Magnetic Metal–Organic Framework Enhanced Inorganic Coagulation for Water Purification

Green water treatment technologies are widely popular, and magnetic coagulation is one of the most popular methods and has been successfully applied in industry. Among them, magnetic seeds are crucial for the flocculation of contaminants. The objective of this work was to investigate the potential of magnetic metal–organic frameworks (MMOFs) as a seed in assisting polymeric ferric sulfate (PFS) flocculant, specifically exploring their applicability in algal-contaminated water. Scanning electron microscopy, transmission electron microscopy, energy-dispersive spectroscopy, Fourier transform infrared spectroscopy, X-ray diffraction, ferrite timing spectroscopy, and flocculation tests were used to characterize the structure and flocculation properties of MMOFs and PFS (PFS-MMOFs) composites, highlighting the stability of magnetic seed MMOFs and the flocculation effect of the composites. The results show that MMOFs have good dispersion and stability in acidic PFS solutions, which are favorable for engineering applications. MMOFs and PFS are bonded by hydrogen bonds, which enhance the polarity and dispersion of MMOFs, as well as the molecular chains of PFS. In the presence of MMOFs, it affected the distribution of iron species in the PFS, which means that the performance of coagulation may be changed. Coagulation with PFS-MMOFs was effective under different hydraulic conditions. It also showed better results than PFS in terms of dissolved organic carbon (DOC) removal and ultraviolet absorption value at 254 nm (UV254). In addition, the PFS-MMOFs in algal-infested waters were superior to the PFS. Overall, the findings tested in this study indicated that MMOFs are good magnetic seeds for remediation of water pollution in conjunction with PFS, potentially enhancing conventional coagulation

Application of a New Architecture Neural Network in Determination of Flocculant Dosing for Better Controlling Drinking Water Quality

In drinking water plants, accurate control of flocculation dosing not only improves the level of operation automation, thus reducing the chemical cost, but also strengthens the monitoring of pollutants in the whole water system. In this study, we used feedforward signal and feedback signal data to establish a back-propagation (BP) model for the prediction of flocculant dosing. We examined the effect of the particle swarm optimization (PSO) algorithm and data type on the simulation performance of the model. The results showed that the parameters, such as the learning factor, population size, and number of generations, significantly affected the simulation. The best optimization conditions were attained at a learning factor of 1.4, population size of 20, 20 generations, 8 feedforward signals and 1 feedback signal as input data, 6 hidden layer nodes, and 1 output node. The coefficient of determination (R2) between the predicted and measured values was 0.68, and the root mean square error (RMSE) was lower than 20%, showing a good prediction result. Weak time-delay data enhanced the model accuracy, which increased the R2 to 0.73. Overall, with the hybridized data, PSO, and weak time-delay data, the new architecture neural network was able to predict flocculant dosing

Application of a New Architecture Neural Network in Determination of Flocculant Dosing for Better Controlling Drinking Water Quality

In drinking water plants, accurate control of flocculation dosing not only improves the level of operation automation, thus reducing the chemical cost, but also strengthens the monitoring of pollutants in the whole water system. In this study, we used feedforward signal and feedback signal data to establish a back-propagation (BP) model for the prediction of flocculant dosing. We examined the effect of the particle swarm optimization (PSO) algorithm and data type on the simulation performance of the model. The results showed that the parameters, such as the learning factor, population size, and number of generations, significantly affected the simulation. The best optimization conditions were attained at a learning factor of 1.4, population size of 20, 20 generations, 8 feedforward signals and 1 feedback signal as input data, 6 hidden layer nodes, and 1 output node. The coefficient of determination (R2) between the predicted and measured values was 0.68, and the root mean square error (RMSE) was lower than 20%, showing a good prediction result. Weak time-delay data enhanced the model accuracy, which increased the R2 to 0.73. Overall, with the hybridized data, PSO, and weak time-delay data, the new architecture neural network was able to predict flocculant dosing

Genome-Wide Significant, Replicated and Functional Risk Variants for Alzheimer’s Disease

