13 results on '"S, Vailati"'
Search Results
2. Preclinical study of the antimyotonic efficacy of safinamide in the myotonic mouse model.
- Author
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Canfora I, Altamura C, Desaphy JF, Boccanegra B, Vailati S, Caccia C, Melloni E, Padoani G, De Luca A, and Pierno S
- Abstract
Mexiletine is the first choice drug in the treatment of non-dystrophic myotonias. However, 30% of patients experience little benefit from mexiletine due to poor tolerability, contraindications and limited efficacy likely based on pharmacogenetic profile. Safinamide inhibits neuronal voltage-gated sodium and calcium channels and shows anticonvulsant activity, in addition to a reversible monoamine oxidase-B inhibition. We evaluated the preclinical effects of safinamide in an animal model of Myotonia Congenita, the ADR (arrested development of righting response) mouse. In vitro studies were performed using the two intracellular microelectrodes technique in current clamp mode. We analyzed sarcolemma excitability in skeletal muscle fibers isolated from male and female ADR (adr/adr) and from Wild-Type (wt/wt) mice, before and after the application of safinamide and the reference compound mexiletine. In ADR mice, the maximum number of action potentials (N-spikes) elicited by a fixed current is higher with respect to that of WT mice. Myotonic muscles show an involuntary firing of action potential called after-discharges. A more potent activity of safinamide compared to mexiletine has been demonstrated in reducing N-spikes and the after-discharges in myotonic muscle fibers. The time of righting reflex (TRR) before and after administration of safinamide and mexiletine was evaluated in vivo in ADR mice. Safinamide was able to reduce the TRR in ADR mice to a greater extent than mexiletine. In conclusion, safinamide counteracted the abnormal muscle hyperexcitability in myotonic mice both in vitro and in vivo suggesting it as an effective drug to be indicated in Myotonia Congenita., Competing Interests: Declaration of competing interest Silvia Vailati, Elsa Melloni, Gloria Padoani are employees of Zambon SpA, and Carla Caccia is a consultant of Zambon SpA. The International patent application PCT/EP2019/063733 entitled “Safinamide for treating myotonia” was filed on May 28, 2019 in the name of Zambon S.p.A. Designated inventors are Desaphy J.F., Pierno S., Conte D., Melloni E., Vailati S., Padoani G., and Caccia C., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2024
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3. Structural Unfolding of G-Quadruplexes: From Small Molecules to Antisense Strategies.
- Author
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Fracchioni G, Vailati S, Grazioli M, and Pirota V
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- Humans, Small Molecule Libraries chemistry, Small Molecule Libraries pharmacology, Ligands, G-Quadruplexes, Oligonucleotides, Antisense chemistry
- Abstract
G-quadruplexes (G4s) are non-canonical nucleic acid secondary structures that have gathered significant interest in medicinal chemistry over the past two decades due to their unique structural features and potential roles in a variety of biological processes and disorders. Traditionally, research efforts have focused on stabilizing G4s, while in recent years, the attention has progressively shifted to G4 destabilization, unveiling new therapeutic perspectives. This review provides an in-depth overview of recent advances in the development of small molecules, starting with the controversial role of TMPyP4. Moreover, we described effective metal complexes in addition to G4-disrupting small molecules as well as good G4 stabilizing ligands that can destabilize G4s in response to external stimuli. Finally, we presented antisense strategies as a promising approach for destabilizing G4s, with a particular focus on 2'-OMe antisense oligonucleotide, peptide nucleic acid, and locked nucleic acid. Overall, this review emphasizes the importance of understanding G4 dynamics as well as ongoing efforts to develop selective G4-unfolding strategies that can modulate their biological function and therapeutic potential.
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- 2024
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4. In Vivo Efficacy and Toxicity of an Antimicrobial Peptide in a Model of Endotoxin-Induced Pulmonary Inflammation.
