Fundamental Study of CO2 Adsorption from Natural Gas using Activated Carbon

This proposed PhD project focuses on addressing the fundamental mechanism of carbon dioxide (CO2) adsorption within activated carbon (AC), which plays an important role in natural gas separation. A systematic study of CO2 adsorption was conducted with AC, which was constructed with representative pore models. The effects of temperature, CO2 potential models and geometrical properties, and presence of other gas components (in natural gas) on the adsorption behaviours were studied via Monte Carlo simulation

A constrained optimisation approach for designing reliable robust H∞ control systems

This research addresses passive fault-tolerant control problems for linear uncertain systems via reliable state feedback and output feedback robust H∞ controllers. Structured uncertainties considered are required to satisfy integral quadratic constraints. These controllers are to obtain an absolutely stable closed-loop system with a specified disturbance attenuation level. Solutions to these control problems involve solving parameterised Riccati equation(s). A feasible set of parameters used to solve the Riccati equation(s) is computed using a differential evolution algorithm

Exploring factors influencing low back pain in people with non-dysvascular lower limb amputation: a national survey

Background: Chronic low back pain (LBP) is a common musculoskeletal impairment in people with lower limb amputation. Given the multifactorial nature of LBP, exploring the factors influencing the presence and intensity of LBP is warranted. Objective: To investigate which physical, personal, and amputee-specific factors predicted presence and intensity of low back pain (LBP) in persons with non-dysvascular transfemoral (TFA) and transtibial amputation (TTA). Design: A retrospective cross-sectional survey. Setting: A national random sample of people with non-dysvascular TFA and TTA. Participants: Participants (N = 526) with unilateral TFA and TTA due to non-dysvascular aetiology (i.e. trauma, tumours, and congenital causes) and a minimum prosthesis usage of one year since amputation were invited to participate in the survey. The data from 208 participants (43.4% response rate) were used for multivariate regression analysis Methods (Independent variables): Personal (i.e. age, body mass, gender, work status, and presence of comorbid conditions), amputee-specific (i.e. level of amputation, years of prosthesis use, presence of phantom limb pain, residual limb problems, and non-amputated limb pain), and physical factors (i.e. pain provoking postures including standing, bending, lifting, walking,sitting, sit-to stand, and climbing stairs). Main outcome measures (Dependent variables): LBP presence and intensity. Results: A multivariate logistic regression model showed that the presence of two or more comorbid conditions (prevalence odds ratio (POR) = 4.34, p = .01), residual limb problems (POR 22 = 3.76, p<.01), and phantom limb pain (POR = 2.46, p = .01) influenced the presence of LBP. Given the high LBP prevalence (63%) in the study, there is a tendency for overestimation of PORand the results must be interpreted with caution. In those with LBP, the presence of residual limb problems (beta = 0.21, p = .01), and experiencing LBP symptoms during sit-to-stand task (beta = 0.22, p = .03) were positively associated with LBP intensity, while being employed demonstrated a negative association (beta = - 0.18, p = .03) in the multivariate linear regression model. Conclusions: Rehabilitation professionals should be cognisant of the influence that comorbid conditions, residual limb problems, and phantom pain have on the presence of LBP in people with non-dysvascular lower limb amputation. Further prospective studies could investigate the underlying causal mechanisms of LBP

18th-Century Blues: Exploring the Melancholy Mind

'Before Depression' is a three-year research project by the English departments of the Universities of Northumbria and Sunderland and funded by the Leverhulme Trust. This exhibition brings together a range of artists who treated 'the blues' in their work. They include the influential Albrecht Durer, William Hogarth, Joshua Reynolds, George Romney, Joseph Wright, Thomas Rowlandson, William Blake, Maria Cosway, Thomas Jones, Jacob van Ruisdael, Caspar David Friedrich, Charles Le Brun, Johann Caspar Lavater, John Constable, John Martin and local artist Luke Clennell. Some were themselves depressive, some were interested in medical matters connected with the condition, some painted melancholy scenes, some even made fun of 'depression' for satirical purposes, and some painted friends and well-known figures who we know suffered from periodic low spirits. 18th-Century Blues offers a sometimes lively, sometimes sombre but, we hope, always thought-provoking insight into how people dealt with a common human experience two hundred years ago. Works are kindly loaned by The National Gallery, London; Tate; The National Portrait Gallery; The British Museum, London; The Wellcome Library, London; The Whitworth Art Gallery, University of Manchester; Derby Museums and Art Gallery; The Laing Art Gallery, Newcastle upon Tyne (Tyne and Wear Museums); The Hatton Gallery, Newcastle University and Petworth House, The Egremont Collection (acquired in lieu of tax by HM Treasury in 1957 and subsequently transferred to The National Trust)

Identification and functional characterization of G6PC2 coding variants influencing glycemic traits define an effector transcript at the G6PC2-ABCB11 locus.

