bluuebunny/crossref_metadata_2025_split huggingface dataset:
113-LB: Home Diabetes Regimen and Admission HbA1c as Predictors of Hospital Glycemic Control: A Pooled Analysis of Inpatient Clinical Trials
Authors: URRUTIA MARIA A. , GUO YI , FAYFMAN MAYA , VELLANKI PRIYATHAMA , GALINDO RODOLFO J. , MIGDAL ALEXANDRA , DAVIS GEORGIA , ANZOLA ISABEL , ALBURY BONNIE S. , SCIOSCIA MARIA F. , ZAMUDIO KARLA W. , UMPIERREZ GUILLERMO E. , PASQUEL FRANCISCO J. 
Published: June 2020

Glycated hemoglobin (HbA1c) on admission has been suggested as a predictor of glycemic control in the hospital. However, no studies have examined the interaction of pre-admission patient characteristics (i.e., complexity of home regimen or diabetes duration) and HbA1c on inpatient glycemic control. We pooled data from eight randomized controlled trials of patients assigned to a standardized basal-bolus insulin regimen in the hospital. Patients were categorized according to: A) increasing home regimen complexity [group 1: diet alone or ≤1 oral antihyperglycemic drugs (OADs) (n=338, 39%); group 2: two or more OADs (n=177, 20%); and group 3: insulin based regimens (n=356, 41%) and B) admission HbA1c categories (&lt;7%, 7-9%, or &gt;9%). Logistic regression models adjusting for age, gender, BMI, admission BG, and hospital service (medicine vs. surgery) were constructed to determine associations between home regimen complexity, diabetes duration, HbA1c and inpatient glycemic control. Compared to patients treated at home with OADs, patients using insulin had a longer duration of diabetes and higher admission HbA1c (both p&lt;0.001). Compared to group 1 (reference), patients on insulin were less likely to achieve target glycemic control (mean BG 70-180 mg/dl without hypoglycemia) regardless of admission HbA1c [HbA1c &lt;7% adjusted odd ratio (aOR) 0.36 (0.16, 0.81); HbA1c 7-9% aOR 0.5 (0.30, 0.91), or HbA1c &gt;9% aOR 0.44 (0.24, 0.83), and had higher risk for hypoglycemia (all p&lt;0.05). Patients with a longer duration of diabetes (&gt;10 years) were less likely to achieve good glycemic control compared to patients with shorter duration of diabetes irrespective of home regimen complexity. Though admission HbA1c has been proposed as a predictor of inpatient glycemic control, our data show patients requiring complex therapy with insulin at home are less likely to achieve inpatient glucose targets independent of admission HbA1c.

Disclosure
M.A. Urrutia: None. Y. Guo: None. M. Fayfman: None. P. Vellanki: Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc. R.J. Galindo: Advisory Panel; Self; Lilly Diabetes. Consultant; Self; Valeritas, Inc. Research Support; Self; Novo Nordisk Inc. Other Relationship; Self; UpToDate. A. Migdal: None. G. Davis: None. I. Anzola: None. B.S. Albury: None. M.F. Scioscia: None. K.W. Zamudio: None. G.E. Umpierrez: None. F.J. Pasquel: Advisory Panel; Self; AstraZeneca, Eli Lilly and Company. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Merck Sharp & Dohme Corp. Research Support; Self; Dexcom, Inc., Merck Sharp & Dohme Corp., National Institutes of Health.
1133-P: Association of Higher Baseline BNP Levels with a Greater Reduction in Plasma Volume and Increase in Beta-Hydroxybutyrate via the SGLT2 Inhibitor Tofogliflozin in Type 2 Diabetes
Authors: YOSHIDA AKIHIRO , MATSUBAYASHI YASUHIRO , NOJIMA TOSHIAKI , SUGANAMI HIDEKI , OE MOMOKO , FUJIHARA KAZUYA , TANAKA SHIRO , KAKU KOHEI , SONE HIROHITO 
Published: June 2020

