Myosin Heavy Chains
Myosin Light Chains
Myosin Type II
Myosin Type V
Nonmuscle Myosin Type IIA
Myosin Type I
Nonmuscle Myosin Type IIB
Cardiomyopathy, Hypertrophic, Familial
Molecular Sequence Data
Death, Sudden, Cardiac
Molecular Motor Proteins
Amino Acid Sequence
Myosin Type III
Rheumatic Heart Disease
Heterocyclic Compounds with 4 or More Rings
Adrenergic beta-2 Receptor Antagonists
Cardiac Pacing, Artificial
Electrophoresis, Polyacrylamide Gel
Disease Models, Animal
Ventricular Function, Left
Enterovirus B, Human
Cardiac Imaging Techniques
Cyclic AMP-Dependent Protein Kinases
Cardiac Output, Low
Gene Expression Regulation
Muscle Fibers, Skeletal
Out-of-Hospital Cardiac Arrest
Heart Defects, Congenital
Promoter Regions, Genetic
Heart Conduction System
Cardiac Resynchronization Therapy
Ventricular Dysfunction, Left
Mice, Inbred Strains
Regulatory Sequences, Nucleic Acid
Myosin Type IV
Muscle Fibers, Slow-Twitch
Protein Structure, Tertiary
Muscle Fibers, Fast-Twitch
Polymerase Chain Reaction
Hypertrophy, Left Ventricular
Atrial Natriuretic Factor
Altered cardiac excitation-contraction coupling in mutant mice with familial hypertrophic cardiomyopathy. (1/275)Excitation-contraction coupling in cardiac muscle of familial hypertrophic cardiomyopathy (FHC) remains poorly understood, despite the fact that the genetic alterations are well defined. We characterized calcium cycling and contractile activation in trabeculae from a mutant mouse model of FHC (Arg403Gln knockin, alpha-myosin heavy chain). Wild-type mice of the same strain and age ( approximately 20 weeks old) served as controls. During twitch contractions, peak intracellular Ca2+ ([Ca2+]i) was higher in mutant muscles than in the wild-type (P < 0.05), but force development was equivalent in the two groups. Ca2+ transient amplitude increased dramatically in both groups as stimulation rate increased from 0.2 to 4 Hz. Nevertheless, developed force fell at the higher stimulation rates in the mutants but not in controls (P < 0.05). The steady-state force-[Ca2+]i relationship was less steep in mutants (Hill coefficient, 2.94 +/- 0.27 vs. 5.28 +/- 0.64; P > 0.003), with no changes in the [Ca2+]i required for 50% activation or maximal Ca2+-activated force. Thus, calcium cycling and myofilament properties are both altered in FHC mutant mice: more Ca2+ is mobilized to generate force, but this does not suffice to maintain contractility at high stimulation rates. (+info)
A post-transcriptional compensatory pathway in heterozygous ventricular myosin light chain 2-deficient mice results in lack of gene dosage effect during normal cardiac growth or hypertrophy. (2/275)Our previous study of homozygous mutants of the ventricular specific isoform of myosin light chain 2 (mlc-2v) demonstrated that mlc-2v plays an essential role in murine heart development (Chen, J., Kubalak, S. W., Minamisawa, S., Price, R. L., Becker, K. D., Hickey, R., Ross, J., Jr., and Chien, K. R. (1998) J. Biol. Chem. 273, 1252-1256). As gene dosage of some myofibrillar proteins can affect muscle function, we have analyzed heterozygous mutants in depth. Ventricles of heterozygous mutants displayed a 50% reduction in mlc-2v mRNA, yet expressed normal levels of protein both under basal conditions and following induction of cardiac hypertrophy by aortic constriction. Heterozygous mutants exhibited cardiac function comparable to that of wild-type littermate controls both prior to and following aortic constriction. There were no significant differences in contractility and responses to calcium between wild-type and heterozygous unloaded cardiomyocytes. We conclude that heterozygous mutants show neither a molecular nor a physiological cardiac phenotype either at base line or following hypertrophic stimuli. These results suggest that post-transcriptional compensatory mechanisms play a major role in maintaining the level of MLC-2v protein in murine hearts. In addition, as our mlc-2v knockout mutants were created by a knock-in of Cre recombinase into the endogenous mlc-2v locus, this study demonstrates that heterozygous mlc-2v cre knock-in mice are appropriate for ventricular specific gene targeting. (+info)
The CACC box and myocyte enhancer factor-2 sites within the myosin light chain 2 slow promoter cooperate in regulating nerve-specific transcription in skeletal muscle. (3/275)Previous experiments showed that activity of the -800-base pair MLC2slow promoter was 75-fold higher in the innervated soleus (SOL) compared with the noninnervated SOL muscles. Using in vivo DNA injection of MLC2slow promoter-luciferase constructs, the aim of this project was to identify regulatory sites and potential transcription factors important for slow nerve-dependent gene expression. Three sites within the proximal promoter (myocyte enhancer factor-2 (MEF2), E-box, and CACC box) were individually mutated, and the effect on luciferase expression was determined. There was no change in luciferase expression in the SOL and extensor digitorum longus (EDL) muscles when the E-box was mutated. In contrast, the MEF2 mutation resulted in a 30-fold decrease in expression in the innervated SOL muscles (10.3 versus 0.36 normalized relative light units (RLUs)). Transactivation of the MLC2slow promoter by overexpressing MEF2 was only seen in the innervated SOL (676,340 versus 2,225,957 RLUs; p < 0.01) with no effect in noninnervated SOL or EDL muscles. These findings suggest that the active MLC2slow promoter is sensitive to MEF2 levels, but MEF2 levels alone do not determine nerve-dependent expression. Mutation of the CACC box resulted in a significant up-regulation in the EDL muscles (0.23 versus 4.08 normalized RLUs). With the CACC box mutated, overexpression of MEF2 was sufficient to transactivate the MLC2slow promoter in noninnervated SOL muscles (27,536 versus 1, 605,797 RLUs). Results from electrophoretic mobility shift and supershift assays confirm MEF2 protein binding to the MEF2 site and demonstrate specific binding to the CACC sequence. These results suggest a model for nerve-dependent regulation of the MLC2slow promoter in which derepression occurs through the CACC box followed by quantitative expression through enhanced MEF2 activation. (+info)
The effect of removing the N-terminal extension of the Drosophila myosin regulatory light chain upon flight ability and the contractile dynamics of indirect flight muscle. (4/275)The Drosophila myosin regulatory light chain (DMLC2) is homologous to MLC2s of vertebrate organisms, except for the presence of a unique 46-amino acid N-terminal extension. To study the role of the DMLC2 N-terminal extension in Drosophila flight muscle, we constructed a truncated form of the Dmlc2 gene lacking amino acids 2-46 (Dmlc2(Delta2-46)). The mutant gene was expressed in vivo, with no wild-type Dmlc2 gene expression, via P-element-mediated germline transformation. Expression of the truncated DMLC2 rescues the recessive lethality and dominant flightless phenotype of the Dmlc2 null, with no discernible effect on indirect flight muscle (IFM) sarcomere assembly. Homozygous Dmlc2(Delta2-46) flies have reduced IFM dynamic stiffness and elastic modulus at the frequency of maximum power output. The viscous modulus, a measure of the fly's ability to perform oscillatory work, was not significantly affected in Dmlc2(Delta2-46) IFM. In vivo flight performance measurements of Dmlc2(Delta2-46) flies using a visual closed-loop flight arena show deficits in maximum metabolic power (P(*)(CO(2))), mechanical power (P(*)(mech)), and flight force. However, mutant flies were capable of generating flight force levels comparable to body weight, thus enabling them to fly, albeit with diminished performance. The reduction in elastic modulus in Dmlc2(Delta2-46) skinned fibers is consistent with the N-terminal extension being a link between the thick and thin filaments that is parallel to the cross-bridges. Removal of this parallel link causes an unfavorable shift in the resonant properties of the flight system, thus leading to attenuated flight performance. (+info)
