Most abundant proteins in COBRA venom; basic polypeptides of 57 to 62 amino acids with four disulfide bonds and a molecular weight of less than 7000; causes skeletal and cardiac muscle contraction, interferes with neuromuscular and ganglionic transmission, depolarizes nerve, muscle and blood cell membranes, thus causing hemolysis.
A family of extremely venomous snakes, comprising coral snakes, cobras, mambas, kraits, and sea snakes. They are widely distributed, being found in the southern United States, South America, Africa, southern Asia, Australia, and the Pacific Islands. The elapids include three subfamilies: Elapinae, Hydrophiinae, and Lauticaudinae. Like the viperids, they have venom fangs in the front part of the upper jaw. The mambas of Africa are the most dangerous of all snakes by virtue of their size, speed, and highly toxic venom. (Goin, Goin, and Zug, Introduction to Herpetology, 3d ed, p329-33)
Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.
Venoms from snakes of the family Elapidae, including cobras, kraits, mambas, coral, tiger, and Australian snakes. The venoms contain polypeptide toxins of various kinds, cytolytic, hemolytic, and neurotoxic factors, but fewer enzymes than viper or crotalid venoms. Many of the toxins have been characterized.
Agents that have a damaging effect on the HEART. Such damage can occur from ALKYLATING AGENTS; FREE RADICALS; or metabolites from OXIDATIVE STRESS and in some cases is countered by CARDIOTONIC AGENTS. Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Solutions or mixtures of toxic and nontoxic substances elaborated by snake (Ophidia) salivary glands for the purpose of killing prey or disabling predators and delivered by grooved or hollow fangs. They usually contain enzymes, toxins, and other factors.
Limbless REPTILES of the suborder Serpentes.
Toxins, contained in cobra (Naja) venom that block cholinergic receptors; two specific proteins have been described, the small (short, Type I) and the large (long, Type II) which also exist in other Elapid venoms.
Lipids containing at least one monosaccharide residue and either a sphingoid or a ceramide (CERAMIDES). They are subdivided into NEUTRAL GLYCOSPHINGOLIPIDS comprising monoglycosyl- and oligoglycosylsphingoids and monoglycosyl- and oligoglycosylceramides; and ACIDIC GLYCOSPHINGOLIPIDS which comprises sialosylglycosylsphingolipids (GANGLIOSIDES); SULFOGLYCOSPHINGOLIPIDS (formerly known as sulfatides), glycuronoglycosphingolipids, and phospho- and phosphonoglycosphingolipids. (From IUPAC's webpage)
A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.
Heart failure caused by abnormal myocardial contraction during SYSTOLE leading to defective cardiac emptying.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
The physiological renewal, repair, or replacement of tissue.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
Elongated, spindle-shaped, quiescent myoblasts lying in close contact with adult skeletal muscle. They are thought to play a role in muscle repair and regeneration.
Embryonic (precursor) cells of the myogenic lineage that develop from the MESODERM. They undergo proliferation, migrate to their various sites, and then differentiate into the appropriate form of myocytes (MYOCYTES, SKELETAL; MYOCYTES, CARDIAC; MYOCYTES, SMOOTH MUSCLE).
Developmental events leading to the formation of adult muscular system, which includes differentiation of the various types of muscle cell precursors, migration of myoblasts, activation of myogenesis and development of muscle anchorage.
A peptide which is a homopolymer of lysine.
A malignant form of polymorphic ventricular tachycardia that is characterized by HEART RATE between 200 and 250 beats per minute, and QRS complexes with changing amplitude and twisting of the points. The term also describes the syndrome of tachycardia with prolonged ventricular repolarization, long QT intervals exceeding 500 milliseconds or BRADYCARDIA. Torsades de pointes may be self-limited or may progress to VENTRICULAR FIBRILLATION.
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)
Exclusive legal rights or privileges applied to inventions, plants, etc.
Diseases of domestic and wild horses of the species Equus caballus.
Large, hoofed mammals of the family EQUIDAE. Horses are active day and night with most of the day spent seeking and consuming food. Feeding peaks occur in the early morning and late afternoon, and there are several daily periods of rest.
Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as AGAR or GELATIN.
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.
The profession of writing. Also the identity of the writer as the creator of a literary production.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
A 235-kDa cytoplasmic protein that is also found in platelets. It has been localized to regions of cell-substrate adhesion. It binds to INTEGRINS; VINCULIN; and ACTINS and appears to participate in generating a transmembrane connection between the extracellular matrix and the cytoskeleton.
Fibrous bands or cords of CONNECTIVE TISSUE at the ends of SKELETAL MUSCLE FIBERS that serve to attach the MUSCLES to bones and other structures.
STRIATED MUSCLE cell components which anchor the MYOFIBRILS from the Z-bands to the SARCOLEMMA and EXTRACELLULAR MATRIX. Costameric proteins include the proteins of FOCAL ADHESIONS.
Contractile tissue that produces movement in animals.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Phospholipases that hydrolyze the acyl group attached to the 2-position of PHOSPHOGLYCERIDES.
Phospholipases that hydrolyze one of the acyl groups of phosphoglycerides or glycerophosphatidates.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Paired, segmented masses of MESENCHYME located on either side of the developing spinal cord (neural tube). Somites derive from PARAXIAL MESODERM and continue to increase in number during ORGANOGENESIS. Somites give rise to SKELETON (sclerotome); MUSCLES (myotome); and DERMIS (dermatome).
A myogenic regulatory factor that controls myogenesis. Though it is not clear how its function differs from the other myogenic regulatory factors, MyoD appears to be related to fusion and terminal differentiation of the muscle cell.
A paired box transcription factor that is involved in EMBRYONIC DEVELOPMENT of the CENTRAL NERVOUS SYSTEM and SKELETAL MUSCLE.
A genus of FLAVIVIRIDAE causing parenterally-transmitted HEPATITIS C which is associated with transfusions and drug abuse. Hepatitis C virus is the type species.
INFLAMMATION of the LIVER in humans caused by a member of the HEPATOVIRUS genus, HUMAN HEPATITIS A VIRUS. It can be transmitted through fecal contamination of food or water.
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally, and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
Ribonucleic acid that makes up the genetic material of viruses.
A layer of acellular matrix that lies beneath the CORNEAL EPITHELIUM and above the CORNEAL STROMA. It consists of randomly arranged COLLAGEN fibers in a condensed bed of intercellular substance. It provides stability and strength to the cornea.
The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos.

Skeletal myogenesis by human embryonic stem cells. (1/115)

We have examined the myogenic potential of human embryonic stem (hES) cells in a xeno-transplantation animal model. Here we show that precursors differentiated from hES cells can undergo myogenesis in an adult environment and give rise to a range of cell types in the myogenic lineage. This study provides direct evidences that hES cells can regenerate both muscle and satellite cells in vivo and are another promising cell type for treating muscle degenerative disorders in addition to other myogenic cell types.  (+info)

Beta-cardiotoxin: a new three-finger toxin from Ophiophagus hannah (king cobra) venom with beta-blocker activity. (2/115)

Snake venoms have provided a number of novel ligands with therapeutic potential. We have constructed a partial cDNA library from the mRNA of Ophiophagus hannah (king cobra) venom gland tissue and identified five new genes encoding proteins belonging to the three-finger toxin family of snake venom proteins. We have isolated and characterized one of these beta-sheet containing proteins with a mass of 7012.43 +/- 0.91 Da from the venom. The protein was nonlethal up to a dose of 10 mg/kg when injected intraperitoneally into Swiss albino mice. However, it induces labored breathing and death at a dose of 100 mg/kg. It does not show any hemolytic or anticoagulant activity. It caused a dose-dependent decrease of heart rate in vivo (anesthetized Sprague-Dawley rats) and also ex vivo (Langendorff isolated rat heart). This is in contrast to classical cardiotoxins from snake venom that increase the heart rate in animals. Radioligand displacement studies showed that this protein targets beta-adrenergic receptors with a binding affinity (Ki) of 5.3 and 2.3 microM toward beta1 and beta2 subtypes, respectively, to bring about its effect, and hence, it was named as beta-cardiotoxin. This is the first report of a natural exogenous beta-blocker.  (+info)

Functional analysis of homeodomain-containing transcription factor Lbx1 in satellite cells of mouse skeletal muscle. (3/115)

