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Symmetrel (Amantadine)

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Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body. Generic Symmetrel is used to treat and prevent influenza A (viral infection). Generic Symmetrel is also used to treat Parkinson's disease and "Parkinson-like" symptoms such as stiffness and shaking that may be caused by the use of certain drugs.

Other names for this medication:

Similar Products:
Famvir, Rebetol, Sustiva, Combivir, Epivir, Retrovir


Also known as:  Amantadine.


Generic Symmetrel is an antiviral medication. It blocks the actions of viruses in your body.

Generic name of Generic Symmetrel is Amantadine.

Symmetrel is also known as Amantadine.

Brand name of Generic Symmetrel is Symmetrel.


Take this medicine with a full glass of water. If you are taking Generic Symmetrel to treat influenza A, start taking the medication within 24-48 hours after flu symptoms begin.

Do not stop taking it suddenly.


If you overdose Generic Symmetrel and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Symmetrel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Be careful with Generic Symmetrel while you are pregnant or have nurseling. Generic Symmetrel can pass in breast milk and harm your baby.

Do not use Generic Symmetrel if you are allergic to Generic Symmetrel components.

Do not use FluMist nasal influenza "live vaccine" while you are being treated with Generic Symmetrel and for at least 48 hours after you stop taking Generic Symmetrel. The nasal vaccine may not be as effective if you receive it while you are taking Generic Symmetrel.

Be careful with Generic Symmetrel if you have epilepsy or other seizure disorder, congestive heart failure, kidney or liver disease, low blood pressure, eczema, glaucoma, or a history of mental illness, suicide attempt, or drug/alcohol addiction.

Be careful with Generic Symmetrel if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Symmetrel if you take atropine (Atreza, Sal-Tropine, and others); dicyclomine (Bentyl); glycopyrrolate (Robinul); hyoscyamine (Anaspaz, Levbid, Levsin, Nulev, and others); mepenzolate (Cantil); methscopolamine (Pamine); propantheline (Pro-Banthine); scopolamine (Maldemar, Scopace, Transderm-Scop); quinine (Qualaquin); quinidine (Cardioquin, Quinaglute); diuretic (water pill) such as triamterene (Dyrenium), hydrochlorothiazide (HCTZ, Dyazide, HydroDiuril, Hyzaar, Lopressor, Vasoretic, Zestoretic); phenothiazines such as prochlorperazine (Compazine), thioridazine (Mellaril), and others.

Avoid alcohol.

Do not stop taking it suddenly.

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The management of acute extrapyramidal effects (EPEs) induced by antipsychotic drugs is reviewed. EPEs associated with antipsychotics include acute dystonias, pseudoparkinsonism, and akathisia. Acute dystonias consist of abnormal muscle spasms and postures and usually occur three to five days after antipsychotic therapy begins or the dosage is increased. Acute dystonias should be treated with anticholinergic medications or benzodiazepines. Antipsychotic-induced pseudoparkinsonism has the same clinical appearance as idiopathic parkinsonism. Symptoms generally appear within the first three months. Pseudoparkinsonism is managed by lowering the anti-psychotic dosage or by adding an anticholinergic agent or a mantadine; switching to a low-potency agent or an atypical antipsychotic may also help. Akathisia is characterized by subjective feelings of restlessness and anxiety and objective signs of motor activity, such as inability to sit still. This EPE appears days to weeks after antipsychotic exposure begins and can be difficult to manage. If reduction of the antipsychotic dosage or a switch to a less potent antipsychotic is not practical or effective, an anticholinergic, beta-blocker, or benzodiazepine may be added. Lipophilic beta-blockers, especially propranolol and metoprolol, appear to be the most effective treatments. Anticholinergic agents are commonly given to prevent acute dystonias, especially in high-risk patients, but long-term prophylaxis is controversial. Atypical antipsychotics may have less potential to induce EPEs. Options in the management of antipsychotic-associated EPEs include using the lowest effective dosage of antipsychotic, treating the reactions with medications, and changing the antipsychotic to one with less potential for inducing EPEs.