A fluorescent reporter gene as a marker for ventricular specification in ES-derived cardiac cells. (5/275)We have established a CGR8 embryonic stem (ES) cell clone (MLC2ECFP) which expresses the enhanced cyan variant of Aequorea victoria green fluorescent protein (ECFP) under the transcriptional control of the ventricular myosin light chain 2 (MLC2v) promoter. Using epifluorescence imaging of vital embryoid bodies (EB) and reverse transcription-polymerase chain reaction (RT-PCR), we found that the MLC2v promoter is switched on as early as day 7 and is accompanied by formation of cell clusters featuring a bright ECFP blue fluorescence. The fluorescent areas within the EBs were all beating on day 8. MLC2ECFP ES cells showed the same time course of cardiac differentiation as mock ES cells as assessed by RT-PCR of genes encoding cardiac-specific transcription factors and contractile proteins. The MLC2v promoter conferred ventricular specificity to ECFP expression within the EB as revealed by MLC2v co-staining of ECFP fluorescent cells. MLC2ECFP-derived cardiac cells still undergo cell division on day 12 after isolation from EBs but withdraw from the cell cycle on day 16. This ES cell clone provides a powerful cell model to study the signalling roads of factors regulating cardiac cell proliferation and terminal differentiation with a view to using them for experimental cell therapy. (+info)
Adverse effects of constitutively active alpha(1B)-adrenergic receptors after pressure overload in mouse hearts. (6/275)Cardiac hypertrophy and function were studied 6 wk after constriction of the thoracic aorta (TAC) in transgenic (TG) mice expressing constitutively active mutant alpha(1B)-adrenergic receptors (ARs) in the heart. Hearts from sham-operated TG animals and nontransgenic littermates (WT) were similar in size, but hearts from TAC/TG mice were larger than those from TAC/WT mice, and atrial natriuretic peptide mRNA expression was also higher. Lung weight was markedly increased in TAC/TG animals, and the incidence of left atrial thrombus formation was significantly higher. Ventricular contractility in anesthetized animals, although it was increased in TAC/WT hearts, was unchanged in TAC/TG hearts, implying cardiac decompensation and progression to failure in TG mice. There was no increase in alpha(1A)-AR mRNA expression in TAC/WT hearts, and expression was significantly reduced in TAC/TG hearts. These findings show that cardiac expression of constitutively actively mutant alpha(1B)-ARs is detrimental in terms of hypertrophy and cardiac function after pressure overload and that increased alpha(1A)-AR mRNA expression is not a feature of the hypertrophic response in this murine model. (+info)
The calcineurin-NFAT pathway and muscle fiber-type gene expression. (7/275)To test for a role of the calcineurin-NFAT (nuclear factor of activated T cells) pathway in the regulation of fiber type-specific gene expression, slow and fast muscle-specific promoters were examined in C2C12 myotubes and in slow and fast muscle in the presence of calcineurin or NFAT2 expression plasmids. Overexpression of active calcineurin in myotubes induced both fast and slow muscle-specific promoters but not non-muscle-specific reporters. Overexpression of NFAT2 in myotubes did not activate muscle-specific promoters, although it strongly activated an NFAT reporter. Thus overexpression of active calcineurin activates transcription of muscle-specific promoters in vitro but likely not via the NFAT2 transcription factor. Slow myosin light chain 2 (MLC2) and fast sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA1) reporter genes injected into rat soleus (slow) and extensor digitorum longus (EDL) (fast) muscles were not activated by coinjection of activated calcineurin or NFAT2 expression plasmids. However, an NFAT reporter was strongly activated by overexpression of NFAT2 in both muscle types. Calcineurin and NFAT protein expression and binding activity to NFAT oligonucleotides were different in slow vs. fast muscle. Taken together, these results indicate that neither calcineurin nor NFAT appear to have dominant roles in the induction and/or maintenance of slow or fast fiber type in adult skeletal muscle. Furthermore, different pathways may be involved in muscle-specific gene expression in vitro vs. in vivo. (+info)
Altered cross-bridge characteristics following haemodynamic overload in rabbit hearts expressing V3 myosin. (8/275)1. Our goal in this study was to evaluate the effect of haemodynamic overload on cross-bridge (XBr) kinetics in the rabbit heart independently of myosin heavy chain (MHC) isoforms, which are known to modulate kinetics in small mammals. We applied a myothermal-mechanical protocol to isometrically contracting papillary muscles from two rabbit heart populations: (1) surgically induced right ventricular pressure overload (PO), and (2) sustained treatment with propylthiouracil (PTU). Both treatments resulted in a 100 % V3 MHC profile. 2. XBr force-time integral (FTI), evaluated during the peak of the twitch from muscle FTI and tension-dependent heat, was greater in the PO hearts (0.80 +/- 0.10 versus 0.45 +/- 0.05 pN s, means +/- S.E.M., P = 0.01). 3. Within the framework of a two-state XBr model, the PO XBr developed more force while attached (5.8 +/- 0.9 versus 2.7 +/- 0.3 pN), with a lower cycling rate (0.89 +/- 0.10 versus 1.50 +/- 0.14 s(-1)) and duty cycle (0.14 +/- 0.03 versus 0.24 +/- 0.02). 4. Only the ventricular isoforms of myosin light chain 1 and 2 and cardiac troponin I (cTnI) were expressed, with no difference in cTnI phosphorylation between the PO and PTU samples. The troponin T (TnT) isoform compositions in the PO and PTU samples were significantly different (P = 0.001), with TnT2 comprising 2.29 +/- 0.03 % in PO hearts versus 0.98 +/- 0.01 % in PTU hearts of total TnT. 5. This study demonstrates that MHC does not mediate dramatic alterations in XBr function induced by haemodynamic overload. Our findings support the likelihood that differences among other thick and thin filament proteins underlie these XBr alterations. (+info)
The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.
Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.
Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.
Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.
In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.
The exact cause of HCM is not fully understood, but it is thought to be related to a combination of genetic and environmental factors. Some people with HCM have a family history of the condition, and it is also more common in certain populations such as athletes and individuals with a history of hypertension or diabetes.
Symptoms of HCM can vary from person to person and may include shortness of breath, fatigue, palpitations, and chest pain. In some cases, HCM may not cause any symptoms at all and may be detected only through a physical examination or diagnostic tests such as an echocardiogram or electrocardiogram (ECG).
Treatment for HCM typically focuses on managing symptoms and reducing the risk of complications. This may include medications to reduce blood pressure, control arrhythmias, or improve heart function, as well as lifestyle modifications such as regular exercise and a healthy diet. In some cases, surgery or other procedures may be necessary to treat HCM.
Prognosis for individuals with HCM varies depending on the severity of the condition and the presence of any complications. With appropriate treatment and management, many people with HCM can lead active and fulfilling lives, but it is important to receive regular monitoring and care from a healthcare provider to manage the condition effectively.
Examples of autoimmune diseases include:
1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.
The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.
HFCM is caused by mutations in genes that encode proteins involved in the structure and function of the heart muscle. These mutations can be inherited from one's parents or can occur spontaneously. The condition typically affects multiple members of a family, and the age of onset and severity of symptoms can vary widely.
HFCM is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as echocardiography, electrocardiography, and cardiac MRI. Treatment options for HFCM include medications to manage symptoms, lifestyle modifications such as regular exercise and a healthy diet, and in some cases, surgery or other procedures to repair or replace damaged heart tissue.
