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At least 649 records · Page 36Linked to original sources
PubMed2004

Choline pivaloyl esters improve in rats cognitive and memory performances impaired by scopolamine treatment or lesions of the nucleus basalis of Meynert.

The effects of two choline pivaloyl esters, [2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium iodide (1) and [2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium 2,2-dimethylpropionate (2), on learning and memory impairments induced in rats by scopolamine or lesions of nucleus basalis magnocellularis (NBM) have been evaluated by object recognition and Morris water maze tests in comparison with Tacrine (THA). Both 1 and 2 restored discrimination in object recognition test for assessing working-episodic memory and improved spatial memory in scopolamine or NBM-lesioned rats as well. The positive effects produced by 1 and 2 on cognitive and memory deficits were well comparable with those evoked by THA, used as reference compound.

Acetylcholinesterase↗
PubMed2006

Anti-proliferative properties of prenylated flavonoids from hops (Humulus lupulus L.) in human prostate cancer cell lines.

Chalcones xanthohumol (X) and desmethylxanthohumol (DMX), present in hops (Humulus lupulus L.), and the corresponding flavanones isoxanthohumol (IX, from X), 8-prenylnaringenin (8-PN, from DMX), and 6-prenylnaringenin (6-PN, from DMX), have been examined in vitro for their anti-proliferative activity on human prostate cancer cells PC-3 and DU145. X proved to be the most active compound in inhibiting the growth of the cell lines with IC50 values of 12.3+/-1.1 microM for DU145 and 13.2+/-1.1 microM for PC-3. 6-PN was the second most active growth inhibitor, particularly in PC-3 cells (IC50 of 18.4+/-1.2 microM). 8-PN, a highly potent phytoestrogen, exhibited pronounced anti-proliferative effects on PC-3 and DU145 (IC50 of 33.5+/-1.0 and 43.1+/-1.2 microM, respectively), and IX gave comparable activities (IC50 of 45.2+/-1.1 microM for PC-3 and 47.4+/-1.1 microM for DU145). DMX was the least active compound. It was evidenced for the first time that this family of prenylated flavonoids from hops effectively inhibits proliferation of prostate cancer cells in vitro.

Cell Line, Tumor↗
PubMed2004

Xanthohumol metabolites in faeces of rats.

Xanthohumol (1), isolated from hop, was fed to rats in a dose of 1000 mg kg(-1) body weight. The faeces of the animals were collected after 24 and 48 h and analysed for metabolites of 1. Approximately 89% of the recovered flavonoid-compounds consisted of unchanged 1. Sixteen metabolites and six previously known metabolites were isolated and characterized by coupling techniques (HPLC-NMR, HPLC-MS and HPLC-DAD). Their structures were elucidated by spectroscopic methods, especially using NMR spectroscopy. Twenty metabolites had a modified chalcone structure and two metabolites were flavanone derivatives.

Animals↗
PubMed2004

Xanthohumol and related prenylflavonoids from hops and beer: to your good health!

Xanthohumol (3'-[3,3-dimethyl allyl]-2',4',4-trihydroxy-6'-methoxychalcone) is the principal prenylated flavonoid of the female inflorescences of the hop plant ('hops'), an ingredient of beer. Human exposure to xanthohumol and related prenylflavonoids, such as 8-prenylnaringenin and isoxanthohumol, is primarily through beer consumption. Xanthohumol has been characterized a 'broad-spectrum' cancer chemopreventive agent in in vitro studies, while 8-prenylnaringenin enjoys fame as the most potent phytoestrogen known to date. These biological activities suggest that prenylflavonoids from hops have potential for application in cancer prevention programs and in prevention or treatment of (post-)menopausal 'hot flashes' and osteoporosis. Xanthohumol and 8-prenylnaringenin are metabolized into many flavonoid derivatives with modified 3,3-dimethyl allyl (prenyl) moieties. Xanthohumol is formed in lupulin glands by a specialized branch of flavonoid biosynthesis that involves prenylation and O-methylation of the polyketide intermediate chalconaringenin. Although a lupulin gland-specific chalcone synthase is known, the aromatic prenyltransferase and O-methyltransferase participating in xanthohumol have not been identified. The prenylflavonoid pathway is a possible target for breeding or biotechnological modification of hops with the aim of increasing xanthohumol levels for beer brewing and 8-prenylnaringenin levels for pharmaceutical production.