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Because of adverse reactions, early efforts to introduce high affinity competitive or use-dependent NMDA receptor antagonists into patients suffering from stroke, head trauma or epilepsy met with failure. Later it was discovered that both low affinity use-dependent NMDA receptor antagonists and compounds with selective affinity for the NR2B receptor subunit met the criteria for safe administration into patients. Furthermore, these low affinity antagonists exhibit significant mechanistic differences from their higher affinity counterparts. Success of the latter is attested to the ability of the following low affinity compounds to be marketed: 1) Cough suppressant-dextromethorphan (available for decades); 2) Parkinson's disease--amantadine, memantine and budipine; 3) Dementia--memantine; and 4) Epilepsy--felbamate. Moreover, Phase III clinical trials are ongoing with remacemide for epilepsy and Huntington's disease and head trauma for HU-211. A host of compounds are or were under evaluation for the possible treatment of stroke, head trauma, hyperalgesia and various neurodegenerative disorders. Despite the fact that other drugs with associated NMDA receptor mechanisms have reached clinical status, this review focuses only on those competitive and use-dependent NMDA receptor antagonists that reached clinical trails. The ensuing discussions link the in vivo pharmacological investigations that led to the success/mistakes/ failures for eventual testing of promising compounds in the clinic.

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Adoption of values for MCIDs based upon 0.4 of the SD of the change in score from baseline on the sMMSE, BADLS and NPI in the first 127 participants to complete DOMINO yielded MCIDs of 1.4 points for sMMSE, 3.5 for BADLS and 8.0 for NPI.

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The therapeutic effects of UDP-glucose (UDPG), an endogenous agonist of GPR17 that may promote the self-repair of white matter, glial cell line-derived neurotrophic factor (GDNF), a neurotrophic factor correlated with the growth and survival of nerve cells, and memantine, an antagonist of NMDA receptors, were evaluated for functional improvement of neonatal rats with experimental periventricular leukomalacia (PVL). Five day-old neonatal rat pups were subjected to an ischemia-induced model of PVL. The pups were then randomly divided into sham, PVL, PVL plus UDPG, PVL plus GDNF, and PVL plus memantine groups. All pups were weighed and the age at first eye opening recorded. Pathological changes and myelin sheath formation in the white matter were assessed under both light and electron microscopy on day 7 and 21 after induction of PVL. Values of escape latency (EL) and swimming distance (SD) in Morris water maze test, and the modified inclined plane scores in Rivlin inclined plane test were recorded for rats on day 26. Pups in the PVL group were found to be significantly lower in weight (p<0.05), delayed in age at first eye opening (p<0.01), and impaired in their inclined plane (p<0.01) and Morris water maze (p<0.01) performance compared with those in the sham, UDPG, GDNF and memantine groups. Histopathological grading of the white matter classified all pups in the PVL group with significantly more severe injury (p<0.01), and the number and thickness of their myelin sheaths were significantly less (p<0.01), compared to the UDPG, GDNF, memantine, or sham groups. These results indicate that treatment with UDPG, GDNF, and memantine may significantly improve long-term prognosis in neonatal rats with cerebral white matter injury, characteristic of PVL.

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In vitro assays showed effective growth inhibition of both drugs on F98 and 9L cell lines. F98 organotypic cultures showed reduced growth of tumors treated with radiation and riluzole in comparison with untreated cultures or cultures treated with radiation or riluzole alone. Three separate efficacy experiments all showed that localized delivery of riluzole or memantine is efficacious against the 9L gliosarcoma tumor in vivo. Systemic riluzole monotherapy was ineffective; however, riluzole given with RT resulted in improved survival.

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Nine hundred and seventy-two patients from six European centres were evaluated by means of individual patient meta-analysis, using mixed models with centres and the centre-treatment interaction fitted as random variables.

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The younger age (beta = -0.23; p < 0.001), more educated (beta = 0.26; p < 0.001) and the greater deterioration of ADL (beta = 0.24; p < 0.001) were associated with a greater decline in all patients. The drugs had a beneficial effect (beta = -0.18; p = 0.011) in the group with lower and slower decline (RAD < 5%).

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Pharmacological treatments that are administered to adults in the postacute stage after a traumatic brain injury (TBI) (≥4 weeks after injury) have the potential to reduce persistent cognitive and behavioral problems. While a variety of treatments have been examined, the findings have yet to be consolidated, hampering advances in the treatment of TBI. A meta-analysis of research that has investigated the cognitive and behavioral effects of pharmacological treatments administered in the later stage after TBI was therefore conducted. The PubMed and PsycINFO databases were searched, and Cohen d effect sizes, percent overlap, and failsafe N statistics were calculated for each treatment. Both randomized controlled trials and open-label studies (prospective and retrospective) were included. Nineteen treatments were investigated by 30 independent studies, comprising 395 participants with TBI in the treatment groups and 137 control subjects. When treated in the postacute period, 1 dopaminergic agent (methylphenidate) improved behavior (anger/aggression, psychosocial function) and 1 cholinergic agent (donepezil) improved cognition (memory, attention). In addition, when the injury-to-treatment interval was broadened to include studies that administered treatment just before the postacute period, 2 dopaminergic agents (methylphenidate, amantadine) showed clinically useful treatment benefits for behavior, whereas 1 serotonergic agent (sertraline) markedly impaired cognition and psychomotor speed.

