To better understand the EEG education provided to adult neurology residents by surveying program directors of adult neurology residency programs in the United States.
 
  An online survey focused on characteristics of neurology residency programs and their EEG teaching systems was distributed to the 161 adult neurology residency program directors listed in the Accreditation Council for Graduate Medical Education website at the time of the study.
 
  Forty-seven (29%) out of the 161 program directors completed the survey. Most of the participating programs (89%) were academic. The mean number of 1-month EEG rotations required to graduate was 1.7 (range 0-4, median 1.75). EEG rotations involved the inpatient and outpatient setting in 91% and 70% of programs, respectively. The average number of EEGs read during a typical EEG rotation varied from more than 40, in about one-third of programs, to 0-10, in about 14% of programs. There was significant variability in the requirements for successful completion of EEG rotations, and most program directors (64%) reported not utilizing objective measures to assess EEG milestones. The most commonly used educational methods were didactics throughout the year (95%) and EEG teaching during EEG rotations (93%). The most commonly reported barriers to EEG education were insufficient EEG exposure (32%) and ineffective didactics (11%); possible solutions are summarized.
 
  Our study identified a lack of consistency in teaching and evaluating residents during residency and presented EEG education barriers alongside possible solutions. We encourage program directors across the country to re-evaluate their EEG teaching systems in order to optimize EEG education.
 Our study identified a lack of consistency in teaching and evaluating residents during residency and presented EEG education barriers alongside possible solutions. We encourage program directors across the country to re-evaluate their EEG teaching systems in order to optimize EEG education.
  Since the last epidemiologic review of neuromyelitis optica/neuromyelitis optica spectrum disorder (NMO/NMOSD), 22 additional studies have been conducted. We systematically review the worldwide prevalence, incidence, and basic demographic characteristics of NMOSD and provide a critical overview of studies.
 
  PubMed, Ovid MEDLINE, and Embase using Medical Subject Headings and keyword search terms and reference lists of retrieved articles were searched from 1999 until August 2019. We collected data on the country; region; methods of case assessment and aquaporin-4 antibody (AQP4-Ab) test; study period; limitations; incidence (per 100,000 person-years); prevalence (per 100,000 persons); and age-, sex-, and ethnic group-specific incidence or prevalence.
 
  We identified 33 relevant articles. The results indicated the highest estimates of incidence and prevalence of NMOSD in Afro-Caribbean region (0.73/100 000 person-years [95% CI 0.45-1.01] and 10/100 000 persons [95% CI 6.8-13.2]). The lowest incidence and prevmethods and NMO/NMOSD definitions, highlighting the need for specifically designed epidemiologic studies to identify genetic effects and etiologic factors.Hypersensitivity pneumonitis (HP) typically presents with interstitial inflammation and granulomas induced by an aberrant immune response to inhaled Ags in sensitized individuals. Although IL-17A is involved in the development of HP, the cellular sources of IL-17A and the mechanisms by which IL-17A contributes to granuloma formation remain unclear. Recent studies report that γδ T cells produce IL-17A and exhibit memory properties in various diseases. Therefore, we focused on IL-17A-secreting memory γδ T cells in the sensitization phase and aimed to elucidate the mechanisms by which IL-17A contributes to granuloma formation in HP. We induced a mouse model of HP using pigeon dropping extract (PDE) in wild-type and IL-17A knockout (IL-17A-/-) mice. IL-17A-/- mice exhibited reduced granulomatous areas, attenuated aggregation of CD11b+ alveolar macrophages, and reduced levels of CCL2, CCL4, and CCL5 in the bronchoalveolar lavage fluid. Among IL-17A+ cells, more γδ T cells than CD4+ cells were detected after intranasal PDE administration. Interestingly, the expansion of IL-17A-secreting Vγ4+ or Vγ1-Vγ4- cells of convalescent mice was enhanced in response to the sensitizing Ag. Additionally, coculture of macrophages with PDE and Vγ4+ cells purified from PDE-exposed convalescent mice produced significantly more IL-17A than coculture with Vγ4+ cells from naive mice. Our findings demonstrate that in the sensitization phase of HP, IL-17A-secreting memory γδ T cells play a pivotal role. Furthermore, we characterized the IL-17A/CCL2, CCL4, CCL5/CD11b+ alveolar macrophage axis, which underlies granuloma formation in HP. These findings may lead to new clinical examinations or therapeutic targets for HP.ADP-ribosylation factor (Arf) family consisting of six family members, Arf1-Arf6, belongs to Ras superfamily and orchestrates vesicle trafficking under the control of guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins. It is well established that brefeldin A, a potent inhibitor of ArfGEFs, blocks cytokine secretion from activated T cells, suggesting that the Arf pathway plays important roles in T cell functions. In this study, because Arf1 and Arf6 are the best-characterized members among Arf family, we established T lineage-specific Arf1-deficient, Arf6-deficient, and Arf1/6 double-deficient mice to understand physiological roles of the Arf pathway in the immune system. Contrary to our expectation, Arf deficiency had little or no impact on cytokine secretion from the activated T cells. In contrast, the lack of both Arf1 and Arf6, but neither Arf1 nor Arf6 deficiency alone, rendered naive T cells susceptible to apoptosis upon TCR stimulation because of imbalanced expression of Bcl-2 family members. We further demonstrate that Arf1/6 deficiency in T cells alleviates autoimmune diseases like colitis and experimental autoimmune encephalomyelitis, whereas Ab response under Th2-polarizing conditions is seemingly normal.  https://www.selleckchem.com/products/BIBF1120.html  Our findings reveal an unexpected role for the Arf pathway in the survival of T cells during TCR-induced activation and its potential as a therapeutic target in the autoimmune diseases.