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https://www.readbyqxmd.com/read/30218876/cr-vi-removal-using-different-reducing-agents-combined-with-fly-ash-leachate-a-comparative-study-of-their-efficiency-and-potential-mechanisms
#1
Shengxin Zhao, Zhonglin Chen, Binyuan Wang, Jimin Shen, Jinna Zhang, Dongmei Li
Remediation of high concentrations of Cr(VI) in wastewater involves its chemical reduction to Cr(III), a product with low toxicity that can be easily removed. To date, NaBH4 has rarely been used to reduce Cr(VI). This article reports a comparative study of Cr(VI) removal by NaBH4 and five sulfur-based reducing agents (FeSO4 , Na2 S2 O5 , NaHSO3 , Na2 S2 O3 , and Na2 SO3 ). The potential mechanisms of Cr(VI) removal by these six reducing agents with and without fly ash leachate (FAL) are also discussed. The results revealed that the reduction and subsequent removal of Cr(VI) are influenced by the hydrolysis and ionization of the reducing agents in solution...
September 8, 2018: Chemosphere
https://www.readbyqxmd.com/read/30208701/trends-in-micropollutant-biotransformation-along-a-solids-retention-time-gradient
#2
Stefan Achermann, Per Fal Aring S, A Joss, Cresten Mansfeldt, Yujie Men, Bernadette Vogler, Kathrin Fenner
For many polar organic micropollutants, biotransformation by activated sludge microorganisms is a major removal process during wastewater treatment. However, our current understanding of how wastewater treatment operations influence microbial communities and their micropollutant biotransformation potential is limited, leaving major parts of observed variability in biotransformation rates across treatment facilities unexplained. Here, we present biotransformation rate constants for 42 micropollutants belonging to different chemical classes along a gradient of solids retention time (SRT)...
September 13, 2018: Environmental Science & Technology
https://www.readbyqxmd.com/read/30195799/translating-sod1-gene-silencing-toward-the-clinic-a-highly-efficacious-off-target-free-and-biomarker-supported-strategy-for-fals
#3
Tommaso Iannitti, Joseph M Scarrott, Shibi Likhite, Ian R P Coldicott, Katherine E Lewis, Paul R Heath, Adrian Higginbottom, Monika A Myszczynska, Marta Milo, Guillaume M Hautbergue, Kathrin Meyer, Brian K Kaspar, Laura Ferraiuolo, Pamela J Shaw, Mimoun Azzouz
Of familial amyotrophic lateral sclerosis (fALS) cases, 20% are caused by mutations in the gene encoding human cytosolic Cu/Zn superoxide dismutase (hSOD1). Efficient translation of the therapeutic potential of RNAi for the treatment of SOD1-ALS patients requires the development of vectors that are free of significant off-target effects and with reliable biomarkers to discern sufficient target engagement and correct dosing. Using adeno-associated virus serotype 9 to deliver RNAi against hSOD1 in the SOD1G93A mouse model, we found that intrathecal injection of the therapeutic vector via the cisterna magna delayed onset of disease, decreased motor neuron death at end stage by up to 88%, and prolonged the median survival of SOD1G93A mice by up to 42%...
September 7, 2018: Molecular Therapy. Nucleic Acids
https://www.readbyqxmd.com/read/30176652/pneumococcal-vaccination-in-the-adult-population-in-poland-the-up-to-date-analysis
#4
Andrzej M Fal, Dorota M Fal, Dorota Kiedik, Barbara Gad-Karpierz
No abstract text is available yet for this article.
2018: Wiadomości Lekarskie: Organ Polskiego Towarzystwa Lekarskiego
https://www.readbyqxmd.com/read/30176351/single-chain-variable-fragment-antibodies-directed-against-sod1-ameliorate-disease-in-mutant-sod1-transgenic-mice
#5
Ghanashyam D Ghadge, Brian K Kay, Claire Drigotas, Raymond P Roos
Mutations in Cu/Zn superoxide dismutase (SOD1) are the cause of ~20% of cases of familial ALS (FALS), which comprise ~10% of the overall total number of cases of ALS. Mutant (mt) SOD1 is thought to cause FALS through a gain and not loss in function, perhaps as a result of the mutant protein's misfolding and aggregation. Previously we used a phage display library to raise single chain variable fragment antibodies (scFvs) against SOD1, which were found to decrease aggregation of mtSOD1 and toxicity in vitro. In the present study, we show that two scFvs directed against SOD1 ameliorate disease in G93A mtSOD1 transgenic mice and also decrease motor neuron loss, microgliosis, astrocytosis, as well as SOD1 burden and aggregation...
