During Ama treatment, PD-PGs showed a decrease in risky choices and an increase in non-risky choices (t(9)=-2.40, P<0.05 and t(9)=2,67, P<0.05 uncorrected, respectively). Between-group comparison showed a significant decrease in risky choices for PD-PG with respect to PD-CTR (t(22)=-4.16, P<0.01), and a decreased accuracy for positive words in comparison between PD-PG and PD-ICD (t(17)=-7,49, P<0.01) and PD-PG and PD-CTR (t(22)=-4.29, P<0.01). No within- and between-group differences were observed for Stroop task.
Nuclear birefringence of neutral red or rivanol stained cell suspensions from rat spleen has been investigated. Polyclonal or monoclonal mitogens produced an increased birefringence of the nucleus following 30 min in vitro stimulation at 37 degrees C. The nuclear birefringence increased by 62.2% [p less than 0.001], when the cells were incubated in the supernatants of a previously phytohemaglutinin stimulated culture. Amantadine, a potent phytohemagglutinin inhibitor, was unable to prevent the effect of the supernatant, but heating for 1 h at 56 degrees C destroyed its activity. The results suggest that increase in nuclear birefringence is mediated by a soluble factor which is released in the course of lymphocyte activation. The nuclear birefringence of surviving cells from human spleens obtained within 6 to 24 h post mortem increases after in vitro stimulation.
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Descriptive study of use and prescription of cholinesterase inhibitors and/or memantine in 2011 according to 2 databases: Farm@drid (pharmacy billing records for the Region of Madrid) and BIFAP (database for pharmacoepidemiology research in primary care, with diagnosis and prescription records). We tested the comparability of drug use results from each database using the chi-square test and prevalence ratios. The prevalence of dementia in Madrid was estimated based on the dose per 100 inhabitants/day, adjusting the result for data obtained from BIFAP on combination treatment in the general population (0.37%) and the percentage of dementia patients undergoing treatment (41.13%).
Three types of hyperalgesia can occur during the postoperative period: primary hyperalgesia, which disappears with wound healing, secondary or central hyperalgesia, which can lead to chronic pain, and opiate-induced hyperalgesia. Different drugs, most of which are NMDA receptors antagonists, are used to decrease or prevent the risk of central or opiate-induced hyperalgesia. However, it is difficult to determine whether they are really effective and at which dosage: the results of most published studies are difficult to interpret because of methodological problems. The two most frequent of those are: absence of objective measurement of secondary hyperalgesia and difficulties targeting an at risk population.
To describe a patient with neuroleptic malignant syndrome (NMS) induced by risperidone, an atypical antipsychotic, and to review the available literature related to risperidone-associated NMS.
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To assess the benefits and harms of antiviral treatment for chronic hepatitis C in patients with HIV.
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Memantine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist used to treat Alzheimer's disease. We investigated memantine pharmacokinetics after oral, IV and patch administration in rats, and compared memantine pharmacokinetics after multiple- or single-dose oral and transdermal administration. Venous blood was collected at preset intervals in single- and multiple-dose studies. Non-compartmental pharmacokinetics was analysed for all formulations. The oral, IV and patch memantine doses were 10 mg/kg, 2 mg/kg and 8.21 ± 0.89 mg/kg, respectively. The maximum plasma concentration was lower and the half-life longer after patch administration than oral and IV administration. Memantine bioavailability was 41 and 63% for oral and patch administration, respectively. Steady state was achieved around 24 hr for oral and patch administration. The mean AUC increased after oral or patch administration from single to multiple dose. The memantine patch formulation displayed a longer duration of action and lower peak plasma concentration. However, drug exposure was similar to the oral formulation at each dose. Additionally, the memantine patch formulation displayed a smaller interindividual variability and lower accumulation than the oral formulation.
