Cobra Cardiotoxin Proteins: 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.Elapidae: 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)Cobra Venoms: 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.Elapid Venoms: 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.Cardiotoxins: 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.Amino Acid Sequence: 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.Protein Structure, Secondary: 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.Molecular Sequence Data: 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.Protein Conformation: 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).

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)

 (+info)

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)

*Jameson's mamba

Its other components include cardiotoxins, and fasciculins. Its venom may also have hemotoxic and myotoxic components to it. ...

*List of dangerous snakes

... and cardiotoxins. Two forms of "cytotoxin II" (cardiotoxin) were found in the venom of this species. The crude venom of this ... Its venom consists mainly of postsynaptic neurotoxins and cardiotoxins. Four cardiotoxin-analogues I, II, III, and IV, account ... The venom of this species also contains myotoxins and cardiotoxins. The median lethal dose (LD50) is 0.28-0.33 mg per gram of ... Research has shown its venom is purely a neurotoxin, with no apparent necrotizing components and no cardiotoxins. These snakes ...

*Eastern green mamba

The venom consists of both neurotoxins and cardiotoxins. The toxicity of individual specimens can vary greatly based on several ... The venom consists of both pre-synaptic and postsynaptic neurotoxins (dendrotoxins), cardiotoxins, calcicludine, and ...

*Equatorial spitting cobra

The venom may also consist of cardiotoxins and cytotoxins. The venom of the Equatorial spitting cobra exhibited the common ... Cardiotoxins represented 40% of the snakes venom protein. This species presented an IV LD50 of 0.50 µg/g mouse. http://www. ...

*Mamba

Their venoms consist mostly of neurotoxins (known as dendrotoxins). Besides the neurotoxins, they also carry cardiotoxins and ...

*Chinese cobra

Its venom consists mainly of postsynaptic neurotoxins and cardiotoxins. Four cardiotoxin-analogues I, II, III, and IV, account ... Using I-labelled cobra venom (Naja atra), 1 μg/g mice, its isolated I-neurotoxin (0.2 μg/g) or cardiotoxin (4 μg/g), it has ... the neurotoxin was more rapidly absorbed than either crude venom or cardiotoxin. Although this is not a spitting cobra, some ... Cardiotoxin-analogue III and phospholipase A2" (PDF). Journal of Biological Chemistry. 256 (17): 9279-9282. PMID 7263715. ...

*Three-finger toxin

These cardiotoxins also often have generalized cytotoxic effects and are sometimes known as cytolysins. The protein targets in ... The cardiotoxin/cytolysin 3FTx subgroup has a somewhat different set of functionally significant residues due to its distinct ... Others, including the second-largest 3FTx subgroup, are cardiotoxins. Many of the most well-characterized 3FTx proteins exert ... Another class, called the beta-cardiotoxins, causes decreased heart rate and are thought to function as beta blockers, ...

*Monocled cobra

Fletcher, J. E.; Jiang, M.-S.; Gong, Q.-H.; Yudkowsky, M. L.; Wieland, S. J. (1991). "Effects of a cardiotoxin from Naja naja ... The venom of this species also contains myotoxins and cardiotoxins. In case of intravenous injection the LD50 tested in mice is ...

*Harlequin poison frog

O. histrionica, along with O. speciosa, produces cardiotoxins known as histrionicotoxins. These moderate to highly toxic ...

*Cardiotoxicity

Cardiotoxins are the second most toxic venom while neurotoxins are the first". Circulation. 121 (5): 675-83. doi:10.1161/ ...

*KCNIP1

"Evidence showing an intermolecular interaction between KChIP proteins and Taiwan cobra cardiotoxins". Biochem. Biophys. Res. ...

*Javan spitting cobra

However, the main components of its venom are cardiotoxins with cytotoxic activity. In fact, polypeptide cardiotoxins make up ... Ma, D; Armugam A; Jeyaseelan K. (15 August 2002). "Cytotoxic potency of cardiotoxin from Naja sputatrix: development of a new ... postsynaptic neurotoxins and polypeptide cardiotoxins, meaning although the venom may be potent, it may not be particularly ...

*KCNIP2

"Evidence showing an intermolecular interaction between KChIP proteins and Taiwan cobra cardiotoxins". Biochemical and ...

*KCNIP4

"Evidence showing an intermolecular interaction between KChIP proteins and Taiwan cobra cardiotoxins". Biochem. Biophys. Res. ...

*Indian cobra

The Indian cobra's venom mainly contains a powerful post-synaptic neurotoxin and cardiotoxin. The venom acts on the synaptic ... ISBN 81-901873-0-9. Achyuthan, K. E.; Ramachandran, L. K. (1981). "Cardiotoxin of the Indian cobra (Naja naja) is a ...

*Three-finger protein

Another large subfamily of 3FTx proteins is the cardiotoxins (also known as cytotoxins or cytolysins); this group is directly ...