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The emergence of pandemic H1N1 influenza viruses in April 2009 and the continuous evolution of highly pathogenic H5N1 influenza viruses underscore the urgency of novel approaches to chemotherapy for human influenza infection. Anti-influenza drugs are currently limited to the neuraminidase inhibitors (oseltamivir and zanamivir) and to M2 ion channel blockers (amantadine and rimantadine), although resistance to the latter class develops rapidly. Potential targets for the development of new anti-influenza agents include the viral polymerase (and endonuclease), the hemagglutinin, and the non-structural protein NS1. The limitations of monotherapy and the emergence of drug-resistant variants make combination chemotherapy the logical therapeutic option. Here we review the experimental data on combination chemotherapy with currently available agents and the development of new agents and therapy targets.

symmetrel reviews

To evaluate the long-term safety and efficacy of memantine use as treatment of HIV-associated cognitive impairment.

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The effect of AP and DMAA on the activity of Ro4-1284-induced PGO waves in lateral geniculate body (CGL) of cats is bidirectional. Higher doses decrease, whereas lower doses increase the intensity of PGO waves. DMAA inhibitis PGO activity in a dose-dependent manner. SP antagonizes AP inhibiting activity but does not affect the action of DMAA. The present study deals with the effect of AP and DMAA, the compounds stimulating central dopamine receptors, on the function of serotonin neurons.

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A ionization technique in mass spectrometry called Direct Analysis in Real Time Mass Spectrometry (DART TOF-MS) coupled with a Direct Binding Assay was used to identify and characterize anti-viral components of an elderberry fruit (Sambucus nigra L.) extract without either derivatization or separation by standard chromatographic techniques. The elderberry extract inhibited Human Influenza A (H1N1) infection in vitro with an IC(50) value of 252+/-34 microg/mL. The Direct Binding Assay established that flavonoids from the elderberry extract bind to H1N1 virions and, when bound, block the ability of the viruses to infect host cells. Two compounds were identified, 5,7,3',4'-tetra-O-methylquercetin (1) and 5,7-dihydroxy-4-oxo-2-(3,4,5-trihydroxyphenyl)chroman-3-yl-3,4,5-trihydroxycyclohexanecarboxylate (2), as H1N1-bound chemical species. Compound 1 and dihydromyricetin (3), the corresponding 3-hydroxyflavonone of 2, were synthesized and shown to inhibit H1N1 infection in vitro by binding to H1N1 virions, blocking host cell entry and/or recognition. Compound 1 gave an IC(50) of 0.13 microg/mL (0.36 microM) for H1N1 infection inhibition, while dihydromyricetin (3) achieved an IC(50) of 2.8 microg/mL (8.7 microM). The H1N1 inhibition activities of the elderberry flavonoids compare favorably to the known anti-influenza activities of Oseltamivir (Tamiflu; 0.32 microM) and Amantadine (27 microM).

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The quality of the evidence combined with a lack of knowledge about the safety of amantadine and the limited benefits of rimantadine, do not indicate that amantadine and rimantadine compared to control (placebo or paracetamol) could be useful in preventing, treating and shortening the duration of influenza A in children and the elderly.

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To determine the clinical efficacy and safety of memantine for people with Alzheimer's disease, or vascular or mixed dementia.

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Convulsions induced on mice by a dose of 200 mg/kg i.p. of amantadine (Ama) or 1-adamantylcyclopentanamine (Ad1) were studied with tricyclic antidepressants (imipramine, desipramine, chlorimipramine), possessing antiglutamatergic properties, or with GABA-linoleamide, a centrally acting GABAergic drug, or with glycine-linoleamide, a centrally acting glycinergic drug, or with glutamic acid palmitamide, a centrally acting glutamatergic drug. The results of these studies could suggest the existence of important glutamatergic and anti-GABAergic components and, probably, of a slight antiglycinergic activity in the pharmacological action profile of the Ad1. Moderate glutamatergic and anti-GABAergic components could operate in the Ama's mechanism of action.

