Water Treatment Using Advanced Oxidation Processes: Application Perspectives

Advanced oxidation processes (AOPs) using hydroxyl radicals and other oxidative radical species are being studied extensively for removal of organic compounds from various waste streams. However, large scale applications of these highly effective technologies in water and wastewater treatment are still very limited due to cost and inadequate information about the resultant water quality. This study focuses on the evaluation of the upstream processing and downstream post treatment analysis of selective AOPs. In the first stage of research, the performance of a proprietary catalyst (VN-TiO2) was compared with the industry standard P25 TiO2, for the use in a pilot-scale immobilized photocatalytic reactor. Using a dip coated fibreglass disk support in the VN-TiO2 solution and calcining, porous films with high surface area were produced. Although films formed by VN-TiO2 on fibreglass disks had a reaction rate 50% lower than that of P25, the VN-TiO2 disks were mechanically robust in the reactor, compared to those coated with P25. The addition of 15% P25 in the VN-TiO2 solution increased the reaction rate by 40%, while maintaining the mechanical stability. Reuse potential of both catalysts (VN-TiO2 and P25) was tested, and the rates of deactivation were comparable for both catalysts. Deactivation occurred possibly due to sustained adsorption of intermediates as well as loss of active sites due to heat treatment for reactivation. The low cost of the fibreglass, as compared to commonly used borosilicate glass, in combination with the VN-TiO2 catalyst is ideal for testing pilot scale reactor designs. In the second stage of the study two bioassays were used to evaluate and compare the toxicity of bisphenol A, and its degradation intermediates formed in three AOPs, namely UV/H2O2, ozonation, and photocatalysis. Two assays were used in evaluating water quality, namely the Ames Test for mutagenicity and the YES assay for estrogencity. Both UV/H2O2 and ozonation removed less than 10% of the initial total organic carbon (TOC), whereas photocatalysis resulted in a 50% reduction of TOC indicating a significant difference in intermediate formation. No mutagenicity was found over the entire tested range of BPA degradation in any of the AOPs. Estrogenicity steadily decreased in accordance with BPA degradation, and was below the limit of detection for photocatalysis. UV/H2O2 and ozonation results indicated the possible formation of intermediates with slight estrogenic activity as estrogenicity reached a plateau with a constant value at 15% of initial estrogenicity, while BPA continued to degrade with time. The work demonstrated effective use of bioassay tools in determining performances of AOPs

Nutrient Supply and Mercury Dynamics in Marine Ecosystems: A Conceptual Model

There is increasing interest and concern over the impacts of mercury (Hg) inputs to marine 32 ecosystems. One of the challenges in assessing these effects is that the cycling and trophic 33 transfer of Hg are strongly linked to other contaminants and disturbances. In addition to Hg, a 34 major problem facing coastal waters is the impacts of elevated nutrient, particularly nitrogen 35 (N), inputs. Increases in nutrient loading alter coastal ecosystems in ways that should change 36 the transport, transformations and fate of Hg, including increases in fixation of organic carbon 37 and deposition to sediments, decreases in the redox status of sediments and changes in fish 38 habitat. In this paper we present a conceptual model which suggests that increases in loading 39 of reactive N to marine ecosystems might alter Hg dynamics, decreasing bioavailabilty and 40 trophic transfer. This conceptual model is most applicable to coastal waters, but may also be 41 relevant to the pelagic ocean. We present information from case studies that both support and 42 challenge this conceptual model, including marine observations across a nutrient gradient; 43 results of a nutrient‐trophic transfer Hg model for pelagic and coastal ecosystems; observations 44 of Hg species, and nutrients from coastal sediments in the northeastern U.S.; and an analysis of 45 fish Hg concentrations in estuaries under different nutrient loadings. These case studies suggest 46 that changes in nutrient loading can impact Hg dynamics in coastal and open ocean ecosystems. 47 Unfortunately none of the case studies is comprehensive; each only addresses a portion of the 48 conceptual model and has limitations. Nevertheless, our conceptual model has important 49 management implications. Many estuaries near developed areas are impaired due to elevated 50 nutrient inputs. Widespread efforts are underway to control N loading and restore coastal 51 ecosystem function. An unintended consequence of nutrient control measures could be to 3 exacerbate 52 problems associated with Hg contamination. Additional focused research and 53 monitoring are needed to critically examine the link between nutrient supply and Hg 54 contamination of marine waters

