1.

Record Nr.

UNICAMPANIAVAN00274644

Autore

Gupta, Vijay K.

Titolo

Computation and Approximation / Vijay Gupta, Michael Th. Rassias

Pubbl/distr/stampa

Cham, : Springer, 2021

Descrizione fisica

vii, 99 p. : ill. ; 24 cm

Altri autori (Persone)

Rassias, Michael Th. <1987- >

Soggetti

26A15 - Continuity and related questions (modulus of continuity, semicontinuity, discontinuities, etc.) for real functions in one variable [MSC 2020]

41A10 - Approximation by polynomials [MSC 2020]

41A25 - Rate of convergence, degree of approximation [MSC 2020]

41A36 - Approximation by positive operators [MSC 2020]

Lingua di pubblicazione

Inglese

Formato

Materiale a stampa

Livello bibliografico

Monografia



2.

Record Nr.

UNINA9910220036503321

Autore

Laura Lossi

Titolo

Reelin-Related Neurological Disorders and Animal Models

Pubbl/distr/stampa

Frontiers Media SA, 2017

Descrizione fisica

1 online resource (179 p.)

Collana

Frontiers Research Topics

Soggetti

Neurosciences

Lingua di pubblicazione

Inglese

Formato

Materiale a stampa

Livello bibliografico

Monografia

Sommario/riassunto

The Reeler mutation was so named because of the alterations in gait that characterize homozygous mice. Several decades after the description of the Reeler phenotype, the mutated protein was discovered and named Reelin (Reln). Reln controls a number of fundamental steps in embryonic and postnatal brain development. A prominent embryonic function is the control of radial neuronal migration. As a consequence, homozygous Reeler mutants show disrupted cell layering in cortical brain structures. Reln also promotes postnatal neuronal maturation. Heterozygous mutants exhibit defects in dendrite extension and synapse formation, correlating with behavioral and cognitive deficits that are detectable at adult ages. The Reln-encoding gene is highly conserved between mice and humans. In humans, homozygous RELN mutations cause lissencephaly with cerebellar hypoplasia, a severe neuronal migration disorder that is reminiscent of the Reeler phenotype. In addition, RELN deficiency or dysfunction is also correlated with psychiatric and cognitive disorders, such as schizophrenia, bipolar disorder and autism, as well as some forms of epilepsy and Alzheimer's disease. Despite the wealth of anatomical studies of the Reeler mouse brain, and the molecular dissection of Reln signaling mechanisms, the consequences of Reln deficiency on the development and function of the human brain are not yet completely understood. This Research Topic include reviews that summarize our current knowledge of the molecular aspects of Reln



function, original articles that advance our understanding of its expression and function in different brain regions, and reviews that critically assess the potential role of Reln in human psychiatric and cognitive disorders.