Thermally conductive but electrically insulating polymer composites are highly desirable for thermal management applications because of their wide range of utilization, ease of processing, and low cost. However, the traditional approaches to thermally conductive polymer composites usually suffer from the low thermal conductivity enhancement and/or the deterioration of electrical insulating property. In this study, using cellulose nanofiber‐supported 3D interconnected boron nitride nanosheet (3D–C–BNNS) aerogels, a novel method for highly thermally conductive but electrically insulating epoxy nanocomposites is reported. The nanocomposites exhibit thermal conductivity enhancement of about 1400% at a low BNNS loading of 9.6 vol%. In addition, the epoxy nanocomposites are still highly insulating, having a volume electrical resistivity of 1015 Ω cm. The strong potential application for thermal management has been demonstrated by the surface temperature variations of the nanocomposites with time during heating and cooling.

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IntroductionStudies have demonstrated that mesenchymal stromal cells (MSCs) could reverse acute and chronic kidney injury by a paracrine or endocrine mechanism, and microvesicles (MVs) have been regarded as a crucial means of intercellular communication. In the current study, we focused on the therapeutic effects of human Wharton-Jelly MSCs derived microvesicles (hWJMSC-MVs) in renal ischemia/reperfusion injury and its potential mechanisms.MethodsMVs isolated from conditioned medium were injected intravenously in rats immediately after ischemia of the left kidney for 60 minutes. The animals were sacrificed at 24 hours, 48 hours and 2 weeks after reperfusion. The infiltration of inflammatory cells was identified by the immunostaining of CD68+ cells. ELISA was employed to determine the inflammatory factors in the kidney and serum von Willebrand Factor (VWF). Tubular cell proliferation and apoptosis were identified by immunostaining. Renal fibrosis was assessed by Masson’s tri-chrome straining and alpha-smooth muscle actin (α-SMA) staining. The CX3CL1 expression in the kidney was measured by immunostaining and Western blot, respectively. In vitro, human umbilical vein endothelial cells were treated with or without MVs for 24 or 48 hours under hypoxia injury to test the CX3CL1 by immunostaining and Western blot.ResultsAfter administration of hWJMSC-MVs in acute kidney injury (AKI) rats, renal cell apoptosis was mitigated and proliferation was enhanced, inflammation was also alleviated in the first 48 hours. MVs also could suppress the expression of CX3CL1 and decrease the number of CD68+ macrophages in the kidney. In the late period, improvement of renal function and abrogation of renal fibrosis were observed. In vitro, MVs could down-regulate the expression of CX3CL1 in human umbilical vein endothelial cells under hypoxia injury at 24 or 48 hours.ConclusionsA single administration of MVs immediately after ischemic AKI could ameliorate renal injury in both the acute and chronic stage, and the anti-inflammatory property of MVs through suppression of CX3CL1 may be a potential mechanism. This establishes a substantial foundation for future research and treatment.

The continuous evolution toward semiconductor technology in the "more-than-Moore" era and rapidly increasing power density of modern electronic devices call for advanced thermal interface materials (TIMs). Here, we report a novel strategy to construct flexible polymer nanocomposite TIMs for advanced thermal management applications. First, aligned polyvinyl alcohol (PVA) supported and interconnected 2D boron nitride nanosheets (BNNSs) composite fiber membranes were fabricated by electrospinning. Then, the nanocomposite TIMs were constructed by rolling the PVA/BNNS composite fiber membranes to form cylinders and subsequently vacuum-assisted impregnation of polydimethylsiloxane (PDMS) into the porous cylinders. The nanocomposite TIMs not only exhibit a superhigh through-plane thermal conductivity enhancement of about 10 times at a low BNNS loading of 15.6 vol % in comparison with the pristine PDMS but also show excellent electrical insulating property (i.e., high volume electrical resistivity). The outstanding thermal management capability of the nanocomposite TIMs was practically confirmed by capturing the surface temperature variations of a working LED chip integrated with the nanocomposite TIMs.

Several studies suggest that mesenchymal stem cells (MSCs) possess antitumor properties; however, the exact mechanisms remain unclear. Recently, microvesicles (MVs) are considered as a novel avenue intercellular communication, which may be a mediator in MSCs-related antitumor effect. In the present study, we evaluated whether MVs derived from human umbilical cord Wharton’s jelly mesenchymal stem cells (hWJMSCs) may inhibit bladder tumor T24 cells growth using cell culture and the BALB/c nu/nu mice xenograft model. CCK-8 assay and Ki-67 immunostaining were performed to estimate cell proliferation in vitro and in vivo. Flow cytometry and TUNEL assay were used to assess cell cycle and apoptosis. To study the conceivable mechanism by which hWJMSC-MVs attenuate bladder tumor T24 cells, we estimated the expression of Akt/p-Akt, p-p53, p21 and cleaved Caspase 3 by Western blot technique after exposing T24 cells to hWJMSC-MVs for 24, 48 and 72h. Our data indicated that hWJMSC-MVs can inhibit T24 cells proliferative viability via cell cycle arrest and induce apoptosis in T24 cells in vitro and in vivo. This study showed that hWJMSC-MVs down-regulated phosphorylation of Akt protein kinase and up-regulated cleaved Caspase 3 during the process of anti-proliferation and pro-apoptosis in T24 cells. These results demonstrate that hWJMSC-MVs play a vital role in hWJMSC-induced antitumor effect and may be a novel tool for cancer therapy as a new mechanism of cell-to-cell communication.

