The role of childhood social position in adult type 2 diabetes: Evidence from the English Longitudinal Study of Ageing

Copyright @ 2014 Pikhartova et al. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.This article has been made available through the Brunel Open Access Publishing Fund.Background: Socioeconomic circumstances in childhood and early adulthood may influence the later onset of chronic disease, although such research is limited for type 2 diabetes and its risk factors at the different stages of life. The main aim of the present study is to examine the role of childhood social position and later inflammatory markers and health behaviours in developing type 2 diabetes at older ages using a pathway analytic approach. Methods. Data on childhood and adult life circumstances of 2,994 men and 4,021 women from English Longitudinal Study of Ageing (ELSA) were used to evaluate their association with diabetes at age 50 years and more. The cases of diabetes were based on having increased blood levels of glycated haemoglobin and/or self-reported medication for diabetes and/or being diagnosed with type 2 diabetes. Father's job when ELSA participants were aged 14 years was used as the measure of childhood social position. Current social characteristics, health behaviours and inflammatory biomarkers were used as potential mediators in the statistical analysis to assess direct and indirect effects of childhood circumstances on diabetes in later life. Results: 12.6 per cent of participants were classified as having diabetes. A disadvantaged social position in childhood, as measured by father's manual occupation, was associated at conventional levels of statistical significance with an increased risk of type 2 diabetes in adulthood, both directly and indirectly through inflammation, adulthood social position and a risk score constructed from adult health behaviours including tobacco smoking and limited physical activity. The direct effect of childhood social position was reduced by mediation analysis (standardised coefficient decreased from 0.089 to 0.043) but remained statistically significant (p = 0.035). All three indirect pathways made a statistically significantly contribution to the overall effect of childhood social position on adulthood type 2 diabetes. Conclusions: Childhood social position influences adult diabetes directly and indirectly through inflammatory markers, adulthood social position and adult health behaviours. © 2014Pikhartova et al.; licensee BioMed Central Ltd.Economic and Social Research Council-funded International Centre for Life Course Studies in Society and Health (RES-596-28-0001)

Multigene analyses resolve early diverging lineages in the Rhodymeniophycidae (Florideophyceae, Rhodophyta).

Multigene phylogenetic analyses were directed at resolving the earliest divergences in the red algal subclass Rhodymeniophycidae. The inclusion of key taxa (new to science and/or previously lacking molecular data), additional sequence data (SSU, LSU, EF2, rbcL, COI-5P), and phylogenetic analyses removing the most variable sites (site stripping) have provided resolution for the first time at these deep nodes. The earliest diverging lineage within the subclass was the enigmatic Catenellopsis oligarthra from New Zealand (Catenellopsidaceae), which is here placed in the Catenellopsidales ord. nov. In our analyses Atractophora hypnoides was not allied with the other included Bonnemaisoniales, but resolved as sister to the Peyssonneliales, and is here assigned to Atractophoraceae fam. nov. in the Atractophorales ord. nov. Inclusion of Acrothesaurum gemellifilum gen. et sp. nov. from Tasmania has greatly improved our understanding of the Acrosymphytales, to which we assign three families, the Acrosymphytaceae, Acrothesauraceae fam. nov. and Schimmelmanniaceae fam. nov. This article is protected by copyright. All rights reserved

Analysis of chloroplast genomes and a supermatrix inform reclassification of the Rhodomelaceae (Rhodophyta).

With over a thousand species, the Rhodomelaceae is the most species-rich family of red algae. While its genera have been assigned to 14 tribes, the high-level classification of the family has never been evaluated with a molecular phylogeny. Here, we reassess its classification by integrating genome-scale phylogenetic analysis with observations of the morphological characters of clades. In order to resolve relationships among the main lineages of the family we constructed a phylogeny with 55 chloroplast genomes (52 newly determined). The majority of branches were resolved with full bootstrap support. We then added 266 rbcL, 125 18S rRNA gene and 143 cox1 sequences to construct a comprehensive phylogeny containing nearly half of all known species in the family (407 species in 89 genera). These analyses suggest the same subdivision into higher-level lineages, but included many branches with moderate or poor support. The circumscription for nine of the 13 previously described tribes was supported, but the Lophothalieae, Polysiphonieae, Pterosiphonieae and Herposiphonieae required revision, and five new tribes and one resurrected tribe were segregated from them. Rhizoid anatomy is highlighted as a key diagnostic character for the morphological delineation of several lineages. This work provides the most extensive phylogenetic analysis of the Rhodomelaceae to date and successfully resolves the relationships among major clades of the family. Our data show that organellar genomes obtained through high-throughput sequencing produce well-resolved phylogenies of difficult groups, and their more general application in algal systematics will likely permit deciphering questions about classification at many taxonomic levels

Analysis of chloroplast genomes and a supermatrix inform reclassification of the Rhodomelaceae (Rhodophyta).

