Are adolescents more likely to have antenatal anxiety disorders than adult women? A comparison between two samples.

BACKGROUND: The literature reports that teenage pregnancy is considered a risk factor for anxiety disorders (ADs). However, research on this topic is limited. This study aimed to investigate if pregnant adolescents presented a greater likelihood of having ADs by comparing two samples of pregnant women in a southern city of Brazil. We also observed the prevalence rates of antenatal ADs among adolescents and adult women. METHODS: In this cross-sectional study, we evaluated 1852 women from two different studies: 995 pregnant adolescents attending prenatal care in the public health system (convenience sample) and 857 pregnant women from a population-based study. We used the Mini International Neuropsychiatric Interview (MINI Plus) to assess antenatal ADs, using the Social Anxiety Disorder (SAD) and Generalized Anxiety Disorder (GAD) modules. The primary aim of this study was tested through multivariate analysis using Poisson regression. RESULTS: The prevalence of ADs was 11.0 % among pregnant adolescents and 13.8 % among adult pregnant women. Both samples presented similar rates of ADs (p = 0.065). In the adjusted analysis, maternal age did not predict antenatal ADs (PR = 0.97; p = 0.853). LIMITATIONS: Considering the particularities of each study where the samples came from, it was not possible to include other ADs such as panic disorder or phobias. CONCLUSIONS: Our findings suggest that pregnancy in adolescence does not increase the likelihood of antenatal ADs. However, we emphasize the importance of an adequate psychological screening and care in pregnancy in order to prevent possible psychiatric disorders.

Influence of different surface treatments on two-body wear and fracture load of monolithic CAD/CAM ceramics.

OBJECTIVES: To investigate two-body wear (2BW) and fracture load (FL) of monolithic ceramics after different surface pretreatments. MATERIALS AND METHODS: Zirconia (MOZ), lithium-disilicate (LIT), and leucite-reinforced (LEU) specimens (n = 60/group) were manufactured with CAD/CAM-technology and underwent (n = 15/subgroup): 1) grinding + polishing (GrPo), 2) grinding + glazing (GrGz), 3) grinding (Gr), or 4) glazing (Gz). Scanning electron microscope (n = 3/subgroup) and 3D measurements of the ceramic crowns and antagonists (N = 180) were performed to determine 2BW before and after 120,000/1,200,000 masticatory cycles. FL was examined for all specimens (N = 180). Data were analyzed using Kolmogorov-Smirnov, one-way ANOVA, Scheffé post hoc, Kruskal-Wallis, Mann-Whitney-U, and Wilcoxon (p < 0.05). RESULTS: MOZ presented the highest FL independent on pretreatment (6960-9250 N), while LEU (1405-2320 N) showed the lowest (p < 0.001). Ceramic and antagonist wear increased between 120,000 and 1,200,000 masticatory cycles (p < 0.001). For pretreatments GrPo, GrGz, and Gz, MOZ showed the lowest wear of the ceramic, while causing the highest antagonist wear (p < 0.001). GrPo resulted in the lowest wear for MOZ (p < 0.001), with Gr leading to the highest antagonist wear (p = 0.008). LIT specimens presented the highest wear of the ceramic and antagonist after Gz (p < 0.001), while GrPo resulted in the lowest antagonist wear (p < 0.001). GrGz led to the highest antagonist wear for LEU (p < 0.001). CONCLUSIONS: With FL exceeding maximum masticatory forces, the three tested ceramics can be recommended for restorations, even in posterior regions. While glazing resulted in higher wear and impaired FL, polishing improved mechanical properties while largely preserving the antagonist. CLINICAL RELEVANCE: While surface pretreatment after grinding is vital to ensure a ceramic's optimal mechanical properties, glazing and polishing varies with regard to material properties, costs, and time.

Circulating AQP4-specific auto-antibodies alone can induce neuromyelitis optica spectrum disorder in the rat.

It is well established that the binding of pathogenic aquaporin-4 (AQP4)-specific autoantibodies to astrocytes may initiate a cascade of events culminating in the destruction of these cells and in the formation of large tissue-destructive lesions typical for patients with neuromyelitis optica spectrum disorders (NMOSD). To date, not a single experimental study has shown that the systemic presence of the antibody alone can induce any damage to the central nervous system (CNS), while pathological studies on brains of NMOSD patients suggested that there might be ways for antibody entry and subsequent tissue damage. Here, we systemically applied a highly pathogenic, monoclonal antibody with high affinity to AQP4 over prolonged period of time to rats, and show that AQP4-abs can enter the CNS on their own, via circumventricular organs and meningeal or parenchymal blood vessels, that these antibodies initiate the formation of radically different lesions with AQP4 loss, depending on their mode and site of entry, and that lesion formation is much more efficient in the presence of encephalitogenic T-cell responses. We further demonstrate that the established tissue-destructive lesions trigger the formation of additional lesions by short and far reaching effects on blood vessels and their branches, and that AQP4-abs have profound effects on the AQP4 expression in peripheral tissues which counter-act possible titer loss by antibody absorption outside the CNS. Cumulatively, these data indicate that directly induced pathological changes caused by AQP4-abs inside and outside the CNS are efficient drivers of disease evolution in seropositive organisms.

