October 26, 2016

Urine metabolome profiling of immune-mediated inflammatory diseases

BMC Medicine

RESEARCH ARTICLE

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OPEN PEER REVIEW

Arnald Alonso,

Antonio JuliàEmail author View ORCID ID profile,

Maria Vinaixa,

Eugeni Domènech,

Antonio Fernández-Nebro,

Juan D. Cañete,

Carlos Ferrándiz,

Jesús Tornero,

Javier P. Gisbert,

Pilar Nos,

Ana Gutiérrez Casbas,

Lluís Puig,

Isidoro González-Álvaro,

José A. Pinto-Tasende,

Ricardo Blanco,

Miguel A. Rodríguez,

Antoni Beltran,

Xavier Correig,

Sara MarsalEmail author and

for the IMID Consortium

BMC Medicine201614:133

DOI: 10.1186/s12916-016-0681-8

Open Peer Review reports

Abstract

Background

Immune-mediated inflammatory diseases (IMIDs) are a group of complex and prevalent diseases where disease diagnostic and activity monitoring is highly challenging. The determination of the metabolite profiles of biological samples is becoming a powerful approach to identify new biomarkers of clinical utility. In order to identify new metabolite biomarkers of diagnosis and disease activity, we have performed the first large-scale profiling of the urine metabolome of the six most prevalent IMIDs: rheumatoid arthritis, psoriatic arthritis, psoriasis, systemic lupus erythematosus, Crohn’s disease, and ulcerative colitis.

Open Access Review Article

Arch Toxicol (2016). doi:10.1007/s00204-016-1876-7

Arathi KizhedathEmail author
Simon Wilkinson
Jarka Glassey

Abstract

Biopharmaceuticals, monoclonal antibody (mAb)-based therapeutics in particular, have positively impacted millions of lives. MAbs and related therapeutics are highly desirable from a biopharmaceutical perspective as they are highly target specific and well tolerated within the human system. Nevertheless, several mAbs have been discontinued or withdrawn based either on their inability to demonstrate efficacy and/or due to adverse effects.

Mast cell desensitization inhibits calcium flux and aberrantly remodels actin

J Clin Invest. 2016. doi:10.1172/JCI87492.

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W.X. Gladys Ang,1 Alison M. Church,2 Mike Kulis,3 Hae Woong Choi,4 A. Wesley Burks,3and Soman N. Abraham1,4,5,6

First published September 26, 2016 - More info

Research Article Immunology

Data on the oral CRTh2 antagonist QAW039 (fevipiprant) in patients with uncontrolled allergic asthma

. 2016 Dec; 9: 199–205.

Published online 2016 Aug 29. doi: 10.1016/j.dib.2016.08.039

PMCID: PMC5021787

Veit J. Erpenbeck,a,⁎ Todor A. Popov,b David Miller,c Steven F. Weinstein,d Sheldon Spector,e Baldur Magnusson,aWande Osuntokun,f Paul Goldsmith,f Markus Weiss,a and Jutta Beierg

Author information ► Article notes ► Copyright and License information ►

Abstract

This article contains data on clinical endpoints (Peak Flow Expiratory Rate, fractional exhaled nitric oxide and total IgE serum levels) and plasma pharmacokinetic parameters concerning the use of the oral CRTh2 antagonist QAW039 (fevipiprant) in mild to moderate asthma patients.

Asthma-related deaths

Multidisciplinary Respiratory Medicine

REVIEW

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Gennaro D’AmatoEmail author,

Carolina Vitale,

Antonio Molino,

Anna Stanziola,

Alessandro Sanduzzi,

Alessandro Vatrella,

Mauro Mormile,

Maurizia Lanza,

Giovanna Calabrese,

Leonardo Antonicelli and

Maria D’Amato

Multidisciplinary Respiratory Medicine201611:37

DOI: 10.1186/s40248-016-0073-0

Abstract

Despite major advances in the treatment of asthma and the development of several asthma guidelines, people still die of asthma currently. According to WHO estimates, approximately 250,000 people die prematurely each year from asthma. Trends of asthma mortality rates vary very widely across countries, age and ethnic groups. Several risk factors have been associated with asthma mortality, including a history of near-fatal asthma requiring intubation and mechanical ventilation, hospitalization or emergency care visit for asthma in the past year, currently using or having recently stopped using oral corticosteroids (a marker of event severity), not currently using inhaled corticosteroids, a history of psychiatric disease or psychosocial problems, poor adherence with asthma medications and/or poor adherence with (or lack of) a written asthma action plan, food allergy in a patient with asthma.

Respiratory Research

RESEARCH

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Thomas SouthworthEmail author,

Jonathan Plumb,

Vandana Gupta,

James Pearson,

Isabel Ramis,

Martin D. Lehner,

Montserrat Miralpeix and

Dave Singh

Respiratory Research201617:124

DOI: 10.1186/s12931-016-0436-2

Abstract

Background

Phosphatidylinositol 3-kinase delta (PI3Kδ) and Janus-activated kinases (JAK) are both novel anti-inflammatory targets in asthma that affect lymphocyte activation. We have investigated the anti-inflammatory effects of PI3Kδ and JAK inhibition on cytokine release from asthma bronchoalveolar lavage (BAL) cells and T-cell activation, and measured lung PI3Kδ and JAK signalling pathway expression.

Acta Derm Venereol 2016; XX: XX–XX.

DOI: 10.2340/00015555-2366

Hjalte H. Andersen, Lars Arendt-Nielsen and Parisa Gazerani*

SMI®, Department of Health Science and Technology, School of Medicine, Aalborg University, Denmark

Recent discoveries in itch neurophysiology include itch-selective neuronal pathways, the clinically relevant non-histaminergic pathway, and elucidation of the notable similarities and differences between itch and pain. Potential involvement of glial cells in itch processing and the possibility of glial modulation of chronic itch have recently been identified, similarly to the established glial modulation of pain processing.