Asymptotic Hyperstability of a Class of Linear Systems under Impulsive Controls Subject to an Integral Popovian Constraint

This paper is focused on the study of the important property of the asymptotic hyperstability of a class of continuous-time dynamic systems. The presence of a parallel connection of a strictly stable subsystem to an asymptotically hyperstable one in the feed-forward loop is allowed while it has also admitted the generation of a finite or infinite number of impulsive control actions which can be combined with a general form of nonimpulsive controls. The asymptotic hyperstability property is guaranteed under a set of sufficiency-type conditions for the impulsive controls.

An Algebraic Preservation Theorem for Aleph-Zero Categorical Quantified Constraint Satisfaction

23 p. -- An extended abstract of this work appears in the proceedings of the 2012 ACM/IEEE Symposium on Logic in Computer Science

Beyond Q-Resolution and Prenex Form: a Proof System for Quantified Constraint Satisfaction

We consider the quanti fied constraint satisfaction problem (QCSP) which is to decide, given a structure and a first-order sentence (not assumed here to be in prenex form) built from conjunction and quanti fication, whether or not the sentence is true on the structure. We present a proof system for certifying the falsity of QCSP instances and develop its basic theory; for instance, we provide an algorithmic interpretation of its behavior. Our proof system places the established Q-resolution proof system in a broader context, and also allows us to derive QCSP tractability results.

Muscle wasting in myotonic dystrophies: a model of premature aging

Myotonic dystrophy type 1 (DM1 or Steinert's disease) and type 2 (DM2) are multisystem disorders of genetic origin. Progressive muscular weakness, atrophy and myotonia are the most prominent neuromuscular features of these diseases, while other clinical manifestations such as cardiomyopathy, insulin resistance and cataracts are also common. From a clinical perspective, most DM symptoms are interpreted as a result of an accelerated aging (cataracts, muscular weakness and atrophy, cognitive decline, metabolic dysfunction, etc.), including an increased risk of developing tumors. From this point of view, DM1 could be described as a progeroid syndrome since a notable age dependent dysfunction of all systems occurs. The underlying molecular disorder in DM1 consists of the existence of a pathological (CTG) triplet expansion in the 3' untranslated region (UTR) of the Dystrophia ll/Iyotonica Protein Kinase (DMPK) gene, whereas (CCTG)n repeats in the first intron of the Cellular Nucleic acid Binding Protein/Zinc Finger Protein 9 (CNBP/ZNF9) gene cause DM2. The expansions are transcribed into (CUG)n and (CCUG)n-containing RNA, respectively, which form secondary structures and sequester RNA binding proteins, such as the splicing factor muscleblind-like protein (MBNL), forming nuclear aggregates known as foci. Other splicing factors, such as CUGBP, are also disrupted, leading to a spliceopathy of a large number of downstream genes linked to the clinical features of these diseases. Skeletal muscle regeneration relies on muscle progenitor cells, known as satellite cells, which are activated after muscle damage, and which proliferate and differentiate to muscle cells, thus regenerating the damaged tissue. Satellite cell dysfunction seems to be a common feature of both age-dependent muscle degeneration (sarcopenia) and muscle wasting in DM and other muscle degenerative diseases. This review aims to describe the cellular, molecular and macrostructural processes involved in the muscular degeneration seen in DM patients, highlighting the similarities found with muscle aging.