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In comparison to the well-developed proton-exchange-membrane fuel cells, anion-exchange-membrane fuel cells (AEMFCs) permit adoption of platinum-group-metal (PGM)-free catalysts due to the alkaline environment, giving a substantial cost reduction. However, previous AEMFCs have generally shown unsatisfactory performances due to the lack of effective PGM-free catalysts that can endure harsh fuel cell conditions. Here we report a plasma-assisted synthesis of high-quality nickel nitride (Ni

Platinum on carbon (Pt/C) catalyst is commercially adopted in fuel cells but it undergoes formidable active-site poisoning by carbon monoxide (CO). In particular, given the sluggish kinetics of hydrogen oxidation reaction (HOR) in anion-exchange membrane fuel cell (AEMFC), the issues of Pt poisoning and slow rate would combine mutually, notably worsening the device performances. Here we overcome these challenges through incorporating cobalt (Co) into molybdenum-nickel alloy (MoNi

Reactive oxygen species (ROS), especially hydrogen peroxide (H2O2), have recently been reported to cause a significant increase in the production and expression of matrix metalloproteinases (MMPs), which are closely correlated with lung cancer metastasis. The aim of the present study is to determine the inhibitory effects of a polysaccharide isolated from Ulva prolifera O.F. Muller (U. prolifera) on the invasive potential of non-small cell lung cancer (NSCLC) cells, and further to explore the underlying mechanisms connected to that potential. The data showed that increased MMP-9 resulting from H2O2 exposure was mediated by activating mitogen-activated protein kinases (MAPKs). Pre-treatment with polysaccharides suppressed the activation of H2O2-mediated MAPK pathways and cell invasion. Hence, MMP-9 production triggered by H2O2 was demonstrated by activating MAPK signaling in a Myc-dependent manner. Taken together, these results suggested that polysaccharides suppress H2O2-induced cell invasion by inhibiting Myc-mediated MMP-9 gene transcription through the MAPK signaling pathway in A549 and NCI-H1650 cells. Our data also suggested that polysaccharides may be useful in minimizing the development of lung cancer metastasis. In the future, pretreatment with polysaccharides because of their antioxidant properties might be beneficial to enhance surgical outcomes.

Reactive oxygen species (ROS), especially hydrogen peroxide (H2O2), have recently been reported to cause a significant increase in the production and expression of matrix metalloproteinases (MMPs), which are closely correlated with lung cancer metastasis. The aim of the present study is to determine the inhibitory effects of a polysaccharide isolated from Ulva prolifera O.F. Müller (U. prolifera) on the invasive potential of non-small cell lung cancer (NSCLC) cells, and further to explore the underlying mechanisms connected to that potential. The data showed that increased MMP-9 resulting from H2O2 exposure was mediated by activating mitogen-activated protein kinases (MAPKs). Pre-treatment with polysaccharides suppressed the activation of H2O2-mediated MAPK pathways and cell invasion. Hence, MMP-9 production triggered by H2O2 was demonstrated by activating MAPK signaling in a Myc-dependent manner. Taken together, these results suggested that polysaccharides suppress H2O2-induced cell invasion by inhibiting Myc-mediated MMP-9 gene transcription through the MAPK signaling pathway in A549 and NCI-H1650 cells. Our data also suggested that polysaccharides may be useful in minimizing the development of lung cancer metastasis. In the future, pretreatment with polysaccharides because of their antioxidant properties might be beneficial to enhance surgical outcomes.

Correction for ‘Polysaccharides from Ulva prolifera O.F. Müller inhibit cell proliferation via activating MAPK signaling in A549 and H1650 cells’ by Juan Juan Yang et al., Food Funct., 2021, 12, 6915–6924, https://doi.org/10.1039/D1FO00294E.

Sortilin is found to regulate proliferation and death of different cells, while its role in regulating keratinocyte proliferation and apoptosis is still unknown. In this study, we found that sortilin levels significantly increased in psoriasis patients, and sortilin suppression eliminated the proliferation of HaCaT cells induced by M5 cocktail solution and enhanced the levels of cleaved caspase 3 protein and the Bax/Bcl-2 ratio; however, levels of p-PI3K and p-AKT were decreased. In addition, sortilin silencing remitted the characteristic changes associated with psoriasis-like skin lesions. In summary, suppressed sortilin expression helped inhibit keratinocyte proliferation in HaCaT cells by inactivating PI3K/AKT signaling, which provides a new target for the therapy of psoriasis.

Some representative steel structural buildings at home and abroad were discussed from the point of view of architectural form and function, structural system and construction, engineering cost and environmental protection et al. Then the common character of excellent designs and the deficiency of some controversial designs were separately summarized. The essential of steel structural buildings was generalized. Furthermore the criteria of excellent design in the current engineering construction were proposed and expounded from three aspects. At last how to produce excellent designs was explored.

To discuss the application of automated DNA image cytometry (ICM) and fluorescence in situ hybridization (FISH) in the diagnosis of urothelial carcinoma of bladder.From August 2008 to March 2009, 60 volunteers with informed consent were divided into two groups, 40 patients proven as urothelial carcinoma of bladder by pathology and 20 healthy individuals as control. Urine was collected and tested by cytology, ICM and FISH.Overall sensitivity of FISH was significantly higher in detection of malignancy than that of ICM (82.5% vs 62.5%, P0.05) and that of urine cytology (82.5% vs 25.0%, P0.05), while ICM was more sensitive to diagnose urothelial carcinoma of bladder than urine cytology (62.5% vs 25.0%, P0.05). Specificities of urine cytology, ICM and FISH were 100% in diagnosis of urothelial carcinoma of bladder (P0.05). Sensitivities of urine cytology, ICM and FISH have no correlation with pathological stage (P0.05), but have significant correlation with grade (P0.05).ICM and FISH have the same specificity as urine cytology in diagnosis of urothelial carcinoma of bladder, but they have significantly higher sensitivity than urine cytology. FISH has the highest sensitivity among three diagnostic methods. Therefore, FISH may become a newly non-invasive technique for the diagnosis and surveillance of urothelial carcinoma of bladder.

To investigate the expression of extracellular matrix metalloproteinase induced (EMMPRIN) in the interface tissue, and explore the role of EMMPRIN in the aseptic loosening of prostheses.Immunohistochemistry was performed to characterize the EMMPRIN-expressing cells at sites of interface tissue around aseptic loosened hip prostheses in 16 cases. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to study the existence of EMMPRIN mRNA in interface tissue samples. And it was followed up by computer assisted image analysis in order to detect the A values of their expression. Synovium of hip joint of 8 femoral neck fracture were in control group.Strong immunostaining of EMMPRIN was found in the macrophages and fibroblasts of lining-like layers and vascular endothelium of synovial membrane-like interface tissue around loosened prostheses. Expression of EMMPRIN was significantly higher in interface tissue than the control synovium (z=-3.252, P=0.001). RT-PCR of interface tissue samples disclosed the presence of EMMPRIN mRNA of 14 cases. In interface tissue, the A value of EMMPRIN increased significantly compared to control synovium (P0.01).Over-expression of EMMPRIN up-regulates the production of matrix metalloproteinase (MMPs) in the interface tissue. And it can promote the bone destruction around prostheses. Thereby it may be one of methods to prevent and treat aseptic loosening of prostheses by repression the biology activity of EMMPRIN.