. PI18/286) and the Research Ethics Committee of the Balearic Islands (IB3950/19 PI). Data distribution will be anonymous. Results will be disseminated via conferences and papers published in peer-reviewed, open-access journals. ClinicalTrials.gov Registry (NCT03951350).ClinicalTrials.gov Registry (NCT03951350). Although cardiovascular disease (CVD) is a common comorbidity associated with chronic obstructive pulmonary disease (COPD), it is unknown how to improve prediction of cardiovascular (CV) risk in individuals with COPD. Traditional CV risk scores have been tested in different populations but not uniquely in COPD. 5-Ethynyl-2'-deoxyuridine chemical The potential of alternative markers to improve CV risk prediction in individuals with COPD is unknown. We aimed to determine the predictive value of conventional CVD risk factors in COPD and to determine if additional markers improve prediction beyond conventional factors. Data from the Evaluation of the Role of Inflammation in Chronic Airways disease cohort, which enrolled 729 individuals with Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II-IV COPD were used. Linked hospital episode statistics and survival data were prospectively collected for a median 4.6 years of follow-up. Five UK centres interested in COPD. Population-based sample including 714 individuals with spirefined by the 6MWT improves prediction of CV hospitalisation in individuals with COPD. ID 11101.ID 11101. Evidence indicates that people with the common inflammatory skin diseases atopic eczema or psoriasis are at increased risk of mental illness. However, the reasons for the relationship between skin disease and common mental disorders (ie, depression and anxiety) or severe mental illnesses (ie, schizophrenia, bipolar disorder and other psychoses) are unclear. Therefore, we aim to synthesise the available evidence regarding the risk factors for mental illness in adults with atopic eczema or psoriasis. We will conduct a systematic review of randomised controlled trials, cohort, case-control and cross-sectional studies. We will search the following databases from inception to March 2020 Medline, Embase, Global Health, Scopus, the Cochrane Library, Web of Science, Base, PsycInfo, the Global Resource of Eczema Trials, and the grey literature databases Open Grey, PsycExtra and the New York Academy of Medicine Grey Literature Report. We will also search the bibliographies of eligible studies and relevant systematic reviews to identify additional relevant studies. Citation searching of large summary papers will be used to further identify relevant publications. Two reviewers will initially review study titles and abstracts for eligibility, followed by full text screening. We will extract data using a standardised data extraction form. We will assess the risk of bias of included studies using the Quality in Prognosis Studies tool. We will synthesise data narratively, and if studies are sufficiently homogenous, we will consider a meta-analysis. We will assess the quality of the evidence using the Grading of Recommendations, Assessment, Development and Evaluation framework. Ethical approval is not required for a systematic review. Results of the review will be published in a peer-reviewed journal and disseminated through conferences. CRD42020163941.CRD42020163941. The incidence and prevalence of chronic inflammatory bowel diseases in childhood and adolescence is increasing and varies internationally. The systematic literature review aims to describe international epidemiological trends of chronic inflammatory bowel diseases in the child and adolescence age. A period from 1970 to 2019 will be taken into account when searching for suitable studies as well as geographical differences in the development of incidences will be presented. The literature databases PubMed and Embase will be searched for the period from 01 January 1970 to 31 December 2019 using linked keywords. A manual search in bibliographies of already published and relevant systematic reviews will complete the systematic literature search. The included studies will be combined in a qualitative and quantitative synthesis and statistically evaluated. Ethical approval is not required for this study as it is a systematicreview. The results will be submitted to peer-reviewed journals and presented in national andinternational meetings. This research received no specific grant from any funding agency inthe public, commercial or not-for-profit sectors. This systematic review protocol was registeredwith the International Prospective Register of Systematic Reviews (PROSPERO-NRCRD42020168644).Ethical approval is not required for this study as it is a systematicreview. The results will be submitted to peer-reviewed journals and presented in national andinternational meetings. This research received no specific grant from any funding agency inthe public, commercial or not-for-profit sectors. This systematic review protocol was registeredwith the International Prospective Register of Systematic Reviews (PROSPERO-NRCRD42020168644).Compositions of proteins and lipids within cilia and on the ciliary membrane are maintained to be distinct from those of the cytoplasm and plasma membrane, respectively, by the presence of the ciliary gate. INPP5E is a phosphoinositide 5-phosphatase that is localized on the ciliary membrane by anchorage via its C-terminal prenyl moiety. In addition, the ciliary membrane localization of INPP5E is determined by the small GTPase ARL13B. However, it remained unclear as to how ARL13B participates in the localization of INPP5E. We here show that wild-type INPP5E, INPP5E(WT), in ARL13B-knockout cells and an INPP5E mutant defective in ARL13B binding, INPP5E(ΔCTS), in control cells were unable to show steady-state localization on the ciliary membrane. However, not only INPP5E(WT) but also INPP5E(ΔCTS) was able to rescue the abnormal localization of ciliary proteins in INPP5E-knockout cells. Analysis using the chemically induced dimerization system demonstrated that INPP5E(WT) in ARL13B-knockout cells and INPP5E(ΔCTS) in control cells were able to enter cilia, but neither was retained on the ciliary membrane due to the lack of the INPP5E-ARL13B interaction. Thus, our data demonstrate that binding of INPP5E to ARL13B is essential for its steady-state localization on the ciliary membrane but is dispensable for its entry into cilia.