calan drug classification
The use of field effect transistors (FETs) in biomedical research has been in rapid progression in recent years. The present study aims to demonstrate a quantitative use of these devices in pharmacological bioassays. FETs were made as a 4 x 4 matrix of gates with a width of 200 microm separating each gate. The surface of the FETs (silicon oxide), covered with a layer of laminin, fibronectin, or nitro cellulose was suitable for cell adhesion. The cultured dissociated cardiac myocytes were spontaneously active within 24 to 48 h after initial plating. Simultaneous intracellular patch clamp recordings were used to verify the electrophysiological signals of cells that were coupled to the gates. All positive chronotropes (isoproterenol, norepinephrine) and negative chronotropes (verapamil, carbamylcholine, SDZ PCO400) showed their characteristic effects on heart cells in terms of changes of beat frequency. As the myocytes were in a complete syncitium on each FET, the cells need not be directly coupled to the gate in order to detect any ionic changes. This enables global cellular responses to be analyzed. The system also offers an opportunity to study the interconnections and communications between different cells. Furthermore, the changes of signal shapes in the presence of different agents could also be detected. The present study demonstrates how versatile and sensitive this recording system is in distinguishing different ionic signal shapes. The authors believe that this system has the potential to replace some currently employed in vitro methods, offering an alternative, which can substantially reduce animal use in pharmacological experiments.
We studied the interaction between the multidrug transporter, P-glycoprotein, and two compounds that interact with it: vinblastine, a classical substrate of the pump, and verapamil, a classical reverser. Steady-state levels of accumulation of these two drugs were determined in a multidrug resistant P388 leukemia cell line, P388/ADR. The time course of accumulation of these drugs, and the effect of energy starvation and the presence of chloroquine on the level of their steady-state accumulation were quite disparate. Vinblastine inhibited the accumulation of verapamil whereas it enhanced the accumulation of daunomycin, another classic substrate of P-glycoprotein. Verapamil did not compete with the intracellular binding sites of vinblastine. In all these aspects, vinblastine behaved as a typical substrate of P-glycoprotein but verapamil did not. Our data suggest that verapamil is a reverser of P-glycoprotein but that its intracellular accumulation is not affected by this membrane-bound transporter.
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Recent data suggest that endothelin (ET) production is enhanced in coronary atherosclerotic lesions. In several studies, an anti-atherosclerotic effect has been attributed to calcium-channel antagonists. This study aimed to investigate whether ET release from cultured human coronary artery smooth muscle and endothelial cells is influenced by the calcium-channel antagonists diltiazem and verapamil. Coronary plaque smooth-muscle cells (SMCs) were isolated from primary stenosis plaque material. Normal coronary smooth muscle and endothelial cells were obtained from organ donors. Addition of diltiazem (5, 15, 25, 50, or 100 micrograms/ml) and verapamil (0.25, 2.5, 25, 50, or 75 micrograms/ml) to the culture medium induced in all three cell types a dose-dependent reduction in ET secretion (coronary plaque SMCs: diltiazem 98.1 +/- 1.5, 94.9 +/- 5.0, 82.0 +/- 6.4**, 63.3 +/- 3.7***, 38.9 +/- 2.4***; control 108.4 +/- 2.8; verapamil 97.0 +/- 7.7, 91.9 +/- 5.5, 67.3 +/- 4.5**, 30.6 +/- 3.0***, 27.6 +/- 2.2***; control 103.4 +/- 6.1 pg/10(4) cells, n = 6; normal coronary SMCs: diltiazem 9.6 +/- 0.7, 8.7 +/- 0.6, 5.4 +/- 0.5***; 3.7 +/- 0.5***, 3.2 +/- 0.4***; control 10.7 +/- 0.5; verapamil 10.3 +/- 0.9, 10.0 +/- 0.7, 6.6 +/- 0.5***, 4.0 +/- 0.3***, 3.0 +/- 0.3***; control 11.1 +/- 0.6 pg/10(4) cells, n = 6; means +/- SEM, **p < 0.01, ***p < 0.001 vs. control). These data suggest that ET release from cultured coronary smooth muscle and endothelial cells is decreased by diltiazem and verapamil. In further studies, it remains to be elucidated whether the local application of diltiazem or verapamil might have a beneficial effect on the progression of coronary atherosclerosis.