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The lower weight, the prolonged mean values of EL and swimming distance and the reduced maximum inclined plane degree were observed in the PVL group compared to those in the sham-operated, GDNF-treated and memantine-treated groups. There were no significant differences in the weight, the values of EI and swimming distance and the maximum inclined plane degree between the two treatment groups and the sham-operated group.
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We studied on mental symptoms which developed during the treatment of Parkinson's disease. Hallucination, delusion, and/or delirious state were observed in 23 (22.8%) of 101 cases. The cases with mental symptoms were studied for the incidence, detail of the symptoms, and the factors involved in their development.
Fatigue is a significant factor in the lives of many MS patients and the most commonly reported symptom in many studies. Fatigue is an important symptom to consider because it affects patients' social lives, occupations, and activities of daily living. Efforts to predict fatigue have been mixed, but it appears to be related to overall quality of life and mood. From a pathophysiologic perspective, fatigue in MS is multifactorial and complex,involving dysregulation of the immune system, changes in the nervous system related to the disease process, neuroendocrine and neurotransmitter changes, and other factors such as physical deconditioning, sleep disturbance, pain, and medication side effects. Various attempts to assess fatigue have been made, and many measures are now available for use in clinical practice and research. In clinical practice, these measures help guide treatment considerations. Recent research has provided valuable strategies to ameliorate fatigue in MS, and although many patients continue to experience fatigue despite interventions, many receive substantial relief.Nonpharmacologic approaches-considered the first step in treatment-include exercise programs, cooling, dietary considerations, and energy conservation strategies. For patients who continue to experience significant fatigue, several medications (although not specifically approved for use in the reduction of MS-related fatigue) have proved effective in this regard.The first-line agents include amantadine for mild fatigue and modafinil for more severe cases. Second-line agents include pemoline and antidepressant medications. Other pharmacologic agents have also shown some promise.
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Data were extracted, pooled where possible, and weighted mean differences, standardized mean differences or odds ratios were estimated. Intention-to-treat (ITT) and observed cases (OC) analyses are reported, where data were available.
To evaluate the pharmacokinetics of amantadine in children with impaired consciousness from acquired brain injury.
Literature was accessed through MEDLINE (1950-August 2007) using the MeSH terms amantadine, brain injuries, cognition, and arousal. PubMed (through August 2007) terms included amantadine, traumatic brain injury, and cerebral injury.
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Prospective controlled trials evaluating the safety and possible positive effects of memantine on antipsychotic induced weight gain are needed.
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We previously reported that some N-methyl-D-aspartate (NMDA)-receptor antagonists enhanced histamine neuron activity in rodents. Here, we have investigated the effects of memantine, an NMDA-receptor antagonist used for the treatment of Alzheimer's disease, on histaminergic neurotransmission. In vitro, memantine antagonized native NMDA receptors with a micromolar potency but had no effect at recombinant human histamine receptors. In vivo, a single administration of memantine increased histamine neuron activity, as shown by the 60% increase of tele-methylhistamine (t-MeHA) levels observed in the brain of mice. This increase occurred with an ED(50) of 0.3 ± 0.1 mg/kg, similar to that found on inhibition of ex vivo [(3)H]dizocilpine maleate (MK-801) binding (1.8 ± 1.3 mg/kg). Two days after pretreatment of mice with memantine at 5 mg/kg twice daily for 5 days, t-MeHA levels were enhanced by 50 ± 7% (p < 0.001), indicating a long-lasting activation of histamine neurons. Quantitative polymerase chain reaction analysis was used to explore genes involved in this persistent effect. H(3) receptor mRNAs were strongly increased, but the density of H(3) receptor binding sites was increased solely in hypothalamus (by 141 ± 24%). Up-regulations of brain-derived neurotrophic factor and NMDA-receptor 1 subunit mRNAs were also found but were restricted to hippocampus. mRNA expression of α7-nicotinic receptors remained unchanged in any region. Considering the well established cognitive effects of histamine neurons, the increase in brain t-MeHA levels after single or repeated administration of therapeutic doses of memantine suggests that the drug exerts its beneficial effects on cognitive deficits of Alzheimer's disease, at least partly, by activating histamine neurons.
