464 research outputs found
Reminiscence of Rose McColl (Woolf)
No full textA typed biography of Rose McColl (Nee Woolf) by an unknown author. Rosa was born around 1904 in Glasgow, Scotland. She married John McCool and had one child, Ian McColl. She died March 4, 1958 at the age of 54 in Vancouver, BC. The collection also contains a photo of her
Furthering the benefits of DBT for eating disorders: a lived experience correspondence on McColl et al.
No full textAbstract This Correspondence article provides a lived experience perspective on McColl et al.‘s study, which examines the use of Dialectical Behaviour Therapy for individuals with eating disorders. Drawing on experiences of DBT treatment for longstanding and severe anorexia, the author critically engages with the study’s findings, highlighting both the strengths and limitations of the treatment approach McColl et al. describe. While DBT has shown promise in addressing the emotional dysregulation and distress tolerance that underlie many eating disorder behaviours, the author emphasises the need for further adaptation to cater to the complexities of co-occurring physical, psychological, and neurodivergent conditions. The benefits of DBT for eating disorders are explored through personal reflections which emphasise the value and importance of skill-development, therapeutic validation, and motivation to build a “life worth living”. Additional, co-produced research is required to further develop the evidence for DBT-based approaches, with particular attention needed in addressing language, stigma, cultural biases, and exclusionary research and clinical practices. Writing from a UK context, the author ends by advocating for the reinstatement of DBT within national guidelines for eating disorder treatment, highlighting its transdiagnostic relevance and potential to provide comprehensive, holistic support for those with more complex presentations
Correction: Corrigendum: Adrenergic-mediated loss of splenic marginal zone B cells contributes to infection susceptibility after stroke
No full textNature Communications 8 Article number: 15051 (2017); Published: 19 April 2017; Updated: 18 August 2017 The affiliation details for Barry W. McColl are incorrect in this Article. The correct affiliation details for this author are given below: The Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK.</jats:p
Tertiary Lymphoid Organs Are Associated With Bacterial Dysbiosis in Chronic Rhinosinusitis
No full textFirst published: 15 May 2025Sathish Paramasivan, Ahmed Bassiouni, Nicholas A. Bokulich, Mahnaz Ramezanpour, Clare Cooksley, J. Gregory Caporasso, Shaun R. McColl, Peter-JohnWormald, Alkis J. Psaltis, Sarah Vreugd
CC chemokine ligand-5 (CCL5/RANTES) and CC chemokine ligand-18 (CCL18/PARC) are specific markers of refractory unstable angina pectoris and are transiently raised during severe ischemic symptoms
No full textBackgroundChemokines play an important role in atherogenesis and in ischemic injury and repair; however, prospective data on individual chemokines in unstable angina pectoris (UAP) are scarce. Therefore, we assessed chemokine patterns in a prospective cohort of patients with UAP.Methods and resultsPlasma samples of 54 patients with Braunwald class IIIB UAP were examined at baseline for 11 chemokines and 5 inflammatory mediators via multiplex analysis. Levels of CC chemokine ligand (CCL)-5 (also known as RANTES [regulated on activation, normally T-cell expressed, and secreted]; 32.7 versus 23.1 ng/mL, P=0.018) and CCL18 (also known as PARC [pulmonary and activation-regulated chemokine]; 104.4 versus 53.7 ng/mL, P=0.011) were significantly elevated in patients with refractory ischemic symptoms versus stabilized patients. Temporal monitoring by ELISA of CCL5, CCL18, and soluble CD40 ligand (sCD40) levels revealed a drop in CCL5 and sCD40L levels in all UAP patients from day 2 onward (CCL5 12.1 ng/mL, PConclusionsWe are the first to report that CCL18 and CCL5 are transiently raised during episodes of UAP, and peak levels of both chemokines are indicative of refractory symptoms. Because levels of both chemokines, as well as of cognate receptor expression by circulating peripheral blood mononuclear cells, are increased during cardiac ischemia, this may point to an involvement of CCL5/CCL18 in the pathophysiology of UAP and/or post-UAP responses.A.O. Kraaijeveld, S.C.A. de Jager, W.J. de Jager, B.J. Prakken, S.R. McColl, I. Haspels, H. Putter, T.J.C. van Berkel, L. Nagelkerken, J.W. Jukema and E.A.L. Biesse