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Systematic reviews of randomized, controlled trials in patients with influenza suggest a lack of evidence about the effects of antiviral therapy on several patient-important outcomes of influenza.

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Our results show a male predominance and an early age of disease onset. MSA-P was the predominant subtype. Our results are similar to the European MSA series.

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The current study found that initial symptom severity and female gender were associated with use of medication in recovery from sports-related concussion among variables available for study.

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This case report describes a 15-year-old male patient with spastic diplegic cerebral palsy, Gross Motor Function Classification System Level III, who developed severe new cognitive and motoric impairments after the administration of haloperidol. He received this dopamine antagonist and typical antipsychotic medication for an acute postoperative episode of agitation. He improved when he received the dopamine agonists amantadine and carbidopa/levodopa. This case suggests that dopamine blockade may be deleterious for individuals with cerebral palsy. Potential explanations for the events observed in this case are also presented.

symmetrel drug summary

Administration of memantine either attenuated (5 mg/kg) or blocked (10 mg/kg) the expression of withdrawal-potentiated startle during naloxone (2.5 mg/kg)-precipitated withdrawal from a single dose of morphine sulfate (10 mg/kg). Pre-treatment with the NMDA receptor antagonist also inhibited the exacerbation of withdrawal-potentiated startle across repeated acute opiate exposures. Memantine blocked the expression of acute dependence, but was less effective in inhibiting its escalation, when hyperalgesia was used as a measure of withdrawal. These doses of memantine did not affect startle responding or nociception in otherwise drug-free animals. Data from additional control groups indicated that the effects of memantine on the expression of withdrawal were not influenced by nonspecific interactions between the NMDA antagonist and either morphine or naloxone.

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No study was identified which met inclusion criteria for this review, however there is an on-going randomised controlled study being conducted in the UK and data are expected in 2009.

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The National Institute for Health Research Health Technology Assessment programme.

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Levodopa provides the most effective symptomatic treatment for Parkinson's disease (PD). Initiation of treatment of PD too early and/or very aggressive treatment with large doses of levodopa results in severe motor fluctuations and dyskinesias in 30% of patients with PD. Chronic levodopa treatment over a period of 9 years or more will invariably result in disabling motor fluctuations in 90% of PD patients. The motor fluctuations and associated dyskinesia are due to progressive dopamine denervation, an unregulated pattern of release of dopamine in the synapse, fluctuating levels of receptor sensitivity, and fluctuating levels of dopamine receptor stimulation. Once the dyskinesias are established, they are difficult to treat. The current medical therapy is a by-product of several explorative open-label trials, as well as a few blinded and double-label placebo-controlled clinical trials, of varying duration in a small number of patients. These studies suggest that amantadine, a glutamate antagonist, may be the most effective, easily available, and inexpensive medical treatment for levodopa-induced dyskinesia. Several other drugs, already approved for other medical ailments, also have been tried but not evaluated in large-scale clinical trials. None of these drugs is approved by the US Food and Drug Administration specifically for levodopa-induced dyskinesia. By far, the most effective treatment of levodopa-induced dyskinesia appears to be deep brain stimulation, with globus pallidus interna or the subthalamic nucleus as the two major targets of placement of electrodes.

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This study reports the genetic characterization of a highly pathogenic avian influenza virus subtype H5N1 isolated from a moribund domestic duck in central Vietnam during 2012. In the moribund duck's flock, within 6 days after vaccination with a commercial H5N1 vaccine (Re-5) to 59-day-old birds, 120 out of 2,000 ducks died. Genetic analysis revealed a substantial number of mutations in the HA gene of the isolate in comparison with the vaccine strains, Re-1 and Re-5. Similar mutations were also found in selected Vietnamese H5N1 strains isolated since 2009. Mutations in the HA gene involved positions at antigenic sites associated with antibody binding and also neutralizing epitopes, with some of the mutations resulting in the modification of N-linked glycosylation of the HA. Those mutations may be related to the escape of virus from antibody binding and the infection of poultry, interpretations which may be confirmed through a reverse genetics approach. The virus also carried an amino acid substitution in the M2, which conferred a reduced susceptibility to amantadine, but no neuraminidase inhibitor resistance markers were found in the viral NA gene. Additional information including vaccination history in the farm and the surrounding area is needed to fully understand the background of this outbreak. Such understanding and expanded monitoring of the H5N1 influenza viruses circulating in Vietnam is an urgent need to provide updated information to improve effective vaccine strain selection and vaccination protocols, aiding disease control, and biosecurity to prevent H5N1 infection in both poultry and humans.

