Cellular thermosetting fluoropolymers and process for making them

Thermosetting fluoropolymer foams are made by mixing fluid from thermosetting fluoropolymer components having a substantial fluoride content, placing the mixture in a pressure tight chamber, filling the chamber with a gas, at a relatively low pressure, that is unreactive with the fluoropolymer components, allowing the mixture to gel, removing the gelled fluoropolymer from the chamber and therafter heating the fluoropolymer at a relatively low temperature to simultaneously cure and foam the fluoropolymer. The resulting fluoropolymer product is closed celled with the cells storing the gas employed for foaming. The fluoropolymer resins employed may be any thermosetting fluoropolymer including fluoroepoxies, fluoropolyurethanes and fluoroacrylates

Cellular thermosetting fluorodiepoxide polymers

Thermosetting fluoropolymer foams are made by mixing fluid form thermosetting fluoropolymer components having a substantial fluorine content, placing the mixture in a pressure tight chamber, filling the chamber with a gas, at relatively low pressure, that is unreactive with the fluoropolymer components, allowing the mixture to gel, removing the gelled fluoropolymer from the chamber and thereafter heating the fluoropolymer at a relatively low temperature to simultaneously sure and foam the fluoropolymer. The resulting fluoropolymer product is closed celled with the cells storing the gas employed for foaming. The fluoropolymer resins employed may be any thermosetting fluoropolymer including fluoroepoxies, fluoropolyurethanes and fluoroacrylates

Methods of using fluoroepoxy compounds as adhesives for fluoroplastic adherends and products made therefrom

Fluoroepoxy compounds are made by reacting a fluoroepoxy resin with an effective curing agent, such as an adduct amine, and, while the compound is sufficiently liquid to wet a fluoroplastic surface, it may be applied to a fluoroplastic adherend, such as a Teflon, to be employed as an adhesive, to form various fluoroplastic products, without requiring any surface treatment of the adherend. The compounds are intentionally formulated with high fluorine contents, normally above 46% by weight, preferably for bonding fluoroplastics with a high F-content, above 55% by weight

Viability of Non-Coplanar VMAT for Liver SBRT as Compared to Coplanar VMAT and Beam Orientation Optimized 4π IMRT.

PurposeThe 4π static non-coplanar radiotherapy delivery technique has demonstrated better normal tissue sparing and dose conformity than the clinically used volumetric modulated arc therapy (VMAT). It is unclear whether this is a fundamental limitation of VMAT delivery or the coplanar nature of its typical clinical plans. The dosimetry and the limits of normal tissue toxicity constrained dose escalation of coplanar VMAT, non-coplanar VMAT and 4π radiotherapy are quantified in this study.Methods and materialsClinical stereotactic body radiation therapy plans for 20 liver patients receiving 30-60 Gy using coplanar VMAT (cVMAT) were re-planned using 3-4 partial non-coplanar arcs (nVMAT) and 4π with 20 intensity-modulated non-coplanar fields. The conformity number (CN), homogeneity index (HI), 50% dose spillage volume (R50), normal liver volume receiving >15 Gy (VL>15), dose to organs at risk (OARs), and tumor control probability (TCP) were compared for all three treatment plans. The maximum tolerable dose (MTD) yielding a normal liver normal tissue control probability (NTCP) below 1%, 5%, and 10% was calculated with the Lyman-Kutcher-Burman model for each plan, as well as the resulting survival fractions at one, two, three, and four years.ResultsCompared to cVMAT, the nVMAT and 4π plans reduced VL>15 by an average of 5 cm3 and 80 cm3, respectively. 4π reduced the 50% dose spillage volume by ~23% compared to both VMAT plans, and either significantly decreased or maintained OAR doses. The 4π MTDs and survival fractions were significantly higher than both cVMAT and nVMAT (p<0.05) for all normal liver NTCP limits used in this study.ConclusionsThe 4π technique provides significantly better OAR sparing than both cVMAT and vMAT and enables more clinically relevant dose escalation for tumor local control. Therefore, despite the current accessibility of nVMAT, it is not a viable alternative to 4π for liver SBRT

A Simple Model for Cavity Enhanced Slow Lights in Vertical Cavity Surface Emission Lasers