Satellite cells are usually mitotically quiescent muscle stem cells, located between the sarcolemma and the basement membrane of muscle fibers. When muscles are damaged, satellite cells become activated, proliferate and differentiate to form multinucleate myofibers. The molecular mechanisms underlying these processes are poorly understood. In the present study, we found that, following treatment with cardiotoxin, homeodomain-containing transcription factor Lbx1 was strongly expressed in the satellite cells of regenerating adult skeletal muscle. Our immunohistochemical and northern blot analyses indicate that Lbx1 is expressed in activated but not quiescent satellite cells. In vitro, this Lbx1 expression was gradually downregulated when satellite cells differentiate into mature myofibers. Transfection and forced expression of Lbx1 in satellite-cell-derived C2C12 myoblast cells resulted in severe depression of myogenic differentiation and incomplete myotube formation, concomitantly with the activation of the paired-box transcription factor Pax7 and depression of the myogenic regulatory factor MyoD. Moreover, knockdown of Lbx1 in in-vitro-cultured satellite cells resulted in downregulation of Pax7. These results suggest that Lbx1 plays important roles in differentiation and maintenance of satellite cells of mature myofibers, probably through the regulation of Pax7.  (+info)

Structural reengineering of imatinib to decrease cardiac risk in cancer therapy. (4/115)

Imatinib, a selective, small-molecule tyrosine kinase inhibitor, has life-saving clinical activity in certain cancers, but questions have been raised about the potential for cardiac toxicity through inhibition of its target, ABL kinase. In this issue of the JCI, Fernandez et al. describe a novel method by which the ABL-inhibitory activity of imatinib was deleted by modifying its chemical structure (see the related article beginning on page 4044). The anticancer activity of the reengineered agent, called WBZ_4, was instead preserved against gastrointestinal stromal tumors in both in vitro and in vivo models via inhibition of KIT tyrosine kinase, and the desired safety was demonstrated with less cardiotoxicity of WBZ_4 compared with imatinib via the inhibition of JNK. The study shows that structural reengineering of a kinase-inhibitory drug to improve tolerability while preserving efficacy is feasible.  (+info)

An anticancer C-Kit kinase inhibitor is reengineered to make it more active and less cardiotoxic. (5/115)

Targeting kinases is central to drug-based cancer therapy but remains challenging because the drugs often lack specificity, which may cause toxic side effects. Modulating side effects is difficult because kinases are evolutionarily and hence structurally related. The lack of specificity of the anticancer drug imatinib enables it to be used to treat chronic myeloid leukemia, where its target is the Bcr-Abl kinase, as well as a proportion of gastrointestinal stromal tumors (GISTs), where its target is the C-Kit kinase. However, imatinib also has cardiotoxic effects traceable to its impact on the C-Abl kinase. Motivated by this finding, we made a modification to imatinib that hampers Bcr-Abl inhibition; refocuses the impact on the C-Kit kinase; and promotes inhibition of an additional target, JNK, a change that is required to reinforce prevention of cardiotoxicity. We established the molecular blueprint for target discrimination in vitro using spectrophotometric and colorimetric assays and through a phage-displayed kinase screening library. We demonstrated controlled inhibitory impact on C-Kit kinase in human cell lines and established the therapeutic impact of the engineered compound in a novel GIST mouse model, revealing a marked reduction of cardiotoxicity. These findings identify the reengineered imatinib as an agent to treat GISTs with curbed side effects and reveal a bottom-up approach to control drug specificity.  (+info)

Comparative genomics identifies genes mediating cardiotoxicity in the embryonic zebrafish heart. (6/115)

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Atrial dysfunction as a marker of iron cardiotoxicity in thalassemia major. (7/115)

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Mechanisms responsible for reduced cardiotoxicity of mitoxantrone compared to doxorubicin examined in isolated guinea-pig heart preparations. (8/115)

We reported previously that doxorubicin, an anticancer agent that has an anthracycline structure, alters Ca2+ releasing and uptake mechanisms in the sarcoplasmic reticulum of myocardial cells. These effects of doxorubicin are apparently related to its cardiotoxicity. Mitoxantrone is a similar anticancer agent with an anthracenedion structure that has been shown to be significantly less cardiotoxic. In the present study, the effects of mitoxantrone on the functions of the sarcoplasmic reticulum were examined in isolated muscle preparations obtained from the guinea-pig heart. In electrically-stimulated left atrial muscle preparations, incubation in vitro for 4 hr with 30 or 100 microM mitoxantrone significantly prolonged the time to the peak of twitch tension, markedly increased the developed tension observed at lower stimulation frequencies, thereby attenuating the slope of positive force-frequency relationships, and increased the postrest contraction observed after a 60-sec quiescent period. In myocytes isolated from ventricular muscles, 30 microM mitoxantrone increased the peak and the size of intracellular Ca2+ concentrations ([Ca2+] i), and prolonged the time to peak [Ca2+]i. In skinned muscle fiber preparations obtained from the left ventricular muscle, 30 muM mitoxantrone significantly increased the caffeine-induced contraction without affecting the Ca2+ sensitivity of contractile proteins. These results suggest that mitoxantrone enhances Ca2+ release from the sarcoplasmic reticulum in isolated atrial muscle preparations obtained from the guinea-pig heart. Apparent enhancement of the sarcoplasmic reticulum functions, in contrast to anthracyclines that has been shown to suppress these functions, seems to explain the relative lack of marked cardiotoxicity of mitoxantrone.  (+info)