calan 180 mg
Hypotensive drugs can normalize blood pressure and control it for a long time but their effect has some specific features. In hypertension of the 2-3 degree, beta-blockers are more effective than blockers of Ca channels, ACE, diuretics and nitroglycerin. Hypertensive patients on beta-adrenergic drugs maintenance have sometimes hypertensive crises which should be managed with nitroglycerin, ACE drugs (enap, as a rule) and diuretics (less frequently).
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Effects of beta-blockers (propranolol, penbutolol) and calcium antagonists (nifedipine, verapamil, diltiazem) were studied in 73 patients with hypertrophic cardiomyopathy (HC). Clinical data, ECG and echo-CG findings were assessed. It was found that beta-adrenoblockers and calcium antagonists improve quality of life in one-third of the patients. Penbutolol and nifedipine did so in half of the patients. Neither beta-adrenoblockers nor calcium antagonists decrease myocardial hypertrophy. Calcium antagonists may result in lowering of myocardial contractility while beta-adrenoblockers may increase the ejection fraction. Diltiazem produced a positive effect on diastolic function but had many side effects. Nifedipine increased lethality compared with verapamil and propranolol.
calan dosage forms
The aim of the study was to investigate comparative contractility of isolated radial artery segments (n = 50). Phosphodiesterase inhibitor (papaverine) was used in 15 segments; dihydropyridine calcium channel antagonist (adalat) was used in 12 segments; calmodulin inhibitor (aminazine) was used in 13 segments; and "nitromixture" (5 mg verapamil hydrochloride, 2.5 mg nitroglycerine, 500-UN heparin, and 300 mL isosmotic Krebs solution) was used in 10 segments. Effect of hyposmotic solution for the morphometric properties of radial artery was analyzed in 22 arterial segments. The data didn't show statistical differences between drugs: "nitromixture" decreased tone by 100 ± 2% (n = 10), papaverine by 100 ± 11% (n = 15), adalat by 95 ± 6.1% (n = 12) and aminazine by 92 ± 11.3% (n = 13) (p > 0.05). The most effective drug in duration was adalat (n = 12, 90 ± 6.5 minutes) versus "nitromixture" (n = 10, 60 ± 9.3 minutes), papaverine (n = 15, 60 ± 4.3 minutes) and aminazine (n = 13, 50 ± 3.2 minutes) (p < 0.05).
The purpose of this study was to characterize blood-brain barrier (BBB) transport of oxycodone, a cationic opioid agonist, via the pyrilamine transporter, a putative organic cation transporter, using conditionally immortalized rat brain capillary endothelial cells (TR-BBB13). Oxycodone and [3H]pyrilamine were both transported into TR-BBB13 cells in a temperature- and concentration-dependent manner with Km values of 89 and 28 microM, respectively. The initial uptake of oxycodone was significantly enhanced by preloading with pyrilamine and vice versa. Furthermore, mutual uptake inhibition by oxycodone and pyrilamine suggests that a common mechanism is involved in their transport. Transport of both substrates was inhibited by type II cations (quinidine, verapamil, and amantadine), but not by classic organic cation transporter (OCT) substrates and/or inhibitors (tetraethylammonium, 1-methyl-4-phenylpyridinium, and corticosterone), substrates of OCTN1 (ergothioneine) and OCTN2 (L-carnitine), or organic anions. The transport was inhibited by metabolic inhibitors (rotenone and sodium azide) but was insensitive to extracellular sodium and membrane potential for both substrates. Furthermore, the transport of both substrates was increased at alkaline extracellular pH and decreased in the presence of a protonophore (carbonyl cyanide-p-trifluoromethoxyphenylhydrazone). Intracellular acidification induced with ammonium chloride enhanced the uptakes, suggesting that the transport is driven by an oppositely directed proton gradient. The brain uptake of oxycodone measured by in situ rat brain perfusion was increased in alkaline perfusate and was significantly inhibited by pyrilamine. These results suggest that blood-brain barrier transport of oxycodone is at least partly mediated by a common transporter with pyrilamine, and this transporter is an energy-dependent, proton-coupled antiporter.