Genome-wide association studies (GWASs) have reported numerous associations between risk variants and Alzheimer’s disease (AD). However, these associations do not necessarily indicate a causal relationship. If the risk variants can be demonstrated to be biologically functional, the possibility of a causal relationship would be increased. In this article, we reviewed all of the published GWASs to extract the genome-wide significant (p \u3c 5×10−8) and replicated associations between risk variants and AD or AD-biomarkers. The regulatory effects of these risk variants on the expression of a novel class of non-coding RNAs (piRNAs) and protein-coding RNAs (mRNAs), the alteration of proteins caused by these variants, the associations between AD and these variants in our own sample, the expression of piRNAs, mRNAs and proteins in human brains targeted by these variants, the expression correlations between the risk genes and APOE, the pathways and networks that the risk genes belonged to, and the possible long non-coding RNAs (LncRNAs) that might regulate the risk genes were analyzed, to investigate the potential biological functions of the risk variants and explore the potential mechanisms underlying the SNP-AD associations. We found replicated and significant associations for AD or AD-biomarkers, surprisingly, only at 17 SNPs located in 11 genes/snRNAs/LncRNAs in eight genomic regions. Most of these 17 SNPs enriched some AD-related pathways or networks, and were potentially functional in regulating piRNAs and mRNAs; some SNPs were associated with AD in our sample, and some SNPs altered protein structures. Most of the protein-coding genes regulated by the risk SNPs were expressed in human brain and correlated with APOE expression. We conclude that these variants were most robust risk markers for AD, and their contributions to AD risk was likely to be causal. As expected, APOE and the lipoprotein metabolism pathway possess the highest weight among these contributions

Transcriptome-Wide piRNA Profiling in Human Brains for Aging Genetic Factors

OBJECTIVE: Piwi-interacting RNAs (piRNAs) represent a molecular feature shared by all nonaging biological systems, including the germline and somatic cancer stem cells, which display an indefinite renewal capacity and lifespan-stable genomic integrity and are potentially immortal. Here, we tested the hypothesis that piRNA is a critical genetic determinant of aging in humans. METHODS: Expression of transcriptome-wide piRNAs (n=24k) was profiled in the human prefrontal cortex of 12 subjects (84.9±9.5, range 68-100, years of age) using microarray technology. We examined the correlation between these piRNAs\u27 expression levels and age, adjusting for covariates including disease status. RESULTS: A total of 9,453 piRNAs were detected in brain. Including seven intergenic and three intronic piRNAs, ten piRNAs were significantly associated with age after correction for multiple testing (|r|=0.9; 1.9×10≤p≤9.9×10). CONCLUSION: We conclude that piRNAs might play a potential role in determining the years of survival of humans. The underlying mechanisms might involve the suppression of transposable elements (TEs) and expression regulation of aging-associated genes

Image3_Morroniside attenuates nucleus pulposus cell senescence to alleviate intervertebral disc degeneration via inhibiting ROS-Hippo-p53 pathway.jpg

Intervertebral disc (IVD) degeneration (IVDD) which is highly prevalent within the elderly population, is a leading cause of chronic low back pain and disability. Nucleus pulposus (NP) cell senescence plays an indispensable role in the pathogenesis of IVDD. Morroniside is a major iridoid glycoside and one of the quality control metrics of Cornus officinalis Siebold & Zucc (CO). An increasing body of evidence suggests that morroniside and CO-containing formulae share many similar biological effects, including anti-inflammatory, anti-oxidative, and anti-apoptotic properties. In a previous study, we reported that Liuwei Dihuang Decoction, a CO-containing formula, is effective for treating IVDD by targeting p53 expression; however, the therapeutic role of morroniside on IVDD remains obscure. In this study, we assessed the pharmacological effects of morroniside on NP cell senescence and IVDD pathogenesis using a lumbar spine instability surgery-induced mouse IVDD model and an in vitro H2O2-induced NP cell senescence model. Our results demonstrated that morroniside administration could significantly ameliorate mouse IVDD progression, concomitant with substantial improvement in extracellular matrix metabolism and histological grading score. Importantly, in vivo and in vitro experiments revealed that morroniside could significantly reduce the increase in SA-β-gal activities and the expression of p53 and p21, which are the most widely used indicators of senescence. Mechanistically, morroniside suppressed ROS-induced aberrant activation of Hippo signaling by inhibiting Mst1/2 and Lats1/2 phosphorylation and reversing Yap/Taz reduction, whereas blockade of Hippo signaling by Yap/Taz inhibitor-1 or Yap/Taz siRNAs could antagonize the anti-senescence effect of morroniside on H2O2-induced NP cell senescence model by increasing p53 expression and activity. Moreover, the inhibition of Hippo signaling in the IVD tissues by morroniside was further verified in mouse IVDD model. Taken together, our findings suggest that morroniside protects against NP cell senescence to alleviate IVDD progression by inhibiting the ROS-Hippo-p53 pathway, providing a potential novel therapeutic approach for IVDD.</p