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Cresti L, Cappello G, Vailati S, Melloni E, Brunetti J, Falciani C, Bracci L, and Pini A
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- Mice, Animals, Antimicrobial Peptides, Lipopolysaccharides toxicity, Cytokines, Peptides, Inflammation drug therapy, Bronchoalveolar Lavage Fluid, Endotoxins toxicity, Pneumonia chemically induced, Pneumonia drug therapy
- Abstract
SET-M33 is a synthetic peptide that is being developed as a new antibiotic against major Gram-negative bacteria. Here we report two in vivo studies to assess the toxicity and efficacy of the peptide in a murine model of pulmonary inflammation. First, we present the toxicity study in which SET-M33 was administered to CD-1 mice by snout inhalation exposure for 1 h/day for 7 days at doses of 5 and 20 mg/kg/day. The results showed adverse clinical signs and effects on body weight at the higher dose, as well as some treatment-related histopathology findings (lungs and bronchi, nose/turbinates, larynx and tracheal bifurcation). On this basis, the no observable adverse effect level (NOAEL) was considered to be 5 mg/kg/day. We then report an efficacy study of the peptide in an endotoxin (LPS)-induced pulmonary inflammation model. Intratracheal administration of SET-M33 at 0.5, 2 and 5 mg/kg significantly inhibited BAL neutrophil cell counts after an LPS challenge. A significant reduction in pro-inflammatory cytokines, KC, MIP-1α, IP-10, MCP-1 and TNF-α was also recorded after SET-M33 administration.
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- 2023
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5. Safety evaluations of a synthetic antimicrobial peptide administered intravenously in rats and dogs.
- Author
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Cresti L, Falciani C, Cappello G, Brunetti J, Vailati S, Melloni E, Bracci L, and Pini A
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- Rats, Dogs, Animals, Microbial Sensitivity Tests, Anti-Bacterial Agents toxicity, Peptides, Dose-Response Relationship, Drug, Antimicrobial Peptides, Anti-Infective Agents toxicity
- Abstract
The antimicrobial peptide SET-M33 is under study for the development of a new antibiotic against major Gram-negative pathogens. Here we report the toxicological evaluation of SET-M33 administered intravenously to rats and dogs. Dose range finding experiments determined the doses to use in toxicokinetic evaluation, clinical biochemistry analysis, necroscopy and in neurological and respiratory measurements. Clinical laboratory investigations in dogs and rats showed a dose-related increase in creatinine and urea levels, indicating that the kidneys are the target organ. This was also confirmed by necroscopy studies of animal tissues, where signs of degeneration and regeneration were found in kidney when SET-M33 was administered at the highest doses in the two animal species. Neurological toxicity measurements by the Irwin method and respiratory function evaluation in rats did not reveal any toxic effect even at the highest dose. Finally, repeated administration of SET-M33 by short infusion in dogs revealed a no-observed-adverse-effect-level of 0.5 mg/kg/day., (© 2022. The Author(s).)
- Published
- 2022
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6. An Eight-Year Survey on Aflatoxin B1 Indicates High Feed Safety in Animal Feed and Forages in Northern Italy.
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Ferrari L, Fumagalli F, Rizzi N, Grandi E, Vailati S, Manoni M, Ottoboni M, Cheli F, and Pinotti L
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- Animals, Aflatoxin B1 analysis, Food Contamination analysis, Animal Feed analysis, Aflatoxins analysis, Mycotoxins analysis
- Abstract
Aflatoxins (AFs) remain the main concern for the agricultural and dairy industries due to their effects on the performances and quality of livestock production. Aflatoxins are always unavoidable and should be monitored. The objective of this paper is to bring to light a significant volume of data on AF contamination in several animal feed ingredients in Northern Italy. The Regional Breeders Association of Lombardy has been conducting a survey program to monitor mycotoxin contamination in animal feeds, and in this paper, we present data relating to AFB1 contamination. In most cases (95%), the concentrations were low enough to ensure compliance with the European Union's (EU's) maximum admitted levels for animal feed ingredients. However, the data show a high variability in AF contamination between different matrices and, within the same matrix, a high variability year over year. High levels of AFs were detected in maize and cotton, especially in the central part of the second decade of this century, i.e., 2015-2018, which has shown a higher risk of AF contamination in feed materials in Northern Italy. Variability due to climate change and the international commodity market affect future prospects to predict the presence of AFs. Supplier monitoring and control and reduced buying of contaminated raw materials, as well as performing analyses of each batch, help reduce AF spread.