Molodavkin G.M.; Sorokina A.V.; Yavorskii A.N.; Lyubimov B.I.; Burov Y.V., 1986: The electrophysiological and morphological analysis of the cardiotoxic effect of ethanol in rats
The cardiac effects of treatment for malignancy are likely to become an increasing problem over the coming decades. This issue is multifactorial and reflects the evolution of cancer from a malignant illness to a chronic disease, as well as the widespread use of cardiotoxic agents. Two groups of patients seem to be especially at risk. In survivors of childhood cancer, the risk for recurrence or progression of malignancy rapidly diminishes after a decade, and cardiac complications are the main cause of cancer-related mortality that is unrelated to recurrence (1). In adults, several of the most common malignancies (especially breast cancer and lymphoma) are often treated with anthracyclines and/or radiotherapy (2). Breast cancer is the most common source of cardiac problems, reflecting its frequency, the cardiotoxic effects of specific chemotherapy, and the consequences of radiation to the left breast. Improvements in detection and therapy have led to ,2 million American women who will have ...
A look at the following clinical trial: Effectiveness of Using Biomarkers to Detect and Identify Cardiotoxicity and Describe Treatment (PREDICT)
hERG assay is used for screening of compounds acting as potential ligands or blockers of hERG channel which is an indication for cardiotoxicity.
PMID- 29303721 OWN - NLM STAT- MEDLINE DCOM- 20180110 LR - 20180110 IS - 1474-547X (Electronic) IS - 0140-6736 (Linking) VI - 390 IP - 10114 DP - 2018 Dec 23 TI - Concerns about cardiotoxicity in the HERA trial. PG - 2767 LID - S0140-6736(17)31954-2 [pii] LID - 10.1016/S0140-6736(17)31954-2 [doi] FAU - Levy, Antonin AU - Levy A AD - Department of Radiation Oncology, Gustave Roussy Cancer Campus, Villejuif 94800, France; Faculte de Medecine, Universite Paris-Saclay, Kremlin Bicetre, France; INSERM U1030, Molecular Radiotherapy, Gustave Roussy Cancer Campus, Villejuif, France. Electronic address: [email protected] FAU - Chargari, Cyrus AU - Chargari C AD - Department of Radiation Oncology, Gustave Roussy Cancer Campus, Villejuif 94800, France; Faculte de Medecine, Universite Paris-Saclay, Kremlin Bicetre, France; INSERM U1030, Molecular Radiotherapy, Gustave Roussy Cancer Campus, Villejuif, France; Institut de Recherche Biomedicale des Armees, Bretigny sur Orge, France. FAU - Deutsch, Eric AU - ...
5-Fluorouracil is a key element to the treatment of colon cancer. But it is also one of the most cardiotoxic chemotherapies, and the management of those th
Greenmedinfo.com - Natural Health Resource - The worlds most widely referenced, open access, natural medicine database, with 30,000+ study abstracts and growing daily
by Jon Cole and Meghan Spyres Photo by Chris Benseler on Flickr Jon: Meghan, thank you for joining me on this post. Ive wanted to write about the
INTRODUCTION Our children are being relentlessly exposed to a cardiotoxic environment. High calorically dense, fat-enriched foods, and technologically aided
We have shown previously that PLNR9C leads to DCM, heart failure, and premature death in heterozygous humans and transgenic mice (PLN+/++TgPLNR9C).4 PLNR9C prevents phosphorylation of coexpressed PLNwt and thereby decelerates diastolic Ca2+ transport into the SR via SERCA2a (Figure 3A). Unlike the nearly normal inhibitory effect that is measured in transfected HEK-293 cells when PLNR9C is present together with PLNwt, SERCA2a inhibition by PLNR9C alone is weak (Figure 3C and 3E). Thus, cardiomyocyte expression of PLNR9C alone (PLN−/−+TgPLNR9C) results in SR Ca2+ uptake rates that are faster than those in wild-type myocytes and almost as fast as those in PLN−/− myocytes (Figure 3A and 3C). The acceleration of SR Ca2+ reuptake kinetics as a result of PLNwt ablation was accompanied by an improved morphological and functional phenotype of the hearts (Figures 1 and 2⇑); lower expression of atrial natriuretic peptide, brain natriuretic peptide, and β-myosin heavy chain (Figure IC of the ...
OncologyPRO is the home of ESMOs educational & scientific resources, with exclusive content for ESMO members such as ESMOs Congresses webcasts,
This 2012 Cardiovascular Research paper by J Ma, etc utilizes the following products and services from Vector Biolabs: Rho family, small GTP binding protein Rac1 Adenovirus, b-gal/LacZ Adenovirus.
Cancer treatment with doxorubicin (DOX) can induce cumulative dose-dependent cardiotoxicity. Currently, there are no specific biomarkers that can identify patients at risk during the initial doses of chemotherapy. The aim of this study was to examine plasma cytokines/chemokines and potential cardiovascular biomarkers for the prediction of DOX-induced cardiotoxicity. Plasma samples were collected before (T0), and after the first (T1) and the second (T2) cycles of DOX-based chemotherapy of 27 breast cancer patients, including five patients who presented with ,10% decline of left ventricular ejection fraction (LVEF), five patients with LVEF decline of 5-10%, and 17 patients who maintained normal LVEF at the end of chemotherapy (240 mg/m2 cumulative dose of DOX from four cycles of treatment ...
Our quality TIMKEN NUP305E.TVP bearing is top in the world. We have large inventory now. Delivery time: 5-7days. NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP NUP305E.TVP 4T-30305D 4T-30305D 4T-30305D 4T-30305D 4T-30305D 4T-30305D 4T-30305D 4T-30305D ... condition monitoring and technical supports. we can assure the quality of the SKF 7305 BECBP bearings we provide, ZENEO Bearings ...
Over the last 40 years, a significant advance has been made in the treatment of childhood and adult cancers. However, the increase of the survival rate points out medium- and long-term adverse effects that constitute a serious limitation for the quality of life in adults survived from a childhood ca …
Bitolterol mesylate (Tornalate) is a short-acting β2 adrenergic receptor agonist used for the relief of bronchospasm in conditions such as asthma and COPD. In these disorders there is a narrowing of the airways (bronchi and their ramifications) that carry air to the lungs. Muscle spasm and inflammation within the bronchi get worse this narrowing. Bitolterol relaxes the smooth muscles present continuously around the bronchi and bronchioles facilitating the flow of air through them. Bitolterol is a prodrug of colterol. It has a rapid onset of action (2-5 minutes) and may last up to 6-8 hours. The drug, alone or in co-administration with theophylline, doesnt show cardiotoxic effect. The U.S. Food and Drug Administration (FDA) approved bitolterol in December 1984. The drug was withdrawn from the market by Élan Pharmaceuticals in 2001. Nathan RA, Bodman SF, Storms WW, Mingo TS (June 1986). Bitolterol mesylate aerosol in adults with steroid-dependent asthma: a comparison with isoproterenol ...
Abstract: Cardiotoxicity is unfortunately a common side effect of many modern chemotherapeutic agents. The mechanisms that underlie these detrimental effects
A case of congestive heart failure in a child with Wilms tumor treated with Adriamycin is presented and discussed. The role of Adriamycin in the production of cardiotoxicity is reviewed.
Cómo evaluar la presencia de TVP desde la Urgencia?, ¿Cansado que el traumatólogo te derive todo por sospecha de TVP?. De esta forma ahorraremos mucho tiempo a nuestros pacientes, sin mencionar el riesgo de dejar anticoagulación por la duda como estilan en algunos lugares ...
Cardiomyopathy is a clinical problem that occurs in the hearts of type 2 diabetic patients as well as cancer patients undergoing doxorubicin chemotherapy. The number of diabetic cancer patients is increasing but surprisingly the cardiac damaging effects of doxorubicin, a commonly used chemotherapeutic drug, on diabetic hearts have not been well-examined. As the signaling mechanisms of the doxorubicin-induced cardiomyopathy in type 2 diabetic heart are largely unknown, this study examined the molecular signaling pathways that are responsible for the doxorubicin-induced cardiotoxicity in type 2 diabetic hearts. Male 14- to 18-week-old db/db mice were used as the type 2 diabetic model, and age-matched non-diabetic db/+ mice served as controls. The db/+ non-diabetic and db/db diabetic mice were randomly assigned to the following groups: db/+CON, db/+DOX-5d, db/+DOX-7d, db/dbCON, db/dbDOX-5d, and db/dbDOX-7d. Mice assigned to doxorubicin (DOX) group were exposed to an intraperitoneal (i.p.) injection of DOX
2016 Annual Meeting: Extracellular Matrix Impregnated with Adipose Derived Stem Cells in Skeletal Muscle Regeneration following Volumetric Muscle Loss in a Murine Model
Nakamori S, Jang J, Tschabrunn CM, Pierce P, Goddu B, Rodriguez J, Ngo LH, Tung NM, Manning WJ, Nezafat R. Noncontrast CMR for Detecting Early Myocardial Tissue Injury in a Swine Model of Anthracycline-Induced Cardiotoxicity. JACC Cardiovasc Imaging. 2019 10; 12(10):2085-2087 ...