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The influence of small Alu-like RNA, isolated from specific RNP complexes (alpha-RNP), on the activity of RNA polymerase III in cell-free system has been studied. The RNAs transcribed in vitro from Alu-DNA template (BLUR, 8) were isolated and subjected to polyacrylamide gel electrophoresis. A specific stimulation of RNA polymerase III activity by alpha-RNA was demonstrated.
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Oseltamivir was administered to 803 patients with influenza A (A+Os group) and 684 patients with influenza B (B+Os group). Amantadine was administered to 676 patients with influenza A (A+Am group).
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Tardive Tourette syndrome is an extrapyramidal symptom which appears after long-term neuroleptic use. We report two cases of this syndrome and review case reports to introduce this extrapyramidal symptom. The first case is a 40-year-old male with schizophrenia. After 6 years of neuroleptic therapy, he began to have barking and grunting vocalizations and show neck and shoulderjerking. The second case is a 53-year-old male with alcoholism. Sulpride was prescribed for three years to treat mood symptoms. Oral dyskinesia appeared after sulpride was stopped. About five weeks after amantadine and trihexyphenidyl hydrochloride was started, he began to have grunting vocalizations and show neck jerking. The involuntary movement disappeared quickly after intraveneous administration of haloperidol. Including our two cases, there are 17 case reports of tardive Tourette syndrome. Twelve cases were schizophrenic patients. In addition to typical movements, patients had coplolalia in 6 cases, and oral dyskinesia in 9 cases. In 8 cases, tardive Tourette syndrome appeared during neuroleptic treatment, and in 9 cases the syndrome appeared after neuroleptics were stopped. Our two cases and previous case reports showed that tardive Tourette syndrome appeared after long-term neuroleptic therapy, it was improved transiently by an increase of neuroleptics and exacerbated by their decrease, it was exacerbated by dopaminergic and anticholinergic drugs, and tardive dyskinesia was often seen concomitantly, indicating that tardive Tourette syndrome has a similar pathophysiology to tardive dyskinesia. Tardive Tourette syndrome should not be misdiagnosed as an exacerbation of schizophrenic symptoms responsive to an increase of neuroleptics. This side effect should be recognized widely and treated properly.
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A study of an outbreak of acute respiratory disease was done at the "Carlos Font Pupo" Old People's Home. Las Tunas Province, where 30 diseased old individuals were detected; grippe was diagnosed to two of them. General attack rate was 8.6%. Curative treatment with amantadine was administered to 29 old patients and chemoprophylaxis to 26, for a total of 55 old individuals treated. The evolution of the patients was satisfactory and none new case was observed. Diarrhea was the only one secondary reaction observed in a patient under chemoprophylactic treatment. The need to carry on performing similar studies is pointed out.
Caregivers of Alzheimer's disease patients treated with memantine have reported improved frontal lobe behaviors. The present study examined these possible improvements in executive functioning using rater-blinded scoring of a clock-drawing test. Fifty-one Alzheimer's disease patients were treated with open-label memantine for 10 weeks. Clock drawing and Mini-Mental State Examination data were collected before and after treatment. Clock drawing improved significantly with treatment, whereas Mini-Mental State Examination data did not. Twenty-seven patients judged as improved in frontal lobe behaviors by caregivers demonstrated a statistically significant improvement in clock drawing to command, whereas 24 patients judged to be unchanged or worse with memantine in their frontal lobe behaviors had no change in their clock drawing and had worsening on their Mini-Mental State Examination. The current findings suggest that memantine improves frontal lobe behavior in some Alzheimer's disease patients and that clock drawing to command may be sensitive to these improvements.