August 31, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/30175474/hydrogen-sulfide-improves-postischemic-neoangiogenesis-in-the-hind-limb-of-cystathionine-%C3%AE-synthase-mutant-mice-via-ppar-%C3%AE-vegf-axis
#6
Avisek Majumder, Mahavir Singh, Akash K George, Jyotirmaya Behera, Neetu Tyagi, Suresh C Tyagi
Neoangiogenesis is a fundamental process which helps to meet energy requirements, tissue growth, and wound healing. Although previous studies showed that Peroxisome proliferator-activated receptor (PPAR-γ) regulates neoangiogenesis via upregulation of vascular endothelial growth factor (VEGF), and both VEGF and PPAR-γ expressions were inhibited during hyperhomocysteinemic (HHcy), whether these two processes could trigger pathological effects in skeletal muscle via compromising neoangiogenesis has not been studied yet...
September 2018: Physiological Reports
https://www.readbyqxmd.com/read/30153567/exposure-of-endothelium-to-biomimetic-flow-waveforms-yields-identification-of-mir-199a-5p-as-a-potent-regulator-of-arteriogenesis
#7
Joshua L Heuslein, Catherine M Gorick, Stephanie P McDonnell, Ji Song, Brian H Annex, Richard J Price
Arteriogenesis, the growth of endogenous collateral arteries bypassing arterial occlusion(s), is a fundamental shear stress-induced adaptation with implications for treating peripheral arterial disease (PAD). Nonetheless, endothelial mechano-signaling during arteriogenesis is incompletely understood. Here we tested the hypothesis that a mechanosensitive microRNA, miR-199a-5p, regulates perfusion recovery and collateral arteriogenesis following femoral arterial ligation (FAL) via control of monocyte recruitment and pro-arteriogenic gene expression...
September 7, 2018: Molecular Therapy. Nucleic Acids
https://www.readbyqxmd.com/read/30135376/low-infrared-emissivity-coating-based-on-graphene-surface-modified-flaky-aluminum
#8
Lihua He, Yan Zhao, Liying Xing, Pinggui Liu, Youwei Zhang, Zhiyong Wang
A low infrared emissivity coating was prepared using graphene surface-modified flaky aluminum complex powders (rGO-FAl) as fillers. The flaky aluminum powders were coated with graphene through chemical bonding. Compared with pure flaky aluminum, the Vis-NIR diffuse reflectance of rGO-FAl complex powders was significantly decreased, which was beneficial to the low glossiness of the coating. After the modification, the glossiness at 60° of the coating with 40% (mass fraction) pigments decreased from 12.8 to 6...
August 22, 2018: Materials
https://www.readbyqxmd.com/read/30131665/ionic-homeostasis-maintenance-in-als-focus-on-new-therapeutic-targets
#9
REVIEW
Rossana Sirabella, Valeria Valsecchi, Serenella Anzilotti, Ornella Cuomo, Antonio Vinciguerra, Pasquale Cepparulo, Paola Brancaccio, Natascia Guida, Nicolas Blondeau, Lorella M T Canzoniero, Cristina Franco, Salvatore Amoroso, Lucio Annunziato, Giuseppe Pignataro
Amyotrophic lateral sclerosis (ALS) is one of the most threatening neurodegenerative disease since it causes muscular paralysis for the loss of Motor Neurons in the spinal cord, brainstem and motor cortex. Up until now, no effective pharmacological treatment is available. Two forms of ALS have been described so far: 90% of the cases presents the sporadic form (sALS) whereas the remaining 10% of the cases displays the familiar form (fALS). Approximately 20% of fALS is associated with inherited mutations in the Cu, Zn-superoxide dismutase 1 (SOD1) gene...
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/30127392/modeling-sporadic-als-in-ipsc-derived-motor-neurons-identifies-a-potential-therapeutic-agent
#10
Koki Fujimori, Mitsuru Ishikawa, Asako Otomo, Naoki Atsuta, Ryoichi Nakamura, Tetsuya Akiyama, Shinji Hadano, Masashi Aoki, Hideyuki Saya, Gen Sobue, Hideyuki Okano
Amyotrophic lateral sclerosis (ALS) is a heterogeneous motor neuron disease for which no effective treatment is available, despite decades of research into SOD1-mutant familial ALS (FALS). The majority of ALS patients have no familial history, making the modeling of sporadic ALS (SALS) essential to the development of ALS therapeutics. However, as mutations underlying ALS pathogenesis have not yet been identified, it remains difficult to establish useful models of SALS. Using induced pluripotent stem cell (iPSC) technology to generate stem and differentiated cells retaining the patients' full genetic information, we have established a large number of in vitro cellular models of SALS...