*Western green mamba

The venom consists mainly of both pre-synaptic and post-synaptic neurotoxins, cardiotoxins, and fasciculins. The toxicity of ... Its venom is a highly potent mixture of rapid-acting presynaptic and postsynaptic neurotoxins (dendrotoxins), cardiotoxins and ...

*Caspian cobra

S. (1999). "Two forms of cytotoxin II (cardiotoxin) from Naja naja oxiana in aqueous solution. Spatial structures with tightly ...

*Philippine cobra

Research has shown its venom is purely a neurotoxin, with no apparent necrotizing components and no cardiotoxins. These snakes ...

*Snake venom

Snake example: Okinawan habu (Trimeresurus flavoviridis) Cardiotoxins: Cardiotoxins are components that are specifically toxic ... Polypeptide toxins (molecular weight 5-10 KDa) include cytotoxins, cardiotoxins, and postsynaptic neurotoxins (such as α- ...

*Spotlight Innovation

The company also licensed a cardiotoxin therapy for acute and chronic nephropathy in 2015. In January, 2015, Celtic Biotech ...

*Black-necked spitting cobra

Fryklund, Linda; Eaker, David (July 1975). "Complete covalent structure of a cardiotoxin from the venom of Naja nigricollis ( ... and cardiotoxins. Bite symptoms include severe external hemorrhaging and tissue necrosis around the bite area and difficulty ...

*Black mamba

The black mamba's venom is composed of neurotoxins (dendrotoxin) and cardiotoxins as well as other toxins such as fasciculins. ...

*Elapidae

Their venom is mainly neurotoxic, although many of them also possess several other types of toxins, including cardiotoxins and ...

*King cobra

Rajagopalan, N.; Pung, Y.F.; Zhu, Y.Z.; Wong, P.T.H.; Kumar, P.P.; Kini, R.M. (2007). "β-Cardiotoxin: A new three-finger toxin ...

