Intercalation of alkylviologen dications into the layered vanadium pentoxide

A novel series of inorganic–organic intercalation compounds were prepared by intercalating of alkylviologen dications into the layered vanadium pentoxide in the system of two phases of the liquid and the solid, and characterized by the techniques of X-ray diffraction (XRD), FT infrared (FTIR), X-ray photoelectron spectroscopy (XPS) and UV/vis diffuse reflectance spectroscopy (DRS).     

Actomyosin contractility in olfactory placode neurons opens the skin epithelium to form the zebrafish nostril

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Inhibition of the lymphoid tyrosine phosphatase: The effect of zinc(II) ions and chelating ligand fragments on enzymatic activity

A 96-member chelator fragment library (CFL-1.1) was screened to identify inhibitors of the lymphoid tyrosine phosphatase in the absence and presence of zinc acetate. Fragments that inhibit LYP activity more potently in the presence of zinc, fragments that rescue LYP activity in the presence of inhibitory concentrations of zinc, and fragments that inhibit LYP activity independent of zinc concentration were identified. Of these, 1,2-dihydroxynaphthalene was the most potent inhibitor with an IC₅₀ value of 2.52 ± 0.06 μM after 2 h of incubation. LYP inhibition by 1,2-dihydroxynaphthalene was very similar to inhibition by 1,2-naphthoquinone (IC₅₀ = 1.10 ± 0.03 µM), indicating that the oxidized quinone species is likely the active inhibitor. The inhibition was time-dependent, consistent with covalent modification of the enzyme.     

Synthesis,biological evaluation and in silico studies of 5-(3-methoxybenzylidene)thiazolidine-2,4-dione analogues as PTP1B inhibitors

PTP1B (protein tyrosine phosphatase 1B) dephosphorylates the insulin receptor substrate and thus acts as a negative regulator of the insulin and leptin signalling pathway. Recently, it has been considered as a new therapeutic target of intervention for the treatment of type2 diabetes. A series of aryl/alkylsulfonyloxy-5-(3-methoxybenzylidene)thiazolidine-2,4-dione derivatives were synthesized, screened in vitro for their PTP1B inhibitory activity and in vivo for anti-hyperglycaemic activity. Docking results further helped in understanding the nature of interactions governing the binding mode of ligands inside the active site of PTP1B. Among the synthesized compounds, 13 and 16 were found to be potent PTP1B inhibitors having IC₅₀ of 7.31 and 8.73 μM respectively. Significant lowering of blood glucose level was observed in some of the synthesized compounds in in vivo study.     

Chemoenzymatic synthesis of ADP-d-glycero-β-d-manno-heptose and study of the substrate specificity of HldE

An efficient one-pot three enzymes strategy for chemoenzymatic synthesis of ADP-d-glycero-β-d-manno-heptose (ADP-d, d-heptose) was reported using chemically synthesized d, d-heptose-7-phosphate and the ADP-d, d-heptose biosynthetic enzymes HldE and GmhB. Moreover, the result of investigating substrate specificity of the kinase action of HldE revealed that HldE had highly restricted substrate specificity towards structurally modified heptose-7-phosphate analogs.     

Nitensidine A,a guanidine alkaloid from Pterogyne nitens,is a novel substrate for human ABC transporter ABCB1

The Pterogyne nitens (Fabaceae) tree, native to South America, has been found to produce guanidine alkaloids as well as bioactive flavonols such as kaempferol, quercetin, and rutin. In the present study, we examined the possibility of interaction between human ATP-binding cassette (ABC) transporter ABCB1 and four guanidine alkaloids isolated from P. nitens (i.e., galegine, nitensidine A, pterogynidine, and pterogynine) using human T cell lymphoblast-like leukemia cell line CCRF-CEM and its multi-drug resistant (MDR) counterpart CEM/ADR5000. In XTT assays, CEM/ADR5000 cells were resistant to the four guanidine alkaloids compared to CCRF-CEM cells, although the four guanidine alkaloids exhibited some level of cytotoxicity against both CCRF-CEM and CEM/ADR5000 cells. In ATPase assays, three of the four guanidine alkaloids were found to stimulate the ATPase activity of ABCB1. Notably, nitensidine A was clearly found to stimulate the ATPase activity of ABCB1 as strongly as the control drug, verapamil. Furthermore, the cytotoxic effect of nitensidine A on CEM/ADR5000 cells was synergistically enhanced by verapamil. Nitensidine A inhibited the extrusion of calcein by ABCB1. In the present study, the possibility of interaction between ABCB1 and two synthetic nitensidine A analogs (nitensidine AT and AU) were examined to gain insight into the mechanism by which nitensidine A stimulates the ATPase activity of ABCB1. The ABCB1-dependent ATPase activity stimulated by nitensidine A was greatly reduced by substituting sulfur (S) or oxygen (O) for the imino nitrogen atom (N) in nitensidine A. Molecular docking studies on human ABCB1 showed that, guanidine alkaloids from P. nitens dock to the same binding pocket as verapamil. Nitensidine A and its analogs exhibit similar binding energies to verapamil. Taken together, this research clearly indicates that nitensidine A is a novel substrate for ABCB1. The present results also suggest that the number, binding site, and polymerization degree of the isoprenyl moiety in the guanidine alkaloids and the imino nitrogen atom cooperatively contribute to their stimulation of ABCB1's ATPase activity.     

