Crystallization Kinetics of Modified Nanocellulose/Monomer Casting Nylon Composites.

Polyisocyanate and caprolactone were used to chemically functionalize nanocellulose (CNF). Composites of CNF, caprolactone-modified nanocellulose (CNF-CL) and polyisocyanate-modified nanocellulose (CNF-JQ)/MC nylon were fabricated by anionic ring-opening polymerization. The effects of the crystal structure, crystal morphology and crystallization process of MC nylon composites have been characterized by wide-angle X-ray diffraction (WAXD), polarized optical microscopy(POM) and differential scanning calorimetry (DSC). Isothermal crystallization kinetics were analyzed using the Avrami equation, and the crystallization rate, half-time, and Avrami exponent were calculated. The results show that the nucleation effects of CNF-JQ/MC nylon composites is increased with the CNF-JQ increase, and it is best compared with MC nylon, CNF/MC nylon and CNF-CL/MC nylon composites, so CNF-JQ can play the role of effective nucleating agent in MC nylon. We also discussed the non-isothermal crystallization of the composites. Analysis of the Jeziorny and Mo model demonstrates that the Zc values of CNF, CNF-CL, CNF-JQ/MC nylon composites increase, and the F(T) values decrease in order. This indicates that CNF-JQ can better promote the crystallization rate of non-isothermal crystallization of MC nylon. The results of this work demonstrate that CNF-JQ can be an effective nucleation agent and increase the crystallization rate of MC nylon compared with CNF-CL. The activation energy of the composites was studied using the kissing method, and the results showed that CNF-CL decreased the activation energy of MC nylon, and CNF and CNF-JQ increased the activation energy of MC nylon.

Preparation of a Ceramifiable Phenolic Foam and Its Ceramization Behavior.

Ceramifiable phenolic foam (GC-PF) with a low ceramization temperature has been prepared by incorporation of low melting point glass frits (LMG) containing B2O3 and Na2O as main components into a phenolic resin matrix. Fourier transform infrared spectrometry, X-ray diffractometry, and scanning electron microscopy were used for assessment of the structure, phase composition, and morphology of GC-PF before and after combustion analysis, respectively. A glassy ceramic protective layer is formed when GC-PF is exposed to flame or a high temperature environment. The presence of LMG not only reduces the level of defects in the phenolic foam cell wall (gas escape pore), but also promotes the generation of a glassy ceramic protective layer that could inhibit heat feedback from the combustion zone and reduce the rate of formation of volatile fuel fragments. Thermogravimetric analysis and differential scanning calorimetry were used to establish that GC-PF exhibits excellent thermal stability. Limiting oxygen index (LOI) determination suggests that GC-PF displays good flame retardancy. The LOI of GC-PF was as high as 45.6%, and the char residue at 900 °C was six times greater than that for ordinary phenolic foam (O-PF). The area of the raw material matrix of GC-PF after combustion for 60 s was about 1.7 times larger than that for O-PF. A possible mode of formation of glassy ceramics has been proposed.

Aquaporin 1 alleviates acute kidney injury via PI3K-mediated macrophage M2 polarization.

BACKGROUND: Lipopolysaccharide (LPS)-induced acute kidney injury (AKI) is associated with an abnormal immune response. Accumulating evidence has demonstrated that aquaporin 1 (AQP1) prevents kidney tissue injury in LPS-induced AKI by mediating immune response. However, the underlying mechanisms remain obscure. Macrophages as immune cells with multiple phenotypes are important mediators in tissue homeostasis and host defense. We propose that macrophage polarization is implicated in AQP1-mediated immune response. METHODS: Herein we established sepsis-induced AKI model rats through intraperitoneal injection of LPS into Wistar rats to reveal immune mechanism of damage. We also used LPS-induced mouse RAW264.7 cells to elucidate the molecular mechanism of macropage polarization. RESULTS: Histopathology showed that renal tubular epithelial cells in the model group were swollen, inflammatory exudation was obvious and the inflammatory factors, interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were increased. Western blotting showed PI3K was upregulated in the model group. Serum creatinine and urea nitrogen increased after LPS injection. Renal AQP1 mRNA is downregulated and serum AQP1 protein increased first and then decreased in LPS-induced AKI rats. M2 macrophage markers (Arg-1, CD206) were increased in repair stage. In addition, treatment of murine macrophages (RAW264.7) with AQP1 siRNA resulted in decreased PI3K activation and M2 polarization, but increased IL-6 and TNF-α. Moreover, inhibiting PI3K with wortmannin imitated the results of AQP1 silencing. CONCLUSIONS: Macrophage M2 polarization is likely the cellular mechanism underlying the anti-AKI property of AQP1, and PI3K activation is involved in the AQP1-induced M2 phenotype switch.