*Osteopontin

"Expression profiling of cytokines and related genes in regenerating skeletal muscle after cardiotoxin injection: a role for ...
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 ...
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
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 ...
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 ...
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 ...
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 ...
2016 Annual Meeting: Extracellular Matrix Impregnated with Adipose Derived Stem Cells in Skeletal Muscle Regeneration following Volumetric Muscle Loss in a Murine Model
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 ...
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
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 ...
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 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
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.
Background: Doxorubicin (DOX), a widely used anticancer drug, has been associated with cardiotoxicity. Recently, DOX-induced cardiotoxicity has been attributed to topoisomerase II (TOPII)-β expression and activity. In our study, we investigated the effect of inhibiting TOPII in attenuating the DOX induced cardiotoxicity. Method: H9c2 cardiomyoblasts were treated with 1 or 2 µM DOX (+/-) 1 µM ETO. Cardiotoxicity was assessed by examining cell viability using the MTT assay, hypertrophy of crystal violet stained cardiomyoblasts and ROS production. Results: DOX induced a dose dependent increase in cardiotoxicity as indicated by the significant reduction in cell viability (71.77 ± 9.25% 2 µM DOX vs. 100% control, P,0.05), ROS production and hypertrophy. Stimulation of H9c2 cardiomyoblasts with both 2 µM DOX and 1µM ETO did not show a significant difference in cell viability, ROS production or hypertrophy. Conclusion: DOX induced cardiotoxicity in H9c2 cardiomyoblasts was not exacerbated in the ...
c-MET Regulates Myoblast Motility and Myocyte Fusion during Adult Skeletal Muscle Regeneration. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Results Doxorubicin decreased calpain activities in cultured neonatal mouse cardiomyocytes and in vivomouse hearts, which correlated with down-regulation of calpain-1 and calpain-2 proteins. Over-expression of calpastatin or treatment with pharmacological calpain inhibitors aggravated apoptosis in neonatal and adult cardiomyocytes caused by doxorubicin. On the while, over-expression of calpain-2 but not calpain-1 decreased doxorubicin-induced apoptosis in cardiomyocytes. The pro-apoptotic effects of calpain inhibition were concerned with down-regulation of AKT protein and mRNA expression, and a concomitant reduction in GSK-3 beta phosphorylation (Ser9) in doxorubicin-treated cardiomyocytes. Inhibiting AKT further increased doxorubicin-induced cardiac injuries, suggesting the effects of calpain inhibition may be mediated through inactivating the AKT signalling. In an in vivomodel of doxorubicin-induced cardiotoxicity, overexpression of calpastatin aggravated myocardial dysfunction in transgenic ...
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 ...
Patients over the age of 60 years with classical Hodgkin lymphoma (cHL) often experience treatment-related toxicities with standard frontline chemotherapy or multiagent regimens, said Christopher A. Yasenchak, MD, who added that a novel combination with brentuximab vedotin (Adcetris) and nivolumab (Opdivo) could provide a more tolerable option for this population.
Food and Drug Administration has expanded the indication for brentuximab vedotin - in combination with chemotherapy - to certain types of peripheral T-cell lymp
Brentuximab vedotin is a type of targeted therapy used in the treatment of Hodgkin lymphoma and systemic anaplastic large cell lymphoma.
Evidence-based recommendations on brentuximab vedotin (Adcetris) for treating relapsed or refractory CD30‑positive Hodgkin lymphoma in adults
Bupivacaine-induced myocardial depression and pulmonary edema: a case report.: Central nervous system and cardiovascular toxicity are well-known side effects of
When DArcy Wentworth Thompsons On Growth and Form was published 100 years ago, it raised the question of how biological forms arise during development and across evolution. In light of the advances in molecular and cellular biology since then, a succinct modern view of the question states: how do genes encode geometry? Our new special issue is packed with articles that use mathematical and physical approaches to gain insights into cell and tissue patterning, morphogenesis and dynamics, and that provide a physical framework to capture these processes operating across scales.. Read the Editorial by guest editors Thomas Lecuit and L. Mahadevan, as they provide a perspective on the influence of DArcy Thompsons work and an overview of the articles in this issue.. ...
For patients who complete 16 cycles of brentuximab vedotin, re-initiation of brentuximab vedotin may be permitted at the joint discretion of the sponsor and investigator. For patients who complete 48 weeks of reference theraphy, initiation of subsequent standard-of-care theraphy should be discussed with the study doctor ...
Results: Median time to relapse after ASCT was 6.7 mos (range, 0-131). Pts received a median 9 cycles of Brentuximab Vedotin. The ORR was 75% (76/102 pts), with complete remissions (CRs) in 34 pts (33%). At time of analysis (July 2012), the median time from first dose was 29.5 mos (range, 1.8-36.9). 60/102 pts (59%) were alive at the time of last follow up and median overall survival (OS) has not been reached. The estimated 24-mo OS was 65% (95% CI: 55, 74). The median OS by best clinical response was 31.6 mos for pts with partial remission (PR, n=42), 20.6 mos for pts with stable disease (SD, n=22), and 10.2 mos for pts with progressive disease (PD, n=3); median OS for pts with CR (n=34) has not been reached. Evaluation of demographic and baseline characteristics found that pts with a baseline ECOG score of 0 were the only subgroup with a significantly more favorable OS following Brentuximab Vedotin treatment (24-mo OS: 81% vs. 47% for ECOG scores of 0 vs 1, respectively). There was no ...
