions for treating heart failure. This antibody was raised against a peptide corresponding to residues 1—46 of rabbit Cav1. The white line indicates the position of intensity readings along a WGA blue labelled t-tubule. We thank Isuru Dilshan and Cherrie Kong for laboratory assistance, Professor Stephen Munn, Helen Gibbs and Janice Langlands for assistance in obtaining donor tissue and transplant recipients and donor families for donating tissue.

Performed the experiments: DJC. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Abstract Background The cardiac myocyte t-tubular system ensures rapid, uniform cell activation and several experimental lines of evidence suggest changes in the t-tubular system and associated excitation-contraction coupling proteins may occur in heart failure.

Szydlowska K, Tymianski M. Calcium, ischemia and excitotoxicity. Regulation and pharmacology of the mitochondrial permeability transition pore. Zamzami N, Kroemer G. Nat Rev Mol Cell Biol. Local control of mitochondrial membrane potential, permeability transition pore and reactive oxygen species by calcium and calmodulin in rat ventricular myocytes.

Characterization of a calmodulin kinase II inhibitor protein in brain. CaMKII determines mitochondrial stress responses in heart. Mitochondrial electron transport complex I is a potential source of oxygen free radicals in the failing myocardium. Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Oxidative stress and mitochondrial DNA damage in heart failure. Circ J. The mitochondrial calcium uniporter is a highly selective ion channel. Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter.

A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporter. Rutter GA, Rizzuto R.

http://ivangorbachev.com/best-phone-tracker-pixel-4.php Trends Biochem Sci. Quantification of calcium signal transmission from sarco-endoplasmic reticulum to the mitochondria. Mitochondria as sensors and regulators of calcium signalling. Ru, a specific mitochondrial calcium uptake inhibitor, improves cardiac post-ischaemic functional recovery in rats in vivo. Br J Pharmacol. T-tubule remodeling during transition from hypertrophy to heart failure. Orphaned ryanodine receptors in the failing heart. Disrupted junctional membrane complexes and hyperactive ryanodine receptors after acute junctophilin knockdown in mice.

PLoS Biol. In vivo suppression of microRNA prevents the transition toward decompensated hypertrophy in aortic-constricted mice. Tuning cardiac performance in ischemic heart disease and failure by modulating myofilament function. J Mol Med Berl. Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease. Defects in ankyrin-based membrane protein targeting pathways underlie atrial fibrillation. Ankyrin-B reduction enhances Ca spark-mediated SR Ca release promoting cardiac myocyte arrhythmic activity.

Heart Rhythm. Ankyrin-B protein in heart failure: identification of a new component of metazoan cardioprotection. The giant protein titin. Emerging roles in physiology and pathophysiology. Altered expression of titin and contractile proteins in failing human myocardium. The role of the cytoskeleton in left ventricular pressure overload hypertrophy and failure.

Cardiac hypertrophy and reduced contractility in hearts deficient in the titin kinase region. Membrane organization of the dystrophin-glycoprotein complex. Emery AE. Muscular dystrophy into the new millennium. Neuromuscul Disord. The heart in human dystrophinopathies. Lohan J, Ohlendieck K.

Biochim Biophys Acta. Biochem Biophys Res Commun. Properties of cardiac cells from dystrophic mouse. The muscular dystrophies. Leaky RyR2 trigger ventricular arrhythmias in Duchenne muscular dystrophy. Mol Endocrinol. Currie S. Crossref Google Scholar De Koninck P, Schulman H. Diabetes increases mortality after myocardial infarction by oxidizing camkii. Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure.

Aldosterone stimulates matrix metalloproteinases and reactive oxygen species in adult rat ventricular cardiomyocytes. CaMKII in myocardial hypertrophy and heart failure. Currie S, Smith GL. FEBS Lett. The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure.

Calmodulin kinase II inhibition protects against myocardial cell apoptosis in vivo. Death, cardiac dysfunction, and arrhythmias are increased by calmodulin kinase II in calcineurin cardiomyopathy. The delta isoform of CaM kinase II is required for pathological cardiac hypertrophy and remodeling after pressure overload. Acta Pharmacol Sin. Molecular aspects of adrenergic signal transduction in cardiac failure. Cloning of the gene and cDNA for mammalian beta-adrenergic receptor and homology with rhodopsin.

Excitation-Contraction Coupling

Removal of phosphorylation sites from the beta 2-adrenergic receptor delays onset of agonist-promoted desensitization. Receptors and G proteins as primary components of transmembrane signal transduction. Part 1. G-protein-coupled receptors: structure and function. Quantification of beta-adrenoceptors and beta-adrenoceptor kinase on protein and mRNA levels in heart failure.

Altered expression of beta-adrenergic receptor kinase and beta 1-adrenergic receptors in the failing human heart. G protein-coupled receptor kinases in normal and failing myocardium. Carvedilol inhibits the mitochondrial permeability transition by an antioxidant mechanism. Cardiovasc Toxicol. Carvedilol inhibits mitochondrial oxygen consumption and superoxide production during calcium overload in isolated heart mitochondria.

Epac mediates beta-adrenergic receptor-induced cardiomyocyte hypertrophy. Epac enhances excitation-transcription coupling in cardiac myocytes. Cardiotoxic and cardioprotective features of chronic beta-adrenergic signaling. Identification of intracellular receptor proteins for activated protein kinase C. PKC-alpha regulates cardiac contractility and propensity toward heart failure.

Dorn GW, Force T. Protein kinase cascades in the regulation of cardiac hypertrophy. Cardiotrophic effects of protein kinase C epsilon: analysis by in vivo modulation of PKCepsilon translocation. Three-dimensional solution structure of the calcium-signaling protein apo-SA1 as determined by NMR. S proteins: structure, functions and pathology. Redox modifications of the C-terminal cysteine residue cause structural changes in SA1 and SB proteins.

Curr Chem Biol. SA1: a regulator of myocardial contractility. SA1 increases the gain of excitation-contraction coupling in isolated rabbit ventricular cardiomyocytes. Mol Cell Biol. Impaired cardiac contractility response to hemodynamic stress in SA1-deficient mice. SA1 deficiency results in prolonged ventricular repolarization in response to sympathetic activation. Gen Physiol Biophys. Lack of SA1 in mice confers a gender-dependent hypertensive phenotype and increased mortality after myocardial infarction.

Cardiac SA1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction. SA1 genetically targeted therapy reverses dysfunction of human failing cardiomyocytes. Cardiac adenoviral SA1 gene delivery rescues failing myocardium. Calcineurin and human heart failure.

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy. Calcineurin expression, activation, and function in cardiac pressure-overload hypertrophy. Targeted inhibition of calcineurin prevents agonist-induced cardiomyocyte hypertrophy. Requirement of nuclear factor of activated T-cells in calcineurin-mediated cardiomyocyte hypertrophy. Circ Heart Fail. Calcineurin in human heart hypertrophy. Differential activation of signal transduction pathways in human hearts with hypertrophy versus advanced heart failure.

Prevention of cardiac hypertrophy in mice by calcineurin inhibition. Impaired cardiac hypertrophic response in Calcineurin Abeta -deficient mice. Sudden death prevention in patients with advanced ventricular dysfunction. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction.