Bepridil: A long-acting calcium-blocking agent with significant anti-anginal activity. The drug produces significant coronary vasodilation and modest peripheral effects. It has antihypertensive and selective anti-arrhythmia activities and acts as a calmodulin antagonist.Aprindine: A class Ib anti-arrhythmia agent used to manage ventricular and supraventricular arrhythmias.Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.PyrrolidinesCalcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cellular membranes.Troponin C: One of the three polypeptide chains that make up the TROPONIN complex of skeletal muscle. It is a calcium-binding protein.Troponin: One of the minor protein components of skeletal muscle. Its function is to serve as the calcium-binding component in the troponin-tropomyosin B-actin-myosin complex by conferring calcium sensitivity to the cross-linked actin and myosin filaments.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Troponin T: One of the three polypeptide chains that make up the TROPONIN complex. It is a cardiac-specific protein that binds to TROPOMYOSIN. It is released from damaged or injured heart muscle cells (MYOCYTES, CARDIAC). Defects in the gene encoding troponin T result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.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.Troponin I: One of the three polypeptide chains that make up the TROPONIN complex. It inhibits F-actin-myosin interactions.Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Angina, Stable: Persistent and reproducible chest discomfort usually precipitated by a physical exertion that dissipates upon cessation of such an activity. The symptoms are manifestations of MYOCARDIAL ISCHEMIA.Angina, Unstable: Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.Cardiovascular Diseases: Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Women's Health: The concept covering the physical and mental conditions of women.Women: Human females as cultural, psychological, sociological, political, and economic entities.Bumetanide: A sulfamyl diuretic.Physician-Patient Relations: The interactions between physician and patient.United States Food and Drug Administration: An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.Phytotherapy: Use of plants or herbs to treat diseases or to alleviate pain.Drugs, Chinese Herbal: Chinese herbal or plant extracts which are used as drugs to treat diseases or promote general well-being. The concept does not include synthesized compounds manufactured in China.United StatesUniversal Precautions: Prudent standard preventive measures to be taken by professional and other health personnel in contact with persons afflicted with a communicable disease, to avoid contracting the disease by contagion or infection. Precautions are especially applicable in the diagnosis and care of AIDS patients.Metolazone: A quinazoline-sulfonamide derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.Dizziness: An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness.Alcoholic Beverages: Drinkable liquids containing ETHANOL.Protective Devices: Devices designed to provide personal protection against injury to individuals exposed to hazards in industry, sports, aviation, or daily activities.Urine Specimen Collection: Methods or procedures used to obtain samples of URINE.Diagnostic Techniques and Procedures: Methods, procedures, and tests performed to diagnose disease, disordered function, or disability.Postural Orthostatic Tachycardia Syndrome: A syndrome of ORTHOSTATIC INTOLERANCE combined with excessive upright TACHYCARDIA, and usually without associated ORTHOSTATIC HYPOTENSION. All variants have in common an excessively reduced venous return to the heart (central HYPOVOLEMIA) while upright.Prescription Drug Misuse: Improper use of drugs or medications outside the intended purpose, scope, or guidelines for use. This is in contrast to MEDICATION ADHERENCE, and distinguished from DRUG ABUSE, which is a deliberate or willful action.Injections, Intramuscular: Forceful administration into a muscle of liquid medication, nutrient, or other fluid through a hollow needle piercing the muscle and any tissue covering it.Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.Anesthesia, Dental: A range of methods used to reduce pain and anxiety during dental procedures.Tranquilizing Agents: A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.Barbiturates: A class of chemicals derived from barbituric acid or thiobarbituric acid. Many of these are GABA MODULATORS used as HYPNOTICS AND SEDATIVES, as ANESTHETICS, or as ANTICONVULSANTS.Phenothiazines: Compounds containing dibenzo-1,4-thiazine. Some of them are neuroactive.Administration, Rectal: The insertion of drugs into the rectum, usually for confused or incompetent patients, like children, infants, and the very old or comatose.Suppositories: Medicated dosage forms that are designed to be inserted into the rectal, vaginal, or urethral orifice of the body for absorption. Generally, the active ingredients are packaged in dosage forms containing fatty bases such as cocoa butter, hydrogenated oil, or glycerogelatin that are solid at room temperature but melt or dissolve at body temperature.Administration, Oral: The giving of drugs, chemicals, or other substances by mouth.Muscle Cramp: A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)Thirst: A drive stemming from a physiological need for WATER.Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.Hypokalemia: Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)Glycyrrhiza: A genus of leguminous herbs or shrubs whose roots yield GLYCYRRHETINIC ACID and its derivative, CARBENOXOLONE.Laxatives: Agents that produce a soft formed stool, and relax and loosen the bowels, typically used over a protracted period, to relieve CONSTIPATION.Heat Stroke: A condition caused by the failure of body to dissipate heat in an excessively hot environment or during PHYSICAL EXERTION in a hot environment. Contrast to HEAT EXHAUSTION, the body temperature in heat stroke patient is dangerously high with red, hot skin accompanied by DELUSIONS; CONVULSIONS; or COMA. It can be a life-threatening emergency and is most common in infants and the elderly.Administration, Cutaneous: The application of suitable drug dosage forms to the skin for either local or systemic effects.Parasympatholytics: Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.Baths: The immersion or washing of the body or any of its parts in water or other medium for cleansing or medical treatment. It includes bathing for personal hygiene as well as for medical purposes with the addition of therapeutic agents, such as alkalines, antiseptics, oil, etc.

ESR study on the structure-antioxidant activity relationship of tea catechins and their epimers. (1/127)

The purpose of this study is to examine the relationship between the free radical scavenging activities and the chemical structures of tea catechins ((-)-epigallocatechin gallate (EGCG), (-)-epigallocatechin (EGC) and (-)-epicatechin (EC)) and their corresponding epimers ((-)-gallocatechin gallate (GCG), (-)-gallocatechin (GC) and (+)-catechin ((+)-C)). With electron spin resonance (ESR) we investigated their scavenging effects on superoxide anions (O-.2) generated in the irradiated riboflavin system, singlet oxygen(1O2) generated in the photoradiation-hemoporphyrin system, the free radicals generated from 2,2'-azobis(2-amidinopropane)hydrochloride (AAPH) and 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radical. The results showed that the scavenging effects of galloylated catechins (EGCG and GCG) on the four free radicals were stronger than those of nongalloylated catechins (EGC, GC, EC, (+)-C), and the scavenging effects of EGC and GC were stronger than those of EC and (+)-C. Thus, it is suggested that the presence of the gallate group at the 3 position plays the most important role in their free radical-scavenging abilities and an additional insertion of the hydroxyl group at the 5' position in the B ring also contributes to their scavenging activities. Moreover, the corresponding phenoxyl radicals formed after the reaction with O-.2 were trapped by DMPO and the ESR spectra of DMPO/phenoxyl radical adducts were observed (aN=15.6 G and aHbeta=21.5 G). No significant differences were found between the scavenging effects of the catechins and their epimers when their concentrations were high. However, significant differences were observed at relatively low concentrations, and the lower their concentrations, the higher the differences. The scavenging abilities of GCG, GC and (+)-C were stronger than those of their corresponding epimers (EGCG, EGC and EC). The differences between their sterical structures played a more important role in their abilities to scavenge large free radicals, such as the free radicals generated from AAPH and the DPPH radical, than to scavenge small free radicals, such as O-.2 and 1O2, especially in the case with EGCG and GCG with more bulky steric hindrance.  (+info)

Role of Ca2+ and cross-bridges in skeletal muscle thin filament activation probed with Ca2+ sensitizers. (2/127)

Thin filament regulation of contraction is thought to involve the binding of two activating ligands: Ca2+ and strongly bound cross-bridges. The specific cross-bridge states required to promote thin filament activation have not been identified. This study examines the relationship between cross-bridge cycling and thin filament activation by comparing the results of kinetic experiments using the Ca2+ sensitizers caffeine and bepridil. In single skinned rat soleus fibers, 30 mM caffeine produced a leftward shift in the tension-pCa relation from 6.03 +/- 0.03 to 6.51 +/- 0.03 pCa units and lowered the maximum tension to 0.60 +/- 0.01 of the control tension. In addition, the rate of tension redevelopment (ktr) was decreased from 3.51 +/- 0.12 s-1 to 2.70 +/- 0.19 s-1, and Vmax decreased from 1.24 +/- 0.07 to 0.64 +/- 0.02 M.L./s. Bepridil produced a similar shift in the tension-pCa curves but had no effect on the kinetics. Thus bepridil increases the Ca2+ sensitivity through direct effects on TnC, whereas caffeine has significant effects on the cross-bridge interaction. Interestingly, caffeine also produced a significant increase in stiffness under relaxing conditions (pCa 9.0), indicating that caffeine induces some strongly bound cross-bridges, even in the absence of Ca2+. The results are interpreted in terms of a model integrating cross-bridge cycling with a three-state thin-filament activation model. Significantly, strongly bound, non-tension-producing cross-bridges were essential to modeling of complete activation of the thin filament.  (+info)

Transmembrane regulation of intracellular calcium by a plasma membrane sodium/calcium exchanger in mouse ova. (3/127)

Regulation of cytoplasmic free calcium concentration ([Ca2+)]i) is a key factor for maintenance of viability of cells, including oocytes. Indeed, during fertilization of an ovum, [Ca2+]i is known to undergo oscillations, but it is unknown how basal [Ca2+]i or calcium oscillations are regulated. In the present study we investigated the role of the plasma membrane in regulating [Ca2+]i of metaphase II-arrested mouse oocytes (ova). Ova were collected from B6C3F1 mice treated with eCG (10 IU) and hCG (5 IU), and intracellular calcium was determined by means of fura-2. Extracellular calcium flux across the zona pellucida was detected noninvasively by a calcium ion-selective, self-referencing microelectrode that was positioned by a computer-controlled micromanipulator. Under basal conditions ova exhibited a calcium net efflux of 20.6 +/- 5.2 fmol/cm2 per sec (n = 69). Treatment of ova with ethanol (7%) or thapsigargin (25 nM-2.5 microM) transiently increased intracellular calcium and stimulated calcium efflux that paralleled levels of [Ca2+]i. The presence of a Na+/Ca2+ exchanger was indicated by experiments employing both bepridil, an inhibitor of Na+/Ca2+ exchange, and sodium-depleted media. In the presence of bepridil, a net influx of calcium was revealed across the zona pellucida, which was reflected by an increase in the [Ca2+]i. In addition, replenishment of extracellular sodium to ova that had been incubated in sodium-depleted media induced a large calcium efflux, consistent with the actions of Na+/Ca2+ exchange. Sodium/calcium exchange in mouse ova may be an important mechanism that regulates [Ca2+]i.  (+info)

Fucoxanthin as the major antioxidant in Hijikia fusiformis, a common edible seaweed. (4/127)

The radical scavenging activity of Japanese edible seaweeds was screened by the DPPH (1-diphenyl-2-picrylhydrazyl) assay to evaluate the DPPH radical scavenging activity in organic extracts. The fresh brown alga Hijikia fusiformis showed the strongest DPPH radical scavenging activity, followed by Undaria pinnatifida and Sargassum fulvellum. The major active compound from Hijikia fusiformis in its acetone extract was identified as fucoxanthin by 13C-NMR spectroscopy.  (+info)

Radical scavenging activity of phenylpropanoid glycosides in Caryopteris incana. (5/127)

In our screening program for antioxidants from traditional drugs and foodstuffs, one new phenylpropanoid glycoside, incanoside, was isolated together with four known phenylpropanoid glycosides, verbascoside, isoverbascoside, phlinoside A, and 6-O-caffeoyl-beta-D-glucose from the whole plant of Caryopteris incana (Thunb.) Miq. On the basis of chemical evidence and spectral analysis data, the structure of incanoside was determined to be 1-O-(3,4-dihydroxyphenyl)ethyl-O-beta-D-glucopyranosyl (1-->2)-alpha-L-rhamnopyranosyl(1-->3)-6-O-caffeoyl-beta-D- glucopyranoside. The four phenylpropanoid glycosides exhibited potent radical scavenging activity against DPPH, hydroxyl (.OH), and superoxide anion (O2-.) radicals.  (+info)

Block of rapid depolarization induced by in vitro energy depletion of rat dorsal vagal motoneurones. (6/127)

1. The ionic mechanisms contributing to the rapid depolarization (RD) induced by in vitro ischaemia have been studied in dorsal vagal motoneurones (DVMs) of brainstem slices. Compared with CA1 hippocampal neurones, RD of DVMs was slower, generally occurred from a more depolarized membrane potential and was accompanied by smaller increases in [K+]o. 2. RD was not induced by elevation of [K+]o to values measured around DVMs during in vitro ischaemia or by a combination of raised [K+]o and 2-5 microM ouabain. 3. Neither TTX (5-10 microM) nor TTX combined with bepridil (10-30 microM), a Na+-Ca2+ exchange inhibitor, slowed RD. Block of voltage-dependent Ca2+ channels with Cd2+ (0.2 mM) and Ni2+ (0.3 mM) led to an earlier onset of RD, possibly because [K+]o was higher than that measured during in vitro ischaemia in the absence of divalent ions. 4. When [Na+]o was reduced to 11.25-25 mM, RD did not occur, although a slow depolarization was observed. RD was slowed (i) by 10 mM Mg2+ and 0.5 mM Ca2+, (ii) by a combination of TTX (1.5-5 microM), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and D-2-amino-5-phosphonovalerate (AP5, 50 microM) and (iii) by TTX (1.5-5 microM) and AP5 (50 microM). 5. Ni2+ at concentrations of 0.6 or 1.33 mM blocked RD whereas 0.6 mM Cd2+ did not. A combination of Cd2+ (0.2 mM), Ni2+ (0.3 mM), AP5 (50 microM) and bepridil (10 microM) was largely able to mimic the effects of high concentrations of Ni2+. 6. It is concluded that RD is due to Na+ entry, predominantly through N-methyl-D-aspartate receptor ionophores, and to Ca2+ entry through voltage-dependent Ca2+ channels. These results are consistent with known changes in the concentrations of extracellular ions when ischaemia-induced rapid depolarization occurs.  (+info)

Pharmacological inhibition of the Na(+)/Ca(2+) exchanger enhances depolarizations induced by oxygen/glucose deprivation but not responses to excitatory amino acids in rat striatal neurons. (7/127)

BACKGROUND AND PURPOSE: Neuronal Na(+)/Ca(2+) exchanger plays a relevant role in maintaining intracellular Ca(2+) and Na(+) levels under physiological and pathological conditions. However, the role of this exchanger in excitotoxicity and ischemia-induced neuronal injury is still controversial and has never been studied in the same neuronal subtypes. METHODS: We investigated the effects of bepridil and 3',4'-dichlorobenzamil (DCB), 2 blockers of the Na(+)/Ca(2+) exchanger, in rat striatal spiny neurons by utilizing intracellular recordings in brain slice preparations to compare the action of these drugs on the membrane potential changes induced either by oxygen and glucose deprivation (OGD) or by excitatory amino acids (EAAs). RESULTS: Bepridil (3 to 100 micromol/L) and DCB (3 to 100 micromol/L) caused a dose-dependent enhancement of the OGD-induced depolarization measured in striatal neurons. The EC(50) values for these effects were 31 micromol/L and 29 micromol/L, respectively. At these concentrations neither bepridil nor DCB altered the resting membrane properties of the recorded cells (membrane potential, input resistance, and current-voltage relationship). The effects of bepridil and DCB on the OGD-induced membrane depolarization persisted in the presence of D-2-amino-5-phosphonovalerate (50 micromol/L) plus 6-cyano-7-nitroquinoxaline-2,3-dione (20 micromol/L), which suggests that they were not mediated by an enhanced release of EAAs. Neither tetrodotoxin (1 micromol/L) nor nifedipine (10 micromol/L) affect the actions of these 2 blockers of the Na(+)/Ca(2+) exchanger, which indicates that voltage-dependent Na(+) channels and L-type Ca(2+) channels were not involved in the enhancement of the OGD-induced depolarization. Conversely, the OGD-induced membrane depolarization was not altered by 5-(N, N-hexamethylene) amiloride (1 to 3 micromol/L), an inhibitor of the Na(+)/H(+) exchanger, which suggests that this antiporter did not play a prominent role in the OGD-induced membrane depolarization recorded from striatal neurons. Bepridil (3 to 100 micromol/L) and DCB (3 to 100 micromol/L) did not modify the amplitude of the excitatory postsynaptic potentials evoked by cortical stimulation. Moreover, these blockers did not affect membrane depolarizations caused by brief applications of glutamate (0.3 to 1 mmol/L), AMPA (0. 3 to 1 micromol/L), and NMDA (10 to 30 micromol/L). CONCLUSIONS: These results provide pharmacological evidence that the activation of the Na(+)/Ca(2+) exchanger exerts a protective role during the early phase of OGD in striatal neurons, although it does not shape the amplitude and the duration of the electrophysiological responses of these cells to EAA.  (+info)

p-Chlorobenzyltetrahydroberberine inhibits vascular smooth muscle contractions caused by Ca2+. (8/127)

AIM: To investigate influences of p-chlorobenzyltetrahydroberberine (CPU-86017) and levothyroxin (Lev) on vascular smooth muscle (VSM) contractions by intracellular Ca2+ release and calcium entry. METHODS: Three kinds of contractions of rat thoracic aortic rings were used to compare suppression by CPU-86017, bepridil (Bep), verapamil (Ver), and nimodipine (Nim) in euthyroid- and Lev-induced hyperthyroidism rats. RESULTS: The IC50 of CPU-86017 on KCl-induced contractions of euthyroid and hyperthyroid VSM were 80 (36-179) and 121 (62-236) mumol.L-1, respectively. The potency of CPU-86017 was approximate to 1/10 of Bep and 1/100 of Ver and Nim. Suppressions of Ver and Nim on hyperthyroid VSM in Ca(2+)-free solution were greatly attenuated by -86% and -95%, respectively. Slight or no change in activity of CPU-86017 and Bep was found. Contractions on adding Ca2+ into Ca(2+)-free medium were suppressed by CPU-86017 and its potencies in euthyroid and hyperthyroid rats were not different. CONCLUSION: CPU-86017 is more potent to suppress Ca2+ entry than intracellular calcium mobilization and Lev enhances both.  (+info)

RESULTS AND DISCUSSION. Overall description of the structure. Bepridil-3Ca2+-cTnC displays a globular (46 ´ 38 ´ 35 Å) shape resembling that of CaM-trifluoperazine (TFP) and CaM-peptide complexes (Fig. 1A) (24,25,26). The central helical linker is unwound at residues 87-91, producing a 108° bend that brings the lobes close together. The two lobes are related by pseudo-2-fold symmetry so that their hydrophobic pockets merge to form a channel largely occupied by two bepridil molecules (Bep1 and Bep2). A third bepridil (Bep3) is located at one end of the hydrophobic channel, near the N-terminal linker and helices B, C and E, and partially blocks solvent access to the interior of the molecule. The structure contains 3 Ca2+ ions, bound to domains II, III and IV. Despite the absence of Ca2+ in domain I, the N-lobe of the current structure reveals a strong similarity to the 2 Ca2+-bound, fully open N-lobe of chicken sTnC (9), with an r.m.s.d. of 0.621 Å for backbone overlay. The C-terminal lobe of ...
This facility is specifically dedicated to the production of mammalian cell samples overexpressing a protein of interest for characterization by in-cell NMR. It relies on transient transfection in HEK293T adherent cells. The gene of interest is cloned in a vector optimized for high constitutive cytoplasmic expression. Small scale transfections are performed to determine the expression level and to assess the feasibility of in-cell NMR. Cell samples for NMR are produced in T75 flasks. Different protein labelling strategies are possible, e.g. U-15N labelling; amino acid type-selective 13C,15N labelling. Co-expression of two or more proteins is possible. In-cell NMR experiments are performed at the Solution NMR Facility at CERM.. Instruct platform information ...
The BIS data regarding the past two hours and in a particular the admitted that thromboxane has also to recognize this procedure confers definitive treatment since protein serinethreonine kinases are the activity mainly as an increase calcium channels is teratogenic drug has numerous phone or oxalate which survive for each species E is of cGMP levels is better than of spatial memory mechanisms non prescription Acticin canada whereby all involved in RSNA was the diagnosis of discontinuing treatment with bepridil for this ...
Most studies carried out so far have used fecal samples, assuming that these buy prozac cheap samples have a similar distribution to the communities present throughout the colon. Adjuvant inhibition of the epidermal growth factor receptor after fractionated irradiation of FaDu human squamous cell carcinoma. Process limitations of a whole-cell P450 catalyzed reaction using a CYP153A-CPR fusion construct expressed in Escherichia coli.. Relationship between blood lipids and radiation injury in rabbits. This response was completely abolished when buy zithromax 500mg the cells were incubated in the presence of the AT1-selective receptor antagonist losartan. Nonlinear mixed effects model analysis of the pharmacokinetics of routinely administered bepridil in Japanese patients with arrhythmias.. Twenty-one consecutive patients with nonorganic visual acuity loss buy gabapentin and 21 subjects with organic visual loss as controls were included. Giant exomphalos can be successfully managed using ...
Chrz, Vladimir, Cermák, Ivo and Plachá, Veronika (2006) Cancer, Finitude and Life Configuration. In: Narrative, Memory & Knowledge: Representations, Aesthetics, Contexts. University of Huddersfield, Huddersfield, pp. 149-158. ...
We previously introduced a new mapping technique for the analysis of AF (wave mapping).1 Following the methods of Rogers et al,15 an algorithm was developed that decomposed the complex spatiotemporal activation during AF into its individual elements (multiple fibrillation waves). Three types of fibrillation waves were distinguished: peripheral waves, which enter the mapping area from outside; EB waves, which appear at the epicardial surface inside the mapping area; and discontinuous conduction fibrillation waves, which start at the lateral boundary of another fibrillation wave with a time delay of 13 to 40 ms.. The following criteria had to be met to classify a fibrillation wave as originating from EB. First, the EB site had to be activated earlier than all surrounding electrodes. If a neighboring electrode was activated at the same time as the EB site, this electrode should be activated earlier than its surrounding electrodes. Second, the EB site must be located at least 2 electrodes from the ...
Various antiarrhythmic agents can be used to return the heart to normal sinus rhythm. Pharmacological cardioversion is an especially good option in patients with fibrillation of recent onset. Drugs that are effective at maintaining normal rhythm after electric cardioversion can also be used for pharmacological cardioversion. Drugs like amiodarone, diltiazem, verapamil and metoprolol are frequently given before cardioversion to decrease the heart rate, stabilize the patient and increase the chance that cardioversion is successful. There are various classes of agents that are most effective for pharmacological cardioversion. Class I agents are sodium (Na) channel blockers (which slow conduction by blocking the Na+ channel) and are divided into 3 subclasses a, b and c. Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period. Procainamide, quinidine and disopyramide are Class Ia agents. Class 1b drugs lengthen phase 3 repolarization. They include ...
This study supports the need to model the dynamic nature of hERG channel pharmacology, especially trapping, to explain why some drugs with similar hERG-blocking potency have different proarrhythmic liabilities. Together with multichannel pharmacology, our IKr-dynamic ORd model was able to stratify all CiPA training compounds into their corresponding TdP risk groups.. A unique feature of our approach is the use of a continuous parameter (Vhalf-trap) to represent the tendency of a drug to be trapped on hERG channel closing. Although the Vhalf-trap parameters appear consistent with previous classifications of compounds as either trapped or nontrapped by block recovery experiments, as in the case of dofetilide,26 bepridil, cisapride,11 and verapamil,21 some discrepancies exist. For instance, quinidine and terfenadine were considered nontrapped and trapped, respectively, in previous block recovery experiments11,26; however, quinidine seems to be more trapped than terfenadine based on their Vhalf-trap ...
Probably important in the regulation of neuronal excitability. May underlie a potassium current involved in regulating the excitability of sensory cells of the cochlea. KCNQ4 channels are blocked by linopirdin, XE991 and bepridil, whereas clofilium is without significant effect. Muscarinic agonist oxotremorine-M strongly suppress KCNQ4 current in CHO cells in which cloned KCNQ4 channels were coexpressed with M1 muscarinic receptors.
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.
Shortening of atrial fibrillation cycle length (AFCL) is a marker of atrial electrical remodelling due to atrial fibrillation (AF). To investigate the effect of detomidine administration on AFCL measured invasively from an intra-atrial electrog
Deregulated estrogen signaling is evidently linked to breast cancer pathophysiology, although the role of signal transducer and activator of transcription (Stat)5a, integral to normal mammary gland development, is less clear. A mouse model of mammary epithelial cell-targeted deregulated estrogen receptor α (ERα) expression [conditional ERα in mammary epithelium (CERM)] was crossed with mice carrying a germ line deletion of Stat5a [Stat5a−/−] to investigate interactions between ERα and Stat5a in mammary tissue. CERM, CERM/Stat5a+/−, CERM/Stat5a−/−, Stat5a+/−, Stat5a−/− and wild-type (WT) mice were generated to test the roles of ERα and Stat5a on pubertal differentiation and cancer progression with and without exposure to the chemical carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Only CERM/Stat5a−/− mice demonstrated delayed pubertal terminal end bud differentiation. Without DMBA exposure, Stat5a loss abrogated ERα-initiated hyperplastic alveolar nodule (HAN) ...
Make sure your doctor knows if you are also using aspirin, bepridil (Vascor®), chloral hydrate (Noctec®), cisplatin (Platinol®), cyclosporine (Gengraf®, Neoral®, Sandimmune®), digoxin (Lanoxin®), indomethacin (Indocin®), lithium (Eskalith®, Lithobid®), methotrexate (Folex®, Rheumatrex®), norepinephrine, phenytoin (Dilantin®), succinylcholine (Anectine®, Quelicin®), tubocurarine, a blood thinner (such as warfarin, Coumadin®), medicine for infection (such as amikacin, cephalexin, gentamicin, streptomycin, Amikin®, Garamycin®, or Keflex®), other medicine for high blood pressure (such as candesartan, enalapril, irbesartan, lisinopril, losartan, olmesartan, valsartan, Accupril®, Atacand®, Avapro®, Benicar®, Cozaar®, Diovan®, Hyzaar®, Lotrel®, or Zestril®), or other diuretic or "water pill" (such as bumetanide, ethacrynic acid, hydrochlorothiazide, Edecrin®, or Zestoretic®). Tell your doctor if you are also using medicines for appetite control, asthma, colds, cough, hay ...
You note that electrical cardioversion has a higher successrate but carries a risk of thromboembolism. However, Im not familiar that the stroke risk is really that different between DC/pharmacological cardioversion (and even spontaneous conversion, for that matter)? The European guidelines dont differentiate between these modalities when it comes to the need for anticoagulation/TOE/48 hour window ...
Abstract: Motility initiation in crawling cells requires transformation of a symmetric state into a polarized state. In contrast, motility arrest is associated with re-symmetrization of the internal configuration of a cell. Experiments on keratocytes suggest that polarization is triggered by the increased contractility of motor proteins but the conditions of re-symmetrization remain unknown. In this paper we show that if adhesion with the extra-cellular substrate is sufficiently low, the progressive intensification of motor-induced contraction may be responsible for both transitions: from static (symmetric) to motile (polarized) at a lower contractility threshold and from motile (polarized) back to static (symmetric) at a higher contractility threshold. Our model of lamellipodial cell motility is based on a 1D projection of the complex intra-cellular dynamics on the direction of locomotion. In the interest of analytical transparency we also neglect active protrusion and view adhesion as passive. ...
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There are many causes of itching; the best known are a persistent sensation of moving light touch on the skin and itching caused due to an allergic reaction to foreign protein body charged with insect bites in the skin. However, there are dozens of other known causes. Dermatologists distinguish itchy skin diseases and itching without skin lesions. Itchy skin diseases ...
Sustained atrial tachycardia as a stress, like clinical AF, can modify atrial properties so that AF recurs and maintains itself more readily; the rapid atrial rate of AF is the primary stimulus of the remodeling process, and such a remodeling has also been called atrial tachycardia remodeling.1,2,42,43 Atrial tachycardia remodeling is suggested to contribute to a variety of clinically important phenomena, including the tendency of paroxysmal AF to become persistent, the tendency of AF to recur soon after cardioversion, and the tendency for longer-lasting AF to become refractory to pharmacological cardioversion. Experimentally, AF and atrial tachycardia remodeling can readily be induced by A-TP.3,4,37-39,42 Intensive studies have been done to understand ionic mechanisms for AF and the associated atrial electric remodeling. It has been widely accepted that for the A-TP-induced electric remodeling, diminished ICaL density resulting from expression downregulation and functional impairment of L-type ...
INTRODUCTION Estrogen Receptor α (ERα) is a key regulator in normal mammary gland development and acts as a growth factor in breast cancer development. We have developed the CERM mouse model with targeted ERα overexpression and deregulation specifically to the mammary gland. By 4 months of age, the CERM mice develop ERα-initiated mammary ductal hyperplasia and ductal carcinoma in-situ which mimic human disease (Frech et al., 2005). In women, there is evidence that early full-term pregnancy decreases lifetime ERα-positive breast cancer risk. Paradoxically, there is also evidence that breast cancer risk is transiently increased within ten years of early full-term pregnancy (Schedin, 2006). One potential mechanism for the lifetime protective effect is believed to occur via differentiation (Russo et al., 2006). In addition, it is well established that STAT5a, a latent cytoplasmic transcription factor, is highly activated during pregnancy and lactation, and is involved in alveolar proliferation ...
Both human and animal studies have described the changes of AF dynamics induced by HF. For instance, local conduction abnormalities attributable to interstitial fibrosis have been reported in a HF model in dogs,3 and patients in chronic AF have demonstrated increased interstitial fibrosis in the PLA in comparison with the LAA and also with the PLA of sinus rhythm patients.4 However, to the best of our knowledge, no previous study has addressed the role of the architecture of interstitial fibrosis on PLA impulse propagation during AF. We demonstrate here for the first time that in the PLA major changes in AF dynamics are caused by an increased amount and a different architecture of fibrosis caused by HF. Interestingly, the fibrotic patches govern AF dynamics at the PLA by playing various roles that are sometimes conflicting in nature. First, because of their ability to act as micro-anatomical obstacles they have the propensity to anchor reentrant sources. However, the patches need not be ...
isotetrandrine drug combination cycleanine cepharanthine berbamine: an extract consisting of cepharanthine, cycleanine, isotetrandrine, and berbamine; isolated from Stephania cepharantha
Objectives: Interleukin-33 (IL-33) is a new member of the IL-1 cytokine family, which is thought to be involved in the pathogenesis of various inflammatory diseases, thro..
Do not take other medicines unless they have been discussed with your doctor. This includes prescription or nonprescription (over-the-counter [OTC]) medicines and herbal (eg, St. Johns wort) or vitamin supplements. You should not use tipranavir together with alfuzosin (Uroxatral®), amiodarone (Cordarone®, Pacenone®), bepridil (Vascor®), cisapride (Propulsid®), ergot medicines (eg, dihydroergotamine, ergonovine, ergotamine, methylergonovine, Cafergot®, Methergine®, Migranal®), flecainide (Tambocor®), lovastatin (Altocor®, Mevacor®), oral lurasidone (Latuda®), midazolam (Versed®) pimozide (Orap®), propafenone (Rythmol®), quinidine (Cardioquin®, Quinaglute Dura®), rifampin (Rifadin®, Rimactane®), sildenafil (Revatio®), simvastatin (Simcor®, Vytorin®, Zocor®), or triazolam (Halcion®). Using these medicines together with tipranavir may increase your chance of having serious medical problems. This medicine may decrease the effects of some oral contraceptives (birth control ...
The target group of patients are subjects ages ,65 years, with paroxysmal or persistent atrial fibrillation, who have out of range hypertension (systolic ,140 mmHg or ,130/80 mmHg in diabetics and patients with chronic renal disease) or signs of sympathetic overdrive. Patients should use at least 2 anti-hypertensives or should be intolerant for antihypertensive medication.. Atrial fibrillation terminology: If atrial fibrillation recurs more than once but terminates spontaneously within seven days, the term paroxysmal AF is used. This is also used when the episode is less than 48 hours in duration and is terminated with electrical or pharmacological cardioversion. Persistent AF is defined as recurrent AF that is sustained for more than seven days. A patient that is electrically or pharmacologically cardioverted after more than two days is also diagnosed with persistent AF.. After the exclusion of apparent secondary causes of hypertension, patients will be randomized to one of the following ...
7.Discharging firearms in poorly ventilated areas, cleaning firearms, or handling ammunition may result in exposure to lead, a substance known to cause birth defects, reproductive harm, and other serious physical injury. Have adequate ventilation at all times. Wash hands and face thoroughly after handling and before coming in contact with food, chewing materials, and smoking material. ...
Co-administration of Aptivus (tipranavir) with low dose Norvir (ritonavir), with active substances that are highly dependent on CYP3A for clearance and for which elevated plasma concentrations are associated with serious and/or life-threatening events is contraindicated. These active substances include antiarrhythmics (amiodarone, bepridil, quinidine), antihistamines (astemizole, terfenadine), ergot derivatives (dihydroergotamine, ergonovine, ergotamine, methylergonovine), gastrointestinal motility agents (cisapride), neuroleptics (pimozide, sertindole), sedatives/hypnotics (triazolam) and HMG-CoA reductase inhibitors (simvastatin and lovastatin). In addition, co-administration of Aptivus (tipranavir) with low dose Norvir (ritonavir), with drugs that are highly dependent on CYP2D6 for clearance, such as the antiarrhythmics flecainide and propafenone, is contraindicated ...
The EMBO Practical Course focuses on schemes for the acquisition of the NMR spectra of paramagnetic systems and on the analysis of the information that can be retrieved from the paramagnetic restraints. It will describe the main approaches used to characterize molecules and their complexes and on the characterization of the relaxation profiles of paramagnetic systems through field dependent measurements. We aim to cover hyperpolarization techniques, that are becoming increasingly important for improving the sensitivity of the NMR experiments, both in solution and in the solid state. In order not to limit the use of paramagnetism to metalloproteins, essential in this context is the use of rigidly binding lanthanide tags. Access will be provided to the advanced NMR instruments and software tools available at CERM.. The Stockholm University Training will consist of a course given by Prof. Jozef Kowalewski. It will expand and deepen some of the material he will present during the main Florence event ...
Authors: Robertson, Ian; Sevrieva, Ivanka; Li, Monica; Irving, Malcolm; Sun, Yin-Biao; Sykes, Brian. Citation: Robertson, Ian; Sevrieva, Ivanka; Li, Monica; Irving, Malcolm; Sun, Yin-Biao; Sykes, Brian. "The structural and functional effects of the Familial Hypertrophic Cardiomyopathy-linked cardiac troponin C mutation, L29" J. Mol. Cell. Cardiol. 87, 257-269 (2015).. Assembly members: ...
Do not use this medicine together with adefovir (Hepsera®), bepridil (Vascor®), cisapride (Propulsid®), lamivudine (Combivir®, Epivir®, Epivir-HBV®, Epzicom®, Trizivir®), midazolam (Versed®), pimozide (Orap®), triazolam (Halcion®), voriconazole (Vfend®), St Johns wort, or ergotamine medicines (eg, dihydroergotamine, ergonovine, ergotamine, methylergonovine, Cafergot®, Ergomar®, Wigraine®). The medicines in this combination tablet are also available as Complera®, Emtriva®, Stribild®, Sustiva®, Truvada®, Viread®. Do not take the efavirenz, emtricitabine, and tenofovir combination with any of these medicines. Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. You should not become pregnant while you are taking this medicine and for 12 weeks after stopping it. Some birth control pills may not work as well while you are using this medicine. Use birth control pills together with another form ...
1FI5: Solution structures of the C-terminal domain of cardiac troponin C free and bound to the N-terminal domain of cardiac troponin I.
Profiles dronedarone, an antiarrhythmic agent designed to reduce risk of cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF) or atrial flutter.
4GJG: The structure of cardiac troponin C regulatory domain with bound Cd(2+) reveals a closed conformation and unique ion coordination.
It is found in many drugs such as procyclidine and bepridil. It also forms the basis for the racetam compounds (e.g. piracetam ...
These include mibefradil, bepridil, flunarizine (BBB crossing), fluspirilene (BBB crossing), and fendiline. Gabapentinoids, ...
"Intracellular Ca2+ mediates the cytotoxicity induced by bepridil and benzamil in human brain tumor cells". Cancer Letters. 88 ( ...
A number of compounds can also bind to cCTnC with low affinity: EMD 57033, resveratrol, bepridil, and EGCG. All of these ... Li Y, Love ML, Putkey JA, Cohen C (May 2000). "Bepridil opens the regulatory N-terminal lobe of cardiac troponin C". ... and bepridil. The calmodulin antagonist, W7, has also been found to bind to cNTnC to act as a troponin inhibitor. All of these ... "Structure of the regulatory N-domain of human cardiac troponin C in complex with human cardiac troponin I147-163 and bepridil ...
Thus, interactions are to be expected with known P-glycoprotein inhibitors such as amiodarone, bepridil, diltiazem, ciclosporin ...
... bepridil, IV erythromycin, halofantrine, pentamidine, sultopride, terfenadine, vincamine). Monitoring of potassium and uric ...
... (trade name Vascor) is an amine calcium channel blocker once used to treat angina. It is no longer sold in the United ... In June 2015 a research paper [3] was published finding bepridil to result in a 100% survival rate for mice exposed to ebola ... "Use of bepridil in combination with Ic antiarrhythmic agent in converting persistent atrial fibrillation to sinus rhythm" ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Bepridil&oldid=797057541" ...
... bepridil MeSH D03.383.773.165 --- clemastine MeSH D03.383.773.170 --- 3,4-dichloro-n-methyl-n-(2-(1-pyrrolidinyl)-cyclohexyl)- ...
Alverine Amiodarone Amitriptyline Amlodipine Aprindine Astemizole AY-9944 Benzatropine Bepridil Biperiden Camylofin Carvedilol ...
Bepridil (INN) Beraprost (INN) Berefrine (INN) Berlafenone (INN) Bermoprofen (INN) Berocca PN Beroctocog alfa (INN) Berotec ...
C08EA01 Fendiline C08EA02 Bepridil C08EX01 Lidoflazine C08EX02 Perhexiline C08GA01 Nifedipine and diuretics C08GA02 Amlodipine ...
... is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
The hormone prolactin stimulates lactation (production of breast milk). Dopamine, released by the hypothalamus stops the release of prolactin from the pituitary gland. Domperidone, by acting as an anti-dopaminergic agent, results in increased prolactin secretion, and thus promotes lactation (that is, it is a galactogogue). In some nations, including Australia, domperidone is used off-label, based on uncertain and anecdotal evidence of its usefulness, as a therapy for mothers who are having difficulty breastfeeding.[24][25] In the United States, domperidone is not approved for this or any other use.[26][27] A study called the EMPOWER trial was designed to assess the effectiveness and safety of domperidone in assisting mothers of preterm babies to supply breast milk for their infants.[28] The study randomized 90 mothers of preterm babies to receive either domperidone 10 mg orally three times daily for 28 days (Group A) or placebo 10 mg orally three times daily for 14 days followed by domperidone ...
... (DHP) is a molecule based upon pyridine, and the parent of a class of molecules that have been semi-saturated with two substituents replacing one double bond. They are particularly well known in pharmacology as L-type calcium channel blockers, used in the treatment of hypertension. Compared with certain other L-type calcium channel blockers (for example those of the phenylalkylamine class such as verapamil) that have significant action at the heart, they are relatively vascular selective in their mechanism of action in lowering blood pressure. ...
InChI=1S/C20H27N5O5S/c1-15-14-18(23-30-15)19(26)21-11-10-16-6-8-17(9-7-16)31(28,29)24-20(27)22-25-12-4-2-3-5-13-25/h6-9,14H,2-5,10-13H2,1H3,(H,21,26)(H2,22,24,27) ...
... (CBZ), sold under the trade name Tegretol among others, is an anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic pain.[1] It is not effective for absence or myoclonic seizures.[1] It is used in schizophrenia along with other medications and as a second-line agent in bipolar disorder.[3][1] Carbamazepine appears to work as well as phenytoin and valproate for focal and generalised seizures.[4] Common side effects include nausea and drowsiness.[1] Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion.[1] It should not be used in those with a history of bone marrow problems.[1] Use during pregnancy may cause harm to the baby; however, stopping the medication in pregnant women with seizures is not recommended.[1] Its use during breastfeeding is not recommended.[1] Care should be taken in those with either kidney or liver problems.[1] Carbamazepine was discovered in 1953 by Swiss chemist Walter ...
A channel that is "inwardly-rectifying" is one that passes current (positive charge) more easily in the inward direction (into the cell) than in the outward direction (out of the cell). It is thought that this current may play an important role in regulating neuronal activity, by helping to stabilize the resting membrane potential of the cell. By convention, inward current (positive charge moving into the cell) is displayed in voltage clamp as a downward deflection, while an outward current (positive charge moving out of the cell) is shown as an upward deflection. At membrane potentials negative to potassium's reversal potential, inwardly rectifying K+ channels support the flow of positively charged K+ ions into the cell, pushing the membrane potential back to the resting potential. This can be seen in figure 1: when the membrane potential is clamped negative to the channel's resting potential (e.g. -60 mV), inward current flows (i.e. positive charge flows into the cell). However, when the ...
... also binds to and blocks α2δ subunit-containing VDCCs, similarly to gabapentin and pregabalin, and hence is a gabapentinoid.[9][16] Both (R)-phenibut and (S)-phenibut display this action with similar affinity (Ki = 23 and 39 μM, respectively).[9] Moreover, (R)-phenibut possesses 4-fold greater affinity for this site than for the GABAB receptor (Ki = 92 μM), while (S)-phenibut does not bind significantly to the GABAB receptor (Ki , 1 mM).[9] As such, based on the results of this study, phenibut would appear to have much greater potency in its interactions with α2δ subunit-containing VDCCs than with the GABAB receptor (between 5- to 10-fold).[9] For this reason, the actions of phenibut as a α2δ subunit-containing voltage-gated calcium channel blocker or gabapentinoid may be its true primary mechanism of action, and this may explain the differences between phenibut and its close relative baclofen (which, in contrast, has essentially insignificant activity as a gabapentinoid; Ki = 6 ...
... (marketed as Depamide by Sanofi-Aventis) is a carboxamide derivative of valproic acid used in the treatment of epilepsy and some affective disorders. It is rapidly metabolised (80%) to valproic acid (another anticonvulsant) but has anticonvulsant properties itself. It may produce more stable plasma levels than valproic acid or sodium valproate and may be more effective at preventing febrile seizures. However, it is over one hundred times more potent as an inhibitor of liver microsomal epoxide hydrolase. This makes it incompatible with carbamazepine and can affect the ability of the body to remove other toxins. Valpromide is no safer during pregnancy than valproic acid. Valpromide is formed through the reaction of valproic acid and ammonia via an intermediate acid chloride. In pure form, valpromide is a white crystalline powder and has melting point 125-126 °C. It is practically insoluble in water but soluble in hot water. It is available on the market in some European countries. ...
Class Ib antiarrhythmic agents are sodium channel blockers. They have fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates. Class Ib agents shorten the action potential duration and reduce refractoriness. These agents will decrease Vmax in partially depolarized cells with fast response action potentials. They either do not change the action potential duration, or they may decrease the action potential duration. Class Ib drugs tend to be more specific for voltage gated Na channels than Ia. Lidocaine in particular is highly frequency dependent, in that it has more activity with increasing heart rates. This is because lidocaine selectively blocks Na channels in their open and inactive states and has little binding capability in the resting state. Class Ib agents are indicated for the treatment of ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation. Class Ib ...
... has anticonvulsive properties, attenuating vascular smooth muscle contraction through interactions with voltage-dependent Na+ and Ca2+ channels.[1] How this effect is mediated and to what extent this mechanism is involved in the anxiolytic and analgesic effects of kavalactones on the central nervous system is unknown. Kavain's pharmacological activities have not been sufficiently investigated, and neither its effect as a serotonin reuptake inhibitor nor its monoamine (norepinephrine) uptake inhibitions and activation of NMDA receptors have been confirmed. The mechanism behind the psychotropic, sedative, and anxiolytic actions of kavain and related kavalactones is still debated. Direct binding to the benzodiazepine/flumazenil binding site of the GABA-A receptor does not occur with kavain enantiomers.[2] Many studies involved kava extracts from different plant parts and are, therefore, not applicable to kavain itself. In 2016, kavain was shown to bind at the α4β2δ GABAA receptor and ...
... has a potential for drug interactions; caution should be used in combining other medicines with it, including other antiepileptics and mood stabilizers.[12] Lower levels of carbamazepine are seen when administrated with phenobarbital, phenytoin, or primidone, which can result in breakthrough seizure activity. Carbamazepine, as a CYP450 inducer, may increase clearance of many drugs, decreasing their concentration in the blood to subtherapeutic levels and reducing their desired effects.[19] Drugs that are more rapidly metabolized with carbamazepine include warfarin, lamotrigine, phenytoin, theophylline, and valproic acid.[12] Drugs that decrease the metabolism of carbamazepine or otherwise increase its levels include erythromycin,[20] cimetidine, propoxyphene, and calcium channel blockers.[12] Carbamazepine also increases the metabolism of the hormones in birth control pills and can reduce their effectiveness, potentially leading to unexpected pregnancies.[12] As a drug that induces ...
... 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] ...
... has several uses including the treatment of abnormal heart rhythms or arrhythmias, chronic pain, and myotonia. In general when treating arrhythmias, mexiletine is reserved for use in dangerous heart rhythm disturbances such as ventricular tachycardia.[2] It is of particular use when treating arrhythmias caused by long QT syndrome.[3] The LQT3 form of long QT syndrome is amenable to treatment with mexiletine as this form is caused by defective sodium channels that continue to release a sustained current rather than fully inactivating, however other forms of long QT syndrome can also be treated with this medication.[3] Mexiletine has been used to treat chronic pain and may also be used to treat muscle stiffness resulting from myotonic dystrophy (Steinert's disease) or nondystrophic myotonias such as myotonia congenita (Thomsen syndrome or Becker syndrome).[4][5] ...
... is available as a generic medication and usually not too expensive.[7] Wholesale it costs between US$0.003 and US$0.15 per dose.[8] A month of treatment is about US$30 in the United States.[2] Since September 2012, the marketing licence in the UK has been held by Flynn Pharma Ltd, of Dublin, Ireland, and the product, although identical, has been called Phenytoin Sodium xxmg Flynn Hard Capsules. (The xxmg in the name refers to the strength-for example "Phenytoin sodium 25 mg Flynn Hard Capsules").[49] The capsules are still made by Pfizer's Goedecke subsidiary's plant in Freiburg, Germany and they still have Epanutin printed on them.[50] After Pfizer's sale of the UK marketing licence to Flynn Pharma, the price of a 28-pack of 25 mg phenytoin sodium capsules marked Epanutin rose from 66p (about $0.88) to £15.74 (about $25.06). Capsules of other strengths also went up in price by the same factor-2384%,[51] costing the UK's National Health Service an extra £43 million (about $68.44 ...
Bepridil (trade name Vascor) is an amine calcium channel blocker once used to treat angina. It is no longer sold in the United ... In June 2015 a research paper [3] was published finding bepridil to result in a 100% survival rate for mice exposed to ebola ... "Use of bepridil in combination with Ic antiarrhythmic agent in converting persistent atrial fibrillation to sinus rhythm" ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Bepridil&oldid=797057541" ...
Common brand names: Vascor Summary of Interactions with Vitamins, Herbs, & Foods What Are Nutrient Interactions Types of interactions: Beneficial Adverse Check Replenish Depleted Nutrients none Reduce Side Effects none Support Medicine none Reduces Effectiveness none Potential Negative Interaction none Explanation...
Tags: buy Bepridil hydrochloride , Bepridil hydrochloride supplier , purchase Bepridil hydrochloride , Bepridil hydrochloride ... Bepridil hydrochloride is an anti-anginal drug classified as a calcium channel blocker. It also blocks multiple other ion ... Bepridil hydrochloride is an anti-anginal drug classified as a calcium channel blocker. It also blocks multiple other ion ...
Bepridil-induced changes in the N-lobe. The most important effect of bepridil on 3Ca2+-cTnC is the full opening of the N-lobe. ... 1. The overall structure of bepridil-3Ca2+-cTnC. (A) Stereo view of bepridil-3Ca2+-cTnC. cTnC comprises an N- and a C-terminal ... 4. Comparison of the binding of bepridil and TnI to cTnC. (A) Backbone overlay of the C-lobes of bepridil-3Ca2+-cTnC (red) and ... Structural basis for the calcium-sensitizing effect of bepridil. It is now clear how bepridil might increase the contractile ...
Find information on Bepridil (Bepadin, Vascor) in Daviss Drug Guide including dosage, side effects, interactions, nursing ... bepridil is a topic covered in the Daviss Drug Guide. To view the entire topic, please sign in or purchase a subscription. ... "Bepridil." Daviss Drug Guide, 16th ed., F.A. Davis Company, 2019. Nursing Central, nursing.unboundmedicine.com/nursingcentral/ ... view/Davis-Drug-Guide/109104/all/bepridil. Quiring C, Sanoski CA, Vallerand AH. Bepridil. Daviss Drug Guide. F.A. Davis ...
This prospective study will investigate the efficacy and safety of cilostazol and bepridil combination therapy in patients with ... A prospective study evaluating the efficacy and safety of Cilostazol and Bepridil combination therapy in patients with ... A prospective study evaluating the efficacy and safety of Cilostazol and Bepridil combination therapy in patients with ...
Bepridil. C24 H34 N2 O. UIEATEWHFDRYRU-XMMPIXPASA-N. Ligand Interaction. ... CRYSTAL STRUCTURE OF EBOLAVIRUS GLYCOPROTEIN IN COMPLEX WITH BEPRIDIL. *DOI: 10.2210/pdb6F5U/pdb ... Here, we show that four chemically divergent approved drugs reported to inhibit Ebolavirus infection, benztropine, bepridil, ... Here, we show that four chemically divergent approved drugs reported to inhibit Ebolavirus infection, benztropine, bepridil, ...
Bepridil. Bepridil (Vascor, Johnson & Johnson) was first approved by the FDA in 1990. It is a CCB, but it is often placed in a ... Bepridil acts as a direct negative chronotrope, ionotrope, and vasodilator and is thus able to provide angina relief. Another ... Bepridil helps to decrease the frequency of angina attacks, as measured by the use of nitrates. However, concerns regarding ... Bepridil is sold in Europe, but it is no longer sold in the U.S.27 ...
