Association Between Residential Greenness and Cardiovascular Disease Risk

Background Exposure to green vegetation has been linked to positive health, but the pathophysiological processes affected by exposure to vegetation remain unclear. To study the relationship between greenness and cardiovascular disease, we examined the association between residential greenness and biomarkers of cardiovascular injury and disease risk in susceptible individuals. Methods and Results In this cross-sectional study of 408 individuals recruited from a preventive cardiology clinic, we measured biomarkers of cardiovascular injury and risk in participant blood and urine. We estimated greenness from satellite-derived normalized difference vegetation index ( NDVI ) in zones with radii of 250 m and 1 km surrounding the participants' residences. We used generalized estimating equations to examine associations between greenness and cardiovascular disease biomarkers. We adjusted for residential clustering, demographic, clinical, and environmental variables. In fully adjusted models, contemporaneous NDVI within 250 m of participant residence was inversely associated with urinary levels of epinephrine (-6.9%; 95% confidence interval, -11.5, -2.0/0.1 NDVI ) and F2-isoprostane (-9.0%; 95% confidence interval, -15.1, -2.5/0.1 NDVI ). We found stronger associations between NDVI and urinary epinephrine in women, those not on β-blockers, and those who had not previously experienced a myocardial infarction. Of the 15 subtypes of circulating angiogenic cells examined, 11 were inversely associated (8.0-15.6% decrease/0.1 NDVI ), whereas 2 were positively associated (37.6-45.8% increase/0.1 NDVI ) with contemporaneous NDVI . Conclusions Independent of age, sex, race, smoking status, neighborhood deprivation, statin use, and roadway exposure, residential greenness is associated with lower levels of sympathetic activation, reduced oxidative stress, and higher angiogenic capacity

Characteristics and Outcomes of Adults Hospitalized with SARS-CoV-2 Community-Acquired Pneumonia in Louisville, Kentucky

Background: Patients infected with the novel coronavirus SARS-CoV-2 are frequently hospitalized with community-acquired pneumonia (CAP). The objective of this study was to define the clinical characteristics and outcomes of hospitalized patients with SARS-CoV-2 CAP in the city of Louisville, KY. Methods: This was a retrospective observational study of 700 patients with SARS-CoV-2 infection hospitalized to eight of the adult hospitals in the city of Louisville. Patients with 1) a positive RT-PCR for SARS-CoV-2, 2) fever, cough, or shortness of breath, and 3) an infiltrate at chest imaging were defined as having SARS-CoV-2 CAP. Demographic characteristics of the study population were compared with census data from the city of Louisville. For each patient more than 500 variables were abstracted from electronic medical records and recorded using Research Electronic Data Capture software. Data was analyzed by descriptive and inferential statistics using R version 3.4.0. Results: SARS-CoV-2 CAP was identified in 632 (90%) patients hospitalized with COVID-19. The median age of the patients was 63 years, 53% were females, 31% were black and 12% Hispanic. The most frequent comorbidities were hypertension (56%), obesity (50%), and diabetes (33%). Mortality was 17% for the total population and 34% for the 249 patients admitted to ICU. For each category of race, ethnicity and comorbidities, the proportion of hospitalized patients with SARS-CoV-2 CAP was significantly different when compared to the Louisville population (p \u3c 0.001). Conclusion: Patients of black race, Hispanic ethnicity, and patients with history of hypertension, obesity or diabetes are overrepresented among hospitalized patients with SARS-CoV-2 CAP when compared to the Louisville population. Hospitalized patients with SARS-CoV-2 CAP are likely to require ICU care, with death occurring in approximately one of six hospitalizations

No difference in clinical outcomes for African American and White patients hospitalized with SARS-CoV-2 pneumonia in Louisville, Kentucky

Introduction: Current literature indicates that African American individuals are at increased risk of becoming infected with the SARS-CoV-2 virus and suffer higher SARS-CoV-2-related mortality rates. However, there is a lack of consensus as to how the clinical outcomes of African American patients differ from those of other groups. The objective of this study was to define the clinical outcomes of African American and White hospitalized patients with SARS-CoV-2 community-acquired pneumonia (CAP) in Louisville, Kentucky. Methods: This was a retrospective cohort study of hospitalized patients with SARS-CoV-2 CAP at eight hospitals in Louisville, Kentucky. Severity of CAP at time of hospitalization was evaluated using the pneumonia severity index (PSI), CURB-65 score and SARS-CoV-2 viral load. The following thirteen clinical outcomes were compared: discharge alive to home, time to home discharge, admission to the ICU, length of ICU stay, need for invasive mechanical ventilation (IMV), duration of IMV, development of acute respiratory distress syndrome (ARDS), development of septic shock, need for vasopressors, development of cardiovascular events, time to cardiovascular events, in-hospital mortality, and time to death. Results: A total of 541 patients were eligible for this study, 343 White (63%) and 198 African American (37%). None of the thirteen clinical outcomes were statistically significantly different between the two groups. Conclusions: This study indicates that African American and White patients do not have different clinical outcomes after the point of hospitalization due to SARS-CoV-2 CAP

