Background As the COVID-19 pandemic developed, reports of neurological dysfunctions spanning the central and peripheral nervous systems have emerged. The spectrum of acute neurological dysfunctions may implicate direct viral invasion, para-infectious complications, neurological manifestations of systemic diseases, or co-incident neurological dysfunction in the context of high SARS-CoV-2 prevalence. A rapid and pragmatic approach to understanding the prevalence, phenotypes, pathophysiology and prognostic implications of COVID-19 neurological syndromes is urgently needed. Methods The Global Consortium to Study Neurological dysfunction in COVID-19 (GCS-NeuroCOVID), endorsed by the Neurocritical Care Society (NCS), was rapidly established to address this need in a tiered approach. Tier-1 consists of focused, pragmatic, low-cost, observational common data element (CDE) collection, which can be launched immediately at many sites in the first phase of this pandemic and is designed for expedited ethical board review ates of each neurological finding divided by the average census of COVID-19 positive patients over the study period. Secondary outcomes include in-hospital, 30 and 90-day morality, discharge modified Rankin score, ventilator-free survival, ventilator days, discharge disposition, and hospital length of stay. Results In a one-month period (3/27/20-4/27/20) the GCS-NeuroCOVID consortium was able to recruit 71 adult study sites, representing 17 countries and 5 continents and 34 pediatrics study sites. Conclusions This is one of the first large-scale global research collaboratives urgently assembled to evaluate acute neurological events in the context of a pandemic. The innovative and pragmatic tiered study approach has allowed for rapid recruitment and activation of numerous sites across the world-an approach essential to capture real-time critical neurological data to inform treatment strategies in this pandemic crisis.Despite the pervasive nature of various forms of impairment associated with attention-deficit/hyperactivity disorder (ADHD), the precise nature of their associations with ADHD and related sluggish cognitive tempo (SCT), particularly at the heterogeneous item level, remains ambiguous. Using innovative network analysis techniques, we sought to identify and examine the concurrent validity of ADHD and SCT bridge items (i.e., those demonstrating the most robust relations with various forms of impairment) with respect to Overall, Home-School, and Community-Leisure impairment domains. Parents of a nationally representative sample of 1742 children (50.17% male) aged 6-17 years completed rating scales of ADHD, SCT, and impairment. learn more Assessment of Bridge Expected Influence suggested eight bridge items primarily from impulsive and Task Completion (i.e., overlapping SCT and inattentive) domains that demonstrated relations with impairment in school performance, completing chores at home, interacting with family members, following rules, and playing sports. Sum scores only including bridge items exhibited relations with Overall, Home-School, and Community-Leisure impairment domains comparable to that of sum scores including all items. Bridge impairment areas were generally consistent across “Childhood” (6-11 years) and “Adolescence” (12-17 years). Problems listening and slowness emerged as bridge items in Childhood, whereas difficulties following through on instructions, problems waiting one’s turn, and social withdrawal emerged in Adolescence. Given the comparable validity of ADHD- and SCT-related bridge items versus all items, bridge items, together, may be the most efficient indicators of impairment. Further clarification is needed across development to inform personalized assessment and intervention protocols that account for item-level heterogeneity in ADHD, SCT, and impairment phenotypes.Heightened reward sensitivity has been proposed as a risk factor for developing behavioral disorders whereas heightened punishment sensitivity has been related to the development of anxiety disorders in youth. Combining a cross-sectional (n = 696, mean age = 16.14) and prospective (n = 598, mean age = 20.20) approach, this study tested the hypotheses that an attentional bias for punishing cues is involved in the development of anxiety disorders and an attentional bias for rewarding cues in the development of behavioral disorders. A spatial orientation task was used to examine the relation between an attentional bias for punishing cues and an attentional bias for rewarding cues with anxiety and behavioral problems in a subsample of a large prospective population cohort study. Our study indicates that attentional biases to general cues of punishment and reward do not seem to be important risk factors for the development of anxiety or behavioral problems respectively. It might be that attentional biases play a role in the maintenance of psychological problems. This remains open for future research.Scleroderma (systemic sclerosis; SSc) is a complex and highly heterogeneous multisystem rheumatic disease characterized by vascular abnormality, immunologic derangement, and excessive deposition of extracellular matrix (ECM) proteins. To date, the etiology of this life-threatening disorder remains not fully clear. More and more studies show epigenetic modifications play a vital role. The aberrant epigenetic status of certain molecules such as Fli-1, BMPRII, NRP1, CD70, CD40L, CD11A, FOXP3, KLF5, DKK1, SFRP1, and so on contributes to the pathogenesis of progressive vasculopathy, autoimmune dysfunction, and tissue fibrosis in SSc. Meanwhile, numerous miRNAs including miR-21, miR-29a, miR-196a, miR-202-3p, miR-150, miR-let-7a, and others are involved in the process. In addition, the abnormal epigenetic biomarker levels of CD11a, Foxp3, HDAC2, miR-30b, miR-142-3p, miR-150, miR-5196 in SSc are closely correlated with disease severity. In this chapter, we not only review new advancements on the epigenetic mechanisms involved in the pathogenesis of SSc and potential epigenetic biomarkers, but also discuss the therapeutic potential of epigenetic targeting therapeutics such as DNA methylation inhibitors, histone acetylase inhibitors, and miRNA replacement.