Wow guys thanks so much for your insight. Its so hard to know what to do. I keep reading articles about people that cannot loose weight. This is not our case. Im still struggling, I think that I am also over-loading my body Im eating all the time. At least every 2 hrs. If not I feel weak and angry. Its crazy I used to look at food and put weight on. Now I eat like a horse no kidding and nothing. Ive read article about the hunter- gatherer Paleo diet basically all organic. High in Protein, Meats, Fish, Eggs, Vegs, Fruits, Alomond milk (instead of Rice Milk). But this eliminates Rice, Patatoes and Dairy, Soy. Apparantely Celiacs that are not seeing any results just with Gluten free diets should try it. Another word of advice is to try taking a probiotic - i was using Florea you take it before eating as it helps build the intestine, and glutamine it helps promote recover. Ive noticed that the last few days since i run out i feel weaker. So try this. I know how you feel its a battle every day to ...
0014]Accordingly, the present disclosure relates to a method for predicting organ toxicity comprising steps of: listing of drug-induced organ injuries, obtaining molecular mechanisms of toxicity followed by tabulating underlying biochemical pathways of said drugs which precipitates organ injury, identifying biomolecules, inferring biochemical pathways and modeling kinetics of enzymes involved in these pathways to obtain a homeostatic in silico model, perturbing the model and designing assays to measure the perturbation, applying the assays to a chemical or set of chemicals to generate new assay data, and feeding the new assay data to the model for predicting toxicity and organ damage; a system for predicting organ toxicity said system comprising: storage element having list of drug-induced organ injury along with their molecular mechanisms of toxicity and underlying biochemical pathways, in silico model component configured to represent normal organ, in vitro assays designed to quantitatively ...
TKIs are a major class of cancer therapeutics, with revenues from these drugs annually reaching billions of dollars (19). However, many TKIs, like other chemotherapeutics, exhibit substantial cardiotoxicities (3). Our results demonstrate that hiPSC-CMs can assess TKI cardiotoxicity in a high-throughput fashion. We evaluated 21 FDA-approved TKIs using hiPSC-CMs derived from 11 healthy individuals and 2 patients receiving TKIs as cancer therapy. From the data obtained, we developed a cardiac safety index integrating TKI-induced cytotoxicity measurements, contractility assessments, and literature-reported TKI blood plasma concentrations in patients. We also validated the negative effects of known cardiotoxic TKIs.. Previous studies evaluated TKI cardiotoxicity using animals and other in vitro models (20). Sorafenib, one of the three most cytotoxic TKIs in our study, induces cardiomyocyte death and contractility defects in the zebrafish heart and causes ventricular dysfunction and heart failure ...
Thermal processing of meat products generates cardiotoxic compounds capable of inducing heart failure in both humans and laboratory animals. Such compounds may be present in broiler diets because supplements such as meat meal (MM), which are commonly
Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. [PubChem]
OBJECTIVE Considering that global left ventricular systolic radial strain is a sensitive technique for the early detection of left ventricular dysfunction due to antineoplastics and the analysis of segmental myocardial contractility, we evaluated this technique for early detection of trastuzumab-related cardiotoxicity by comparing it with cardiac structural damage. METHODS Groups of six mice were injected with trastuzumab or doxorubicin, used either as single agents or in combination. Cardiac function was evaluated by transthoracic echocardiography measurements before and after treatment for 2 or 7 days, by using a Vevo 2100 high-resolution imaging system. After echocardiography, mice were euthanized, and hearts were processed for histological evaluations, such as cardiac fibrosis, apoptosis, capillary density, and inflammatory response. RESULTS Trastuzumab-related cardiotoxicity was detected early by 2D strain imaging. Radial strain was reduced after 2 days in mice treated with trastuzumab alone
TY - JOUR. T1 - Cardiotoxicity with immune system targeting drugs. T2 - A meta-analysis of anti-PD/PD-L1 immunotherapy randomized clinical trials. AU - Rahouma, Mohamed. AU - Karim, Nagla Abdel. AU - Baudo, Massimo. AU - Yahia, Maha. AU - Kamel, Mohamed. AU - Eldessouki, Ihab. AU - Abouarab, Ahmed. AU - Saad, Ihab. AU - Elmously, Adham. AU - Gray, Katherine D.. AU - Ghaly, Galal. AU - Gaber, Ola. AU - Kamal, Mona. AU - A Hassan, Ayah. AU - Rahouma, Mostafa. AU - DAscenzo, Fabrizio. AU - Morris, John. AU - Mohamed, Abdelrahman. AU - Girardi, Leonard. AU - Gaudino, Mario. PY - 2019/5/15. Y1 - 2019/5/15. N2 - Background: With antiprogrammed death receptor-1 (anti-PD-L1) therapy, a recent meta-analysis reported higher incidence of cutaneous, endocrine and gastrointestinal complications especially with dual anti-PD-L1 immunotherapy (IMM). Methods: Our primary outcome was assessment of all cardiotoxicity grades in IMM compared with different treatments, thus a systemic review and a meta-analysis on ...
Cardio-oncology is an emerging field of cardiology that focuses on cardiovascular diseases in patients with cancer. The classic cardio-oncology paradigm is the prevention, diagnosis and treatment of cardiotoxicity resulting from chemotherapy and/or radiotherapy. Diagnosis and treatment of primary and metastatic cardiac tumours as well as cardiac amyloidosis can be considered less classical cardio-oncology objectives.
Training set will consist of sera of 30 patients who has reached an end point. Training set will be sequenced using next generation sequencing.. Training set will be used to derive a miRNA signature capable of separating early cardiotoxicity patients from healthy ones. MiRNA signature will be validated using validation set. ...
At any time during the study, if your doctor thinks it is necessary, you will have an ECG and/or ECHO or MUGA scan.. If you stop receiving chemotherapy during your participation in this study, you will still be asked to complete the above tests and procedures listed at the 12-month (end-of-study visit) visit. Other tests and procedures scheduled during the study may not be performed because you are no longer receiving chemotherapy treatment. Your study doctor and the research staff will go over this information with you if this happens.. Research Test Results:. The primary biomarkers being tested in this study are the BNP and TnI. Both the BNP and TnI look at the function of your heart. The BNP and TnI will both be tested at MD Anderson.. The results of the biomarker tests will be kept separately from your other tests results, and will not affect your treatment in any way. The only reason your biomarker test results would be shared with your cancer doctor would be if the study doctor thinks the ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
Specific target organ toxicity - single exposure : Not available Ingredient disclosure. Comments: This classification comes from an automated conversion of the classification established under the Controlled Products Regulations. The complete classification under the Hazardous Products Regulations will be determined at a later date.. ...
Technology Appraisal Guidance No. 446. Source: National Institute for Health and Care Excellence. 1. Guidance. 1.1 Brentuximab vedotin is recommended as an option for treating CD30-positive Hodgkin lymphoma in adults, only if:. they have relapsed or refractory disease after autologous stem cell transplant and. the company provides brentuximab vedotin at the price agreed with NHS England in the commercial access agreement.. 1.2 Brentuximab vedotin is recommended for use within the Cancer Drugs Fund as an option for treating CD30-positive Hodgkin lymphoma in adults, only if:. ...
Trastuzumab is a drug used for the treatment of metastatic breast cancer patients. Due to blockage of the human epidermal growth factor receptor 2 signaling in cardiac myocytes, cardiotoxicity has been observed. There are many studies that investigated risk factors for trastuzumab-induced cardiotoxicity, but no study has been published for factors on the time to cardiotoxicity. This study aimed to investigate the factors for the time to occur trastuzumab-induced cardiotoxicity. From January 2014 to December 2015, a retrospective study was performed with breast cancer patients who were treated with trastuzumab. Associations between presence of and time to cardiotoxicity and various factors were analyzed. Based on multivariate models, it was found that baseline left ventricular ejection fraction (LVEF) < 62.5% (AHR 5.96, 95% CI 2543-13.95) and anthracycline-based chemotherapy (AHR 7.90, 95% CI 1.05-59.71) were significant factors for time to cardiotoxicity after adjusting other confounding ...
This manuscript describes a detailed protocol to induce acute skeletal muscle regeneration in adult mice and subsequent manipulations...