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Glutamate is the major transmitter candidate between inner hair cells and the afferent neurons of the mammalian cochlea. We investigated the action of memantine (1-amino-3,5-dimethyl-adamantane) and the quinoxaline derivative caroverine [1-diethylaminoethyl-3,8-(p-methoxybenzyl)-1,2-dihydro-quinoxaline-dione] on the glutamatergic transmission in the guinea pig cochlea utilizing extracellular recording techniques and microiontophoretic ejection of substances. While memantine was able to inhibit the NMDA (N-methyl-D-aspartate)-induced firing, the AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid)-stimulated activity was unaffected. In contrast, caroverine could block both NMDA- as well as AMPA-induced firing. As memantine and caroverine are currently in clinical use, these substances could be introduced to the treatment of several cochlear disorders.

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Using recombinant receptor expression in Xenopus laevis oocytes and two electrode voltage clamp recordings we characterized pharmacological properties of rat NR1/NR2A NMDARs with altered CTDs. We assessed the effects of truncating [at residue Iso1098; NR2A(trunC)] and deleting [from residue Phe822; NR2A(delC)] the CTD of NR2A NMDAR subunits on agonist potencies, channel block by Mg(2+) and memantine and potentiation of NMDAR-mediated responses by chelating contaminating divalent cations.

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Immunocompromised patients are at increased risk of complications of influenza virus infection. We report on two critically ill patients on immunosuppressive medication with influenza pneumonia. In both patients, oseltamivir monotherapy did not result in clearance of the virus after 18 and five days, respectively. After adding zanamivir and amantadine to the treatment, PCRs on pharyngeal and/or plasma specimens turned negative in both patients after four and three days, respectively. We suggest, that in critically ill patients with influenza A H1N1 infection, treatment efficacy should be monitored closely and treatment with a combination of antiviral drugs should be considered.

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symmetrel buy 2016-03-04

A 62-year-old male, was admitted on Oct. 7, 1987 because of productive cough and dyspnea. He worked for an iron factory, where pneumoconiosis was regarded as an occupational disease, for 40 years. No abnormal finding had been noted on his mass screening chest roentgenograms. He was well until three years ago when hypertension and Parkinsonism were noted. Since then he was treated with beta blockers, L-DOPA, amantadine and bromocriptine. Two weeks before admission, he suddenly complained of dyspnea and productive cough. His chest roentgenograms showed diffuse reticulonodular infiltration in both lung fields. The partial pressure of oxygen of the arterial blood was 65.9 Torr. The first transbronchial lung biopsy obtained from right B8 on Sept. 29, 1987 (before the admission) revealed some epithelioid granulomas and the second biopsy obtained from right B10 on Oct. 14, 1987 demonstrated bronchiolar edema and infiltration of inflammatory cells. Fibrotic changes associated with carbon dust between airways and vessels were also noted. Lymphocyte stimulation index by bromocriptine was 362%, and that by amantadine, 139%, L-DOPA, 150%, respectively. After ceasing the administration of bromocriptine, productive cough, dyspnea and the reticulonodular shadows diminished gradually. These findings strongly suggest that the interstitial pulmonary lesions are bromocriptine-induced interstitial pneumonitis. His occupational exposure to inorganic dust may be buy symmetrel a predisposing factor.

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These cell lines provide the basis of simple, rapid, and objective assays that involve virus quantitation such as determination of viral titer, assessment of antiviral susceptibility, and determination of antibody neutralization titer. These buy symmetrel cell lines could be very useful for influenza virus researchers and vaccine manufacturers.

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The objective Prograf Medication Assistance Program was addressed through the development of a structured critically appraised topic. This included a clinical scenario, structured question, literature search strategy, critical appraisal, results, evidence summary, commentary, and bottom-line conclusions. Participants included consultant and resident neurologists, a medical librarian, clinical epidemiologists, and content experts in the disciplines of neurocritical care and physical medicine and rehabilitation.

