Sociodemographic and socioeconomic differences in sleep duration and insomnia-related symptoms in Finnish adults

ABSTRACT: BACKGROUND: Poor sleep tends to be patterned by sociodemographic and socioeconomic factors. The aim of this study was to examine the associations of sociodemographic and socioeconomic factors with sleep duration and insomnia-related symptoms across life course. METHODS: We used cross-sectional Health 2000 Survey (2000-2001) among a total of 5,578 adult Finns, aged 30-79 years, representative of adult Finnish population. Data about sociodemographic and socioeconomic circumstances, insomnia-related symptoms over the previous month as well as average sleep duration were collected by questionnaires. Multinomial logistic regression models were adjusted first for gender and age, second for sociodemographic factors, and third for all covariates simultaneously. RESULTS: On average 70% of Finnish adults slept 7-8 hours a day. Frequent insomnia-related symptoms were more prevalent among women (14%) than men (10%). Not being married, not having children, having low education, low income, being unemployed, and being a disability retiree were associated with frequent insomnia-related symptoms. Similar factors were associated with short and long sleep duration. However, childhood socioeconomic position was mostly unrelated to sleep in adulthood except parental education had some associations with short sleep duration. CONCLUSIONS: Disadvantaged socioeconomic position in adulthood, in particular income and employment status, is associated with poorer sleep. When promoting optimal sleep duration and better sleep quality, families with low incomes, unemployed people, and disability retirees should be targeted. Key words: marital status; parental status; education; employment status; household income; residential area; insomnia-related symptoms; sleep duration; life course; self-perceived health.     

Distribution of naive and memory T-cells in photoprovoked and spontaneous skin lesions of discoid lupus erythematosus and polymorphous light eruption

Immune response to ultraviolet radiation-modified skin antigens has been suggested as a pathomechanism of skin lesions in discoid lupus erythematosus and polymorphous light eruption. In order to elucidate the role of T-lymphocyte subsets in this response, we studied the distribution of CD45RO+, CD45RA+ and CD31+ cells and the endothelial expression of adhesion molecules E-selectin/P-selectin, intercellular adhesion molecule-1 and CD31 antigen in photoprovoked and spontaneous skin lesions. Typically, CD45RA+ cells were the prevailing inflammatory cell population of discoid lupus erythematosus, whereas CD45RO+ cells prevailed in both diseases and in healthy controls. Epidermotrophism of any T-cell subsets was more typical of discoid lupus erythematosus, whereas no major differences in endothelial adhesion molecule expression was found between the 2 diseases. Strong keratinocyte ICAM-1 expression was associated with adjacent CD45RO+ cell infiltrates, not with CD45RA+ or CD31+ cell infiltrates. We conclude that the cellular immune response to UV radiation is dissimilar in discoid lupus erythematosus and polymorphous light eruption.     

Analysis of Cdh22 expression and function in the developing mouse brain

Classical cadherins are important cell adhesion molecules specifying and separating brain nuclei and developmental compartments. Cadherin‐22 (Cdh22) belongs to type II subfamily of classical cadherins, and is expressed at the midbrain‐hindbrain boundary during early embryogenesis. In Fgfr1 mutant mouse embryos, which have a disturbed midbrain‐hindbrain border, Cdh22 is down‐regulated. Here, we studied expression of Cdh22 in developing mouse brain in more detail and compared it to expression of related family members. This revealed both complementary and overlapping patterns of Cdh22, Cdh11, Cdh8, and Cdh6 expression in distinct regions of the forebrain and midbrain. We used a mutated allele of Cdh22 to study its function in brain development. Loss of Cdh22 caused reduced postnatal viability. Despite strong Cdh22 expression in the developing brain, we did not observe defects in compartmentalization or abnormalities in the midbrain and forebrain nuclei in Cdh22 mutants. This may be explained by functional redundancy between type II cadherins. Developmental Dynamics 240:1989–2001, 2011. © 2011 Wiley‐Liss, Inc.     

The i blood group antigen as a marker for umbilical cord blood-derived mesenchymal stem cells

Multipotent mesenchymal stem cells (MSCs) offer great promise for future regenerative and anti-inflammatory therapies. However, there is a lack of methods to quickly and efficiently isolate, characterize, and ex vivo expand desired cell populations for therapeutic purposes. Single markers to identify cell populations have not been characterized; instead, all characterizations rely on panels of functional and phenotypical properties. Glycan epitopes can be used for identifying and isolating specific cell types from heterogeneous populations, on the basis of their cell-type specific expression and prominent cell surface localization. We have now studied in detail the cell surface expression of the blood group i epitope (linear poly-N-acetyllactosamine chain) in umbilical cord blood (UCB)-derived MSCs. We used flow cytometry and mass spectrometric glycan analysis and discovered that linear poly-N-acetyllactosamine structures are expressed in UCB-derived MSCs, but not in cells differentiated from them. We further verified the findings by mass spectrometric glycan analysis. Gene expression analysis indicated that the stem-cell specific expression of the i antigen is determined by β3-N-acetylglucosaminyltransferase 5. The i antigen is a ligand for the galectin family of soluble lectins. We found concomitant cell surface expression of galectin-3, which has been reported to mediate the immunosuppressive effects exerted by MSCs. The i antigen may serve as an endogenous ligand for this immunosuppressive agent in the MSC microenvironment. Based on these findings, we suggest that linear poly-N-acetyllactosamine could be used as a novel UCB-MSC marker either alone or within an array of MSC markers.     