Human antibodies against the myelin oligodendrocyte glycoprotein can cause complement-dependent demyelination.

BACKGROUND: Antibodies to the myelin oligodendrocyte glycoprotein (MOG) are associated with a subset of inflammatory demyelinating diseases of the central nervous system such as acute disseminated encephalomyelitis and neuromyelitis optica spectrum disorders. However, whether human MOG antibodies are pathogenic or an epiphenomenon is still not completely clear. Although MOG is highly conserved within mammals, previous findings showed that not all human MOG antibodies bind to rodent MOG. We therefore hypothesized that human MOG antibody-mediated pathology in animal models may only be evident using species-specific MOG antibodies. METHODS: We screened 80 human MOG antibody-positive samples for their reactivity to mouse and rat MOG using either a live cell-based assay or immunohistochemistry on murine, rat, and human brain tissue. Selected samples reactive to either human MOG or rodent MOG were subsequently tested for their ability to induce complement-mediated damage in murine organotypic brain slices or enhance demyelination in an experimental autoimmune encephalitis (EAE) model in Lewis rats. The MOG monoclonal antibody 8-18-C5 was used as a positive control. RESULTS: Overall, we found that only a subset of human MOG antibodies are reactive to mouse (48/80, 60%) or rat (14/80, 18%) MOG. Purified serum antibodies from 10 human MOG antibody-positive patients (8/10 reactive to mouse MOG, 6/10 reactive to rat MOG), 3 human MOG-negative patients, and 3 healthy controls were tested on murine organotypic brain slices. Purified IgG from one patient with high titers of anti-human, mouse, and rat MOG antibodies and robust binding to myelin tissue produced significant, complement-mediated myelin loss in organotypic brain slices, but not in the EAE model. Monoclonal 8-18-C5 MOG antibody caused complement-mediated demyelination in both the organotypic brain slice model and in EAE. CONCLUSION: This study shows that a subset of human MOG antibodies can induce complement-dependent pathogenic effects in a murine ex vivo animal model. Moreover, a high titer of species-specific MOG antibodies may be critical for demyelinating effects in mouse and rat animal models. Therefore, both the reactivity and titer of human MOG antibodies must be considered for future pathogenicity studies.

Association between perception of maternal bonding styles and social anxiety disorder among young women.

OBJECTIVE: To evaluate the association between social anxiety disorder (SAD) and perceived maternal bonding styles among young women during pregnancy and 30 months after childbirth. METHODS: A cohort of young women from the city of Pelotas, Brazil was followed up from pregnancy to 30 months postpartum. The Mini Neuropsychiatric Interview Plus was used to assess SAD and the Parental Bonding Instrument was administered to measure maternal bonding styles. Poisson regression with robust variance was used for multivariable analysis. RESULTS: After adjusting for potential confounding factors, SAD prevalence was 6.39 times higher among young women who perceived their mothers as neglectful (prevalence ratio [PR] 6.39; 95% confidence interval [95%CI] 1.2-32.0), and 5.57 times higher in women who perceived their mothers as affectionless controlling (PR = 5.57; 95%CI 1.5-19.7) when compared with those who received optimal care. CONCLUSION: Maternal bonding style may have an influence on the development of SAD. Therefore, support and early prevention strategies should be offered to the family.

Cognitive and language performance in children is associated with maternal social anxiety disorder: A study of young mothers in southern Brazil.

BACKGROUND: It has been shown that maternal mental health is associated with poorer skills development in the offspring. However, the evidence evaluating the association between social anxiety disorder (SAD) and cognitive or language development, is scarce. AIM: To evaluate the association between maternal SAD and performance in cognitive and language tests in 30-month old children. STUDY DESIGN: This was a cohort study involving young women evaluated since pregnancy. SUBJECTS: We evaluated 520 mother-child dyads who received prenatal medical assistance through the National Public Health System in a southern Brazilian city, from October 2009 to March 2011. OUTCOME MEASURES: We used the Mini Neuropsychiatric Interview Plus (MINI Plus) to assess SAD among young mothers. Cognitive and language performance in their offspring was analyzed using the Bayley Scales of Infant and Toddler Development - 3rd Edition. RESULTS: We found an association between maternal SAD and performance in cognitive and language tests. Children of mothers with SAD had in average 4.5 less points in the Bayley scale, when compared to those with mothers without SAD: in the cognitive (ß=-4.53 [95% CI -7.8; -1.1] p=0.008) and language subscales (ß=-4.54 [95% CI -9.0; -0.5] p=0.047). CONCLUSIONS: Our findings suggest that children with mothers suffering from SAD have poorer cognitive abilities and language skills.