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In this study, we monitored gene expression profiles using cDNA microarrays after an acute systemic administration of the high affinity N-methyl-D-aspartate (NMDA) uncompetitive antagonist MK-801 (1 mg/kg; 4 h), and the clinically used moderate affinity antagonist memantine (25 mg/kg; 4 h) in adult rat brains. From a microarray containing 1090 known genes, 13 genes were regulated by both treatments of which 12 were upregulated and one was downregulated. In addition, 28 and 34 genes were regulated (> or = 1.5- or < or = 0.67-fold change) by either memantine or MK-801, respectively. Genes commonly regulated by both treatments and not previously reported were confirmed by in situ hybridization (ISH) and include regenerating liver inhibitory factor-1 (RL/IF-1), GDP-dissociation inhibitor 1 (GDI-1), neural visinin Ca2+-binding protein 2 (NVP-2), neuromedin B receptor, and Na+/K+ transporting ATPase 2beta. ISH with memantine (5-50 mg/kg) revealed regulation of these genes in other cortical and hippocampal regions. RL/IF-1 induction occurred at 1 h and returned to basal levels by 8 h, consistent with the profile of an immediate early gene. Western blot analysis showed increases (approximately Amaryl 4 Mg Price 30-65%) in GDI-1 protein present in both cytosolic and membrane fractions that were significant in the 84-kDa Rab bound form, suggesting that memantine influences Ras-like GTPase function. Genes regulated by a 5 mg/kg dose of memantine might be important in its therapeutic effects. These findings increase the number of known, differentially altered genes after treatment of uncompetitive NMDA receptor antagonists and suggest broader actions of these agents than previously realized.

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The study population consisted of 53 HBsAg-negative patients with chronic hepatitis C treated with IFN/ribavirin or IFN/ribavirin/amantadine. Nine patients experienced a viral breakthrough (BT), 30 were non-responders (NR) and 14 were responders (R). HBV-DNA detection by PCR was performed using primers specific for the S Zyrtec Gel Caps region of the HBV genome and HCV-RNA detection by PCR with primers localised in both the 5'NC and core region of HCV genome, before, during and after treatment. Viral genome sequences were also studied.

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We enrolled 4443 participants, aged 3-97 years, who had influenza-kit-positive results during seasons 2007-12, including 2135 with influenza A, 534 with Vermox How To Buy A/H1N1, and 1643 with influenza B. Eligible subjects completed a questionnaire to identify past influenza infection and vaccination history. For the diagnosis of current influenza infection, subjects were examined, and pharyngeal swabs were collected and tested using the Capilia flu rapid diagnosis kit to confirm influenza infection. An interim analysis was performed using clinician-based surveillance data for the entire four seasons of influenza infection in Japan.

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(1) Oseltamivir, an oral antiviral agent, has been marketed in the European Union for the prevention and treatment of suspected influenza during epidemics. (2) Three prevention trials done in the general population showed moderate effects, with a 3.5-4% reduction (in absolute values) in serologically confirmed episodes of 'flu. According to one trial, oseltamivir was moderately effective as a prophylactic for close contacts of 'flu cases (6.6% in absolute values). (3) There are three placebo-controlled double-blind trials evaluating oseltamivir as a treatment for 'flu, two in adults and one in children. (4) At Levitra Online Pagamento Paypal a dose of 75 mg twice a day, oseltamivir shortened symptoms by about 24 hours. There was no evidence that oseltamivir prevented complications that need antibiotic therapy. Influenza virus isolates from adult patients belonged to type A in more than 90% of cases. There is no sound evidence that oseltamivir is effective against type B influenza virus. (5) There was no reduction in the frequency of complications in a trial in at-risk adults with chronic respiratory or cardiovascular disorders, or in a trial in asthmatic children. (6) Patients receiving oseltamivir in clinical trials were more likely to suffer nausea and vomiting than patients given placebo. (7) Oseltamivir has not been compared with oral amantadine or inhaled zanamivir. (8) It is best to use amantadine when prophylaxis is needed during epidemics. In the curative setting, the poor risk-benefit ratio of oseltamivir, zanamivir, and amantadine, argues against the use of these drugs.

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Both treatments significantly reduced the baseline level of depression and anxiety according to MADRS and HAM-A, which were the primary measures (p < .0001). There was no significant difference between the memantine and escitalopram groups. Assessed cognitive functioning scores were primarily within the normative range and were unchanged in both groups. Quality-of-life Vantin Antibiotic Medication outcomes equally improved in both treatment groups.

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These data suggest benefit of 13.3 mg/24 h versus 4.6 mg/24 h rivastigmine patch, regardless of concomitant memantine use. The incidence of adverse events with highdose patch Imitrex 50 Mg Price was similar in memantine-treated patients and those not receiving memantine.

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A Bactrim Dosage Uti 3 Days MEDLINE search restricted to English-language literature published from 1966 through 1994 and an extensive review of journals was conducted.

