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Leveraging bright and stable carbon dots (CDs) for blue light‐emitting diodes (LEDs) is a prospective but challenging topic. Aggregation‐caused quenching (ACQ) of CDs and device engineering of CDs‐LEDs are two issues. Here, blue CDs with quantum yield of 59.75% are synthesized. Hydrogen bonds increase rigidity and facilitate luminescence, while polymer chains increase spatial resistance and resist ACQ. Then, solution‐processed blue CDs‐LEDs are assembled by blending CDs into poly(N‐vinylcarbazole) (PVK) as light‐emitting layer (EML). Furthermore, several other materials are also employed as the second host to reduce injection barrier, facilitate carriers' transport, and balance carriers' distribution. In particular, the blue CDs‐LED based on the co‐host system of PVK and 4‐[1‐[4‐[bis(4‐methylphenyl)amino]phenyl]cyclohexyl]‐N‐(3‐methylphenyl)‐N‐(4‐methylphenyl)benzenamine (TAPC) achieves a maximum brightness up to 827.60 cd m−2. This work is a step forward for applying CDs in LEDs. [ABSTRACT FROM AUTHOR]

Ji S, Liu M, Chen J, Yin L, Sha G, Chen H, Liu Z, Li L. The fate of glomerular mesangial IgA deposition in the donated kidney after allograft transplantation. Clin Transplant 2004 DOI: 10.1111/j.1399-0012.2004.00206.x © Blackwell Munksgaard, 2004 To investigate the fate of the mesangial IgA deposits in the donor kidney after allograft transplantation. Routine pre-transplant cadaveric donor kidney biopsy and repeated renal biopsies were performed at months 1, 3, and 6 after renal transplantation. The patients, 342 in number, were divided into IgA positive deposition kidney group (group A, n = 83) and non-IgA deposition kidney group (group B, n = 259). There were no significant differences between the two groups’ sex, age, time of hemodialysis, warm ischemia time, cold ischemia time, complement-dependent cytotoxicity, level of panel-reactive assay, and the distribution of original disease. Recipients in group A received donor kidney with glomerular mesangial proliferation and marked diffuse granular IgA deposition. All of them showed edema, nephrotic range protienuria, microhematuria, hypoalbuminemia, hypertension, and delayed graft function. Borderline change was higher in group A than in group B, 37.3 and 16.2% (p < 0.001), respectively. Acute allograft rejection was higher in group A than in group B, 31.3 and 19.3% (p < 0.001), respectively. The glomerular mesangial IgA deposits gradually disappeared from the mesangial regions in grafts of acute rejection. Graft survival in both groups was not significant, being 93.8 and 95.6% in 1 yr, and 86.7 and 88.3% in 3 yr. Clinical features of the recipients which received from donor kidney with glomerular mesangial proliferation and marked diffuse granular IgA deposition: edema, proteinuria, microhematuria, hypoalbuminemia, hypertension, and delayed graft function. The presence of IgA deposits on donated kidney, by a possible increase of the immunogenicity of these kidneys, might be a cause of increased rejection. There were no significant differences between the two groups on long-term allograft survival. [ABSTRACT FROM AUTHOR]