We develop a simple model for the slow lights in Vertical Cavity Surface Emission Lasers (VCSELs), with the combination of cavity and population pulsation effects. The dependences of probe signal power, injection bias current and wavelength detuning for the group delays are demonstrated numerically and experimentally. Up to 65 ps group delays and up to 10 GHz modulation frequency can be achieved in the room temperature at the wavelength of 1.3 $\mu$m. The most significant feature of our VCSEL device is that the length of active region is only several $\mu$m long. Based on the experimental parameters of quantum dot VCSEL structures, we show that the resonance effect of laser cavity plays a significant role to enhance the group delays

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Role of Aβ-RAGE interaction in oxidative stress and cPLA2 activation in astrocytes and cerebral endothelial cells

Blood–brain barrier (BBB) dysfunctions have been implicated in the progression of Alzheimer's disease. Cerebral endothelial cells (CECs) and astrocytes are the main cell components of the BBB. Although amyloid-β oligomers (Aβ42) have been reported to mediate oxidative damage to the CECs and astrocytes and trigger the downstream mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway, the cell surface binding site for Aβ42 and exact sequence of these events have yet to be elucidated. In this study, the receptor for advanced glycation endproducts (RAGE) was postulated to function as a signal transducing cell surface receptor for Aβ42 to induce reactive oxygen species (ROS) generation from NADPH oxidase and trigger downstream pathways for the phosphorylation of extracellular signal-regulated kinases (ERK1/2) and cytosolic phospholipase A2 (cPLA2). We found that Aβ42 competed with the anti-RAGE antibody (AbRAGE) to bind to RAGE on the surfaces of CECs and primary astrocytes. In addition, AbRAGE abrogate Aβ42-induced ROS production and the colocalization between the cytosolic (p47-phox) and membrane (gp91-phox) subunits of NADPH oxidase in both cell types. AbRAGE as well as NADPH oxidase inhibitor and ROS scavenger suppressed Aβ42-induced ERK1/2 and cPLA2 phosphorylation in CECs. At the same time, only AbRAGE, but neither NADPH oxidase inhibitor nor ROS scavenger, inhibited the ERK1/2 pathway and cPLA2 phosphorylation in primary astrocytes. Therefore, this study demonstrates that NADPH oxidase complex assembly and ROS production are not required for Aβ42 binding to RAGE at astrocytic surface leading to sequential phosphorylation of ERK1/2 and cPLA2, and suggests the presence of two different RAGE-dependent downstream pathways in the CECs and astrocytes

Phase Diagram of Integer Quantum Hall Effect

The phase diagram of integer quantum Hall effect is numerically determined in the tight-binding model, which can account for overall features of recently obtained experimental phase diagram. In particular, the quantum Hall plateaus are terminated by two distinct insulating phases, characterized by the Hall resistance with classic and quantized values, respectively, which is also in good agreement with experiments.Comment: 4 pages, RevTex, 4 PostScript figures; one new figure is added; minor modifications in the tex

Spin-charge separation in the single hole doped Mott antiferromagnet

The motion of a single hole in a Mott antiferromagnet is investigated based on the t-J model. An exact expression of the energy spectrum is obtained, in which the irreparable phase string effect [Phys. Rev. Lett. 77, 5102 (1996)] is explicitly present. By identifying the phase string effect with spin backflow, we point out that spin-charge separation must exist in such a system: the doped hole has to decay into a neutral spinon and a spinless holon, together with the phase string. We show that while the spinon remains coherent, the holon motion is deterred by the phase string, resulting in its localization in space. We calculate the electron spectral function which explains the line shape of the spectral function as well as the ``quasiparticle'' spectrum observed in angle-resolved photoemission experiments. Other analytic and numerical approaches are discussed based on the present framework.Comment: 16 pages, 9 figures; references updated; to appear in Phys. Rev.

Goal-Based Daylighting Design Using an Interactive Simulation Method

This paper proposes an interactive goal-based method for designing day lit buildings. The lighting simulation tool which supports this process is a hybrid global illumination rendering method which efficiently computes annual daylighting metrics. The goal-based method uses a knowledge base populated using a set of previously completed simulations that quantify the effects of various façade design modifications. The knowledge base guides a simple algorithm over an iterative design process. The current knowledge base includes information about window size, shape, location on the façade, and simple shading devices. Three case studies are given in which this iterative optimization method was applied; all resulted in improved daylighting performance