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Six point calibration curves, ranging from 0.5 μM to 20 μM of polyamines in water and ethanol/water (50:50), were used to establish instrument response. The method was validated by analysis of fortified Arbutus spirits. Samples of Arbutus and grape pomace spirits were also analyzed. Linear responses were observed for all polyamines and were similar in water, hydro-alcoholic solutions and fortified Arbutus spirits. Putrescine the simple polyamine was detected only in grape pomace distillate samples.

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Considering a societal perspective over 3 years, this analysis shows that memantine ER combined with an AChEI provides better clinical outcomes and lower costs than AChEI monotherapy. Discounted average savings were estimated at $18,355 and $20,947 per patient and quality-adjusted life-years (QALYs) increased by an average of 0.12 and 0.13 from a societal and healthcare payer perspective, respectively. Patients on combination therapy spent an average of 4 months longer living at home and spend less time in moderate-severe and severe stages of the disease.

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N-methyl-D-aspartate (NMDA) receptor channels are implicated in a wide range of physiological and pathophysiological processes, and a large number of pharmacological agents have been introduced that target the receptor via diverse mechanisms of action. Amongst others, subunit selectivity (in particular for the NR2B receptor subunit) and rapid unblocking kinetics have been put forward as favourable pharmacological properties of NMDA receptor-targeting drugs. Here, we describe a pharmacological characterization of human recombinant NMDA receptors expressed in Xenopus oocytes in an electrophysiological set-up. Using this approach, we compare inhibitor potencies of several known NMDA receptor ligands as well as unblocking kinetic properties of selected compounds. All compounds tested had similar potencies at receptors containing NR2A or NR2B receptors with the exception of traxoprodil, which was selective for NR2B. The rank order of potency was (+)MK-801 > phencyclidine (PCP) ≈ traxoprodil > memantine ≈ ketamine > duloxetine. In line with its proposed rapid dissociation properties, the relatively well-tolerated drug memantine exhibits markedly faster unblocking than ketamine and PCP, similar to the low-affinity compound, duloxetine. Electrophysiological recording in Xenopus oocytes thus allows a relatively convenient comparison of key pharmacological parameters at recombinant human NMDA receptors.

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Amantadine, injected into mice, produces dose-dependent mydriasis. The pupillary dilation caused by amantadine is not abolished by pretreatment with reserpine, or by combined pretreatment with reserpine and alpha-methyl-p-tyrosine, although the mydriasis is reduced by approximately 25%. Thus, release of catecholamines from nerve terminals can account for only 25% of amantadine-produced mydriasis. Haloperidol and phentolamine can partially block the effect of amantadine, but, when given after reserpine, neither of the antagonists increases the blockade produced by reserpine alone. We conclude that the catecholaminergic system contributes only partially to the pupillary effect of amantadine, and that other mechanisms appear to be involved.

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This study assessed the frequency of PS in patients with MCP, the phenotype of these patients, and their response to anti-Parkinson medication, during a 1-year period.

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To investigate to what extent antagonists of spinal neurotransmitters interact with the effects of sacral neuromodulation in a rat model of a chronically hyperactive urinary bladder.

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A structure-function analysis of the influenza A virus M2 ion channel protein was performed. The M2 protein of human influenza virus A/Udorn/72 and mutants containing changes on one face of the putative alpha helix of the M2 transmembrane (TM) domain, several of which lead to amantadine resistance when found in virus, were expressed in oocytes of Xenopus laevis. The membrane currents of oocytes expressing mutant M2 ion channels were measured at both normal and low pH, and the amantadine-resistant mutant containing the change of alanine at residue 30 to threonine was found to have a significantly attenuated low pH activation response. The specific activity of the channel current of the amantadine-resistant mutants was investigated by measuring the membrane current of individual oocytes followed by quantification of the amount of M2 protein expressed in these single oocytes by immunoblotting analysis. The data indicate that changing residues on this face of the putative alpha helix of the M2 TM domain alters properties of the M2 ion channel. Some of the M2 proteins containing changes in the TM domain were found to be modified by addition of an N-linked carbohydrate chain at an asparagine residue that is membrane proximal and which is not modified in the wild-type M2 protein. These N-linked carbohydrate chains were further modified by addition of polylactosaminoglycan. A glycosylated M2 mutant protein (M2 + V, A30T) exhibited an ion channel activity with a voltage-activated, time-dependent kinetic component. Prevention of carbohydrate addition did not affect the altered channel activity. The ability of the M2 protein to tolerate deletions in the TM domain was examined by expressing three mutants (del29-31, del28-31, and del27-31) containing deletions of three, four, and five residues in the TM domain. No ion channel activity was detected from expression of M2 del29-31 and del27-31, whereas expression of M2 del28-31 resulted in an ion channel activity that was activated by hyperpolarization (and not low pH) and was resistant to amantadine block. Examination of the oligomeric form of M2 del28-31 indicated that the oligomer is different from wild-type M2, and the data were consistent with M2 del28-31 forming a pentamer.