In summary, Cardiomyopathy, Hypertrophic, Familial (HFCM) is a genetic disorder that affects the heart muscle, leading to thickening of the heart muscle and potentially causing heart failure and other complications. It is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle, and can be inherited or caused by spontaneous mutations in genes that encode proteins involved in heart muscle structure and function.
Medical Term: Cardiomegaly
Definition: An abnormal enlargement of the heart.
Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.
Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.
Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.
Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.
Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
Some examples of the use of 'Death, Sudden, Cardiac' in medical contexts include:
1. Sudden cardiac death (SCD) is a major public health concern, affecting thousands of people each year in the United States alone. It is often caused by inherited heart conditions, such as hypertrophic cardiomyopathy or long QT syndrome.
2. The risk of sudden cardiac death is higher for individuals with a family history of heart disease or other pre-existing cardiovascular conditions.
3. Sudden cardiac death can be prevented by prompt recognition and treatment of underlying heart conditions, as well as by avoiding certain risk factors such as smoking, physical inactivity, and an unhealthy diet.
4. Cardiopulmonary resuscitation (CPR) and automated external defibrillators (AEDs) can be effective in restoring a normal heart rhythm during sudden cardiac death, especially when used promptly after the onset of symptoms.
There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:
1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.
It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.
There are several possible causes of dilated cardiomyopathy, including:
1. Coronary artery disease: This is the most common cause of dilated cardiomyopathy, and it occurs when the coronary arteries become narrowed or blocked, leading to a decrease in blood flow to the heart muscle.
2. High blood pressure: Prolonged high blood pressure can cause the heart muscle to become weakened and enlarged.
3. Heart valve disease: Dysfunctional heart valves can lead to an increased workload on the heart, which can cause dilated cardiomyopathy.
4. Congenital heart defects: Some congenital heart defects can lead to an enlarged heart and dilated cardiomyopathy.
5. Alcohol abuse: Chronic alcohol abuse can damage the heart muscle and lead to dilated cardiomyopathy.
6. Viral infections: Some viral infections, such as myocarditis, can cause inflammation of the heart muscle and lead to dilated cardiomyopathy.
7. Genetic disorders: Certain genetic disorders, such as hypertrophic cardiomyopathy, can cause dilated cardiomyopathy.
8. Obesity: Obesity is a risk factor for developing dilated cardiomyopathy, particularly in younger people.
9. Diabetes: Diabetes can increase the risk of developing dilated cardiomyopathy, especially if left untreated or poorly controlled.
10. Age: Dilated cardiomyopathy is more common in older adults, with the majority of cases occurring in people over the age of 65.
It's important to note that many people with these risk factors will not develop dilated cardiomyopathy, and some people without any known risk factors can still develop the condition. If you suspect you or someone you know may have dilated cardiomyopathy, it's important to consult a healthcare professional for proper diagnosis and treatment.
Treatment for rheumatic heart disease typically involves antibiotics to prevent further damage and medications to manage symptoms such as high blood pressure, swelling, and shortness of breath. In severe cases, surgery may be necessary to repair or replace damaged valves.
Prevention of rheumatic heart disease involves early diagnosis and treatment of rheumatic fever, as well as maintaining good cardiovascular health through a healthy diet, regular exercise, and not smoking.
Some common symptoms of rheumatic heart disease include:
* Shortness of breath
* Swelling in the legs, ankles, and feet
* Chest pain or discomfort
* Dizziness or lightheadedness
* Irregular heartbeat
Some common risk factors for developing rheumatic heart disease include:
* Previous exposure to group A streptococcus bacteria, which can cause rheumatic fever
* Family history of rheumatic heart disease
* Poor living conditions or overcrowding, which can increase the risk of exposure to group A streptococcus bacteria
* Malnutrition or a diet low in certain nutrients, such as vitamin D and iron.
There are several possible causes of cardiac tamponade, including:
1. Trauma: Blunt chest trauma, such as a car accident or fall, can cause bleeding within the pericardial sac and lead to cardiac tamponade.
2. Infection: Bacterial, viral, or fungal infections can spread to the pericardial sac and cause inflammation and fluid accumulation.
3. Ischemia: Reduced blood flow to the heart muscle, such as during a heart attack, can lead to inflammation and fluid accumulation within the pericardial sac.
4. Cancer: Cancer that has spread to the pericardial sac can cause fluid accumulation and cardiac tamponade.
5. Hemodynamic instability: Severe hypotension or tachycardia can cause fluid to seep into the pericardial sac, leading to cardiac tamponade.
The symptoms of cardiac tamponade may include:
1. Chest pain: Pain in the chest that worsens with deep breathing or coughing.
2. Shortness of breath: Difficulty breathing due to compression of the heart.
3. Fatigue: Weakness and tiredness due to decreased cardiac output.
4. Palpitations: Abnormal heart rhythms.
5. Low blood pressure: Hypotension.
Cardiac tamponade is a medical emergency that requires prompt treatment to prevent cardiac failure and death. Treatment options may include:
1. Pericardiocentesis: Insertion of a needle into the pericardial sac to drain excess fluid.
2. Surgical drainage: Surgical removal of fluid and any underlying cause of tamponade.
3. Diuretics: Medications to increase urine production and reduce fluid buildup in the body.
4. Inotropes: Medications to increase heart contractility.
5. Mechanical support: Use of a device such as an intra-aortic balloon pump or an implantable cardioverter-defibrillator to support the heart.
In some cases, cardiac tamponade may be a sign of a more serious underlying condition that requires long-term management. It is important to work with a healthcare provider to develop a treatment plan that addresses the underlying cause of the tamponade and helps to prevent recurrences.
There are two main types of heart failure:
1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.
Symptoms of heart failure may include:
* Shortness of breath
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness
Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).
It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.
There are many different types of heart diseases, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries, which supply blood to the heart muscle, leading to chest pain or a heart attack.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, leading to fatigue, shortness of breath, and swelling in the legs.
3. Arrhythmias: Abnormal heart rhythms, such as atrial fibrillation or ventricular tachycardia, which can cause palpitations, dizziness, and shortness of breath.
4. Heart valve disease: Problems with the heart valves, which can lead to blood leaking back into the chambers or not being pumped effectively.
5. Cardiomyopathy: Disease of the heart muscle, which can lead to weakened heart function and heart failure.
6. Heart murmurs: Abnormal sounds heard during a heartbeat, which can be caused by defects in the heart valves or abnormal blood flow.
7. Congenital heart disease: Heart defects present at birth, such as holes in the heart or abnormal blood vessels.
8. Myocardial infarction (heart attack): Damage to the heart muscle due to a lack of oxygen, often caused by a blockage in a coronary artery.
9. Cardiac tamponade: Fluid accumulation around the heart, which can cause compression of the heart and lead to cardiac arrest.
10. Endocarditis: Infection of the inner lining of the heart, which can cause fever, fatigue, and heart valve damage.
Heart diseases can be diagnosed through various tests such as electrocardiogram (ECG), echocardiogram, stress test, and blood tests. Treatment options depend on the specific condition and may include lifestyle changes, medication, surgery, or a combination of these.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
The most common cause of hyperthyroidism is an autoimmune disorder called Graves' disease, which causes the thyroid gland to produce too much thyroxine (T4) and triiodothyronine (T3). Other causes include inflammation of the thyroid gland (thyroiditis), thyroid nodules, and certain medications.
Symptoms of hyperthyroidism can vary depending on the severity of the condition, but may include:
* Rapid weight loss
* Nervousness or irritability
* Increased heart rate
* Heat intolerance
* Changes in menstrual cycle
* Muscle weakness
If left untreated, hyperthyroidism can lead to more serious complications such as heart problems, bone loss, and eye problems. Treatment options for hyperthyroidism include medications to reduce hormone production, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.
