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Most of As (80.3-82.9%) sequestered by Fe plaque was in the form of arsenate (As(V)), and the associated As(V) on Fe plaque was 11.0% higher under P0 treatment than under P150 treatment. In addition, the abundance of aioA gene was 73.5% higher under P0 treatment than under P150 treatment, and the dominant aioA at genus level was Rhizobium and Rhodoferax. In general, P0 treatment led to higher root oxidation activity, which improved the formation of Fe plaque; and P0 treatment also improved the abundance of aioA gene in rhizosphere, thus increased the oxidation of As; so, P0 treatment indirectly enhanced As sequestration on Fe plaque, and that in turn reduced As accumulation in brown rice.Esophageal cancer (EC) is a deadly malignancy worldwide with a high incidence and exhibits unevenly geographic prevalence, which suggests that environmental factors are deeply involved in the development of EC. Although the carcinogenesis of nitrosamines in the esophagus has been identified by tremendous toxicological data, the role of nitrosamines in the genesis of human EC has so far proved inconclusive largely due to a lack of convincing evidences. In this study, urinary nitrosamines in population controls and cases with esophageal precancerous lesions, including reflux esophagitis (RE) accompanying with basal cell hyperplasia (BCH) and dysplasia (DYS), and esophageal squamous cell carcinoma (ESCC) were detected by a SPE-LC-MS/MS method and the associated risk was evaluated. Higher excretion concentrations of N-nitrosomethylethylamine (NMEA) in the RE/BCH patients, NMEA and N-nitrosodibutylamine (NDBA) in the DYS patients, and NMEA, NDBA, N-nitrosopyrrolidine (NPyr) and N-nitrosomorpholine (NMor) in the ESCC patients were observed compared with the controls (p less then .05). And with the progression of esophageal lesion, the exposure complexity increased in terms of the categories of nitrosamines. Furthermore, the observed positive associations between the hazardous exposure of NMEA, NDBA and NPyr and the increased risk of ESCC, and between NMEA and NDBA and RE/BCH were established. find more These findings provided direct evidence to support the hypothesis that exposure to nitrosamines are involved in the carcinogenesis of esophageal epithelia in this high incidence area from the perspective of endogenous exposure assessment. However, discoveries in this study need to be confirmed by systematic researches in the future. And the dose-response relationships, the reference ranges or cutoff values to predict the risks of nitrosamines exposure also need to be defined.In this study, nano-silica (Nano-SiO2), oxidized (O-CNTs) and graphitized multi-walled carbon nanotubes (G-CNTs) were applied as model adsorbents to study the adsorption, desorption and coadsorption behaviors of sulfamerazine (SMR), Pb(II) and benzoic acid (BA). The results showed that charge assisted H-bond (CAHB) formation played an important role in adsorption of SMR and BA on O-riched nanomaterials. The adsorption capacities of Pb(II) on CNTs were 21.46- 26.77 times higher than that on Nano-SiO2, which was mainly attributed to surface complexation and cation-π interaction. link2 The fraction of Pb2+ adsorbed in the inside channel of CNTs should not be ignored. In coexisting systems, the absolute sorption inhibition of the SMR (ΔQeSMR) was compared with the amount of competitor adsorbed. Competitive sorption was observed as indicated by adding Pb(II) decreased adsorption of SMR on Nano-SiO2 (ΔQeSMR > 0), but hardly affected SMR adsorption on CNTs (ΔQeSMR ≈ 0) which was attributed to cation-π interaction. In addition, CAHB formed between SMR and Nano-SiO2 (ΔpKa ≈ 4.34) was weaker than that formed between SMR and O-CNTs (ΔpKa ≈ 3.15), which also consequently resulted in stronger competition of Pb(II) to SMR on Nano-SiO2 than that on O-CNTs. Moreover, coexisting BA increased adsorption of SMR on Nano-SiO2 and G-CNTs (ΔQeSMR less then 0), but did not result in an apparent competition on SMR adsorption by O-CNTs (ΔQeSMR ≈ 0). These results emphasize that the environmental behaviors of a certain pollutant should be assessed carefully by considering the presence of other pollutants.Interspecies model represents an established approach for the response data gap filling for regulatory agencies and researchers. link3 We propose a novel approach of intraspecies modeling within the animals of the same species, instead of animals from different species. The proposed intraspecies model is capable of more precise extrapolation of data than the interspecies model, as animals under the same species share a similar mechanism of action (MOA) and target sites for the response. Along with the advantage of better prediction over the interspecies model, the intraspecies model has all the significant features like recognition of MOA, species-specific toxicity, reduction of animal experimentation, and money and time. To establish and test the intraspecies modeling approach, we have modeled ecotoxicity of organic chemicals to three avian species Anas platyrhynchos, Colinus virginianus, and Phasianus colchicus. The intraspecies models offer to identify the mechanistic interpretation of the ecotoxicity of the studied chemicals along with the toxicity data gap filling. The success of the intraspecies modeling relies on connecting the missing dots of toxicity for the regulatory purposes, especially when there is a scarcity of ecotoxicity experimental data and in silico models for avian species.Background mir-RNAs play a role in regulating bone homeostasis. In this study we assessed the functional role of mir-RNA 150 in bone homeostasis. We also assess the effects of miR-150 