Community Health Worker-led Implementation of the Stanford Youth Diabetes Coaching Program in Underserved Latinx Communities.

BACKGROUND: The Stanford Youth Diabetes Coaching Program (SYDCP) is an evidence-based program led by health care professionals to teach healthy youth who then coach family members with diabetes or other chronic conditions. This purpose of this study is to evaluate a Community Health Worker (CHW)-led implementation of the SYDCP for low-income Latinx students from underserved agricultural communities. METHOD: CHWs were trained and virtually led 10 training sessions virtually during the COVID-19 for Latinx students who were recruited from high schools in agricultural regions of Washington state. Feasibility measures include recruitment, retention, class attendance, and successful coaching of a family member or friend. Acceptability was measured by responses on the post-training survey. Effectiveness was evaluated by pre-post changes in measures used in prior studies of the SYDCP such as level of activation and diabetes knowledge. RESULTS: Thirty-four students were recruited, 28 completed the training and 23 returned both pre- and post-surveys. Over 80% of students attended 7 or more classes. All met with a family or friend and 74% met with them weekly. Approximately 80% of the students rated the program's usefulness as "very good" or "excellent." Pre-post increases in diabetes knowledge, nutrition-related behaviors, resilience, and activation were significant and similar to those observed in prior published studies of the SYDCP. CONCLUSIONS: Findings support the feasibility, acceptability, and effectiveness of a CHW-led implementation of the SYDCP in underserved Latinx communities using a virtual remote model.

Receptor for advanced glycation end-products axis and coronavirus disease 2019 in inflammatory bowel diseases: A dangerous liaison?

Compelling evidence supports the crucial role of the receptor for advanced glycation end-products (RAGE) axis activation in many clinical entities. Since the beginning of the coronavirus disease 2019 pandemic, there is an increasing concern about the risk and handling of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in inflammatory gastrointestinal disorders, such as inflammatory bowel diseases (IBD). However, clinical data raised during pandemic suggests that IBD patients do not have an increased risk of contracting SARS-CoV-2 infection or develop a more severe course of infection. In the present review, we intend to highlight how two potentially important contributors to the inflammatory response to SARS-CoV-2 infection in IBD patients, the RAGE axis activation as well as the cross-talk with the renin-angiotensin system, are dampened by the high expression of soluble forms of both RAGE and the angiotensin-converting enzyme (ACE) 2. The soluble form of RAGE functions as a decoy for its ligands, and soluble ACE2 seems to be an additionally attenuating contributor to RAGE axis activation, particularly by avoiding the transactivation of the RAGE axis that can be produced by the virus-mediated imbalance of the ACE/angiotensin II/angiotensin II receptor type 1 pathway.

Advanced-glycation end-products axis: A contributor to the risk of severe illness from COVID-19 in diabetes patients.

Compelling pieces of evidence derived from both clinical and experimental research has demonstrated the crucial role of the receptor for advanced-glycation end-products (RAGE) in orchestrating a plethora of proinflammatory cellular responses leading to many of the complications and end-organ damages reported in patients with diabetes mellitus (DM). During the coronavirus disease 2019 (COVID-19) pandemic, many clinical reports have pointed out that DM increases the risk of COVID-19 complications, hospitalization requirements, as well as the overall severe acute respiratory syndrome coronavirus 2 case-fatality rate. In the present review, we intend to focus on how the basal activation state of the RAGE axis in common preexisting conditions in DM patients such as endothelial dysfunction and hyperglycemia-related prothrombotic phenotype, as well as the contribution of RAGE signaling in lung inflammation, may then lead to the increased mortality risk of COVID-19 in these patients. Additionally, the cross-talk between the RAGE axis with either another severe acute respiratory syndrome coronavirus 2 receptor molecule different of angiotensin-converting enzyme 2 or the renin-angiotensin system imbalance produced by viral infection, as well as the role of this multi-ligand receptor on the obesity-associated low-grade inflammation in the higher risk for severe illness reported in diabetes patients with COVID-19, are also discussed.