Apnea of prematurity (AOP) is a common problem affecting premature infants, likely secondary to a “physiologic” immaturity of respiratory control that may be exacerbated by neonatal disease. These include altered ventilatory responses to hypoxia, hypercapnia, and altered sleep states, while the roles of gastroesophageal reflux and anemia remain controversial. Standard clinical management of the obstructive subtype of AOP includes prone positioning and continuous positive or nasal intermittent positive pressure ventilation to prevent pharyngeal collapse and alveolar atelectasis, while methylxanthine therapy is a mainstay of treatment of central apnea by stimulating the central nervous system and respiratory muscle function. Other therapies, including kangaroo care, red blood cell transfusions, and CO₂ inhalation, require further study. The physiology and pathophysiology behind AOP are discussed, including the laryngeal chemoreflex and sensitivity to inhibitory neurotransmitters, as are the mechanisms by which different therapies may work and the potential long-term neurodevelopmental consequences of AOP and its treatment.

Psoriasis is a complex, chronic relapsing and inflammatory skin disorder with a prevalence of approximately 2% in the general population worldwide. Psoriasis can be triggered by infections, physical injury and certain drugs. The most common type of psoriasis is psoriasis vulgaris, which primarily features dry, well-demarcated, raised red lesions with adherent silvery scales on the skin and joints. Over the past few decades, scientific research has helped us reveal that innate and adaptive immune cells contribute to the chronic inflammatory pathological process of psoriasis. In particular, dysfunctional helper T cells (Th1, Th17, Th22, and Treg cells) are indispensable factors in psoriasis development. When stimulated by certain triggers, antigen-presenting cells (APCs) can release pro-inflammatory factors (IL-23, IFN-α and IL-12), which further activate naive T cells and polarize them into distinct helper T cell subsets that produce numerous cytokines, such as TNF, IFN-γ, IL-17 and IL-22, which act on keratinocytes to amplify psoriatic inflammation. In this review, we describe the function of helper T cells in psoriasis and summarize currently targeted anti-psoriatic therapies.

CONTEXT: Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in childhood. Exploring the risk factors for ADHD is helpful in preventing ADHD. OBJECTIVE: To explore the association between maternal smoking during pregnancy and the occurrence of ADHD in offspring. DATA SOURCES: PubMed, Embase, and Cochrane Library were searched from inception to May 2017 for studies. STUDY SELECTION: Cohort or case-control studies in which the association between maternal smoking and ADHD in offspring were investigated were eligible if they included odds ratios (ORs), hazard ratios, or risk ratios and 95% confidence intervals (CIs). DATA EXTRACTION: Two investigators independently extracted data on definition of exposure and outcome, number of cases and total sample population, and potential confounders adjusted. Any dose-relationship data for smoking and ADHD risk were also extracted. RESULTS: Fifteen cohort studies and 5 case-control studies with 50 044 cases and 2 998 059 participants were included. Smoking during pregnancy increased the risk of offspring ADHD (OR: 1.60; 95% CI: 1.45–1.76). The risk of ADHD was greater for children whose mothers were heavy smokers (OR: 1.75; 95% CI: 1.51–2.02) than for those mothers were light smokers (OR: 1.54; 95% CI: 1.40–1.70). LIMITATIONS: The limitations of our study included different assessment tools of ADHD and a lack of objective biological measures for maternal smoking. CONCLUSIONS: With our meta-analysis, we provide evidence for an association between maternal smoking and offspring ADHD but do not solve the causality issues concerning potential confounding by other risk factors. More high-quality studies are needed to establish whether the association with smoking is causal.

The etiology of non-genetic intellectual disability (ID) is not fully known, and we aimed to identify the prenatal, perinatal and neonatal risk factors for ID. PubMed and Embase databases were searched for studies that examined the association between pre-, peri- and neonatal factors and ID risk (keywords “intellectual disability” or “mental retardation” or “ID” or “MR” in combination with “prenatal” or “pregnancy” or “obstetric” or “perinatal” or “neonatal”. The last search was updated on September 15, 2015. Summary effect estimates (pooled odds ratios) were calculated for each risk factor using random effects models, with tests for heterogeneity and publication bias. Seventeen studies with 55,344 patients and 5,723,749 control individuals were eligible for inclusion in our analysis, and 16 potential risk factors were analyzed. Ten prenatal factors (advanced maternal age, maternal black race, low maternal education, third or more parity, maternal alcohol use, maternal tobacco use, maternal diabetes, maternal hypertension, maternal epilepsy and maternal asthma), one perinatal factor (preterm birth) and two neonatal factors (male sex and low birth weight) were significantly associated with increased risk of ID. This systemic review and meta-analysis provides a comprehensive evidence-based assessment of the risk factors for ID. Future studies are encouraged to focus on perinatal and neonatal risk factors and the combined effects of multiple factors.