Myocardial ischemia (MI) is a worldwide epidemic. Compound Danshen Tablets (CDTs), an herbal compound preparation, are widely used to treat MI in China. In this study, we aimed to explore novel biomarkers to increase the understanding of MI and investigate therapeutic mechanisms of CDT by using a metabolomic approach. Plasma extracts from sham, MI model, CDT- and western medicines (isosorbide dinitrate, verapamil, propranolol, captopril, and trimethazine)-treated rats were analyzed by ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS). The orthogonal partial least square (OPLS) model was built to find metabolites expressed in significantly different amounts between MI and sham rats. Meanwhile, partial least squares discriminant analysis (PLS-DA) was used to investigate CDT's protective effects. The results showed that CDT presented protective effects on MI by reversing potential biomarkers to sham levels, especially for the four metabolites in the pathway of purine metabolism (hypoxanthine, xanthine, inosine and allantoin).
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Peripheral arterial disease (PAD) causes considerable morbidity and mortality. Hypertension is a risk factor for PAD. Treatment for hypertension must be compatible with the symptoms of PAD. Controversy regarding the effects of beta-blockade for hypertension in patients with PAD has led many physicians to stop prescribing beta-blockers. Little is known about the effects of other classes of anti-hypertensive drugs in the presence of PAD. This is an update of a Cochrane review first published in 2003.
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The importance of cytosolic free calcium level intracellular Ca(2+), [Ca(2+)]i, in neutrophil activation prompted us to investigate changes in [Ca(2+)]i of neutrophils caused by methylmercury (MeHg), which has been shown to have immunomodulatory properties. We have shown in this paper that MeHg increased [Ca(2+)]i in the mouse peritoneal neutrophil. The L-type calcium channel blocker verapamil can decrease the elevated [Ca(2+)]i caused by 10 microM MeHg, suggesting that Ca(2+)-influx through L-type Ca(2+) channel mediates the effect of MeHg. Moreover, MeHg potently decreased nitric oxide (NO) production but also the protein and mRNA level of NO synthase induced by lipopolysaccharide. Both verapamil (1 microM) and H-89 (10 microM) can antagonize the inhibitory effect of MeHg (10 microM) on NO production. These findings lead us to conclude that MeHg inhibits NO production mediated at least in part by Ca(2+)-activated adenylate cyclase-cAMP-protein kinase A pathway.
calan generic name
P-glycoprotein functions as an ATP-driven efflux pump for antitumor agents. C219 is a monoclonal antibody which recognizes regions near both ATP binding domains in each half of P-glycoprotein. In this study, we have demonstrated that C219 inhibits the ATPase activity of P-glycoprotein based on the following findings: 1) the inhibition of total ATPase activity by C219 was selective to P-glycoprotein-positive membranes; 2) the C219-sensitive fraction of ATPase correlated the expression of P-glycoprotein; and 3) modulators of P-glycoprotein ATPase, verapamil and cyclosporin A, affected the C219-sensitive fraction of ATPase. The photolabeling of P-glycoprotein with 8-azido-[alpha-32P]ATP was inhibited by C219, suggesting that the inhibition of ATP binding by C219 reduced the activity. Since C219 interacts with P-glycoprotein ATPase, C219 might become a useful tool for studying the role of P-glycoprotein ATPase.