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- 2022
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7. Activity of fosfomycin/colistin combinations against planktonic and biofilm Gram-negative pathogens.
- Author
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Boncompagni SR, Micieli M, Di Maggio T, Aiezza N, Antonelli A, Giani T, Padoani G, Vailati S, Pallecchi L, and Rossolini GM
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- Anti-Bacterial Agents pharmacology, Biofilms, Drug Resistance, Multiple, Bacterial, Drug Synergism, Klebsiella pneumoniae, Microbial Sensitivity Tests, Plankton, Colistin pharmacology, Fosfomycin pharmacology
- Abstract
Objectives: To investigate the in vitro activity of fosfomycin, colistin and combinations thereof against planktonic and biofilm cultures of Gram-negative pathogens, mostly showing MDR phenotypes, at concentrations achievable via inhalation of aerosolized drugs., Methods: Activity against planktonic cultures was tested by the chequerboard assay with 130 strains, including 52 Pseudomonas aeruginosa, 47 Klebsiella pneumoniae, 19 Escherichia coli, 7 Stenotrophomonas maltophilia and 5 Acinetobacter baumannii. Activity against biofilm cultures was tested by biofilm chequerboard and quantitative antibiofilm assays with a subset of 20 strains. In addition, 10 of these strains were tested in mutant prevention concentration (MPC) assays., Results: Against planktonic cultures, synergism between fosfomycin and colistin was detected with a minority (10%) of strains (eight K. pneumoniae and five P. aeruginosa), while antagonism was never observed. Synergism between fosfomycin and colistin against biofilms was observed with the majority of tested strains (16/20 in biofilm chequerboard assays, and 18/20 in the quantitative antibiofilm assays), including representatives of each species and regardless of their resistance genotype or phenotype. Furthermore, combination of fosfomycin and colistin was found to significantly reduce the MPC of individual drugs., Conclusions: Fosfomycin and colistin in combination, at concentrations achievable via inhalation of nebulized drugs, showed notable synergy against MDR Gram-negative pathogens grown in biofilm, and were able to reduce the emergence of fosfomycin- and colistin-resistant subpopulations., (© The Author(s) 2022. Published by Oxford University Press on behalf of British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
- Published
- 2022
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8. Effects of safinamide on the glutamatergic striatal network in experimental Parkinson's disease.