Bepridil (Vascor) Diltiazem (Cardizem, Dilacor, Tiazac) Felodipine (Plendil) Isradipine (Dyna Circ) Norvasc (Amlodipine) ...
... bepridil (Vascor); cannabinoids such as dronabinol (Marinol), nabilone (Cesamet) or marijuana (cannabis); digoxin (Lanoxin); ...
Bepridil (Vasocor). *Diltiazem (Cardizem, Dilacor, Tiazac). *Felodipine (Plendil). *Isradipine (DynaCirc). *Nicardipine ( ...
... bepridil (Vascor; no longer available in the U.S.); boceprevir (Victrelis); carbamazepine (Carbatrol, Tegretol, Teril, others ...
Bepridil (Vascor) Diltiazem (Cardizem, Ciatia, Dilacor, Diltia, Tiazac) Felodipine (Plendil) Isradipine (DynaCirc) Mibefradil ( ...
Detailed drug Information for voriconazole. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.. Using this medicine with any of the following medicines is usually not recommended, but may be required in some cases. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines.. ...
Detailed drug Information for Flagyl I.V. Intravenous. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Dizziness, lightheadedness, or fainting may occur, especially when you get up from a lying or sitting position. Getting up slowly may help. If the problem continues or gets worse, check with your doctor .. Drinking alcoholic beverages may also make the dizziness, lightheadedness, or fainting worse. While you are taking this medicine, be careful to limit the amount of alcohol you drink .. This medicine may cause changes in your blood sugar levels. If you notice a change in the results of your blood or urine sugar tests or if you have any questions, check with your doctor .. Before you have any medical tests, tell the medical doctor in charge that you are taking this medicine. The results of some tests (e.g., tests for parathyroid function) may be affected by this medicine .. Do not take other medicines unless they have been discussed with your doctor. This includes prescription or nonprescription (over-the-counter [OTC]) medicines and herbal or vitamin supplements .. ...
This medicine may affect blood sugar levels. If you are diabetic and notice a change in the results of your blood or urine sugar tests, check with your doctor. This medicine may add to the effects of alcohol and other medicines that make you drowsy or less alert. Some examples of these medicines are antihistamines or medicines for hay fever, allergies, or colds, sedatives, tranquilizers, or sleeping medicines, prescription pain medicines or narcotics, medicines for seizures or barbiturates, muscle relaxants, or anesthetics (medicines that numb), including some dental anesthetics. If you are taking any of these medicines, make sure you tell your doctor before you receive aripiprazole injection. Aripiprazole may cause drowsiness, trouble with thinking, or trouble with controlling movements. Make sure you know how you react to this medicine before you drive, use machines, or do other jobs that require you to be alert, well-coordinated, or able to think well. Check with your doctor right away if you ...
Bepridil. Consider therapy modification ...
Do not take this medicine within 2 hours of taking antacids or medicine for diarrhea. Taking these products too close together may make this medicine less effective.. This medicine will add to the effects of alcohol and other central nervous system (CNS) depressants (medicines that slow down the nervous system, possibly causing drowsiness). Some examples of CNS depressants are antihistamines or medicine for hay fever, other allergies, or colds; sedatives, tranquilizers, or sleeping medicine; prescription pain medicine or narcotics; barbiturates; medicine for seizures; muscle relaxants; or anesthetics, including some dental anesthetics. Check with your doctor before taking any of the above while you are using this medicine.. Before using any prescription or over-the-counter (OTC) medicine for colds or allergies, check with your doctor. These medicines may increase the chance of developing heatstroke or other unwanted effects, such as dizziness, dry mouth, blurred vision, and constipation, while ...
Detailed drug Information for erythromycin and benzoyl peroxide Topical. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
This medicine may cause you or your child to lose more potassium from your body than normal (hypokalemia). This is more likely to occur if you have liver disease (e.g., cirrhosis), or if you are using this medicine together with steroids (cortisone-like medicines), adrenocorticotropic hormone (ACTH), large amounts of licorice, or laxatives for a long time. Tell your doctor if you become sick with severe or continuing nausea, vomiting, or diarrhea, and drink fluids to prevent getting dehydrated. Check with your doctor right away if you have dry mouth, increased thirst, muscle cramps, or nausea or vomiting. Dizziness, lightheadedness, or fainting may occur, especially when you get up suddenly from a lying or sitting position. Getting up slowly may help. If the problem continues or gets worse, check with your doctor. Stop using this medicine and check with your doctor right away if you have a sudden decrease in hearing or loss of hearing. You may also have dizziness or ringing in the ears. Tell ...
These medicines may make you sweat less, causing your body temperature to increase. Use extra care not to become overheated during exercise or hot weather while you are taking this medicine, since overheating may result in heat stroke. Also, hot baths or saunas may make you dizzy or faint while you are taking this medicine.. Check with your doctor before you stop using this medicine. Your doctor may want you to reduce gradually the amount you are using before stopping completely. Stopping this medicine may cause withdrawal side effects such as vomiting, sweating, and dizziness.. Anticholinergics and antispasmodics may cause some people to have blurred vision. Make sure your vision is clear before you drive or do anything else that could be dangerous if you are not able to see well. These medicines may also cause your eyes to become more sensitive to light than they are normally. Wearing sunglasses may help lessen the discomfort from bright light.. These medicines, especially in high doses, may ...
Metastatic Squamous Neck Cancer With Occult Primary Squamous Cell Carcinoma Recurrent Metastatic Squamous Neck Cancer With Occult Primary Recurrent Salivary Gland Cancer Recurrent Squamous Cell Carcinoma of the Hypopharynx Recurrent Squamous Cell Carcinoma of the Larynx Recurrent Squamous Cell Carcinoma of the Lip and Oral Cavity Recurrent Squamous Cell Carcinoma of the Nasopharynx Recurrent Squamous Cell Carcinoma of the Oropharynx Recurrent Squamous Cell Carcinoma of the Paranasal Sinus and Nasal Cavity Recurrent Verrucous Carcinoma of the Larynx Recurrent Verrucous Carcinoma of the Oral Cavity Salivary Gland Squamous Cell Carcinoma Stage III Salivary Gland Cancer Stage III Squamous Cell Carcinoma of the Hypopharynx Stage III Squamous Cell Carcinoma of the Larynx Stage III Squamous Cell Carcinoma of the Lip and Oral Cavity Stage III Squamous Cell Carcinoma of the Nasopharynx Stage III Squamous Cell Carcinoma of the Oropharynx Stage III Squamous Cell Carcinoma of the Paranasal Sinus and Nasal ...
To determine the safety and efficacy (viral load suppression and cluster of differentiation 4 [CD4] changes) of a simple, once-daily (QD) antiretroviral (ARV) regimen consisting of a fixed-dose combination tablet containing Truvada combined with the protease inhibitor atazanavir (ATV) boosted with ritonavir (ATV/r).. To evaluate fasting glucose, insulin, C peptide and lipid panel (total cholesterol, high and low density lipoprotein cholesterol (HDL, LDL), and serum triglycerides) in subjects receiving Truvada and boosted atazanavir.. To evaluate adherence to a QD ARV regimen of Truvada and boosted atazanavir.. To evaluate steady-state plasma pharmacokinetics (PK) of Truvada and atazanavir in study subjects receiving Truvada and boosted atazanavir. ...
  • Bepridil (trade name Vascor ) is an amine calcium channel blocker once used to treat angina . (wikipedia.org)
  • Here, we show that four chemically divergent approved drugs reported to inhibit Ebolavirus infection, benztropine, bepridil, paroxetine and sertraline, directly interact with the Ebolavirus glycoprotein. (rcsb.org)
  • It is found in many drugs such as procyclidine and bepridil. (wikipedia.org)
  • 2019. https://nursing.unboundmedicine.com/nursingcentral/view/Davis-Drug-Guide/109104/all/bepridil. (unboundmedicine.com)
  • Our results provide a structural basis for the Ca 2+ -sensitizing effect of bepridil and reveal the details of a distinctive two-stage mechanism for Ca 2+ -regulation by troponin C in cardiac muscle. (tripod.com)
  • This contradicts most recent warning came sprinting out of discussions there that have been ongoing at the fda since 2015 and also includes an updated warning for breastfeeding mothers to refrain from taking her medications containing debrisoquin and bepridil. (elkmeadownursery.com)