Aquaporin-1 attenuates macrophage-mediated inflammatory responses by inhibiting p38 mitogen-activated protein kinase activation in lipopolysaccharide-induced acute kidney injury.

OBJECTIVE: This study was designed to investigate the role of AQP1 in the development of LPS-induced AKI and its potential regulatory mechanisms in the inflammatory responses of macrophages. METHODS: Male Wistar rats were injected intraperitoneally with LPS, and biochemical and histological renal damage was assessed. The levels of inflammatory mediators, macrophage markers and AQP1 in blood and kidney tissues were assessed by ELISA. RTPCR was used to assess changes in the relative levels of AQP1 mRNA induced by LPS. Western blot and immunofluorescence analyses were performed to assay the activation of the p38 MAPK and NF-κB pathways, respectively. The same detection methods were used in vitro to determine the regulatory mechanisms underlying AQP1 function. RESULTS: AQP1 mRNA levels were dramatically decreased in AKI rats following the increased expression of inflammatory factors. In vitro experiments demonstrated that silencing the AQP1 gene increased inflammatory mediator secretion, altered the classical activation of macrophages, greatly enhanced the phosphorylation of p38 and accelerated the translocation of NF-κB. Furthermore, these results were blocked by doramapimod, a p38 inhibitor. Therefore, these effects were mediated by the increased phosphorylation of p38 MAPK. CONCLUSION: Our results suggest that altered AQP1 expression may be associated with the development of inflammation in AKI. AQP1 plays a protective role in modulating acute renal injury and can attenuate macrophage-mediated inflammatory responses by downregulating p38 MAPK activity in LPS-induced RAW264.7 cells. The pharmacological targeting of AQP1-mediated p38 MAPK signalling may provide a novel treatment approach for AKI.

The Preparation and Properties of Terephthalyl-Alcohol-Modified Phenolic Foam with High Heat Aging Resistance.

In this experiment, terephthalyl alcohol was used as a modifier to modify phenol under both acidic and alkaline conditions to obtain modified phenols with different molecular structures. Subsequently, the modified phenols reacted with paraformaldehyde in an alkaline environment. After foaming and curing, a modified phenolic foam with high heat aging resistance was obtained. The molecular structure was characterized via Fourier transform infrared spectrometry (FT-IR) and nuclear magnetic resonance spectroscopy (13C NMR). The results showed that two different structures of phenolic resin can be successfully prepared under different conditions of acid and alkali. The modified phenolic foam was tested by thermogravimetric analysis. In addition, the modified phenolic foam was tested for mass change rate, dimensional change rate, powdering rate, water absorption rate, and compressive strength before and after aging. The results show that the modified phenolic foam has excellent performance. After heat aging for 24 h, the mass loss rate of the modified phenolic foam obtained by acid catalysis was as low as 4.5%, the pulverization rate was only increased by 3.2%, and the water absorption of the modified phenolic foam increased by 0.77%, which is one-third that of the phenolic foam. Compared with the phenolic foam, the modified phenolic foam shows good heat aging resistance.

Preparation and Properties of Acetoacetic Ester-Terminated Polyether Pre-Synthesis Modified Phenolic Foam.

In the present study, acetoacetic ester-terminated polyether was selected as a modifier to prepare a new type of polyether phenolic resin, which was successfully prepared by pre-synthesis modification. It is used to prepare interpenetrating cross-linked network structure modified phenolic foam with excellent mechanical properties. Fourier transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance (¹H NMR, 13C NMR) were used to characterize the molecular structure of the polyether phenolic resin. The results showed that the acetoacetic ester-terminated polyether successfully modified the phenolic resin and introduced a polyether skeleton into the resin structure. The effect of changing the added amount of acetoacetic ester-terminated polyether from 10% to 20% of the phenol content on the mechanical properties and microstructure of the modified phenolic foam was investigated. The results showed that when the amount of acetoacetic ester-terminated polyether was 16% the amount of phenol, this resulted in the best toughness of the modified foam, which had a bending deflection that could be increased to more than three times that of the base phenolic foam. The modified phenolic foam cell diameter was reduced by 36.3%, and the distribution was more uniform, which formed a denser network structure than that of the base phenolic foam. The bending strength was increased by 0.85 MPa, and the pulverization rate was as low as 1.3%.