In pregnant women, untreated hyperthyroidism can increase the risk of miscarriage, preterm labor, and intellectual disability in the baby. Treatment options for pregnant women with hyperthyroidism are similar to those for non-pregnant adults, but may need to be adjusted to avoid harm to the developing fetus.
It is important for individuals suspected of having hyperthyroidism to seek medical attention as soon as possible to receive proper diagnosis and treatment. Early treatment can help prevent complications and improve quality of life.
There are two types of heart arrest:
1. Asystole - This is when the heart stops functioning completely and there is no electrical activity in the heart.
2. Pulseless ventricular tachycardia or fibrillation - This is when the heart is still functioning but there is no pulse and the rhythm is abnormal.
Heart arrest can be diagnosed through various tests such as electrocardiogram (ECG), blood tests, and echocardiography. Treatment options for heart arrest include cardiopulmonary resuscitation (CPR), defibrillation, and medications to restore a normal heart rhythm.
In severe cases of heart arrest, the patient may require advanced life support measures such as mechanical ventilation and cardiac support devices. The prognosis for heart arrest is generally poor, especially if it is not treated promptly and effectively. However, with proper treatment and support, some patients can recover and regain normal heart function.
There are different types of myocardial infarctions, including:
1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.
Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.
Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.
Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.
Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.
Hypothyroidism can be diagnosed through a series of blood tests that measure the levels of thyroid hormones in the body. Treatment typically involves taking synthetic thyroid hormone medication to replace the missing hormones. With proper treatment, most people with hypothyroidism can lead normal, healthy lives.
Hypothyroidism is a relatively common condition, affecting about 4.6 million people in the United States alone. Women are more likely to develop hypothyroidism than men, and it is most commonly diagnosed in middle-aged women.
Some of the symptoms of Hypothyroidism include:
1. Fatigue or tiredness
2. Weight gain
3. Dry skin
5. Depression or anxiety
6. Memory problems
7. Muscle aches and stiffness
8. Heavy or irregular menstrual periods
9. Pale, dry, or rough skin
10. Hair loss or thinning
11. Cold intolerance
12. Slowed speech and movements
It's important to note that some people may not experience any symptoms at all, especially in the early stages of the condition. However, if left untreated, hypothyroidism can lead to more severe complications such as heart disease, mental health problems, and infertility.
Coxsackievirus infections are a group of viral diseases caused by enteroviruses, primarily Coxsackie A and B viruses. These infections can affect various parts of the body, including the gastrointestinal tract, skin, and nervous system.
Types of Coxsackievirus Infections:
1. Hand, Foot, and Mouth Disease (HFMD): This is a common viral illness that affects children under the age of 10, causing fever, mouth sores, and a rash with blisters on the hands and feet.
2. Herpangina: A severe form of HFMD characterized by small ulcers in the mouth and throat.
3. Aseptic Meningitis: An inflammation of the meninges (protective membranes) around the brain and spinal cord, often caused by Coxsackievirus B.
4. Myocarditis: Inflammation of the heart muscle caused by Coxsackievirus B.
5. Pericarditis: Inflammation of the membrane surrounding the heart (pericardium) caused by Coxsackievirus B.
6. Pleurodynia (also known as Coxsackievirus pleurisy): A sudden onset of chest pain, fever, and cough caused by Coxsackievirus A.
7. Meningoradiculitis: Inflammation of the meninges and spinal nerves caused by Coxsackievirus B.
Symptoms of Coxsackievirus Infections:
The symptoms of coxsackievirus infections can vary depending on the type of infection and the individual affected. Common symptoms include:
* Muscle pain
* Sore throat
* Mouth sores (in HFMD)
* Rash (in HFMD)
* Blisters (in HFMD)
* Seizures (in severe cases)
* Meningitis (inflammation of the membranes surrounding the brain and spinal cord)
* Encephalitis (inflammation of the brain)
* Myocarditis (inflammation of the heart muscle)
* Pericarditis (inflammation of the membrane surrounding the heart)
* Pleurodynia (chest pain, fever, and cough)
* Meningoradiculitis (inflammation of the meninges and spinal nerves)
Diagnosis of Coxsackievirus Infections:
The diagnosis of coxsackievirus infections is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include:
* Blood tests to detect the presence of antibodies against the virus
* PCR (polymerase chain reaction) to detect the genetic material of the virus in respiratory or gastrointestinal secretions
* Culture of the virus from respiratory or gastrointestinal secretions
* Imaging studies such as X-rays, CT scans, MRI scans to evaluate the extent of inflammation or damage to organs.
Treatment and Management of Coxsackievirus Infections:
There is no specific treatment for coxsackievirus infections, but supportive care may be provided to manage symptoms and prevent complications. Supportive care may include:
* Rest and hydration
* Pain management with over-the-counter pain medications or prescription medications
* Antihistamines to reduce fever and relieve itching
* Antiviral medications in severe cases
* Oxygen therapy if necessary
* Intravenous fluids if dehydration is present.
Prevention of Coxsackievirus Infections:
Prevention of coxsackievirus infections is important, especially for high-risk individuals such as children and people with weakened immune systems. Prevention measures include:
* Practicing good hygiene, such as washing hands frequently, especially after using the bathroom or before eating
* Avoiding close contact with people who are sick
* Avoiding sharing food, drinks, or personal items with people who are sick
* Keeping children home from school or daycare if they are experiencing symptoms of a coxsackievirus infection
* Practicing safe sex to prevent the spread of the virus through sexual contact.
Complications of Coxsackievirus Infections:
Coxsackievirus infections can lead to complications, especially in high-risk individuals. Complications may include:
* Meningitis or encephalitis, which can be life-threatening
* Myocarditis, which can lead to heart failure
* Pericarditis, which can cause chest pain and difficulty breathing
* Retinitis, which can cause blindness
* Gastrointestinal bleeding
* Kidney damage or failure.
Prognosis for Coxsackievirus Infections:
The prognosis for coxsackievirus infections is generally good for most people, especially those with mild symptoms. However, high-risk individuals, such as children and people with weakened immune systems, may experience more severe illness and have a poorer prognosis.
Prevention of Coxsackievirus Infections:
Prevention is key to avoiding coxsackievirus infections. Some ways to prevent the spread of the virus include:
* Practicing good hygiene, such as washing your hands frequently and avoiding sharing personal items with people who are sick
* Avoiding close contact with people who are sick
* Keeping children home from school or daycare if they are experiencing symptoms of a coxsackievirus infection
* Practicing safe sex to prevent the spread of the virus through sexual contact.
Treatment of Coxsackievirus Infections:
There is no specific treatment for coxsackievirus infections, but symptoms can be managed with over-the-counter medications and home remedies. Some ways to manage symptoms include:
* Taking over-the-counter pain relievers, such as acetaminophen or ibuprofen, to reduce fever and relieve headache and body aches
* Drinking plenty of fluids to stay hydrated
* Resting and avoiding strenuous activities until symptoms improve
* Using a humidifier to relieve dryness and discomfort in the throat and nose.
Complications of Coxsackievirus Infections:
Coxsackievirus infections can lead to complications, such as:
* Meningitis: an inflammation of the protective membranes that cover the brain and spinal cord
* Encephalitis: an inflammation of the brain
* Myocarditis: an inflammation of the heart muscle
* Pericarditis: an inflammation of the membrane surrounding the heart
* Pleurodynia: a painful inflammation of the lining of the chest cavity.
It's important to seek medical attention if you or your child experiences any of these complications, as they can be serious and potentially life-threatening.