Reduced plasma volume (PV) to decrease ventricular filling pressure and increased beta-hydroxybutyrate (BHB) as a substitute for the energy source by SGLT2 inhibitors (SGLT2is) might contribute to preserving the heart in type 2 diabetes mellitus (T2DM). However, the impact of SGLT2is on PV and BHB is little known according to cardiac workload. We investigated the effect of long-term treatment with the SGLT2i, tofogliflozin, on PV and BHB according to baseline brain natriuretic peptide (BNP) levels in T2DM. Analyzed were 774 T2DM patients who received tofogliflozin for 52 weeks as mono- and add-on-therapy in two phase-3 studies. Percent change in estimated PV (%ΔePV) was calculated by the Strauss formula: {100*(pre Hb/post Hb)*[(100 - post Ht)/(100 - pre Ht)] - 100}. We divided patients into two groups (Quartiles 1-3[Q1-3] and Quartile 4[Q4]) according to baseline BNP. Differences in characteristics were analyzed using unpaired t-test, wilcoxon rank sum test or Fisher’s exact test. Differences in changes between groups were analyzed using an analysis of covariance model. Multivariate analysis evaluated the association of baseline BNP with changed variables. Baseline characteristics were: male (71 vs. 52% *, * p&lt;0.05, Q1-3 vs. Q4), age (mean: 57 vs. 64 y *), HbA1c (8.1 vs. 8.0%), BMI (26 vs. 25 kg/m2 *), BNP (median: 9 vs. 27 pg/mL *) and BHB (45 vs. 54 µmol/L). Reduction in Ln-transformed BNP (ln-BNP) was greater in Q4 (least square mean: -0.5 ln[pg/mL]) than in Q1-3 (-0.1) as was %ΔePV (Q4 [-6 %] vs. Q1-3 [-4]). Increase in Ln-transformed BHB (ln-BHB) was larger n Q4 (+0.7 ln[µmol/L]) than in Q1-3 (+0.5). Changes in HbA1c, body weight and blood pressure were similar. Q4 was independently correlated with the greater reduction in %ΔePV and increase in ln-BHB. Results suggested that reduced PV and increased BHB might be greater in T2DM patients with higher baseline BNP levels after long-term tofogliflozin therapy.

Disclosure
A. Yoshida: Employee; Self; Kowa Company, Ltd. Y. Matsubayashi: None. T. Nojima: Employee; Self; Kowa Company, Ltd. H. Suganami: Employee; Self; Kowa Company, Ltd. M. Oe: Employee; Self; Kowa Company, Ltd. K. Fujihara: None. S. Tanaka: None. K. Kaku: Advisory Panel; Self; Nippon Boehringer Ingelheim Co. Ltd., Novo Nordisk Inc. Consultant; Self; Sanwa Kagaku Kenkyusho. Research Support; Self; Taisho Pharmaceutical Co., Ltd. Speaker’s Bureau; Self; Astellas Pharma Inc., AstraZeneca, Daiichi Sankyo, Eli Lilly Japan K.K., Kowa Company, Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Ono Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. H. Sone: Research Support; Self; Kyowa Hakko Kirin Co., Ltd., Novartis AG, Ono Pharmaceutical Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co.
1134-P: The Secretome of Visceral Adipose Cells Induces Apoptosis of Cardiac Progenitor Cells in Human Obesity: Protective Effects of the SGLT2 Inhibitor Dapagliflozin
Authors: PORRO STEFANIA , PERRINI SEBASTIO , CACCIOPPOLI CRISTINA , DORIA ROSSELLA , GENCHI VALENTINA ANNAMARIA , SCHIPANI ROSSELLA , CIGNARELLI ANGELO , NATALICCHIO ANNALISA , LAVIOLA LUIGI , GIORGINO FRANCESCO 
Published: June 2020

This study aimed to assess whether the secretome from abdominal visceral (AV) and epicardial (E) adipose stem cells (ASC), ASC-derived mature adipocytes, and isolated AV mature adipocytes may affect the viability of cardiac progenitor cells (CPC) in human obesity, and whether dapagliflozin (DAPA) may reduce the proapoptotic effects in injured CPC. ASC were isolated from AV and E adipose tissue biopsies of nondiabetic subjects with varying levels of BMI and used before and after differentiation into adipocytes in vitro. CPC were isolated from right auricle biopsies of non-obese (Ob) subjects, preincubated in the presence or absence of 10 uM DAPA, and exposed or not to conditioned media (CM) of AV-ASC, E-ASC, AV-ASC-derived adipocytes and isolated AV mature adipocytes. The CM of AV-ASC and differentiated adipocytes from Ob subjects induced CPC apoptosis after 4-8-24 h (p&lt;0.05). In addition, exposure of CPC to CM of Ob AV-ASC and mature adipocytes resulted in marked inhibition of insulin-stimulated Akt phosphorylation (Akt-Ph) (p&lt;0.05). In contrast, the CM of AV-ASC and differentiated adipocytes from non-Ob subjects did not induce apoptosis nor impaired insulin signaling. Similarly, the CM of AV mature adipocytes isolated from Ob subjects induced a marked apoptosis of CPC (p&lt;0.05) and inhibited insulin-stimulated Akt-Ph, whereas no effects were observed when CPC were exposed to CM of mature adipocytes isolated from non-Ob subjects. Of note, the CM of E-ASC isolated from Ob subjects also induced CPC apoptosis and impaired insulin-stimulated Akt-Ph (p&lt;0.05), while these effects were not observed when CPC were exposed to CM of E-ASC from non-Ob subjects. The proapoptotic effects of the CM in the CPC were inhibited when these cells were pretreated with DAPA (p&lt;0.05).
In conclusion, the secretome of adipose cells from Ob subjects impairs insulin action and viability of the CPC, and these effects can be counteracted by DAPA.

