Learning Moore Machines from Input-Output Traces

The problem of learning automata from example traces (but no equivalence or membership queries) is fundamental in automata learning theory and practice. In this paper we study this problem for finite state machines with inputs and outputs, and in particular for Moore machines. We develop three algorithms for solving this problem: (1) the PTAP algorithm, which transforms a set of input-output traces into an incomplete Moore machine and then completes the machine with self-loops; (2) the PRPNI algorithm, which uses the well-known RPNI algorithm for automata learning to learn a product of automata encoding a Moore machine; and (3) the MooreMI algorithm, which directly learns a Moore machine using PTAP extended with state merging. We prove that MooreMI has the fundamental identification in the limit property. We also compare the algorithms experimentally in terms of the size of the learned machine and several notions of accuracy, introduced in this paper. Finally, we compare with OSTIA, an algorithm that learns a more general class of transducers, and find that OSTIA generally does not learn a Moore machine, even when fed with a characteristic sample

Neurofibromatosis: analysis of clinical cases and new diagnostic criteria

Neurofibromatoses are a group of genetic disorders with predisposing for central and peripheral nervous system tumor development. The group includes three entities: neurofibromatosis type I, neurofibromatosis type II and schwannomatosis, which are characterized by gradual phenotype development and have a partially overlapping spectrum of manifestations, which complicates diagnosis establishing, especially at the stage of clinical onset. At the same time, the emergence of new pathogenetic therapy and the high risk of transmission to descendants actualize the necessity of early diagnosis. DNA tests allow us to reliably confirm the presumed diagnosis. This article presents a review of neurofibromatoses, their clinical features and courses, modern diagnostic criteria and indications for DNA tests

Нейрофиброматоз: анализ клинических случаев и новые диагностические критерии

Neurofibromatoses are a group of genetic disorders with predisposing for central and peripheral nervous system tumor development. The group includes three entities: neurofibromatosis type I, neurofibromatosis type II and schwannomatosis, which are characterized by gradual phenotype development and have a partially overlapping spectrum of manifestations, which complicates diagnosis establishing, especially at the stage of clinical onset. At the same time, the emergence of new pathogenetic therapy and the high risk of transmission to descendants actualize the necessity of early diagnosis. DNA tests allow us to reliably confirm the presumed diagnosis. This article presents a review of neurofibromatoses, their clinical features and courses, modern diagnostic criteria and indications for DNA tests.Нейрофиброматозы – группа наследственных заболеваний, которые характеризуются развитием опухолей центральной и периферической нервной системы. Включают 3 нозологии: нейрофиброматоз I типа, нейрофиброматоз II типа и шванноматоз. Эти заболевания отличаются динамическим развитием и имеют схожие клинические проявления, что осложняет постановку клинического диагноза, особенно на этапе клинического дебюта. В то же время появление новых методов патогенетической терапии и высокий риск передачи заболевания потомству обусловливают необходимость ранней диагностики. Одним из методов подтверждения предполагаемого диагноза является молекулярно-генетическое тестирование. В данной статье приведен анализ данных литературы, посвященных особенностям клинического течения нейрофиброматозов, актуальные диагностические критерии, а также показания к проведению молекулярно-генетической диагностики

EFFICACY OF RUFINAMIDE IN THE TREATMENT OF DRUG-RESISTANT FOCAL EPILEPSIES IN PAEDIATRIC PRACTICE

Among drug-resistant epilepsies, epileptic syndromes, characterized by combination of several types of seizures, are considered to be the most difficult in terms of treatment. Lennox–Gastaut syndrome is one of them. It manifests with polymorphic seizures (tonic axial, myatonic, atypical absence seizures, status epilepticus of minor motor seizures, myoclonic, generalized convulsive, and focal seizures). This is a heterogeneous disease, represented by a complex of clinical and electroencephalographic manifestations with various etiology. Current review is devoted to a novel antiepileptic drug rufinamide, which has a new mechanism of action. The drug has been registered in Russia in 2015. The authors also describe their own experience of rufinamide usage in the treatment of drug-resistant focal epilepsy as a part of multicomponent therapy for polymorphic seizures. One patient achieved clinical remission for 16 months; the second one had more than 50 % decrease in seizures frequency with a remission of drop-attacks

ATTENTION DEFICIT HYPERACTIVITY DISORDER: COMORBIDITIES, EMPHASIS ON CONCURRENCE WITH EPILEPSY

Attention deficit hyperactivity disorder (ADHD) is the most common cause of behavioral disorders and learning problems at preschool and school ages. Patients with ADHD are frequently found to have comorbidities that present additional diagnostic and therapeutic problems and result in an even greater decrease in quality of life in patients. Thus, ADHD is frequently concurrent with epilepsy; in this case, not only the manifestations of ADHD are more common in epilepsy, but the latter is more often encountered in patients with ADHD than in those as a whole. The authors consider the epidemiological factors and causes, which may lead to a concurrence of these two diseases in the same patient, the principles of diagnosis and differential diagnosis of ADHD in epileptic patients, the specific features of treatment in this patient category. At the same time, the authors place emphasis on the fact that some antiepileptic drugs, such as barbiturates, may cause symptoms that mimic ADHD (in these cases, inattention and hyperactivity are adverse reactions of therapy and lessen or disappear after drug discontinuation) or enhance the manifestations of ADHD in patients with a concurrence of these two diseases. On the other hand, care should be also taken to choose drugs for the treatment of ADHD due to the possible higher frequency of seizures. So preference should be given to the drugs having no negative effect on the course of comorbidities or those having a positive therapeutic effect against both diseases