August 20, 2018: Nature Medicine
https://www.readbyqxmd.com/read/30110532/investigation-of-anti-sod1-antibodies-yields-new-structural-insight-into-sod1-misfolding-and-surprising-behavior-of-the-antibodies-themselves
#11
Ryan S Atlasi, Ravinder Malik, Christian I Corrales, Laura Tzeplaeff, Julian P Whitelegge, Neil R Cashman, Gal Bitan
Mutations in Cu/Zn-superoxide dismutase (SOD1) gene are linked to 10-20% of familial amyotrophic lateral sclerosis (fALS) cases. The mutations cause misfolding and self-assembly of SOD1 into toxic oligomers and aggregates, resulting in motor neuron degeneration. The molecular mechanisms underlying SOD1 aggregation and toxicity are unclear. Characterization of misfolded SOD1 is particularly challenging because of its metastable nature. Antibodies against misfolded SOD1 are useful tools for this purpose, provided their specificity and selectivity are well-characterized...
August 30, 2018: ACS Chemical Biology
https://www.readbyqxmd.com/read/30038021/endoplasmic-reticulum-stress-leads-to-accumulation-of-wild-type-sod1-aggregates-associated-with-sporadic-amyotrophic-lateral-sclerosis
#12
Danilo B Medinas, Pablo Rozas, Francisca Martínez Traub, Ute Woehlbier, Robert H Brown, Daryl A Bosco, Claudio Hetz
Abnormal modifications to mutant superoxide dismutase 1 (SOD1) are linked to familial amyotrophic lateral sclerosis (fALS). Misfolding of wild-type SOD1 (SOD1WT ) is also observed in postmortem tissue of a subset of sporadic ALS (sALS) cases, but cellular and molecular mechanisms generating abnormal SOD1WT species are unknown. We analyzed aberrant human SOD1WT species over the lifetime of transgenic mice and found the accumulation of disulfide-cross-linked high-molecular-weight SOD1WT aggregates during aging...
August 7, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/30030593/dysregulation-of-a-novel-mir-1825-tbcb-tuba4a-pathway-in-sporadic-and-familial-als
#13
Anika M Helferich, Sarah J Brockmann, Jörg Reinders, Dhruva Deshpande, Karlheinz Holzmann, David Brenner, Peter M Andersen, Susanne Petri, Dietmar R Thal, Jens Michaelis, Markus Otto, Steffen Just, Albert C Ludolph, Karin M Danzer, Axel Freischmidt, Jochen H Weishaupt
Genetic and functional studies suggest diverse pathways being affected in the neurodegenerative disease amyotrophic lateral sclerosis (ALS), while knowledge about converging disease mechanisms is rare. We detected a downregulation of microRNA-1825 in CNS and extra-CNS system organs of both sporadic (sALS) and familial ALS (fALS) patients. Combined transcriptomic and proteomic analysis revealed that reduced levels of microRNA-1825 caused a translational upregulation of tubulin-folding cofactor b (TBCB). Moreover, we found that excess TBCB led to depolymerization and degradation of tubulin alpha-4A (TUBA4A), which is encoded by a known ALS gene...
July 20, 2018: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/30014505/neurofilament-light-a-candidate-biomarker-of-presymptomatic-amyotrophic-lateral-sclerosis-and-phenoconversion
#14
Michael Benatar, Joanne Wuu, Peter M Andersen, Vittoria Lombardi, Andrea Malaspina
OBJECTIVE: To evaluate neurofilament light (NfL) as a biomarker of the presymptomatic phase of amyotrophic lateral sclerosis (ALS). METHODS: The study population includes 84 individuals at risk for developing ALS, 34 controls, 17 ALS patients, and 10 phenoconverters (at-risk individuals observed both before and after the emergence of clinically manifest disease). At-risk individuals are enrolled through Pre-Symptomatic Familial ALS (Pre-fALS), a longitudinal natural history and biomarker study of individuals who are carriers of any ALS-associated gene mutation (in SOD1, C9orf72, TARDBP, FUS, VCP, etc), but who, at the time of enrollment, demonstrated no clinical symptoms or signs (including electromyographic evidence) of manifest disease...
