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Studies of people living with HIV who are homeless or unstably housed show a high prevalence of food insufficiency (>50%) and associated poor health outcomes; however, most evidence is in the form of cross-sectional studies. To better understand this issue, we conducted a longitudinal study to examine the impact of food insufficiency and housing instability on overall physical and mental health-related quality of life (HRQoL) among people living with HIV in Ontario. Six hundred and two adults living with HIV were enrolled in the Positive Spaces, Healthy Places study and followed from 2006 to 2009. Interviewer-administered questionnaires were used, and generalized linear mixed-effects models constructed to examine longitudinal associations between food insufficiency, housing instability and physical and mental HRQoL. At baseline, 57% of participants were classified as food insufficient. After adjusting for potential confounders, longitudinal analyses revealed a significant, negative association between food insufficiency and physical and mental HRQoL outcomes, respectively [effect size (ES) with 95% confidence interval (CI): (ES = −2.1, CI = −3.9,−0.3); (ES = −3.5, CI = −6.1,−1.5)]. Furthermore, difficulties meeting housing costs were shown to have additional negative impacts on mental HRQoL. Food insufficiency is highly prevalent among people living with HIV in Ontario, particularly for those with unstable housing. This vulnerable group of individuals is in urgent need of changes to current housing programmes, services and policies, as well as careful consideration of their unmet nutritional needs. [ABSTRACT FROM AUTHOR]

Koornstra J J, Rijcken F E M, de Jong S, Hollema H, de Vries E G E & Kleibeuker J H (2004) Histopathology 44, 9–17 Assessment of apoptosis by M30 immunoreactivity and the correlation with morphological criteria in normal colorectal mucosa, adenomas and carcinomas : To investigate the monoclonal antibody M30 for the assessment of apoptosis in colorectal tissues. Although Terminal deoxyribonucleotidyl transferase mediated nick end labelling (TUNEL) and in-situ end labelling (ISEL) are the methods most often used to demonstrate and quantify apoptosis in histological tissue sections, the interpretation and specificity of these techniques have been controversial. Immunohistochemistry using the monoclonal antibody M30 that recognizes caspase-cleaved cytokeratin 18 is considered to be a promising alternative but has yet to be validated against a generally accepted standard. : Paraffin sections of normal colonic mucosa ( n = 30), normal mucosa obtained from resection margins from carcinomas ( n = 30), colorectal adenomas ( n = 84) and carcinomas ( n = 40) were studied. Apoptosis of epithelial cells was assessed by M30 immunoreactivity and morphological criteria and expressed as a proportion of the total number of cells counted (apoptotic index). Mean apoptotic indices using M30 were 0.18 ± 0.04% in normal mucosa, 0.42 ± 0.04% in adenomas and 1.97 ± 0.24% in carcinomas. Using morphological criteria, these indices were 0.23 ± 0.03%, 0.62 ± 0.06% and 1.78 ± 0.19%, respectively. Apoptotic counts were higher in normal mucosa obtained from resection margins than in genuinely normal mucosa using the M30 antibody. Apoptotic indices obtained by M30 immunoreactivity and morphological criteria were positively correlated ( r = 0.71, P < 0.01). : Assessment of apoptotic cells by M30 immunoreactivity correlates well with morphological criteria. Apoptotic indices increase in the course of the adenoma–carcinoma sequence. Apoptosis in normal mucosa obtained from resection margins differs from genuinely normal mucosa necessitating caution when interpreting studies of apoptosis in normal colonic mucosa. Our findings support the use of the M30 method in the study of apoptosis in colorectal tissues. [ABSTRACT FROM AUTHOR]

Background: Fundic gland polyps (FGPs) occur in both syndromic and sporadic form. Syndromic FGPs arise through mutations in the adenomatous polyposis coli (APC) gene, whereas sporadic FGPs are caused by Β-catenin gene mutations. Dysplasia in sporadic FGPs, found less often than in syndromic FGPs, was recently associated with APC rather than Β-catenin mutations. These data suggest different functional consequences of APC and Β-catenin mutations. To investigate this hypothesis, we examined proliferative activity, degree of apoptosis, β-catenin expression and p53 expression in syndromic and sporadic FGPs. Methods: Syndromic FGPs ( n = 9) from familial adenomatous polyposis (FAP) patients and sporadic FGPs ( n = 18) were studied. Proliferative activity, apoptotic cell death and expression of β-catenin and p53 were examined by immunohistochemistry. In FGPs containing dysplasia, areas with and without dysplasia were compared. Results: Syndromic and sporadic FGPs without dysplasia exhibited similar proliferative activity, degree of apoptosis, β-catenin and p53 expression. Dysplasia was observed more often in syndromic (4/9) than in sporadic FGPs (1/18). Within FGPs containing dysplasia, dysplastic areas showed abnormal nuclear β-catenin staining in 3/5 cases and higher rates of cell proliferation and apoptosis than non-dysplastic areas. Overexpression of p53 was not observed. Conclusion: The finding of similar rates of proliferation and apoptosis in syndromic and sporadic FGPs does not support the hypothesis that APC and Β-catenin gene mutations have different functional consequences in FGPs. The association of dysplasia with relatively high cell turnover rates and nuclear expression of Β- catenin indicates activation of the Wnt-APC-β-catenin pathway in dysplasia. The finding of dysplasia in some but not all syndromic FGPs suggests the involvement of other genes in addition to the APC gene in the development of dysplasia in FGPs. [ABSTRACT FROM AUTHOR]