- Author
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Sciaccaluga M, Mazzocchetti P, Bastioli G, Ghiglieri V, Cardinale A, Mosci P, Caccia C, Keywood C, Melloni E, Padoani G, Vailati S, Picconi B, Calabresi P, and Tozzi A
- Subjects
- Alanine pharmacology, Alanine therapeutic use, Animals, Antiparkinson Agents pharmacology, Benzylamines pharmacology, Corpus Striatum metabolism, Dose-Response Relationship, Drug, Excitatory Postsynaptic Potentials drug effects, Excitatory Postsynaptic Potentials physiology, Levodopa pharmacology, Levodopa therapeutic use, Male, Nerve Net metabolism, Organ Culture Techniques, Oxidopamine toxicity, Parkinsonian Disorders chemically induced, Parkinsonian Disorders metabolism, Rats, Rats, Wistar, Alanine analogs & derivatives, Antiparkinson Agents therapeutic use, Benzylamines therapeutic use, Corpus Striatum drug effects, Glutamic Acid metabolism, Nerve Net drug effects, Parkinsonian Disorders drug therapy
- Abstract
Objective: The aim of the study was to evaluate electrophysiological effects of safinamide on the intrinsic and synaptic properties of striatal spiny projection neurons (SPNs) and to characterize the possible therapeutic antiparkinsonian effect of this drug in dopamine (DA) denervated rats before and during levodopa (l-DOPA) treatment., Background: Current therapeutic options in Parkinson's disease (PD) are primarily DA replacement strategies that usually cause progressive motor fluctuations and l-DOPA-induced dyskinesia (LIDs) as a consequence of SPNs glutamate-induced hyperactivity. As a reversible and use-dependent inhibitor of voltage-gated sodium channels, safinamide reduces the release of glutamate and possibly optimize the effect of l-DOPA therapy in PD., Methods: Electrophysiological effects of safinamide (1-100 μM) were investigated by patch-clamp recordings in striatal slices of naïve, 6-hydroxydopamine (6-OHDA)-lesioned DA-denervated rats and DA-denervated animals chronically treated with l-DOPA. LIDs were assessed in vivo with and without chronic safinamide treatment and measured by scoring the l-DOPA-induced abnormal involuntary movements (AIMs). Motor deficit was evaluated with the stepping test., Results: Safinamide reduced the SPNs firing rate and glutamatergic synaptic transmission in all groups, showing a dose-dependent effect with half maximal inhibitory concentration (IC
50 ) values in the therapeutic range (3-5 μM). Chronic co-administration of safinamide plus l-DOPA in DA-denervated animals favored the recovery of corticostriatal long-term synaptic potentiation (LTP) and depotentiation of excitatory synaptic transmission also reducing motor deficits before the onset of LIDs., Conclusions: Safinamide, at a clinically relevant dose, optimizes the effect of l-DOPA therapy in experimental PD reducing SPNs excitability and modulating synaptic transmission. Co-administration of safinamide and l-DOPA ameliorates motor deficits., Competing Interests: Declaration of competing interest Charlotte Keywood, Elsa Melloni, Gloria Padoani, Silvia Vailati are employees of Zambon SpA and Carla Caccia is a consultant of Zambon SpA., (Copyright © 2020 Elsevier Ltd. All rights reserved.)- Published
- 2020
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9. Safinamide's potential in treating nondystrophic myotonias: Inhibition of skeletal muscle voltage-gated sodium channels and skeletal muscle hyperexcitability in vitro and in vivo.
- Author
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Desaphy JF, Farinato A, Altamura C, De Bellis M, Imbrici P, Tarantino N, Caccia C, Melloni E, Padoani G, Vailati S, Keywood C, Carratù MR, De Luca A, Conte D, and Pierno S
- Subjects
- Action Potentials drug effects, Alanine pharmacology, Animals, HEK293 Cells, Humans, Male, Rats, Rats, Wistar, Alanine analogs & derivatives, Benzylamines pharmacology, Muscle, Skeletal drug effects, Myotonia, NAV1.4 Voltage-Gated Sodium Channel drug effects
- Abstract
The antiarrhythmic sodium-channel blocker mexiletine is used to treat patients with myotonia. However, around 30% of patients do not benefit from mexiletine due to poor tolerability or suboptimal response. Safinamide is an add-on therapy to levodopa for Parkinson's disease. In addition to MAOB inhibition, safinamide inhibits neuronal sodium channels, conferring anticonvulsant activity in models of epilepsy. Here, we investigated the effects of safinamide on skeletal muscle hNa
