Nonthermal treatment with cold atmospheric plasma (CAP) is a promising option for local treatment of chronic-inflammatory and precancerous lesions as well as various mucosal cancer diseases, besides its primary indication for wound healing and antiseptics. Atmospheric pressure plasma jets (APPJs) are versatile plasma sources, some of which are well-characterized and medically approved. The characterization of APPJs, however, is often based on the treatment of simple solutions or even studies on the plasma effluent itself. To better assess the in vivo effects of CAP treatment, this study aims to recapitulate and study the physicochemical tissue-level effects of APPJ treatment on human primary mucosal tissue and tissue models. High resolution on-tissue infrared (IR) thermography and a first-time-performed spatially resolved optical emission spectroscopy (OES) of the APPJ emissions did not identify potentially tissue-harming effects. In this study, electron-spinresonance (ESR) spectroscopy on human tissue samples, treated with different CAP doses, enabled the measurement and the distribution of CAP-derived radicals in the tissues. The results correlate plasma dosage and the generation of radical species with cell viability and cell proliferation of primary human fibroblasts while demonstrating apoptosis-independent antiproliferative cell effects. Moreover, a dose-dependent increase of cells in the G1 phase of the cell cycle was observed, stressing the likely important role of cell cycle regulation for antiproliferative CAP mechanisms. This study introduces suitable methods for CAP monitoring on tissues and contributes to a better understanding of tissue-derived plasma effects of APPJs.

Background. This scoping review with narrative synthesis aimed to analyze scholarly peer-reviewed articles reporting on improving communication with patients discharged from the emergency department with noncardiac chest pain and qualitatively narrate on and summarize items that can be used in guiding communication with patients discharged from the emergency department with noncardiac chest pain. Methods. The databases of EMBASE/PubMed, Scopus, COCHRANE, CInAHL/EBESCO, UW libraries, and Google Scholar were searched using relevant MeSH and key terms up to February 06, 2020. The selected articles were analyzed for their contents. Items guiding discharge communication were summarized qualitatively. Results. Twenty-five articles were eligible for full review. These were published in between 1994 and 2020. Of those, 16 (64.0%) originated from the United States and 4 (16%) used some interventional design. A total of 45 different items that could be used in guiding discharge communication with patients presenting to the emergency department with chest pain were identified from the studies included in this review. Items were grouped under 6 categories that were related to initial assessment (8 items), information on diagnosis (7 items), information on discharge (9 items), follow-up suggestions (7 items), symptoms that promote return to the emergency department (7 items), and treatment plan (7 items). Conclusion. Communication with patients discharged from the emergency department with noncardiac chest pain can be improved. Results of this investigation might be helpful in guiding quality improvement projects aimed for further improvement of communication with patients discharged from the emergency department with noncardiac chest pain.

Diabetes induced hyperglycemia increases the risk of cardiovascular complications as it impacts vascular endothelial cells causing vascular dysfunction. Endothelial progenitor cells (EPCs) have been suggested to participate in the repair of vascular endothelial cells once they are impacted by hyperglycemia in diabetic patients. This research aims to test the EPC subtype blood outgrowth endothelial cells (BOECs) and their ability to survive and function under chronic hyperglycemic conditions. For that, we studied BOECs viability, response to shear stress, angiogenesis ability, and barrier function under normoglycemic (5.5mM) and hyperglycemic (25mM) conditions. The results have shown significant effects of chronic hyperglycemic conditions on cell proliferation (n=3, p<0.05), and migration (n=3, p<0.05) which were decreased when compared to control. Cells responses to shear stress were not affected under these conditions. There was a trend towards an increase in permeability as indicated by barrier function assays. The decrease in those endothelial cell functions might impact the repair mechanisms needed in diabetic patients to protect from vascular complications. Further investigations are required to establish therapeutic targets to improve EPCs repair function.