Disclosure
S. Porro: None. S. Perrini: None. C. Caccioppoli: None. R. Doria: None. V. Genchi: None. R. Schipani: None. A. Cignarelli: None. A. Natalicchio: Consultant; Self; AstraZeneca, Novo Nordisk Inc., Sanofi-Aventis. L. Laviola: Advisory Panel; Self; Abbott, AstraZeneca, Boehringer Ingelheim International GmbH, Eli Lilly and Company, Novo Nordisk Inc., Roche Diabetes Care, Sanofi-Aventis. Speaker’s Bureau; Self; Abbott, Medtronic. F. Giorgino: Advisory Panel; Self; AstraZeneca, Eli Lilly and Company, Novo Nordisk Inc., Roche Diabetes Care, Sanofi. Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., LifeScan, Inc., MedImmune, Merck Sharp & Dohme Corp., Roche Diabetes Care, Sanofi. Research Support; Self; Eli Lilly and Company, LifeScan, Inc., Takeda Development Centre Europe Ltd.
1136-P: Glucose Kinetics during Oral Glucose Challenge following Administration of Exenatide and Dapagliflozin Alone and in Combination in Type 2 Diabetes
Authors: ALATRACH MARIAM , AGYIN CHRISTINA , LAICHUTHAI NITCHAKARN , LAVRYNENKO OLGA , ADAMS JOHN M. , ABDUL-GHANI MUHAMMAD , TRIPLITT CURTIS L. , DEFRONZO RALPH A. , CERSOSIMO EUGENIO 
Published: June 2020

Aim: To examine the effect of SGLT2i on endogenous glucose production (EGP), tissue glucose disappearance (Rd), and urinary glucose excretion (UGE) following glucose ingestion.
Study Design: 28 type 2 diabetes [T2D] patients (Age= 51±2 y; BMI=31.2±0.7; A1C=7.9±0.2%) received 8-hour 3-3H-glucose infusion after an overnight fast. Previously shown, EGP suppression by dapagliflozin (DAPA) compared to placebo (PCB) (Δ=-0.02±0.02 vs. -0.45±0.03, p&lt;0.01 mg/kg.min) was impaired. On a separate day, subjects were randomized to receive 5-hour double-isotope (IV 3-[3H]-glucose and oral [14C]-glucose) OGTT (75-g) preceded by PCB, DAPA 10 mg, EXEN 5 µg, or DAPA+EXEN. Oral [RaO], EGP, Total and Tissue Rd, and UGE were calculated.
Results: During 0-300-min, RaO was 65 g in DAPA, 59 g in PCB, 46 g in EXEN, and 48 g in DAPA+EXEN. UGE was 31±4 g in DAPA and 30±4 g in DAPA+EXEN, but only 3±1 g in EXEN and 10±3 g in PCB (p&lt;0.001 vs. DAPA and DAPA+EXEN).
Conclusion: The post-OGTT rise in PG was significantly reduced after DAPA+EXEN vs. each drug alone. This resulted from lower oral glucose appearance with greater UGE. During the OGTT, EGP suppression with DAPA (Δ = -0.8±0.1 mg/kg.min) was less than with PCB, EXEN, and DAPA/EXEN (p&lt;0.05-0.01), while EGP suppression with DAPA/EXEN was similar to PCB but required a higher rise in insulin (p&lt;0.05). Tissue glucose clearance was unchanged by any therapy.

