The role of non-thermal plasma technique in NOx treatment : a review

Non-thermal plasma (NTP) has been introduced over the past several years as a promising method for nitrogen oxide (NOx) removal. The intent, when using NTP, is to selectively transfer input electrical energy to the electrons, and to not expend this in heating the entire gas stream, which generates free radicals through collisions, and promotes the desired chemical changes in the exhaust gases. The generated active species react with the pollutant molecules and decompose them. This paper reviews and summarizes relevant literature regarding various aspects of the application of NTP technology on NOx removal from exhaust gases. A comprehensive description of available scientific literature on NOx removal using NTP technology is presented, including various types of NTP, e.g. dielectric barrier discharge, corona discharge and electron beam. Furthermore, the combination of NTP with catalyst and adsorbent for better NOx removal efficiency is presented in detail. The removal of NOx from both simulated gases and real diesel engines is also considered in this review paper. As NTP is a new technique and is not yet commercialized, there is a need for more studies to be performed in this field

Performance evaluation of non-thermal plasma on particulate matter, ozone and CO2 correlation for diesel exhaust emission reduction

This study is seeking to investigate the effect of non-thermal plasma technology in the abatement of particulate matter (PM) from the actual diesel exhaust. Ozone (O3) strongly promotes PM oxidation, the main product of which is carbon dioxide (CO2). PM oxidation into the less harmful product (CO2) is the main objective whiles the correlation between PM, O3 and CO2 is considered. A dielectric barrier discharge reactor has been designed with pulsed power technology to produce plasma inside the diesel exhaust. To characterise the system under varied conditions, a range of applied voltages from 11 kVPP to 21kVPP at repetition rates of 2.5, 5, 7.5 and 10 kHz, have been experimentally investigated. The results show that by increasing the applied voltage and repetition rate, higher discharge power and CO2 dissociation can be achieved. The PM removal efficiency of more than 50% has been obtained during the experiments and high concentrations of ozone on the order of a few hundreds of ppm have been observed at high discharge powers. Furthermore, O3, CO2 and PM concentrations at different plasma states have been analysed for time dependence. Based on this analysis, an inverse relationship between ozone concentration and PM removal has been found and the role of ozone in PM removal in plasma treatment of diesel exhaust has been highlighted

CFD Simulation of a shell and multiple tubes condensing heat exchanger in a modified microwave plant applied for reprocessing End of Life Tires (ELTs)

Data Availability Statement: The data that support the findings of this study are openly available in BURA at https://bura.brunel.ac.uk/.Copyright © 2023 The Authors. The condensation heat exchanger has a critical role in the microwave reduction process to separate and capture valuable by-products after the microwave reactor. This study aims to perform a computational fluid dynamics (CFD) simulation of a condenser to assess the heat transfer performance of the heat exchanger comprehensively. The type of heat exchanger used for this study is based upon an existing industrial-scale condenser taken from a conventional thermal pyrolysis end of tires (ELT) reprocessing plant and repurposed for integration into a 1500 kg/h ELT microwave reduction process. The condenser is a shell-and-multiple-tube heat exchanger in which the syngas passes through the tubes while cold water from a cooling tower is placed inside the shell. After the simulation, the effects of inlet temperatures and mass flow rates of the gas and water are investigated. The results show that the heat transfer rate is 58 kW for the inlet air velocity of 0.25 m/s and increases due to the convective heat transfer by 32% and 55% when the air velocity rises to 0.5 and 1 m/s, respectively, for the inlet gas and water temperatures of 80 and 15°C, respectively. Additionally, because the outlet air temperature and the inlet water temperature are strongly correlated with convective heat transfer, the outlet air temperature is equivalent to 17.2, 22.3, and 29.5°C when the inlet water temperature is 15, 20, and 25°C, respectively

Research Report 2008–2009

The NHMRC Clinical Trials Centre at the University of Sydney runs large multicentre investigator-initiated clinical trials, takes part in trials of national and international collaborative trial groups and contributes expertise to trials run by others. It also: • undertakes research into trial methods and is recognised through publications as a leader in trial methodology • reviews and synthesises evidence from completed trials, and is at the forefront of developments in methods, such as prospective meta-analysis • advises on trial design and operation, and randomises patients and analyses data for other groups conducting trials, particularly through its Outreach program • takes a lead in proposing new directions for trial research in Australia, particularly with regard to integrating clinical trials with national policy and clinical practice • offers placements for postgraduate students in all of these areas • runs short courses in the design and conduct of clinical trials as part of its undertaking to train people for Australian medical research. Core funding is provided by the NHMRC, and specific projects are funded by government, public and private institutions and the pharmaceutical industry. The CTC is at two sites in Camperdown in inner Sydney — the Medical Foundation Building on Parramatta Road and on Mallett Street. This report covers the CTC’s achievements for the biennium 2008–200

Autism genetic database (AGD): a comprehensive database including autism susceptibility gene-CNVs integrated with known noncoding RNAs and fragile sites

