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Abstract: It has been reported that mesenchymal stem cells (MSCs) can transdifferentiate into Schwann cell-like cells by a series of treatments with a reducing agent, retinoic acid and a combination of trophic factors in vitro, and can transdifferentiate into myelin-forming cells to repair the demyelinated rat spinal cord in vivo. We now report that when co-cultured with dorsal root ganglion (DRG) neurons, MSCs were induced to transdifferentiate into Schwann cell-like cells that had ensheathed DRG axons. Following differentiation, MSCs underwent morphological changes similar to those of cultured Schwann cells and express GFAP and S100, the marker of Schwann cells. Moreover, 6 weeks later, MSCs wrapped their membrane around DRG axons. Further, initiation of myelination was observed in the co-cultured DRG neurons, which was determined by signals to MBP and this initiation of axon myelination by MSCs is similar to that of Schwann cells. However, electron micrographs show that no compact myelin was present in the MSCs co-cultures, whereas the Schwann cells co-cultures had formed a multilammelar myelin sheath around the axon. These indicate that the release of cytokine by DRG neurons may promote the transdifferentiation of MSCs, but is not sufficient to elicit compact myelination by transdifferentiated MSCs. These results improve our understanding in the mechanism of MSC transdifferentiation, and the mechanism underlying ensheathment and myelination by transdifferentiated MSCs. [Copyright &y& Elsevier]

The defects in perovskite crystals and the penetration of moisture/oxygen into the perovskite layer are major problems for perovskite solar cells (PSCs) to achieve long-term stability and high power conversion efficiency (PCE). However, there is still a lack of multifunctional passivation materials to solve these problems. Herein, for the first time, we report oleyl amine-coated PbSO 4 (PbO) 4 quantum-dots (QDs), as a passivation material with dual functions to simultaneously passivate the surface defects and block the penetration of moisture/oxygen into the perovskite layer for stable and efficient PSCs. The PbSO 4 (PbO) 4 QDs significantly reduce the defect density of the as-prepared CH 3 NH 3 PbI 3 films by passivating under-coordinated Pb ions and I anions and effectively enhance charge extraction efficiency at the TiO 2 /CH 3 NH 3 PbI 3 and CH 3 NH 3 PbI 3 /spiro-OMeTAD interfaces. Moreover, the hydrogen bond between H atoms of the OA and I atoms of the perovskite and the interface electric field at CH 3 NH 3 PbI 3 /OA interface also contribute to the improvement of efficiency and stability of PSCs. Finally, higher PCE (20.02%) is achieved by the PSCs with OA-coated PbSO 4 (PbO) 4 QDs compared to that (16.86%) of the PSCs without OA-coated PbSO 4 (PbO) 4 , corresponding to a 18.7% enhancement. Moreover, the PSCs with OA-coated PbSO 4 (PbO) 4 QDs maintain 90% of initial efficiency after operation for 280 h, indicating better stability than the PSCs without PbSO 4 (PbO) 4 QDs. Device structure and charge separation diagram. Image 1 • Oleyl amine (OA) coated-PbSO 4 (PbO) 4 quantum-dots are synthesized. • PbSO 4 (PbO) 4 QDs passivate defect states in perovskite crystals. • OA results in an interfacial electric field for charge extraction. • The efficiency and stability of the PSCs are significantly improved. [ABSTRACT FROM AUTHOR]

To improve the power conversion efficiency (PCE) and stability of inverted perovskite solar cells (PSCs) prepared in humid air (RH = 55%), a new zinc oxide (ZnO):TIPD composite film is inserted between PCBM layer and Ag electrode for the first time. Compared to the single PCBM layer, the formed PCBM/ZnO:TIPD electron transport layer (ETL) has better coverage on the perovskite layer and more effective charge extraction ability from the perovskite layer. The insertion of ZnO:TIPD film effectively suppress the charge recombination at perovskite/ETL interface. Besides, the PCBM/ZnO:TIPD layer has better ability to prevent moisture from penetrating into the perovskite layer than single PCBM film. For these reasons, the PCE and stability of the PSCs with the PCBM/ZnO:TIPD are significantly improved compared to the PSCs with single PCBM (or ZnO:TIPD) layer. The highest efficiency of the cell with PCBM/ZnO:TIPD ETL reaches (13.7 ± 0.4)% in ambient atmosphere, which is 1.20 times that of the PSCs with PCBM only. • The ZnO:TIPD composite film are fabricated for the first time. • The effect of the ZnO:TIPD film on charge separation and extraction is studied. • The efficiency and stability of the perovskite solar cells are significantly improved. [ABSTRACT FROM AUTHOR]

