Quantifying effective slip length over micropatterned hydrophobic surfaces

We employ micro-particle image velocimetry ($\mu$-PIV) to investigate laminar micro-flows in hydrophobic microstructured channels, in particular the slip length. These microchannels consist of longitudinal micro-grooves, which can trap air and prompt a shear-free boundary condition and thus slippage enhancement. Our measurements reveal an increase of the slip length when the width of the micro-grooves is enlarged. The result of the slip length is smaller than the analytical prediction by Philip et al. [1] for an infinitely large and textured channel comprised of alternating shear-free and no-slip boundary conditions. The smaller slip length (as compared to the prediction) can be attributed to the confinement of the microchannel and the bending of the meniscus (liquid-gas interface). Our experimental studies suggest that the curvature of the meniscus plays an important role in microflows over hydrophobic micro-ridges.Comment: 8 page

The Zipping-wetting Dynamics at the Breakdown of Superhydrophobicity

Under some conditions water droplets can completely wet micro-structured superhydrophobic surfaces. The dynamics of this rapid process is investigated with ultra-high-speed imaging. Depending on the scales of the micro-structure, the wetting fronts propagate smoothly and circularly or – more interestingly – in a stepwise manner for a smaller periodicity of the microstructure. The latter phenomenon leads to a growing square-shaped wetted area: liquid laterally enters a new row on a slow timescale of milliseconds, once it happens the row then fills itself towards the sides in microseconds (“zipping”)

Spontaneous Breakdown of Superhydrophobicity

In some cases water droplets can completely wet micro-structured superhydrophobic surfaces. The {\it dynamics} of this rapid process is analyzed by ultra-high-speed imaging. Depending on the scales of the micro-structure, the wetting fronts propagate smoothly and circularly or -- more interestingly -- in a {\it stepwise} manner, leading to a growing {\it square-shaped} wetted area: entering a new row perpendicular to the direction of front propagation takes milliseconds, whereas once this has happened, the row itself fills in microseconds ({\it ``zipping''})Comment: Accepted for publication in Physical Review Letter

Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress neuropathology in two murine models of AD, Tg2576 and 3xTg. Previously, a genetic deficiency of C1q in the Tg2576 mouse model showed an accumulation of fibrillar plaques similar to the complement sufficient Tg2576, but reactive glia were significantly decreased and neuronal integrity was improved suggesting detrimental consequences for complement activation in AD. The goal of this study was to define the role of the classical complement activation pathway in the progression of pathology in the 3xTg mouse that develops tangles in addition to fibrillar plaques (more closely reflecting human AD pathology) and to assess the influence of complement in a model of AD with a higher level of complement hemolytic activity.</p> <p>Methods</p> <p>3xTg mice deficient in C1q (3xTgQ-/-) were generated, and both 3xTg and 3xTgQ-/- were backcrossed to the BUB mouse strain which has higher in vitro hemolytic complement activity. Mice were aged and perfused, and brain sections stained for pathological markers or analyzed for proinflammatory marker expression.</p> <p>Results</p> <p>3xTgQ-/- mice showed similar amounts of fibrillar amyloid, reactive glia and hyperphosphorylated tau as the C1q-sufficient 3xTg at the ages analyzed. However, 3xTg and 3xTgQ-/- on the BUB background developed pathology earlier than on the original 3xTg background, although the presence of C1q had no effect on neuropathological and pro-inflammatory markers. In contrast to that seen in other transgenic models of AD, C1q, C4 and C3 immunoreactivity was undetectable on the plaques of 3xTg in any background, although C3 was associated with reactive astrocytes surrounding the plaques. Importantly, properdin a component of the alternative complement pathway was associated with plaques in all models.</p> <p>Conclusions</p> <p>In contrast to previously investigated transgenic models of AD, development of neuropathology in 3xTg mice, which progresses much slower than other murine models, may not be influenced by fibrillar amyloid mediated activation of the classical complement pathway, suggesting that the alternative complement pathway activation or a C3-independent cleavage of C5 could account for the detrimental effects in these mice that are prevented by the C5a receptor antagonist. Furthermore, the paucity of complement activation may be a factor in the slower kinetics of progression of pathology in the 3xTg model of this disease.</p