Diabetes-related molecular signatures in infrared spectra of human saliva

WOS: 000290261500001PubMed ID: 20630088Background: There is an ongoing need for improvements in non-invasive, point-of-care tools for the diagnosis and prognosis of diabetes mellitus. Ideally, such technologies would allow for community screening. Methods: In this study, we employed infrared spectroscopy as a novel diagnostic tool in the prediction of diabetic status by analyzing the molecular and sub-molecular spectral signatures of saliva collected from subjects with diabetes (n = 39) and healthy controls (n = 22). Results: Spectral analysis revealed differences in several major metabolic components - lipid, proteins, glucose, thiocyanate and carboxylate - that clearly demarcate healthy and diseased saliva. The overall accuracy for the diagnosis of diabetes based on infrared spectroscopy was 100% on the training set and 88.2% on the validation set. Therefore, we have established that infrared spectroscopy can be used to generate complex biochemical profiles in saliva and identify several potential diabetes-associated spectral features. Conclusions: Infrared spectroscopy may represent an appropriate tool with which to identify novel diseases mechanisms, risk factors for diabetic complications and markers of therapeutic efficacy. Further study into the potential utility of infrared spectroscopy as diagnostic and prognostic tool for diabetes is warranted

Diabetic Gastroparesis: Principles and Current Trends in Management

<p><strong>Article full text</strong></p><p> </p><p><br> The full text of this article can be found <a href="https://link.springer.com/article/10.1007/s13300-018-0454-9"><b>here</b>.</a><br> <br> <strong>Provide enhanced digital features for this article</strong><br> If you are an author of this publication and would like to provide additional enhanced digital features for your article then please contact <u>[email protected]</u>.<br> <br> The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.<br> <br> Other enhanced features include, but are not limited to:<br> • Slide decks<br> • Videos and animations<br> • Audio abstracts<br> • Audio slides<u></u></p> <p> </p

Circulating angiogenic stem cells in type 2 diabetes are associated with glycemic control and endothelial dysfunction

Circulating angiogenic cells (CACs) of various described phenotypes participate in the regeneration of the damaged endothelium, but the abundance of these cells is highly influenced by external cues including diabetes. It is not entirely clear which CAC populations are most reflective of endothelial function nor which are impacted by diabetes. To answer these questions, we enrolled a human cohort with variable CVD risk and determined relationships between stratified levels of CACs and indices of diabetes and vascular function. We also determined associations between CAC functional markers and diabetes and identified proangiogenic molecules which are impacted by diabetes. We found that subjects with low levels of CD34+ /AC133+ /CD31+ /CD45dim cells (CAC-3) had a significantly higher incidence of diabetes (p = 0.004), higher HbA1c levels (p = 0.049) and higher CVD risk scores. Furthermore, there was an association between low CAC-3 levels and impaired vascular function (p = 0.023). These cells from diabetics had reduced levels of CXCR4 and VEGFR2, while diabetics had higher levels of certain cytokines and pro-angiogenic molecules. These results suggest that quantitative and functional defects of CD34+ /AC133+ /CD31+ /CD45dim cells are associated with diabetes and vascular impairment and that this cell type may be a prognostic indicator of CVD and vascular dysfunction

Depletion of Circulating CD34+/KDR+ Cells in Type 2 Diabetes is Associated With Glycemic Control