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Arterial tone in muscular conduit arteries may influence pressure wave reflection through changes in diameter and pulse wave velocity. We examined the relative specificity of vasodilator drugs for radial artery and forearm resistance vessels during intrabrachial arterial infusion. The nitric oxide (NO) donors, nitroglycerine and nitroprusside, and brain natriuretic peptide were compared with the α-adrenergic antagonist phentolamine, calcium-channel antagonist verapamil, and hydralazine. Radial artery diameter was measured by high resolution ultrasound, forearm blood flow by strain gauge plethysmography, and pulse wave velocity by pressure recording cuffs placed over the distal brachial and radial arteries. Norepinephrine was used to constrict the radial artery to generate a greater range of vasodilator tone when examining pulse wave velocity. Despite dilating resistance vasculature, phentolamine and verapamil had little effect on radial artery diameter (mean dilation <9%). By contrast, for comparable actions on resistance vessels, nitroglycerine and nitroprusside but not brain natriuretic peptide had powerful actions to dilate the radial artery (dilations of 31.3 ± 3.6%, 23.6 ± 3.1%, and 9.8 ± 2.0% for nitroglycerine, nitroprusside, and brain natriuretic peptide, respectively). Changes in pulse wave velocity followed those in arterial diameter irrespective of the signaling pathway used to modulate arterial tone (R=-0.89, P<0.05). Basal tone in human muscular arteries is relatively unaffected by α-adrenergic or calcium-channel blockade, but is functionally or directly antagonized by NO donors. The differential response to NO donors suggests that there is potential to manipulate the downstream pathway to confer greater specificity for large arteries with a resultant decrease in pressure wave reflection and systolic blood pressure.
Rottlerin has been widely accepted as a specific inhibitor of protein kinase C delta (PKC delta); however, recent data suggest that the specificity of this compound become a question. Herein, we address this issue using a lens organ culture system, as PKC delta might regulate the gap junction permeability in lens. Interestingly, we found that rottlerin induced the degradation of connexin50 more rapidly than that of PKC delta. Furthermore, comparison of rottlerin with a protonophore, carbonylcyanide-4-(trifluoromethoxy)-phenylhydrazone (FCCP) that shares many characteristics with rottlerin, showed that both rottlerin and FCCP dramatically increased lens weight over time. This increase in lens weight was partially reversed by depletion of extracellular calcium with ethyleneglycoltetraacetic acid (EGTA) or by blocking L-type calcium channels with verapamil, suggesting rottlerin may induce calcium influx. Indeed, the rapid degradation of connexin50 (but not PKC delta) induced by rottlerin and FCCP was blocked by EGTA. In addition, rottlerin and FCCP also induced degradation of connexin46, filensin, vimentin and CP49. In order to determine whether this protein degradation is associated with the decrease of ATP due to uncoupling mitochondria by rottlerin, ATP content in lenses with different treatments were examined. The result indicated that EGTA had no effect on lens ATP content. Taken together, these data suggest that rottlerin, like FCCP, induces calcium influx, leading to protein degradation and cleavage in the lens, and that this effect is unrelated to the inhibition of PKC delta. Thus, extreme caution must be taken when considering use of rottlerin as a PKC delta inhibitor.
The obstruction was at first treated with verapamil, later with sotalol. The pericardial effusion was interpreted as part of a postcardiotomy syndrome. The effusion regressed under steroid administration, and the LVOT and mitral regurgitation also decreased. A provocation test five months postoperatively no longer brought about an outflow gradient. The good results were still present 12 months postoperatively.
