Mohamed, Essa A.

Rural populations are underrepresented in cognitive impairment research and have limited resources for education about brain and cognitive health, Alzheimer's disease and related dementias, or caregiving. As our Outreach, Recruitment, and Engagement team aimed to expand activities into more rural communities, we also wanted to better understand the characteristics of the communities surrounding our center and gain insight into the social exposome of the areas. The goal of the manuscript is to reflect on our experience and share measures that were useful in this effort, which can be further enriched and adjusted by other outreach teams.

Abstract Introduction Obstructive sleep apnea (OSA) has been linked to metabolic syndrome, heart failure, atrial fibrillation, and hypertension. Although ethnic differences related to OSA have been reported, no studies have evaluated the impact of OSA among Greek-Americans. Methods This prospective cross-sectional study, in partnership with the Greek-American community, employed a community-based participatory research framework. Individuals who were of Greek descent and ≥18 years of age were recruited. Anthropometric measurements, Mallampati score, BMI, and adiposity (DEXA scan) were determined. All subjects were administered the Epworth Sleepiness Scale (ESS) and underwent home sleep apnea test (WatchPAT ONE), using a desaturation threshold of 4% as diagnostic. Descriptive statistics were computed to describe the study population and data were analyzed using the student t-test and chi-squared test. Results A 76 Greeks, 34 males (44.8%) and 42 females (55.2%), were enrolled in this study with a mean ± SD age and BMI of 42.6±17.5 years (p< 0.01) and 27±6 kg/m2, respectively. A total of 22 (29%; 14 males and 8 females) individuals were diagnosed with OSA, of whom 13 (59.1%) had mild, 5 (22.7%) had moderate and 4 (18.2%) had severe OSA. Subjects with OSA were older (58.8±11.9 vs 36.0±15.1 years, p< 0.01), had higher BMI (32±7 vs 25±4 kg/m2, p< 0.01), larger neck circumference (40±4 vs 35±4 cm, p< 0.01) and higher waist-to-hip ratio (0.94±0.08 vs 0.84±0.07, p< 0.01). Body fat percentage was significantly higher among those with versus without OSA (38.8±9.6 vs 34.0±9.2%; p=0.04) while Mallampati and ESS scores were similar. Conclusion This is the first study to assess sleep metrics of Greek-Americans suffering from OSA. Characteristics of those with OSA are similar to other populations. However, the commonly used ESS screening appears to have limited application in this cohort of subjects. Greek-Americans with elevated body fat percentage when associated with concurrent OSA, may be at higher risk of developing cardiometabolic adverse events. Additional studies are required to further elucidate the effect of sleep physiology, cardiometabolic dysfunction and health outcomes. Support (if any) This work was supported by a grant from Sleep Number Corporation to Mayo Clinic, by WatchPATs provided by Zoll Itamar, and by the National Institutes of Health HL160619.

