oncussions are a common cause of brain injury occurring in more than 1 million Americans each year and disproportionately involving older adults. 1-4 The subacute consequences vary widely and include fatigue, headache, irritability, insomnia, inattention, photophobia, vertigo, and cognitive difficulties. 5-9 Most patients recover from a concussion within weeks, although some can develop lingering mood disorders or chronic neuropsychiatric disorders. 10-14 The extent of complications after a concussion is uncertain, and effective pharmacologic treatments remain elusive. 15-17 Unfortunately, many medical treatments for traumatic brain injury that showed promise in animal models have subsequently failed in human clinical trials. 18-22 Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) are a class of medications prescribed for the treatment of hyperlipidemia. 23,24 Preclinical data suggest that statin use might mitigate injury-related brain edema, oxidative stress, amyloid protein aggregation, and neuroinflammation. 25-29 The potential neuroprotective benefits from statins have also been speculated and include preserved cerebral blood flow, leading to decreased risks of Alzheimer disease, vascular dementia, and age-related cognitive decline. 30-35 Together, these findings suggest that statin use could contribute to microvascular homeostasis and immune modulation independent of systemic lipid levels. However, statins do not improve cognition for patients already diagnosed as having dementia. 36-38 IMPORTANCE Concussions are an acute injury that may lead to chronic disability, while statin use might improve neurologic recovery. OBJECTIVE To test whether statin use is associated with an increased or decreased risk of subsequent dementia after a concussion.
Chronic obstructive pulmonary disease (COPD) is characterized by fixed airflow limitation and progressive decline of lung function and punctuated by occasional exacerbations. The disease pathogenesis may involve activation of the bone marrow stimulating mobilization and lung-homing of progenitor cells. We investigated the hypothesis that lower circulating numbers of vascular endothelial progenitor cells (VEPCs) are a consequence of increased lung-sequestration in COPD. Nonatopic, current or ex-smokers with diagnosed COPD and nonatopic, nonsmoking normal controls were enrolled. Blood and induced sputum extracted primitive hemopoietic progenitors (HPCs) and VEPC were enumerated by flow cytometry. Migration and adhesive responses to fibronectin were assessed. In sputum, VEPC numbers were significantly greater in COPD compared to normal controls. In blood, VEPCs were significantly lower in COPD versus normal controls. There were no differences in HPC levels between the two groups in either compartment. Functionally, there was a greater migrational responsiveness of progenitors from COPD subjects to stromal cell-derived factor-1alpha (SDF-1α) compared to normal controls. This was associated with greater numbers of CXCR4+ progenitors in sputum from COPD. Increased migrational responsiveness of progenitor cells may promote lung-homing of VEPC in COPD which may disrupt maintenance and repair of the airways and contribute to COPD disease pathogenesis.
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