We investigated anaerobic threshold (< theta(L)) gas exchange kinetics and maximal oxygen uptake (VO2,max) among older men with reduced left ventricular end-diastolic filling (LVDF). Ten men (mean age, 73 years) with LVDF impairment and low fitness, but without other cardiovascular dysfunction were studied. Treatments compared to control included: 5 days, high intensity exercise training protocol; 5 days, calcium channel blockade (240 mg verapamil); 21 days, detraining/washout; and 5 days, combined treatments. Results indicated no changes in resting left ventricular systolic function with any treatment. Significant resting diastolic function changes included increased early:late flow velocity (control, 0.87; training, 1.28; verapamil, 1.32), and a decreased isovolumic relaxation time (control, 0.10 s; training, 0.08 s; verapamil, 0.08 s). The combined treatments were not additive. Sub-threshold oxygen uptake kinetics (tauVO2, s) were significantly faster following either training or verapamil (tauVO2,control, 62+/-12; tauVO2,training, 44+/-9; tauVO2,verapamil, 48+/-10) and combined treatments (tauVO2, 41+/- 8). V O2,max (ml kg(-1) min(-1)) was significantly increased (control, 21.8+/-2.2; training, 27.3+/-2.2; verapamil, 25.2+/-3.4; combined treatments, 26.9+/-2.3). Increasing ventricular preload with either exercise training or calcium channel blockade was coincident with faster tauVO2 and increased VO2,max.
calan eeze review
Male out-patients excluding those taking other drugs known to raise PRL, renal failure and known primary hypothyroidism (1265 eligible subjects). Control subjects were drawn from eligible out-patients not taking verapamil.
Many patients with potentially life-threatening cardiac conditions presenting with transient loss of consciousness are referred first to neurology clinics. Therefore, neurologists must remain competent to interpret electrocardiograms (ECGs) and in particular be able to identify those rare conditions that predict sudden cardiac death. A 12-lead ECG is cheap and readily available, and can give essential diagnostic information. Here the authors review abnormalities in, and indications for, the ECG in neurological practice.
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Peyronie's disease (PD) is a connective tissue disorder characterized by a fibrous plaque involving the tunica albuginea of the penis. The inelastic fibrous plaque leads to a penile curvature. Several Authors have suggested an immunological genesis of this disease, others have linked PD with Dupuytren's contracture. Signs of this disease are curvature, penile pain, penile deformity, difficulty with coitus, shortening, hinging, narrowing and erectile dysfunction. The natural history of PD and the clinical course can develop from spontaneous resolution of symptoms to progressive penile deformity and impotence. Surgical treatment is indicated when patients fail the conservative medical treatment and however, only in case of disease stabilization with a condition of impossibility of penetration. The medical treatment is indicated in the development stage of PD for at least one year after diagnosis and whenever in case of penile pain. Current non-surgical therapy includes vitamin-E, verapamil, para-aminobenzoate, propoleum, colchicine, carnitine, tamoxifen, interferons, collagenase, hyaluronidase, cortisone, pentoxifylline, superoxide dismutase, iontophoresis, radiation, extracorporeal shock wave therapy (ESWT) and the penile extender. The etiology of this fibrotic disease is not widely known, although in recent years pathophysiological knowledge has evolved and new studies propose the penile trauma as cause of the disease. The penile trauma results in a delamination of the tunica albuginea with a consequent small hematoma, then the process evolves as an inflammation with accumulation of inflammatory cells and production of reactive oxygen species (ROS). In the course of the inflammation, Peyronie's disease occurs due to the activation of nuclear factor kappa-B, that induces the production of inducible nitric oxide synthase (iNOS), with an increase of nitric oxide, leading to increased production of peroxynitrite anion. All these processes result in the proliferation of fibroblasts and myo-fibroblasts and excessive production of collagen between the layers of the tunica albuginea (penile plaque). Referring to the current knowledge of inflammatory and oxidative mechanisms of PD, a possible therapeutic strategy is then analyzed.
Action potential and bipolar electrograms were recorded at epicardial and endocardial sites of coronary-perfused canine RV wedge preparations, together with a pseudo-ECG. The transient outward potassium current agonist NS5806 (5 μM) and the Ca(2+)-channel blocker verapamil (2 μM) were used to pharmacologically mimic the BrS genetic defect.