v 1.4 sodium channels and in models of myotonia, in-vitro and in-vivo. Using patch-clamp, we showed that safinamide reversibly inhibited sodium currents in HEK293T cells transfected with hNav1.4. At the holding potential (hp) of -120 mV, the half-maximum inhibitory concentrations (IC50 ) were 160 and 33 μM at stimulation frequencies of 0.1 and 10 Hz, respectively. The calculated affinity constants of safinamide were dependent on channel state: 420 μM for closed channels and 9 μM for fast-inactivated channels. The p.F1586C mutation in hNav1.4 greatly impaired safinamide inhibition, suggesting that the drug binds to the local anesthetic receptor site in the channel pore. In a condition mimicking myotonia, i.e. hp. of -90 mV and 50-Hz stimulation, safinamide inhibited INa with an IC50 of 6 μM, being two-fold more potent than mexiletine. Using the two-intracellular microelectrodes current-clamp method, action potential firing was recorded in vitro in rat skeletal muscle fibers in presence of the chloride channel blocker, 9-anthracene carboxylic acid (9-AC), to increase excitability. Safinamide counteracted muscle fiber hyperexcitability with an IC50 of 13 μM. In vivo, oral safinamide was tested in the rat model of myotonia. In this model, intraperitoneal injection of 9-AC greatly increased the time of righting reflex (TRR) due to development of muscle stiffness. Safinamide counteracted 9-AC induced TRR increase with an ED50 of 1.2 mg/kg, which is 7 times lower than that previously determined for mexiletine. In conclusion, safinamide is a potent voltage and frequency dependent blocker of skeletal muscle sodium channels. Accordingly, the drug was able to counteract abnormal muscle hyperexcitability induced by 9-AC, both in vitro and in vivo. Thus, this study suggests that safinamide may have potential in treating myotonia and warrants further preclinical and human studies to fully evaluate this possibility., Competing Interests: Declaration of Competing Interest Charlotte Keywood, Elsa Melloni, Gloria Padoani, Silvia Vailati are employees of Zambon S.p.A. and Carla Caccia is a consultant of Zambon S.p.A. The International patent application PCT/EP2019/063733 entitled “Safinamide for treating myotonia” was filed on May 28, 2019 in the name of Zambon S.p.A. Designated inventors are Desaphy J.F., Pierno S., Conte D., Melloni E., Vailati S., Padoani G., and Caccia C., (Copyright © 2020 Elsevier Inc. All rights reserved.)- Published
- 2020
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10. Safinamide inhibits in vivo glutamate release in a rat model of Parkinson's disease.
- Author
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Pisanò CA, Brugnoli A, Novello S, Caccia C, Keywood C, Melloni E, Vailati S, Padoani G, and Morari M
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- Alanine pharmacology, Alanine therapeutic use, Animals, Benzylamines pharmacology, Excitatory Amino Acid Antagonists pharmacology, Male, Oxidopamine toxicity, Parkinsonian Disorders chemically induced, Rats, Rats, Sprague-Dawley, Alanine analogs & derivatives, Benzylamines therapeutic use, Excitatory Amino Acid Antagonists therapeutic use, Glutamic Acid metabolism, Parkinsonian Disorders drug therapy, Parkinsonian Disorders metabolism
- Abstract
To investigate whether the reversible MAO-B inhibitor and sodium channel blocker safinamide impairs glutamate release under parkinsonian conditions in vivo, and this effect is dependent on MAO-B inhibition, safinamide (and rasagiline as a comparator) were administered to 6-hydroxydopamine hemilesioned rats, a model of Parkinson's disease, and haloperidol-treated rats, a model of neuroleptic-induced parkinsonism. A microdialysis probe was implanted in the dopamine-depleted dorsolateral striatum, globus pallidus, subthalamic nucleus or substantia nigra reticulata of 6-hydroxydopamine hemilesioned rats. Glutamate and GABA release was stimulated by reverse dialysis of veratridine, and safinamide or rasagiline were acutely administered before veratridine at doses inhibiting MAO-B >50%. A microdialysis probe was implanted in the substantia nigra reticulata of naïve rats to monitor glutamate and GABA release following acute haloperidol and safinamide administration. Safinamide inhibited the veratridine-evoked glutamate release in the globus pallidus and subthalamic nucleus but not in the striatum and substantia nigra. Moreover, it reduced pallidal and nigral GABA release. Conversely, rasagiline failed to modify the veratridine-induced glutamate and GABA release in the basal ganglia. Safinamide also inhibited the haloperidol-induced nigral glutamate release. MAO-B inhibitors safinamide and rasagiline differ in their abilities to inhibit depolarization-evoked glutamate release in the basal ganglia of parkinsonian rats. The ineffectiveness of rasagiline suggests that MAO-B inhibition does not contribute to the antiglutamatergic activity of safinamide. The glutamate-inhibiting action of safinamide within the subthalamo-external pallidal loop, which shows abnormal activity in Parkinson's disease, might contribute to its therapeutic actions of improving motor performance without provoking troublesome dyskinesia., (Copyright © 2020 Elsevier Ltd. All rights reserved.)