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Direct DNA inoculations have been used to demonstrate that in vivo transfections can be used to elicit protective immune responses. The direct inoculation of an H7 haemagglutinin-expressing DNA protected chickens against lethal challenge with an H7N7 influenza virus. Three-week-old chickens were vaccinated by inoculating 100 micrograms of plasma DNA by each of three routes (intravenous, intraperitoneal and subcutaneous). One month later, chickens were boosted with 100 micrograms of DNA by each of the three routes. At 1-2 weeks postboost, chickens were challenged via the nares with 100 lethal doses of an H7N7 virus. Low to undetectable levels of H7-specific antibodies were present postvaccination and boost. High titres of H7-specific antibodies appeared within 1 week of challenge. In a series of four experiments, 50% (28/56) of the DNA-vaccinated and < 2% (1/67) of the control chickens survived the challenge. This exceptionally simple method of immunization holds high promise for the development of subunit vaccines.

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These results are the first to indicate that the H2 allele of the extended MAPT haplotype negatively affects the course of psychotic symptoms in AD independently of disease severity. It will be important for future research to examine MAPT transcription in people with AD with and without psychotic symptoms to understand the exact mechanisms underlying these findings.

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Glutamate is a major neurotransmitter in the central nervous system (CNS). Large amount of glutamate can overstimulate N-methyl-D-aspartate receptor (NMDAR), causing neuronal injury and death. Recently, NMDAR has been reported to be found in the lungs. The aim of this study is to examine the effects of memantine, a NMDAR channel blocker, on bleomycin-induced lung injury mice.

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Influenza A viruses of subtype H3N2 were primarily isolated in CACO-2 and then passaged in parallel in CACO-2 and MDCK cells. Structural properties of passaged virus variants were compared and analyzed for evolutionary relationships.

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The effects of competitive and noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists were evaluated in an inbred line of Syrian golden hamsters, in which sustained dystonic postures of limbs and trunk can be initiated by handling or mild environmental stimuli. In this model of paroxysmal dystonia, the noncompetitive NMDA receptor antagonists memantine and MK-801 (dizocilpine) delayed the progression of dystonic attacks in a dose-dependent fashion. The novel competitive NMDA receptor antagonist CGP 37849 (DL-[E]-2-amino-4-methyl-5-phosphono-3-pentenoic acid) was more effective than memantine and MK-801, because it retarded not only the progression but also reduced the severity of the dystonic movements. All compounds exhibited antidystonic effects at doses which did not cause marked ataxia or sedation. The data indicate that NMDA receptor antagonists might be interesting candidates for treatment of dystonia.

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Alzheimer's disease is already an international problem of enormous significance, with an estimated 500,000 sufferers in the UK alone. There are currently four licensed compounds available for the symptomatic treatment of mild to moderate Alzheimer's disease, yet there is still considerable debate over their effectiveness. A variety of anti-dementia agents affecting the various aspects of the disease are in development and the debate will continue over the potential rationing of such treatments in the future. Drugs developed from the cholinergic and glutamatergic hypotheses will be discussed, and a number of other potential treatments aimed at reducing the oxidative stress and inflammatory response associated with dementia will be reviewed. The arrival of these new treatments for Alzheimer's disease has focused attention on the management of dementia in general and has provided the catalyst for the widespread development of memory clinics to enable proper assessment of patients with dementing disorders, providing hope for both patients and carers.

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Biogenic polyamines in drinks have been implicated in undesirable physiological effects. Methods for their detection and quantification usually involve derivatization, pre-concentration and clean-up. To assist the evaluation of the potential risk of distillates, it was important to develop a simple and fast analytical method, which is described in this study.

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In this randomized double-blind parallel-group study, 68 patients with moderate to severe AD (Mini-Mental State Examination score of 8-14) received memantine (20 mg/day) or saffron extract (30 mg/day) capsules for 12 months. Participants were evaluated every month by Severe Cognitive Impairment Rating Scale (SCIRS) and Functional Assessment Staging (FAST) in addition to recording the probable adverse events.