20 results match your criteria: "Univ. of Edinburgh[Affiliation]"

Background: The choroid plexus is an important structure within the ventricular system. Schizophrenia has been associated with morphological changes to the choroid plexus but the presence and extent of alterations at different illness stages is unclear.

Methods: We examined choroid plexus volumes in participants at clinical high-risk for psychosis (N = 110), participants with first-episode psychosis (N = 37), participants with schizophrenia (N = 28), clinical (N = 38) and non-clinical controls (N = 75).

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Genomic selection strategies to increase genetic gain in tea breeding programs.

Plant Genome

March 2023

The Roslin Institute and Royal (Dick) School of Veterinary Studies, The Univ. of Edinburgh, Easter Bush Campus, Midlothian, EH25 9RG, UK.

Tea [Camellia sinensis (L.) O. Kuntze] is mainly grown in low- to middle-income countries (LMIC) and is a global commodity.

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Aim: Language disturbances are a candidate biomarker for the early detection of psychosis. Temporal and prosodic abnormalities have been observed in schizophrenia patients, while there is conflicting evidence whether such deficits are present in participants meeting clinical high-risk for psychosis (CHR-P) criteria.

Methods: Clinical interviews from CHR-P participants (n = 50) were examined for temporal and prosodic metrics and compared against a group of healthy controls (n = 17) and participants with affective disorders and substance abuse (n = 23).

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Hippocampal structural alterations in early-stage psychosis: Specificity and relationship to clinical outcomes.

Neuroimage Clin

August 2022

Institute for Neuroscience and Psychology, Univ. of Glasgow, UK; Department of Child and Adolescent Psychiatry, Charité Universitätsmedizin, Berlin, Germany. Electronic address:

Hippocampal dysfunctions are a core feature of schizophrenia, but conflicting evidence exists whether volumetric and morphological changes are present in early-stage psychosis and to what extent these deficits are related to clinical trajectories. In this study, we recruited individuals at clinical high risk for psychosis (CHR-P) (n = 108), patients with a first episode of psychosis (FEP) (n = 37), healthy controls (HC) (n = 70) as well as a psychiatric control group with substance abuse and affective disorders (CHR-N: n = 38). MRI-data at baseline were obtained and volumetric as well as vertex analyses of the hippocampus were carried out.

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Article Synopsis
  • DNA methylation (DNAm) has a significant link to various diseases and is a potential factor in predicting mortality, particularly when combined with clinical risk factors.
  • In a study involving 15,013 participants over 10 years, researchers identified specific CpGs associated with all-cause mortality, cardiovascular, and cancer death in both European and African ancestry groups.
  • The study developed a DNAm-based prediction model that improved cancer death risk prediction, found potential causal relationships between certain CpGs and longevity, and highlighted their relevance in immune and cancer-related pathways.
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The relationship between cognitive deficits and impaired short-term functional outcome in clinical high-risk for psychosis participants: A machine learning and modelling approach.

Schizophr Res

May 2021

Institute for Neuroscience and Psychology, Univ. of Glasgow, United Kingdom of Great Britain and Northern Ireland; Department of Child and Adolescent Psychiatry, Charité Universitätsmedizin, Berlin, Germany. Electronic address:

Poor functional outcomes are common in individuals at clinical high-risk for psychosis (CHR-P), but the contribution of cognitive deficits remains unclear. We examined the potential utility of cognitive variables in predictive models of functioning at baseline and follow-up with machine learning methods. Additional models fitted on baseline functioning variables were used as a benchmark to evaluate model performance.

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Corticosterone affects physiology and behavior both during normal daily processes but also in response to environmental challenges and is known to mediate life history trade-offs. Many studies have investigated patterns of corticosterone production at targeted times of year, while ignoring underlying annual profiles. We aimed to understand the annual regulation of hypothalamic-pituitary-adrenal (HPA) axis function of both migrant (Zonotrichia leucophrys gambelii; n = 926) and resident (Z.

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Grey-matter abnormalities in clinical high-risk participants for psychosis.

Schizophr Res

December 2020

Institute for Neuroscience and Psychology, Univ. of Glasgow, UK; Charité Universitätsmedizin, Department of Child and Adolescent Psychiatry, Berlin, Germany. Electronic address:

The current study examined the presence of abnormalities in cortical grey-matter (GM) in a sample of clinical high-risk (CHR) participants and examined relationships with psychosocial functioning and neurocognition. CHR-participants (n = 114), participants who did not fulfil CHR-criteria (CHR-negative) (n = 39) as well as a group of healthy controls (HC) (n = 49) were recruited. CHR-status was assessed using the Comprehensive Assessment of At-Risk Mental State (CAARMS) and the Schizophrenia Proneness Interview, Adult Version (SPI-A).

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Acute inhibition of NCC does not activate distal electrogenic Na+ reabsorption or kaliuresis.

Am J Physiol Renal Physiol

February 2014

Univ. of Edinburgh/BHF Centre for Cardiovascular Science, Rm. W3.33B, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.

Na(+) reabsorption from the distal renal tubule involves electroneutral and electrogenic pathways, with the latter promoting K(+) excretion. The relative activities of these two pathways are tightly controlled, participating in the minute-to-minute regulation of systemic K(+) balance. The pathways are interdependent: the activity of the NaCl cotransporter (NCC) in the distal convoluted tubule influences the activity of the epithelial Na(+) channel (ENaC) downstream.

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Endothelial progenitor cells in patients with chronic obstructive pulmonary disease.

Am J Physiol Lung Cell Mol Physiol

December 2013

BHF/Univ. Centre for Cardiovascular Science, The Univ. of Edinburgh, Scottish Centre for Regenerative Medicine, Little France Crescent, Edinburgh EH16 4UU, UK.