- Published
- 2020
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11. Safinamide Modulates Striatal Glutamatergic Signaling in a Rat Model of Levodopa-Induced Dyskinesia.
- Author
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Gardoni F, Morari M, Kulisevsky J, Brugnoli A, Novello S, Pisanò CA, Caccia C, Mellone M, Melloni E, Padoani G, Sosti V, Vailati S, and Keywood C
- Subjects
- Alanine pharmacology, Animals, Antiparkinson Agents pharmacology, Corpus Striatum drug effects, Disease Models, Animal, Dopamine Agents pharmacology, Male, Oxidopamine pharmacology, Parkinson Disease drug therapy, Rats, Rats, Sprague-Dawley, Alanine analogs & derivatives, Benzylamines pharmacology, Dyskinesia, Drug-Induced drug therapy, Excitatory Amino Acid Agents pharmacology, Levodopa pharmacology, Signal Transduction drug effects
- Abstract
Safinamide (Xadago) is a novel dual-mechanism drug that has been approved in the European Union and United States as add-on treatment to levodopa in Parkinson's disease therapy. In addition to its selective and reversible monoamine oxidase B inhibition, safinamide through use-dependent sodium channel blockade reduces overactive glutamatergic transmission in basal ganglia, which is believed to contribute to motor symptoms and complications including levodopa-induced dyskinesia (LID). The present study investigated the effects of safinamide on the development of LID in 6-hydroxydopamine (6-OHDA)-lesioned rats, evaluating behavioral, molecular, and neurochemical parameters associated with LID appearance. 6-OHDA-lesioned rats were treated with saline, levodopa (6 mg/kg), or levodopa plus safinamide (15 mg/kg) for 21 days. Abnormal involuntary movements, motor performance, molecular composition of the striatal glutamatergic synapse, glutamate, and GABA release were analyzed. In the striatum, safinamide prevented the rearrangement of the subunit composition of N -methyl-d-aspartate receptors and the levodopa-induced increase of glutamate release associated with dyskinesia without affecting the levodopa-stimulated motor performance and dyskinesia. Overall, these findings suggest that the striatal glutamate-modulating component of safinamide's activity may contribute to its clinical effects, where its long-term use as levodopa add-on therapy significantly improves motor function and "on" time without troublesome dyskinesia., (Copyright © 2018 by The American Society for Pharmacology and Experimental Therapeutics.)
- Published
- 2018
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12. Safinamide Differentially Modulates In Vivo Glutamate and GABA Release in the Rat Hippocampus and Basal Ganglia.
