A review of fouling mechanisms, control strategies and real-time fouling monitoring techniques in forward osmosis

Forward osmosis has gained tremendous attention in the field of desalination and wastewater treatment. However, membrane fouling is an inevitable issue. Membrane fouling leads to flux decline, can cause operational problems and can result in negative consequences that can damage the membrane. Hereby, we attempt to review the different types of fouling in forward osmosis, cleaning and control strategies for fouling mitigation, and the impact of membrane hydrophilicity, charge and morphology on fouling. The fundamentals of biofouling, organic, colloidal and inorganic fouling are discussed with a focus on recent studies. We also review some of the in-situ real-time online fouling monitoring technologies for real-time fouling monitoring that can be applicable to future research on forward osmosis fouling studies. A brief discussion on critical flux and the coupled effects of fouling and concentration polarization is also provided

A review of fouling mechanisms, control strategies and real-time fouling monitoring techniques in forward osmosis

© 2019 by the authors. Forward osmosis has gained tremendous attention in the field of desalination and wastewater treatment. However, membrane fouling is an inevitable issue. Membrane fouling leads to flux decline, can cause operational problems and can result in negative consequences that can damage the membrane. Hereby, we attempt to review the different types of fouling in forward osmosis, cleaning and control strategies for fouling mitigation, and the impact of membrane hydrophilicity, charge and morphology on fouling. The fundamentals of biofouling, organic, colloidal and inorganic fouling are discussed with a focus on recent studies. We also review some of the in-situ real-time online fouling monitoring technologies for real-time fouling monitoring that can be applicable to future research on forward osmosis fouling studies. A brief discussion on critical flux and the coupled effects of fouling and concentration polarization is also provided

Whole transcriptome in silico screening implicates cardiovascular and infectious disease in the mechanism of action underlying atypical antipsychotic side effects

Background: Stroke/thromboembolic events, infections, and death are all significantly increased by antipsychotics in dementia but little is known about why they can be harmful. Using a novel application of a drug repurposing paradigm, we aimed to identify potential mechanisms underlying adverse events. Methods: Whole transcriptome signatures were generated for SH-SY5Y cells treated with amisulpride, risperidone, and volinanserin using RNA sequencing. Bioinformatic analysis was performed that scored the association between antipsychotic signatures and expression data from 415,252 samples in the National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO) repository. Results: Atherosclerosis, venous thromboembolism, and influenza NCBI GEO-derived samples scored positively against antipsychotic signatures. Pathways enriched in antipsychotic signatures were linked to the cardiovascular and immune systems (eg, brain derived neurotrophic factor [BDNF], platelet derived growth factor receptor [PDGFR]-beta, tumor necrosis factor [TNF], transforming growth factor [TGF]-beta, selenoamino acid metabolism, and influenza infection). Conclusions: These findings for the first time mechanistically link antipsychotics to specific cardiovascular and infectious diseases which are known side effects of their use in dementia, providing new information to explain related adverse events.This article is freely available via Open Access. Click on the Publisher URL to access it via the publisher's site.This work was generously supported by the Wellcome Trust Institu tional Strategic Support Award (204909/Z/16/Z) and in part through the MRC Proximity to Discovery: Industry Engagement Fund (External Collaboration, Innovation and Entrepreneurism: Translational Medicine in Exeter 2 (EXCITEME2) ref. MC_PC_16072.published version, accepted version (12 month embargo), submitted versio

A Leptin Fragment Mirrors the Cognitive Enhancing and Neuroprotective Actions of Leptin

J.H. is funded by The Anonymous Trust and Cunningham Trust. GD is funded by ARUK, DR received a University of St Andrews Research Internship. JAA is funded by the Carnegie Trust.A key pathology of Alzheimer’s disease (AD) is amyloid β (Aβ) accumulation which triggers synaptic impairments and neuronal death. Metabolic disruption is common in AD and recent evidence implicates impaired leptin function in AD. Thus the leptin system may be a novel therapeutic target in AD. Indeed, leptin has cognitive enhancing properties and it prevents the aberrant effects of Aβ on hippocampal synaptic function and neuronal viability. However as leptin is a large peptide, development of smaller leptin-mimetics may be the best therapeutic approach. Thus, we have examined the cognitive enhancing and neuroprotective properties of known bioactive leptin fragments. Here we show that the leptin (116-130) fragment, but not leptin (22-56), mirrored the ability of leptin to promote AMPA receptor trafficking to synapses and facilitate activity-dependent hippocampal synaptic plasticity. Administration of leptin (116-130) also mirrored the cognitive enhancing effects of leptin as it enhanced performance in episodic-like memory tests. Moreover, leptin (116-130) prevented hippocampal synaptic disruption and neuronal cell death in models of amyloid toxicity. These findings establish further the importance of the leptin system as a therapeutic target in AD.PostprintPeer reviewe