Genome wide association studies (GWAS) for fasting glucose (FG) and insulin (FI) have identified common variant signals which explain 4.8% and 1.2% of trait variance, respectively. It is hypothesized that low-frequency and rare variants could contribute substantially to unexplained genetic variance. To test this, we analyzed exome-array data from up to 33,231 non-diabetic individuals of European ancestry. We found exome-wide significant (P<5×10-7) evidence for two loci not previously highlighted by common variant GWAS: GLP1R (p.Ala316Thr, minor allele frequency (MAF)=1.5%) influencing FG levels, and URB2 (p.Glu594Val, MAF = 0.1%) influencing FI levels. Coding variant associations can highlight potential effector genes at (non-coding) GWAS signals. At the G6PC2/ABCB11 locus, we identified multiple coding variants in G6PC2 (p.Val219Leu, p.His177Tyr, and p.Tyr207Ser) influencing FG levels, conditionally independent of each other and the non-coding GWAS signal. In vitro assays demonstrate that these associated coding alleles result in reduced protein abundance via proteasomal degradation, establishing G6PC2 as an effector gene at this locus. Reconciliation of single-variant associations and functional effects was only possible when haplotype phase was considered. In contrast to earlier reports suggesting that, paradoxically, glucose-raising alleles at this locus are protective against type 2 diabetes (T2D), the p.Val219Leu G6PC2 variant displayed a modest but directionally consistent association with T2D risk. Coding variant associations for glycemic traits in GWAS signals highlight PCSK1, RREB1, and ZHX3 as likely effector transcripts. These coding variant association signals do not have a major impact on the trait variance explained, but they do provide valuable biological insights

Identification of neural networks that contribute to motion sickness through principal components analysis of fos labeling induced by galvanic vestibular stimulation

Motion sickness is a complex condition that includes both overt signs (e.g., vomiting) and more covert symptoms (e.g., anxiety and foreboding). The neural pathways that mediate these signs and symptoms are yet to identified. This study mapped the distribution of c-fos protein (Fos)-like immunoreactivity elicited during a galvanic vestibular stimulation paradigm that is known to induce motion sickness in felines. A principal components analysis was used to identify networks of neurons activated during this stimulus paradigm from functional correlations between Fos labeling in different nuclei. This analysis identified five principal components (neural networks) that accounted for greater than 95% of the variance in Fos labeling. Two of the components were correlated with the severity of motion sickness symptoms, and likely participated in generating the overt signs of the condition. One of these networks included neurons in locus coeruleus, medial, inferior and lateral vestibular nuclei, lateral nucleus tractus solitarius, medial parabrachial nucleus and periaqueductal gray. The second included neurons in the superior vestibular nucleus, precerebellar nuclei, periaqueductal gray, and parabrachial nuclei, with weaker associations of raphe nuclei. Three additional components (networks) were also identified that were not correlated with the severity of motion sickness symptoms. These networks likely mediated the covert aspects of motion sickness, such as affective components. The identification of five statistically independent component networks associated with the development of motion sickness provides an opportunity to consider, in network activation dimensions, the complex progression of signs and symptoms that are precipitated in provocative environments. Similar methodology can be used to parse the neural networks that mediate other complex responses to environmental stimuli. © 2014 Balaban et al

Vitamin K1 intake is associated with lower risk for all-cause and cardiovascular disease mortality in community-dwelling older Australian women

