Health Disparities of Coronavirus Disease 2019 in Texas, March-July 2020.

OBJECTIVES: Although disparities in coronavirus disease 2019 (COVID-19) prevalence are known, knowledge of the recent surge of COVID-19 in Texas and factors affecting fatality rates is limited. Understanding the health disparities associated with COVID-19 can help healthcare professionals determine the populations that are most in need of COVID-19 preventive care and treatment. The aim of this study was to assess COVID-19-related case and mortality rates. METHODS: Our cross-sectional analysis used Texas Department of State Health Services COVID-19 case surveillance counts. Case, hospitalization, and mortality counts were obtained from March to July 2020. RESULTS: From March to July 2020, there were 420,397 COVID-19-related cases and 6954 deaths in Texas. There were 3277 new cases and 104 deaths in March, and 261,876 new cases and 3660 deaths in July. The number of new COVID-19 cases was the highest from March to April (relative risk 1.77, 95% confidence interval [CI] 1.76-1.78). Although the death rate in June was a 30% increase over the rate in May, death rates nearly tripled by the end of July, for a total of 3660 deaths. Of the 3958 deaths, demographic data were available for 753 deaths. Of these, 440 were male, 16 Asian, 95 Black, 221 Hispanic, 325 White, and 96 were "Other" or "Unknown." Males were associated with a slightly higher chance of acquiring COVID-19 than females (odds ratio [OR] 1.11, 95% CI 1.09-1.14) and nearly a 29% higher chance of dying of COVID-19 compared with females (OR 1.29, 95% CI 1.11-1.49). Bivariate analysis revealed that the probability of acquiring COVID-19 was 12% higher in older adults compared with individuals younger than 65 years old (OR 1.12, 95% CI 1.08-1.16), and older adults had an 18.8 times higher risk of death when compared with the rate of younger individuals (OR 18.79, 95% CI 15.93-22.15). Hispanics and Blacks were 70% and 48%, respectively, more likely to contract COVID-19 than Whites. All races had lower significant chance of death when compared with Whites. At the end of July, there was a total of 430,485 Texas COVID-19 cases and 6387 fatalities (8.8% of all cases and 4% of all deaths in the United States.). Case fatality ratios were the highest in older adults. As we continued to observe data, in contrast to previous study time points, we found that Asians and Hispanics had no significant difference in COVID mortality rates and were comparable in terms of mortality odds and death case ratios when compared with Whites. CONCLUSIONS: This time period represents the highest COVID-19 surge time in Texas. Although our data consist of a short time period of population-level data in an ongoing pandemic and are limited by information reported to the Texas Department of State Health Services, older age, male sex, Hispanics, and Blacks are currently associated with higher infection rates, whereas older age, male sex, and Whites are associated with higher mortality rates. Clinicians and decision makers should be aware of the COVID-19 health disparities and risk factors for mortality to better promote targeted interventions and allocate resources accordingly.

Salvianolic Acid B (Sal B) Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Cell Death by Activating Glutaredoxin 1 (Grx1).

Protein glutathionylation, defined as the formation of protein mixed disulfides (PSSG) between cysteine residues and glutathione (GSH), can lead to cell death. Glutaredoxin 1 (Grx1) is a thiol repair enzyme which catalyzes the reduction of PSSG. Therefore, Grx1 exerts strong anti-apoptotic effects by improving the redox state, especially in times of oxidative stress. However, there is currently no compound that is identified as a Grx1 activator. In this study, we identified and characterized Salvianolic acid B (Sal B), a natural compound, as a Grx1 inducer, which potently protected retinal pigment epithelial (RPE) cells from oxidative injury. Our results showed that treatment with Sal B protected primary human RPE cells from H2O2-induced cell damage. Interestingly, we found Sal B pretreatment upregulated Grx1 expression in RPE cells in a time- and dose-dependent manner. Furthermore, NF-E2-related factor 2 (Nrf2), the key transcription factor that regulates the expression of Grx1, was activated in Sal B treated RPE cells. Further investigation showed that knockdown of Grx1 by small interfering RNA (siRNA) significantly reduced the protective effects of Sal B. We conclude that Sal B protects RPE cells against H2O2-induced cell injury through Grx1 induction by activating Nrf2 pathway, thus preventing lethal accumulation of PSSG and reversing oxidative damage.