Anticarcinogenic Agents↗
PubMed2004

Lack of in vitro protection by a common sunscreen ingredient on UVA-induced cytotoxicity in keratinocytes.

As an extension of our previous investigations on sunscreen ingredients, the present work was aimed at assessing the possible protective effects of a common UVA-absorbing agent, Parsol 1789 (4-tert-butyl-4'-methoxydibenzoylmethane) in contact with human keratinocytes under UVA illumination. Cell viability was evaluated by determining lactate dehydrogenase (LDH) release, uptake of propidium iodide and fluorescein diacetate, total protein content and percentage of cell detachment. Apoptosis was detected by recognition of translocated phosphatidylserine using annexin V-FITC uptake. Oxidative stress was evaluated through the carboxy-H2DCFDA assay while the total oxyradical scavenging capacity (TOSC) assay was used for determining the total antioxidant capacity level in these cells. Lipid peroxidation was also assessed by checking hydroperoxide (HP) levels. The results obtained show that UVA exposure induces significant cell mortality, decrease in protein concentration, release of LDH, increase in apoptosis, oxidative stress and lipid peroxidation with a concomitant reduction in the response of the antioxidant cellular defense system. The presence of 10 microM Parsol 1789 did not minimize these UVA-induced effects, on the contrary, for some parameters measured such as lipid hydroperoxides, there was a significant enhancement. Furthermore, the presence of glutathione (GSH) alone decreased the level of ROS and lipid hydroperoxides, but in combination with Parsol 1789, this protective effect was reduced. The overall results indicate that the compound does not protect these cells from UVA exposure under our experimental conditions confirming previous findings on the lack of photoprotective efficiency of this sunscreen in contact with biologically relevant molecules. However, the biological role and significance of these results to the consequences of sunscreen use in humans are not known, hence extrapolation from laboratory experiments must be done with caution.

Annexin A5↗
PubMed1984

Propafenone for refractory ventricular arrhythmias: correlation with drug plasma levels during long-term treatment.

The efficacy of propafenone, a new antiarrhythmic drug, was studied in 21 patients with ventricular arrhythmias refractory to previous antiarrhythmic medications. Group A included 10 patients with chronic ventricular premature complexes (VPCs), 6 of whom had nonsustained ventricular tachycardia (VT) and 4 of whom had recurrent, sustained VT; all received propafenone, 900 mg/day. Group B included 11 patients, all with chronic VPCs, 9 of whom had nonsustained VT and 5 of whom had sustained VT; all received propafenone, 450 mg/day. Drug efficacy was evaluated as a 70% or greater reduction in VPC frequency with complex VPC abolition in ambulatory monitoring and suppression of nonsustained VT and sustained VT during a follow-up period up to 154 +/- 58 days in group A and 96 +/- 42 days in group B. Drug plasma levels were measured during chronic therapy in pharmacologic steady state. In group A, propafenone reduced the frequency of chronic VPCs in 9 patients and abolished nonsustained VT in 4 of 6 and sustained VT in 3 of 4; in group B, propafenone reduced the frequency of chronic VPCs in 6 patients and abolished nonsustained VT in 6 of 9 and sustained VT in 3 of 5. Two patients with recurrences of sustained VT in this group were later successfully treated with propafenone, 900 mg/day; overall, 8 of 9 patients with recurrences of sustained VT were successfully treated with 900 mg/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Clinical pharmacology of propafenone: pharmacokinetics, metabolism and concentration-response relations.

Propafenone is a promising new antiarrhythmic agent marketed in Europe for the past 7 years. The drug is remarkable for great interindividual variability in its pharmacokinetic and pharmacodynamic properties. Propafenone undergoes extensive presystemic clearance that appears to be saturable, with bioavailability increasing as dosage increases. The drug is highly protein bound. Elimination half-life is 5 to 8 hours in most patients, although a range of 2 to 32 hours has been reported. Propafenone slows intracardiac conduction in a concentration-dependent manner. It is a weak beta-adrenergic blocker, but this property is of uncertain clinical significance. The major metabolic pathway for propafenone begins with aromatic ring hydroxylation, a pathway that may be determined by genetic factors.