Brentuximab vedotin - Intravenous : Brentuximab vedotin is used on its own or together with other medicines to treat cancer of the blood and lymph tissue.
The goal of this clinical research study is learn more about the safety of SGN-35 (brentuximab vedotin) in patients who participated in 2009-0851, were on placebo, and whose HL has gotten worse. Another goal of this study is to allow other patients with HL and ALCL whose disease has come back or is not getting better on another treatment, access to brentuximab vedotin.
I have read the article by Cardinale and colleagues1 with great interest and congratulate the authors for the completion of a burdensome work and the excellent presentation of their results. As the authors have correctly stated, early preclinical cardiac injury should be looked for soon after anthracycline treatment to effectively treat this disorder from its onset, before its overt clinical expression. However, I would like to point out one aspect that needs further clarification. The authors have reported that the overall incidence of cardiotoxicity is 9%. Previous researches have reported that anthracycline promotes cancer cell death via regulator of G-protein signaling 6 (RGS6)-mediated activation of ataxia telangiectasia-mutated serine/threonine protein kinase and the resultant upregulation of tumor suppressor p53, leading to an apoptosis pathway underlying its cytotoxic activity. The ability of RGS6 to promote p53 activation in response to anthracycline is independent of RGS6 interaction ...
The drug being tested in this study is called brentuximab vedotin. Brentuximab vedotin is being tested to treat pediatric participants who have advanced stage, newly diagnosed, classical CD30+ HL. This study will assess the safety, tolerability, and anti-tumor activity, as well as recommended dose of brentuximab vedotin in combination with a multiagent chemotherapy regimen that is based on a current standard of care (SOC) first-line treatment regimen for newly diagnosed HL. The study will enroll approximately 55 evaluable participants. The study will be conducted in 2 phases, Phase 1 and Phase 2. Phase 1 study will enroll up to 12 participants to determine the recommended dose. Once the recommended dose is identified additional participants will be enrolled into phase 2 so that the total number of evaluable participants will be approximately 55, including participants treated at recommended dose in Phase 1. Participants will be enrolled in the following 2 dose Cohorts: • Brentuximab vedotin 48 ...
Seattle Genetics Highlights Updated Progression-Free Survival and Overall Survival Data from ADCETRIS® (Brentuximab Vedotin) Frontline PTCL Phase 1 Clinical Trial at the ESMO 2014 Congress
City of Hope research-led study reports on five-year survival data, suggests that the targeted therapy brentuximab vedotin (BV) should be standard of care for patients with relapsed or treatment-resistant Hodgkin lymphoma.
Seattle Genetics Reports Data from Phase I Trial of ADCETRIS ® (Brentuximab Vedotin) in Front-line Mature T-Cell Lymphomas (MTCL) -100 Percent Objective Response Rate, Including 88 Percent
Adult patients with CD30+ relapsed/refractory (R/R) Hodgkin Lymphoma (HL) after ASCT - National Institute for Health and Care Excellence (NICE) recommend long-term funding for brentuximab vedotin
In this study, we have shown that Id-mutant mice, unlike Id3-null mice, display a muscle regeneration phenotype using the cardiotoxin-induced TA muscle regeneration paradigm. The Id1 and Id3 proteins were markedly upregulated in the injured skeletal muscle of WT mice within 24 h, as were BMPR-II and pSmad1/5/8. Hindlimb injection of the BMP antagonist Noggin reduced the amounts of pSmad1/5/8 and both Id1 and Id3 at 24 h after cardiotoxin injury, suggesting that BMP signaling was responsible for their expression. These proteins were also expressed in the satellite cell-derived myogenic cell line C2C12 (3) when actively proliferating as myoblasts, but were all reduced on differentiation into myotubes. Immunofluorescent microscopy revealed that pSmad1/5/8, Id1, and Id3 were all detectable in the nuclei of many Pax7+ myoblasts in the injured mouse hindlimb at day 3 post-cardiotoxin injection. Finally, we showed that the Id-mutant mice, but not Id3-null mice, displayed a reduced number of ...
5-Fluorouracil (5-FU) is a commonly used anti-neoplastic agent. 5-FU has been not uncommonly associated with cardiotoxicity, although the many potentially causative mechanisms are yet to be established. Here, we present the case of a 61-year-old gemstone miner who developed symptomatic sinus bradycardia while receiving a continuous 5-FU infusion combined with radiotherapy for locally advanced rectal cancer. This dysrhythmia is an unusual type of 5-FU toxicity, our case being the second described. We review the actions of 5-FU and the various proposed mechanisms of its cardiotoxic effects ...
A paper published in 2011 indicates that taking two 220 mg naproxen tablets every day after age 70 substantially diminishes the development of Alzheimers disease, but only in asymptomatic individuals after two to three years on this regimen. By contrast, NSAIDs including naproxen had an adverse effect on patients with signs of AD pathogenesis, including those at the very early stages of cognitive impairment. Unfortunately, this trial (ADAPT) was not continued as long as it should have been because of health concerns about the cardiotoxic effects of one of the NSAIDs undergoing testing (celecoxib, Celebrex). However, clearly anyone with a family history of early-onset Alzheimers disease or over the age of 60 should definitely consider taking daily naproxen as a preventive measure as long as no cognitive defects are already apparent, and they have the consent of their physician. Naproxen has a good overall safety profile and is available over the counter in the United States (Aleve). However, ...
TY - JOUR. T1 - Adult rat myocardial slices. T2 - A tool for studies of comparative cardiotoxicity. AU - Parrish, A. R.. AU - Dorr, Robert T. AU - Gandolfi, A Jay. AU - Brendel, K.. PY - 1994. Y1 - 1994. N2 - The applicability of myocardial slices in comparative cardiotoxicity studies was investigated using the known cardiotoxicants allylamine (AAM) and doxorubicin (DOX). Precision-cut adult rat myocardial slices are a recently developed in vitro system. Previously, it has been demonstrated that myocardial slices are viable for up to 24 hr in organ culture. Myocardial slices exhibited a concentration- and time-dependent loss of viability in response to exposure to AAM or DOX (10-7, 10-6 or 10-5 m) during 24 hr in culture, as assessed by biochemical parameters including protein synthesis, ATP content, lipid peroxidation and the loss of the cytosolic enzyme creatine kinase. Protein synthesis and ATP content were sensitive indicators of slice viability, while lipid peroxidation was affected only by ...
1.Sánchez G, Cervantes G y Maldonado J. Linfomas No Hodgkin. Med Int Mex 2004; 20: 111-23. 2.Estrada D, Rajdev L and Sparado J. Lymphoma, Non-Hodgkin. Emedicine. Last Updated: June 24, 2004. 3.Ng R, Better N, Green MD. Anticancer agents and cardiotoxicity. Semin Oncol. 2006; 33 (1): 2-14. 4.Youssef G, Links M. The prevention and management of cardiovascular complications of chemotherapy in patients with cancer. Am J Cardiovasc Drugs. 2005; 5 (4): 233-43. 5.Pasca A, Pereiro G, Mansilla S y Lastiri H. Toxicidad miocardiaca por antraciclinas. Rev Fed Arg Cardiol 2000; 29:319-325. 6.Suter T and Meier B. Detection of anthracycline- induced cardiotoxicity: is there light at the end of the tunnel?. Editorial. Annals of Oncology. 2002; 13: 647-649. 7.Cvetkovic RS, Scott LJ. Dexrazoxane a review of its use for cardioprotection during anthracycline chemotherapy. Drugs. 2005; 65 (7): 1005-24. 8.Gianni L, Haerman E, Lipshultz S, Minotti G, sarvazyan N and Sawyer D.Anthracycline Cardiotoxicity: From Bench ...
There are many possible causes of cardiac toxicity. In cancer patients, cardiac toxicity may be caused by radiation to the chest and chemotherapy drugs.
Explore more about content imaging systems designed to assess cytotoxic effect of compounds on pertinent human cardiac cells, derived from induced pluripotent stem cells.
A session at the 64th Annual Scientific Session of the American College of Cardiology evaluated the cardiotoxic outcomes of treatment in cancer survivors.
MYTH: Synthroid (synthetic thyroid or T4, Thyroxine) works and is more effective than thyroid glandular.The truth: Synthroid is cardiotoxic, shrinks...
Its venom consists of both neurotoxins and cardiotoxins. Symptoms of envenomation include swelling of the bite site, dizziness ...
The 3FTx family consists of two major categories, neurotoxins and cardiotoxins. LNTX belongs to the neurotoxin family; other ...
The compounds consist of neurotoxins, cardiotoxin, nephrotoxin, hemolytic toxic, phosphodiesterases, phospholipase, histamine, ...
It has the most potent venom of its kind, it is mainly composed of neurotoxins, cardiotoxins and myotoxins and additional ...