Disclosure
M. Alatrach: None. C. Agyin: None. N. Laichuthai: None. O. Lavrynenko: None. J.M. Adams: None. M. Abdul-Ghani: None. C.L. Triplitt: Speaker’s Bureau; Self; AstraZeneca, Janssen Pharmaceuticals, Inc., Lilly Diabetes, Xeris Pharmaceuticals, Inc. R.A. DeFronzo: None. E. Cersosimo: None.
1140-P: Empagliflozin Attenuates Fasting and Postprandial Hyperglycemia in Totally Pancreatectomized Patients: A Randomized, Double-Blinded, Placebo-Controlled Crossover Trial
Authors: BAEKDAL MILLE , LUND ASGER , NIELSEN SOPHIE W. , STORKHOLM JAN H. , HANSEN CARSTEN , VILSBØLL TINA , KNOP FILIP K. 
Published: June 2020

Insulin remains the only glucose-lowering treatment modality recommended in totally pancreatectomized (PX) patients. We investigated the effects of the sodium glucose transporter 2 (SGLT2) inhibitor empagliflozin on fasting and postprandial glucose concentrations in PX patients. In a randomized, double-blinded, placebo-controlled crossover study, 10 PX patients (age 65.7±6.4 [mean±SD] years; BMI 23.8±4.3 kg/m2) and 10 CTRLs (age 65±7.8 years; BMI 24.3±3.5 kg/m2) underwent a 3-hour liquid mixed meal test (MMT) preceded by two doses of 25 mg empagliflozin (administered the night before and on the morning of the MMT) and placebo, respectively. Basal insulin was administered as usual; no bolus insulin was administered during study days. Empagliflozin lowered fasting plasma glucose compared to placebo (5.0±0.5 vs. 7.9±0.9 mmol/l [mean±SEM], P=0.029) and postprandial plasma glucose excursions as assessed by baseline-subtracted area under curve (999±96 vs. 1,235±69 min×pmol/l, P=0.034) in the PX patients. In CTRLs, empagliflozin lowered fasting plasma glucose compared to placebo (5.2±0.1 vs. 5.5±0.1 mmol/l, P=0.021) without affecting postprandial glucose excursions significantly. Empagliflozin acutely and effectively decreases fasting plasma glucose and attenuates postprandial hyperglycemia in PX patients.

Disclosure
M. Baekdal: None. A. Lund: Speaker’s Bureau; Self; AstraZeneca, Novo Nordisk A/S, Sanofi. S.W. Nielsen: None. J.H. Storkholm: None. C. Hansen: None. T. Vilsbøll: Advisory Panel; Self; AstraZeneca, Mundipharma International, Novo Nordisk A/S, Sun Pharmaceutical Industries Ltd. Consultant; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Lilly Diabetes, Medscape, Merck Sharp & Dohme Corp., Sanofi. F.K. Knop: Advisory Panel; Self; AstraZeneca, Merck Sharp & Dohme Corp., Mundipharma International, Novo Nordisk A/S, Sanofi. Consultant; Self; Carmot Therapeutics, Inc., Eli Lilly and Company, Novo Nordisk A/S. Research Support; Self; AstraZeneca, Gubra, Novo Nordisk A/S, Sanofi, Zealand Pharma A/S. Speaker’s Bureau; Self; AstraZeneca, Lupin Pharmaceuticals, Inc., Merck Sharp & Dohme Corp., Norgine B.V., Novo Nordisk A/S.
1146-P: The Effects of the SGLT2 Inhibitor Empagliflozin on Fatty Liver in Diet-Induced Obese Mice
Authors: WANG WEI , GUO WANRONG , JIAN YING , SHEN YUNFENG , XU FEN 
Published: June 2020

SGLT2 inhibitors (SGLT2Is), which are known to reduce blood glucose by inhibiting the reabsorption of renal glucose and promoting the excretion of urine glucose, are a kind of novel antidiabetic drugs for the treatment of type 2 diabetes and were reported to have multiple beneficial effects on the complications of diabetes. However, whether and how SGLT2Is improve obesity-related fatty liver remains unclear. In our study, 8-week-old C57BL/6 mice were fed on a normal diet or a high-fat diet for 16 weeks. After the diet induction, they were divided randomly into four groups: the normal chow diet group (NC group), the normal diet + empagliflozin group (NCE group), the high-fat diet group (HFD group) and the high-fat diet + empagliflozin group (HFDE group). The NCE group and the HFDE group were administered empagliflozin by oral gavage for 4 weeks, while the NC group and the HFD group were administered the same amount of cosolvent. After four-week treatment, body weight and fasting blood glucose of HFDE group were significantly improved when compared to HFD group. In addition, improved glucose tolerance and insulin sensitivity were observed in HFDE group. Both the energy intake and water intake increased significantly after empagliflozin intervention. What’s more, daily urine volume was remarkably increased by empagliflozin. Although there was no difference in total body fat mass between HFD group and HFDE group, the weight of subcutaneous adipose tissue and brown adipose tissue were significantly reduced. Importantly, liver weight was also statistically reduced in HFDE group compared with the HFD group. Oil red O staining showed that the hepatic steatosis in the HFDE group was ameliorated compared to HFD group.
In conclusion, empagliflozin could significantly reduce the body weight and liver weight, and improve fasting blood glucose and hepatic steatosis. The underlying mechanism will be further explored.

