Recognition of UK Insolvency Proceedings Post-Brexit: The Impact of a ‘No Deal’ Scenario

This paper examines the impact of a ‘no deal’ or ‘hard’ Brexit on the recognition of insolvency proceedings commenced in the UK by the remaining Member States of the European Union (‘EU’) post-Brexit. The paper considers the framework currently implemented by the Recast European Insolvency Regulation and the possible approaches when it will cease to apply to proceedings commenced post-Brexit. The paper identifies that there will be no overarching framework in the event that ‘no deal’ is reached between the UK and EU for post-Brexit arrangements, resulting in reliance on individual Member States’ domestic laws to determine recognition of insolvency proceedings commenced in the UK. The paper sets out the contrasting approaches of five of the UK’s key trading partners in the EU: France, Germany, Ireland, the Netherlands and Spain. The paper concludes that UK insolvency proceedings will not be recognised in a consistent manner in these Member States, which will be detrimental to stakeholders in, and ultimately the economies of, the UK and these Member States. In doing so, the paper underlines the importance of an agreement being reached between the UK and the EU on the recognition of cross-border insolvency proceedings for the benefit of all parties

Association between a longer duration of illness, age and lower frontal lobe grey matter volume in schizophrenia

The frontal lobe has an extended maturation period and may be vulnerable to the long-term effects of schizophrenia. We tested this hypothesis by studying the relationship between duration of illness (DoI), grey matter (GM) and cerebro-spinal fluid (CSF) volume across the whole brain. Sixty-four patients with schizophrenia and 25 healthy controls underwent structural MRI scanning and neuropsychological assessment. We performed regression analyses in patients to examine the relationship between DoI and GM and CSF volumes across the whole brain, and correlations in controls between age and GM or CSF volume of the regions where GM or CSF volumes were associated with DoI in patients. Correlations were also performed between GM volume in the regions associated with DoI and neuropsychological performance. A longer DoI was associated with lower GM volume in the left dorsomedial prefrontal cortex (PFC), right middle frontal cortex, left fusiform gyrus (FG) and left cerebellum (lobule III). Additionally, age was inversely associated with GM volume in the left dorsomedial PFC in patients, and in the left FG and CSF excess near the left cerebellum in healthy controls. Greater GM volume in the left dorsomedial PFC was associated with better working memory, attention and psychomotor speed in patients. Our findings suggest that the right middle frontal cortex is particularly vulnerable to the long-term effect of schizophrenia illness whereas the dorsomedial PFC, FG and cerebellum are affected by both a long DoI and aging. The effect of illness chronicity on GM volume in the left dorsomedial PFC may be extended to brain structure–neuropsychological function relationships

Endothelial Cell Capture of Heparin-Binding Growth Factors under Flow

Circulation is an important delivery method for both natural and synthetic molecules, but microenvironment interactions, regulated by endothelial cells and critical to the molecule's fate, are difficult to interpret using traditional approaches. In this work, we analyzed and predicted growth factor capture under flow using computer modeling and a three-dimensional experimental approach that includes pertinent circulation characteristics such as pulsatile flow, competing binding interactions, and limited bioavailability. An understanding of the controlling features of this process was desired. The experimental module consisted of a bioreactor with synthetic endothelial-lined hollow fibers under flow. The physical design of the system was incorporated into the model parameters. The heparin-binding growth factor fibroblast growth factor-2 (FGF-2) was used for both the experiments and simulations. Our computational model was composed of three parts: (1) media flow equations, (2) mass transport equations and (3) cell surface reaction equations. The model is based on the flow and reactions within a single hollow fiber and was scaled linearly by the total number of fibers for comparison with experimental results. Our model predicted, and experiments confirmed, that removal of heparan sulfate (HS) from the system would result in a dramatic loss of binding by heparin-binding proteins, but not by proteins that do not bind heparin. The model further predicted a significant loss of bound protein at flow rates only slightly higher than average capillary flow rates, corroborated experimentally, suggesting that the probability of capture in a single pass at high flow rates is extremely low. Several other key parameters were investigated with the coupling between receptors and proteoglycans shown to have a critical impact on successful capture. The combined system offers opportunities to examine circulation capture in a straightforward quantitative manner that should prove advantageous for biologicals or drug delivery investigations

Genetic variation in Fcγ receptor IIa and risk of coronary heart disease: negative results from two large independent populations

