117 research outputs found
Orientations of the lamellar phase of block copolymer melts under oscillatory shear flow
We develop a theory to describe the reorientation phenomena in the lamellar
phase of block copolymer melt under reciprocating shear flow. We show that
similar to the steady-shear, the oscillating flow anisotropically suppresses
fluctuations and gives rise to the parallel-perpendicular orientation
transition. The experimentally observed high-frequency reverse transition is
explained in terms of interaction between the melt and the shear-cell walls.Comment: RevTex, 3 pages, 1 figure, submitted to PR
Shear induced instabilities in layered liquids
Motivated by the experimentally observed shear-induced destabilization and
reorientation of smectic A like systems, we consider an extended formulation of
smectic A hydrodynamics. We include both, the smectic layering (via the layer
displacement u and the layer normal p) and the director n of the underlying
nematic order in our macroscopic hydrodynamic description and allow both
directions to differ in non equilibrium situations. In an homeotropically
aligned sample the nematic director does couple to an applied simple shear,
whereas the smectic layering stays unchanged. This difference leads to a finite
(but usually small) angle between n and p, which we find to be equivalent to an
effective dilatation of the layers. This effective dilatation leads, above a
certain threshold, to an undulation instability of the layers. We generalize
our earlier approach [Rheol. Acta, vol.39(3), 15] and include the cross
couplings with the velocity field and the order parameters for orientational
and positional order and show how the order parameters interact with the
undulation instability. We explore the influence of various material parameters
on the instability. Comparing our results to recent experiments and molecular
dynamic simulations, we find a good qualitative agreement.Comment: 15 pages, 12 figures, accepted for publication in PR
Apolipoprotein E4 influences amyloid deposition but not cell loss after traumatic brain injury in a mouse model of Alzheimer's disease
The epsilon4 allele of apolipoprotein E (APOE) and traumatic brain injury (TBI) are both risk factors for the development of Alzheimer's disease (AD). These factors may act synergistically, in that APOE4+ individuals are more likely to develop dementia after TBI. Because the mechanism underlying these effects is unclear, we questioned whether APOE4 and TBI interact either through effects on amyloid-beta (Abeta) or by enhancing cell death/tissue injury. We assessed the effects of TBI in PDAPP mice (transgenic mice that develop AD-like pathology) expressing human APOE3 (PDAPP:E3), human APOE4 (PDAPP:E4), or no APOE (PDAPP:E-/-). Mice were subjected to a unilateral cortical impact injury at 9-10 months of age and allowed to survive for 3 months. Abeta load, hippocampal/cortical volumes, and hippocampal CA3 cell loss were quantified using stereological methods. All of the groups contained mice with Abeta-immunoreactive deposits (56% PDAPP:E4, 20% PDAPP:E3, 75% PDAPP:E-/-), but thioflavine-S-positive Abeta (amyloid) was present only in the molecular layer of the dentate gyrus in the PDAPP:E4 mice (44%). In contrast, our previous studies showed that in the absence of TBI, PDAPP:E3 and PDAPP:E4 mice have little to no Abeta deposition at this age. After TBI, all of the Abeta deposits present in PDAPP:E3 and PDAPP:E-/- mice were diffuse plaques. In contrast to the effect of APOE4 on amyloid, PDAPP:E3, PDAPP:E4, and PDAPP:E-/- mice did not differ in the amount of brain tissue or cell loss. These data support the hypothesis that APOE4 influences the neurodegenerative cascade after TBI via an effect on Abeta
Influence of confinement on the orientational phase transitions in the lamellar phase of a block copolymer melt under shear flow
In this work we incorporate some real-system effects into the theory of
orientational phase transitions under shear flow (M. E. Cates and S. T. Milner,
Phys. Rev. Lett. v.62, p.1856 (1989) and G. H. Fredrickson, J. Rheol. v.38,
p.1045 (1994)). In particular, we study the influence of the shear-cell
boundaries on the orientation of the lamellar phase. We predict that at low
shear rates the parallel orientation appears to be stable. We show that there
is a critical value of the shear rate at which the parallel orientation loses
its stability and the perpendicular one appears immediately below the spinodal.
We associate this transition with a crossover from the fluctuation to the
mean-field behaviour. At lower temperatures the stability of the parallel
orientation is restored. We find that the region of stability of the
perpendicular orientation rapidly decreases as shear rate increases. This
behaviour might be misinterpreted as an additional perpendicular to parallel
transition recently discussed in literature.Comment: 25 pages, 4 figures, submitted to Phys. Rev.
Tracking Membrane Protein Association in Model Membranes
Membrane proteins are essential in the exchange processes of cells. In spite of great breakthrough in soluble proteins studies, membrane proteins structures, functions and interactions are still a challenge because of the difficulties related to their hydrophobic properties. Most of the experiments are performed with detergent-solubilized membrane proteins. However widely used micellar systems are far from the biological two-dimensions membrane. The development of new biomimetic membrane systems is fundamental to tackle this issue
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Missense mutation of Brain Derived Neurotrophic Factor (BDNF) alters neurocognitive performance in patients with mild traumatic brain injury: a longitudinal study
The predictability of neurocognitive outcomes in patients with traumatic brain injury is not straightforward. The extent and nature of recovery in patients with mild traumatic brain injury (mTBI) are usually heterogeneous and not substantially explained by the commonly known demographic and injury-related prognostic factors despite having sustained similar injuries or injury severity. Hence, this study evaluated the effects and association of the Brain Derived Neurotrophic Factor (BDNF) missense mutations in relation to neurocognitive performance among patients with mTBI. 48 patients with mTBI were prospectively recruited and MRI scans of the brain were performed within an average 10.1 (SD 4.2) hours post trauma with assessment of their neuropsychological performance post full Glasgow Coma Scale (GCS) recovery. Neurocognitive assessments were repeated again at 6 months follow-up. The paired t-test, Cohen’s d effect size and repeated measure ANOVA were performed to delineate statistically significant differences between the groups [wildtype G allele (Val homozygotes) vs. minor A allele (Met carriers)] and their neuropsychological performance across the time point (T1 = baseline/ admission vs. T2 = 6th month follow-up). Minor A allele carriers in this study generally performed more poorly on neuropsychological testing in comparison wildtype G allele group at both time points. Significant mean differences were observed among the wildtype group in the domains of memory (M = -11.44, SD = 10.0, p = .01, d = 1.22), executive function (M = -11.56, SD = 11.7, p = .02, d = 1.05) and overall performance (M = -6.89 SD = 5.3, p = .00, d = 1.39), while the minor A allele carriers showed significant mean differences in the domains of attention (M = -11.0, SD = 13.1, p = .00, d = .86) and overall cognitive performance (M = -5.25, SD = 8.1, p = .01, d = .66).The minor A allele carriers in comparison to the wildtype G allele group, showed considerably lower scores at admission and remained impaired in most domains across the timepoints, although delayed signs of recovery were noted to be significant in the domains attention and overall cognition. In conclusion, the current study has demonstrated the role of the BDNF rs6265 Val66Met polymorphism in influencing specific neurocognitive outcomes in patients with mTBI. Findings were more detrimentally profound among Met allele carriers
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