<p>Abstract</p> <p>Background</p> <p>Autism is a highly heritable complex neurodevelopmental disorder, therefore identifying its genetic basis has been challenging. To date, numerous susceptibility genes and chromosomal abnormalities have been reported in association with autism, but most discoveries either fail to be replicated or account for a small effect. Thus, in most cases the underlying causative genetic mechanisms are not fully understood. In the present work, the Autism Genetic Database (AGD) was developed as a literature-driven, web-based, and easy to access database designed with the aim of creating a comprehensive repository for all the currently reported genes and genomic copy number variations (CNVs) associated with autism in order to further facilitate the assessment of these autism susceptibility genetic factors.</p> <p>Description</p> <p>AGD is a relational database that organizes data resulting from exhaustive literature searches for reported susceptibility genes and CNVs associated with autism. Furthermore, genomic information about human fragile sites and noncoding RNAs was also downloaded and parsed from miRBase, snoRNA-LBME-db, piRNABank, and the MIT/ICBP siRNA database. A web client genome browser enables viewing of the features while a web client query tool provides access to more specific information for the features. When applicable, links to external databases including GenBank, PubMed, miRBase, snoRNA-LBME-db, piRNABank, and the MIT siRNA database are provided.</p> <p>Conclusion</p> <p>AGD comprises a comprehensive list of susceptibility genes and copy number variations reported to-date in association with autism, as well as all known human noncoding RNA genes and fragile sites. Such a unique and inclusive autism genetic database will facilitate the evaluation of autism susceptibility factors in relation to known human noncoding RNAs and fragile sites, impacting on human diseases. As a result, this new autism database offers a valuable tool for the research community to evaluate genetic findings for this complex multifactorial disorder in an integrated format. AGD provides a genome browser and a web based query client for conveniently selecting features of interest. Access to AGD is freely available at <url>http://wren.bcf.ku.edu/</url>.</p

An Integrated Meta-Analysis of Two Variants in HOXA1/HOXB1 and Their Effect on the Risk of Autism Spectrum Disorders

BACKGROUND: HOXA1 and HOXB1 have been strongly posed as candidate genes for autism spectrum disorders (ASD) given their important role in the development of hindbrain. The A218G (rs10951154) in HOXA1 and the insertion variant in HOXB1 (nINS/INS, rs72338773) were of special interest for ASD but with inconclusive results. Thus, we conducted a meta-analysis integrating case-control and transmission/disequilibrium test (TDT) studies to clearly discern the effect of these two variants in ASD. METHODS AND FINDINGS: Multiple electronic databases were searched to identify studies assessing the A218G and/or nINS/INS variant in ASD. Data from case-control and TDT studies were analyzed in an allelic model using the Catmap software. A total of 10 and 7 reports were found to be eligible for meta-analyses of A218G and nINS/INS variant, respectively. In overall meta-analysis, the pooled OR for the 218G allele and the INS allele was 0.97 (95% CI = 0.76-1.25, P(heterogeneity) = 0.029) and 1.14 (95% CI = 0.97-1.33, P(heterogeneity) = 0.269), respectively. No significant association was also identified between these two variants and ASD risk in stratified analysis. Further, cumulative meta-analysis in chronologic order showed the inclination toward null-significant association for both variants with continual adding studies. Additionally, although the between-study heterogeneity regarding the A218G is not explained by study design, ethnicity, and sample size, the sensitive analysis indicated the stability of the result. CONCLUSIONS: This meta-analysis suggests the HOXA1 A218G and HOXB1 nINS/INS variants may not contribute significantly to ASD risk

Autism-Associated Gene Expression in Peripheral Leucocytes Commonly Observed between Subjects with Autism and Healthy Women Having Autistic Children

Autism spectrum disorder (ASD) is a severe neuropsychiatric disorder which has complex pathobiology with profound influences of genetic factors in its development. Although the numerous autism susceptible genes were identified, the etiology of autism is not fully explained. Using DNA microarray, we examined gene expression profiling in peripheral blood from 21 individuals in each of the four groups; young adults with ASD, age- and gender-matched healthy subjects (ASD control), healthy mothers having children with ASD (asdMO), and asdMO control. There was no blood relationship between ASD and asdMO. Comparing the ASD group with control, 19 genes were found to be significantly changed. These genes were mainly involved in cell morphology, cellular assembly and organization, and nerve system development and function. In addition, the asdMO group possessed a unique gene expression signature shown as significant alterations of protein synthesis despite of their nonautistic diagnostic status. Moreover, an ASD-associated gene expression signature was commonly observed in both individuals with ASD and asdMO. This unique gene expression profiling detected in peripheral leukocytes from affected subjects with ASD and unaffected mothers having ASD children suggest that a genetic predisposition to ASD may be detectable even in peripheral cells. Altered expression of several autism candidate genes such as FMR-1 and MECP2, could be detected in leukocytes. Taken together, these findings suggest that the ASD-associated genes identified in leukocytes are informative to explore the genetic, epigenetic, and environmental background of ASD and might become potential tools to assess the crucial factors related to the clinical onset of the disorder

