We fabricated silver nanowire (AgNW)-coated cellulose papers with a hierarchical structure by an efficient and facile dip-coating process, and investigated their microstructures, electrical conductivity and electromagnetic interference (EMI) shielding effectiveness. SEM images confirm that AgNWs are coated dominantly on the paper surfaces, although they exist partially in the inner parts of the cellulose papers, which demonstrates that the AgNW density gradually decreases in thickness direction of the AgNW/cellulose papers. This result is supported by the anisotropic apparent electrical conductivity of the AgNW/cellulose papers depending on in-plane or thickness direction. Even for a AgNW/cellulose paper obtained by a single dip-coating cycle, the apparent electrical conductivity in the in-plane direction of 0.34 S/cm is achieved, which is far higher than the neat cellulose paper with ∼10(-11) S/cm. In addition, the apparent electrical conductivity of the papers in the in-plane direction increases significantly from 0.34 to 67.51 S/cm with increasing the number of dip-coating cycle. Moreover, although the AgNW/cellulose paper with 67.51 S/cm possesses 0.53 vol % AgNW only, it exhibits high EMI shielding performance of ∼48.6 dB at 1 GHz. This indicates that the cellulose paper structure is highly effective to form a conductive AgNW network. Overall, it can be concluded that the AgNW/cellulose papers with high flexibility and low density can be used as electrically conductive components and EMI shielding elements in advanced application areas.

IL-1β-secreting nucleotide-binding oligomerization domain protein 3 (NLRP3) inflammasomes play a pivotal role in triggering innate immune responses in metabolic disease. We investigated the role of soluble uric acid in NLRP3 inflammasome activation in macrophages to demonstrate the effect of systemic hyperuricemia on progressive kidney damage in type 2 diabetes. THP-1 cells, human acute monocytic leukemia cells, were cultured to obtain macrophages, and HK-2 cells, human renal proximal tubule cells, were cultured and stimulated with uric acid. In vivo, we designed four rat groups as follows: 1) Long-Evans Tokushima Otsuka (LETO); 2) Otsuka Long-Evans Tokushima Fatty (OLETF); 3) OLETF+high-fructose diet (HFD) for 16 wk; and 4) OLETF+HFD+allopurinol (10 mg/dl administered in the drinking water). Soluble uric acid stimulated NLRP3 inflammasomes to produce IL-1β in macrophages. Uric acid-induced MitoSOX mediates NLRP3 activation and IL-1β secretion. IL-1β from macrophages activates NF-κB in cocultured proximal tubular cells. In vivo, intrarenal IL-1β expression and macrophage infiltration increased in HFD-fed OLETF rats. Lowering the serum uric acid level resulted in improving the albuminuria, tubular injury, macrophage infiltration, and renal IL-1β (60% of HFD-fed OLETF) independently of glycemic control. Direct activation of proximal tubular cells by uric acid resulted in (C-X-C motif) ligand 12 and high mobility group box-1 release and accelerated macrophage recruitment and the M1 phenotype. Taken together, these data support direct roles of hyperuricemia in activating NLRP3 inflammasomes in macrophages, promoting chemokine signaling in the proximal tubule and contributing to the progression of diabetic nephropathy through cross talk between macrophages and proximal tubular cells.

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Background/Aims: Recent evidence has shown that an inflammatory process is involved in the development and progression of diabetic nephropathy. This study examined the impact of activated intrarenal lymphocytes in this inflammatory process. Methods: We studied T cell recruitment in mice with streptozotocin (STZ)-induced diabetes by flow cytometry and immunohistochemistry. The kidney biopsy specimens from patients with type 2 diabetes mellitus and diabetic nephropathy were evaluated by immunohistochemistry. Results: In flow cytometry, intrarenal CD3+ T cells were significantly increased in proteinuric mice at 20 weeks after STZ injection. However, the population of T cells and B cells in diabetic spleen was not different from that of control mice. Immunohistochemistry also showed a marked infiltration of interstitial CD4+, CD8+ T cells in diabetic kidney. Interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) mRNA expression was significantly increased in diabetic mouse kidney compared with controls. Interestingly, flow cytometry analysis of kidney-derived mononuclear cells from diabetic mice showed significantly increased production of IFN-γ and TNF-α by CD3+ T cells. Type 2 diabetic patients also showed a marked increase in CD4+, CD8+ and CD20+ cells in interstitium, and the number of CD4+ and CD20+ cells correlated with the amount of proteinuria. Conclusion: Our results clearly showed that aberrant intrarenal infiltration and the activation of T cells in interstitium are the underlying immunopathological mechanisms of diabetic kidney injury.

Mesenchymal stem cell (MSC) has been implied to have the therapeutic potential on chronic kidney disease (CKD). However, the underlying mechanism is still unclear and administration frequency of MSCs could be an issue in a chronic disease model. We evaluated the effect of repeated administration of MSCs on a remnant kidney model. MSCs from 5-week male Sprague-Dawley rats were infused by tail vein into 7-week female 5/6 nephrectomized rats after tagging with a fluorescent probe, chloromethyl-1,1-dioctadecyl-3,3,3',3'-tetramethyl- indocarbocyanine perchlorate (CM-Dil). Effect of weekly administration of MSCs was compared with the effect of once injection of MSCs and mesangial cells (MCs) at 1 and 5 weeks, respectively. Engraftment of MSCs into the kidney was evaluated by the presence of CM-Dil fluorescence or SRY gene expression. Weekly MSCs administration showed significant improvement in systolic blood pressure (SBP), urinary protein excretion amount, and serum creatinine level at 5 weeks, whereas once MSCs or MCs administration did not. Although once MSCs administration attenuated glomerulosclerosis and infiltration of ED-1 positive cells at 5 weeks as compared with MCs, weekly MSC administration led to a more significant improvement. Renal SRY gene expression and presence of CM-Dil-tagged cells could be confirmed at 1 week after injection of MSCs or weekly injected group, but not at 5 weeks after once injection. MSCs attenuated cortical expression of interleukin (IL)-6 and elevated the expression of IL-10, but these effects were only sustained in the weekly group. Thus, repeated administration of MSCs improves the protective effect on remnant kidney injury, but primarily via the paracrine effect rather than differentiation.