Multifunctional Epoxy-based copolymers can be used as chain-extender (CE) to increase the molecular weight and create branching in polylactides (PLA). In this study, the effect of a multifunctional epoxy-acrylic-styrene copolymer on the properties of PLA/Thermoplastic Starch (PLA/TPS) blends was investigated. The PLA/TPS blends were prepared by twin-screw extrusion. The drystarch and plasticizers were mixed together in the first half of the extruder to complete starch gelatinization. Water was removed by devolatilization at midex-truder and the PLA matrix was mixed with the water-free TPS in the latter portion of the compounding process. The standard blends comprised 27% TPS in the PLA matrix. The TPS phase itself comprised 36% plasticizer in the form of glycerol or sorbitol. A maleic anhydride grafted PLA (PLAg) was also used in selected blends to examine the effect of interfacial modification on the morphology of chain-extended blends. The blends were injection molded into standard test bars and their tensile properties were measured. Differential scanning calorimetry was carried out to examine the effect of chain extension on PLA's ability to crystallize. Oscillatory-shear rheology was used to monitor changes in blend viscosity. Finally, scanning electron microscopy on microtomed and acid-etched samples was carried out to assess the blend morphology. It was found that the combination of interfacial modification and chain-extension strategies led to greatly improved ductility. The viscosity of the PLA/TPS blends was also dramatically increased by adding a small amount of epoxy-based chain extender. This is of great interest for polymer processing techniques (such as foaming or film blowing) that require high melt strength.
Humic substances (HS) were extracted from the sediments of four Sudbury area lakes, namely, Tilton, Clearwater, Silver, and Ramsey Lakes, with the aid of 0.1 M Na4P2O7 and 0.5 M NaOH solutions. The HS (humic and fulvic acids) were purified and characterized using the methods of elemental analysis, visible spectroscopy (E4/E6 ratio), FTIR, and solid-state 13C CPMAS NMR. A substantial amount of information with regard to the composition and chemical nature of lake sediment HS was obtained. The results obtained for the Sudbury area lake sediments were compared with one another and with HS from other sources, such as soils. The elemental composition, atomic ratios, E4/E6 ratios, and FTIR and NMR features of the samples from the above lakes were found to be nearly identical, suggesting that HS formed in the Sudbury area have similar chemical properties. Compared with soil HS, the Sudbury lake sediments HS have undergone a low degree of aromatic condensation and are considerably more aliphatic in nature. Keywords: humic substances, characterization, lake sediments, extraction, 13C NMR.
The midbrain ventrolateral periaqueductal gray (VL-PAG) is a key component that mediates pain modulation. Although spinal cord glial cells appear to play an important role in chronic pain development, the precise mechanisms involving descending facilitation pathways from the PAG following nerve injury are poorly understood. This study shows that cellular events that occur during glial activation in the VL-PAG may promote descending facilitation from the PAG during neuropathic pain. Chronic constriction nerve injury (CCI) was induced by ligature construction of the sciatic nerve in male Sprague-Dawley rats. Behavioral responses to noxious mechanical (paw withdrawal threshold; PWT) and thermal (paw withdrawal latency; PWL) stimuli were evaluated. After CCI, immunohistochemical and Western blot analysis of microglia and astrocytes in the VL-PAG showed morphological and quantitative changes indicative of activation in microglia and astrocytes. Intra-VL-PAG injection of microglial or astrocytic inhibitors attenuated PWT and PWL at days 7 and 14, respectively, following CCI. We also evaluated the effects of intra-VL-PAG administration of the phosphorylated p38 mitogen-activated protein kinase (p-p38 MAPK) inhibitor SB 203580 at day 7 after CCI. This treatment abolished microglial activation and produced a significant time-dependent attenuation of PWT and PWL. Western blot analysis showed localized expression of p-p38 in the VL-PAG after CCI. P-p38 was expressed in labeled microglia of the VL-PAG but was not present in astrocytes and neurons on day 7 after CCI. These results demonstrate that CCI-induced neuropathic pain is associated with glial activation in the VL-PAG, which likely participates in descending pain facilitation through the p38 MAPK signaling pathway.
The objective of this study was to investigate the role of miR-148a-3p in lupus nephritis (LN) based on data from previous studies and a microRNA assay. We evaluated the miR-148a-3p expression level in LN renal tissues and blood serum to determine its clinicopathological significance and effect on glomerular cell proliferation. Then, we collected renal glomeruli from LN mice and determined the miR-148a-3p, proliferating cell nuclear antigen (PCNA), and PCNA/Thy1 expression. We performed functional analyses of miR-148a-3p in vitro and in vivo. We also investigated the target gene of miR-148a-3p in LN. The results showed that miR-148a-3p expression levels were significantly higher not only in glomeruli but also in the blood serum during LN and increased in the glomeruli of LN mice and that at the same time there was positive correlation between miR-148a-3p and PCNA expression of glomruli. Overexpression of miR-148a-3p accelerated cell proliferation and PCNA expression, while a miR-148a-3p inhibitor inhibited cell proliferation via the Akt/cyclin D1 pathway. Furthermore, miR-148a-3p overexpression reduced the phosphatase and tensin homology deleted on chromosome ten (PTEN) expression level, while miR-148a-3p silencing increased its expression in high-mobility group box 1 (HMGB1)-induced mouse mesangial cells (MMCs). Luciferase assays demonstrated that miR-148a-3p could directly bind to the PTEN 3'-UTR. PTEN overexpression inhibited MMC proliferation considerably, resembling the results observed during miR-148a-3p inhibition. Reducing miR-148a-3p expression upregulated PTEN in the glomeruli and improved renal function in LN mice. Thus miR-148a-3p may promote proliferation and contribute to LN progression by targeting PTEN.
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