At the end, Jairaj discloses to Ajay that he is going to have a heart attack from cardiotoxin, which he had used to kill Maya, ... Ajay's possessiveness and his affair with Ritu made him kill Maya and made it look like a heart attack by using a cardiotoxin ... He feels Maya's presence around him and gradually gets clues including the bottle of cardiotoxin (TH-16) which he had used to ...
Aconitine is a potent neurotoxin and cardiotoxin that causes persistent depolarization of neuronal sodium channels in ...
... (CTX III, also known as cytotoxin 3) is a sixty amino-acid polypeptide toxin from the Taiwan Cobra Naja atra. ... "Cardiotoxin III induces apoptosis in K562 cells through a mitochondrial-mediated pathway". Clin. Exp. Pharmacol. Physiol. 32 ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Cardiotoxin_III&oldid=899751861" ...
While botulinum toxin is generally considered safe in a clinical setting, there can be serious side effects from its use. The use of botulinum toxin A in cerebral palsy children is safe in the upper and lower limb muscles.[5][6] Most commonly, botulinum toxin can be injected into the wrong muscle group or with time spread from the injection site, causing temporary paralysis of unintended muscles. Side effects from cosmetic use generally result from unintended paralysis of facial muscles. These include partial facial paralysis, muscle weakness, and trouble swallowing. Side effects are not limited to direct paralysis however, and can also include headaches, flu-like symptoms, and allergic reactions.[41] Just as cosmetic treatments only last a number of months, paralysis side-effects can have the same durations.[citation needed] At least in some cases, these effects are reported to dissipate in the weeks after treatment.[citation needed] Bruising at the site of injection is not a side effect of the ...
Cardiotoxin III. *note: some toxins are produced by lower species and pass through intermediate species ...
No animal species is immune to the acute toxic effects of aflatoxins. Adult humans have a high tolerance for aflatoxin exposure and rarely succumb to acute aflatoxicosis,[23] but children are particularly affected, and their exposure can lead to stunted growth and delayed development, in addition to all the symptoms mentioned below.[4] High-level aflatoxin exposure produces an acute hepatic necrosis (acute aflatoxicosis), resulting later in cirrhosis or carcinoma of the liver. Acute liver failure is made manifest by bleeding, edema, alteration in digestion, changes to the absorption and/or metabolism of nutrients, and mental changes and/or coma.[23] Chronic, subclinical exposure does not lead to symptoms so dramatic as acute aflatoxicosis. Chronic exposure increases the risk of developing liver and gallbladder cancer,[24] as aflatoxin metabolites may intercalate into DNA and alkylate the bases through epoxide moiety. This is thought to cause mutations in the p53 gene, an important gene in ...
... s are often distinguished from other chemical agents by their method of production-the word toxin does not specify method of delivery (compare with venom and the broader meaning of poison-all substances that can also cause disturbances to organisms). It simply means it is a biologically produced poison. There was an ongoing terminological dispute between NATO and the Warsaw Pact over whether to call a toxin a biological or chemical agent, in which the NATO opted for biological agent, and the Warsaw Pact, like most other countries in the world, for chemical agent.[citation needed] According to an International Committee of the Red Cross review of the Biological Weapons Convention, "Toxins are poisonous products of organisms; unlike biological agents, they are inanimate and not capable of reproducing themselves", and "Since the signing of the Constitution, there have been no disputes among the parties regarding the definition of biological agents or toxins".[4] According to Title 18 of the ...
Cardiotoxin III. *note: some toxins are produced by lower species and pass through intermediate species ...
The first three steps outline the travel of tetanus from the peripheral nervous system to where it is taken up to the CNS and has its final effect. The last three steps document the changes necessary for the final mechanism of the neurotoxin. Transport to the CNS inhibitory interneurons begins with the B-chain mediating the neurospecific binding of TeNT to the nerve terminal membrane. It binds to GT1b polysialogangliosides, similarly to the botulinum neurotoxin. It also binds to another poorly characterized GPI anchored protein receptor more specific to TeNT.[10][11] Both the ganglioside and the GPI anchored protein are located in lipid microdomains and both are requisite for specific TeNT binding.[11] Once it is bound the neurotoxin is then endocytosed into the nerve and begins to travel through the axon to the spinal neurons. The next step, transcytosis from the axon into the CNS inhibitory interneuron, is one of the least understood parts of TeNT action. At least two pathways are involved, ...
... acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the surface of target cells. The B subunit can also bind to cells lacking GM1. The toxin then most likely binds to other types of glycans, such as Lewis Y and Lewis X, attached to proteins instead of lipids.[7][8][9] Once bound, the entire toxin complex is endocytosed by the cell and the cholera toxin A1 (CTA1) chain is released by the reduction of a disulfide bridge. The endosome is moved to the Golgi apparatus, where the A1 protein is recognized by the endoplasmic reticulum chaperone, protein disulfide isomerase. The A1 chain is then unfolded and delivered to the membrane, where Ero1 triggers the release of the A1 protein by oxidation of protein disulfide isomerase complex.[10] As the A1 protein moves from the ER into the cytoplasm by the Sec61 channel, it refolds and avoids deactivation as a result of ubiquitination. CTA1 is then free to bind with a human partner protein ...
... occludes the pore of calcium-activated voltage-gated shaker K+ channels by binding to one of four independent, overlapping binding sites.[6][7] It binds both to the open and the closed states. In addition, the block is enhanced as the ionic strength is lowered.[8] This block occurs as the Asn 30 on the CTX interacts with the Asp 381 on the K+ channel.[9] The blockade of K+ channels by the charybdotoxin peptide causes neuronal hyperexcitability. Mutations of the Lys31Gln and the Asn30Gln had the effect of lessening the CTX block of the pore on the shaker channel.[9] ...
LPS acts as the prototypical endotoxin because it binds the CD14/TLR4/MD2 receptor complex in many cell types, but especially in monocytes, dendritic cells, macrophages and B cells, which promotes the secretion of pro-inflammatory cytokines, nitric oxide, and eicosanoids.[16] As part of the cellular stress response, superoxide is one of the major reactive oxygen species induced by LPS in various cell types that express TLR (toll-like receptor). LPS is also an exogenous pyrogen (fever-inducing substance). Being of crucial importance to Gram-negative bacteria, these molecules make candidate targets for new antimicrobial agents. Some researchers doubt reports of generalized toxic effects attributed to all lipopolysaccharides, in particular, for cyanobacteria.[17] LPS function has been under experimental research for several years due to its role in activating many transcription factors. LPS also produces many types of mediators involved in septic shock. Humans are much more sensitive to LPS than ...
Cardiotoxin III, from Chinese cobra. Environmental toxins[edit]. See also: Environmental toxicology ...
Cardiotoxin III(英语:Cardiotoxin III). *注:一些挂名在某物种下的毒素其实
Độc tố (enterotoxin (độc tố đường ruột)/neurotoxin (độc tố thần kinh)/hemotoxin (huyết độc tố)/cardiotoxin (độc tố gây ung thư ...
Their venom is mainly neurotoxic, although many of them also possess several other types of toxins, including cardiotoxins and ...
টক্সিন"' ( প্রাচীন গ্রিক: শব্দτοξικόν toxikon(টক্সিকন) থেকে এর উৎপত্তি) হচ্ছে এক প্রকার বিষাক্ত পদার্থ যা উৎপন্ন হয় জীব বা জীবকোষের অভ্যন্তরে।[১][২] টক্সিকেন্ট কৃত্রিমভাবে জীবকোষের বাইরে প্রস্তুত করা যায়। এই কাজটি প্রথম করেন জৈব রসায়নবিদ লুডউইক ব্রেইজের।(১৮৪৯-১৯১৯)[৩] টক্সিন হতে পারে small molecule, পেপটাইড অথবা প্রোটিন। এগুলো রোগ তৈরী করতে, শরীরের টিস্যুকে ধ্বংস করে দিতে সক্ষম। জৈব macromolecule ...
Cardiotoxin III (CTX III, also known as cytotoxin 3) is a sixty amino-acid polypeptide toxin from the Taiwan Cobra Naja atra. ... "Cardiotoxin III induces apoptosis in K562 cells through a mitochondrial-mediated pathway". Clin. Exp. Pharmacol. Physiol. 32 ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Cardiotoxin_III&oldid=899751861" ...
A common cytolytic region in myotoxins, hemolysins, cardiotoxins and antibacterial peptides.. Kini RM1, Evans HJ. ...