terms of a graceful failure. [1] These devices have been applied in many high-tech fields such as hybrid electric vehicles, electrical defibrillators, pulsed power systems, and power grids. Nevertheless, the inferior energy density of the polymer dielectrics significantly restrains the development of film capacitors in the future applications. For instance, the commercial benchmark poly mer dielectric biaxially oriented polypropylene (BOPP) only possesses an energy density of <4 J cm −3 , [2] which leads to the cumbrous volume and cost in the practical applications. For example, film capacitors occupy ≈35% the volume and ≈40% the cost of the power inverters in hybrid electric vehicles. [3] The energy density (U e ) of dielectric materials can be derived from U e = ∫EdD , where E is the applied electric field and D denotes the electrical displacement. For linear dielectrics, the formula evolves into U e = 1/2ε 0 ε r E b 2 , where ε 0 is the vacuum permittivity, and ε r and E b are the dielectric constant and breakdown strength of dielectrics, respectively. Clearly, U e depends on the dielectric constant and breakdown strength of dielectrics, where E b is more important because of its quadratic relationship to U e .Boron nitride nanosheets (BNNSs), a 2D nanomaterial with a wide bandgap (≈6 eV), have proved to be an intriguing dopant in dielectric polymer nanocomposites for the interest of enhancing dielectric strength and energy efficiency, because they are of high intrinsic breakdown voltage, can serve as efficient scattering centers for charge carriers, and possess large electrical resistance, in addition to their great thermal conductivity and mechanical strength. [4] To make use of the exceptional effects of BNNSs on dielectric polymers, a straightforward approach is to homogeneously disperse such nanosheets in the polymer matrices to impede charge conduction. In princi ple, with increasing the population density of BNNSs in the polymer matrices, the transport of charge carriers becomes increasingly constrained by these 2D topological barriers, leading to better dielectric performance. A strain forced orientation (i.e., mechanical stretching) of the BNNSs along the film direction is usually applied as an extra step to further enlarge the coverage of the embedded nanofillers in the transverse plane direction, and hence improve the dielectric performance of the composite film. [5] However, with increasing the feed Polymer dielectrics such as poly(vinylidene fluoride) (PVDF) have drawn tremendous attention in high energy density capacitors because of their high dielectric constant and ease of processing. However, the discharged energy density attained with these materials is restrained by the inferior breakdown strength and electric resistivity. Herein, PVDF composite films with a nanosized interlayer of assembled boron nitride nanosheets (BNNSs) that is aligned along the in-plane direction are prepared through a simple layer-by-layer solution-casting process. Compared to the pristine PVDF, the composite films ...

Background Cardiac dysfunction in failing hearts of human patients and animal models is associated with both microtubule densification and T-tubule remodeling. Our objective was to investigate whether microtubule densification contributes to T-tubule remodeling and excitation-contraction coupling dysfunction in heart disease. Methods and Results In a mouse model of pressure overload-induced cardiomyopathy by transaortic banding (TAB), colchicine, a microtubule depolymerizer, significantly ameliorated T-tubule remodeling and cardiac dysfunction. In cultured cardiomyocytes, microtubule depolymerization with nocodazole or colchicine profoundly attenuated T-tubule impairment, whereas microtubule polymerization/stabilization with taxol accelerated T-tubule remodeling. In situ immunofluorescence of heart tissue sections demonstrated significant disorganization of JP2, a protein that bridges the T-tubule and sarcoplasmic reticulum membranes, in TAB hearts as well as in human failing hearts, while colchicine injection significantly preserved the distribution of JP2 in TAB hearts. In isolated mouse cardiomyocytes, prolonged culture or treatment with taxol resulted in pronounced redistribution of JP2 from T-tubules to the peripheral plasma membrane, without changing total JP2 expression. Nocodazole treatment antagonized JP2 redistribution. Moreover, overexpression of a dominant-negative mutant of Kinesin 1, a microtubule motor protein responsible for anterograde trafficking of proteins, protected against JP2 redistribution and T-tubule remodeling in culture. Finally, nocodazole treatment improved Ca2+ handling in cultured myocytes by increasing the amplitude of Ca2+ transients and reducing the frequency of Ca2+ sparks. Conclusions Our data identify a mechanistic link between microtubule densification and T-tubule remodeling and reveal microtubule-mediated JP2 redistribution as a novel mechanism for T-tubule disruption, loss of E-C coupling, and heart failure.

Our data identify a critical role for JP2 in T-tubule and excitation-contraction coupling maturation during development.