134 research outputs found

    Green synthesis of novel biocomposites from treated cellulosic fibers and recycled bio-plastic polylactic acid

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    This study investigated mechanical properties of biocomposites developed from recycled polylactic acid (PLA) from packaging industry and treated cellulosic fibers from pulp and paper solid waste. Microwave and enzymatic treatments were used for extraction and surface modification of hydrophilic cellulosic fibers. Enzymatic treatment was specifically performed for activation of hydroxyl groups and improvement of adhesion between matrix and fibers including controlling the length of cellulosic fibers with size reduction of around 50% (142 and 127 mm for primary and mixed biosolids, respectively) as compared to microwave treatment. Microwave treatment produced cellulosic fibers of 293 and 341 mm, for primary and mixed biosolids, respectively. Mechanical properties of biocomposites with 2% (w/w) of treated cellulosic fibers (Young's Modulus 887.83 MPa with tensile strain at breakpoint of 7.22%, tensile stress at yield 41.35 MPa) was enhanced in comparison to the recycled PLA (Young's Modulus 644.47 ± 30.086 MPa with tensile strain at breakpoint of 6.01 ± 0.83%, tensile stress at yield of 29.49 ± 3.64 MPa). Scanning electron microscopy revealed size reduction of cellulosic fibers. X-ray diffraction and Fourier transform infrared spectroscopy confirmed strong mechanical properties of novel biocomposites.The authors are sincerely thankful to the Natural Sciences and Engineering Research Council of Canada (Discovery Grant 355254 and NSERC CRD Grant), and CRIBIQ for financial support. We would like to thank Mr. R. Fortin and Colin Jacob Vaillancourt from Gaudreau Environment for providing rPLA samples. Likewise, the support of Ozymes Inc. is equally appreciated for valuable comments during the experimental planning from industrial perspective. Financial assistance by the ‘Fonds de recherche du Quebec- Nature et technologies (FRQNT)’ and INRS-ETE has been thankfully acknowledged by K Hegde.info:eu-repo/semantics/publishedVersio

    Microglial Expression of the Wnt Signaling Modulator DKK2 Differs between Human Alzheimer's Disease Brains and Mouse Neurodegeneration Models

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    Wnt signaling is crucial for synapse and cognitive function. Indeed, deficient Wnt signaling is causally related to increased expression of DKK1, an endogenous negative Wnt regulator, and synapse loss, both of which likely contribute to cognitive decline in Alzheimer's disease (AD). Increasingly, AD research efforts have probed the neuroinflammatory role of microglia, the resident immune cells of the CNS, which have furthermore been shown to be modulated by Wnt signaling. The DKK1 homolog DKK2 has been previously identified as an activated response and/or disease-associated microglia (DAM/ARM) gene in a mouse model of AD. Here, we performed a detailed analysis of DKK2 in mouse models of neurodegeneration, and in human AD brain. In APP/PS1 and APPNL-G-F AD mouse model brains as well as in SOD1G93A ALS mouse model spinal cords, but not in control littermates, we demonstrated significant microgliosis and microglial Dkk2 mRNA upregulation in a disease-stage-dependent manner. In the AD models, these DAM/ARM Dkk2+ microglia preferentially accumulated close to βAmyloid plaques. Furthermore, recombinant DKK2 treatment of rat hippocampal primary neurons blocked WNT7a-induced dendritic spine and synapse formation, indicative of an anti-synaptic effect similar to that of DKK1. In stark contrast, no such microglial DKK2 upregulation was detected in the postmortem human frontal cortex from individuals diagnosed with AD or pathologic aging. In summary, the difference in microglial expression of the DAM/ARM gene DKK2 between mouse models and human AD brain highlights the increasingly recognized limitations of using mouse models to recapitulate facets of human neurodegenerative disease.Significance StatementThe endogenous negative Wnt regulator Dkk2 is significantly upregulated at the mRNA level in microglia of Alzheimer's disease (AD) mouse models, implying that microglia derived Dkk2 protein may detrimentally contribute to a reduced Wnt signaling tone in the AD brain, a known pathophysiological manifestation. Indeed, recombinant DKK2 prevented Wnt-dependent synapse formation in cultured neurons. However, DKK2 upregulation was not recapitulated in postmortem human AD brains. The success of neurodegeneration animal models has relied on pathophysiology that for the most part correctly modelled human disease. Increasingly, however, limitations to the validity of mouse models to recapitulate human neurodegenerative disease have become apparent, as evidenced by the present study by the difference in microglial DKK2 expression between AD mouse models and human AD brain

    Intermediate follow-up following intravascular stenting for treatment of coarctation of the aorta

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    Background : We report a multiinstitutional study on intermediate-term outcome of intravascular stenting for treatment of coarctation of the aorta using integrated arch imaging (IAI) techniques. Methods and Results : Medical records of 578 patients from 17 institutions were reviewed. A total of 588 procedures were performed between May 1989 and Aug 2005. About 27% (160/588) procedures were followed up by further IAI of their aorta (MRI/CT/repeat cardiac catheterization) after initial stent procedures. Abnormal imaging studies included: the presence of dissection or aneurysm formation, stent fracture, or the presence of reobstruction within the stent (instent restenosis or significant intimal build-up within the stent). Forty-one abnormal imaging studies were reported in the intermediate follow-up at median 12 months (0.5–92 months). Smaller postintervention of the aorta (CoA) diameter and an increased persistent systolic pressure gradient were associated with encountering abnormal follow-up imaging studies. Aortic wall abnormalities included dissections ( n = 5) and aneurysm ( n = 13). The risk of encountering aortic wall abnormalities increased with larger percent increase in CoA diameter poststent implant, increasing balloon/coarc ratio, and performing prestent angioplasty. Stent restenosis was observed in 5/6 parts encountering stent fracture and neointimal buildup ( n = 16). Small CoA diameter poststent implant and increased poststent residual pressure gradient increased the likelihood of encountering instent restenosis at intermediate follow-up. Conclusions : Abnormalities were observed at intermediate follow-up following IS placement for treatment of native and recurrent coarctation of the aorta. Not exceeding a balloon:coarctation ratio of 3.5 and avoidance of prestent angioplasty decreased the likelihood of encountering an abnormal follow-up imaging study in patients undergoing intravascular stent placement for the treatment of coarctation of the aorta. We recommend IAI for all patients undergoing IS placement for treatment of CoA. © 2007 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/57392/1/21191_ftp.pd
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