Examining palliative and end of life care research in Ireland within a global context: a systematic mapping review of the evidence

Background: Globally the state of palliative care research remains uncertain. Questions remain regarding impact, funding, and research priorities. Building upon previous research, this review examines palliative care research in Ireland and contributes to a wider international debate on the state of palliative care research. Methods: A systematic mapping review was undertaken. Eight bibliographic databases and thesis repositories were searched from May 2012 to April 2017. Palliative care related search terms were combined with "Ireland" or "Irish" to increase search sensitivity. Inclusion criteria were applied by two independent reviewers. Descriptive analysis was completed using IBM SPSS v23. Thematic analysis was undertaken using a data-driven approach to develop new themes. Results: In total, 808 studies were screened and 151 papers from 117 studies were included for review. The top two areas of research focus included: (1) specific groups, services, and settings (n = 70); and (2) identification, communication and education (n = 37). A diverse variety of research methods were used including mixed methods (25%), surveys (22%), interviews (20%), and reviews (17%). One randomised control trial was conducted. The predominance of research papers focused solely on health care professionals (n = 35%), and the community setting was the most frequent location for data collection (41%). The majority of data was collected across the two jurisdictions of the Republic of Ireland (ROI) and Northern Ireland (NI) (37%), and 23% of studies included data outside of Ireland and the UK. The most frequent sources of funding were: consortiums (n = 40); government (n = 24); and philanthropic bodies (n = 20). Forty percent (n = 60) of papers were either unfunded or did not acknowledge a funder. Conclusions: There is a continued increase in palliative care research in Ireland with increased collaborative working nationally and internationally. The quantity and impact of research has increased from the previous review, which can be attributed to significant investment in research funding and collaborative networks. However, research gaps continue to exist including out of hours' care, physical and psychological symptom control, intervention studies, and the patient and family perspective. Areas for attention include the need to ensure knowledge exchange and demonstrate impact of the research on patient and family carer outcomes. © 2018 The Author(s)

Palliative and end-of-life educational interventions for staff working in long-term care facilities: An integrative review of the literature

Background: Given the increase in the number of deaths within long-term care facilities (LTCFs), the need for palliative and end-of-life (EOL) care education among such facilities has been increasing. As such, a systematic synthesis of global palliative and EOL care educational approaches and evaluation can aid further educational development. Objective: To synthesise the current literature on palliative and EOL care educational interventions for staff working in LTCFs and identify barriers to, and facilitators of, intervention implementation. Methods: The study used an integrative review framework wherein indexed databases, namely, CINAHL, EMBASE, MEDLINE, PsycINFO, Web of Science, Cochrane Library and Japan Medical Abstract Society, were systematically searched for studies published in English and Japanese between 2007 and 2019. Search terms that are related to palliative care, LTCF, and education were combined to increase search sensitivity. The quality of the papers was assessed using Joanna Briggs Institute Critical Appraisal Tools and the Mixed-Methods Appraisal Tool. Results: A total of 52 studies were included in the review. Our results suggested that although studies in this area and setting have been evolving, suboptimal developmental research and educational practices, global variability and unstandardised approaches to education and lacking viewpoints from service users have remained. Barriers to intervention implementation were also reported due to the specific characteristics of LTCFs, which include high staff turnover and considerable variation in professional skills and experience. Conclusions: Given the different LTCF types, systems and policies across each country or region, further research on standardised educational interventions with contextual considerations using large-scale studies with robust methodology is needed to meet the increasing demand for palliative and EOL care among the global ageing population. Implications for practice: Palliative and EOL care educational intervention for LTCF staff need to include more consideration of context, organisational culture and the user involvement throughout the process of education and research to enhance the quality of care in this complex setting. © 2020 The Authors. International Journal of Older People Nursing published by John Wiley & Sons Lt

Small habitat matrix: How does it work?

We present herein our perspective of a novel Small Habitats Matrix (SHM) concept showing how small habitats on private lands are untapped but can be valuable for mitigating ecological degradation. Grounded by the realities in Sabah, Malaysian Borneo, we model a discontinuous “stepping stones” linkage that includes both terrestrial and aquatic habitats to illustrate exactly how the SHM can be deployed. Taken together, the SHM is expected to optimize the meta-population vitality in monoculture landscapes for aerial, arboreal, terrestrial and aquatic wildlife communities. We also provide the tangible cost estimates and discuss how such a concept is both economically affordable and plausible to complement global conservation initiatives. By proposing a practical approach to conservation in the rapidly developing tropics, we present a perspective from “ground zero” that reaches out to fellow scientists, funders, activists and pro-environmental land owners who often ask, “What more can we do?

The metabolic syndrome- associated small G protein ARL15 plays a role in adipocyte differentiation and adiponectin secretion.