Triptolide Inhibited Cytotoxicity of Differentiated PC12 Cells Induced by Amyloid-Beta25–35 via the Autophagy Pathway

Evidence shows that an abnormal deposition of amyloid beta-peptide_25–35 (Aβ_25–35) was the primary cause of the pathogenesis of Alzheimer’s disease (AD). And the elimination of Aβ_25–35 is considered an important target for the treatment of AD. Triptolide (TP), isolated from Tripterygium wilfordii Hook.f. (TWHF), has been shown to possess a broad spectrum of biological profiles, including neurotrophic and neuroprotective effects. In our study investigating the effect and potential mechanism of triptolide on cytotoxicity of differentiated rat pheochromocytoma cell line (the PC12 cell line is often used as a neuronal developmental model) induced by Amyloid-Beta_25–35 (Aβ_25–35), we used 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) assay, flow cytometry, Western blot, and acridine orange staining to detect whether triptolide could inhibit Aβ_25–35–induced cell apoptosis. We focused on the potential role of the autophagy pathway in Aβ_25–35-treated differentiated PC12 cells. Our experiments show that cell viability is significantly decreased, and the apoptosis increased in Aβ_25–35-treated differentiated PC12 cells. Meanwhile, Aβ_25–35 treatment increased the expression of microtubule-associated protein light chain 3 II (LC3 II), which indicates an activation of autophagy. However, triptolide could protect differentiated PC12 cells against Aβ_25–35-induced cytotoxicity and attenuate Aβ_25–35-induced differentiated PC12 cell apoptosis. Triptolide could also suppress the level of autophagy. In order to assess the effect of autophagy on the protective effects of triptolide in differentiated PC12 cells treated with Aβ_25–35, we used 3-Methyladenine (3-MA, an autophagy inhibitor) and rapamycin (an autophagy activator). MTT assay showed that 3-MA elevated cell viability compared with the Aβ_25–35-treated group and rapamycin inhibits the protection of triptolide. These results suggest that triptolide will repair the neurological damage in AD caused by deposition of Aβ_25–35 via the autophagy pathway, all of which may provide an exciting view of the potential application of triptolide or TWHF as a future research for AD.     

Examining the impact factors of urban residential energy consumption and CO2 emissions in China – Evidence from city-level data

Rapid urbanization has exerted substantial pressure on China’s energy system and contributed to climate change. To find the key drivers of urban residential energy consumption and CO₂ emissions, this paper uses an extended Stochastic Impacts by Regression on Population, Affluence and Technology (STIRPAT) model that employs city-level data to examine the influences of population scale, income level, population compactness and price on house-based residential energy consumption, energy-related CO₂ emissions and private vehicle ownership. The empirical results indicate that factors such as population scale, affluence, and population compactness can lead to increases in residential energy consumption and CO₂ emissions. In terms of transportation, income and population scale positively drive the growth of private vehicle ownership, while the fuel price negatively influences private vehicle ownership. Moreover, population scale is the most important factor in residential energy consumption and CO₂ emissions. Finally, policy recommendations are suggested for China’s urban development strategy and urban design and to encourage technology innovations that reduce residential energy consumption and CO₂ emissions.     

Appearance can be deceptive: shrubby native mangrove species contributes more to soil carbon sequestration than fast-growing exotic species

Plant and Soil - A dominant species of steppe in northern China, Stipa grandis, is gradually being replaced by S. krylovii due to climate change events. The aim of this study was...