Anti-Arrhythmia Agents↗
PubMed1984

Block of sodium currents by antiarrhythmic agents: analysis of the electrophysiologic effects of propafenone in heart muscle.

Antiarrhythmic efficacy may result from the ability of class I drugs to depress cardiac sodium currents (INa). Drug interaction with sodium channels could underlie INa blockade and can be defined in terms of the law of mass action which is modulated by many experimental conditions. As exemplified by propafenone, INa blockade occurs in 2 forms: tonic and phasic inhibition. Steady-state phasic (or use-dependent) INa blockade is determined by the interstimulus interval and reflects a labile equilibrium between drug occupancy of and dissociation from a channel-associated binding site. The drug-specific kinetics of the latter process together with the duration of the diastole determine the accumulation of blocked, that is, nonconductive, channels. Several lines of evidence suggest that tonic and phasic INa blockade are not 2 different manifestations of the same molecular event. Decreasing resting potential or reducing extracellular Na+ concentration strongly accentuates tonic blockade, whereas phasic blockade is comparatively less affected by these interventions. Consistent with this special susceptibility are individual concentration-response relations characterized by different apparent dissociation constants and Hill (nH) coefficients. Cardiac sodium channels presumably possess less drug affinity under resting conditions. Their binding of drugs no longer seems to be an allosteric process during repetitive stimulation, but could be characterized by 1:1 stoichiometry.

Action Potentials↗
PubMed1984

Effect of propafenone on left ventricular ejection fraction.

The effects of orally administered propafenone on ejection fraction (EF) determined by radionuclide angiography were studied in 2 groups of patients receiving different dosing regimens. Fourteen group A patients had no clinical evidence of left ventricular (LV) dysfunction and were not receiving digoxin therapy. In this group a mean daily dosage of 879 mg resulted in a decrease in resting LVEF from 52 +/- 9% to 48 +/- 11% (p less than 0.05). Eight group B patients had clinical radionuclide evidence of LV dysfunction and were receiving digoxin therapy. In this group, a daily dosage of propafenone of 600 mg/day resulted in no significant change in LVEF. No clinically significant effects on cardiac compensation were evident in either group. These data suggest a negative inotropic effect that is either related to propafenone dosage or at least partially attenuated by digoxin therapy. Further studies are necessary to define precisely the effects of propafenone on LV function.

Aged↗
PubMed1984

Antiarrhythmic and electrophysiologic effects of oral propafenone.

Twenty-six patients had ventricular tachycardia initiated at control electrophysiologic study and had a repeat study during oral propafenone therapy. Ten patients had had sustained ventricular tachycardia, 6 cardiac arrest and 10 symptomatic, nonsustained ventricular tachycardia. Twenty-two patients had heart disease, 18 of whom had coronary artery disease. During propafenone therapy, ventricular tachycardia could not be initiated during programmed ventricular stimulation in 5 patients, and in 21 patients the cycle length of induced ventricular tachycardia increased from 246 +/- 42 ms at control to 355 +/- 96 ms (p less than 0.001). Seventeen patients were discharged with propafenone therapy and have been followed for a mean of 11 months. No symptomatic ventricular tachycardia recurred in the 5 patients without inducible ventricular tachycardia during drug treatment. Six of 12 patients with inducible ventricular tachycardia during the drug study have remained asymptomatic. In conclusion, propafenone substantially prolongs the cycle length of ventricular tachycardia, and initiation of ventricular tachycardia by programmed ventricular stimulation at drug study does not preclude a favorable clinical outcome.

Adult↗
PubMed1984

Effect of propafenone in the Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up.