Ive only been able to find one paper so far using cardiotoxin to injure myoblasts in culture (they used it on C2C12 myotubes ... Cardiotoxin on myoblasts - posted in Tissue and Cell Culture: ... Ive only been able to find one paper so far using cardiotoxin ... Also tagged with one or more of these keywords: cardiotoxin, myoblast, C2C12, primary. Protocols and Techniques Forums → ... Cardiotoxin on myoblasts. Started by assembler01, Oct 05 2012 01:00 PM ...
In regenerating muscle, β-synemin is first expressed at the sarcolemma and in the cytoplasm at day 5 following cardiotoxin ... Beta-synemin expression in cardiotoxin-injected rat skeletal muscle. BMC Musculoskeletal Disorders 8: 40. ... and co-localization studies for α-dystrobrevin and β-synemin were performed in regenerating muscle following cardiotoxin ...
Cobra venom contains cardiotoxins (CTXs) that induce tissue necrosis and systolic heart arrest in bitten victims. CTX-induced ... Non-cytotoxic cobra cardiotoxin A5 binds to avß3 integrin and inhibit bone resorption. Identification of cardiotoxins as nonRGD ... Interaction of cardiotoxins with membranes: a molecular modeling study. Biophys J 2002; 83:144-53.CrossRefPubMedGoogle Scholar ... Possible mechanisms of action of cobra snake venom cardiotoxins and bee venom melittin. Toxicon 1993; 31:669-695.CrossRefPubMed ...
C.-M. Chien, S.-Y. Chang, K.-L. Lin, C.-C. Chiu, L.-S. Chang, and S.-R. Lin, "Taiwan cobra cardiotoxin III inhibits Src kinase ... L.-W. Chen, P.-H. Kao, Y.-S. Fu, S.-R. Lin, and L.-S. Chang, "Membrane-damaging activity of Taiwan cobra cardiotoxin 3 is ... Ameliorating Adriamycin-Induced Chronic Kidney Disease in Rats by Orally Administrated Cardiotoxin from Naja naja atra Venom. ... C.-C. Hung, S.-H. Wu, and S.-H. Chiou, "Sequence characterization of cardiotoxins from Taiwan cobra: isolation of a new isoform ...
1. Cardiotoxin Injection in the Tibialis Anterior Muscle. *Prepare a 10 μM working solution of cardiotoxin (CTX) by diluting ... Cardiotoxin from Naja mossambica mossambica. SIGMA ALDRICH. C9759. Syringe For Insulin BD Micro-Fine+ Needle 30 G x 8 mm - Da ... Chang, C. C., Chuang, S. T., Lee, C. Y., Wei, J. W. Role of cardiotoxin and phospholipase A in the blockade of nerve conduction ... Induction of Acute Skeletal Muscle Regeneration by Cardiotoxin Injection. doi: 10.3791/54515 Published: January 1, 2017 ...
Cardiotoxin, Naja nigricollis A cytolytic toxin that causes depolarization of skeletal muscle fibers in vitro. - Find MSDS or ... We are offering Cardiotoxin, Naja pallida (Cat. No. 217503) as a possible alternative. Please read the alternative product ... Cardiotoxin, Naja nigricollis MSDS (material safety data sheet) or SDS, CoA and CoQ, dossiers, brochures and other available ...
A cardiotoxin-like basic polypeptide from the venom of Naja naja atra is homologous to cardiotoxins from the same venom, but ... Harvey, A L and Hayashi, K (1987) Depolarization of skeletal muscle cells in culture by a cardiotoxin-like basic polypeptide ... To determine if it acts like the cardiotoxins its depolarizing ability was measured. It was about 10 times less potent than the ... Depolarization of skeletal muscle cells in culture by a cardiotoxin-like basic polypeptide from the venom of the Taiwan cobra ( ...
Cardiotoxin-4b (CTX-4b), isolated from Naja naja sputatrix venom, shows lethality in several cell types. Employing murine ... Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early ... Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early calpain ...
Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.. ...
Its venom consists of both neurotoxins and cardiotoxins. Symptoms of envenomation include swelling of the bite site, dizziness ...
The 3FTx family consists of two major categories, neurotoxins and cardiotoxins. LNTX belongs to the neurotoxin family; other ...
Cardiotoxin muscle injury. Eight hours after the blood exchange procedure, mice were injured by intramuscular injections of CTX ... One day after the blood exchange, tibiallis anterior (TA) hind leg muscles of all mice were injured by cardiotoxin (CTX) and 5 ...
The expression of cardiotoxin fusion protein with a yield of about 35 mg/liter culture was confirmed by highly specific anti- ... The expression of cardiotoxin fusion protein with a yield of about 35 mg/liter culture was confirmed by highly specific anti- ... The expression of cardiotoxin fusion protein with a yield of about 35 mg/liter culture was confirmed by highly specific anti- ... The expression of cardiotoxin fusion protein with a yield of about 35 mg/liter culture was confirmed by highly specific anti- ...
In regenerating muscle, β-synemin is first expressed at the sarcolemma and in the cytoplasm at day 5 following cardiotoxin ... and co-localization studies for α-dystrobrevin and β-synemin were performed in regenerating muscle following cardiotoxin ... Immunohistochemistry of β-synemin and ATPase staining on muscle sections after injection with cardiotoxin. (A) 10 μm transverse ...
Cardiotoxins in Horses May 28, 2017. Learn about several substances that can cause heart muscle damage and death in horses. ...
Muscle injury was induced by a 100-µl injection of a 10 µM cardiotoxin (CTX) solution (cardiotoxin 1 from Naja naja atra, part ... Cardiotoxin Injury.. Cardiotoxin injury was induced similar to what was described by Garry et al. (2000), with slight ... cardiotoxin. ELISA. enzyme-linked immunosorbent assay. FSD. follistatin domain. FSH. follicle-stimulating hormone. FST288. ... Cardiotoxin Injury/Hind Limb Immobilization.. Lower limb muscles were injured using the aforementioned protocol. Following the ...
Cardiotoxin experiments. 50 μl of 10 μM cardiotoxin (Sigma-Aldrich) were injected into the calf muscles of 8- to 12-week-old ... we injected gastrocnemius muscles of 2-month-old mice with cardiotoxin and analyzed muscle fiber morphology 5, 10 and 21 days ...
Muscle injury with cardiotoxin. Cardiotoxin (CTX; Sigma) was prepared in PBS (10 μM) and 50 μl was injected percutaneously into ... Therefore, we induced injury by injection of cardiotoxin (CTX) into Pax7+/CE;R26ReGFP-DTA/lacZ EDL muscle grafts that had ... B-E) Fluorescent microscopy on cross-sections of established Pax7+/CE;R26ReGFP-DTA/lacz EDL grafts four weeks post-cardiotoxin ... Absence of the myogenic response to acute injury in satellite cell-ablated mice. (A) Tamoxifen (tmx) and cardiotoxin (CTX) ...
After 15 days of irradiation, the tibialis anterior (TA) muscle was injected with cardiotoxin (CTX), and muscles were harvested ...
The multiplicity of cardiotoxins from Naja naja atra (Taiwan cobra) venom. ... The multiplicity of cardiotoxins from Naja naja atra (Taiwan cobra) venom. Four novel cardiotoxins were isolated from Naja naja ... Analysis on the secondary structure of pre-mRNAs of N. naja atra cardiotoxin 4 gene and N. naja sputatrix cardiotoxin 3 gene ... The hypervariable segments encoded by the second and third exon of cardiotoxin genes are located at or near the tips of loop ...
Although Naja naja atra cardiotoxin 3 (CTX3) and cardiotoxin 4 (CTX4) showed different cytotoxicity toward human neuroblastoma ... abstract = "Although Naja naja atra cardiotoxin 3 (CTX3) and cardiotoxin 4 (CTX4) showed different cytotoxicity toward human ... N2 - Although Naja naja atra cardiotoxin 3 (CTX3) and cardiotoxin 4 (CTX4) showed different cytotoxicity toward human ... AB - Although Naja naja atra cardiotoxin 3 (CTX3) and cardiotoxin 4 (CTX4) showed different cytotoxicity toward human ...
JAK1/STAT1/STAT3 were activated during cardiotoxin-induced muscle regeneration. (A) After the injection of cardiotoxin (CTX), ... Cardiotoxin-induced muscle injury and regeneration. TA muscles of 6-8-wk-old C57BL/6 mice were injected with 25 μl of 10 μM ... JAK1/STAT1/STAT3 are up-regulated and activated in cardiotoxin-induced regenerating muscles. Because MSC-derived primary ... muscles in response to cardiotoxin-induced muscle injury (Charge and Rudnicki, 2004). In this injury-induced muscle ...
Cardiotoxin molecular toxicology modeling. US20070082332 *. Jan 8, 2003. Apr 12, 2007. Gene Logic, Inc.. Molecular ...
This page includes the following topics and synonyms: Systolic Dysfunction, Left Ventricular Dysfunction, Left Ventricular Failure, Systolic Heart Failure, Left Ventricular Systolic Dysfunction, Heart Failure with Reduced Ejection Fraction.
Cardiotoxins / adverse effects, pharmacology, therapeutic use. Controlled Clinical Trials as Topic. Databases, Factual. Female ...
Cardiotoxin-induced skeletal muscle injury elicits profound changes in anabolic and stress signaling, and muscle fiber type ...
Cardiotoxin injury was induced by injecting 20 μL of a 10 μM cardiotoxin solution in PBS into tibialis anterior or ... Cardiotoxin injection and histology. Wild-type mice were sedated (3% isoflurane, 0.8 L/min O2) and then injected with 1 mg/kg ... Cardiotoxin was released down the midline of the muscle to induce a homogeneous area of injury at the center of the muscle. ... Three hours after cardiotoxin injury muscle was evaluated for Evans blue dye uptake (Figure 8A). Fluorescence imaging showed a ...