Disruption of the neurexin 1 gene is associated with schizophrenia

Deletions within the neurexin 1 gene (NRXN1; 2p16.3) are associated with autism and have also been reported in two families with schizophrenia. We examined NRXN1, and the closely related NRXN2 and NRXN3 genes, for copy number variants (CNVs) in 2977 schizophrenia patients and 33 746 controls from seven European populations (Iceland, Finland, Norway, Germany, The Netherlands, Italy and UK) using microarray data. We found 66 deletions and 5 duplications in NRXN1, including a de novo deletion: 12 deletions and 2 duplications occurred in schizophrenia cases (0.47%) compared to 49 and 3 (0.15%) in controls. There was no common breakpoint and the CNVs varied from 18 to 420 kb. No CNVs were found in NRXN2 or NRXN3. We performed a Cochran-Mantel-Haenszel exact test to estimate association between all CNVs and schizophrenia (P = 0.13; OR = 1.73; 95% CI 0.81-3.50). Because the penetrance of NRXN1 CNVs may vary according to the level of functional impact on the gene, we next restricted the association analysis to CNVs that disrupt exons (0.24% of cases and 0.015% of controls). These were significantly associated with a high odds ratio (P = 0.0027; OR 8.97, 95% CI 1.8-51.9). We conclude that NRXN1 deletions affecting exons confer risk of schizophrenia.     

NAV3 copy number changes and target genes in basal and squamous cell cancers

The neuron navigator 3 (NAV3) gene on chromosome 12q21 encodes a microtubule plus end tracking protein and belongs to the navigator family of cytoskeletal regulators. Loss of heterozygosity on 12q has previously been suggested to be associated with poor prognosis in cancers of epithelial origin. In this study, we characterized copy number changes of NAV3 in 24 basal cell cancers (BCCs), eight squamous cell cancers (SCCs) and eight non-malignant inflammatory skin lesions by fluorescent in situ hybridization. To identify genes affected by NAV3, we used oligo siRNA gene silencing and gene microarrays to analyse gene expression profiles at several time points post-transfection in primary human keratinocytes. We found NAV3 copy number loss and decreased protein expression in 21% of the BCCs and 25% of the SCCs. In the nodular/superficial BCC subgroup, low-level NAV3 amplification was also observed. NAV3 aberrations were independent of the known chromosome 6 amplifications in BCC. Chromosome 12 polysomy was detected in 33% and 25% of the invasive type of BCC and SCC, respectively. Silencing of NAV3 in primary human keratinocytes revealed 22 differentially expressed genes, mostly related to inflammation. The most relevant of these were validated with qPCR or immunohistochemistry. This pilot study suggests that NAV3 is a novel cancer-associated gene that contributes to the pathogenesis of a subgroup of BCC and SCC.     

Antibodies to retroviral proteins in autoimmune connective tissue disease. Relation to clinical manifestations and ribonucleoprotein autoantibodies

Objective. To study the relationship between antibodies that recognize human retroviral proteins and the presence of clinical features and ribonucleoprotein antibodies in patients with autoimmune connective tissue diseases (CTDs). Methods. Antibodies against native human immunodeficiency virus type 1 (HIV-1) and human T cell leukemia/lymphoma virus type I, recombinant HIV-1 Nef protein, and ribonucleoprotein antigens were determined by immunoblot of sera from 65 prospectively studied patients with definite or suspected CTDs of autoimmune type. Results. Antibodies to retroviral proteins (ARP), most frequently to HIV Gag proteins p55 and p24, were found in 64% of 22 patients with systemic lupus erythematosus (SLE), in 63% of 8 patients with discoid LE (DLE), in 75% of 8 patients with mixed connective tissue disease (MCTD), and in 26% of 19 individuals with chronic biologically false-positive (CBFP) seroreactions, but not in 8 patients with subacute cutaneous lupus erythematosus. No clear correlation of ARP with antibodies to any specific small nuclear RNP antigen was observed. The most striking finding was that recurrent infections, both in LE patients and in those with CBFP reactions and widespread, acral discoid skin lesions, occurred significantly more often in ARP-positive patients. Conclusion. The occurrence of antibodies reacting with human retroviral proteins is associated with severe skin lesions and recurrent infections in SLE, DLE, and MCTD patients, and with a disposition toward developing systemic disease in CBFP reactors.