Cxcr4-ccr7 heterodimerization is a driver of breast cancer progression
No full textData source: Supplementary materials, https://www.mdpi.com/article/10.3390/life11101049/s1Metastatic breast cancer has one of the highest mortality rates among women in western society. Chemokine receptors CXCR4 and CCR7 have been shown to be linked to the metastatic spread of breast cancer, however, their precise function and underlying molecular pathways leading to the acquisition of the pro-metastatic properties remain poorly understood. We demonstrate here that the CXCR4 and CCR7 receptor ligands, CXCL12 and CCL19, cooperatively bind and selectively elicit synergistic signalling responses in invasive breast cancer cell lines as well as primary mammary human tumour cells. Furthermore, for the first time, we have documented the presence of CXCR4-CCR7 heterodimers in advanced primary mammary mouse and human tumours where number of CXCR4-CCR7 complexes directly correlate with the severity of the disease. The functional significance of the CXCR4-CCR7 association was also demonstrated when their forced heterodimerization led to the acquisition of invasive phenotype in non-metastatic breast cancer cells. Taken together, our data establish the CXCR4-CCR7 receptor complex as a new functional unit, which is responsible for the acquisition of breast cancer cell metastatic phenotype and which may serve as a novel biomarker for invasive mammary tumours.Valentina Poltavets, Jessica W. Faulkner, Deepak Dhatrak, Robert J. Whitfield, Shaun R. McColl and Marina Kochetkov
Regulatory T cells are paramount effectors in progesterone regulation of embryo implantation and fetal growth
No full textPublished: June 8, 2023Progesterone (P4) is essential for embryo implantation, but the extent to which the pro-gestational effects of P4 depend on the maternal immune compartment is unknown. Here, we investigate whether regulatory T cells (Treg cells) act to mediate luteal phase P4 effects on uterine receptivity in mice. P4 antagonist RU486 administered to mice on days 0.5 and 2.5 post coitum (dpc) to model luteal phase P4 deficiency caused fewer CD4+Foxp3+ Treg cells and impaired Treg functional competence, along with dysfunctional uterine vascular remodeling and perturbed placental development in mid-gestation. These effects were linked with fetal loss and fetal growth restriction, accompanied by a Th1/CD8-skewed T cell profile. Adoptive transfer at implantation of Treg cells - but not T conventional (Tconv) cells - alleviated fetal loss and fetal growth restriction by mitigating adverse effects of reduced P4 signaling on uterine blood vessel remodeling and placental structure, and restoring maternal T cell imbalance. These findings demonstrate an essential role for Treg cells in mediating P4 effects at implantation, and indicate that Treg cells are a sensitive and critical effector mechanism through which P4 drives uterine receptivity to support robust placental development and fetal growth.Ella S. Green, Lachlan M. Moldenhauer, Holly M. Groome, David J. Sharkey, Peck Y. Chin, Alison S. Care, Rebecca L. Robker, Shaun R. McColl, and Sarah A., Robertso
RoMEO Studies 5: IPR issues for OAI Data and Service Providers
