4,961 research outputs found
Surface Characterization of Chemically Modified Wood: Dynamic Wettability1
Dynamic wettability of chemically modified yellow-poplar veneer was investigated with sessile water droplets in this study. Dynamic contact angle, decay ratio, spreading ratio, and their changing rates (the wetting slope and K value) were used to illustrate the dynamic wetting process. Dynamic contact angle (α) and droplet height decay ratio (DRh) followed the first order exponential decay equation, whereas the droplet base-diameter spreading ratio (SRφ) fitted the Boltzmann sigmoid model. Wetting behavior of Epolene G-3015 [a maleated polypropylene (MAPP) copolymer with a high molecular weight]-treated wood surface was independent of the retention and wetting time. The retention effect on wetting slopes of >, DRh, and SRφ on poly(ethylene and maleic anhydride) (PEMA)-treated specimens was opposite to that on Epolene E-43 (a MAPP copolymer with a low molecular weight)-treated specimens. Based on these two models, the wetting slope and K value were used to interpret the kinetics of wetting. Therefore, these methods were helpful to characterize the dynamic wettability of wood surfaces modified with different coupling agents
Surface and Interfacial Characterization of Wood-PVC Composite: Imaging Morphology and Wetting Behavior1
An imaging technique was used to investigate wetting behavior of wood-PVC composites in this study. Two-dimensional and time-dependent profiles of water droplets on maleated wood surface and wood-PVC interface were observed. Experimental results indicated that coupling agents Epolene E-43 (a maleated polypropylene copolymer with low molecular weight)- and polyethylene-maleic anhydride (PEMA)- treated veneers had a hydrophilic surface, whereas the coupling agent Epolene G-3015 (a maleated polypropylene copolymer with high molecular weight)-treated veneer had a hydrophobic surface. For E-43- and PEMA-treated veneers, a water droplet had an elliptical shape after initial contact with the wood surface. However, a sessile droplet on G-3015-treated specimens was closer to a circular shape. During wetting, contact angle changes on E-43- and PEMA-treated specimens were larger than those on G-3015- treated specimens. Contact angles on maleated specimens with heat treatment and maleated interphases were almost independent of wetting time. Initial contact angle was influenced by coupling agent type, acid number, and retention and directions of wood grains. Initial contact angle decreased with increase of E-43 retention, but it was proportional to PEMA retention. However, it was independent of G-3015 retention. Wettability of fractured wood-PVC interface was similar to that of maleated wood surface with heat treatment. Thus, the interfacial characteristics of wood-PVC interface can be simulated with maleated wood surface with heat treatment
Chemical Coupling in Wood Fiber and Polymer Composites: A Review of Coupling Agents and Treatments
Coupling agents in wood fiber and polymer composites (WFPC) play a very important role in improving the compatibility and adhesion between polar wood fibers and non-polar polymeric matrices. In this paper, we review coupling agents, pretrcatment, and mixing technology for wood fiber and polymer currently used in the manufacture of WFPC. So far, over forty coupling agents have been used in production and research. These agents are classified as organic, inorganic, and organic-inorganic groups, among which organic agents are better than inorganic agents because of stronger interfacial adhesion. The most popular coupling agents currently being used include isocyanates, anhydrides, silanes, and anhydride-modified copolymers. Coupling agents are usually coated on the surface of wood fiber, polymer or both by compounding, blending, soaking, spraying, or other methods. Three basic processes suitable for coupling treatment are discussed: directly coating during mixing and fully or partly pretreating before mixing. The pretreatment of wood fiber and polymer by coating or grafting is the preferred method to improve the mechanical properties of WFPC.
Relationship between intact HIV-1 proviruses in circulating CD4+ T cells and rebound viruses emerging during treatment interruption.
Combination antiretroviral therapy controls but does not cure HIV-1 infection because a small fraction of cells harbor latent viruses that can produce rebound viremia when therapy is interrupted. The circulating latent virus reservoir has been documented by a variety of methods, most prominently by viral outgrowth assays (VOAs) in which CD4+ T cells are activated to produce virus in vitro, or more recently by amplifying proviral near full-length (NFL) sequences from DNA. Analysis of samples obtained in clinical studies in which individuals underwent analytical treatment interruption (ATI), showed little if any overlap between circulating latent viruses obtained from outgrowth cultures and rebound viruses from plasma. To determine whether intact proviruses amplified from DNA are more closely related to rebound viruses than those obtained from VOAs, we assayed 12 individuals who underwent ATI after infusion of a combination of two monoclonal anti-HIV-1 antibodies. A total of 435 intact proviruses obtained by NFL sequencing were compared with 650 latent viruses from VOAs and 246 plasma rebound viruses. Although, intact NFL and outgrowth culture sequences showed similar levels of stability and diversity with 39% overlap, the size of the reservoir estimated from NFL sequencing was larger than and did not correlate with VOAs. Finally, intact proviruses documented by NFL sequencing showed no sequence overlap with rebound viruses; however, they appear to contribute to recombinant viruses found in plasma during rebound
Endpoint Estimates for N-dimensional Hardy Operators and Their Commutators
In this paper, it is proved that the higher dimensional Hardy operator is
bounded from Hardy space to Lebesgue space. The endpoint estimate for the
commutator generated by Hardy operator and (central) BMO function is also
discussed.Comment: 8 page
Recommended from our members
Characterization of Intact Proviruses in Blood and Lymph Node from HIV-Infected Individuals Undergoing Analytical Treatment Interruption.
The role of lymphoid tissue as a potential source of HIV-1 rebound following interruption of antiretroviral therapy (ART) is uncertain. To address this issue, we compared the latent viruses obtained from CD4+ T cells in peripheral blood and lymph nodes to viruses emerging during treatment interruption. Latent viruses were characterized by sequencing near-full-length (NFL) proviral DNA and env from viral outgrowth assays (VOAs). Five HIV-1-infected individuals on ART were studied, four of whom participated in a clinical trial of a TLR9 agonist that included an analytical treatment interruption. We found that 98% of intact or replication-competent clonal sequences overlapped between blood and lymph node. In contrast, there was no overlap between 205 latent reservoir and 125 rebound sequences in the four individuals who underwent treatment interruption. However, rebound viruses could be accounted for by recombination. The data suggest that CD4+ T cells carrying latent viruses circulate between blood and lymphoid tissues in individuals on ART and support the idea that recombination may play a role in the emergence of rebound viremia.IMPORTANCE HIV-1 persists as a latent infection in CD4+ T cells that can be found in lymphoid tissues in infected individuals during ART. However, the importance of this tissue reservoir and its contribution to viral rebound upon ART interruption are not clear. In this study, we sought to compare latent HIV-1 from blood and lymph node CD4+ T cells from five HIV-1-infected individuals. Further, we analyzed the contribution of lymph node viruses to viral rebound. We observed that the frequencies of intact proviruses were the same in blood and lymph node. Moreover, expanded clones of T cells bearing identical proviruses were found in blood and lymph node. These latent reservoir sequences did not appear to be the direct origin of rebound virus. Instead, latent proviruses were found to contribute to the rebound compartment by recombination
- …