PMID- 29303722 OWN - NLM STAT- MEDLINE DCOM- 20180110 LR - 20180111 IS - 1474-547X (Electronic) IS - 0140-6736 (Linking) VI - 390 IP - 10114 DP - 2018 Dec 23 TI - Concerns about cardiotoxicity in the HERA trial - Authors reply. PG - 2767-2768 LID - S0140-6736(17)31940-2 [pii] LID - 10.1016/S0140-6736(17)31940-2 [doi] FAU - Cameron, David A AU - Cameron DA AD - Edinburgh Cancer Centre, Western General Hospital, Edinburgh EH4 2XU, UK. Electronic address: [email protected] FAU - Gelber, Richard D AU - Gelber RD AD - Edinburgh Cancer Centre, Western General Hospital, Edinburgh EH4 2XU, UK. FAU - Procter, Marion AU - Procter M AD - Edinburgh Cancer Centre, Western General Hospital, Edinburgh EH4 2XU, UK. FAU - Suter, Thomas AU - Suter T AD - Edinburgh Cancer Centre, Western General Hospital, Edinburgh EH4 2XU, UK. LA - eng PT - Letter PT - Comment PL - England TA - Lancet JT - Lancet (London, England) JID - 2985213R RN - 0 (Antineoplastic Agents) RN - P188ANX8CK (Trastuzumab) SB - AIM SB - IM CON - ...
Sigma-Aldrich offers abstracts and full-text articles by [Rongrong Li, He Ma, Xiaojin Zhang, Chuanfu Li, Jingwei Xiong, Ting Lu, Yu Mao, Juncheng Dai, Li Liu, Zhengnian Ding].
Introduction With an ageing population, the incidence of cancer is rising.1 This, coupled with the development of newer and more effective cancer treatments, has led to an increasing number of cancer survivors. Unfortunately, many of these treatments can be cardiotoxic, and prevention, early detection, long-term m ...
TY - JOUR. T1 - Cost-effectiveness of strain-targeted cardioprotection for prevention of chemotherapy-induced cardiotoxicity. AU - Nolan, Mark T.. AU - Plana, Juan Carlos. AU - Thavendiranathan, Paaladinesh. AU - Shaw, Leslee. AU - Si, Lei. AU - Marwick, Thomas H.. PY - 2016/6/1. Y1 - 2016/6/1. N2 - Background: Cancer chemotherapy increases the risk of heart failure. This cost-effectiveness model compared strain-guided cardioprotection with other protective strategies using a health care payer perspective and five-year time horizon. Methods: Three cardioprotection strategies were assessed: 1) usual care (EF-guided cardioprotection, EFGCP) with cardioprotection initiated on diagnosis of LVEF-defined cardiotoxicity (EF-CTX), 2) universal cardioprotection (UCP) for all such patients, and 3) strain-guided cardioprotection (SGCP - treatment of patients with subclinical cardiotoxicity [S-CTX]). A Markov model, informed by the published literature on transitional probabilities, costs and ...
Takeda Receives European Commission Approval of ADCETRIS® (brentuximab vedotin) for Consolidation Treatment in Post-Transplant Hodgkin Lymphoma
The wide spectrum of anthracycline activity as well as the unique cumulative dose related cardiac toxicity pose a significant clinical challenge. These drugs, particularly doxorubicin (AdriamycinR),...
Daunorubicin (DNR) and doxorubicin (DOX) are two of the most effective anthracycline drugs known for the treatment of systemic neoplasms and solid tumors. However, their clinical use is hampered due to profound cardiotoxicity ...
Radcliffe Cardiology article authored by Michele Russo covering topics - Anticancer drugs-induced cardiotoxicity, heart failure, anthracyclines & on other cardiology field
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In some countries, you might find that the Women on Web website is censored. Here you can read about several ways you… Read more » ...
In some countries, you might find that the Women on Web website is censored. Here you can read about several ways you… Lees meer » ...
2015 Elsevier Inc. High-dose chemotherapy regimens using cyclophosphamide (CY) are frequently associated with cardiotoxicity that could lead to myocyte damage and congestive heart failure. However, the mechanisms regulating the cardiotoxic effects of CY remain unclear. Because CY is converted to an unsaturated aldehyde acrolein, a toxic, reactive CY metabolite that induces extensive protein modification and myocardial injury, we examined the role of glutathione S-transferase P (GSTP), an acrolein-metabolizing enzyme, in CY cardiotoxicity in wild-type (WT) and GSTP-null mice. Treatment with CY (100-300. mg/kg) increased plasma levels of creatine kinase-MB isoform (CK·MB) and heart-to-body weight ratio to a significantly greater extent in GSTP-null than WT mice. In addition to modest yet significant echocardiographic changes following acute CY-treatment, GSTP insufficiency was associated with greater phosphorylation of c-Jun and p38 as well as greater accumulation of albumin and protein-acrolein ...
Side effects on cardiac ion channels causing lethal arrhythmias are one major reason for drug withdrawals from the market. Field potential (FP) recording from cardiomyocytes, is a well-suited tool to assess such cardiotoxic effects of drug candidates in preclinical drug development, but it is currently limited to the spontaneous beating of the cardiomyocytes and manual analysis. Herein, we present a novel optogenetic cardiotoxicity screening system suited for the parallel automated frequency-dependent analysis of drug effects on FP recorded from human-induced pluripotent stem cell-derived cardiomyocytes. For the expression of the light-sensitive cation channel Channelrhodopsin-2, we optimised protocols using virus transduction or transient mRNA transfection. Optical stimulation was performed with a new light-emitting diode lid for a 96-well FP recording system. This enabled reliable pacing at physiologically relevant heart rates and robust recording of FP. Thereby we detected rate-dependent effects of
Side effects on cardiac ion channels causing lethal arrhythmias are one major reason for drug withdrawals from the market. Field potential (FP) recording from cardiomyocytes, is a well-suited tool to assess such cardiotoxic effects of drug candidates in preclinical drug development, but it is currently limited to the spontaneous beating of the cardiomyocytes and manual analysis. Herein, we present a novel optogenetic cardiotoxicity screening system suited for the parallel automated frequency-dependent analysis of drug effects on FP recorded from human-induced pluripotent stem cell-derived cardiomyocytes. For the expression of the light-sensitive cation channel Channelrhodopsin-2, we optimised protocols using virus transduction or transient mRNA transfection. Optical stimulation was performed with a new light-emitting diode lid for a 96-well FP recording system. This enabled reliable pacing at physiologically relevant heart rates and robust recording of FP. Thereby we detected rate-dependent effects of
