Supplementary Material, Focus_Group_Questions - Does the Design of Settings Where Acute Care Is Delivered Meet the Needs of Older People? Perspectives of Patients, Family Carers, and Staff

<p>Supplementary Material, Focus_Group_Questions for Does the Design of Settings Where Acute Care Is Delivered Meet the Needs of Older People? Perspectives of Patients, Family Carers, and Staff by Annette Haywood, Sarah Barnes, Hazel Marsh and Stuart G. Parker in HERD: Health Environments Research & Design Journal</p

Supplementary Material, Topic_guide_for_qualitative_interviews_with_Older_People_and_their_Family_Carer(s) - Does the Design of Settings Where Acute Care Is Delivered Meet the Needs of Older People? Perspectives of Patients, Family Carers, and Staff

<p>Supplementary Material, Topic_guide_for_qualitative_interviews_with_Older_People_and_their_Family_Carer(s) for Does the Design of Settings Where Acute Care Is Delivered Meet the Needs of Older People? Perspectives of Patients, Family Carers, and Staff by Annette Haywood, Sarah Barnes, Hazel Marsh and Stuart G. Parker in HERD: Health Environments Research & Design Journal</p

A systematic review of discharge arrangements for older people

A systematic review of discharge arrangements for older peopl

Tumour necrosis factor gene complex polymorphisms and haplotypes in chronic obstructive pulmonary disease

We aimed to examine the role of tumour necrosis factor gene complex polymorphisms in subjects with chronic obstructive pulmonary disease (COPD). We hypothesized that individuals possessing polymorphic variants associated with higher TNF secretion would be more susceptible to and/or have more severe disease. Patients with COPD and population controls underwent detailed clinical phenotyping. Genotyping for the tumour necrosis factor-308 and the lymphotoxin alpha NcoI (LTα) polymorphisms was carried out by ‘blinded’ laboratory staff. 361 individuals (220 cases and 141 controls) were recruited. We showed an association between the LTαNcol polymorphism and forced vital capacity (FVC) in a population of older adults with and without COPD. The LTαNcol*2 allele was associated with poorer lung function, under a codominant model, with a fall in FVC (expressed as a percentage of its predicted value) of 3.7% for each copy of the LTαNcol*2 allele possessed (for FVC, regression coefficient (95% CI) = -3.73 (-7.01to -0.44), p=0.026; for FEV1 regression coefficient = -3.56 (-7.80 to 0.70), p = 0.101. However, there was no difference in genotype distribution between the case and control populations. This study adds weight to the suggestion that the TNF gene complex is involved in physiological alterations (FVC) that may affect the development and severity of COPD. The absence of a significant association between the TNF gene-complex polymorphisms in this study does not rule out a modest effect of these polymorphisms on the risk of COPD, as much larger studies are needed to detect modest gene effects on binary disease endpoints

PLAUR polymorphisms and lung function in UK smokers

Background: We have previously identified Urokinase Plasminogen Activator Receptor (PLAUR) as an asthma susceptibility gene. In the current study we tested the hypothesis that PLAUR single nucleotide polymorphisms (SNPs) determine baseline lung function and contribute to the development of Chronic Obstructive Pulmonary Disease (COPD) in smokers. Methods: 25 PLAUR SNPs were genotyped in COPD subjects and individuals with smoking history (n = 992). Linear regression was used to determine the effects of polymorphism on baseline lung function (FEV[subscript 1], FEV[subscript 1]/FVC) in all smokers. Genotype frequencies were compared in spirometry defined smoking controls (n = 176) versus COPD cases (n = 599) and COPD severity (GOLD stratification) using logistic regression. Results: Five SNPs showed a significant association (p < 0.01) with baseline lung function; rs2302524(Lys220Arg) and rs2283628(intron 3) were associated with lower and higher FEV[subscript 1] respectively. rs740587(-22346), rs11668247(-20040) and rs344779(-3666) in the 5'region were associated with increased FEV[subscript 1]/FVC ratio. rs740587 was also protective for COPD susceptibility and rs11668247 was protective for COPD severity although no allele dose relationship was apparent. Interestingly, several of these associations were driven by male smokers not females. Conclusion: This study provides tentative evidence that the asthma associated gene PLAUR also influences baseline lung function in smokers. However the case-control analyses do not support the conclusion that PLAUR is a major COPD susceptibility gene in smokers. PLAUR is a key serine protease receptor involved in the generation of plasmin and has been implicated in airway remodelling

<i>AGER</i> isoform expression in three HBEC donors using RNA Seq.

<p>Structure and abundance of known <i>AGER</i> isoforms in three human bronchial epithelial cell donors illustrating heterogeneity in expression levels. Percentage abundances (% FPKM) were calculated for each donor. Transcripts for full length and soluble <i>AGER</i> were identified at similar low abundancies. FPKM; fragments per kilobase of transcript per million mapped reads.</p

<i>AGER</i> mRNA expression levels in total lung and airway cells.

<p>Q-PCR analysis identified <i>AGER</i> mRNA was highly expressed in total lung and at lower levels in human airway smooth muscle cells (HASM) cells, human bronchial epithelial cells (HBEC) and the BEAS-2BR1 bronchial epithelial cell line, (n = 3).</p

Immunohistochemical analysis of RAGE expression in healthy and COPD lung.

<p>In healthy lung tissue, RAGE was found to be localised to the cytoplasm and membrane. RAGE expression was high in the pneumocytes of alveolar regions (a). The bronchial epithelium showed variable weak to moderate staining (e). In lung tissue of individuals with COPD, RAGE was very strongly immunopositive in the membrane and cytoplasm of the pneumocytes in the alveolar regions (b). The bronchial epithelium from individuals with COPD was weak or immunonegative for the RAGE protein (f). All isotype controls were negative (c, d, g and h). Representative images of one healthy and one COPD lung shown. x10 magnification.</p

Gene expression array data of 38 fetal lungs for the <i>AGER</i> probes.

<p>Expression intensities for the <i>AGER</i> probes 210081_at and 217046_s_at were plotted against the gestational age of each fetal lung sample and showed an increase in expression with fetal lung age. RMA; Robust Multi-array Average. Affymetrix U133 Plus 2 expression array probe 210081_at probes for exon 8 of AGER mRNA whilst 217046_s_at probes AGER exons 7–11’.</p

Fetal lung gene array data for <i>AGER</i> expression across Pseudoglandular and Canalicular stages.

<p>Fetal lung gene array data for <i>AGER</i> expression across Pseudoglandular and Canalicular stages.</p