Nutrient Supply and Mercury Dynamics in Marine Ecosystems: A Conceptual Model

There is increasing interest and concern over the impacts of mercury (Hg) inputs to marine ecosystems. One of the challenges in assessing these effects is that the cycling and trophic transfer of Hg are strongly linked to other contaminants and disturbances. In addition to Hg, a major problem facing coastal waters is the impacts of elevated nutrient, particularly nitrogen (N), inputs. Increases in nutrient loading alter coastal ecosystems in ways that should change the transport, transformations and fate of Hg, including increases in fixation of organic carbon and deposition to sediments, decreases in the redox status of sediments and changes in fish habitat. In this paper we present a conceptual model which suggests that increases in loading of reactive N to marine ecosystems might alter Hg dynamics, decreasing bioavailabilty and trophic transfer. This conceptual model is most applicable to coastal waters, but may also be relevant to the pelagic ocean. We present information from case studies that both support and challenge this conceptual model, including marine observations across a nutrient gradient; results of a nutrient‐trophic transfer Hg model for pelagic and coastal ecosystems; observations of Hg species, and nutrients from coastal sediments in the northeastern U.S.; and an analysis of fish Hg concentrations in estuaries under different nutrient loadings. These case studies suggest that changes in nutrient loading can impact Hg dynamics in coastal and open ocean ecosystems. Unfortunately none of the case studies is comprehensive; each only addresses a portion of the conceptual model and has limitations. Nevertheless, our conceptual model has important management implications. Many estuaries near developed areas are impaired due to elevated nutrient inputs. Widespread efforts are underway to control N loading and restore coastal ecosystem function. An unintended consequence of nutrient control measures could be to exacerbate problems associated with Hg contamination. Additional focused research and monitoring are needed to critically examine the link between nutrient supply and Hg contamination of marine waters

Polymorphisms within autophagy-related genes as susceptibility biomarkers for multiple myeloma: a meta-analysis of three large cohorts and functional characterization

Functional data used in this project have been meticulously catalogued and archived in the BBMRI-NL data infrastructure (https://hfgp.bbmri.nl/, accessed on 12 February 2020) using the MOLGENIS open-source platform for scientific data.Multiple myeloma (MM) arises following malignant proliferation of plasma cells in the bone marrow, that secrete high amounts of specific monoclonal immunoglobulins or light chains, resulting in the massive production of unfolded or misfolded proteins. Autophagy can have a dual role in tumorigenesis, by eliminating these abnormal proteins to avoid cancer development, but also ensuring MM cell survival and promoting resistance to treatments. To date no studies have determined the impact of genetic variation in autophagy-related genes on MM risk. We performed meta-analysis of germline genetic data on 234 autophagy-related genes from three independent study populations including 13,387 subjects of European ancestry (6863 MM patients and 6524 controls) and examined correlations of statistically significant single nucleotide polymorphisms (SNPs; p < 1 × 10−9) with immune responses in whole blood, peripheral blood mononuclear cells (PBMCs), and monocyte-derived macrophages (MDM) from a large population of healthy donors from the Human Functional Genomic Project (HFGP). We identified SNPs in six loci, CD46, IKBKE, PARK2, ULK4, ATG5, and CDKN2A associated with MM risk (p = 4.47 × 10−4−5.79 × 10−14). Mechanistically, we found that the ULK4rs6599175 SNP correlated with circulating concentrations of vitamin D3 (p = 4.0 × 10−4), whereas the IKBKErs17433804 SNP correlated with the number of transitional CD24+CD38+ B cells (p = 4.8 × 10−4) and circulating serum concentrations of Monocyte hemoattractant Protein (MCP)-2 (p = 3.6 × 10−4). We also found that the CD46rs1142469 SNP corre lated with numbers of CD19+ B cells, CD19+CD3− B cells, CD5+ IgD− cells, IgM− cells, IgD−IgM− cells, and CD4−CD8− PBMCs (p = 4.9 × 10−4−8.6 × 10−4 ) and circulating concentrations of interleukin (IL)-20 (p = 0.00082). Finally, we observed that the CDKN2Ars2811710 SNP correlated with levels of CD4+EMCD45RO+CD27− cells (p = 9.3 × 10−4 ). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3−, MCP-2−, and IL20-dependent pathways.This work was supported by the European Union’s Horizon 2020 research and innovation program, N° 856620 and by grants from the Instituto de Salud Carlos III and FEDER (Madrid, Spain; PI17/02256 and PI20/01845), Consejería de Transformación Económica, Industria, Conocimiento y Universidades and FEDER (PY20/01282), from the CRIS foundation against cancer, from the Cancer Network of Excellence (RD12/10 Red de Cáncer), from the Dietmar Hopp Foundation and the German Ministry of Education and Science (BMBF: CLIOMMICS [01ZX1309]), and from National Cancer Institute of the National Institutes of Health under award numbers: R01CA186646, U01CA249955 (EEB).This work was also funded d by Portuguese National funds, through the Foundation for Science and Technology (FCT)—project UIDB/50026/2020 and UIDP/50026/2020 and by the project NORTE-01-0145-FEDER-000055, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF)