Common genetic variants at the ARL15 locus are associated with plasma adiponectin, insulin and HDL cholesterol concentrations, obesity, and coronary atherosclerosis. The ARL15 gene encodes a small GTP-binding protein whose function is currently unknown. In this study adipocyte-autonomous roles for ARL15 were investigated using conditional knockdown of Arl15 in murine 3T3-L1 (pre)adipocytes. Arl15 knockdown in differentiated adipocytes impaired adiponectin secretion but not adipsin secretion or insulin action, while in preadipocytes it impaired adipogenesis. In differentiated adipocytes GFP-tagged ARL15 localized predominantly to the Golgi with lower levels detected at the plasma membrane and intracellular vesicles, suggesting involvement in intracellular trafficking. Sequencing of ARL15 in 375 severely insulin resistant patients identified four rare heterozygous variants, including an early nonsense mutation in a proband with femorogluteal lipodystrophy and non classical congenital adrenal hyperplasia, and an essential splice site mutation in a proband with partial lipodystrophy and a history of childhood yolk sac tumour. No nonsense or essential splice site mutations were found in 2,479 controls, while five such variants were found in the ExAC database. These findings provide evidence that ARL15 plays a role in adipocyte differentiation and adiponectin secretion, and raise the possibility that human ARL15 haploinsufficiency predisposes to lipodystrophy

Truncation of POC1A associated with short stature and extreme insulin resistance.

We describe a female proband with primordial dwarfism, skeletal dysplasia, facial dysmorphism, extreme dyslipidaemic insulin resistance and fatty liver associated with a novel homozygous frameshift mutation in POC1A, predicted to affect two of the three protein products of the gene. POC1A encodes a protein associated with centrioles throughout the cell cycle and implicated in both mitotic spindle and primary ciliary function. Three homozygous mutations affecting all isoforms of POC1A have recently been implicated in a similar syndrome of primordial dwarfism, although no detailed metabolic phenotypes were described. Primary cells from the proband we describe exhibited increased centrosome amplification and multipolar spindle formation during mitosis, but showed normal DNA content, arguing against mitotic skipping, cleavage failure or cell fusion. Despite evidence of increased DNA damage in cells with supernumerary centrosomes, no aneuploidy was detected. Extensive centrosome clustering both at mitotic spindles and in primary cilia mitigated the consequences of centrosome amplification, and primary ciliary formation was normal. Although further metabolic studies of patients with POC1A mutations are warranted, we suggest that POC1A may be added to ALMS1 and PCNT as examples of centrosomal or pericentriolar proteins whose dysfunction leads to extreme dyslipidaemic insulin resistance. Further investigation of links between these molecular defects and adipose tissue dysfunction is likely to yield insights into mechanisms of adipose tissue maintenance and regeneration that are critical to metabolic health.This work was supported by the Wellcome Trust [grant numbers WT098498, WT098051,WT095515, and WT091310]; the Medical Research Council [MRC_MC_UU_12012/5]; the United Kingdom National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre.This is the final version of the article. It first appeared from Bioscientifica via http://dx.doi.org/10.1530/JME-15-009

The candidate genes TAF5L, TCF7, PDCD1, IL6 and ICAM1 cannot be excluded from having effects in type 1 diabetes.

BACKGROUND: As genes associated with immune-mediated diseases have an increased prior probability of being associated with other immune-mediated diseases, we tested three such genes, IL23R, IRF5 and CD40, for an association with type 1 diabetes. In addition, we tested seven genes, TAF5L, PDCD1, TCF7, IL12B, IL6, ICAM1 and TBX21, with published marginal or inconsistent evidence of an association with type 1 diabetes. METHODS: We genotyped reported polymorphisms of the ten genes, nonsynonymous SNPs (nsSNPs) and, for the IL12B and IL6 regions, tag SNPs in up to 7,888 case, 8,858 control and 3,142 parent-child trio samples. In addition, we analysed data from the Wellcome Trust Case Control Consortium genome-wide association study to determine whether there was any further evidence of an association in each gene region. RESULTS: We found some evidence of associations between type 1 diabetes and TAF5L, PDCD1, TCF7 and IL6 (ORs = 1.05 - 1.13; P = 0.0291 - 4.16 x 10-4). No evidence of an association was obtained for IL12B, IRF5, IL23R, ICAM1, TBX21 and CD40, although there was some evidence of an association (OR = 1.10; P = 0.0257) from the genome-wide association study for the ICAM1 region. CONCLUSION: We failed to exclude the possibility of some effect in type 1 diabetes for TAF5L, PDCD1, TCF7, IL6 and ICAM1. Additional studies, of these and other candidate genes, employing much larger sample sizes and analysis of additional polymorphisms in each gene and its flanking region will be required to ascertain their contributions to type 1 diabetes susceptibility.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Polymorphism discovery and association analyses of the interferon genes in type 1 diabetes.

BACKGROUND: The aetiology of the autoimmune disease type 1 diabetes (T1D) involves many genetic and environmental factors. Evidence suggests that innate immune responses, including the action of interferons, may also play a role in the initiation and/or pathogenic process of autoimmunity. In the present report, we have adopted a linkage disequilibrium (LD) mapping approach to test for an association between T1D and three regions encompassing 13 interferon alpha (IFNA) genes, interferon omega-1 (IFNW1), interferon beta-1 (IFNB1), interferon gamma (IFNG) and the interferon consensus-sequence binding protein 1 (ICSBP1). RESULTS: We identified 238 variants, most, single nucleotide polymorphisms (SNPs), by sequencing IFNA, IFNB1, IFNW1 and ICSBP1, 98 of which where novel when compared to dbSNP build 124. We used polymorphisms identified in the SeattleSNP database for INFG. A set of tag SNPs was selected for each of the interferon and interferon-related genes to test for an association between T1D and this complex gene family. A total of 45 tag SNPs were selected and genotyped in a collection of 472 multiplex families. CONCLUSION: We have developed informative sets of SNPs for the interferon and interferon related genes. No statistical evidence of a major association between T1D and any of the interferon and interferon related genes tested was found.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are