Background The role of the Fcgamma receptor IIa (FcgammaRIIa), a receptor for C-reactive protein (CRP), the classical acute phase protein, in atherosclerosis is not yet clear. We sought to investigate the association of FcgammaRIIa genotype with risk of coronary heart disease (CHD) in two large population-based samples. Methods FcgammaRIIa-R/H131 polymorphisms were determined in a population of 527 patients with a history of myocardial infarction and 527 age and gender matched controls drawn from a population-based MONICA- Augsburg survey. In the LURIC population, 2227 patients with angiographically proven CHD, defined as having at least one stenosis [greater than or equal to]50%, were compared with 1032 individuals with stenosis H genotype was not independently associated with lower risk of CHD after multivariable adjustments, neither in the MONICA population (odds ratio (OR) 1.08; 95% confidence interval (CI) 0.81 to 1.44), nor in LURIC (OR 0.96; 95% CI 0.81 to 1.14). Conclusion Our results do not confirm an independent relationship between FcgammaRIIa genotypes and risk of CHD in these populations

Preservation and compensation: The functional neuroanatomy of insight and working memory in schizophrenia

Background: Poor insight in schizophrenia has been theorised to reflect a cognitive deficit that is secondary to brain abnormalities, localized in the brain regions that are implicated in higher order cognitive functions, including working memory (WM). This study investigated WM-related neural substrates of preserved and poor insight in schizophrenia. Method: Forty stable schizophrenia outpatients, 20 with preserved and 20 with poor insight (usable data obtained from 18 preserved and 14 poor insight patients), and 20 healthy participants underwent functional magnetic resonance imaging (fMRI) during a parametric 'n-back' task. The three groups were preselected to match on age, education and predicted IQ, and the two patient groups to have distinct insight levels. Performance and fMRI data were analysed to determine how groups of patients with preserved and poor insight differed from each other, and from healthy participants. Results: Poor insight patients showed lower performance accuracy, relative to healthy participants (p. = 0.01) and preserved insight patients (p. = 0.08); the two patient groups were comparable on symptoms and medication. Preserved insight patients, relative to poor insight patients, showed greater activity most consistently in the precuneus and cerebellum (both bilateral) during WM; they also showed greater activity than healthy participants in the inferior-superior frontal gyrus and cerebellum (bilateral). Group differences in brain activity did not co-vary significantly with performance accuracy. Conclusions: The precuneus and cerebellum function contribute to preserved insight in schizophrenia. Preserved insight as well as normal-range WM capacity in schizophrenia sub-groups may be achieved via compensatory neural activity in the frontal cortex and cerebellum. © 2013 Elsevier B.V.Wellcome Trust, UK; NIHR Birmingham and Black Country CLAHRC, UK; Biomedical Research Centre for Mental Health at the Institute of Psychiatry, King's College London; South London and Maudsley NHS Foundation Trust, UK

Simultaneous NO/SO[subscript x] removal using an electrochemical concentrator device

M.S.Jack Winnic

Simulations show FGF-2 binding and internalization under flow.

<p>For the simulations, FGF-2 (1 ng) was introduced into the reservoir (30% nonspecific loss) and sent into the cell-lined hollow fibers under pulsatile flow (0.63 mL/min, 1.26 mm/sec). (A) The sum of all cell surface bound FGF-2 (•) and FGF-2 internalized (○) within the cell-lined hollow fiber are shown. (B, C) Plot of % FGFR bound to FGF-2 versus time at the entrance (•), middle (▴) and at the exit (▪) cell when the diffusion coefficient is 1.67×10⁻¹⁰ (B) or 1.67×10⁻⁹ m²/s (C). The fluid entering the system is essentially free of FGF-2 by 150s after flow is initiated.</p

Simulations predict FGF-2 concentration profile in the cell-lined hollow fiber is impacted by diffusion.

<p>Grayscale images of FGF-2 concentration within the cell-lined hollow fiber (1×10⁴ FGFR/cell and 2.5×10⁵ HSPG/cell) at 44s after FGF-2 (1 ng) addition from the reservoir (30% nonspecific loss) at 0.63 mL/min (1.26 mm/sec) with FGF-2 having a diffusion coefficient of 1.67×10⁻¹⁰ (A) or 1.67×10⁻⁹ m²/s (B). The scale and numbers on the plots indicates the concentration of FGF-2 in ng/mL.</p

Simulations predict cell surface density impacts FGF-2 retention.

<p>Simulations were run for FGF-2 (1ng) added to the system (30% non-specific loss) at 0.63 mL/min pulsatile flow (1.26 mm/sec) for 5 min. (A) Cells expressed either 1×10⁴ FGFR/cell and variable densities of HSPG (○) or 2.5×10⁵ HSPG/cell and variable densities of FGFR (•) on the cell-lined hollow fibers. The amount retained within the system (bound, internalized, and fluid phase FGF-2) is shown. (B) Cells expressed 1×10⁴ FGFR/cell and 2×10³ (•,○), 2×10⁴ (▪,□), or 2×10⁵ (▴,▵) HSPG/cell on the cell-lined hollow fibers and simulation results correspond to entrance cell value at a given time. Filled symbols correspond to % of FGF-2 bound to FGFR which are simultaneously bound to HSPG and open symbols correspond to the #/cell of FGF-2 bound to FGFR and HSPG.</p