Functional Phenotypic Rescue of Caenorhabditis elegans Neuroligin-Deficient Mutants by the Human and Rat NLGN1 Genes

Neuroligins are cell adhesion proteins that interact with neurexins at the synapse. This interaction may contribute to differentiation, plasticity and specificity of synapses. In humans, single mutations in neuroligin encoding genes lead to autism spectrum disorder and/or mental retardation. Caenorhabditis elegans mutants deficient in nlg-1, an orthologue of human neuroligin genes, have defects in different behaviors. Here we show that the expression of human NLGN1 or rat Nlgn1 cDNAs in C. elegans nlg-1 mutants rescues the fructose osmotic strength avoidance and gentle touch response phenotypes. Two specific point mutations in NLGN3 and NLGN4 genes, involved in autistic spectrum disorder, were further characterized in this experimental system. The R451C allele described in NLGN3, was analyzed with both human NLGN1 (R453C) and worm NLG-1 (R437C) proteins, and both were not functional in rescuing the osmotic avoidance behavior and the gentle touch response phenotype. The D396X allele described in NLGN4, which produces a truncated protein, was studied with human NLGN1 (D432X) and they did not rescue any of the behavioral phenotypes analyzed. In addition, RNAi feeding experiments measuring gentle touch response in wild type strain and worms expressing SID-1 in neurons (which increases the response to dsRNA), both fed with bacteria expressing dsRNA for nlg-1, provided evidence for a postsynaptic in vivo function of neuroligins both in muscle cells and neurons, equivalent to that proposed in mammals. This finding was further confirmed generating transgenic nlg-1 deficient mutants expressing NLG-1 under pan-neuronal (nrx-1) or pan-muscular (myo-3) specific promoters. All these results suggest that the nematode could be used as an in vivo model for studying particular synaptic mechanisms with proteins orthologues of humans involved in pervasive developmental disorders

Gene expression biomarkers of response to citalopram treatment in major depressive disorder

There is significant variability in antidepressant treatment outcome, with ∼30–40% of patients with major depressive disorder (MDD) not presenting with adequate response even following several trials. To identify potential biomarkers of response, we investigated peripheral gene expression patterns of response to antidepressant treatment in MDD. We did this using Affymetrix HG-U133 Plus2 microarrays in blood samples, from untreated individuals with MDD (N=63) ascertained at a community outpatient clinic, pre and post 8-week treatment with citalopram, and used a regression model to assess the impact of gene expression differences on antidepressant response. We carried out technical validation of significant probesets by quantitative reverse transcriptase PCR and conducted central nervous system follow-up of the most significant result in post-mortem brain samples from 15 subjects who died during a current MDD episode and 11 sudden-death controls. A total of 32 probesets were differentially expressed according to response to citalopram treatment following false discovery rate correction. Interferon regulatory factor 7 (IRF7) was the most significant differentially expressed gene and its expression was upregulated by citalopram treatment in individuals who responded to treatment. We found these results to be concordant with our observation of decreased expression of IRF7 in the prefrontal cortex of MDDs with negative toxicological evidence for antidepressant treatment at the time of death. These findings point to IRF7 as a gene of interest in studies investigating genomic factors associated with antidepressant response

SnoRNA Snord116 (Pwcr1/MBII-85) Deletion Causes Growth Deficiency and Hyperphagia in Mice

Prader-Willi syndrome (PWS) is the leading genetic cause of obesity. After initial severe hypotonia, PWS children become hyperphagic and morbidly obese, if intake is not restricted. Short stature with abnormal growth hormone secretion, hypogonadism, cognitive impairment, anxiety and behavior problems are other features. PWS is caused by lack of expression of imprinted genes in a ∼4 mb region of chromosome band 15q11.2. Our previous translocation studies predicted a major role for the C/D box small nucleolar RNA cluster SNORD116 (PWCR1/HBII-85) in PWS. To test this hypothesis, we created a ∼150 kb deletion of the >40 copies of Snord116 (Pwcr1/MBII-85) in C57BL/6 mice. Snord116del mice with paternally derived deletion lack expression of this snoRNA. They have early-onset postnatal growth deficiency, but normal fertility and lifespan. While pituitary structure and somatotrophs are normal, liver Igf1 mRNA is decreased. In cognitive and behavior tests, Snord116del mice are deficient in motor learning and have increased anxiety. Around three months of age, they develop hyperphagia, but stay lean on regular and high-fat diet. On reduced caloric intake, Snord116del mice maintain their weight better than wild-type littermates, excluding increased energy requirement as a cause of hyperphagia. Normal compensatory feeding after fasting, and ability to maintain body temperature in the cold indicate normal energy homeostasis regulation. Metabolic chamber studies reveal that Snord116del mice maintain energy homeostasis by altered fuel usage. Prolonged mealtime and increased circulating ghrelin indicate a defect in meal termination mechanism. Snord116del mice, the first snoRNA deletion animal model, reveal a novel role for a non-coding RNA in growth and feeding regulation