Project researcher: Dr Ilsa Haeusler, Academic Foundation Doctor Ilsas main project during the AFP was to undertake a systematic literature review to investigate the effects of antimalarial drugs on cardiac adverse events. She wanted to determine whether antimalarial drugs, particularly quinoline antimalarials, caused cardiovascular side effects such as prolongation of the QT interval on the electrocardiogram. The project allowed her to learn the fundamentals of systematic reviewing, particularly in terms of literature search, reference acquisition, database design and analysis. The review was large with many variables having been extracted, so dealing with the volume of data was a key learning point. This was a fantastic opportunity to learn about standardised ways of carrying out a systematic review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The question of cardiotoxic effects of antimalarial drugs is very relevant to clinical practice on ...
Singulex will be featuring a highly sensitive Cardiac Troponin I (cTnI) immunoassay kit for preclinical toxicity and safety assessment at the Society of Toxicology meeting in San Francisco CA. Cardiotoxicity alerts and recent drug recalls have generated concerns for regulatory agencies and pharmaceutical companies. As a result there is an increased pressure to implement more sensitive detection methods that allow for early and robust cardiotoxicity assessment during drug development.
This poster describes the use of the new EarlyTox™ Cardiotoxicity Kit for improved assay performance with iPSC-derived cardiomyocytes. The dye has minimal non-specific toxicity, provides a larger signal window, and is more suitable for longer term studies than other dyes. Characterization was done with a FLIPR® Tetra System and data generated on the SpectraMax® i3 Multi-Mode Microplate Platform.
Anthracycline chemotherapeutic agents are commonly employed in thetreatment of lymphoma; however, their efficacy in combating themalignancy comes at a cost-they are cardiotoxic and are known to causecardioditis and cardiomyopathy. A study presented at the recentRadiological Society of North America annual scientific conferencesought to determine a relation between myocardial FDG metabolism withFDG PET/CT scanning and the use of anthracycline chemotherapeuticagents.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Whilst receiving mitoxantrone the chances of you getting an infection are increased. If you begin to have any symptoms of infection, such as fever, chills, sore throat, cough, pain with urinating, or urinating more often, please call your GP or neurology team. MSers who are treated with mitoxantrone are known to be at increased risk of developing a specific type of leukaemia in the future; this an uncommon complication, occurring in approximately 1 in 200-400 subjects with MS who are treated with Mitoxantrone. Clearly female MSers who are pregnant, are trying to become pregnant, or are breastfeeding should not be treated with mitoxantrone because it may harm the baby. You should use birth control while taking mitoxantrone to avoid becoming pregnant. We may have to adjust the dose of mitoxantrone depending on your blood counts. As mitoxantrone is potentially cardiotoxic, or can damage the heart. you will need to have regular testing of your heart and blood to help avoid this serious side effects. ...
In the current issue of ONCOLOGY, Hershman and Shao provide a comprehensive review of anthracycline-induced cardiotoxicity (AIC). Risk factors for AIC include age (??18 or ??65 years) at time of treatment, increasing cumulative dose or dose intensity of anthracyclines, mediastinal radiation therapy (RT), and female gender.[1-4] The Surveillance, Epidemiology and End Results (SEER)-Medicare database showed […]. ...
Dr. Gorin lectures frequently on genetics, cell and molecular biology, and the peripheral nervous system. He has authored many publications on neurological topics, and also serves as a journal scientific reviewer and neuromuscular evaluation consultant.. Dr. Gorins research interests focus on nerve and skeletal muscle regeneration and rheumatoid arthritis. He has patents pending for two cancer drugs.. ...
Thermoforming machine - TVP 64 / TVP 67. Automatic vacuum and pressure high performance thermoforming machine with separate stations for thermoforming, stamping and vertical stacking of the final product in a conveyor belt.
Request to participate using Be Involved at Wake Forest Baptist Medical Center for: Testing Brentuximab Vedotin at a treatment for Hodgkins Disease in children
We hope to determine the importance of different genes (including B receptors) in anthracycline-induced cardiomyopathy. This has important benefits to p
Our study is the largest prospective placebo controlled study of the cardiac effects of VEGFR-TKIs and the first in a non-cancer-bearing population. As such, our population presents a unique opportunity to study patients naïve to the effects of prior cardiotoxic regimens and with a relatively low baseline prevalence of CV disease. We found the incidence of significant LVEF decline occurring in the first 6 months of treatment in patients treated with sunitinib or sorafenib to be low. In sensitivity analyses using alternative definitions of cardiac dysfunction, this remained low, with only very modest differences when we considered person-years in our analyses. The number of late declines in LVEF was also not statistically different among the three groups.. It is critical to note that in E2805, patients were carefully screened and those with baseline CV comorbidities were excluded from study participation. As such, these patients may have a lower prevalence of CV disease compared to metastatic ...
BioAssay record AID 735493 submitted by ChEMBL: Activation of SIRT1 in human MCF7 cells assessed as reduction in doxorubicin-induced acetyl-p53 level up to 100 uM after 6 hrs by Western blotting analysis.