Coxsackievirus infections are common and can cause a range of symptoms, from mild to severe. Prevention is key, and taking steps such as washing your hands frequently, avoiding close contact with people who are sick, and keeping children home from school or daycare when they are ill can help reduce the risk of transmission. If you suspect that you or your child has a coxsackievirus infection, it's important to seek medical attention if symptoms worsen or if complications develop. With prompt and appropriate treatment, most people with coxsackievirus infections recover fully.
Cardiac output is typically measured using invasive or non-invasive methods. Invasive methods involve inserting a catheter into the heart to directly measure cardiac output. Non-invasive methods include echocardiography, MRI, and CT scans. These tests can provide an estimate of cardiac output based on the volume of blood being pumped out of the heart and the rate at which it is being pumped.
There are several factors that can contribute to low cardiac output. These include:
1. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs, leading to fatigue and shortness of breath.
2. Anemia: A low red blood cell count can reduce the amount of oxygen being delivered to the body's tissues, leading to fatigue and weakness.
3. Medication side effects: Certain medications, such as beta blockers, can slow down the heart rate and reduce cardiac output.
4. Sepsis: A severe infection can lead to inflammation throughout the body, which can affect the heart's ability to pump blood effectively.
5. Myocardial infarction (heart attack): This occurs when the heart muscle is damaged due to a lack of oxygen, leading to reduced cardiac output.
Low cardiac output can cause a range of symptoms, including:
1. Fatigue and weakness
2. Dizziness and lightheadedness
3. Shortness of breath
4. Pale skin
5. Decreased urine output
6. Confusion and disorientation
The treatment of low cardiac output depends on the underlying cause. Treatment may include:
1. Medications to increase heart rate and contractility
2. Diuretics to reduce fluid buildup in the body
3. Oxygen therapy to increase oxygenation of tissues
4. Mechanical support devices, such as intra-aortic balloon pumps or ventricular assist devices
5. Surgery to repair or replace damaged heart tissue
6. Lifestyle changes, such as a healthy diet and regular exercise, to improve cardiovascular health.
Preventing low cardiac output involves managing any underlying medical conditions, taking medications as directed, and making lifestyle changes to improve cardiovascular health. This may include:
1. Monitoring and controlling blood pressure
2. Managing diabetes and other chronic conditions
3. Avoiding substances that can damage the heart, such as tobacco and excessive alcohol
4. Exercising regularly
5. Eating a healthy diet that is low in saturated fats and cholesterol
6. Maintaining a healthy weight.
OHCA is a life-threatening medical emergency that requires immediate attention and treatment. If not treated promptly, OHCA can lead to brain damage, disability, or even death.
The symptoms of OHCA are similar to those of in-hospital cardiac arrest, and may include:
* Loss of consciousness (fainting)
* No breathing or abnormal breathing (gasping or gurgling sounds)
* No pulse or a very weak pulse
* Blue lips and skin (cyanosis)
If you suspect someone has experienced OHCA, it is important to call emergency services immediately. While waiting for help to arrive, follow these steps:
1. Check the person's airway, breathing, and pulse. If the person is not breathing or has no pulse, begin CPR (cardiopulmonary resuscitation) immediately.
2. Provide rescue breaths and chest compressions until emergency medical services arrive.
3. Use an automated external defibrillator (AED) if one is available and the person is in cardiac arrest.
4. Keep the person warm and comfortable, as hypothermia can worsen the condition.
5. Provide reassurance and support to the person's family and loved ones.
OHCA is a medical emergency that requires prompt treatment and attention. If you suspect someone has experienced OHCA, call emergency services immediately and provide appropriate care until help arrives.
During ventricular remodeling, the heart muscle becomes thicker and less flexible, leading to a decrease in the heart's ability to fill with blood and pump it out to the body. This can lead to shortness of breath, fatigue, and swelling in the legs and feet.
Ventricular remodeling is a natural response to injury, but it can also be exacerbated by factors such as high blood pressure, diabetes, and obesity. Treatment for ventricular remodeling typically involves medications and lifestyle changes, such as exercise and a healthy diet, to help manage symptoms and slow the progression of the condition. In some cases, surgery or other procedures may be necessary to repair or replace damaged heart tissue.
The process of ventricular remodeling is complex and involves multiple cellular and molecular mechanisms. It is thought to be driven by a variety of factors, including changes in gene expression, inflammation, and the activity of various signaling pathways.
Overall, ventricular remodeling is an important condition that can have significant consequences for patients with heart disease. Understanding its causes and mechanisms is crucial for developing effective treatments and improving outcomes for those affected by this condition.
Types of congenital heart defects include:
1. Ventricular septal defect (VSD): A hole in the wall between the two lower chambers of the heart, allowing abnormal blood flow.
2. Atrial septal defect (ASD): A hole in the wall between the two upper chambers of the heart, also allowing abnormal blood flow.
3. Tetralogy of Fallot: A combination of four heart defects, including VSD, pulmonary stenosis (narrowing of the pulmonary valve), and abnormal development of the infundibulum (a part of the heart that connects the ventricles to the pulmonary artery).
4. Transposition of the great vessels: A condition in which the aorta and/or pulmonary artery are placed in the wrong position, disrupting blood flow.
5. Hypoplastic left heart syndrome (HLHS): A severe defect in which the left side of the heart is underdeveloped, resulting in insufficient blood flow to the body.
6. Pulmonary atresia: A condition in which the pulmonary valve does not form properly, blocking blood flow to the lungs.
7. Truncus arteriosus: A rare defect in which a single artery instead of two (aorta and pulmonary artery) arises from the heart.
8. Double-outlet right ventricle: A condition in which both the aorta and the pulmonary artery arise from the right ventricle instead of the left ventricle.
Causes of congenital heart defects are not fully understood, but genetics, environmental factors, and viral infections during pregnancy may play a role. Diagnosis is typically made through fetal echocardiography or cardiac ultrasound during pregnancy or after birth. Treatment depends on the type and severity of the defect and may include medication, surgery, or heart transplantation. With advances in medical technology and treatment, many children with congenital heart disease can lead active, healthy lives into adulthood.
There are several potential causes of LVD, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.
Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.
Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.
Heart neoplasms, also known as cardiac tumors, are abnormal growths that occur within the heart muscle or on the surface of the heart. These tumors can be benign (non-cancerous) or malignant (cancerous). Malignant heart tumors are rare but can be aggressive and potentially life-threatening.
Types of Heart Neoplasms:
1. Benign tumors: These include fibromas, lipomas, and teratomas, which are usually slow-growing and do not spread to other parts of the body.
2. Malignant tumors: These include sarcomas, carcinomas, and lymphomas, which can be more aggressive and may spread to other parts of the body.
Causes and Risk Factors:
The exact cause of heart neoplasms is not fully understood, but several factors have been linked to an increased risk of developing these tumors. These include:
1. Genetic mutations: Some heart neoplasms may be caused by inherited genetic mutations.
2. Viral infections: Some viruses, such as human T-lymphotropic virus (HTLV-1), have been linked to an increased risk of developing heart tumors.
3. Radiation exposure: Radiation therapy to the chest area can increase the risk of developing heart tumors.
4. Previous heart surgery: People who have had previous heart surgery may be at higher risk of developing heart neoplasms.
Symptoms and Diagnosis:
The symptoms of heart neoplasms can vary depending on the size and location of the tumor. They may include:
1. Chest pain or discomfort
2. Shortness of breath
5. Swelling in the legs, ankles, or feet
Diagnosis is typically made through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and cardiac imaging studies. A biopsy may be necessary to confirm the diagnosis.