Image1_Morroniside attenuates nucleus pulposus cell senescence to alleviate intervertebral disc degeneration via inhibiting ROS-Hippo-p53 pathway.jpg

Intervertebral disc (IVD) degeneration (IVDD) which is highly prevalent within the elderly population, is a leading cause of chronic low back pain and disability. Nucleus pulposus (NP) cell senescence plays an indispensable role in the pathogenesis of IVDD. Morroniside is a major iridoid glycoside and one of the quality control metrics of Cornus officinalis Siebold & Zucc (CO). An increasing body of evidence suggests that morroniside and CO-containing formulae share many similar biological effects, including anti-inflammatory, anti-oxidative, and anti-apoptotic properties. In a previous study, we reported that Liuwei Dihuang Decoction, a CO-containing formula, is effective for treating IVDD by targeting p53 expression; however, the therapeutic role of morroniside on IVDD remains obscure. In this study, we assessed the pharmacological effects of morroniside on NP cell senescence and IVDD pathogenesis using a lumbar spine instability surgery-induced mouse IVDD model and an in vitro H2O2-induced NP cell senescence model. Our results demonstrated that morroniside administration could significantly ameliorate mouse IVDD progression, concomitant with substantial improvement in extracellular matrix metabolism and histological grading score. Importantly, in vivo and in vitro experiments revealed that morroniside could significantly reduce the increase in SA-β-gal activities and the expression of p53 and p21, which are the most widely used indicators of senescence. Mechanistically, morroniside suppressed ROS-induced aberrant activation of Hippo signaling by inhibiting Mst1/2 and Lats1/2 phosphorylation and reversing Yap/Taz reduction, whereas blockade of Hippo signaling by Yap/Taz inhibitor-1 or Yap/Taz siRNAs could antagonize the anti-senescence effect of morroniside on H2O2-induced NP cell senescence model by increasing p53 expression and activity. Moreover, the inhibition of Hippo signaling in the IVD tissues by morroniside was further verified in mouse IVDD model. Taken together, our findings suggest that morroniside protects against NP cell senescence to alleviate IVDD progression by inhibiting the ROS-Hippo-p53 pathway, providing a potential novel therapeutic approach for IVDD.</p

Image2_Morroniside attenuates nucleus pulposus cell senescence to alleviate intervertebral disc degeneration via inhibiting ROS-Hippo-p53 pathway.jpg

Intervertebral disc (IVD) degeneration (IVDD) which is highly prevalent within the elderly population, is a leading cause of chronic low back pain and disability. Nucleus pulposus (NP) cell senescence plays an indispensable role in the pathogenesis of IVDD. Morroniside is a major iridoid glycoside and one of the quality control metrics of Cornus officinalis Siebold & Zucc (CO). An increasing body of evidence suggests that morroniside and CO-containing formulae share many similar biological effects, including anti-inflammatory, anti-oxidative, and anti-apoptotic properties. In a previous study, we reported that Liuwei Dihuang Decoction, a CO-containing formula, is effective for treating IVDD by targeting p53 expression; however, the therapeutic role of morroniside on IVDD remains obscure. In this study, we assessed the pharmacological effects of morroniside on NP cell senescence and IVDD pathogenesis using a lumbar spine instability surgery-induced mouse IVDD model and an in vitro H2O2-induced NP cell senescence model. Our results demonstrated that morroniside administration could significantly ameliorate mouse IVDD progression, concomitant with substantial improvement in extracellular matrix metabolism and histological grading score. Importantly, in vivo and in vitro experiments revealed that morroniside could significantly reduce the increase in SA-β-gal activities and the expression of p53 and p21, which are the most widely used indicators of senescence. Mechanistically, morroniside suppressed ROS-induced aberrant activation of Hippo signaling by inhibiting Mst1/2 and Lats1/2 phosphorylation and reversing Yap/Taz reduction, whereas blockade of Hippo signaling by Yap/Taz inhibitor-1 or Yap/Taz siRNAs could antagonize the anti-senescence effect of morroniside on H2O2-induced NP cell senescence model by increasing p53 expression and activity. Moreover, the inhibition of Hippo signaling in the IVD tissues by morroniside was further verified in mouse IVDD model. Taken together, our findings suggest that morroniside protects against NP cell senescence to alleviate IVDD progression by inhibiting the ROS-Hippo-p53 pathway, providing a potential novel therapeutic approach for IVDD.</p