1,723,014 research outputs found
Amedeo Avogadro Come Ritratto Da Eligio Perucca in Un Articolo Del 1957 (Amedeo Avogadro as Portrayed by Eligio Perucca in an Article of 1957)
No full textItalian Abstract: Eligio Perucca, che è stato professore di Fisica al Politecnico di Torino, ha scritto e pubblicato nel 1957 sul Nuovo Cimento, un articolo sulla vita e le opere di Amedeo Avogadro. Quello di Perucca è un lavoro che non solo ci riporta fatti e riferimenti bibliografici, ma che ci fornisce un ritratto appassionato di Amedeo, anzi di Aimé, come ogni tanto il professore del Politecnico chiama Avogadro. Questo articolo discute proprio il ritratto scritto da Perucca, che usiamo come guida per conoscere il lavoro scientifico di Amedeo Avogadro, lavoro che fu di un chimico-fisico di “quando la chimica fisica era scienza non ancora nata”. Commentando l’articolo di Perucca, verranno aggiunti molti cenni storici al Piemonte ed alle vite di tanti altri illustri scienziati del tempo ed alcune digressioni di fisica.
English Abstract: Eligio Perucca, who was professor of Physics at the Polytechnic of Turin, wrote and published in 1957 on the Nuovo Cimento, an article on life and works of Amedeo Avogadro. The article by Perucca is a work that not only brings us facts and scientific references, but that gives us a passionate portrait of Amedeo, or Aimé, as sometime the professor of the Polytechnic calls Avogadro. This article discusses this portrait made by Perucca, which we use as a guide to know Amedeo Avogadro and his scientific work, a work that was of a "chemical-physicist when the chemical-physics was not born yet." Commenting on this article by Perucca, many historical notes will be added about Piedmont and the lives of many other illustrious scientists of the time and some digressions on physics.
Note: Downloadable document is available in Italian
Age-Related Changes in Pharmacokinetics: Predictability and Assessment Methods
No full textAlthough there have been relatively few studies of the pharmacokinetics of antiepileptic drugs (AEDs) in old age, available evidence indicates that the clearance of most old and new generation AEDs is reduced on average by about 20-40% in elderly patients compared with nonelderly adults. Depending on the pharmacokinetic characteristics of the drug, the reduction in clearance can be ascribed to a physiological reduction in rate of drug metabolism, to a decrease in renal excretion rate, or to both. Studies have consistently demonstrated that interindividual pharmacokinetic variability in old age is particularly prominent, due not only to the influence of aging-related physiological changes, but also to the impact of comorbidities and drug-drug interactions. For extensively metabolized drugs, there are no reliable tools to predict with a high degree of accuracy the pharmacokinetic behavior of an AED in an individual patient. With renally eliminated drugs, determination of creatinine clearance may provide a useful clue in predicting individual changes in drug clearance and the consequent need for dosage adjustment. In the therapeutic setting, measurement of serum AED concentrations can be valuable in individualizing dosage in an elderly person, even though it should be remembered that in the case of drugs that are highly bound to plasma proteins the total serum concentration may underestimate the level of unbound, pharmacologically active drug. Because aging is also associated with important pharmacodynamic changes that may alter the relationship between serum drug concentration and pharmacological effects, pharmacokinetic measurements alone are not a substitute for the need to monitor clinical response carefully and to adjust dosage accordingly. © 2006 Elsevier Inc. All rights reserved
Pauli letter collection: letter to Wolfgang Pauli
No full textPerucca sends a reprint on a unified system of units. He gives his views on it
Identifying mutations in epilepsy genes: Impact on treatment selection
No full textThe last decade saw impressive advances not only in the discovery of gene mutations causing epilepsy, but also in unraveling the molecular mechanisms underlying the clinical manifestations of the disease. Increasing evidence is emerging that understanding these mechanisms is relevant for selection of the most appropriate treatment in the affected individual(s). The present article discusses the therapeutic implications of epilepsy causing variants affecting a broad range of targets, from ion channels to genes controlling cellular metabolism and cell signaling pathways. Identification of a precise genetic etiology can direct physicians to (i) prescribe treatments that correct specific metabolic defects (e.g., the ketogenic diet for GLUT1 deficiency, or pyridoxine for pyridoxine-dependent epilepsies); (ii) avoid antiepileptic drugs (AEDs) that can aggravate the pathogenic defect (e.g., sodium channel blocking drugs in SCN1A-related Dravet syndrome), or (iii) select AEDs that counteract the functional disturbance caused by the gene mutation (e.g., sodium channel blockers for epilepsies due to gain-of-function SCN8A mutations). In some instances, different pathogenic variants of the same gene can have opposite functional effects, which determines whether certain treatments can be beneficial or deleterious (e.g., gain-of-function versus loss-of-function variants in SCN2A determine whether sodium channel blockers improve or worsen seizure control). There are also cases where functional disturbances caused by the gene defect may not be corrected by existing AEDs, but can be countered by medications already available in the market for other indications (e.g., memantine has been used to treat the epileptic encephalopathy caused by a specific gain-of-function GRIN2A mutation), thus making 'drug repurposing' a valuable tool for personalized epilepsy therapies. As our understanding of pathogenic mechanisms improve, opportunities arise for development of treatments targeting the specific gene defect or its consequences. Everolimus, an mTOR inhibitor approved for the treatment of focal seizures associated with tuberous sclerosis complex, is an example of a medication targeting the etiological mechanisms of the disease. Several treatments aimed at correcting specific pathogenic defects responsible for rare genetic epilepsies are currently in development, and range from traditional small molecules to novel approaches involving peptides, antisense oligonucleotides, and gene therapy
El conflicto textil de los trabajadores de Guilford en Comodoro Rivadavia, 1975-1976
No full textFil: Perucca, Pedro. UBA.Fil: Castro, Diego. UBA
Author Response: Does Screening for Adverse Effects Improve Health Outcomes in Epilepsy? A Randomized Trial
No full text
Current trends in antiepileptic drug therapy
No full textOver the last two decades, drug therapy for epilepsy has improved substantially. This can be ascribed to a large extent to three factors, including the demonstration of the advantages of monotherapy; the realization of the need for dosage tailoring, coupled [for some antiepileptic drugs (AEDs)] with control of pharmacokinetic variability through therapeutic drug monitoring; and the introduction of newer agents with improved tolerability profiles. What further advances should we expect for the future? Current trends that are expected to increasingly affect our prescribing patterns include greater reliance on evidence-based medicine and treatment guidelines, a trend that will be facilitated by completion of therapeutically meaningful randomized trials (including cost-effectiveness studies) and high-quality observational studies (including multinational pregnancy registries), as well as initiatives from scientific societies and government organizations aimed at condensing the most relevant information into therapeutic guidelines. The explosion in communication technology will accelerate dissemination of this information and its application to clinical practice. Other factors include a more rational patient-tailored AED selection and dose individualization, aided by characterization of predictors of outcome as defined by clinical parameters (sex, age, epilepsy syndrome, and etiology), pathophysiological mechanisms, and newly discovered genetic markers of outcome; improved definition of the role of new AEDs, resulting in their increased use in newly diagnosed epilepsy; and reappraisal of the value of combination therapy in refractory epilepsies, based on evidence produced by experimental and clinical studies designed to identify favorable pharmacodynamic interactions. Additional important developments may come from the discovery of novel, more efficacious AEDs and from exploration of potential new targets, such as prevention of epileptogenesis
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