No full textThis paper is the fifth in a series of studies emanating from the UK JISC-funded RoMEO Project (Rights Metadata for Open-archiving). It reports the results of two surveys of OAI Data Providers (DPs) and Service Providers (SPs) with regards to the rights issues they face. It finds that very few DPs have rights agreements with depositing authors and that there is no standard approach to the creation of rights metadata. The paper considers the rights protection afforded individual and collections of metadata records under UK Law and contrasts this with DP and SP’s views on the rights status of metadata and how they wish to protect it. The majority of DP and SPs believe that a standard way of describing both the rights status of documents and of metadata would be usefu
A divergent transcriptional landscape underpins the development and functional branching of MAIT cells
No full textMR1-restricted mucosal-associated invariant T (MAIT) cells play a unique role in the immune system. These cells develop intrathymically through a three-stage process, but the events that regulate this are largely unknown. Here, using bulk and single-cell RNA sequencing-based transcriptomic analysis in mice and humans, we studied the changing transcriptional landscape that accompanies transition through each stage. Many transcripts were sharply modulated during MAIT cell development, including SLAM (signaling lymphocytic activation molecule) family members, chemokine receptors, and transcription factors. We also demonstrate that stage 3 "mature" MAIT cells comprise distinct subpopulations including newly arrived transitional stage 3 cells, interferon-γ-producing MAIT1 cells and interleukin-17-producing MAIT17 cells. Moreover, the validity and importance of several transcripts detected in this study are directly demonstrated using specific mutant mice. For example, MAIT cell intrathymic maturation was found to be halted in SLAM-associated protein (SAP)-deficient and CXCR6-deficient mouse models, providing clear evidence for their role in modulating MAIT cell development. These data underpin a model that maps the changing transcriptional landscape and identifies key factors that regulate the process of MAIT cell differentiation, with many parallels between mice and humans.H.-F. Koay, S. Su, D. Amann-Zalcenstein, S.R. Daley, I. Comerford, L. Miosge, C.E. Whyte, I.E. Konstantinov, Y. d’Udekem, T. Baldwin, P.F. Hickey, S.P. Berzins, J.Y.W. Mak, Y. Sontani, C.M. Roots, T. Sidwell, A. Kallies, Z. Chen, S. Nüssing, K. Kedzierska, L.K. Mackay, S.R. McColl, E.K. Deenick, D.P. Fairlie, J. McCluskey, C.C. Goodnow, M.E. Ritchie, G.T. Belz, S.H. Naik, D.G. Pellicci, and D.I. Godfre
MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment
No full text© 2007 Nature Publishing GroupThe cytokine macrophage migration inhibitory factor (MIF) plays a critical role in inflammatory diseases and atherogenesis. We identify the chemokine receptors CXCR2 and CXCR4 as functional receptors for MIF. MIF triggered G(alphai)- and integrin-dependent arrest and chemotaxis of monocytes and T cells, rapid integrin activation and calcium influx through CXCR2 or CXCR4. MIF competed with cognate ligands for CXCR4 and CXCR2 binding, and directly bound to CXCR2. CXCR2 and CD74 formed a receptor complex, and monocyte arrest elicited by MIF in inflamed or atherosclerotic arteries involved both CXCR2 and CD74. In vivo, Mif deficiency impaired monocyte adhesion to the arterial wall in atherosclerosis-prone mice, and MIF-induced leukocyte recruitment required Il8rb (which encodes Cxcr2). Blockade of Mif but not of canonical ligands of Cxcr2 or Cxcr4 in mice with advanced atherosclerosis led to plaque regression and reduced monocyte and T-cell content in plaques. By activating both CXCR2 and CXCR4, MIF displays chemokine-like functions and acts as a major regulator of inflammatory cell recruitment and atherogenesis. Targeting MIF in individuals with manifest atherosclerosis can potentially be used to treat this condition.Jürgen Bernhagen, Regina Krohn, Hongqi Lue, Julia L Gregory, Alma Zernecke, Rory R Koenen, Manfred Dewor, Ivan Georgiev, Andreas Schober, Lin Leng, Teake Kooistra, Günter Fingerle-Rowson, Pietro Ghezzi, Robert Kleemann, Shaun R McColl, Richard Bucala, Michael J Hickey & Christian Webe
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