The electrophysiologic and long-term efficacy of propafenone, a relatively new antiarrhythmic agent, was assessed in 47 patients with accessory pathways. In 23 patients (group I), the electrophysiologic effects were assessed initially. In 19 patients in this group and in 24 additional patients (group II), long-term therapy with oral propafenone was initiated. The mean age of the patients was 38 years in group I and 41 years in group II. The duration of a history of tachycardia in both groups was 12 years (mean); 14 patients previously had had attacks of syncope. During the electrophysiologic study in group I, propafenone did not change the spontaneous sinus rate. Corrected sinus node recovery time as well as the AH interval, HV time, QRS duration and effective refractory periods of the atria and ventricles was significantly prolonged. The effective refractory period of the accessory pathway increased from 238 to 322 ms (p less than 0.02). The 1:1 conduction capacity of the accessory pathway decreased from 231 to 176 beats/min (mean; p less than 0.01). Complete block in the anterograde direction occurred in 6 patients. The shortest RR interval during atrial fibrillation increased from 232 to 303 ms (p less than 0.05). The retrograde refractory period of the accessory pathway was prolonged from 245 to 295 ms (p less than 0.01). Complete or 2:1 retrograde block during basic drive occurred in 3 patients and 1 patient, respectively. In 6 of 15 patients, propafenone made sustained supraventricular tachycardia (SVT) either no longer inducible or nonsustained. The cycle length of induced SVT increased from 324 to 395 ms (p less than 0.01). During long-term administration (follow-up duration 2 to 3 years), 17 of 43 patients did not report any episode of symptomatic tachycardia. In another 18 patients, tachycardia was rare, slower and self-terminating. In only 3 patients, the frequency and severity of attacks had not changed. One patient with dilated cardiomyopathy died suddenly. Side effects necessitating discontinuation of medication were observed in only 2 patients. The remaining side effects, if present, were tolerated, and dosage dependent. In conclusion, propafenone is an effective and well-tolerated antiarrhythmic agent in the long-term management of patients with the Wolff-Parkinson-White syndrome.

Adolescent↗
PubMed1984

Propafenone treatment of recurrent ventricular tachycardia: comparison of continuous electrocardiographic recording and electrophysiologic study in predicting drug efficacy.

Propafenone was administered to 29 patients who had multiple episodes of recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) despite previous antiarrhythmic therapy. All patients had 24-hour continuous electrocardiographic recording and electrophysiologic study in a drug-free control state and while receiving maximum doses of propafenone. During propafenone treatment, the mean frequency of ventricular premature complexes (VPCs) decreased 74% (p less than 0.05). There was more than an 83% decrease in VPC frequency in 17 of 29 patients, and 11 patients had 99 to 100% decreases. Propafenone prevented VT induction at electrophysiologic study in 6 patients, whereas another 12 patients were judged to have satisfactory electrophysiologic responses on the basis of slower VT rates and absence of hemodynamic compromise during VT. After long-term treatment from 2 to 26 months, 9 patients continued propafenone without evidence of recurrent arrhythmia. Six of these 9 patients had not VT induction at electrophysiologic study while receiving propafenone. The decrease in VPC frequency produced by propafenone was a poor predictor of a successful electrophysiologic study and of long-term therapy. In conclusion, propafenone has potential as an effective antiarrhythmic agent, but better methods to stratify risk for recurrence of VT and VF are needed.

Adult↗
PubMed1984

Double-blind placebo-controlled evaluation of propafenone in suppressing ventricular ectopic activity.

The effectiveness of oral propafenone in treating ventricular premature complexes (VPCs) was assessed with a single-blind dose-ranging trial followed by a double-blind, randomized, crossover comparison of propafenone and placebo. Patients subsequently were treated with propafenone for up to 24 months. During dose ranging, the average of individual percent suppressions was 83% at the largest dose (300 mg/8 hours). During the double-blind trial, the effectiveness of propafenone was confirmed, with 7 of 12 patients achieving greater than or equal to 80% reduction in VPCs (p less than 0.05 versus double-blind placebo study). Propafenone was also effective in controlling couplets and nonsustained ventricular tachycardia. Seven patients were treated with propafenone for 24 months, during which effectiveness continued, with mean suppression ranging from 67 to 79% (p less than 0.05 versus initial single-blind placebo). Propafenone prolonged PR and QRS intervals by 16 and 18%, respectively; these prolongations continued during long-term therapy. Propafenone increased serum digoxin levels in 5 of 5 patients (mean increase 83%). Cardiovascular side effects included congestive heart failure (1 patient) and conduction abnormalities (3 patients). Thus, propafenone was effective in the treatment of total and repetitive VPCs. Side effects were few, but congestive heart failure, conduction disturbances and increases in serum digoxin were observed.

Aged↗
PubMed1984

Propafenone: noninvasive evaluation of efficacy.