Treatment and Prognosis:
The treatment of heart neoplasms depends on the type, size, and location of the tumor, as well as the patient's overall health. Treatment options may include:
1. Watchful waiting: Small, benign tumors may not require immediate treatment and can be monitored with regular check-ups.
2. Surgery: Surgical removal of the tumor may be necessary for larger or more aggressive tumors.
3. Chemotherapy: Chemotherapy drugs may be used to shrink the tumor before surgery or to treat any remaining cancer cells after surgery.
4. Radiation therapy: Radiation therapy may be used to treat heart neoplasms that are difficult to remove with surgery or that have returned after previous treatment.
The prognosis for heart neoplasms varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the earlier the diagnosis and treatment, the better the prognosis. However, some heart neoplasms can be aggressive and may have a poor prognosis despite treatment.
Heart neoplasms can cause a variety of complications, including:
1. Heart failure: Tumors that obstruct the heart's pumping activity can lead to heart failure.
2. Arrhythmias: Tumors can disrupt the heart's electrical activity and cause arrhythmias (abnormal heart rhythms).
3. Thrombus formation: Tumors can increase the risk of blood clots forming within the heart.
4. Septicemia: Bacterial infections can occur within the tumor, leading to septicemia (blood poisoning).
5. Respiratory failure: Large tumors can compress the lungs and lead to respiratory failure.
Heart neoplasms are rare but potentially life-threatening conditions that require prompt diagnosis and treatment. While some heart neoplasms are benign, others can be aggressive and may have a poor prognosis despite treatment. It is essential to seek medical attention if symptoms persist or worsen over time, as early detection and treatment can improve outcomes.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
There are several types of heart injuries that can occur, including:
1. Myocardial infarction (heart attack): This occurs when the blood flow to the heart is blocked, causing damage to the heart muscle.
2. Cardiac tamponade: This occurs when fluid accumulates in the space between the heart and the sac that surrounds it, putting pressure on the heart and impeding its ability to function properly.
3. Myocarditis: This is an inflammation of the heart muscle that can be caused by a virus or bacteria.
4. Pericardial tamponade: This occurs when fluid accumulates in the space between the heart and the sac that surrounds it, putting pressure on the heart and impeding its ability to function properly.
5. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs.
6. Coronary artery disease: This occurs when the coronary arteries, which supply blood to the heart, become narrowed or blocked, leading to damage to the heart muscle.
7. Cardiac rupture: This is a rare and severe injury that occurs when the heart muscle tears or ruptures.
Symptoms of heart injuries can include chest pain, shortness of breath, fatigue, and irregular heartbeat. Treatment options for heart injuries depend on the severity of the injury and can range from medications to surgery. In some cases, heart injuries may be fatal if not properly treated.
In conclusion, heart injuries are a serious medical condition that can have long-term consequences if not properly treated. It is important to seek medical attention immediately if symptoms of a heart injury are present.
LVH can lead to a number of complications, including:
1. Heart failure: The enlarged left ventricle can become less efficient at pumping blood throughout the body, leading to heart failure.
2. Arrhythmias: The abnormal electrical activity in the heart can lead to irregular heart rhythms.
3. Sudden cardiac death: In some cases, LVH can increase the risk of sudden cardiac death.
4. Atrial fibrillation: The enlarged left atrium can lead to atrial fibrillation, a common type of arrhythmia.
5. Mitral regurgitation: The enlargement of the left ventricle can cause the mitral valve to become incompetent, leading to mitral regurgitation.
6. Heart valve problems: The enlarged left ventricle can lead to heart valve problems, such as mitral regurgitation or aortic stenosis.
7. Coronary artery disease: LVH can increase the risk of coronary artery disease, which can lead to a heart attack.
8. Pulmonary hypertension: The enlarged left ventricle can lead to pulmonary hypertension, which can further strain the heart and increase the risk of complications.
Evaluation of LVH typically involves a physical examination, medical history, electrocardiogram (ECG), echocardiography, and other diagnostic tests such as stress test or cardiac MRI. Treatment options for LVH depend on the underlying cause and may include medications, lifestyle changes, and in some cases, surgery or other interventions.
Myosin binding protein C, cardiac
John M. Squire
Cardiac excitation-contraction coupling
Myosin light-chain kinase
Richard B. Lanman
Second-harmonic imaging microscopy
UC Davis School of Veterinary Medicine
Sudden cardiac death of athletes
Myosin light chain
Striated muscle tissue
Physiological effects in space
DNA damage theory of aging
Congenital heart defect
Samuel Victor Perry
List of OMIM disorder codes
Actin, cytoplasmic 2
List of autoimmune diseases
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SMART: IGc2 domain annotation
- RT-PCR showed increased mRNA levels of cardiac hypertrophy marker atrial natriuretic peptide, but not BNP, decreased expression of myosin heavy chain isoform MYH6 and unaltered expression of pathological MYH7. (nih.gov)
- Rationale Overexpression of the (+)insert smooth muscle myosin heavy chain (SMMHC) isoform could contribute to airway bronchospasm by increasing the velocity of contraction. (bmj.com)
- 2-4 The smooth muscle myosin heavy chain (SMMHC) (+)insert isoform contains a seven-amino acid insert near the ATP binding site that makes ATPase activity approximately twofold greater than that of the (−)insert isoform. (bmj.com)
- MYBPC3 encodes the cardiac isoform of myosin-binding protein C. Myosin-binding protein C is a myosin-associated protein found in the cross-bridge-bearing zone (C region) of A bands in striated muscle. (origene.com)
- MYBPC3, the cardiac isoform, is expressed exclussively in heart muscle. (origene.com)
- Regulatory phosphorylation of the cardiac isoform in vivo by cAMP-dependent protein kinase (PKA) upon adrenergic stimulation may be linked to modulation of cardiac contraction. (origene.com)
- Myosin light chain 3, or MYL3 for short, consists of a 195 amino acid isoform that is 22 kDa, and is involved in the regulation of Myosin, which is a protein that conducts ATP hydrolysis. (novusbio.com)
- Mutations in the MYH7 gene cause myosin storage myopathy. (medlineplus.gov)
- Mutations in the MYH7 gene lead to the production of an altered cardiac β-myosin heavy chain protein, which is thought to be less able to form thick filaments. (medlineplus.gov)
- Armel TZ, Leinwand LA. Mutations in the beta-myosin rod cause myosin storage myopathy via multiple mechanisms. (medlineplus.gov)
- MYBPC3 gene mutations that cause familial hypertrophic cardiomyopathy lead to an abnormally short or otherwise altered cardiac MyBP-C protein. (nih.gov)
- MYBPC3 gene mutations likely lead to changes in this process, resulting in a left ventricular cardiac muscle that is not compacted but is thick and spongy. (nih.gov)
- Mutations in the myosin 15 gene (MYO15A) have been linked to a form of hereditary deafness in humans. (nih.gov)
- By purifying myosin 15, we can study its characteristics, which helps us understand its function in hair cells and how mutations in this molecule lead to hearing loss. (nih.gov)
- Understanding the molecular basis of HCM-causing mutations in cardiac myosin and cardiac myosin binding protein-C Pathak, D., Nandwani, N., Ruppel, K., Spudich, J. A. CELL PRESS. (stanford.edu)
- Hypertrophic cardiomyopathy (HCM) is a disease of the myocardium caused by mutations in sarcomeric proteins with mechanical roles, such as the molecular motor myosin. (stanford.edu)