5, A and B, a-c). We then stained cardiotoxin-damaged TA muscle sections from day 3, 7, and 14 postinjection (Fig. 5, B, d-l, ... B: uninjured TA muscle (a-c, ×10 fields) and cardiotoxin-damaged TA muscle (d-l, ×20 fields = 0.12 mm2) at D3 (d-f), D7 (g-i), ... Cardiotoxin was injected into the left hindlimb TA muscles of WT, Id3-null, and Id-mutant mice. Groups of mice were killed at 3 ... Cardiotoxin-damaged TA muscle sections at D3 postinjury were costained with antibodies to Pax7 (left) and either p-S1/5/8 (top ...
  • Cardiotoxin III (CTX III, also known as cytotoxin 3 ) is a sixty amino-acid polypeptide toxin from the Taiwan Cobra Naja atra . (wikipedia.org)
  • Actions of cardiotoxins from the southern Chinese cobra (Naja naja atra) on rat cardiac tissue. (springer.com)
  • We are offering Cardiotoxin, Naja pallida (Cat. (merckmillipore.com)
  • A cardiotoxin-like basic polypeptide from the venom of Naja naja atra is homologous to cardiotoxins from the same venom, but much less toxic. (strath.ac.uk)
  • We report here the construction of cardiotoxin V gene, from cobra snake venom (Naja naja atra), by chemically synthesized oligonucleotides and its expression as a glutathione S-transferase-cardiotoxin fusion protein in the inclusion bodies of Escherichia coli. (elsevier.com)
  • GENTAUR antibody-antibodies.com The Marketplace for Antibodies : The multiplicity of cardiotoxins from Naja naja atra (Taiwan cobra) venom. (antibody-antibodies.com)
  • The multiplicity of cardiotoxins from Naja naja atra (Taiwan cobra) venom. (antibody-antibodies.com)
  • Four novel cardiotoxins were isolated from Naja naja atra (Taiwan cobra) venom by successive separation on a SP-Sephadex C-25 column and a reverse phase column. (antibody-antibodies.com)
  • Comparative analyses on the amino acid sequences of cardiotoxins from the venoms of N. naja atra and other Naja species indicated that amino acid substitutions of cardiotoxin isoforms frequently occurred at positions 7-11, 27-32 and 45-47. (antibody-antibodies.com)
  • Analysis on the secondary structure of pre-mRNAs of N. naja atra cardiotoxin 4 gene and N. naja sputatrix cardiotoxin 3 gene has shown that the hypervariable regions of the exon 2 pertain to form intra-exon pairings and are not involved in the formation of intron-exon pairings. (antibody-antibodies.com)
  • Although Naja naja atra cardiotoxin 3 (CTX3) and cardiotoxin 4 (CTX4) showed different cytotoxicity toward human neuroblastoma SK-N-SH cells, the two toxins induced apoptotic death on SK-N-SH cells. (elsevier.com)
  • Its venom consists of both neurotoxins and cardiotoxins. (wikipedia.org)
  • The venom is a combination of neurotoxins and cardiotoxins. (hubpages.com)
  • And also their venom contains neurotoxins and cardiotoxins. (biology-online.org)
  • The present work describes a detailed and reproducible protocol to induce acute skeletal muscle regeneration in mice through a single intramuscular injection of cardiotoxin (CTX). (jove.com)
  • Genetic deletion of miR-206 in mice substantially delayed regeneration induced by cardiotoxin injury. (jci.org)
  • R. Couteaux, J.-C. Mira, and A. d'Albis, "Regeneration of muscles after cardiotoxin injury. (hindawi.com)
  • Gαi2 knockout mice display decreased lean body mass, reduced muscle size, and impaired skeletal muscle regeneration after cardiotoxin-induced injury. (asm.org)
  • This study addressed how Tregcells rein in MFs during regeneration of murine muscle after acute injury with cardiotoxin. (unboundmedicine.com)
  • 10 Mouse MSC-like cells converted to a myogenic phenotype after infusion and homing to cardiotoxin injured skeletal muscle. (ahajournals.org)
  • Viable skNAC(-/-) adult mice had reduced postnatal skeletal muscle growth and impaired regenerative capacity after cardiotoxin-induced injury. (ca.gov)
  • A common cytolytic region in myotoxins, hemolysins, cardiotoxins and antibacterial peptides. (nih.gov)
  • It has the most potent venom of its kind, it is mainly composed of neurotoxins, cardiotoxins and myotoxins and additional hemotoxins, deaths in humans usually occur by heart and respiratory failure, sometimes by cerebral hemorrhage, organ dysfunction and shock. (wikipedia.org)
  • C obra venom contains cardiotoxins (CTXs) that induce tissue necrosis and systolic heart arrest in bitten victims. (springer.com)
  • Brown snake venom contains procoagulants, cardiotoxins and a potent presynaptic neurotoxin ( Textilotoxin ). (lifeinthefastlane.com)
  • Immunoprecipitation and co-localization studies for α-dystrobrevin and β-synemin were performed in regenerating muscle following cardiotoxin injection. (harvard.edu)
  • In regenerating muscle, β-synemin is first expressed at the sarcolemma and in the cytoplasm at day 5 following cardiotoxin injection. (harvard.edu)
  • Immunohistochemistry of β-synemin and ATPase staining on muscle sections after injection with cardiotoxin. (biomedcentral.com)
  • Acute injury was induced by injection of cardiotoxin (CTX) into the belly of the tibialis anterior (TA) muscle. (rupress.org)
  • Possible mechanisms of action of cobra snake venom cardiotoxins and bee venom melittin. (springer.com)
  • These categories are: (i) haemotoxins, which promote haemorrhaging primary to extensive local swelling and necrosis, (ii) neurotoxins, which disable muscle contraction and paralyse the heart as well as hinder respiration, and (iii) cardiotoxins, which elicit specific toxicity to cardiac and muscle cells, causing irreversible depolarization of cell membranes [ 6 ]. (biology-online.org)
  • It was about 10 times less potent than the cardiotoxins. (strath.ac.uk)
  • I would not recommend using oleander extracts without good safety data, because oleander leaves contain several potent cardiotoxins. (sunjournal.com)
  • The second venom category comprises so-called cardiotoxins, which are actually generalized cell-membrane poisons that produce irreversible cell depolarization. (medscape.com)
  • The lab is also identifying some of the mechanisms regulating muscle repair following cardiotoxin-induced injury. (pugetsound.edu)
  • I've only been able to find one paper so far using cardiotoxin to injure myoblasts in culture (they used it on C2C12 myotubes). (protocol-online.org)
  • The hypervariable segments encoded by the second and third exon of cardiotoxin genes are located at or near the tips of loop structure of cardiotoxin molecules. (antibody-antibodies.com)
  • These results, together with the suggestions that the residues at the tips of cardiotoxins' loop structure were involved in the manifestation of the biological activities of cardiotoxins, reflect that the preferential mutations may contribute to alterations in the function of cardiotoxin molecules. (antibody-antibodies.com)
  • Emetine is a cardiotoxin and has been associated with serious cardiotoxicity. (drugs.com)
  • Hider RC, Khader F. Biochemical and pharmacological properties of cardiotoxins isolated from cobra venom. (springer.com)
  • Amino acid sequences of the cardiotoxins were determined by Edman degradation and carboxypeptidase digestion. (antibody-antibodies.com)
  • Neurotoxins cause damage to the nervous system, such as parts of the brain controlling motor functions, while cardiotoxins attack the heart. (biology-online.org)
  • Using muscle-specific gain- and loss-of-function models for PGC-1α in combination with the myotoxic agent cardiotoxin (CTX), we explored the role of this transcriptional coactivator in muscle damage and inflammation. (biomedcentral.com)
  • Anthracyclines such as Adriamycin are considered type 1 cardiotoxins that can cause permanent damage to the heart and is felt to be dose related. (medpagetoday.com)
  • Since the pairings of splice sites and gene architecture were supposed to be associated with intron-exon recognition, it is likely that the preferred loci of mutations occurring with the evolution of cardiotoxin genes would not affect the processing of cardiotoxin precursors. (antibody-antibodies.com)
  • Two distinct types of cardiotoxin as revealed by the structure and activity relationship of their interaction with zwitterionic phospholipid dispersions. (springer.com)
  • Interaction of cardiotoxins with membranes: a molecular modeling study. (springer.com)
  • and the interaction of cardiotoxin with phospholipid vesicles. (thermofisher.com)
  • These cardiotoxins are responsible for more fatal dysrhythmias annually than any other class of medications. (calpoison.org)
  • Lee SC, Guan HH, Wang CH. Structural basis of citrate-dependent and heparin sulfate-mediated cell surface retention of cobra cardiotoxin A3. (springer.com)
  • Ainsi, la compréhension de leur mode d'action à l'échelle moléculaire représente une étape essentielle à l'identification de sondes biologiques du fonctionnement et du développement des organismes, en plus de faciliter la mise au point de dérivés potentiellement utiles comme outils pharmacologiques ou agents thérapeutiques. (inrs.ca)
  • Cardiotoxins: Functional Role of Local Conformational Changes. (ibch.ru)
  • Our alternative/pediatric oncologist ordered a Troponin I level because of the cardiotoxin doxyrubicin. (cancer.org)