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Springer, M. L.

Publications and source records attributed to Springer, M. L..

2 recordsLinked to original sources

JUUL and Combusted Cigarettes Comparably Impair Endothelial Function

ObjectivesJUUL and earlier generation electronic cigarettes (e-cigs) are promoted as being less hazardous than cigarettes. While JUUL Labs, in particular, claims that switching from smoking to vaping has beneficial impacts, the health effects of such products are not well understood. We investigated whether exposure to JUUL and previous generation e-cig aerosol impairs endothelial function comparably to cigarette smoke.\n\nMethodsWe exposed rats to aerosol from Virginia Tobacco flavor JUUL, an e-cig tank system using unflavored freebase nicotine e-liquid, Marlboro Red combustible tobacco cigarettes, or clean air for 10 cycles of 2 second inhalation over 5 minutes. Endothelial function (FMD) was measured pre- and post-exposure. Blood was collected 20 mins post-exposure for serum nicotine analysis.\n\nResultsAerosol/smoke from JUUL, previous generation e-cigs, and cigarettes all impaired FMD. The extent of impairment ranged from 34%-58%, although the differences between groups were insignificant. Nicotine was highest in serum from the JUUL group; for the other e-cig and cigarette groups, nicotine levels were lower and comparable to each other.\n\nConclusionsAerosol from JUUL and previous generation e-cigs impairs endothelial function in rats, comparable to impairment by cigarette smoke.

pharmacology and toxicology

Impaired Therapeutic Efficacy of Bone Marrow Cells from Post-Myocardial Infarction Patients in the TIME and LateTIME Clinical Trials

Implantation of bone marrow-derived cells (BMCs) into mouse hearts post-myocardial infarction (MI) limits cardiac functional decline. However, clinical trials of post-MI BMC therapy have yielded conflicting results. While most laboratory experiments use healthy BMC donor mice, clinical trials use post-MI autologous BMCs. Post-MI mouse BMCs are therapeutically impaired, due to inflammatory changes in BMC composition. Thus, therapeutic efficacy of the BMCs progressively worsens after MI but recovers as donor inflammatory response resolves. The availability of post-MI patient BM mononuclear cells (MNCs) from the TIME and LateTIME clinical trials enabled us to test if human post-MI MNCs undergo a similar period of impaired efficacy. We hypothesized that MNCs from TIME trial patients would be less therapeutic than healthy human donor MNCs when implanted into post-MI mouse hearts, and that therapeutic properties would be restored in MNCs from LateTIME trial patients. Post-MI SCID mice received MNCs from healthy donors, TIME patients, or LateTIME patients. Cardiac function improved considerably in the healthy donor group, but neither the TIME nor LateTIME group showed therapeutic effect. Conclusion: post-MI human MNCs lack therapeutic benefits possessed by healthy MNCs, which may partially explain why BMC clinical trials have been less successful than mouse studies.

physiology