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This study was to investigate the effect of lovastatin on the bioavailability or pharmacokinetics of verapamil and its major metabolite, norverapamil, in rats. The pharmacokinetic parameters of verapamil and norverapamil in rats were measured after the oral administration of verapamil (9 mg/kg) in the presence or absence of lovastatin (0.3 or 1.0 mg/kg). The pharmacokinetic parameters of verapamil were significantly altered by the presence of lovastatin compared to the control group (given verapamil alone). The presence of lovastatin significantly (p < 0.05, 0.3 mg/kg; p < 0.01, 1.0 mg/kg) increased the total area under the plasma concentration-time curve (AUC) of verapamil by 26.5-64.8%, and the peak plasma concentration (C(max)) of verapamil by 34.1-65.9%. Consequently, the relative bioavailability (R.B.) of verapamil was increased by 1.27- to 1.65-fold than that of the control group. However, there was not significant change in the time to reach the peak plasma concentration (T(max)) and the terminal half-life (t(1/2)) of verapamil in the presence of lovastatin. The AUC and C(max) of norverapamil were significantly (p < 0.05) higher than those of presence of 1.0 mg/kg of lovastatin compared with the control group. However, there was no significant change in the metabolite-parent ratio (M.R.) of norverapamil in the presence of lovastatin. The presence of lovastatin significantly enhanced the oral bioavailability of verapamil. The enhanced oral bioavailability of verapamil may be due to inhibition both of the CYP3A-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or in liver by the presence of lovastatin.
calan drug classification
Calcium channel antagonists (CCAs) may either be divided into the dihydropyridines (e.g. amlodipine, felodipine, isradipine, lacidipine, nilvadipine, nifedipine, nicardipine etc.), the phenylalkylamines (e.g. verapamil) and the benzothiazepines (e.g. diltiazem) according to their chemical structure, or into first generation agents (nifedipine, verapamil and diltiazem) and second generation agents (subsequently developed dihydropyridine-derivatives). Second generation CCAs are characterized by greater selectivity for calcium channels in vascular smooth muscle cells than the myocardium, a longer duration of action and a small trough-to-peak variation in plasma concentrations. Heart failure is characterized by decreased cardiac output resulting in inadequate oxygen delivery to peripheral tissues. Although the accompanying neurohormonal activation, leading to vasoconstriction and increased blood pressure, is initially beneficial in increasing tissue perfusion, prolonged activation is detrimental because it increases afterload and further reduces cardiac output. At the level of the myocyte, heart failure is associated with increased intracellular calcium levels which are thought to impair diastolic function. These changes indicate that the CCAs would be beneficial in patients with heart failure. There has been a strong interest and increasing experience in the use of CCAs in patients with heart failure. Despite potential beneficial effects in initial small trials, findings from larger trials suggest that CCA may have detrimental effects upon survival and cardiovascular events. However, this may not necessarily be a 'class b' effect of the CCAs as there is considerable heterogeneity in the chemical structure of individual agents. Clinical experience with different CCAs in patients with heart failure includes trials that evaluated their effects on hemodynamic parameters, exercise tolerance and on symptomatology. However, the most relevant results are those from randomized clinical trials that assessed mortality as the primary endpoint. First generation CCAs have direct negative inotropic effects and even sustained release formulations have not proved any beneficial effect upon survival. With second generation CCAs, some benefit on hemodynamic parameters has been observed but none on survival, alone or in combination with ACE inhibitors. It is noteworthy that although amlodipine had a neutral effect on morbidity and mortality in large, randomized, placebo-controlled trials in patients with heart failure, the drug was well tolerated. There is no specific indication for CCAs (first or second generation) in patients with systolic heart failure, alone or in combination with ACE inhibitors, but amlodipine may be a considered in the management of hypertension or coronary artery disease in patients with heart failure.
We report on a 6-month-old patient with a right bundle, superior axis tachycardia at 197 beats per minute. The tachycardia was unresponsive to adenosine, propranolol, flecainide, or amiodarone, or synchronized cardioversion. Overdrive atrial pacing terminated the tachycardia and since initiating verapamil, no recurrences of his tachycardia have occurred.
calan 120 mg
1) Ca2+ influx through the L-type channels may be the primary source of Ca2+ to stimulate in vivo phasic contractions. 2) Phosphatidylinositol hydrolysis enhances the stimulation of in vivo phasic contractions in the normal ileum. In the inflamed ileum, phosphatidylinositol hydrolysis may be essential to stimulate phasic contractions. 3) Inflammation may downregulate the protein kinase C pathway. 4) Ryanodine stimulates phasic contractions by the release of ACh.