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To make evidence-based recommendations regarding management of tardive syndromes (TDS), including tardive dyskinesias (TDD), by addressing 5 questions: 1) Is withdrawal of dopamine receptor blocking agents (DRBAs) an effective TDS treatment? 2) Does switching from typical to atypical DRBAs reduce TDS symptoms? 3) What is the efficacy of pharmacologic agents in treating TDS? 4) Do patients with TDS benefit from chemodenervation with botulinum toxin? 5) Do patients with TDS benefit from surgical therapy?
There is growing preclinical evidence for the involvement of glutamate in the behavioral actions of nicotine. The aim of this study, was to investigate the role of N-methyl-D-aspartate (NMDA) receptors in the cognitive and subjective effects of smoking in humans. Sixty regular smokers took part in this double-blind placebo controlled study, that investigated the effect of the NMDA-antagonist memantine (40 mg) and the nicotinic-receptor antagonist mecamylamine (10 mg) on smoking-induced improvement in performance of a task of sustained attention and on smoking-induced changes in subjective effects and craving. Increases in subjective ratings of 'buzzed' following smoking were reversed by memantine, but not by mecamylamine. In contrast, improvement on a Rapid Visual Information Processing task by smoking was opposed by mecamylamine, but not by memantine. Smoking reduced craving for cigarettes, but neither drug altered this effect. Our results suggest that glutamatergic mechanisms may have differential involvement in the subjective and cognitive actions of smoking. Further investigations using different ligands are warranted to fully characterize the role of glutamate underlying the consequences of smoking behavior.
Antiviral chemotherapy has come of age. Several compounds, i.e. amantadine, rimantadine, idoxuridine, trifluridine, vidarabine, acyclovir, ribavirin and azidothymidine, have been licensed for clinical use and other promising compounds may follow soon. The search for new antiviral agents has been boosted by the advent of AIDS, but the activity spectrum of the newly developed antivirals not only spans retroviruses but also various other virus infections, i.e. herpes-, adeno-, pox- and rhinovirus infections. Clinical trials have been started with a variety of these new compounds and the prospects for an effective chemotherapy of several viral diseases certainly look bright.
The antispastic agent and N-methyl-D-aspartate (NMDA) receptor antagonist memantine has recently been proposed as a neuroprotective drug for use in patients with dementia syndromes with primarily temporal lobe pathology, e.g. senile dementia of Alzheimer type or dementia in Parkinson's disease. In a quantitative autoradiographic study in human post mortem hippocampus, memantine was able to inhibit binding of the noncompetitive NMDA-antagonist [3H]MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine maleate) with inhibition constants between 3 and 10 microM, being about a factor of 10 more potent than the dissociative anaesthetic and NMDA receptor antagonist (+/-)ketamine. As these inhibition constants are well within the therapeutic concentration range of memantine, antagonism of endogenous glutamate at limbic NMDA receptors may be one molecular mechanism by which memantine is beneficial in dementia syndromes.
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While aminoadamantanes are well-established inhibitors of the influenza A M2 proton channel, the mechanisms by which they are rendered ineffective against M2S31N are unclear. Solid state NMR, isothermal titration calorimetry, electrophysiology, antiviral assays, and molecular dynamics simulations suggest stronger binding interactions for aminoadamantanes to M2WT compared to negligible or weak binding to M2S31N. This is due to reshaping of the M2 pore when N31 is present, which, in contrast to wild-type (WT), leads (A) to the loss of the V27 pocket for the adamantyl cage and to a predominant orientation of the ligand's ammonium group toward the N-terminus and (B) to the lack of a helical kink upon ligand binding. The kink, which reduces the tilt of the C-terminal helical domain relative to the bilayer normal, includes the W41 primary gate for proton conductance and may prevent the gate from opening, representing an alternative view for how these drugs prevent proton conductance.
We are the first in Russia to detect a mutant variant of A H1N1 pan IV resistant to oseltamivir We describe a set of nucleotide polymorphisms which determine a complicated course of the flu in patients with identified A H1N1 pan IV.