Gastrointestinal Issues in Infants and Children with Autism and Developmental Delays

Controversy exists regarding whether gastrointestinal (GI) issues play a role in the symptomatology of autism spectrum disorder (ASD). While some studies have found GI problems to be more prevalent in individuals with ASD, others have reported no such difference. Studies looking at the relationship between GI issues and ASD symptom severity have also had mixed results. The current study examined 112 participants between the age of 17 to 37 months. Participants comprised four groups of 28 children: an ASD and no GI issues group, an ASD with GI problems group, an atypical development and no GI issues group, and an atypical development with GI issues group. The results of the current study suggest that although the prevalence of GI symptoms was higher in participants with ASD than those without, this difference was not significant. The study also found that GI issues were not related to ASD symptom severity or developmental functioning.     

Anti-phospholipid syndrome: Current opinion on mechanisms involved,laboratory characterization and diagnostic aspects

Anti-phospholipid syndrome is a complex and severe clinical situation, associated with symptoms such as recurrent thrombosis, arterial or venous, at any site, pregnancy loss, and other related syndromes. These clinical burdens, are highly variable from patient to patient, and are associated with biological abnormalities, such as the presence of the Lupus Anticoagulant or phospholipid dependent antibodies, confirmed on two occasions at least 12 weeks apart. From the diagnosis standpoint, both, functional (clotting) or immunological assays, are difficult to standardize and to optimize, due to the absence of reference material, or a characteristic clinical group, and international reference preparations. Large cohort studies are necessary for defining the usefulness of each assay, in terms of specificity, sensitivity, accuracy and for following-up the disease evolution. Clotting assays are based on Activated Partial Thromboplastin Time (APTT) and diluted Russell Viper Venom Time (dRVVT), performed at low and high phospholipid concentration, or on 1:1 mixtures of tested sample and a normal plasma pool. They allow evaluation of the paradoxal effects of LAs, which are pro-thrombotic in vivo, and anticoagulant in vivo. Use of synthetic phospholipids improves assay specificities and sensitivities, especially in patients treated with anticoagulants. Immunoassays can also be used for testing phospholipid dependent antibodies, first identified and measured as anti-cardiolipin antibodies, but now characterized as targeted to phospholipid cofactor proteins: mainly β2GP1 (which exposes cryptic epitopes upon binding to phospholipids), and in some cases prothrombin, and more rarely Protein S, Factor XIII, Protein Z or Annexin V. Use of optimized assays designed with well-characterized anionic phospholipids, then complexed with highly purified phospholipid cofactor protein (mainly β2GP1), offers a better link between reactivity and clinical associations, than the former assays which were empirically designed with cardiolipin. Standardization also remains complicated due to the absence of international standards and harmonized quantitation units. Validation on large cohorts of negative and positive patients remains the key approach for defining assay performance and clinical usefulness. Laboratory practice for all these methods is now greatly facilitated thanks to the use of automated instruments and dedicated software. Along with clinical criteria, laboratory assays are of great usefulness for identification and confirmation of the anti-phospholipid syndrome and they allow disease follow-up when appropriate patient management is in place.     

Persistence of autoreactive myelin oligodendrocyte glycoprotein (MOG)-specific T cell repertoires in MOG-expressing mice

Experimental autoimmune encephalomyelitis, an experimental murine model for multiple sclerosis, is induced by stimulation of myelin-specific T lymphocytes. Myelin oligodendrocyte glycoprotein (MOG), a minor component of myelin proteins, is a potent autoantigen which contributes extensively to the anti-myelin response. In the present work, immunoscope analyses and sequencing of the oligoclonal expansions revealed anti-MOG Valpha and Vbeta public repertoires in lymphocytes infiltrating the CNS of wild-type (WT) mice. Moreover, a subset of CNS-infiltrating CD4+ T lymphocytes bearing the public Vbeta8.2 segment have an inflammatory phenotype strongly suggesting that it is encephalitogenic. We then observed that, in lymph node cells of MOG-deficient and WT animals, the Valpha and Vbeta public repertoires expressed by MOG-specific T cells are identical in both strains of mice and correspond to those found in the CNS of WT animals. These findings indicate that the MOG immunodominant determinant is unable to induce tolerance by deletion, and public anti-MOG T cell repertoires are selected for, regardless of the presence of MOG in the thymus and peripheral organs.     

Trends in private and public health insurance for adolescents

Context  Previous studies (1984-1995) of adolescent health insurance have shown little change in the proportion with coverage. Federally mandated expansions in Medicaid were offset by declines in private coverage. Further expansions of Medicaid and implementation of the State Children's Health Insurance Program (SCHIP) have opened new avenues for increasing coverage rates. Objectives  To assess the current health insurance status of adolescents, the demographic and socioeconomic correlates of insurance coverage, and document recent changes in public and private coverage rates. Design, Setting, and Participants  We analyzed data on 12 995 adolescents aged 10 to 18 years, who had been included in the 2002 National Health Interview Survey. We conducted multivariate analyses to assess the independent association of age, sex, race, poverty status, family structure, family size, and region on the likelihood of having insurance coverage. Results are compared with previously published findings on adolescent health insurance coverage spanning 1984 to 1995. Main Outcome Measure  Insurance coverage for adolescents. Results  An estimated 12.2% of adolescents were uninsured in 2002, which is a decrease from 14.1% in 1995 (P<.003). The decrease occurred entirely because of an expansion of public coverage and is concentrated among children in poor (<100% of the federal poverty level) and near-poor (100%-199% of the federal poverty level) families. A substantial decrease in the differences between poor and higher-income groups occurred between 1995 and 2002 due to gains in coverage for adolescents in poor and near-poor families and losses in coverage among those in middle- and upper-income families (=" BORDER="0">200% of the federal poverty level). Specifically, the proportion of adolescents in poor families without coverage declined from 27.4% in 1995 to 19.7% in 2002 (P<.001). The proportion of adolescents in near-poor families without coverage declined from 24.8% in 1995 to 19.2% in 2002 (P<.002). In contrast, the proportion of adolescents in middle- and higher-income families without insurance increased from 4.1% in 1995 to 6.3% in 2002 because availability of insurance through the private market declined (P<.001). Conclusions  A modest but significant reduction in the percentage of adolescents without insurance has occurred since 1995, largely as a result of expansions in public coverage. An even larger reduction in the proportion of adolescents without coverage would have occurred, if not for a reduction in private coverage for adolescents in middle- and higher-income families.      

What about N? A methodological study of sample-size reporting in focus group studies

Background  

Focus group studies are increasingly published in health related journals, but we know little about how researchers use this method, particularly how they determine the number of focus groups to conduct. The methodological literature commonly advises researchers to follow principles of data saturation, although practical advise on how to do this is lacking. Our objectives were firstly, to describe the current status of sample size in focus group studies reported in health journals. Secondly, to assess whether and how researchers explain the number of focus groups they carry out.