- Around half of the HCM-causing genetic variants target contraction modulator cardiac myosin-binding protein C (cMyBP-C), although the underlying pathogenic mechanisms remain unclear since many of these mutations cause no alterations in protein structure and stability. (stanford.edu)
- The genetic basis of cardiac disease in humans ranges from simple mutations to complex genetic traits. (vin.com)
- Two different mutations in the same gene (myosin-binding protein C) have been described with HCM in Maine Coons and Ragdolls. (vin.com)
- In addition to extending our knowledge into the conformational and biological properties of coiled-coil discontinuities, the molecular characterization of the four myosin skip residues also provides a guide to modeling the effects of rod mutations causing cardiac and skeletal myopathies. (rcsb.org)
- To demonstrate the importance of cardiac light chain phosphorylation, we cloned a myosin light chain kinase from a human heart and have identified a gain-in-function mutation in two individuals with cardiac hypertrophy. (nih.gov)
- This condition is characterized by thickening (hypertrophy) of the cardiac muscle. (nih.gov)
- Here we show that HKL blocks agonist-induced and pressure overload-mediated, cardiac hypertrophic responses, and ameliorates pre-existing cardiac hypertrophy, in mice. (nature.com)
- Cardiac hypertrophy is a physiologic or pathologic state of the heart that occurs in response to a variety of intrinsic or extrinsic stimuli. (nature.com)
- At the molecular level cardiac hypertrophy is a consequence of imbalance between the activities of pro- and anti-hypertrophic molecules. (nature.com)
- We have previously demonstrated that Sirt3 is one of the anti-hypertrophic molecules whose deficiency causes development of hypertrophy, whereas cardiac specific overexpression of Sirt3 blocks the hypertrophic response 1 . (nature.com)
- The Interplay between S-Glutathionylation and Phosphorylation of Cardiac Troponin I and Myosin Binding Protein C in End-Stage Human Failing Hearts. (bvsalud.org)
- This was accompanied by the increased oxidation of troponin I and myosin binding protein C, and decreased levels of protein kinases A (PKA)- and C (PKC)-mediated phosphorylation of both proteins . (bvsalud.org)
- This condition is characterized by the formation of protein clumps, which contain a protein called myosin, within certain muscle fibers. (medlineplus.gov)
- The MYH7 gene provides instructions for making a protein known as the cardiac beta (β)-myosin heavy chain. (medlineplus.gov)
- This protein is found in heart (cardiac) muscle and in type I skeletal muscle fibers, one of two types of fibers that make up the muscles that the body uses for movement. (medlineplus.gov)
- In several instances, such as rheumatoid arthritis, multiple sclerosis, and myocarditis, the autoimmune disease can be induced experimentally by administering self-antigen in the presence of adjuvant (col- lagen, myelin basic protein, and cardiac myosin, respec- tively) (3). (cdc.gov)
- Here, we report for the, to our knowledge, first time that α- and β-myosin, as protein crystals, possess different symmetries: the former has C6 symmetry, and the latter has C3v. (nih.gov)
- The MYBPC3 gene provides instructions for making cardiac myosin binding protein C (cardiac MyBP-C), which is found in heart (cardiac) muscle cells. (nih.gov)
- Kulikovskaya I, McClellan GB, Levine R, Winegrad S. Multiple forms of cardiac myosin-binding protein C exist and can regulate thick filament stability. (nih.gov)
- 1 Alternative splicing of the myosin gene produces four isoforms of the smooth muscle heavy chain, two of which, the (−)insert and (+)insert, are in the motor domain of the protein. (bmj.com)
- MyBPC3 (Myosin-binding protein C-cardiac type) is a 140-150 kDa member of the MyBP family, Ig superfamily of proteins. (rndsystems.com)
- We identified a specific cardiac protein that showed selective carbonylation under Dox-induced cardiotoxic conditions in a spontaneously hypertensive rat (SHR) model and this protein was confirmed to be a 140 kDa cardiac myosin binding protein C (MyBPC). (nih.gov)
- We further analyzed and confirmed the carbonylation and degradation of this protein using HL-1 cardiomyocytes under Dox-induced oxidative stress, and a purified recombinant rat cardiac MyBPC under metal-catalyzed oxidative stress conditions. (nih.gov)
- Researchers at the NIH have for the first time purified a key part of myosin 15, a molecular motor protein that helps build healthy hearing structures in the inner ear. (nih.gov)
- Myosin 15 is a molecular motor protein, so called because it can move around within a cell. (nih.gov)
- To gain a better understanding of how myosin 15 works, the researchers set out to produce and purify the protein. (nih.gov)
- Although the cells produced plenty of the protein, the myosin aggregated into large clumps that were useless for biochemical analysis. (nih.gov)
- Nanomechanical Phenotypes in Cardiac Myosin-Binding Protein C Mutants That Cause Hypertrophic Cardiomyopathy. (stanford.edu)
- Fully differentiated cardiac myocytes achieve this by increase in size, enhanced protein synthesis and increased sarcomere organization, in association with reactivation of the fetal gene programme. (nature.com)
- Left ventricular noncompaction cardiomyopathy: cardiac, neuromuscular, and genetic factors. (nih.gov)
- Current research is being conducted on the relationship between Myosin light chain 3 and a multitude of diseases and disorders, including familial hypertrophic cardiomyopathy, congestive heart failure, restrictive cardiomyopathy, dilated cardiomyopathy, diabetes mellitus, and renal failure. (novusbio.com)
- Dilated cardiomyopathy (DCM) of Doberman Pinschers was the first canine cardiac disease to undergo genetic analysis. (vin.com)
- Hypertrophic cardiomyopathy (HCM) of Maine Coons was the first veterinary cardiac disease in which a genetic basis was identified. (vin.com)
- In these cells, cardiac MyBP-C is associated with a structure called the sarcomere, which is the basic unit of muscle contraction. (nih.gov)
- Smooth muscle contraction involves complex interactions between numerous contractile proteins, with actin and myosin playing a central role in this process. (bmj.com)
- It is expressed in cardiac muscle, and contributes both to myosin filament structure by interacting with light meromysin, and the regulation of contraction by binding to myosin subfragment-2, which results in a reduction of actomyosin ATPase activity. (rndsystems.com)
- Myosin light chain 3 has been linked to the RhoA pathway, as well as PKA signaling, growth cone motility, cell adhesion, cardiac muscle contraction, and cytoskeleton remodeling. (novusbio.com)
- The new approach to expressing myosin 15 may also help the study of other types of myosin motors, such as skeletal and cardiac muscle myosins, which could accelerate development of targeted drug therapies for heart disease and other health conditions. (nih.gov)
- Immunohistochemistry-Paraffin: Myosin light chain 3 Antibody [NBP1-88068] - Staining of human skeletal muscle shows moderate to strong cytoplasmic positivity in myocytes. (novusbio.com)
- Here, we show how a spatial gradient of myosin light chain phosphorylation across the heart facilitates torsion by inversely altering tension production and the stretch activation response. (nih.gov)
- A gradient of myosin regulatory light-chain phosphorylation across the ventricular wall supports cardiac torsion. (nih.gov)
- A montage of fluorescence images showing a single actin filament being propelled along a microscope slide by the molecular motor, myosin 15. (nih.gov)
- Multi-color actin filaments were used to determine the direction of myosin 15 movement. (nih.gov)
- suggested candidates include structural and functional proteins such as collagen, actin, and myosin [2-3]. (nih.gov)
- Myosin storage myopathy is a condition that causes muscle weakness (myopathy) that does not worsen or worsens very slowly over time. (medlineplus.gov)
- The signs and symptoms of myosin storage myopathy usually become noticeable in childhood, although they can occur later. (medlineplus.gov)