With over a thousand species, the Rhodomelaceae is the most species-rich family of red algae. While its genera have been assigned to 14 tribes, the high-level classification of the family has never been evaluated with a molecular phylogeny. Here, we reassess its classification by integrating genome-scale phylogenetic analysis with observations of the morphological characters of clades. In order to resolve relationships among the main lineages of the family we constructed a phylogeny with 55 chloroplast genomes (52 newly determined). The majority of branches were resolved with full bootstrap support. We then added 266 rbcL, 125 18S rRNA gene and 143 cox1 sequences to construct a comprehensive phylogeny containing nearly half of all known species in the family (407 species in 89 genera). These analyses suggest the same subdivision into higher-level lineages, but included many branches with moderate or poor support. The circumscription for nine of the 13 previously described tribes was supported, but the Lophothalieae, Polysiphonieae, Pterosiphonieae and Herposiphonieae required revision, and five new tribes and one resurrected tribe were segregated from them. Rhizoid anatomy is highlighted as a key diagnostic character for the morphological delineation of several lineages. This work provides the most extensive phylogenetic analysis of the Rhodomelaceae to date and successfully resolves the relationships among major clades of the family. Our data show that organellar genomes obtained through high-throughput sequencing produce well-resolved phylogenies of difficult groups, and their more general application in algal systematics will likely permit deciphering questions about classification at many taxonomic levels

A new species of Achnanthes (Bacillariophyceae) from a freshwater habitat in a karst landform from south‐central China

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/151953/1/pre12381.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/151953/2/pre12381_am.pd

HLA Genes, Islet Autoantibodies and Residual C-Peptide at the Clinical Onset of Type 1 Diabetes Mellitus and the Risk of Retinopathy 15 Years Later

HLA genes, islet autoantibodies and residual C-peptide were studied to determine the independent association of each exposure with diabetic retinopathy (DR), 15 years after the clinical onset of type 1 diabetes in 15-34 year old individuals.The cohort was identified in 1992 and 1993 by the Diabetes Incidence Study in Sweden (DISS), which investigates incident cases of diabetes for patients between 15 and 34 years of age. Blood samples at diagnosis were analyzed to determine HLA genotype, islet autoantibodies and serum C-peptide. In 2009, fundus photographs were obtained from patient records. Study measures were supplemented with data from the Swedish National Diabetes Registry.The prevalence of DR was 60.2% (148/246). Autoantibodies against the 65 kD isoform of glutamate decarboxylase (GADA) at the onset of clinical diabetes increased the risk of DR 15 years later, relative risk 1.12 for each 100 WHO units/ml, [95% CI 1.02 to 1.23]. This equates to risk estimates of 1.27, [95% CI 1.04 to 1.62] and 1.43, [95% CI 1.06 to 1.94] for participants in the highest 25(th) (GADA>233 WHO units/ml) and 5(th) percentile (GADA>319 WHO units/ml) of GADA, respectively. These were adjusted for duration of diabetes, HbA(1c), treated hypertension, sex, age at diagnosis, HLA and C-peptide. Islet cell autoantibodies, insulinoma-antigen 2 autoantibodies, residual C-peptide and the type 1 diabetes associated haplotypes DQ2, DQ8 and DQ6 were not associated with DR.Increased levels of GADA at the onset of type 1 diabetes were associated with DR 15 years later. These results, if confirmed, could provide additional insights into the pathogenesis of the most common microvascular complication of diabetes and lead to better risk stratification for both patient screenings and DR treatment trials

The Impact of Socio-Demographic and Religious Factors upon Sexual Behavior among Ugandan University Students

INTRODUCTION: More knowledge is needed about structural factors in society that affect risky sexual behaviors. Educational institutions such as universities provide an opportune arena for interventions among young people. The aim of this study was to investigate the relationship between sociodemographic and religious factors and their impact on sexual behavior among university students in Uganda. METHODS: In 2005, 980 university students (response rate 80%) were assessed by a self-administered questionnaire. Validated instruments were used to assess socio-demographic and religious factors and sexual behavior. Logistic regression analyses were applied. RESULTS: Our findings indicated that 37% of the male and 49% of the female students had not previously had sex. Of those with sexual experience, 46% of the males and 23% of the females had had three or more sexual partners, and 32% of the males and 38% of the females did not consistently use condoms. For those who rated religion as less important in their family, the probability of early sexual activity and having had a high number of lifetime partners increased by a statistically significant amount (OR = 1.7; 95% CI: 1.2-2.4 and OR = 1.6; 95% CI: 1.1-2.3, respectively). However, the role of religion seemed to have no impact on condom use. Being of Protestant faith interacted with gender: among those who had debuted sexually, Protestant female students were more likely to have had three or more lifetime partners; the opposite was true for Protestant male students. CONCLUSION: Religion emerged as an important determinant of sexual behavior among Ugandan university students. Our findings correlate with the increasing number of conservative religious injunctions against premarital sex directed at young people in many countries with a high burden. of HIV/AIDS. Such influence of religion must be taken into account in order to gain a deeper understanding of the forces that shape sexual behavior in Uganda