Cardiovascular health disparities are present in several minority racial and ethnic groups including African Americans, who exhibit an increased risk of hypertension compared to non-Hispanic Whites. Somali Americans, a subgroup of African Americans of East African origins, exhibit high rates of diabetes and obesity, conditions often comorbid with impaired blood pressure (BP) regulation. Importantly, it remains unknown whether the disparate cardiovascular risk profile, namely poor nocturnal BP regulation, manifested in African Americans can be applied to Somali Americans. We therefore examined 24-hour BP patterns in Somali Americans compared to White control participants. We hypothesized that Somali Americans would present with heightened nocturnal BP and heart rate (HR). We utilized ambulatory blood pressure monitoring (ABPM) to quantify 24-hour BP patterns in 25 Somali (10 female, 15 male; age: 34 ± 3 years; BMI: 27 ± 1 kg/m2) and 25 White (13 female, 12 male; age: 38 ± 3 years; BMI: 27 ± 1 kg/m2) individuals. Each ABPM recorded a BP reading every 20 minutes throughout the 24-hour period. Subjects were instructed to abstain from caffeine, alcohol, and vigorous exercise during the recording period. From the 24-hour recording, an ambulatory arterial stiffness index (AASI) was calculated as 1 minus the regression slope of systolic (SAP) and diastolic (DAP) arterial pressure. SAP, DAP, and HR obtained between 12:00am and 6:00am were averaged to compute nocturnal means. BP and HR dipping was determined as the percent change between daytime and nocturnal BP and HR. Statistical analysis included independent samples t-tests to determine differences in BP and HR between racial groups (i.e., Somali vs. White). Nocturnal SAP (105 ± 2 vs. 106 ± 3 mmHg, p = 0.364) and DAP (60 ± 1 vs. 58 ± 2 mmHg, p = 0.093) were not different between Somali and White participants. In contrast, nocturnal HR was significantly higher in Somalis compared to Whites (72 ± 2 vs. 64 ± 2 beats/minute, p = 0.009). Similarly, SAP (12 ± 2% vs. 12 ± 1%, p = 0.437) and DAP (18 ± 2% vs. 21 ± 2%, p = 0.127) dipping were comparable between groups, while Somali individuals exhibited blunted HR dipping (11 ± 2% vs. 19 ± 2%, p = 0.008) compared to Whites. AASI (0.32 ± 0.03 vs. 0.24 ± 0.03 a.u., p = 0.031) was higher in Somali compared to White individuals. These findings suggest Somali Americans present with impaired nocturnal cardiovascular regulation and increased arterial stiffness, which may place this racial minority at increased cardiovascular risk. Future work to investigate the mechanistic relationships of cardiovascular dysfunction in Somali Americans is warranted. Research grant from Sleep Number to Mayo Clinic for studies of sleep and cardiovascular risk in Somali Americans, and by NIH R01-HL160619, T32-DK007013, T32-HL007111, and T32-HL105355. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Background The prevalence of excessive daytime sleepiness (EDS) in the general population is reported to be 9 to 28 percent. Various social and biological factors have been reported to contribute to the development of EDS, such as cardiovascular disease, metabolic disorders as well as socioeconomic status. Medically, EDS is associated with poorer prognosis in patients with sleep disorders. However, whether sleepiness is an independent negative prognostic indicator in patients without sleep apnea is poorly understood. Objective To evaluate the relationship between self‐reported excessive daytime sleepiness (assessed by Epworth Sleepiness Scale) and the risk of all‐cause mortality in patients without obstructive sleep apnea (OSA). Methods We performed a retrospective cohort study in a large registry of patients seen at the Mayo Clinic Center for Sleep Medicine between November 17 th , 2009 and April 15 th , 2017. All patients received a diagnostic polysomnography and had completed Epworth Sleepiness Scale (ESS). The primary outcome of all‐cause mortality risk was computed using the Kaplan‐Meier analysis and Cox‐proportional hazard model with age, sex, body mass index (BMI), baseline comorbidities and sleep measurements as confounders. Results A total of 2746 non‐OSA patients were identified. The overall median age (IQR) was computed as 53 (40, 63) with 45% of patients identifying as males. The median follow‐up time was approximately 2.3 years. In a univariate analysis, daytime sleepiness was associated with the female sex, younger age and higher BMI. No significant differences were observed in vascular related diseases between sleepy and non‐sleepy patients. EDS was not significantly associated with all‐cause mortality with an adjusted hazard ratio of 1.23 (95% CI 0.86, 1.76; p =0.257). In addition, there was no significant association of EDS and the risk of all‐cause mortality even after stratifying by sex, age and BMI in non‐OSA patients. Conclusion EDS is not associated with all‐cause mortality in non‐OSA patients. Further prospective studies are needed to confirm this finding. Support or Funding Information This research was supported by NIH HL65176 and NIH HL114024. Kaplan–Meier survival curve of 8 years all‐cause mortality of non‐OSA patients with and without excessive daytime sleepiness (EDS) at baseline. image Kaplan–Meier survival curve of 8 years all‐cause mortality of non‐OSA patients with and without excessive daytime sleepiness (EDS) at baseline. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

