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Kim, Taeyoon,Mays, Jimmy,Chung, Ildoo Elsevier 2018 Polymer Vol.158 No.-
<P><B>Abstract</B></P> <P>Porous biodegradable microspheres were fabricated by successful RAFT polymerization of methyl vinyl ketone onto polycaprolactone followed by an oil/water emulsion-evaporation method, then finally photodegradation of PMVK blocks by UV irradiation. Macro-CTA (chain transfer agent) was synthesized by reacting carboxylic acid-terminated CTA, S-1-dodecyl-S’-(α,α′-dimethyl-α’‘-acetic acid) trithiocarbonate (DDMAT) with hydroxyl terminated polycaprolactone, which was then used for the synthesis of triblock copolymer with methyl vinyl ketone (MVK). The synthesized triblock copolymers were characterized by FT-IR, <SUP>1</SUP>H NMR spectroscopies. Gel permeation chromatography (GPC) was used to evaluate the molecular weight and molecular weight distribution and monitored the photodegradability of the block copolymers. The morphology of microspheres was spherical with smooth surfaces before UV irradiation. However, those from PCL-PMVK triblock copolymers had rough surfaces and porous structures after UV irradiation due to the photodegradation of PMVK blocks as a porous template. The porosity and shape of the microspheres and shape of microspheres were dependent on the PMVK contents and size of microspheres.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Successful RAFT polymerization of triblock copolymers from methyl vinyl ketone onto polycaprolactone. </LI> <LI> Fabrication of porous microspheres by emulsion-evaporation method, followed by the photodegradation of PMVK blocks. </LI> <LI> Novel methods for direct templating fabrication of porous polymers by removing template blocks by UV light. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Kim, Y.,Han, B.,Titlow, W.,Mays, C.E.,Kwon, M.,Ryou, C. Elsevier/North-Holland 2009 Antiviral research Vol.84 No.2
Prion diseases are incurable, transmissible neurodegenerative disorders in humans and animals. Because the disease-associated isoform of prion protein, PrP<SUP>Sc</SUP>, is conformationally converted from cellular prion protein, PrP<SUP>C</SUP>, knockdown of PrP<SUP>C</SUP> expression by RNA interference (RNAi) implicates therapy for prion diseases. In this study, introduction of small interfering (si) and small hairpin (sh) RNAs targeting the prion protein gene (prnp) transcripts triggered specific gene silencing and reduced the PrP<SUP>C</SUP> level in both prion-free and -infected neuroblastoma cell lines. Furthermore, this approach suppressed PrP<SUP>Sc</SUP> formation and ultimately eliminated PrP<SUP>Sc</SUP> from prion-infected cell lines. However, prolonged culture of cured cells resulted in reappearance of PrP<SUP>Sc</SUP> in the cell population, presumably by de novo PrP<SUP>Sc</SUP> formation from residual PrP<SUP>C</SUP> uncontrolled by RNAi and PrP<SUP>Sc</SUP> remained under the detection limit. Protein misfolding cyclic amplification assays further confirmed that lysate of cured cells was sufficient to support PrP<SUP>Sc</SUP> propagation. Our data not only suggest a potential treatment option but also implicate a caveat for using an RNAi approach for prion diseases. These findings provide critical information required to advance RNAi-based prevention and therapy for prion diseases of humans and animals.
Worlanyo E. Gato,Daniel A. Hunter,Shamaya L. Whitby,Christopher A. Mays,Wilson Yau 대한당뇨병학회 2016 Diabetes and Metabolism Journal Vol.40 No.6
Background In recent times, there has been an increase in the incidence of type 2 diabetes mellitus (T2DM) particularly in children. Adipocyte dysfunction provide a critical link between obesity and insulin resistance resulting in diabetes outcome. Further, environmental chemical exposure during early years of life might be a significant contributing factor to the increase in the incidence of T2DM. This study tests the idea that exposure to environmental contaminants (2-aminoanthracene [2AA]) in utero will show effects in the adipose tissue (AT) that signify T2DM vulnerability. 2AA is a polycyclic aromatic hydrocarbon found in a variety of products. Methods To accomplish the study objective, pregnant dams were fed various amounts of 2AA adulterated diets from gestation through postnatal period. The neonates and older offspring were analyzed for diabetic-like genes in the ATs and analysis of serum glucose. Furthermore, weight monitoring, histopathology and immunohistochemical (IHC) staining for CD68 in AT, adipocyte size determination and adiponectin amounts in serum were undertaken. Results Up-regulation of adiponectin and interleukin-6 genes were noted in the pups and older rats. Combination of intrauterine 2AA toxicity with moderate high fat diet exhibited gene expression patterns similar to those of the neonates. Elevated serum glucose levels were noted in treated groups. IHC of the AT indicated no significant malformations; however, CD68+ cells were greater in the animals treated to 2AA. Similarly, mean sizes of the adipocytes were larger in treated and combined 2AA and moderate high fat animals. Adiponectin was reduced in 2AA groups. Conclusion From the preceding, it appears intrauterine 2AA disturbance, when combined with excess fat accumulation will lead to greater risk for the diabetic condition.
Margetts, Peter J.,Bonniaud, Philippe,Liu, Limin,Hoff, Catherine M.,Holmes, Clifford J.,West-Mays, Judith A.,Kelly, Margaret M. American Society of Nephrology 2005 Journal of the American Society of Nephrology Vol.16 No.2
<P>Epithelial mesenchymal transition (EMT), a process involved in many growth and repair functions, has been identified in the peritoneal tissues of patients who undergo peritoneal dialysis. The sequence of changes in gene regulation and cellular events associated with EMT after TGF-beta1-induced peritoneal fibrosis is reported. Sprague-Dawley rats received an intraperitoneal injection of an adenovirus vector that transfers active TGF-beta1 (AdTGF-beta1) or control adenovirus, AdDL. Animals were killed 0 to 21 days after infection. Peritoneal effluent and tissue were analyzed for markers of EMT. In the animals that were treated with AdTGF-beta1, an increase in expression of genes associated with EMT and fibrosis, such as type I collagen A2, alpha-smooth muscle actin, and the zinc finger regulatory protein Snail, was identified. Transition of mesothelial cells 4 to 7 d after infection, with appearance of epithelial cells in the submesothelial zone 7 to 14 d after exposure to AdTGF-beta1, was demonstrated. This phase was associated with disruption of the basement membrane and increased expression of matrix metalloproteinase 2. By 14 to 21 d after infection, there was evidence of restoration of normal submesothelial architecture. These findings suggest that EMT occurs in vivo after TGF-beta1 overexpression in the peritoneum. Cellular changes and gene regulation associated with EMT are evident throughout the fibrogenic process and are not limited to early time points. This further supports the central role of TGF-beta1 in peritoneal fibrosis and provides an important model to study the sequence of events involved in TGF-beta1-induced EMT.</P>