The cardiotoxicity sometimes seen with doxorubicin may be caused by the effects of chemotherapy on the enzyme topoisomerase-IIβ.
マウス・モノクローナル抗体 ab76746 交差種: Hu 適用: WB,IHC-P,Flow Cyt,ICC/IF…Myoferlin抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
Purpose: The antibody-drug conjugate (ADC) brentuximab vedotin comprises a CD30-directed antibody covalently attached to the potent antimicrotubule agent monomethyl auristatin E (MMAE) via a protease-cleavable linker. This study explored the safety, maximum tolerated dose (MTD), and activity of weekly dosing of brentuximab vedotin in patients with relapsed or refractory CD30-positive hematologic malignancies. Experimental Design: In this phase 1 dose-escalation study, brentuximab vedotin was administered intravenously on Days 1, 8, and 15, of each 28-day cycle at doses ranging from 0.4 to 1.4 mg/kg. Forty-four patients were enrolled: 38 with Hodgkin lymphoma, 5 with systemic anaplastic large cell lymphoma, and 1 with peripheral T-cell lymphoma - not otherwise specified. Doses were escalated in increments of 0.2 mg/kg until dose-limiting toxicity (DLT) was observed. Patients were monitored for anti-therapeutic antibodies and pharmacokinetic parameters. Antitumor assessments were performed every 2 ...
Nitric oxide is produced in cardiac microvascular endothelial cells and cardiomyocytes from either constitutive or inducible nitric oxide synthase (NOS), which catalyses the conversion of L-arginine to L-citrulline. Cardiomyocytes principally express endothelial NOS, localized near invaginations of the plasmalemma termed caveolae, and neuronal NOS, localized on the sarcoplasmic reticulum (61). A third isoform, the inducible nitric oxide synthase (iNOS), may be expressed upon stimulation with inflammatory mediators. While NO synthesized by neuronal NOS and endothelial NOS has cardioprotective effects through improvement of perfusion and inhibition of apoptosis, NO derived from iNOS has a cardiotoxic effect through the suppression of muscle wall contractility and induction of apoptosis (62). Nitric oxide is released in a pulsatile manner from the beating heart. Changes in ventricular filling induce parallel increases or decreases in cardiac NO synthesis, which, in turn, modulate the function of ...
In cardiac amyloidosis, myocardial tissue histology reveals among its salient features, the expansion of the extracellular space, the accumulation of amyloid protein, and collagen fiber deposition. At the cellular level, cytoplasmic vacuolization and decline of myofibrils are commonly seen in endomyocardial biopsies from amyloid patients. There is evidence that human amyloidogenic light (AL) chain proteins have a cardiotoxic effect (1), which is associated with impaired cardiomyocyte contractile function and increased cell death. Of similar relevance for transthyretin-related amyloidosis (ATTR) is the fact that transthyretin (TTR) also has a cytotoxic effect (2), causing increased inflammatory and oxidative stress. How well cardiac magnetic resonance (CMR) can identify various aspects of pathological tissue remodeling in cardiac amyloidosis remains a question of intense research interest.. Over the last decade, CMR has identified a series of promising image-based markers tied to cardiomyopathic ...
Title:The Role of Autophagy and Death Pathways in Dose-dependent Isoproterenolinduced Cardiotoxicity VOLUME: 25 ISSUE: 19. Author(s):Alexandra Gyongyosi, Rita Zilinyi, Andras Czegledi, Agnes Tosaki, Arpad Tosaki and Istvan Lekli*. Affiliation:Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Department of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Department of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen. Keywords:Isoproterenol, cardiotoxicity, necrosis, apoptosis, autophagy, β-adrenergic agonist.. Abstract:. Background: Isoproterenol (ISO) is a non-selective β-adrenergic agonist. Our aims were to investigate the autophagy and cell death pathways including apoptosis ...
Seattle Genetics, Inc. (Nasdaq: SGEN) announced today that it has submitted a supplemental Biologics License Application (BLA) to the U.S. Food and Dr
Cobra venom contains cardiotoxins (CTXs) that induce tissue necrosis and systolic heart arrest in bitten victims. CTX-induced membrane pore formation is one of the major mechanisms responsible for...
A 61-year-old man with 5-fluorouracil (5-FU) chemotherapy suffered a cardiopulmonary arrest (CPA). The electrocardiogram showed changes consistent with myocardial infarct..
Potentials of brentuximab vedotin in the treatment of relapse/refractory cutaneous T-cell lymphomas: literature review and authors observation
Perceived resource constraints within the Canadian health care system might threaten adoption of pharmacogenomic testing. We therefore propose prioritizing serious ADRs where delays in access to tests put patients at risk of devastating consequences that also represent substantial cost burdens on the health care system. Pharmacogenomic testing for serious ADRs also holds the most promise for cost effectiveness. We have shown that cost savings associated with the prevention of one such ADR, anthracycline-induced cardiotoxicity, are predicted to outweigh the costs of testing.20 Specifically, severe cases of anthracycline-induced cardiotoxicity cost more than $1 million owing to the need for heart transplants,20 and incorporation of pharmacogenomic testing is estimated to save $495 per patient, representing a 5.7% reduction in costs associated with anthracycline-based cancer treatment.20. Several parameters must be optimized to improve access for our proposed approach to pharmacogenomic testing, ...
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The Research Group on Cell Biology is led by Dra. Pura Muñoz-Cánoves. The group focuses on the molecular mechanisms underlying adult muscle regeneration and growth. They work with mouse muscle stem cells (satellite cells) and isolated cultured myofibers with associated satellite cells, as the best physiological muscle models ex vivo. They use in vivo models for skeletal muscle regeneration and atrophy/hypertrophy in genetically modified mice (Cre-LoxP system) and models of human muscle diseases (DMD), and electroporation techniques to modulating gene expression in mouse muscle at wish.. The main research lines are:. ...