We tested the hypothesis that local inhibition of NOS would 1) alter the kinetics of vasodilation during dynamic forearm (FA) exercise and 2) prolong the time to reach steady state (SS). Subjects (n=22) performed rhythmic FA exercise (20% of maximum) during saline infusion (control) and NOS inhibition (L‐NMMA). Additionally, a subset of subjects performed a third trial of FA exercise during combined inhibition of either 1) NOS and adenosine (aminophylline; n=9), or 2) NOS and prostaglandins (Ketorolac; n=8). Forearm vascular conductance (FVC; ml/min/100mmHg) was calculated from blood flow (ml/min) and blood pressure (mmHg). Vasodilator kinetics were assessed by calculating the slope of the FVC response for every duty cycle between baseline and SS exercise as well as the number of duty cycles (1s contraction/2s relaxation) to reach SS. NOS inhibition reduced the kinetics of vasodilation during dynamic FA exercise (8.5 ± 0.6 vs. 11.1 ± 0.8 FVC/duty cycle; P < 0.001 vs. control) and increased the time to reach SS (25.1 ± 1 vs. 32 ± 1 duty cycles; P < 0.001 vs. control). The kinetics of vasodilation were reduced further with combined inhibition of NOS and adenosine (6.2 ± 0.8 vs. 7.5 ± 0.6 FVC/duty cycle; P < 0.05 vs. L‐NMMA alone), but not with combined inhibition of NOS and prostaglandins. Our data indicate that NOS inhibition blunts the kinetics of vasodilation during dynamic FA exercise and prolongs the time to reach SS.

We tested the hypothesis that elevated sympathetic tone is responsible for lower peak vasoldilation following single muscle contractions in older adults. Younger (n=8; 5M/3F, age 27 ± 2) and older (n=10; 5M/5F, age 69 ± 2) adults performed single forearm contractions at 10, 20 and 40% of maximum during 1) control, 2) sympathetic activation via lower body negative pressure (LBNP; ‐ 20mmHg), and 3) intra‐arterial infusion of phentolamine (α‐adrenergic antagonist). Brachial artery diameter and velocities were measured via Doppler ultrasound and forearm vascular conductance (FVC) was calculated from blood flow (ml/min) and blood pressure (mmHg). Peak vasodilator responses (ΔFVC from baseline) were attenuated in older adults for all intensities ( P < 0.05). LBNP reduced the ΔFVC at 10% (95 ± 18 vs. 60 ± 11), 20% (128 ± 9 vs. 91 ± 18) and 40% (192 ± 21 vs. 133 ± 23; P < 0.01 vs. control) in younger subjects, but not older adults (61 ± 6 vs. 58 ± 10; 99 ± 10 vs. 101 ± 17; 141 ± 17 vs. 129 ± 19, respectively; P = 0.53–0.97). With phentolamine ΔFVC was enhanced in older adults at each contraction intensity (91 ± 12, 136 ± 22, and 181 ± 22, respectively; P < 0.01 vs. control), but not younger adults (87 ± 9, 145 ± 12, and 192 ± 24, respectively; P = 0.31–1.0 vs. control). Our data indicate that overlying α‐adrenergic vasoconstriction plays a significant role in the age‐related decreases in skeletal muscle contraction‐induced rapid vasodilation.

Hepatitis B virus (HBV) genotype E (HBV‐E) accounts for the majority of chronic hepatitis B (CHB) infections in West Africa. We aimed to determine factors associated with HBV‐E‐induced hepatocellular carcinoma (HCC) in West Africa. Data on patients from Burkina Faso who were hepatitis B surface antigen positive (HBsAg+) and had CHB were analyzed. HBV viral load and hepatitis B e antigen (HBeAg) status were measured in 3,885 individuals with CHB without HCC (CHB HCC−) and 59 individuals with CHB with HCC (CHB HCC+). HBV genotyping was performed for 364 subjects with CHB HCC− and 41 subjects with CHB HCC+. Overall, 2.5% of the CHB HCC− group was HBeAg+ compared with 0% of the CHB HCC+ group. Of the 364 patients who were CHB HCC− with available genotyping, the frequencies of HBV genotypes E and C/E were 70.3% and 12.9%, respectively. Age (odds ratio [OR] for older age, 1.08; 95% confidence interval [CI], 1.06‐1.10 per 1‐year increase in age), male sex (OR, 2.03; 95% CI, 1.11‐3.69), and HBV viremia (OR, 1.48; 95% CI, 1.31‐1.67 per 1 log10 IU/mL) were each associated with HCC diagnosis. Patients with genotype E had a lower HBeAg prevalence (6.3% vs. 14.9%), lower HBV viral load, and higher prevalence of cirrhosis (14.5% vs. 4.8%) than patients with genotype C/E. Conclusion: HBV‐E is the most common circulating strain (70.3%) in West African patients. HCC was associated with older age, male sex, and high HBV viral load. It is expected that these results will further inform guidance on clinical management of HBV infection in West Africa.