Background and Hypothesis: Circulating levels of endothelial progenitor cells have been found to be predictive of cardiovascular events and mortality. Although the levels of these cells reflect overall cardiovascular disease (CVD) risk, studies assessing their association with major CVD factors - hypertension, dyslipidemia and diabetes have yielded inconsistent results and the mechanisms contributing to EPC depletion remain unknown. We hypothesized that EPC depletion occurring in diabetes is mediated in part by hyperglycemia or insulin resistance. Methods: Circulating levels of progenitor cells were measured by flow cytometry in 108 diabetic or non-diabetic subjects recruited from the University of Louisville Health System. Reactive hyperemia index (RHI) was measured by the EndoPAT. Demographic information was acquired and blood, plasma and urine were used for biochemical analyses. Subjects were divided into high and low EPC count groups using the median split. Data was analyzed using a Chi-square test, a two-sample rank sum test, and univariable and multivariable logistic regressions. Results: Levels of CD34+/KDR+/CD14−/CD16− cells (EPCs) were associated with the diagnosis of diabetes (p=0.04), but not with other demographic covariates, hypertension or dyslipidemia. Levels of CD34+, AC133+ and CD34+/AC133+/CD45+ cells also displayed significant association with diabetes (p=0.038, 0.014 and 0.038 respectively). RHI was strongly associated with diabetes (p\u3c0.0001) hypertension and dyslipidemia, however, no significant associations were observed between RHI and EPCs. EPC levels were inversely associated with HbA1C (p=0.047) and fasting blood glucose, but not with insulin levels or the HOMA-IR score. In the complete model, the association between EPCs and diabetes was strengthened by the inclusion of RHI, indicating more robust EPC depletion in those with endothelial dysfunction. Conclusion: Circulating EPC levels are a robust index of long-term glycemic control and are associated with hyperglycemia rather than contemporaneous insulin levels or endothelial dysfunction. These findings may help in prognosis and early identification of CVD risk in patients with diabetes, independent of other risk estimates

Illustration of Gut&ndash;Thyroid Axis in Alcohol Use Disorder: Interplay of Gut Dysfunction, Pro-Inflammatory Responses, and Thyroid Function

(1) Background: Heavy and chronic alcohol drinking leads to altered gut dysfunction, coupled with a pro-inflammatory state. Thyroid-associated hormones and proteins may be dysregulated by heavy and chronic alcohol intake; however, the mechanism for altered gut-derived changes in thyroid function has not been studied thus far. This study investigates the role of alcohol-induced gut dysfunction and pro-inflammatory cytokine profile in the thyroid function of patients with alcohol use disorder (AUD). (2) Methods: Male and female AUD patients (n = 44) were divided into Gr.1, patients with normal thyroid-stimulating hormone (TSH) levels (n = 28, 0.8 &le; TSH &le; 3 mIU/L); and Gr.2, patients with clinically elevated TSH levels (n = 16, TSH &gt; 3 mIU/L). Demographics, drinking measures, comprehensive metabolic panels, and candidate thyroid markers (TSH, circulating triiodothyronine (T3), and free thyroxine (fT4)) were analyzed. Gut-dysfunction-associated markers (lipopolysaccharide (LPS), LPS-binding protein (LBP), and soluble LPS-induced pathogen-associated protein (sCD14)), and candidate pro-inflammatory cytokines (IL-1&beta;, TNF-&alpha;, IL-6, IL-8, MCP-1, PAI-1) were also evaluated. (3) Results: Patients in both groups presented with a borderline overweight BMI category. Gr.2 reported numerically higher indices of chronic and heavy drinking patterns than Gr.1. The fT4 levels were elevated, while T3 was within normal limits in both groups. The gut dysfunction markers LBP and sCD14 were numerically elevated in Gr.2 vs. Gr.1, suggesting subtle ongoing changes. Candidate pro-inflammatory cytokines were significantly elevated in Gr.2, including IL-1 &beta;, MCP-1, and PAI-1. Gr.2 showed a strong and statistically significant effect on the gut&ndash;immune&ndash;thyroid response (r = 0.896, 36 p = 0.002) on TSH levels in a multivariate regression model with LBP, sCD14, and PAI-1 levels as upstream variables in the gut&ndash;thyroid pathway. In addition, AUROC analysis demonstrated that many of the cytokines strongly predicted TSH in Gr.2, including IL-6 (area = 0.774, 39 p &lt; 0.001) and TNF-&alpha; (area = 0.708, p = 0.017), among others. This was not observed in Gr.1. Gr.2 demonstrated elevated fT4, as well as TSH, which suggests that there was subclinical thyroiditis with underlying CNS dysfunction and a lack of a negative feedback loop. (4) Conclusions: These findings reveal the toxic effects of heavy and chronic drinking that play a pathological role in thyroid gland dysregulation by employing the gut&ndash;brain axis. These results also emphasize potential directions to carefully evaluate thyroid dysregulation in the overall medical management of AUD