Social inequalities in self-rated health by age: Cross-sectional study of 22 457 middle-aged men and women

<p>Abstract</p> <p>Background</p> <p>We investigate the association between occupational social class and self-rated health (SRH) at different ages in men and women.</p> <p>Methods</p> <p>Cross sectional population study of 22 457 men and women aged 39–79 years living in the general community in Norfolk, United Kingdom, recruited using general practice age-sex registers in 1993–1997. The relationship between self-rated health and social class was examined using logistic regression, with a poor or moderate rating as the outcome.</p> <p>Results</p> <p>The prevalence of poor or moderate (lower) self-rated health increased with increasing age in both men and women. There was a strong social class gradient: in manual classes, men and women under 50 years of age had a prevalence of lower self-rated health similar to that seen in men and women in non-manual social classes over 70 years old. Even after adjustment for age, educational status, and lifestyle factors (body mass index (BMI), smoking, physical activity and alcohol consumption) there was still strong evidence of a social gradient in self-rated health, with unskilled men and women approximately twice as likely to report lower self-rated health as professionals (OR_men= 2.44 (95%CI 1.69, 3.50); OR_women= 1.97 (95%CI 1.45, 2.68).</p> <p>Conclusion</p> <p>There was a strong gradient of decreased SRH with age in both men and women. We found a strong cross-sectional association between SRH and social class, which was independent of education and major health related behaviors. The social class differential in SRH was similar with age. Prospective studies to confirm this association should explore social and emotional as well as physical pathways to inequalities in self reported health.</p

Whispering in our hearts: speaking of another in changing schools

Beneath discussions about race and ethnic relations is an unease, \u27a whispering in our hearts\u27 these debates that need to be understood \u27otherwise\u27. In more recent times, they seem increasingly complex and dangerous as the essential differences that underpin modern notions of identity appear negotiated, contingent, and disjunctive. In this paper, I examine the ways in which teachers and parents in one Melbourne secondary school spoke about these notions in 1988 and 1998. Taking up suggestions in the postcolonial and race literatures, the article argues that the normalised notions which make up these conversations need to be made explicit, and the near silences that negotiate the parameters of these discussions should also be the focus of analysis. While at one level teachers and parents discussed their unease and their excitement about the ways their school had changed, their conversations remained underpinned by taken-for-granted understandings about the ways people belong differently within the school community.<br /

The diagnosis and management of gastric cancer: expert discussion and recommendations from the 12th ESMO/World Congress on Gastrointestinal Cancer, Barcelona, 2010

Well-recognized experts in the field of gastric cancer discussed during the 12th European Society Medical Oncology (ESMO)/World Congress Gastrointestinal Cancer (WCGIC) in Barcelona many important and controversial topics on the diagnosis and management of patients with gastric cancer. This article summarizes the recommendations and expert opinion on gastric cancer. It discusses and reflects on the regional differences in the incidence and care of gastric cancer, the definition of gastro-esophageal junction and its implication for treatment strategies and presents the latest recommendations in the staging and treatment of primary and metastatic gastric cancer. Recognition is given to the need for larger and well-designed clinical trials to answer many open question

Plasma amyloid-β ratios in autosomal dominant Alzheimer's disease: the influence of genotype.

In-vitro studies of autosomal dominant Alzheimer's disease implicate longer amyloid-beta peptides in disease pathogenesis, however less is known about the behaviour of these mutations in-vivo. In this cross-sectional cohort study, we used liquid chromatography-tandem mass spectrometry to analyse 66 plasma samples from individuals who were at-risk of inheriting a mutation or were symptomatic. We tested for differences in amyloid-beta42:38, 42:40 and 38:40 ratios between presenilin1 and amyloid precursor protein carriers. We examined the relationship between plasma and in-vitro models of amyloid-beta processing and tested for associations with parental age at onset. 39 participants were mutation carriers (28 presenilin1 and 11 amyloid precursor protein). Age- and sex-adjusted models showed marked differences in plasma amyloid-beta between genotypes: higher amyloid-beta42:38 in presenilin1 versus amyloid precursor protein (p < 0.001) and non-carriers (p < 0.001); higher amyloid-beta38:40 in amyloid precursor protein versus presenilin1 (p < 0.001) and non-carriers (p < 0.001); while amyloid-beta42:40 was higher in both mutation groups compared to non-carriers (both p < 0.001). Amyloid-beta profiles were reasonably consistent in plasma and cell lines. Within presenilin1, models demonstrated associations between amyloid-beta42:38, 42:40 and 38:40 ratios and parental age at onset. In-vivo differences in amyloid-beta processing between presenilin1 and amyloid precursor protein carriers provide insights into disease pathophysiology, which can inform therapy development