Role of Heparan Sulfates and Glycosphingolipids in the Pore Formation of Basic Polypeptides of Cobra Cardiotoxin | SpringerLinkRole of Heparan Sulfates and Glycosphingolipids in the Pore Formation of Basic Polypeptides of Cobra Cardiotoxin | SpringerLink

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 ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4419-6327-7_12

Cardiotoxins | CTDCardiotoxins | CTD

Induction of LONG QT SYNDROME or TORSADES DE POINTES has been the reason for viewing some drugs as cardiotoxins.. ...
more infohttp://ctdbase.org/detail.go?type=chem&acc=D054715

GENTAUR antibody-antibodies.com The Marketplace for Antibodies : The multiplicity of cardiotoxins from Naja naja atra (Taiwan...GENTAUR antibody-antibodies.com The Marketplace for Antibodies : The multiplicity of cardiotoxins from Naja naja atra (Taiwan...

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 ...
more infohttp://www.antibody-antibodies.com/pubmed-PubMed:10708798-PubMedArticl.html

Plus itPlus it

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 ...
more infohttp://ajpcell.physiology.org/content/298/5/C1087

Biology-Online • View topic - What is the most poisonous snake in da world?Biology-Online • View topic - What is the most poisonous snake in da world?

And also their venom contains neurotoxins and cardiotoxins. Neurotoxins cause damage to the nervous system, such as parts of ... the brain controlling motor functions, while cardiotoxins attack the heart. The roots of education is bitter, but the fruit is ...
more infohttp://www.biology-online.org/biology-forum/about1419.html?hilit=Pungent

couuntries without snakes | Python Junglecouuntries without snakes | Python Jungle

Its venom mainly consists of neuro and cardiotoxins. This means a bite can lead to paralysis of the muscles or even cardiac ... Its venom contains postsynaptic neurotoxins, cardiotoxins, and cytotoxic activity. The Mali cobra is responsible for the most ...
more infohttp://pythonjungle.com/tag/couuntries-without-snakes/

the worlds deadliest snake | Python Junglethe worlds deadliest snake | Python Jungle

Its venom mainly consists of neuro and cardiotoxins. This means a bite can lead to paralysis of the muscles or even cardiac ... Its venom contains postsynaptic neurotoxins, cardiotoxins, and cytotoxic activity. The Mali cobra is responsible for the most ...
more infohttp://pythonjungle.com/tag/the-worlds-deadliest-snake/

Elapidae - WikipediaElapidae - Wikipedia

Their venom is mainly neurotoxic, although many of them also possess several other types of toxins, including cardiotoxins and ...
more infohttps://en.m.wikipedia.org/wiki/Elapid

Cardiotoxin III - WikipediaCardiotoxin III - Wikipedia

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" ...
more infohttps://en.wikipedia.org/wiki/Cardiotoxin_III

A common cytolytic region in myotoxins, hemolysins, cardiotoxins and antibacterial peptides.  - PubMed - NCBIA common cytolytic region in myotoxins, hemolysins, cardiotoxins and antibacterial peptides. - PubMed - NCBI

A common cytolytic region in myotoxins, hemolysins, cardiotoxins and antibacterial peptides.. Kini RM1, Evans HJ. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/2599766?dopt=Abstract

Cardiotoxin on myoblasts: post #1Cardiotoxin on myoblasts: post #1

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 ...
more infohttp://www.protocol-online.org/forums/topic/27199-cardiotoxin-on-myoblasts/

Ameliorating Adriamycin-Induced Chronic Kidney Disease in Rats by Orally Administrated Cardiotoxin from Naja naja atra VenomAmeliorating Adriamycin-Induced Chronic Kidney Disease in Rats by Orally Administrated Cardiotoxin from Naja naja atra Venom

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 ...
more infohttps://www.hindawi.com/journals/ecam/2014/621756/ref/

Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early...Antioxidants: Promising neuroprotection against cardiotoxin-4b-induced cell death which triggers oxidative stress with early...

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 ...
more infohttps://scholarbank.nus.edu.sg/handle/10635/28804

Quarterly Equine Disease Author Bio | The Horse | TheHorse.comQuarterly Equine Disease Author Bio | The Horse | TheHorse.com

Cardiotoxins in Horses May 28, 2017. Learn about several substances that can cause heart muscle damage and death in horses. ...
more infohttp://www.thehorse.com/authors/221/equine-disease-quarterly

Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration | Journal of Pharmacology and Experimental...Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration | Journal of Pharmacology and Experimental...

