Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. Humans with probable prediabetes generate similar autoreactivities, and autoantibodies in islet-cell autoantibody (lCA) -positive sera co-localize to pSC. Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. However, pSC were deleted in spontaneously diabetic NOD mice carrying the CD8+/8.3 T-cell receptor transgene, a T cell receptor commonly expressed in earliest islet infiltrates. Autoimmune targeting of pancreatic nervous system tissue elements seems to be an integral, early part of natural type 1 diabetes.

Work-related asthma is the most common occupational lung disease encountered in clinical practice. In adult asthmatics, work-relatedness can account for 15%–33% of cases, but delays in diagnosis remain common and lead to worse outcomes. Accurate diagnosis of asthma is the first step to managing occupational asthma, which can be sensitizer-induced or irritant-induced asthma. While latency has traditionally been recognized as a hallmark of sensitizer-induced asthma and rapid-onset a defining feature of irritant-induced asthma (as in Reactive Airway Dysfunction Syndrome), there is epidemiological evidence for irritant-induced asthma with latency from chronic moderate exposure. Diagnostic testing while the patient is still in the workplace significantly improves sensitivity. While specific inhalational challenges remain the gold-standard for the diagnosis of occupational asthma, they are not available outside of specialized centers. Commonly available tests including bronchoprovocation challenges and peak flow monitoring are important tools for practicing clinicians. Management of sensitizer-induced occupational asthma is notable for the central importance of removal from the causative agent: ideally, removal of the culprit agent; but if not feasible, this may require changes in the work process or ultimately, removal of the worker from the workplace. While workers' compensation programs may reduce income loss, these are not universal and there can be significant socio-economic impact from work-related asthma. Primary prevention remains the preferred method of reducing the burden of occupational asthma, which may include modification to work processes, better worker education and substitution of sensitizing agents from the workplace with safer compounds.

Background Chronic obstructive pulmonary disease (COPD) is a progressive condition associated with physical and cognitive impairments contributing to difficulty in performing activities of daily living (ADLs) that require dual tasking (eg, walking and talking). Despite evidence showing that cognitive decline occurs among patients with COPD and may contribute to functional limitations and decreased health-related quality of life (HRQL), pulmonary rehabilitation continues to focus mainly on physical training (ie, aerobic and strength exercises). An integrated cognitive and physical training program compared to physical training alone may be more effective in increasing dual-tasking ability among people living with COPD, leading to greater improvements in performance of ADLs and HRQL. Objective The aims of this study are to evaluate the feasibility of an 8-week randomized controlled trial of home-based, cognitive-physical training versus physical training for patients with moderate to severe COPD and derive preliminary estimates of cognitive-physical training intervention efficacy on measures of physical and cognitive function, dual task performance, ADLs, and HRQL. Methods A total of 24 participants with moderate to severe COPD will be recruited and randomized into cognitive-physical training or physical training. All participants will be prescribed an individualized home physical exercise program comprising 5 days of moderate-intensity aerobic exercise (30-50 minutes/session) and 2 days of whole-body strength training per week. The cognitive-physical training group will also perform cognitive training for approximately 60 minutes, 5 days per week via the BrainHQ platform (Posit Science Corporation). Participants will meet once weekly with an exercise professional (via videoconference) who will provide support by reviewing the progression of their training and addressing any queries. Feasibility will be assessed through the recruitment rate, program adherence, satisfaction, attrition, and safety. The intervention efficacy regarding dual task performance, physical function, ADLs, and HRQL will be evaluated at baseline and at 4 and 8 weeks. Descriptive statistics will be used to summarize intervention feasibility. Paired 2-tailed t tests and 2-tailed t tests will be used to compare the changes in the outcome measures over the 8-week study period within and between the 2 randomized groups, respectively. Results Enrollment started in January 2022. It is estimated that the enrollment period will be 24 months long, with data collection to be completed by December 2023. Conclusions A supervised home-based cognitive-physical training program may be an accessible intervention to improve dual-tasking ability in people living with COPD. Evaluating the feasibility and effect estimates is a critical first step to inform future clinical trials evaluating this approach and its effects on physical and cognitive function, ADL performance, and HRQL. Trial Registration ClinicalTrials.gov NCT05140226; https://clinicaltrials.gov/ct2/show/NCT05140226 International Registered Report Identifier (IRRID) DERR1-10.2196/48666

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