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Biomedical subjects

A Cavagna

Publications and source records attributed to A Cavagna.

8 recordsLinked to original sources
PubMed2001

Interface fluctuations under shear.

Coarsening systems under uniform shear display a long time regime characterized by the presence of highly stretched and thin domains. The question then arises whether thermal fluctuations may actually destroy this layered structure. To address this problem in the case of nonconserved dynamics, we study an anisotropic version of the Burgers equation, constructed to describe thermal fluctuations of an interface in the presence of a uniform shear flow. As a result, we find that stretched domains are only marginally stable against thermal fluctuations in d=2, whereas they are stable in d=3.

Journal Article↗
PubMed2000

Energy landscape of a lennard-jones liquid: statistics of stationary points.

Molecular dynamics simulations are used to generate an ensemble of saddles of the potential energy of a Lennard-Jones liquid. Classifying all extrema by their potential energy u and number of unstable directions k, a well-defined relation k(u) is revealed. The degree of instability of typical stationary points vanishes at a threshold potential energy u(th), which lies above the energy of the lowest glassy minima of the system. The energies of the inherent states, as obtained by the Stillinger-Weber method, approach u(th) at a temperature close to the mode-coupling transition temperature T(c).

Journal Article↗
PubMed2000

Ohta-jasnow-kawasaki approximation for nonconserved coarsening under shear

We analytically study coarsening dynamics in a system with nonconserved scalar order parameter, when a uniform time-independent shear flow is present. We use an anisotropic version of the Ohta-Jasnow-Kawasaki approximation to calculate the growth exponents in two and three dimensions: for d=3 the exponents we find are the same as expected on the basis of simple scaling arguments, that is, 3/2 in the flow direction and 1/2 in all the other directions, while for d=2 we find an unusual behavior, in that the domains experience an unlimited narrowing for very large times and a nontrivial dynamical scaling appears. In addition, we consider the case where an oscillatory shear is applied to a two-dimensional system, finding in this case a standard t(1/2) growth, modulated by periodic oscillations. We support our two-dimensional results by means of numerical simulations and we propose to test our predictions by experiments on twisted nematic liquid crystals.

Journal Article↗
PubMed1994

Genetic homogeneity of Pelizaeus-Merzbacher disease: tight linkage to the proteolipoprotein locus in 16 affected families. PMD Clinical Group.

Among the numerous leukodystrophies that have an early onset and no biochemical markers, Pelizaeus-Merzbacher disease (PMD) is one that can be identified using strict clinical criteria and demonstrating an abnormal formation of myelin that is restricted to the CNS in electrophysiological studies and brain magnetic resonance imaging (MRI). In PMD, 12 different base substitutions and one total deletion of the genomic region containing the PLP gene have been reported, but, despite extensive analysis, PLP exon mutations have been found in only 10%-25% of the families analyzed. To test the genetic homogeneity of this disease, we have carried out linkage analysis with polymorphic markers of the PLP genomic region in 16 families selected on strict diagnostic criteria of PMD. We observed a tight linkage of the PMD locus with markers of the PLP gene (cDNA PLP, exon IV polymorphism) and of the Xq22 region (DXS17, DXS94, and DXS287), whereas the markers located more proximally (DXYS1X and DXS3) or distally (DXS11) were not linked to the PMD locus. Multipoint analysis gave a maximal location score for the PMD locus (13.98) and the PLP gene (8.32) in the same interval between DXS94 and DXS287, suggesting that in all families PMD is linked to the PLP locus. Mutations of the extraexonic PLP gene sequences or of another unknown close gene could be involved in PMD. In an attempt to identify molecular defects of this genomic region that are responsible for PMD, these results meant that RFLP analysis could be used to improve genetic counseling for the numerous affected families in which a PLP exon mutation could not be demonstrated.

Adolescent↗
PubMed1993

Pelizaeus-Merzbacher disease: a frameshift deletion/insertion event in the myelin proteolipid gene.

Among the central nervous system (CNS) dysmyelinating disorders, Pelizaeus-Merzbacher disease (PMD) has been individualized by its X-linked mode of inheritance and the existence of corresponding animal models. Mutations in the major myelin proteolipid (PLP) gene coding for PLP and its splicing variant DM20 protein, have been demonstrated in animal mutants and more recently in PMD affected patients. We have identified, in a two-generation PMD affected family, an insertion/deletion event in the exon IV of the PLP gene, leading to the synthesis of predicted truncated PLP and DM20 proteins with altered carboxyl terminal end. This is the first report of a frameshift mutation in the PLP gene in PMD.

Amino Acid Sequence↗