Association between LTA, TNF and AGER Polymorphisms and Late Diabetic Complications

BACKGROUND: Several candidate genes on the short arm of chromosome 6 including the HLA locus, TNF, LTA and AGER could be associated with late diabetic complications. The aim of our study was therefore to explore whether polymorphisms (TNF -308 G-->A, LTA T60N C-->A and AGER -374 T-->A) in these genes alone or together (as haplotypes) increased the risk for diabetic complications. METHODOLOGY/PRINCIPAL FINDINGS: The studied polymorphisms were genotyped in 742 type 1 and 2957 type 2 diabetic patients as well as in 206 non-diabetic control subjects. The Haploview program was used to analyze putative linkage disequilibrium between studied polymorphisms. The TNF, LTA and AGER polymorphisms were associated with the HLA-DQB1 risk genotypes. The AGER -374 A allele was more common in type 1 diabetic patients with than without diabetic nephropathy (31.2 vs. 28.4%, p = 0.007). In a logistic regression analysis, the LTA but not the AGER polymorphism was associated with diabetic nephropathy (OR 2.55[1.11-5.86], p = 0.03). The AGER -374 A allele was associated with increased risk of sight threatening retinopathy in type 2 diabetic patients (1.65[1.11-2.45], p = 0.01) and also with increased risk for macrovascular disease in type 1 diabetic patients (OR 2.05[1.19-3.54], p = 0.01), but with decreased risk for macrovascular disease in type 2 diabetic patients (OR 0.66[0.49-0.90], p = 0.009). The TNF A allele was associated with increased risk for macrovascular complications in type 2 (OR 1.53 [1.04-2.25], p = 0.03, but not in type 1 diabetic patients. CONCLUSIONS/SIGNIFICANCE: The association between diabetic complications and LTA, TNF and AGER polymorphisms is complex, with partly different alleles conferring susceptibility in type 1 and type 2 diabetic patients. We can not exclude the possibility that the genes are part of a large haplotype block that also includes HLA-DQB1 risk genotypes

Vascular Cellular Adhesion Molecule-1 (VCAM-1) Expression in Mice Retinal Vessels Is Affected by Both Hyperglycemia and Hyperlipidemia

BACKGROUND: Inflammation has been proposed to be important in the pathogenesis of diabetic retinopathy. An early feature of inflammation is the release of cytokines leading to increased expression of endothelial activation markers such as vascular cellular adhesion molecule-1 (VCAM-1). Here we investigated the impact of diabetes and dyslipidemia on VCAM-1 expression in mouse retinal vessels, as well as the potential role of tumor necrosis factor-α (TNFα). METHODOLOGY/PRINCIPAL FINDINGS: Expression of VCAM-1 was examined by confocal immunofluorescence microscopy in vessels of wild type (wt), hyperlipidemic (ApoE(-/-)) and TNFα deficient (TNFα(-/-), ApoE(-/-)/TNFα(-/-)) mice. Eight weeks of streptozotocin-induced diabetes resulted in increased VCAM-1 in wt mice, predominantly in small vessels (<10 µm). Diabetic wt mice had higher total retinal TNFα, IL-6 and IL-1β mRNA than controls; as well as higher soluble VCAM-1 (sVCAM-1) in plasma. Lack of TNFα increased higher basal VCAM-1 protein and sVCAM-1, but failed to up-regulate IL-6 and IL-1β mRNA and VCAM-1 protein in response to diabetes. Basal VCAM-1 expression was higher in ApoE(-/-) than in wt mice and both VCAM-1 mRNA and protein levels were further increased by high fat diet. These changes correlated to plasma cholesterol, LDL- and HDL-cholesterol, but not to triglycerides levels. Diabetes, despite further increasing plasma cholesterol in ApoE(-/-) mice, had no effects on VCAM-1 protein expression or on sVCAM-1. However, it increased ICAM-1 mRNA expression in retinal vessels, which correlated to plasma triglycerides. CONCLUSIONS/SIGNIFICANCE: Hyperglycemia triggers an inflammatory response in the retina of normolipidemic mice and up-regulation of VCAM-1 in retinal vessels. Hypercholesterolemia effectively promotes VCAM-1 expression without evident stimulation of inflammation. Diabetes-induced endothelial activation in ApoE(-/-) mice seems driven by elevated plasma triglycerides but not by cholesterol. Results also suggest a complex role for TNFα in the regulation of VCAM-1 expression, being protective under basal conditions but pro-inflammatory in response to diabetes