Long-term medication adherence and preventive vs reactive care utilization among older adults with diabetes.

OBJECTIVES: To assess long-term adherence to oral hypoglycemic agents (OHAs) and determine if adherence affects total health care expenditures of reactive vs preventive services. STUDY DESIGN: Retrospective cohort study. METHODS: This study measured adherence to OHAs using Medical Expenditure Panel Survey 2013-2017 data. Adults 65 years and older who had diabetes and were taking at least 1 OHA were included. Respondents with a medication possession ratio (MPR) of at least 80% were considered adherent. Health care utilization and expenditure were compared among adherent and nonadherent respondents for preventive and reactive services. Utilization data were analyzed using negative binomial regression and expenditure data using γ-family generalized linear regression models. RESULTS: Approximately 67% of the cohort (n = 1279) were adherent. The adherent group had greater health care expenditure overall than nonadherent respondents ($29,985 [95% CI, $27,161-$32,743] vs $24,623 [95% CI, $21,623-$28,122]; P < .05). Although expenditure was higher for prescription medications and office visits, mean emergency department expenditures were higher for adherent respondents. The utilization and proportion of expenditure on preventive vs reactive health care services did not differ by adherence as defined by an MPR of at least 80%. CONCLUSIONS: Increasing adherence provides an opportunity to improve CMS quality ratings. Our finding that adherence does not affect the financial burden of disease might be explained by the increased costs of preventive medication and increased comorbidity burden of these patients. Low adherence to OHAs encourages clinicians to be more proactive in ensuring that prescription medications are refilled regularly. By emphasizing equitable diabetes education and tailoring quality initiatives that minimize racial disparities, adherence can be better achieved.

Cost of Traditional Herbal Medicines for Noncommunicable Diseases in Rural and Urban Communities in South Africa.

OBJECTIVES: This study assessed traditional herbal medicine (THM) and conventional medicine (CM) utilization among participants with noncommunicable disease in South Africa. METHODS: A cross-sectional study of the Prospective Urban and Rural Epidemiological study collected data through face-to-face interviews using structured questionnaires in 2014. Descriptive, bivariate, and multivariate logistic regression were used to determine the effect of sociodemographic and economic factors on THM and CM use. All statistical analyses were conducted using the statistical computing and graphics language "R." RESULTS: Of the total 417 randomly selected participants in this study, 85% were females, 95% with no health insurance, and 81% with monthly incomes of <2000 rand (R) ($137 equivalent) per month. Moreover, 73% spend 5% of their income on THM, and 10% say they are willing to pay >R500 per year on THM to feel better. Age was significantly associated with different spending patterns after controlling for other demographic factors, given that older adults were 82% (odds ratio 0.18; 95% confidence interval 0.02-0.93) less likely to pay >R100 for THM whereas younger adults were 59% (odds ratio 0.41; 95% confidence interval 0.17-0.97) less likely to pay for CM. CONCLUSIONS: The cost of using THM and CM largely differed by age. The economic insight into this study reveals individuals more willing to pay for THM to payors, which can ultimately clue payors into areas for medication optimization from potential drug-drug interactions and adverse events and, therefore, reduce healthcare costs.

Involvement of Nrf2 in Ocular Diseases.

The human body harbors within it an intricate and delicate balance between oxidants and antioxidants. Any disruption in this checks-and-balances system can lead to harmful consequences in various organs and tissues, such as the eye. This review focuses on the effects of oxidative stress and the role of a particular antioxidant system-the Keap1-Nrf2-ARE pathway-on ocular diseases, specifically age-related macular degeneration, cataracts, diabetic retinopathy, and glaucoma. Together, they are the major causes of blindness in the world.