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Taken together, these data suggest these cells will be useful for evaluation of rat Abcb1a-mediated transport and for evaluation of species-specific P-glycoprotein-mediated transport.
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Verapamil effectively decreased the lens calcium concentration, which is accepted as the key element in radiation cataractogenesis. It is therefore concluded that verapamil may reduce the risk of radiation-induced cataract formation.
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Data were extracted by one author (DAL) and checked by the other (GYHL). Potentially eligible studies were excluded when the results presentation prevented adequate extraction of data and enquiries to authors did not yield raw data.
Our observations are consistent with the Hoechst 33342 dye efflux assay isolating a stem cell enriched population which can be further sub-fractionated by CD133 selection. Moreover, the loss of the CDK inhibitor in malignancy is consistent with the hypothesis that neoplastic change originates in the stem cell compartment.
In the present study we assess that the etiology of digitalis intoxication. We try to identify factors and intensity of each association. One thousand fifty patients form Havana City, Cuba were selected, under digitalis therapy. Two groups were made Cases and Controls. Each patient was evaluated by direct interview. There was a significative association (P < 0.01) among digitalis intoxication and; older persons who use high doses of digoxin, other risk factors were underweight, lack of potassium supplement, some associated diseases, combination therapy between digoxin, and furosemide, thyazides, dipyridamole, amiodarone, quinidine, nifedipine or verapamil, cigar smoking, alcohol intake and prior history of digitalis intoxication. The odds ratio (OR) was calculated for each association. We conclude: some factors are responsible for digitalis intoxication, each one contribute partially.
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The uptake of Tc-TF was examined in the MCF7/WT cell line, a wild-type breast cancer cell line that does not exhibit MDR, and its subclonal etoposide resistant cell line MCF7/VP, which expresses high levels of MRP1, one of the multi-drug resistance associated proteins (MRPs), in the presence of increasing concentrations of verapamil, a classical MDR modulator. In the absence of verapamil, MCF7/VP cells showed significantly lower Tc-TF uptake than did MCF7/WT cells, indicating that Tc-TF is a substrate for MRP1. The presence of verapamil enhanced the uptake of Tc-TF in MCF7/VP cells. On the other hand, verapamil also increased tracer uptake in MCF7/WT cells, which was readily appreciated when the uptake values were corrected by viable cell numbers: an approximately 100% increase of Tc-TF uptake was observed in comparison with that in the absence of verapamil in viable MCF7/WT cells whereas a 100-200% increase occurred in viable MCF7/VP cells. In addition, verapamil prolonged the retention of radioactivity in both MCF7/WT cells and MCF7/VP cells.
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Ec.Cr caused atropine-sensitive stimulatory effect in isolated guinea-pig ileum at 3-10mg/ml. In rabbit jejunum preparations, Ec.Cr relaxed spontaneous and K+ (80 mM)-induced contractions as well as shifted Ca++ curves to right, like verapamil. Ec.Cr (3-100mg/kg) induced fall in the arterial blood pressure (BP) of anaesthetized rats, partially blocked in atropinized animals. In endothelium-intact rat aorta, Ec.Cr relaxed phenylephrine (1 microM)-induced contractions, partially antagonized by atropine and also inhibited K+ (80 mM) contractions. In guinea-pig atria, Ec.Cr exhibited a cardio-depressant effect. Ec.Cr (1-10mg/kg) produced diuresis in rats, accompanied by a saluretic effect. It enhanced pentobarbital-induced sleeping time in mice. Bio-assay directed fractionation revealed the separation of spasmogenic and spasmolytic components in the aqueous and organic fractions respectively.