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Of the carbon materials for capacitive deionization (CDI), carbon nanofibers prepared by electrospinning are a good alternative. A convenient method for effectively increasing the mesopore volume and modulate the micro-nano morphology of electrospun fibers still keep on developing. In this study, aiming at the requirement of CDI electrodes, a designed structure of carbon fibers embedded with porous carbon sheets was fabricated successfully. During preparation, instead of common polymer solution and its electrospinning, a triphase solution was carried out for combined electrospinning/electrospray process, which result in a self-supporting mat with high flexibility. Droplets were dispersed on newly formed fibers and solidified into porous sheets. Thus, a binary morphology of fibers and sheets was obtained. The mesopore volume of this work is 0.329 cm3 g−1, about 2.9 times larger than that of activated carbon fibers (ACF). The prepared electrodes exhibited an adsorption capacity of 15.1 mg g−1. The kinetics of electrosorption processes was also studied by Weber-Morris model. In summary, the classic ACF synthesis method was modified in the electrospinning step. An optimized morphology of the carbon mat was obtained, with no extra reagents and no material doping. This study might spark more interest for the advancement of electrospray/electrospinning methods and promote research on phase separation for CDI material preparation. [ABSTRACT FROM AUTHOR]

Copper (Cu) can be harmful to host physiology at high levels, although it is still unclear exactly how it causes nephrotoxicity. Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are associated with heavy metal intoxication. Meanwhile, mitochondria and ER are connected via mitochondria-associated ER membranes (MAM). In order to reveal the crosstalk between them, a total of 144 1-day-old Peking ducks were randomly divided into four groups: control (basal diet), 100 mg/kg Cu, 200 mg/kg Cu, and 400 mg/kg Cu groups. Results found that excessive Cu disrupted MAM integrity, reduced the co-localization of IP3R and VDAC1, and significantly changed the MAM-related factors levels (Grp75, Mfn2, IP3R, MCU, PACS2, and VDAC1), leading to MAM dysfunction. We further found that Cu exposure induced mitochondrial dysfunction via decreasing the ATP level and the expression levels of COX4, TOM20, SIRT1, and OPA1 and up-regulating Parkin expression level. Meanwhile, Cu exposure dramatically increased the expression levels of Grp78, CRT, and ATF4, resulting in ER stress. Overall, these findings demonstrated MAM plays the critical role in Cu-induced kidney mitochondrial dysfunction and ER stress, which deepened our understanding of Cu-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

The article titled "Retraction Note: Insulin-Like Growth Factor Binding Protein-Related Protein 1 Activates Primary Hepatic Stellate Cells via Autophagy Regulated by the PI3K/Akt/mTOR Signaling Pathway" has been retracted by the Editor-in-Chief of Digestive Diseases & Sciences. Concerns were raised about the images presented in the figures, including issues of duplication, similarity, and artifacts. The Editor-in-Chief no longer has confidence in the data presented, and all authors agree with the retraction. Springer Nature, the publisher, remains neutral regarding jurisdictional claims and institutional affiliations. [Extracted from the article]

Background: Autophagy is a self-degrading process. Previously, we showed that insulin-like growth factor binding protein-related protein 1 (IGFBPrP1) is a novel transforming growth factor β1 (TGFβ1)-interacting factor in liver fibrosis; the role of TGFβ1-mediated autophagy in hepatic stellate cells (HSCs) activation has been investigated. However, whether autophagy is regulated by IGFBPrP1 remains unknown.Aims: We investigated the interactions among IGFBPrP1, autophagy, and activation of primary rat HSCs.Methods: Primary HSCs were separated from Sprague Dawley rats by two-step enzymatic digestion, and then, we overexpressed or inhibited IGFBPrP1 expression in HSCs under serum-starved condition. Autophagy inducer rapamycin or inhibitor 3-methyladenine (3MA) was used to assess the relationship between autophagy and HSCs activation.Results: We observed the expression of activation marker α-SMA and autophagy markers such as LC3B and Beclin1, which were significantly increased in HSCs treated with adenovirus vector harboring the IGFBPrP1 gene (AdIGFBPrP1) compared to cells cultured under serum-starved. In comparison, HSCs treated with shIGFBPrP1 showed opposite results. Furthermore, HSCs activation and autophagy increased when cells were treated with rapamycin, whereas opposite results were obtained when cells were treated with 3MA. AdIGFBPrP1 treatment downregulated the phosphorylation of Akt and mTOR.Conclusion: Autophagy was induced in IGFBPrP1-treated primary HSCs, and IGFBPrP1-induced autophagy promoted the activation of HSCs and extracellular matrix expression, the underlying mechanism of which may involve the phosphatidylinositide 3-kinase/Akt/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Carbapenemase-producing Klebsiella pneumoniae have emerged as an important pathogens in nosocomial infections with high mortality rate. Although the modified Hodge test (MHT) is recommended for phenotypic detection of carbapenemase-producing Enterobacteriaceae, high false-positive rates were reported for MHT results. The MHT has acceptable sensitivity (98.0 %), but it lacks specificity (73.6 %). In this study, we incorporated an EDTA disk test into the MHT (MHT-EDTA) to improve the efficiency in phenotypic detection of K. pneumoniae carbapenemase (KPC) of K. pneumoniae isolates. EDTA was used to lyse the cells of 123 carbapenem non-susceptible K. pneumoniae isolates to release the β-lactamases. The MHT-EDTA achieved 100 % sensitivity and specificity for KPC detection among K. pneumoniae isolates as compared to growth patterns of the indicator organism E. coli (ATCC 25922). This method could be carried out as part of routine work to provide useful information for the clinical management of K. pneumoniae infection. [ABSTRACT FROM AUTHOR]

Purple acid phosphatase (PAP) encoding genes are a multigene family. PAPs require iron (Fe) to exert their functions that are involved in diverse biological roles including Fe homeostasis. However, the possible roles of PAPs in response to excess Fe remain unknown. In this study, we attempted to understand the regulation of PAPs by excess Fe in tea plant (Camellia sinensis). A genome-wide investigation of PAP encoding genes identified 19 CsPAP members based on the conserved motifs. The phylogenetic analysis showed that PAPs could be clustered into four groups, of which group II contained two specific cysteine-containing motifs "GGECGV" and "YERTC". To explore the expression patterns of CsPAP genes in response to excessive Fe supply, RNA-sequencing (RNA-seq) analyses were performed to compare their transcript abundances between tea plants that are grown under normal and high iron conditions, respectively. 17 members were shown to be transcribed in both roots and leaves. When supplied with a high amount of iron, the expression levels of four genes were significantly changed. Of which, CsPAP15a, CsPAP23 and CsPAP27c were shown as downregulated, while the highly expressed CsPAP10a was upregulated. Moreover, CsPAP23 was found to be alternatively spliced, suggesting its post-transcriptional regulation. The present work implicates that some CsPAP genes could be associated with the responses of tea plants to the iron regime, which may offer a new direction towards a further understanding of iron homeostasis and provide the potential approaches for crop improvement in terms of iron biofortification. [ABSTRACT FROM AUTHOR]