The pathogenesis of chronic obstructive pulmonary disease is not fully understood. The objective of this study was to compare circulating endothelial progenitor cells in patients with chronic obstructive pulmonary disease to age, sex, and cigarette smoking matched healthy controls. Patients with chronic obstructive pulmonary disease (n = 37) and healthy controls (n = 19) were matched by age, sex, and smoking status.

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An anatomically unbiased approach for analysis of renal BOLD magnetic resonance images.

Am J Physiol Renal Physiol

September 2013

Univ./British Heart Foundation Centre for Cardiovascular Science The Univ. of Edinburgh, Queen's Medical Research Centre, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.

Oxygenation defects may contribute to renal disease progression, but the chronology of events is difficult to define in vivo without recourse to invasive methodologies. Blood oxygen level-dependent magnetic resonance imaging (BOLD MRI) provides an attractive alternative, but the R2* signal is physiologically complex. Postacquisition data analysis often relies on manual selection of region(s) of interest.

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A urine-concentrating defect in 11β-hydroxysteroid dehydrogenase type 2 null mice.

Am J Physiol Renal Physiol

August 2012

BHF Centre for Cardiovascular Science, The Queen's Medical Research Institute, The Univ. of Edinburgh, 47, Little France Crescent, Edinburgh, UK EH16 4TJ.

In aldosterone target tissues, 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) is coexpressed with mineralocorticoid receptors (MR) and protects the receptor from activation by glucocorticoids. Null mutations in the encoding gene, HSD11B2, cause apparent mineralocorticoid excess, in which hypertension is thought to reflect volume expansion secondary to sodium retention. Hsd11b2(-/-) mice are indeed hypertensive, but impaired natriuretic capacity is associated with significant volume contraction, suggestive of a urine concentrating defect.

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Therapeutic targets in liver fibrosis.

Am J Physiol Gastrointest Liver Physiol

May 2011

Univ. of Edinburgh, UK.

Detailed analysis of the cellular and molecular mechanisms that mediate liver fibrosis has provided a framework for therapeutic approaches to prevent, slow down, or even reverse fibrosis and cirrhosis. A pivotal event in the development of liver fibrosis is the activation of quiescent hepatic stellate cells (HSCs) to scar-forming myofibroblast-like cells. Consequently, HSCs and the factors that regulate HSC activation, proliferation, and function represent important antifibrotic targets.

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The overall pattern of the developing kidney is set in large part by the developing ureteric bud/collecting duct system, and dysgenesis of this system accounts for a variety of clinically significant renal diseases. Understanding how the behavior of cells in the developing ureteric bud/collecting duct is controlled is therefore important to understanding the normal and abnormal kidney. Dact proteins have recently been identified as cytoplasmic regulators of intracellular signaling.

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Circulating endothelial progenitor cells are not affected by acute systemic inflammation.

Am J Physiol Heart Circ Physiol

June 2010

Centre for Cardiovascular Science, Univ. of Edinburgh, Chancellor's Bldg., Edinburgh EH16 4SU, UK.

Vascular injury causes acute systemic inflammation and mobilizes endothelial progenitor cells (EPCs) and endothelial cell (EC) colony-forming units (EC-CFUs). Whether such mobilization occurs as part of a nonspecific acute phase response or is a phenomenon specific to vascular injury remains unclear. We aimed to determine the effect of acute systemic inflammation on EPCs and EC-CFU mobilization in the absence of vascular injury.

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Fractional urinary excretion of endothelin-1 is reduced by acute ETB receptor blockade.

Am J Physiol Renal Physiol

November 2007

Centre for Cardiovascular Science, Univ. of Edinburgh, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.

Evidence suggests that urinary excretion of endothelin-1 (ET-1) reflects renal ET-1 production and is independent of systemic ET-1 activity. The influence of ET receptors on urinary ET-1 excretion has not been studied in humans, yet peritubular ETB receptors are abundant within the kidney. We have studied the effects of acute ETA and ETB receptor blockade with BQ-123 and BQ-788, respectively, on urinary ET-1 excretion in a randomized, placebo-controlled, double-blind study in 16 subjects with a wide range of GFRs (15-152 ml/min).

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Genetic manipulation of 11beta-hydroxysteroid dehydrogenases in mice.

Am J Physiol Regul Integr Comp Physiol

September 2005

Univ. of Edinburgh, Molecular Physiology Group, Centre for Cardiovascular Science, Queens Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, UK.

11beta-hydroxysteroid dehydrogenases (HSDs) interconvert active 11-hydroxy glucocorticoids (cortisol, corticosterone) and their inert 11-keto derivatives (cortisone, 11-dehydrocorticosterone). 11beta-HSD type 1 is a predominant reductase that regenerates active glucocorticoids in expressing cells, thus amplifying local glucocorticoid action, whereas 11beta-HSD type 2 catalyzes rapid dehydrogenation, potently inactivating intracellular glucocorticoids. Both isozymes thus regulate receptor activation by substrate availability.

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Mechanisms in adverse reactions to food. The gastrointestinal tract.

Allergy

June 1995

Dept. of Medicine, Univ. of Edinburgh, Western General Hospital, Scotland.

Application of strict diagnostic criteria to celiac disease has led to the realization that there is a wide clinical spectrum within this disease. Normally there are immune reactions to dietary proteins, particularly secretory antibodies of IgA class, low titers of serum antibody and specific down-regulation of IgE and T cell reactivity (oral tolerance). From time to time, abnormal immunity to foods, either as inappropriately high titers of antibodies or qualitatively altered responses, produce disease.

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