ICU Volunteer "Transition Guides": A Prospective Study on Improving the Patient Transfer Experience.

BACKGROUND: This study was conducted to measure the impact of a volunteer "Transition Guide" on patient experience and psychological stress during the transition from ICUs to general medical and surgical wards. METHODS: Between July 2017 and February 2020, medical and surgical patients from nine ICUs at a single tertiary care hospital were accompanied by a uniquely trained volunteer Transition Guide to aid them at the time of transfer to general medical/surgical wards, when available. If a Transition Guide was not available, they were transferred without one. The following day, patients were surveyed with a tool assessing overall satisfaction, multiple aspects in the domain of communication, and psychological stress associated with the transition process. When available, family members and ward nurses who admitted patients from the ICU were surveyed. RESULTS: Target enrollment was 300 patients in each group. Due to COVID-19 and institutional restrictions on volunteers, only 264 underwent transfer with a Guide, while 305 transferred without one. Of all patients approached, 95% with a Guide and 96% without a Guide completed the survey. Patients who were accompanied by a Transition Guide reported a better overall transition, better communication, greater understanding, better resolution of concerns, and less stress than those who did not have a Transition Guide (p < 0.05 for all). CONCLUSION: Among a cohort of formerly critically ill patients subsequently transferred to general medical and surgical wards, the presence of a volunteer Transition Guide significantly improved patient experience, enhanced patient communication and understanding, and reduced stress associated with the transfer process. Hospitals may consider this expanded and specialized role for volunteerism in the health care setting to improve patient-centered outcomes.

Impact of Coffee Consumption on Physiological Markers of Cardiovascular Risk: A Systematic Review.

BACKGROUND: Coffee is one of the most widely consumed beverages globally. A substantial number of observational data suggest an inverse relationship between coffee consumption and the risk for cardiovascular disease. The basis for this association is not clear. In this review, we specifically study the impact of coffee on inflammatory biomarkers as one potential mechanistic basis for this observation. Our objective was to systematically review randomized controlled trials that examined the effects of coffee consumption on selected cardiovascular biomarkers. METHODS: We systematically reviewed bibliographic databases including PubMed (NCBI), Embase (Elsevier), CINAHL (EBSCO), Web of Science (Clarivate Analytics), Cochrane Central Register of Controlled Trials (EBSCO), and CAB Abstracts (Clarivate Analytics). We searched for randomized controlled trials that studied the effect of drinking coffee on inflammatory markers of cardiovascular risk. RESULTS: The search of electronic databases returned 1631 records. After removing duplicate records and ineligible studies, we examined a total of 40 full-text documents, 17 of which were eligible for further analysis. In our review, boiled coffee, in particular, appeared to raise total and low-density lipoprotein cholesterol and apolipoprotein B, but evidence suggests no similar effect for filtered coffee. One study showed a significant increase in blood interleukin 6 levels among individuals who drank caffeinated coffee, compared with individuals consuming no coffee. CONCLUSION: Based on our systematic review of randomized controlled studies, we cannot confidently conclude that an anti-inflammatory effect of coffee is a major contributing factor to the lower all-cause mortality reported in observational studies.

GLP1-derived nonapeptide GLP1(28-36)amide protects pancreatic ß-cells from glucolipotoxicity.

Type 2 diabetes, often associated with obesity, results from a deficiency of insulin production and action manifested in increased blood levels of glucose and lipids that further promote insulin resistance and impair insulin secretion. Glucolipotoxicity caused by elevated plasma glucose and lipid levels is a major cause of impaired glucose-stimulated insulin secretion from pancreatic ß-cells, due to increased oxidative stress, and insulin resistance. Glucagon-like peptide-1 (GLP1), an insulinotropic glucoincretin hormone, is known to promote ß-cell survival via its actions on its G-protein-coupled receptor on ß-cells. Here, we report that a nonapeptide, GLP1(28-36)amide, derived from the C-terminal domain of the insulinotropic GLP1, exerts cytoprotective actions on INS-1 ß-cells and on dispersed human islet cells in vitro in conditions of glucolipotoxicity and increased oxidative stress independently of the GLP1 receptor. The nonapeptide appears to enter preferably stressed, glucolipotoxic cells compared with normal unstressed cells. It targets mitochondria and improves impaired mitochondrial membrane potential, increases cellular ATP levels, inhibits cytochrome c release, caspase activation, and apoptosis, and enhances the viability and survival of INS-1 ß-cells. We propose that GLP1(28-36)amide might be useful in alleviating ß-cell stress and might improve ß-cell functions and survival.