Background and aims: Assessing the relationship between vitamin K1 intakes, using region-specific food databases, with both all-cause, and cardiovascular disease (CVD) mortality warrants further investigation to inform future preventative strategies. Consequently, we examined the aforementioned associations in the Perth Longitudinal Study of Ageing Women (PLSAW). Methods and results: 1436 community-dwelling older Australian women (mean ± SD age 75.2 ± 2.7 years) completed a validated food frequency questionnaire at baseline (1998). Vitamin K1 intake was calculated based on an Australian vitamin K food database, supplemented with published data. All-cause and CVD mortality data was obtained from linked health records. Associations were examined using restricted cubic splines within Cox-proportional hazard models, adjusted for a range of cardiovascular and lifestyle related risk factors. Over 15 years of follow-up, 601 (41.9%) women died, with 236 deaths (16.4%) due to CVD. Compared to women with the lowest vitamin K1 intakes (Quartile 1, median 49.1 μg/day), those with the highest intakes (Quartile 4, median 119.3 g/day) had lower relative hazards for all-cause mortality (HR 0.66 95%CI 0.51–0.86) and CVD mortality (HR 0.61 95%CI 0.41–0.92). A plateau in the inverse association was observed from vitamin K1 intakes of approximately ≥ 80 g/day. Conclusion: Higher vitamin K1 intakes were associated with lower risk for both all-cause and CVD mortality in community-dwelling older women, independent of CVD related risk factors. A higher intake of vitamin K1 rich foods, such as leafy green vegetables, may support cardiovascular health

Vitamin K: Metabolism, genetic influences, and chronic disease outcomes

Vitamin K refers to a group of lipid-soluble vitamins that exist in two natural isoforms; phylloquinone (PK, vitamin K1) and menaquinones (MKs, vitamin K2). Phylloquinone, the primary dietary source, is found abundantly in green vegetables and plant oils. Menaquinones (MK-4 through MK-13) are synthesized by anaerobic bacteria and may be obtained through the diet from fermented foods and animal products (e.g., meats, dairy and eggs). Originally recognized for its role in blood coagulation, vitamin K is an essential cofactor for the posttranslational carboxylation of vitamin K-dependent proteins (VKDPs), which are implicated in various physiological processes including; blood coagulation, calcium homeostasis, as well as metabolic and inflammatory pathways. Therefore, vitamin K has attracted considerable research interest for its potential implications in several diseases. While promising, the specific roles of vitamin K in various health conditions, the quantity of vitamin K (both PK and MKs) required for the function of various VKDPs, and the influence of genetics on vitamin K metabolism, remain unclear. This review aims to (i) provide an overview of the structure, dietary sources, metabolism, and physiological roles of vitamin K, including those relating to; cardiovascular diseases, type 2 diabetes, respiratory conditions, musculoskeletal health and cancer; (ii) discuss the impact of genetic factors on vitamin K status and how such factors modulate the role of vitamin K in the aforementioned chronic diseases; and (iii) outline key directions for future research

Phage N15-Based Vectors for Gene Cloning and Expression in Bacteria and Mammalian Cells

Bacteriophage N15 is the first virus known to deliver linear prophage into Escherichia coli. During its lysogenic cycle, N15 protelomerase (TelN) resolves its telomerase occupancy site (tos) into hairpin telomeres. This protects the N15 prophage from bacterial exonuclease degradation, enabling it to stably replicate as a linear plasmid in E. coli. Interestingly, purely proteinaceous TelN can retain phage DNA linearization and hairpin formation without involving host- or phage-derived intermediates or cofactors in the heterologous environment. This unique feature has led to the advent of synthetic linear DNA vector systems derived from the TelN-tos module for the genetic engineering of bacterial and mammalian cells. This review will focus on the development and advantages of N15-based novel cloning and expression vectors in the bacterial and mammalian environments. To date, N15 is the most widely exploited molecular tool for the development of linear vector systems, especially the production of therapeutically useful miniDNA vectors without a bacterial backbone. Compared to typical circular plasmids, linear N15-based plasmids display remarkable cloning fidelity in propagating unstable repetitive DNA sequences and large genomic fragments. Additionally, TelNlinearized vectors with the relevant origin of replication can replicate extrachromosomally and retain transgenes functionality in bacterial and mammalian cells without compromising host cell viability. Currently, this DNA linearization system has shown robust results in the development of gene delivery vehicles, DNA vaccines and engineering mammalian cells against infectious diseases or cancers, highlighting its multifaceted importance in genetic studies and gene medicine