July 2018: Annals of Neurology
https://www.readbyqxmd.com/read/30008669/screening-for-ccnf-mutations-in-a-chinese-amyotrophic-lateral-sclerosis-cohort
#15
Danyang Tian, Jiao Li, Lu Tang, Nan Zhang, Dongsheng Fan
Previous research has identified CCNF mutations in familial (FALS) and sporadic amyotrophic lateral sclerosis (SALS), as well as in frontotemporal dementia (FTD). The aim of our study was to measure the frequency of CCNF mutations in a Chinese population. In total, 78 FALS patients, 581 SALS patients and 584 controls were included. We found 19 missense mutations, nine synonymous mutations and two intron variants. According to the American College of Medical Genetics and Genomics (ACMG) standards and guidelines for the interpretation of sequence variants, eight variants were judged to be pathogenic or likely pathogenic variants...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29996549/proteomics-and-toxicity-analysis-of-spinal-cord-primary-cultures-upon-hydrogen-sulfide-treatment
#16
Viviana Greco, Alida Spalloni, Victor Corasolla Carregari, Luisa Pieroni, Silvia Persichilli, Nicola B Mercuri, Andrea Urbani, Patrizia Longone
Hydrogen sulfide (H₂S) is an endogenous gasotransmitter recognized as an essential body product with a dual, biphasic action. It can function as an antioxidant and a cytoprotective, but also as a poison with a high probability of causing brain damage when present at noxious levels. In a previous study, we measured toxic liquoral levels of H₂S in sporadic amyotrophic lateral sclerosis (ALS) patients and in the familial ALS (fALS) mouse model, SOD1G93A. In addition, we experimentally demonstrated that H₂S is extremely and selectively toxic to motor neurons, and that it is released by glial cells and increases Ca2+ concentration in motor neurons due to a lack of ATP...
July 10, 2018: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/29982983/pathological-modification-of-tdp-43-in-amyotrophic-lateral-sclerosis-with-sod1-mutations
#17
Gye Sun Jeon, Yu-Mi Shim, Do-Yeon Lee, Jun-Soon Kim, MinJin Kang, So Hyun Ahn, Je-Young Shin, Dongho Geum, Yoon Ho Hong, Jung-Joon Sung
Amyotrophic lateral sclerosis (ALS) is a fatal, adult-onset, progressive neurodegenerative disorder with no known cure. Cu/Zn-superoxide dismutase (SOD1) was the first identified protein associated with familial ALS (fALS). Recently, TAR DNA-binding protein 43 (TDP-43) has been found to be a principal component of ubiquitinated cytoplasmic inclusions in neurons and glia in ALS. However, it remains unclear whether these ALS-linked proteins partly have a shared pathogenesis. Here, we determine the association between mutant SOD1 and the modification of TDP-43 and the relationship of pathologic TDP-43 to neuronal cytotoxicity in SOD1 ALS...
July 7, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29881358/effect-of-mutated-cu-zn-superoxide-dismutase-sod1-g93a-on-modulation-of-transductional-pathway-mediated-by-m1-muscarinic-receptor-in-sk-n-be-and-nsc-34-cells
#18
Simona Damiano, Anna Sasso, Roberta Accetta, Marcellino Monda, Bruno De Luca, Luigi Michele Pavone, Anna Belfiore, Mariarosaria Santillo, Paolo Mondola
The constitutive secretion of antioxidant Cu-Zn Superoxide dismutase (SOD1) has been widely demonstrated in many cellular lines. In addition, we showed that as well as the basal SOD1 secretion, this enzyme is also exported through depolarization of excitable cells by high extracellular K concentration. Recent data showed that SOD1 was able to activate muscarinic M1 receptor producing the activation, via phospholipase C, of ERK1-2 and AKT pathways. It is also known that about 20% of familial amyotrophic lateral sclerosis (fALS) is due to mutations in the gene coding for SOD1...
2018: Frontiers in Physiology
https://www.readbyqxmd.com/read/29869502/in-cell-nmr-in-human-cells-direct-protein-expression-allows-structural-studies-of-protein-folding-and-maturation
#19
Enrico Luchinat, Lucia Banci
Cellular structural biology methods are needed to characterize biological processes at atomic resolution in the physiological environment of the cell. Toward this goal, solution in-cell NMR is a powerful approach because it provides structural and dynamic data on macromolecules inside living cells. Several approaches have been developed for in-cell NMR in cultured human cells, which are needed to study processes related to human diseases that rely on the delivery of exogenous macromolecules to the cells. Such strategies, however, may not be applicable to proteins that are sensitive to the external environment or prone to aggregate and can introduce artifacts during protein purification or delivery...
June 19, 2018: Accounts of Chemical Research
https://www.readbyqxmd.com/read/29861271/a-proposed-mechanism-for-neurodegeneration-in-movement-disorders-characterized-by-metal-dyshomeostasis-and-oxidative-stress
#20
REVIEW
Benjamin Guy Trist, Dominic James Hare, Kay Lorraine Double
Shared molecular pathologies between distinct neurodegenerative disorders offer unique opportunities to identify common mechanisms of neuron death, and apply lessons learned from one disease to another. Neurotoxic superoxide dismutase 1 (SOD1) proteinopathy in SOD1-associated familial amyotrophic lateral sclerosis (fALS) is recapitulated in idiopathic Parkinson disease (PD), suggesting that these two phenotypically distinct disorders share an etiological pathway, and tractable therapeutic target(s). Despite 25 years of research, the molecular determinants underlying SOD1 misfolding and toxicity in fALS remain poorly understood...
July 19, 2018: Cell Chemical Biology
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