Immunological parameters in girls with Turner syndrome

Disturbances in the immune system has been described in Turner syndrome, with an association to low levels of IgG and IgM and decreased levels of T- and B-lymphocytes. Also different autoimmune diseases have been connected to Turner syndrome (45, X), thyroiditis being the most common. Besides the typical features of Turner syndrome (short stature, failure to enter puberty spontaneously and infertility due to ovarian insufficiency) ear problems are common (recurrent otitis media and progressive sensorineural hearing disorder). Levels of IgG, IgA, IgM, IgD and the four IgG subclasses as well as T- and B-lymphocyte subpopulations were investigated in 15 girls with Turners syndrome to examine whether an immunodeficiency may be the cause of their high incidence of otitis media. No major immunological deficiency was found that could explain the increased incidence of otitis media in the young Turner girls

Motivation for or from bilingual education? A comparative study of learner views in the Netherlands

Teaching and Teacher Learning (ICLON

Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

Ischemia-Reperfusion Injury and Pregnancy Initiate Time-Dependent and Robust Signs of Up-Regulation of Cardiac Progenitor Cells

To explore how cardiac regeneration and cell turnover adapts to disease, different forms of stress were studied for their effects on the cardiac progenitor cell markers c-Kit and Isl1, the early cardiomyocyte marker Nkx2.5, and mast cells. Adult female rats were examined during pregnancy, after myocardial infarction and ischemia-reperfusion injury with/out insulin like growth factor-1(IGF-1) and hepatocyte growth factor (HGF). Different cardiac sub-domains were analyzed at one and two weeks post-intervention, both at the mRNA and protein levels. While pregnancy and myocardial infarction up-regulated Nkx2.5 and c-Kit (adjusted for mast cell activation), ischemia-reperfusion injury induced the strongest up-regulation which occurred globally throughout the entire heart and not just around the site of injury. This response seems to be partly mediated by increased endogenous production of IGF-1 and HGF. Contrary to c-Kit, Isl1 was not up-regulated by pregnancy or myocardial infarction while ischemia-reperfusion injury induced not a global but a focal up-regulation in the outflow tract and also in the peri-ischemic region, correlating with the up-regulation of endogenous IGF-1. The addition of IGF-1 and HGF did boost the endogenous expression of IGF and HGF correlating to focal up-regulation of Isl1. c-Kit expression was not further influenced by the exogenous growth factors. This indicates that there is a spatial mismatch between on one hand c-Kit and Nkx2.5 expression and on the other hand Isl1 expression. In conclusion, ischemia-reperfusion injury was the strongest stimulus with both global and focal cardiomyocyte progenitor cell marker up-regulations, correlating to the endogenous up-regulation of the growth factors IGF-1 and HGF. Also pregnancy induced a general up-regulation of c-Kit and early Nkx2.5+ cardiomyocytes throughout the heart. Utilization of these pathways could provide new strategies for the treatment of cardiac disease

Correlates of postpartum depression in first time mothers without previous psychiatric contact

Background Postpartum depression (PPD) is a common disorder after childbirth. The strongest known predictors are a history of depression and/or a history of PPD. However, for a significant proportion of women, PPD constitutes their first depressive episode. This study aimed to gain further insight into the risk factors for PPD in first time mothers without previous psychiatric contact. Methods Women delivering in Uppsala University Hospital, Sweden, from May 2006 to June 2007, were asked to participate and filled out questionnaires five days and six weeks postpartum, containing inter alia the Edinburgh Postnatal Depression Scale (EPDS). Univariate logistic regression models, as well as a path analysis, were performed to unveil the complex interplay between the study variables. Results Of the 653 participating primiparas, 10.3% and 6.4% reported depressive symptoms (EPDS ≥ 12 points) five days and six weeks postpartum, respectively. In the path analysis, a positive association between anxiety proneness and depressive symptoms at five days and six weeks postpartum was identified. For depressive symptoms six weeks after delivery, additional risk factors were detected, namely depressive symptoms five days postpartum and subjective experience of problems with the baby. Caesarean section and assisted vaginal delivery were associated with fewer depressive symptoms at 6 six weeks postpartum. Conclusions Identification of anxiety proneness, delivery mode and problems with the baby as risk factors for self-reported depressive symptoms postpartum in this group of primiparas can be important in helping health care professionals identify women at increased risk of affective disorders in the perinatal period, and provide a base for early intervention. © 2016 Elsevier Masson SA

Antenatal depressive symptoms and early initiation of breastfeeding in association with exclusive breastfeeding six weeks postpartum: A longitudinal population-based study

Background: Depressive symptoms negatively impact on breastfeeding duration, whereas early breastfeeding initiation after birth enhances the chances for a longer breastfeeding period. Our aim was to investigate the interplay between depressive symptoms during pregnancy and late initiation of the first breastfeeding session and their effect on exclusive breastfeeding at six weeks postpartum. Methods: In a longitudinal study design, web-questionnaires including demographic data, breastfeeding information and the Edinburgh Postnatal Depression Scale (EPDS) were completed by 1217 women at pregnancy weeks 17-20, 32 and/or at six weeks postpartum. A multivariable logistic regression model was fitted to estimate the effect of depressive symptoms during pregnancy and the timing of the first breastfeeding session on exclusive breastfeeding at six weeks postpartum. Results: Exclusive breastfeeding at six weeks postpartum was reported by 77% of the women. Depressive symptoms during pregnancy (EPDS> 13); (OR:1.93 [1.28-2.91]) and not accomplishing the first breastfeeding session within two hours after birth (OR: 2.61 [1.80-3.78]), were both associated with not exclusively breastfeeding at six weeks postpartum after adjusting for identified confounders. he combined exposure to depressive symptoms in pregnancy and late breastfeeding initiation was associated with an almost 4-fold increased odds of not exclusive breastfeeding at six weeks postpartum. Conclusions: Women reporting depressive symptoms during pregnancy seem to be more vulnerable to the consequences of a postponed first breastfeeding session on exclusive breastfeeding duration. Consequently, women experiencing depressive symptoms may benefit from targeted breastfeeding support during the first hours after birth. © 2019 The Author(s)