The novel triterpenoid RTA 408 protects human retinal pigment epithelial cells against H2O2-induced cell injury via NF-E2-related factor 2 (Nrf2) activation.

Oxidative stress-induced retinal pigment epithelial (RPE) cell damage is an important factor in the pathogenesis of age-related macular degeneration (AMD). Previous studies have shown that RTA 408, a synthetic triterpenoid compound, potently activates Nrf2. This study aimed to investigate the protective effects of RTA 408 in cultured RPE cells during oxidative stress and to determine the effects of RTA 408 on Nrf2 and its downstream target genes. Primary human RPE cells were pretreated with RTA 408 and then incubated in 200µM H2O2 for 6h. Cell viability was measured with the WST-8 assay. Apoptosis was quantitatively measured by annexin V/propidium iodide (PI) double staining and Hoechst 33342 fluorescent staining. Reduced (GSH) and oxidized glutathione (GSSG) were measured using colorimetric assays. Nrf2 activation and its downstream effects on phase II enzymes were examined by Western blot. Treatment of RPE cells with nanomolar ranges (10 and 100nM) of RTA 408 markedly attenuated H2O2-induced viability loss and apoptosis. RTA 408 pretreatment significantly protected cells from oxidative stress-induced GSH loss, GSSG formation and decreased ROS production. RTA 408 activated Nrf2 and increased the expression of its downstream genes, such as HO-1, NQO1, SOD2, catalase, Grx1, and Trx1. Consequently, the enzyme activities of NQO1, Grx1, and Trx1 were fully protected by RTA 408 pretreatment under oxidative stress. Moreover, knockdown of Nrf2 by siRNA significantly reduced the cytoprotective effects of RTA 408. In conclusion, our data suggest that RTA 408 protect primary human RPE cells from oxidative stress-induced damage by activating Nrf2 and its downstream genes.

Glutaredoxin 1 (Grx1) Protects Human Retinal Pigment Epithelial Cells From Oxidative Damage by Preventing AKT Glutathionylation.

PURPOSE: Glutaredoxin 1 (Grx1) belongs to the oxidoreductase family and is a component of the endogenous antioxidant defense system. However, its physiological function remains largely unknown. In this study, we investigated whether and how Grx1 overexpression protects the retinal pigment epithelial (RPE) cells against H2O2-induced apoptosis. METHODS: Human retinal pigment epithelial (ARPE-19) cells were transfected with either a Grx1-containing plasmid or an empty vector. Primary human RPE cells were transfected with Grx1 small interfering RNA (siRNA) or scrambled siRNA. Cell viability was measured with the WST8 assay. Apoptosis was quantitatively measured by annexin V/propidium iodide (PI) double staining. The level of protein glutathionylation (PSSG) was measured by immunoblotting using anti-PSSG antibody. Protein kinase B (AKT) activation was examined by Western blot. Protein kinase B glutathionylation was detected by immunoprecipitation followed by immunoblotting with anti-PSSG antibody. RESULTS: Glutaredoxin 1 overexpression protected ARPE-19 cells from H2O2-induced cell viability loss. Conversely, Grx1 gene knockdown sensitized primary human RPE cells to H2O2. Assessment of apoptosis indicated that cells transfected with the Grx1-containing plasmid were more resistant to H2O2 with fewer cells undergoing apoptosis as compared to empty vector-transfected cells. Hydrogen peroxide-induced PSSG accumulation was also attenuated by Grx1 enrichment. Furthermore, Grx1 overexpression prevented H2O2-induced AKT glutathionylation, resulting in a sustained phospho-AKT elevation in RPE cells. CONCLUSIONS: Glutaredoxin 1 can protect RPE cells against oxidative stress-induced apoptosis. The mechanism of this protection is associated with its ability to stimulate the phosphorylation of AKT by preventing AKT glutathionylation. Considering Grx1's protective abilities in RPE cells, Grx1 could be a potential pharmacological target for retinal degenerative diseases.