Caesarean sections may be associated with an increased risk of developing AR in childhood.

No abstract

BackgroundWith rates of childhood obesity increasing, physical activity (PA) promotion especially in young children has assumed greater importance. Given the limited effectiveness of most interventions to date, new approaches are needed. The General Systems theory suggests that involving parents as intervention targets may be effective in fostering healthier life styles in children. We describe the development of a parent-focused participatory intervention and the procedures used to evaluate its effectiveness in increasing daily PA in preschoolers.Methods/DesignThirty-seven South German preschools were identified for this study and agreed to participate. Using a two-armed, controlled cluster-randomized trial design we test a participatory intervention with parents as the primary target group and potential agents of behavioural change. Specifically, the intervention is designed to engage parents in the development, refinement and selection of project ideas to promote PA and in incorporating these ideas into daily routines within the preschool community, consisting of children, teachers and parents. Our study is embedded within an existing state-sponsored programme providing structured gym lessons to preschool children. Thus, child-based PA outcomes from the study arm with the parent-focused intervention and the state-sponsored programme are compared with those from the study arm with the state-sponsored programme alone. The evaluation entails baseline measurements of study outcomes as well as follow-up measurements at 6 and 12 months. Accelerometry measures PA intensity over a period of six days, with the mean over six days used as the primary outcome measure. Secondary outcomes include childrens' BMI, a sum of averaged skin fold thickness measurements across multiple sites, and PA behaviour. Longitudinal multilevel models are used to assess within-subject change and between-group differences in study outcomes, adjusted for covariates at the preschool and individual levels. Teacher qualitative interviews monitor the intervention implementation process.DiscussionParticipatory approaches that actively involve parents have the potential to promote PA in ways that might be better tailored to local needs and more sustainable. Our mixed methods approach to assess the intervention efficacy and implementation employing both quantitative and qualitative measures within a cluster-randomized controlled trial may serve as a framework for evaluating public health interventions in preschool settings.Trial Registrationclinicaltrials.gov No: NCT00987532

The evidence on the aetiology of DP is fragmentary and heterogeneous. In addition, factors possibly relevant to the development of DP have not been appreciated in the scientific discussion.

Hintergrund Ein erheblicher Teil der Verläufe des Post-COVID-Syndroms ( COVID „coronavirus disease“) erfüllt die Diagnosekriterien für Myalgische Enzephalomyelitis/Chronisches Fatigue-Syndrom (ME/CFS). In den nächsten Jahren muss deshalb mit einer Verdopplung der Zahl der von ME/CFS Betroffenen gerechnet werden. Ziel der Arbeit Darstellung des aktuellen Wissensstands zu ME/CFS. Material und Methoden Unsystematisches Review der Literatur sowie eigener Arbeiten in Forschung und Patient*innenversorgung. Ergebnisse und Schlussfolgerung Bei ME/CFS handelt es sich um eine zumeist infektinduzierte, in der Regel lebenslang persistierende neuroimmunologische Erkrankung mit mindestens 6 Monate anhaltender Fatigue und dem definierenden Kernmerkmal der Belastungsintoleranz („post-exertional malaise“ [PEM]). Darunter versteht man eine nach (auch leichter) Alltagsanstrengung auftretende Verschlechterung der Beschwerden, die meist erst nach mehreren Stunden oder am Folgetag einsetzt, mindestens 14 h nach Belastung noch spürbar ist und oft mehrere Tage (bis Wochen oder länger) anhält. Des Weiteren bestehen bei ME/CFS Schmerzen, Störungen von Schlaf, Denk- und Merkfähigkeit sowie Fehlregulationen von Kreislauf, Hormon- und Immunsystem. Als eigenständige klinische Entität ist ME/CFS von der chronischen Fatigue abzugrenzen, die als Symptom bei ganz unterschiedlichen Erkrankungen auftritt. Die Diagnose ME/CFS wird anhand etablierter internationaler Diagnosekriterien klinisch gestellt und erfordert zum Ausschluss anderer Diagnosen eine sorgfältige Stufendiagnostik. Eine kausale Therapie für ME/CFS ist nicht etabliert, im Vordergrund steht die Linderung der Beschwerden, die Behandlung der oft begleitenden orthostatischen Intoleranz sowie die Unterstützung beim vorausschauenden Energiemanagement („pacing“).

Although myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has a specific and distinctive profile of clinical features, the disease remains an enigma because causal explanation of the pathobiological matrix is lacking. Several potential disease mechanisms have been identified, including immune abnormalities, inflammatory activation, mitochondrial alterations, endothelial and muscular disturbances, cardiovascular anomalies, and dysfunction of the peripheral and central nervous systems. Yet, it remains unclear whether and how these pathways may be related and orchestrated. Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes). We will test this hypothesis by reviewing, in reference to the current literature, the two most salient and widely accepted features of ME/CFS, and by investigating how these might be linked to dysfunctional neuroglia. From this review we conclude that the multifaceted pathobiology of ME/CFS may be attributable in a unifying manner to neuroglial dysfunction. Because the two key features – post exertional malaise and decreased cerebral blood flow – are also recognized in a subset of patients with post-acute sequelae COVID, we suggest that our findings may also be pertinent to this entity.

Lay Summary: In industrialized societies some babies develop flattening of the back part of their head. It is thought that this comes from sleeping supine, which has been shown to be the safest option for babies. However, this explanation cannot be correct from an evolutionary standpoint: why should safe sleep come at the cost of a misshaped head?Babies in industrialized societies are generally healthy. The medical problems they may be afflicted with are usually well understood. Deformational plagiocephaly presents a notable exception. In many industrialized countries, one in six babies shows posterior flattening of the skull—a feature noteworthy from an evolutionary perspective as the well rounded cranium is part of the ‘Kindchenschema’ evolved to secure care for the infant. It is commonly held that the deformation of the posterior cranium occurs as a consequence of the supine sleep position, now advocated as the safest sleep position for babies by medical experts. This explanation, however, does not fare well in the light of evolutionary theory: why should safe sleep come at the cost of a social handicap? Here, we present an alternative hypothesis that is grounded on evolutionary mismatch theory and exemplifies how evolutionary reasoning can help clarify medical conditions relevant to today’s public health.

In spite of decades of research, the pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is still poorly understood. Several pathomechanisms have been identified, yet, it remains unclear how they are related and which of them may be upstream or downstream.. In this paper, we present a theoretical strategy that may help clarify the causal chain of pathophysiological events in ME/CFS. We propose to focus on the common final histological pathway of ME/CFS and suggest to ask: Which cellular compartment may explain the pathological processes and clinical manifestations observed in ME/CFS? Any functional unit consistently identified through this search may then be a plausible candidate for further exploration.For this "histological" approach we have compiled a list of 22 undisputed clinical and pathophysiological features of ME/CFS that need to be plausibly and most directly explained by the dysfunctional cellular unit in question. For each feature we have searched the literature for pathophysiological explanations and analyzed if they may point to the same functional cellular unit.Through this search we have identified the CNS neuroglia - microglia and astroglia - as the one functional unit in the human body which may best explain all and any of the clinical and pathological features, dysfunctions and observations described for ME/CFS. While this points to neuroinflammation as the central hub in ME/CFS, it also points to a novel understanding of the neuroimmune basis of ME/CFS. After all, the neuroglial cells are now understood as the functional matrix of the human brain connectome which operates beyond and above specific brain centers, receptor units or neurotransmitter systems and integrates innate immune functions with CNS regulatory functions pertaining to autonomous regulation, cellular metabolism and the stress response.