Algoritmo de Gale-Shapley. Variaciones y alternativas

En esta memoria se trata el problema de encontrar un algoritmo que construya un emparejamiento entre dos grupos, entendiendo por emparejamiento la asignacion a cada individuo, de cada grupo, otro individuo. La situaci on inicial de la que parte el problema es la siguiente: Dos grupos, los proponentes y los propuestos, que est an formados por n individuos cada uno, siendo n la dimensi on del problema. El grupo de los proponentes es el encargado de hacer las propuestas a la hora de construir el emparejamiento. El grupo de los propuestos es el encargado de recibir y gestionar las propuestas a la hora de construir el emparejamiento. Cada individuo de cada grupo ordena en una lista, de manera decreciente, a individuos del otro grupo atendiendo a su preferencia a la hora de ser emparejado, a esta lista la llamaremos lista de preferencia del individuo, considerando el quedarse solo la opci on menos preferida de entre las aceptables. El objetivo del problema es crear un emparejamiento en el que cada pareja sea satisfactoria para los individuos que la crean en base a las preferencias de cada uno.

UDP-galactose 4-epimerase (GALE)

UDP-galactose 4-epimerase (GALE; EC 5.1.3.2; UniProt: Q14376) catalyses the interconversion of UDP-galactose and UDP-glucose (figure 1a). In the majority of eukaryotes studied to date, the enzyme is also able to interconvert UDP-N-acetylgalactosamine (UDP-GalNAc) and UDP-N-acetylglucosamine (UDP-GlcNAc) (figure 1b). The first of these reactions occurs as part of the Leloir pathway, which converts galactose into the glycolytic intermediate glucose 6-phosphate. Both reactions are important in the maintenance of UDP-monosaccharide pools and, consequently, in supplying raw materials for the glycosylation of proteins and lipids. The enzyme has attracted considerable research interest because mutations in the corresponding gene are associated with the genetic disease type III galactosemia (OMIN #230350). There is also some interest in using the enzyme as a biocatalyst to interconvert its substrates and related UDP-monosaccharides.

The metastability of human UDP-galactose 4'-epimerase (GALE) is increased by variants associated with type III galactosemia but decreased by substrate and cofactor binding

Type III galactosemia is an inherited disease caused by mutations which affect the activity of UDP-galactose 4'-epimerase (GALE). We evaluated the impact of four disease-associated variants (p.N34S, p.G90E, p.V94M and p.K161N) on the conformational stability and dynamics of GALE. Thermal denaturation studies showed that wild-type GALE denatures at temperatures close to physiological, and disease-associated mutations often reduce GALE's thermal stability. This denaturation is under kinetic control and results partly from dimer dissociation. The natural ligands, NAD(+) and UDP-glucose, stabilize GALE. Proteolysis studies showed that the natural ligands and disease-associated variations affect local dynamics in the N-terminal region of GALE. Proteolysis kinetics followed a two-step irreversible model in which the intact protein is cleaved at Ala38 forming a long-lived intermediate in the first step. NAD(+) reduces the rate of the first step, increasing the amount of undigested protein whereas UDP-glucose reduces the rate of the second step, increasing accumulation of the intermediate. Disease-associated variants affect these rates and the amounts of protein in each state. Our results also suggest communication between domains in GALE. We hypothesize that, in vivo, concentrations of natural ligands modulate GALE stability and that it should be possible to discover compounds which mimic the stabilising effects of the natural ligands overcoming mutation-induced destabilization.

Brucella melitensis 16M: characterisation of the galE gene and mouse immunisation studies with a galE deficient mutant

The galE gene of Streptomyces lividans was used to probe a cosmid library harbouring Brucella melitensis 16M DNA and the nucleotide sequence of a 2.5 kb ClaI fragment which hybridised was determined. An open reading frame encoding a predicted polypeptide with significant homology to UDP-galactose-4-epimerases of Brucella arbortus strain 2308 and other bacterial species was identified. DNA sequences flanking the B. melitensis galE gene shared no identity with other gal genes and, as for B. abortus, were located adjacent to a mazG homologue. A plasmid which encoded the B. melitensis galE open reading frame complemented a galE mutation in Salmonella typhimurium LB5010, as shown by the restoration of smooth lipopolysaccharide (LPS) biosynthesis, sensitivity to phage P22 infection and restoration of UDP-galactose-4-epimerase activity. The galE gene on the B. melitensis 16M chromosome was disrupted by insertional inactivation and these mutants lacked UDP-galactose-4-epimerase activity but no discernible differences in LPS structure between parent and the mutants were observed. One B. melitensis 16M galE mutant, Bm92, was assessed for virulence in CD-1 and BALB/c mice and displayed similar kinetics of invasion and persistence in tissues compared with the parent bacterial strain. CD-1 mice immunised with B. melitensis 16M galE were protected against B. melitensis 16M challenge. Crown Copyright (C) 1999 Published by Elsevier Science B.V.

Contágio no modelo de Allen e Gale com infraestrutura bancária endógena

Neste trabalho investigamos a formação de network considerando agentes cautelosos. O modelo consiste em duas regiões com (n/2) bancos em cada, onde a interligação entre eles ocorre através e depósitos interbancários. Cada banco está sujeito a corrida bancária, ou devido a um choque negativo de agentes impacientes, ou devido a contaminação da corrida de um banco pertencente a infraestrutura bancária. Os bancos podem tentar eliminar a possibilidade de contágio ao fazer um número alto de inter-ligações. Para isso, é necessário uma coordenação entre todos os bancos. Se um banco não se prevenir de um contágio, ele impõe a todos os outros a possibilidade de contágio no pior cenário. Há duas regiões bem definidas de equilíbrio de nash simétrico com network estável, uma na qual todos os bancos se previnem do cenário de contágio no pior cenário e a outra na qual nenhum banco se previne. Devido ao problema de coordenação, o equilíbrio com contágio no pior cenário pode ocorrer mesmo sendo pareto dominado pelo equilíbrio sem contágio. Sob certas condições, o equilíbrio com contágio ocorre com um network pareto eficiente. Neste caso o network eficiente é diferente do network mais resiliente ao contágio.