Brain energy rescue:an emerging therapeutic concept for neurodegenerative disorders of ageing

The brain requires a continuous supply of energy in the form of ATP, most of which is produced from glucose by oxidative phosphorylation in mitochondria, complemented by aerobic glycolysis in the cytoplasm. When glucose levels are limited, ketone bodies generated in the liver and lactate derived from exercising skeletal muscle can also become important energy substrates for the brain. In neurodegenerative disorders of ageing, brain glucose metabolism deteriorates in a progressive, region-specific and disease-specific manner — a problem that is best characterized in Alzheimer disease, where it begins presymptomatically. This Review discusses the status and prospects of therapeutic strategies for countering neurodegenerative disorders of ageing by improving, preserving or rescuing brain energetics. The approaches described include restoring oxidative phosphorylation and glycolysis, increasing insulin sensitivity, correcting mitochondrial dysfunction, ketone-based interventions, acting via hormones that modulate cerebral energetics, RNA therapeutics and complementary multimodal lifestyle changes

A comparative monitoring of maternal and cord serum polychlorinated biphenyls levels from Iranian pregnant women between industrial and urban areas

The aim of this study was to compare maternal and fetal exposure to PCBs in pregnant women from a petrochemical and gas area (PGA) and an urban area (UA), by the analyses of serum samples from mother (MS) and cord (CS). After liquid-liquid extracting, samples were analyzed for 12 PCBs congeners by gas chromatography mass spectrometer. Adjusted multiple linear regression models showed the mean levels (μg/L) of total PCBs in the MS and CS samples from the PGA (1.70 ± 0.81 and 1.19 ± 0.43) were significantly higher than those from UA (1.64 ± 0.75 and 1.07 ± 0.38). PCB 44 was predominant in both MS and CS serum samples, and in both PGA (0.80 ± 0.70 and 0.76 ± 0.67) and UA (0.79 ± 0.39 and 0.67 ± 0.34). A negative correlation was found for PCB 52 as one-unit increase in the cord serum levels was associated with 0.024 g decrease in newborn weight. Similarly, one-unit increase in the maternal serum PCB 18 concentrations were associated with 0.09 and 0.086 cm decrease in newborn height and head circumference. The serum levels of PCB 18 and 52 in the mothers who consumed meat and milk at least 1 meal/week were higher than these who consumed meat and milk never or less than 1 meal/month. The findings in this study indicated that higher maternal exposure to PCBs, as result of living in an industrialized area, leads to higher PCBs accumulation in cord blood, which consequently passes to the developing fetus. These events may cause harmful effects on both them in-utero and afterbirth growth and development. © 2022 Elsevier Lt

Leptin-based hexamers facilitate memory and prevent amyloid-driven AMPA receptor internalisation and neuronal degeneration

Funding: This work was supported by a Medical Research Scotland vacation award for BM, Sulsa Dementia grants to JH & GHD.Key pathological features of Alzheimer’s disease (AD) include build-up of amyloid β (Aβ), which promotes synaptic abnormalities and ultimately leads to neuronal cell death. Metabolic dysfunction is known to influence the risk of developing AD. Impairments in the leptin system have been detected in AD patients, which has fuelled interest in targeting this system to treat AD. Increasing evidence supports pro-cognitive and neuroprotective actions of leptin and these beneficial effects of leptin are mirrored by a bioactive leptin fragment (leptin116-130). Here we extend these studies to examine the potential cognitive enhancing and neuroprotective actions of eight six-amino acid peptides (hexamers) derived from leptin116-130. In this study, we show that four of the hexamers (leptin116-121, 117-122, 118-123 and 120-125) replicate the ability of leptin to promote α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking and facilitate hippocampal synaptic plasticity. Moreover, the pro-cognitive effects of the hexamers were verified in behavioural studies, with administration of leptin117-122 enhancing performance in episodic memory tasks. The bioactive hexamers replicated the neuroprotective actions of leptin by preventing the acute hippocampal synapto-toxic effects of Aβ, and the chronic effects of Aβ on neuronal cell viability, Aβ seeding and tau phosphorylation. These findings provide further evidence to support leptin and leptin-derived peptides as potential therapeutics for AD.Publisher PDFPeer reviewe