Propafenone, a new antiarrhythmic drug, was administered to 60 patients with a history of refractory ventricular tachyarrhythmias, including ventricular fibrillation in 16 and ventricular tachycardia (VT) in 44. A noninvasive protocol was followed utilizing ambulatory monitoring and exercise testing for evaluation of drug effect. The protocol involved acute drug testing with 450 mg of propafenone followed by maintenance therapy with 150 to 300 mg t.i.d. for 4 days. The protocol was completed by 57 patients; in 3 patients side effects developed that necessitated discontinuation of the drug before evaluation. When evaluated by monitoring, 34 patients (60%) responded to the drug, with total elimination of runs of VT, a greater than 90% reduction in couplets and a greater than 50% decrease in the frequency of ventricular premature beats. Based on exercise testing, 36 patients (63%) were deemed responders. When both exercise and monitoring were considered, 30 of 57 patients (53%) responded to propafenone. The acute drug test predicted the response to maintenance therapy in 84% of patients. Propafenone did not change left ventricular function in patients with normal ejection fractions (greater than 50%). However, in those with an ejection fraction less than 50%, propafenone significantly reduced this value (34% vs 29%, p less than 0.01). Side effects occurred in 20 patients (33%) and included nausea, congestive heart failure, aggravation of arrhythmia and conduction abnormalities. Eleven patients have continued on propafenone for an average of 16 months with continued efficacy and freedom from side effects.

Adolescent↗
PubMed1984

European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias.

Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Distance dependence of the tryptophan-disulfide interaction at the triplet level from pulsed phosphorescence studies on a model system.

In the present study the distance dependence of tryptophan-disulfide interaction is examined with a view to both utilizing the interaction as a more quantitative indicator of subtle conformational changes in proteins as well as elucidating the interaction mechanism. To examine perturbations specifically at the indole triplet level 2-(3-indolyl)-ethyl phenyl ketone (IEPK) in which excitation is transferred with high efficiency to the triplet state of the indole moiety was employed. Phosphorescence decays of IEPK excited by a laser pulse in 70/30 (vol/vol) ethanolether at 77 K were measured in the presence of various concentrations of simple disulfides. The nonexponential phosphorescence decays arising from a distribution of fixed chromophoreperturber separations and the steady-state quenching of IEPK were accounted for with an exponential dependence of the quenching rate constant with distance. The small effective Bohr radius (0.8 A) that appears in the exponent emphasizes the localized nature of the interaction. Comparison of the triplet quenching rate constant obtained at quencher contact with IEPK to that estimated in proteins suggests a dependence on the triplet energy of the indole moiety and an endothermic nature for the quenching process. The study predicts that in proteins tryptophan-disulfide interactions are very localized in nature and should give rise to detectable anomalous decays only out to 2 A beyond van der Waals contact between the interacting partners.

Computer Graphics↗
PubMed2000

Effects of TAK-637, a tachykinin receptor antagonist, on the micturition reflex in guinea pigs.

The effects of a new tachykinin NK(1) receptor antagonist, (aR, 9R)-7-[3,5-bis(trifluoromethyl)benzyl]-8,9,10, 11-tetrahydro-9-methyl-5-(4-methylphenyl)-7H-[1,4]diazocino[2,1-g] [1, 7]naphthyridine-6,13-dione (TAK-637), on the micturition reflex were compared with those of drugs used for abnormally frequent micturition or incontinence. TAK-637 showed a characteristic effect on the distension-induced rhythmic bladder contractions in guinea pigs. The systemic administration of TAK-637 decreased the number but not the amplitude of the distension-induced rhythmic bladder contractions. A similar effect was observed in animals in which the spinal cord had been severed. TAK-637 also inhibited the micturition reflex induced by topical application of capsaicin onto the surface of bladder dome. From these results, it is concluded that TAK-637 inhibits sensory transmissions from the bladder evoked by both physiological and nociceptive stimuli by blocking tachykinin NK(1) receptors, possibly at the level of the spinal cord. On the other hand, the other drugs such as oxybutynin, tolterodine, propiverine, and inaperisone showed no effects on the frequency of the distension-induced rhythmic bladder contractions but decreased the contraction amplitude. Therefore, TAK-637 may represent a new class of drugs, which would be effective for abnormally frequent micturition without causing voiding difficulties due to decreased voiding pressure.

Animals↗