Assessment of ROS Production in the Mitochondria of Live Cells

Production of reactive oxygen species (ROS) in the mitochondria plays multiple roles in physiology, and excessive production of ROS leads to the development of various pathologies. ROS in the mitochondria are generated by various enzymes, mainly in the electron transporvt chain, and it is important to identify not only the trigger but also the source of free radical production. It is important to measure mitochondrial ROS in live, intact cells, because activation of ROS production could be initiated by changes in extramitochondrial processes which could be overseen when using isolated mitochondria. Here we describe the approaches, which allow to measure production of ROS in the matrix of mitochondria in live cells. We also demonstrate how to measure kinetic changes in lipid peroxidation in mitochondria of live cells. These methods could be used for understanding the mechanisms of pathology in a variety of disease models and also for testing neuro- or cardioprotective chemicals

The influence of the Cyclin D1 870 G>A polymorphism as an endometrial cancer risk factor

<p>Abstract</p> <p>Background</p> <p>Cyclin D1 is integral for the G1 to S phase of the cell cycle as it regulates cellular proliferation. A polymorphism in cyclin D1, 870 G>A, causes overexpression and supports uncontrollable cellular growth. This polymorphism has been associated with an increased risk of developing many cancers, including endometrial cancer.</p> <p>Methods</p> <p>The 870 G>A polymorphisms (rs605965) in the cyclin D1 gene was genotyped in an Australian endometrial cancer case-control population including 191 cases and 291 controls using real-time PCR analysis. Genotype analysis was performed using chi-squared (χ²) statistics and odds ratios were calculated using unconditional logistic regression, adjusting for potential endometrial cancer risk factors.</p> <p>Results</p> <p>Women homozygous for the variant cyclin D1 870 AA genotype showed a trend for an increased risk of developing endometrial cancer compared to those with the wild-type GG genotype, however this result was not statistically significant (OR 1.692 95% CI (0.939–3.049), p = 0.080). Moreover, the 870 G>A polymorphism was significantly associated with family history of colorectal cancer. Endometrial cancer patients with the homozygous variant AA genotype had a higher frequency of family members with colorectal cancer in comparison to endometrial cancer patients with the GG and combination of GG and GA genotypes (GG versus AA; OR 2.951, 95% CI (1.026–8.491), p = 0.045, and GG+GA versus AA; OR 2.265, 95% CI (1.048–4.894), p = 0.038, respectively).</p> <p>Conclusion</p> <p>These results suggest that the cyclin D1 870 G>A polymorphism is possibly involved in the development of endometrial cancer. A more complex relationship was observed between this polymorphism and familial colorectal cancer.</p

Monocot plastid phylogenomics, timeline, net rates of species diversification, the power of multiâ gene analyses, and a functional model for the origin of monocots

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/1/ajb21178-sup-0009-AppendixS9.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/2/ajb21178-sup-0020-AppendixS20.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/3/ajb21178.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/4/ajb21178-sup-0019-AppendixS19.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/5/ajb21178-sup-0010-AppendixS10.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/6/ajb21178-sup-0002-AppendixS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/7/ajb21178-sup-0006-AppendixS6.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/8/ajb21178-sup-0012-AppendixS12.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/9/ajb21178-sup-0017-AppendixS17.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/10/ajb21178-sup-0007-AppendixS7.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/11/ajb21178-sup-0001-AppendixS1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/12/ajb21178-sup-0003-AppendixS3.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/13/ajb21178-sup-0016-AppendixS16.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/14/ajb21178_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/15/ajb21178-sup-0008-AppendixS8.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/16/ajb21178-sup-0004-AppendixS4.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/17/ajb21178-sup-0018-AppendixS18.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/18/ajb21178-sup-0014-AppendixS14.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/19/ajb21178-sup-0011-AppendixS11.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/20/ajb21178-sup-0005-AppendixS5.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146610/21/ajb21178-sup-0015-AppendixS15.pd