De Novo Truncating Mutations in WASF1 Cause Intellectual Disability with Seizures.

Next-generation sequencing has been invaluable in the elucidation of the genetic etiology of many subtypes of intellectual disability in recent years. Here, using exome sequencing and whole-genome sequencing, we identified three de novo truncating mutations in WAS protein family member 1 (WASF1) in five unrelated individuals with moderate to profound intellectual disability with autistic features and seizures. WASF1, also known as WAVE1, is part of the WAVE complex and acts as a mediator between Rac-GTPase and actin to induce actin polymerization. The three mutations connected by Matchmaker Exchange were c.1516C>T (p.Arg506Ter), which occurs in three unrelated individuals, c.1558C>T (p.Gln520Ter), and c.1482delinsGCCAGG (p.Ile494MetfsTer23). All three variants are predicted to partially or fully disrupt the C-terminal actin-binding WCA domain. Functional studies using fibroblast cells from two affected individuals with the c.1516C>T mutation showed a truncated WASF1 and a defect in actin remodeling. This study provides evidence that de novo heterozygous mutations in WASF1 cause a rare form of intellectual disability

Global patient outcomes after elective surgery: prospective cohort study in 27 low-, middle- and high-income countries.

BACKGROUND: As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. METHODS: We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. RESULTS: A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2-7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. CONCLUSIONS: Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care. STUDY REGISTRATION: ISRCTN5181700

A Phylogenetic Analysis of Human Immunodeficiency Virus Type 1 Sequences in Kiev: Findings Among Key Populations

Background: The human immunodeficiency virus (HIV) epidemic in Ukraine has been driven by a rapid rise among people who inject drugs, but recent studies have shown an increase through sexual transmission. Methods: Protease and reverse transcriptase sequences from 876 new HIV diagnoses (April 2013–March 2015) in Kiev were linked to demographic data. We constructed phylogenetic trees for 794 subtype A1 and 64 subtype B sequences and identified factors associated with transmission clustering. Clusters were defined as ≥2 sequences, ≥80% local branch support, and maximum genetic distance of all sequence pairs in the cluster ≤2.5%. Recent infection was determined through the limiting antigen avidity enzyme immunoassay. Sequences were analyzed for transmitted drug resistance mutations. Results Thirty percent of subtype A1 and 66% of subtype B sequences clustered. Large clusters (maximum 11 sequences) contained mixed risk groups. In univariate analysis, clustering was significantly associated with subtype B compared to A1 (odds ratio [OR], 4.38 [95% confidence interval {CI}, 2.56–7.50]); risk group (OR, 5.65 [95% CI, 3.27–9.75]) for men who have sex with men compared to heterosexual males; recent, compared to long-standing, infection (OR, 2.72 [95% CI, 1.64–4.52]); reported sex work contact (OR, 1.93 [95% CI, 1.07–3.47]); and younger age groups compared with age ≥36 years (OR, 1.83 [95% CI, 1.10–3.05] for age ≤25 years). Females were associated with lower odds of clustering than heterosexual males (OR, 0.49 [95% CI, .31–.77]). In multivariate analysis, risk group, subtype, and age group were independently associated with clustering (P < .001, P = .007, and P = .033, respectively). Eighteen sequences (2.1%) indicated evidence of transmitted drug resistance. Conclusions Our findings suggest high levels of transmission and bridging between risk groups