- Author
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Morari M, Brugnoli A, Pisanò CA, Novello S, Caccia C, Melloni E, Padoani G, Vailati S, and Sardina M
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- Alanine pharmacology, Animals, Basal Ganglia cytology, Hippocampus cytology, Male, Neurons drug effects, Neurons metabolism, Rats, Rats, Sprague-Dawley, Alanine analogs & derivatives, Basal Ganglia drug effects, Basal Ganglia metabolism, Benzylamines pharmacology, Glutamic Acid metabolism, Hippocampus drug effects, Hippocampus metabolism, gamma-Aminobutyric Acid metabolism
- Abstract
Safinamide has been recently approved as an add-on to levodopa therapy for Parkinson disease. In addition to inhibiting monoamine oxidase type B, it blocks sodium channels and modulates glutamate (Glu) release in vitro. Since this property might contribute to the therapeutic action of the drug, we undertook the present study to investigate whether safinamide inhibits Glu release also in vivo and whether this effect is consistent across different brain areas and is selective for glutamatergic neurons. To this aim, in vivo microdialysis was used to monitor the spontaneous and veratridine-induced Glu and GABA release in the hippocampus and basal ganglia of naive, awake rats. Brain levels of safinamide were measured as well. To shed light on the mechanisms underlying the effect of safinamide, sodium currents were measured by patch-clamp recording in rat cortical neurons. Safinamide maximally inhibited the veratridine-induced Glu and GABA release in hippocampus at 15 mg/kg, which reached free brain concentrations of 1.89-1.37 µ M. This dose attenuated veratridine-stimulated Glu (but not GABA) release in subthalamic nucleus, globus pallidus, and substantia nigra reticulata, but not in striatum. Safinamide was ineffective on spontaneous neurotransmitter release. In vitro, safinamide inhibited sodium channels, showing a greater affinity at depolarized (IC
50 = 8 µ M) than at resting (IC50 = 262 µ M) potentials. We conclude that safinamide inhibits in vivo Glu release from stimulated nerve terminals, likely via blockade of sodium channels at subpopulations of neurons with specific firing patterns. These data are consistent with the anticonvulsant and antiparkinsonian actions of safinamide and provide support for the nondopaminergic mechanism of its action., (Copyright © 2018 The Author(s).)- Published
- 2018
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13. Fertility preservation in female cancer patients: a single center experience.
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Sigismondi C, Papaleo E, Viganò P, Vailati S, Candiani M, Ottolina J, Di Mattei VE, and Mangili G
- Subjects
- Adolescent, Adult, Child, Child, Preschool, Counseling, Female, Humans, Middle Aged, Oocyte Retrieval, Fertility Preservation, Neoplasms physiopathology
- Abstract
Advances in cancer treatment allow women to be cured and live longer. However, the necessary chemotherapy and radiotherapy regimens have a negative impact on future fertility. Oncofertility has emerged as a new interdisciplinary field to address the issue of gonadotoxicity associated with cancer treatment and to facilitate fertility preservation, including oocyte and ovarian tissue cryopreservation. These fertility issues are often inadequately addressed, and referral rates to oncofertility centers are low. The aim of this study was to report the 3-year experience of the San Raffaele Oncofertility Unit. A total of 96 patients were referred to the Oncofertility Unit for evaluation after the diagnosis of cancer and before gonadotoxic treatment between April 2011 and June 2014. Of the 96 patients, 30 (31.2%) were affected by breast cancers, 20 (20.8%) by sarcomas, 28 (29.2%) by hematologic malignancies, 13 (13.5%) by central nervous system cancers, 3 (3.1%) by bowel tumors, 1 (1.0%) by Wilms' tumor, and 1 (1.0%) by a thyroid tumor; 47 (49.0%) were referred for oocyte cryopreservation before starting chemotherapy, 20 (20.8%) were referred for ovarian tissue cryopreservation, and 29 (30.2%) were not recruited. The mean time between the patients' counseling and oocyte retrieval was 15 days (range, 2-37 days). The mean time between the laparoscopic surgery and the beginning of treatment was 4 days (range, 2-10 days). The number of patients who were referred increased over time, whereas the rate of patients who were not recruited decreased, showing an improvement in referrals to the Oncofertility Unit and in the patients' counseling and understanding. Our results indicate that an effective multidisciplinary oncofertility team is necessary for prompt referrals and treatment.
- Published
- 2015
- Full Text
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