deficiency on osteoblast and osteoclast differentiation and function using in vivo and in vitro approaches. Methods Wild type (WT) (C57BL/6J) and miR-150 KO mice were compared for a variety of parameters. Micro-CT imaging was conducted to quantify trabecular bone mass inferior to the distal growth plate of the femur. Von Kossa staining was performed for osteoblast culture mineralization. RT-qPCR, biochemical analysis and bone histomorphometry were utilized for quantification of relevant genes and serum protein measurements. Differentiation and function of osteoblasts and osteoclasts was performed using primarily cultures and assessed the cell autonomous response of mir-RNA-150 on cell differentiation and function. Results Mir-150 exhibited expression in a variety of tissues and increases progressively with age. Through micro-CT imaging, we found that KO mice presented reduced bone mass at 4, 8, and 16 weeks of age compared to WT mice. Furthermore, histomorphometric analysis revealed increased trabecular separation, decreased bone thickness, and decreased osteoblast number in KO compared to WT mice. Mir-150 deficiency also correlated with higher bone resorption, accompanied with significant increases in CTX-1 serum levels, and a decrease in cell apoptotic rate ex vivo. Additionally, miR-150 KO mice showed increased osteoblast differentiation and decreased osteoclastogenesis ex vivo. Luciferase assay showed increased Osteoactivin/GPNMB expression in miR-150 KO osteoblasts compared to WT cells. Conclusion Our data suggests that miR-150 influences osteoblast and osteoclast functionality and differentiation; specifically, miR-150 serves as a negative regulator for osteoblasts and a positive regulator for osteoclasts by regulating, at least in part, Osteoactivin/GPNMB expression.Notch 1 through 4 are transmembrane receptors that play a pivotal role in cell differentiation and function; this review addresses the role of Notch signaling in osteoclastogenesis and bone resorption. Notch receptors are activated following interactions with their ligands of the Jagged and Delta-like families. In the skeleton, Notch signaling controls osteoclast differentiation and bone-resorbing activity either directly acting on osteoclast precursors, or indirectly acting on cells of the osteoblast lineage and cells of the immune system. NOTCH1 inhibits osteoclastogenesis, whereas NOTCH2 enhances osteoclast differentiation and function by direct and indirect mechanisms. NOTCH3 induces the expression of RANKL in osteoblasts and osteocytes and as a result induces osteoclast differentiation. There is limited expression of NOTCH4 in skeletal cells. Selected congenital disorders and skeletal malignancies are associated with dysregulated Notch signaling and enhanced bone resorption. In conclusion, Notch signaling is a critical pathway that controls osteoblast and osteoclast differentiation and function and regulates skeletal homeostasis in health and disease.Osteoclasts are derived from mononuclear phagocyte lineage cells and are indispensable for bone resorption. Recent findings suggest that fetal yolk sac macrophage progenitors give rise to neonatal osteoclasts, while hematopoietic stem cell-derived cells, such as monocytes, contribute to maintaining osteoclast syncytia in vivo. Osteoclast differentiation is dependent on macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL) signaling that mediates global epigenetic and transcriptional changes. PU.1 is a transcription factor that establishes cell type-specific enhancer landscapes in osteoclast precursors and mature osteoclasts by collaborating with interferon regulatory factor-8 (IRF8) and nuclear factor of activated T-cells (NFATc1), respectively. Irf8 and Nfatc1 genes are tightly controlled by epigenetic mechanisms such as DNA methylation and histone modifications during osteoclastogenesis. Thus, key transcription factors orchestrate osteoclast-specific transcription regulatory networks through epigenetic modifications. In this review, we discuss recent advances in our understanding of the molecular mechanisms involved in osteoclast development.Background A new combination of amlodipine and celecoxib has been recently introduced in order to relieve the symptoms of osteoarthritis and help treat hypertension that commonly associated with osteoarthritis. Objective The current study is the first to develop and optimize a sensitive, simple and accurate first derivative synchronous spectrofluorimetric method for the simultaneous determination of amlodipine and celecoxib in bulk powder, pharmaceutical preparation and spiked human plasma. Method The method implies the use of synchronous methodology using Δλ = 100 nm and measuring the fluorescence amplitudes of the first derivative each at the zero-crossing point of the other. For amlodipine and celecoxib, the emission wavelengths were at 455 nm and 368 nm, after excitation at 367 nm and 264 nm, respectively. Results The method was found to be linear over a wide concentration ranges of (5-600 ng/ml), (100-2000 ng/ml) with lower limits of detection of (1.16 ng/ml) and (17.16 ng/ml) for amlodipine and celecoxib, respectively. Enhancement of the fluorescence intensity was achieved by complex formation between the studied drugs and the surfactant sodium dodecyl sulfate and optimizing other experimental conditions. The method was further extended for application for determination of the studied drugs in spiked human plasma with excellent % recoveries of (95.20 ± 6.095) and (98.67 ± 6.394) for amlodipine and celecoxib, respectively. Validation of the method was successfully implemented according to recommendations delivered by guidelines of the International Conference on Harmonization.