- Myosin storage myopathy is a rare condition. (medlineplus.gov)
- It is unclear how these changes lead to muscle weakness in people with myosin storage myopathy. (medlineplus.gov)
- Tajsharghi H, Thornell LE, Lindberg C, Lindvall B, Henriksson KG, Oldfors A. Myosin storage myopathy associated with a heterozygous missense mutation in MYH7. (medlineplus.gov)
- Cardiac β-myosin heavy chain is the major component of the thick filament in muscle cell structures called sarcomeres . (medlineplus.gov)
- when the phosphate groups are removed, cardiac MyBP-C is broken down, followed by the breakdown of proteins of the thick filament. (nih.gov)
- The rod of sarcomeric myosins directs thick filament assembly and is characterized by the insertion of four skip residues that introduce discontinuities in the coiled-coil heptad repeats. (rcsb.org)
- By defining the biophysical properties of the rod, the structures and molecular dynamic calculations presented here provide insight into thick filament formation, and highlight the structural differences occurring between the coiled-coils of myosin and the stereotypical tropomyosin. (rcsb.org)
- This abnormal cardiac muscle is weak and cannot contract effectively, causing the varied signs and symptoms of left ventricular noncompaction. (nih.gov)
- FDA has informed Bristol Myers Squibb (NSDQ:GILD) that it has extended its review of mavacamten, an allosteric modulator of cardiac myosin. (drugdiscoverytrends.com)
- Experimental evidence based on genetic fate mapping confirms that cardiac-derived stem or precursor cells (CPCs) contribute to replacement of adult mammalian cardiomyocytes [ 1 ]. (hindawi.com)
- Subsequent to the identification of genetic abnormalities in a number of cardiac diseases in humans, veterinary cardiologists and others began investigating analogous diseases in dogs and cats using a candidate gene approach. (vin.com)
- Several inherited or familial cardiac diseases have now been shown to have a specific genetic basis in both dogs and cats. (vin.com)
- However, with genomic studies growing ever-cheaper, in-roads into the genetic basis of many of the cardiac disease to which specific breeds are predisposed will be made over the coming years. (vin.com)
- It is most probable that cardiac diseases that occur within specific breeds or lines within a breed have a genetic basis. (vin.com)
- These results suggest that HKL is a pharmacological activator of Sirt3 capable of blocking, and even reversing, the cardiac hypertrophic response. (nature.com)
- 1. T cells specific for α-myosin drive immunotherapy-related myocarditis. (nih.gov)
- 3. Cardiac myosin-specific autoimmune T cells contribute to immune-checkpoint-inhibitor-associated myocarditis. (nih.gov)
- 4. Expansion of Disease Specific Cardiac Macrophages in Immune Checkpoint Inhibitor Myocarditis. (nih.gov)
- 6. Myocarditis-inducing epitope of myosin binds constitutively and stably to I-Ak on antigen-presenting cells in the heart. (nih.gov)
- 7. Myosin-induced acute myocarditis is a T cell-mediated disease. (nih.gov)
- 9. Localization of CD8 T cell epitope within cardiac myosin heavy chain-α334-352 that induces autoimmune myocarditis in A/J mice. (nih.gov)
- 16. T cells in cardiac myosin-induced myocarditis. (nih.gov)
- In cardiac muscle sarcomeres, cardiac MyBP-C attaches to thick filaments and keeps them from being broken down prematurely. (nih.gov)
- The positive results are based on patients participating in the expansion phase of Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure (COSMIC-HF), a study that included several secondary end points assessing cardiac function, such as changes in systolic ejection time, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, heart rate, stroke volume, and NT-proBNP. (medscape.com)
- Patients with elevated left ventricular filling pressures and increased systemic vascular resistance in association with a depressed cardiac index are likely to experience an improvement in cardiac index. (nih.gov)
- 5. Impaired thymic tolerance to α-myosin directs autoimmunity to the heart in mice and humans. (nih.gov)
- Dose-dependent oxidative stress by the anthracycline doxorubicin (Dox) and other chemotherapeutic agents causes irreversible cardiac damage, restricting their clinical effectiveness. (nih.gov)
- Moreover, HKL-treatment blocks cardiac fibroblast proliferation and differentiation to myofibroblasts in a Sirt3-dependent manner. (nature.com)
- These cardiac abnormalities can result in a wide range of outcomes from a complete lack of symptoms to sudden cardiac death. (nih.gov)
- In view of previously reported increased capacity for nitric oxide production, we suggested that l-arginine (ARG), the nitric oxide synthase (NOS) substrate, supplementation would improve cardiac function in isoproterenol (ISO)-induced heart failure. (nih.gov)
- Human cardiac-derived progenitor cells (hCPCs) have shown promise in treating heart failure (HF) in adults. (hindawi.com)
- In this study, the differences in symmetry of polarization spectra obtained from α- and β-myosin in various mammalian ventricles and propylthiouracil-treated rats are explored through polarization-dependent second harmonic generation microscopy. (nih.gov)
- (A) MT spectra of cardiac tissue and mitochondria (36mg/ml) at B1 saturation of 1.33 X 10-6 T evaluated at T=37oC. (nih.gov)
- Figures 3A and 4A contain plots of the magnetization spectra of cardiac tissue and mitochondria obtained at 37oC for B1 = 1.33 X 10-6 T (Figure 3A) and 2.45 X 10-6 T (Figure 4A). (nih.gov)
- These events lead to dephosphorylation of myosin light chains, which regulate the contractile state in smooth muscle, and result in vasodilatation. (nih.gov)
- Her work concerned understanding the roles of cardiac myosin using knockout mice. (nih.gov)
- Immunohistochemistry-Paraffin: Myosin light chain 3 Antibody [NBP1-88068] - Analysis in human heart muscle and lymph node tissues. (novusbio.com)
- Immunohistochemistry-Paraffin: Myosin light chain 3 Antibody [NBP1-88068] - Staining of human cerebral cortex shows no positivity in neurons as expected. (novusbio.com)
- Immunohistochemistry-Paraffin: Myosin light chain 3 Antibody [NBP1-88068] - Staining of human lymph node shows no positivity in non-germinal center cells as expected. (novusbio.com)
- however, the effects of pMΦ on cardiac stem cells (CSCs) remain unknown. (mdpi.com)
- Instead, cardiac sympathetic activity may be investigated using systolic time intervals (STI), such as the pre-ejection period. (frontiersin.org)
- To test this idea, the researchers engineered the cells to produce two additional chaperone molecules (UNC45B and HSP90AA1), as well as the myosin 15 motor fragment. (nih.gov)
- Scientists believe that myosin 15 helps to build stereocilia by supplying them with components for assembly, much like a delivery truck. (nih.gov)
- But the molecular structure of myosin 15 and how it functions in stereocilia assembly is still unclear. (nih.gov)
- Assembly of myosin with mutated skip residues in cardiomyocytes shows that the functional importance of each skip residue is associated with rod position and reveals the unique role of the molecular hinge in promoting myosin antiparallel packing. (rcsb.org)
- Mitochondria, effectively a proteinaceous crystal (Figure 1B), makes up to 25% of cardiac tissue volume. (nih.gov)
- (A) Cardiac tissue and mitochondria (36 mg/ml) plotted to demonstrate the saturation power dependence of the MT effect. (nih.gov)
- Plots of cardiac tissue (T=37oC, 7 T) (A) T1 data from inversion-recovery experiments (B) T2 data from CPMG experiments. (nih.gov)
- The raw data shown in these figures suggest that the physiological concentration of mitochondria can support ~ 50% MS effect observed in cardiac tissue. (nih.gov)
- A single-sarcomere line scan further demonstrated that the differences in polarization-spectrum symmetry between α- and β-myosin came from their head regions: the head and neck domains of α- and β-myosin account for the differences in symmetry. (nih.gov)
- The researchers first genetically engineered laboratory-grown cells to make a fragment of mouse myosin 15 that contained the protein's "motor. (nih.gov)