Inhibition of inflammation using diacerein markedly improved renal function in endotoxemic acute kidney injured mice.

BACKGROUND: Inflammation is an important pathogenic component of endotoxemia-induced acute kidney injury (AKI), finally resulting in renal failure. Diacerein is an interleukin-1ß (IL-1ß) inhibitor used for osteoarthritis treatment by exerting anti-inflammatory effects. This study aims to investigate the effects of diacerein on endotoxemia-induced AKI. METHODS: Male C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS, 10 mg/kg) for 24 h prior to diacerein treatment (15 mg/kg/day) for another 48 h. Mice were examined by histological, molecular and biochemical approaches. RESULTS: LPS administration showed a time-dependent increase of IL-1ß expression and secretion in kidney tissues. Diacerein treatment normalized urine volume and osmolarity, reduced blood urea nitrogen (BUN), fractional excretion of sodium (FENa), serum creatinine and osmolarity, and protected renal function in an endotoxemic AKI mice model. In the histopathologic study, diacerein also improved renal tubular damage such as necrosis of the tubular segment. Moreover, diacerein inhibited LPS-induced increase of inflammatory cytokines, such as IL-1ß, tumor necrosis factor-α, monocyte chemoattractant protein-1 and nitric oxide synthase 2. In addition, LPS administration markedly decreased aquaporin 1 (AQP1), AQP2, AQP3, Na,K-ATPase α1, apical type 3 Na/H exchanger and Na-K-2Cl cotransporter expression in the kidney, which was reversed by diacerein treatment. We also found that diacerein or IL-1ß inhibition prevented the secretion of inflammatory cytokines and the decrease of AQP and sodium transporter expression induced by LPS in HK-2 cells. CONCLUSION: Our study demonstrates for the first time that diacerein improves renal function efficiently in endotoxemic AKI mice by suppressing inflammation and altering tubular water and sodium handing. These results suggest that diacerein may be a novel therapeutic agent for the treatment of endotoxemic AKI.

Preparation and Properties of the 3-pentadecyl-phenol In Situ Modified Foamable Phenolic Resin.

In this present study, 3-pentadecyl-phenol was selected as a modifier to prepare a foamable phenolic resin with excellent performance, which was successfully prepared by in situ modification. Fourier transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance (¹H NMR, 13C NMR) were used to test and characterize the molecular structure of the modified resin. The results showed that 3-pentadecyl-phenol successfully modified the molecular structure of phenolic resin with a reduction in the resin gel time. The effect of changing the added amount of 3-pentadecyl-phenol on the mechanical properties, microstructure, and flame retardancy of the modified foam was investigated. The results showed that when the amount of added 3-pentadecyl-phenol was 15% of the total amount of phenol, this resulted in the best toughness of the modified foam, which could be increased to 300% compared to the bending deflection of the unmodified phenolic foam. The cell structure showed that the modified phenolic foam formed a more regular and dense network structure and the closed cell ratio was high. Furthermore, the compressive strength, bending strength, and limited oxygen index were improved, while the water absorption rate was lowered. However, the foam density could be kept below 40 mg/cm³, which does not affect the load.

[Clinical application of micro-implant anchorage for treatment of scissors bite on one-side posterior teeth].

OBJECTIVE: To evaluate the efficiency of micro-implant anchorage (MIA) for posterior teeth intruded and the result of the treatment of scissors bite on one-side posterior teeth. METHODS: The study included 3 females and 1 male. All the overextruding upper posterior teeth were intruded by the MIA. The micro-implant screws were inserted into the buccal and lingual alveolar hone of the maxillary posterior teeth or the buccal alveolar hone of mandibular posterior teeth. About 0.833 N force was used to intrude the overgrowthing upper posterior teeth, and about 0.559 N force was used to draw buecally the low posterior teeth tilting lingually. RESULTS: The overextruding upper posterior teeth were intruded 2.0 mm on average, the low posterior teeth tilting lingually were upreared buccally. All the MIA screws kept stable during the treatment, but there was a slight inflammation around the implant screws. CONCLUSION: MIA could be used as an efficient method to correct scissors bite on one-side posterior teeth with intruding overgrowth upper posterior teeth, or uprearing buccally the tilting low posterior teeth.