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Background The aim of the study was to explore the potential role of IL-37 in nerve repair and immune regulation in peripheral nerve xenograft hosts. Methods Rat nerve xenografts were transplanted into mouse recipients. Transplanted mice received an intraperitoneal injection of IL-37 on the day before transplantation, whereas control mice remained untreated. At postoperative 2, 4, 8, and 12 weeks, the effects of IL-37 were examined on motor function, tissue morphology, and regenerative ability of xenograft nerves. Levels of IL-17 and IL-22 in serum and spleen were measured at 3, 7, 14, and 28 days after nerve transplantation. Results At 12 postoperative weeks, grafted nerves grew well in IL-37 treatment group, as documented by the recovery in function of sciatic nerves compared to untreated controls. In particular, IL-37-treated mice showed more complete neuromorphology, thicker myelin sheath, compact structure, and the increased number of myelinated nerve fibers in histological examination. The number of T helper (Th)17 (CD3 + CD4 + IL-17+) and Th22 (CD3 + CD4 + IL-22+) cells in the spleen was reduced in the IL-37-treated group, as well as serum IL-17 and IL-22 were decreased after IL-37 treatment compared with the untreated group. Conclusions IL-37 attenuates immunomodulatory responses induced by xenografts, contributing to the recovery of nerve function and the prevention of muscle atrophy caused by nerve grafts. [ABSTRACT FROM AUTHOR]

An improved Helferich method is presented. It involves the glycosylation of 4-methylumbelliferone with glycosyl acetates in the presence of boron trifluoride etherate combined with triethylamine, pyridine, or 4-dimethylaminopyridine under mild conditions, followed by deprotection to give fluorogenic 4-methylumbelliferyl glycoside substrates. Due to the use of base, the glycosylation reaction proceeds more easily, is uncommonly α- or β-stereoselective, and affords the corresponding products in moderate to excellent yields (51%–94%) under appropriate conditions. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSCs) are associated with tumor initiation, therapeutic resistance, relapse and metastasis. However, the underlying mechanisms CSCs use to preserve stemness are not yet fully understood. The present study demonstrated that the expression of RAB27A, member RAS oncogene family (Rab27a), which was reported to promote tumor progression by upregulating exocytosis of extracellular vesicles, was higher in mammosphere cells than in adherent MDA-MB-231 breast cancer cells. Downregulation of Rab27A inhibited mammosphere formation by decreasing the proportion of CD44+CD24-/low cells of the MDA-MB-231 cell line. Furthermore, Rab27A overexpression redistributed the cell cycle of breast (b) CSCs. The present study revealed that downregulation of Rab27A enhanced the capacity of metformin, the most widely used oral hypoglycemic drug for the treatment of type II diabetes, to inhibit mammosphere growth. Metformin reduced the expression of Rab27A dose-dependently. These data suggested that Rab27A acts as a mediator of human bCSCs by promoting the growth of mammospheres and that synergistic suppression of Rab27A, alone or in combination with metformin, holds promise for therapeutically targeting bCSCs. [ABSTRACT FROM AUTHOR]

Ni self-assembly has been performed on GaN (0001), Si (111) and sapphire (0001) substrates. Scanning electron microscopy (SEM) images verify that the Si (111) substrate leads to failure of the Ni assembly due to Si–N interlayer formation; the GaN (0001) and sapphire (0001) substrates promote assembly of the Ni particles. This indicates that the GaN/sapphire (0001) substrates are fit for Ni self-assembly. For the Ni assembly process on GaN/sapphire (0001) substrates, three differences are observed from the x-ray diffraction (XRD) patterns: (i) Ni self-assembly on the sapphire (0001) needs a 900 °C annealing temperature, lower than that on the GaN (0001) at 1000 °C, and loses the Ni network structure stage; (ii) the Ni particle shape is spherical for the sapphire (0001) substrate, and truncated-cone for the GaN (0001) substrate; and (iii) a Ni–N interlayer forms between the Ni particles and the GaN (0001) substrate, but an interlayer does not appear for the sapphire (0001) substrate. All these differences are attributed to the interaction between the Ni and the GaN/sapphire (0001) substrates. A model is introduced to explain this mechanism. [ABSTRACT FROM AUTHOR]