Comparing flat and micro-patterned surfaces: Gas permeation and tensile stress measurements

Micro-patterning is a suitable method to produce structured membranes that display increased flux compared to flat membranes. In this work we studied the permeation of four different gases (nitrogen, helium, oxygen and carbon dioxide) through Kraton™ polymer (SBS) membranes. It is possible to cast a micro-patterned membrane with 25 μm high and 30 μm wide lines that has a thickness of 5 μm at its thinnest point. Using this micro-pattern, the experimental diffusive gas flux was increased up to 59% compared to non-patterned membranes with the same polymer volume. Finite element simulations confirm this enhancement. Selectivities are similar for both flat and micro-patterned membranes and in accordance with literature. Tensile stress measurements confirm that the micro-patterned membranes yield only limited loss in mechanical strength. Although only one material and geometry is explored here, this principle is generally applicable to all diffusion-driven processes

Influence of porous substrate on mesopore structure and water permeability of surfactant templated mesoporous silica membranes

The formation of silica films via sol–gel route on disordered mesoporous and macroporous supports is reported. These films are structurally characterised by TEM, XRD, XPS and permporometry. It has been found that the ordered mesoporous silica layer does not grow directly on a mesoporous support. Instead it grows on a structurally disordered interface of 10–20 nm thickness. This observation differs considerably from studies on film formation on dense supports as reported in the literature. Water transport experiments were carried out on the silica films deposited on porous supports. The results suggest that the disordered interface layer of the film deposited on the mesoporous support does not contribute significantly to the total resistance for water transport

Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease

Background: Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress neuropathology in two murine models of AD, Tg2576 and 3xTg. Previously, a genetic deficiency of C1q in the Tg2576 mouse model showed an accumulation of fibrillar plaques similar to the complement sufficient Tg2576, but reactive glia were significantly decreased and neuronal integrity was improved suggesting detrimental consequences for complement activation in AD. The goal of this study was to define the role of the classical complement activation pathway in the progression of pathology in the 3xTg mouse that develops tangles in addition to fibrillar plaques (more closely reflecting human AD pathology) and to assess the influence of complement in a model of AD with a higher level of complement hemolytic activity. Methods: 3xTg mice deficient in C1q (3xTgQ-/-) were generated, and both 3xTg and 3xTgQ-/- were backcrossed to the BUB mouse strain which has higher in vitro hemolytic complement activity. Mice were aged and perfused, and brain sections stained for pathological markers or analyzed for proinflammatory marker expression. Results: 3xTgQ-/- mice showed similar amounts of fibrillar amyloid, reactive glia and hyperphosphorylated tau as the C1q-sufficient 3xTg at the ages analyzed. However, 3xTg and 3xTgQ-/- on the BUB background developed pathology earlier than on the original 3xTg background, although the presence of C1q had no effect on neuropathological and pro-inflammatory markers. In contrast to that seen in other transgenic models of AD, C1q, C4 and C3 immunoreactivity was undetectable on the plaques of 3xTg in any background, although C3 was associated with reactive astrocytes surrounding the plaques. Importantly, properdin a component of the alternative complement pathway was associated with plaques in all models. Conclusions: In contrast to previously investigated transgenic models of AD, development of neuropathology in 3xTg mice, which progresses much slower than other murine models, may not be influenced by fibrillar amyloid mediated activation of the classical complement pathway, suggesting that the alternative complement pathway activation or a C3-independent cleavage of C5 could account for the detrimental effects in these mice that are prevented by the C5a receptor antagonist. Furthermore, the paucity of complement activation may be a factor in the slower kinetics of progression of pathology in the 3xTg model of this disease