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 ...
more infohttp://jpet.aspetjournals.org/content/349/2/355.full

Progressive myopathy and defects in the maintenance of myotendinous junctions in mice that lack talin 1 in skeletal muscle |...Progressive myopathy and defects in the maintenance of myotendinous junctions in mice that lack talin 1 in skeletal muscle |...

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 ...
more infohttp://dev.biologists.org/content/135/11/2043

An absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration | DevelopmentAn absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration | Development

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) ...
more infohttp://dev.biologists.org/content/138/17/3639?ijkey=4345ab60aea7ea2f2cb1c8a9ca732a2c780c67dd&keytype2=tf_ipsecsha

Stem cell-mediated muscle regeneration is enhanced by local isoform of insulin-like growth factor 1 | PNASStem cell-mediated muscle regeneration is enhanced by local isoform of insulin-like growth factor 1 | PNAS

After 15 days of irradiation, the tibialis anterior (TA) muscle was injected with cardiotoxin (CTX), and muscles were harvested ...
more infohttp://www.pnas.org/content/101/5/1206

JAK1-STAT1-STAT3, a key pathway promoting proliferation and preventing premature differentiation of myoblasts | JCBJAK1-STAT1-STAT3, a key pathway promoting proliferation and preventing premature differentiation of myoblasts | JCB

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 ...
more infohttp://jcb.rupress.org/content/179/1/129.long

Patent US6153421 - Cloned genomes of infectious hepatitis C viruses and uses thereof - Google PatentsPatent US6153421 - Cloned genomes of infectious hepatitis C viruses and uses thereof - Google Patents

Cardiotoxin molecular toxicology modeling. US20070082332 *. Jan 8, 2003. Apr 12, 2007. Gene Logic, Inc.. Molecular ...
more infohttp://www.google.com/patents/US6153421?dq=5179747

Systolic DysfunctionSystolic Dysfunction

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.
more infohttp://www.fpnotebook.com/CV/CHF/SystlcDysfnctn.htm

Systolic DysfunctionSystolic Dysfunction

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.
more infohttps://fpnotebook.com/legacy/CV/CHF/SystlcDysfnctn.htm

Time-Dependent Block of Ultrarapid-Delayed Rectifier K+ Currents by Aconitine, a Potent Cardiotoxin, in Heart-Derived H9c2...Time-Dependent Block of Ultrarapid-Delayed Rectifier K+ Currents by Aconitine, a Potent Cardiotoxin, in Heart-Derived H9c2...

Aconitine (ACO), a highly toxic diterpenoid alkaloid, is recognized to have effects on cardiac voltage-gated Na+ channels. However, it remains unknown whether it has any effects on K+ currents. The effects of ACO on ion currents in differentiated clonal cardiac (H9c2) cells and in cultured neonatal rat ventricular myocytes were investigated in this study. In H9c2 cells, ACO suppressed ultrarapid-delayed rectifier K+ current (IKur) in a time- and concentration-dependent fashion. The IC50 value for ACO-induced inhibition of IKur was 1.4μM. ACO could accelerate the inactivation of IKur with no change in the activation time constant of this current. Steady-state inactivation curve of IKur during exposure to ACO could be demonstrated. Recovery from block by ACO was fitted by a single-exponential function. The inhibition of IKur by ACO could still be observed in H9c2 cells preincubated with ruthenium red (30μM). Intracellular dialysis with ACO (30μM) had no effects on IKur. IKur elicited by ...
more infohttp://oxfordindex.oup.com/view/10.1093/toxsci/kfn189

Protocols and Video Articles Authored by Silvia BrunelliProtocols and Video Articles Authored by Silvia Brunelli

Induction of Acute Skeletal Muscle Regeneration by Cardiotoxin Injection ... Induction of Acute Skeletal Muscle Regeneration by Cardiotoxin Injection. Ombretta Guardiola1, Gennaro Andolfi1, Mario Tirone2, ...
more infohttps://www.jove.com/author/Silvia_Brunelli
  • Their venom is mainly neurotoxic , although many of them also possess several other types of toxins , including cardiotoxins and cytotoxins . (wikipedia.org)
  • 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)
  • 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)
  • The second venom category comprises so-called cardiotoxins, which are actually generalized cell-membrane poisons that produce irreversible cell depolarization. (medscape.com)
  • 10 Mouse MSC-like cells converted to a myogenic phenotype after infusion and homing to cardiotoxin injured skeletal muscle. (ahajournals.org)
  • These cardiotoxins are responsible for more fatal dysrhythmias annually than any other class of medications. (calpoison.org)
  • 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)
  • Cardiotoxins: Functional Role of Local Conformational Changes. (ibch.ru)