Velocity autocorrelation function of a Brownian particle

In this article, we present molecular dynamics study of the velocity autocorrelation function (VACF) of a Brownian particle. We compare the results of the simulation with the exact analytic predictions for a compressible fluid from [6] and an approximate result combining the predictions from hydrodynamics at short and long times. The physical quantities which determine the decay were determined from separate bulk simulations of the Lennard-Jones fluid at the same thermodynamic state point.We observe that the long-time regime of the VACF compares well the predictions from the macroscopic hydrodynamics, but the intermediate decay is sensitive to the viscoelastic nature of the solvent.Comment: 7 pages, 6 figure

Evolution of Recrystallization Texture in AISI300 Series Austenitic Stainless Steels After Cold Rolling to Large Strain

The present paper deals with the evolution of texture in austenitic stainless steels during annealing after 95% cold rolling. After 95% cold rolling, the texture is mainly of the brass type {110} along with a scatter towards the S orientation {123} and Goss orientation {011} . Weak evidence of Cu component is observed at this high deformation level. During annealing, recovery is observed before any detectable recrystallization. After recrystallization, the overall texture intensity was weak; however, there are some discernible texture components. There was no existence of the brass component at this stage. Major components are centered on Goss orientation and Cu component {112} as well as the BR component {236} . Also, there are some few orientations which come up after recrystallization i.e. {142} and {012} . With increase in annealing temperature the textural evolution shows emergence of weak texture with another new component i.e. {197} . The evolution of texture was correlated with the deformation texture through twin chain reaction

Congenital disorders of glycosylation in hepatology: the example of polycystic liver disease.

Contains fulltext : 89364.pdf (publisher's version ) (Closed access)Autosomal dominant polycystic liver disease (PCLD) is a rare progressive disorder characterized by an increased liver volume due to many (>20) fluid-filled cysts of biliary origin. Disease causing mutations in PRKCSH or SEC63 are found in approximately 25% of the PCLD patients. Both gene products function in the endoplasmic reticulum, however, the molecular mechanism behind cyst formation remains to be elucidated. As part of the translocon complex, SEC63 plays a role in protein import into the ER and is implicated in the export of unfolded proteins to the cytoplasm during ER-associated degradation (ERAD). PRKCSH codes for the beta-subunit of glucosidase II (hepatocystin), which cleaves two glucose residues of Glc(3)Man(9)GlcNAc(2) N-glycans on proteins. Hepatocystin is thereby directly involved in the protein folding process by regulating protein binding to calnexin/calreticulin in the ER. A separate group of genetic diseases affecting protein N-glycosylation in the ER is formed by the congenital disorders of glycosylation (CDG). In distinct subtypes of this autosomal recessive multisystem disease specific liver symptoms have been reported that overlap with PCLD. Recent research revealed novel insights in PCLD disease pathology such as the absence of hepatocystin from cyst epithelia indicating a two-hit model for PCLD cystogenesis. This opens the way to speculate about a recessive mechanism for PCLD pathophysiology and shared molecular pathways between CDG and PCLD. In this review we will discuss the clinical-genetic features of PCLD and CDG as well as their biochemical pathways with the aim to identify novel directions of research into cystogenesis.1 maart 201