The interplay between Hsf4 and Hsf1 plays an important role in the regulation of lens homeostasis. However, the mechanism of the intermolecular association involved is still unclear. In this paper, we find that reconstitution of Hsf4b into Hsf4 −/− lens epithelial (mLEC/Hsf4 −/− ) cells can simultaneously downregulate Hsp70 expression and upregulate the expression of small heat shock proteins Hsp25 and αB-crystallin at both RNA and protein levels. ChIP assay results indicate Hsf4b, which binds to the promoters of Hsp90α, Hsp70.3, Hsp25 and αB-crystallin but not Hsp70.1, can inhibit Hsf1 binding to Hsp70.3 promoter and the heat shock mediated Hsp70 promoter activity by reducing Hsf1 protein expression. Hsf4b N-terminal hydrophobic region can interact with Hsf1 N-terminal hydrophobic region. Their interaction impairs Hsf1's intramolecular interaction between the N- and C-terminal hydrophobic regions, leading to Hsf1's cytosolic retention and protein degradation. Both lysosome inhibitors (chloroquine, pepstatin A plus E64d) and proteasome inhibitor MG132 can inhibit Hsf4-mediated Hsf1 protein degradation, but MG132 can induce Hsf1 activation as well. Upregulation of Hsf4b can significantly inhibit cisplatin and staurosporine induced lens epithelial cell apoptosis through direct upregulation of Hsp25 and αB-crystallin expression. Taken together, our results imply that upregulation of Hsf4b modulates the expression pattern of heat shock proteins in lens tissue by either directly binding to their promoters or promoting Hsf1 protein degradation. Moreover, upregulation of Hsf4b protects lens cell survival by upregulating anti-apoptotic pathways. These studies reveal a novel regulatory mechanism between Hsf1 and Hsf4b in modulating lens epithelial cell homeostasis. [ABSTRACT FROM AUTHOR]

Abstract: Hsf4b, a key regulator of postnatal lens development, is subjected to posttranslational modifications including phosphorylation. However, the phosphorylation sites in Hsf4b and their biological effects on the transcription activity of Hsf4b are poorly understood. Here we examined 17 potential phosphorylation residues in Hsf4b with alanine-scanning assays and found that a T472A mutation diminished Hsf4b-mediated expression of Hsp25 and αB-crystallin. In contrast, the phosphomimetic mutation of T472D enhanced their expression. Further investigation demonstrated that Hsf4b could interact with nuclear-transporter importin β-1 and Hsc70 via amino acids 246–320 and 320–493, respectively. T472A mutation reduced Hsf4b's interaction with importin β-1, while enhancing its interaction with Hsc70, resulting in Hsf4b cytosolic re-localization, protein instability and transcription activity attenuation. At the upstream, MEK6 was found to interact with Hsf4b and enhance Hsf4b's nuclear translocation and transcription activity, probably by phosphorylation at sites such as T472. Taken together, our results suggest that phosphorylation of Hsf4b at T472 by protein kinases such as MEK6 regulates Hsf4b interaction with the importin β-1-Hsc70 complex, resulting in blockade of its nuclear translocation and transcriptional activity of Hsf4b. [Copyright &y& Elsevier]

Abstract: 16S rRNA methylase-mediated high-level resistance to aminoglycosides has been reported recently in clinical isolates of Gram-negative bacilli from several countries. Twenty-one (6.2%, 21/337) of 337 isolates of Klebsiella pneumoniae from a teaching hospital in Wenzhou, China, were positive for 16S rRNA methylase genes (3 for armA, 13 for rmtB, 5 for both armA and rmtB) and highly resistant to gentamicin, amikacin, and tobramycin (MICs, ≥256 μg/mL). Nineteen of 21 isolates harboring 16S rRNA methyalse genes were extended-spectrum β-lactamase (ESBL) producers. The plasmids harboring 16S rRNA methylase genes from 14 of 21 donors were transferred into the recipients, Escherichia coli J53. The armA and the rmtB usually coexisted with ESBL genes in the same isolate in clinical isolates and cotransferred with ESBL genes on a self-transmissible conjugative plasmid to the recipients. Among 5 isolates harboring both armA and rmtB, the armA genes were located on the chromosomes, and the rmtB genes were located on the plasmids, as determined by Southern hybridization. The result of pulsed-field gel electrophoresis showed that horizontal gene transfer and clonal spread were responsible for the dissemination of the rmtB and the armA genes. 16S rRNA methylase-producing isolates of Klebsiella pneumoniae were commonly identified in the Chinese teaching hospital with coexistence of rmtB and armA genes in the same isolate. [Copyright &y& Elsevier]