Disclosure
W. Wang: None. W. Guo: None. Y. Jian: None. Y. Shen: None. F. Xu: None.
1148-P: Antioxidative Effects of Empagliflozin and Metformin in Type 1 Diabetes Mellitus Patients
Authors: JANIC MIODRAG , LUNDER MOJCA , SABOVIC MISO , JANEZ ANDREJ 
Published: June 2020

Background: Favourable cardiovascular effects of SGLT2 inhibitors have been clearly revealed, whereas the underlying mechanism(s) still remain unknown. We explored the anti-oxidative action of empagliflozin (alone and in combination with metformin) in type 1 diabetes mellitus (T1DM) patients.
Methods: Forty T1DM male patients (age 44.7 ± 2.5 years, BMI 28.3 ± 0.6 kg/m2) were equally randomised into four groups: 1) control (placebo), 2) empagliflozin (25 mg daily), 3) metformin (2000 mg daily) and 4) combination (empagliflozin 25 mg daily and metformin 2000 mg daily). Oxidative stress parameters were assessed at inclusion and after 12 weeks of treatment, comprising of total antioxidative status (TAS), superoxide dismutase (SOD), glutathione peroxidase (GPx), isoprostane, interleukin 6 (IL6) and advanced oxidation protein products (AOPP). One-way analysis of variance (ANOVA) with Bonferroni post-test was used for statistical analysis.
Results: Empagliflozin in combination with metformin significantly improved antioxidative status parameters by increasing TAS for up to 1.07-fold (P&lt;0.01), SOD for up to 1.08-fold (P&lt;0.001) and GPx for up to 1.15-fold (P&lt;0.01), whereas empagliflozin or metformin alone were less effective. The prooxidants significantly decreased in groups treated with empagliflozin alone or empagliflozin in combination with metformin: isoprostane for up to 1.26-fold (P&lt;0.001) and IL6 for up to 1.34-fold (P&lt;0.01); whereas the level of AOPP significantly decreased only in the group treated with empagliflozin and metformin combination (for up to 1.22-fold; P&lt;0.01). The levels of oxidative stress parameters in the control group remained unchanged.
Conclusion: We found that empagliflozin in combination with metformin provided powerful antioxidative defense in T1DM patients. The results could at least partially explain the beneficial effects of the two drugs beyond glucose control. Antioxidant activity should be focused on in further large clinical studies.

Disclosure
M. Janic: None. M. Lunder: None. M. Sabovic: None. A. Janez: None.
1154-P: Ending a Blanket Ban for Insulin-Treated Commercial Pilots: An Interdisciplinary Collaboration
Authors: LORBER DANIEL , FECH-BAUGHMAN SARAH 
Published: June 2020

Background: In 1959, the Department of Transportation enacted safety regulations that included a blanket ban on insulin use by pilots. In 1996, in response to American Diabetes Association® (ADA) advocacy, the Federal Aviation Administration (FAA) began allowing insulin-treated (ITDM) pilots to fly privately. The success of this program led to approximately 500 pilots certified to fly privately with no adverse events related to diabetes. Nonetheless, the ban on insulin use remained intact for commercial pilots. Some ITDM pilots continued working but chose to avoid insulin and accept the resulting increased hyperglycemia and long term complications.
Interventions: The ADA began a strategy of multi-disciplinary interventions to reverse the blanket ban, including engaging “grassroots” and “grasstops” advocates, litigation, and legislative efforts. In 2014, an expert ADA medical panel reviewed relevant National Transportation and Safety Board data and recommended criteria to identify pilots capable of avoiding hypo and hyperglycemia in flight. When the FAA remained reluctant to overturn its longstanding policy, ADA continued its advocacy to encourage the FAA to adopt its recommendations by providing legal and medical support to ITDM pilots engaged in litigation against the FAA. Increasingly accurate continuous glucose monitoring (CGM) technology contributed to the FAA’s decision to overturn the blanket ban. Indeed, the new protocol requires pilots to use a CGM.
Results: In November 2019 the FAA published a new protocol for insulin-treated commercial pilots which eliminates the blanket ban.
Conclusions: The ADA’s unique structure and position enabled it to take the lead in dramatically improving the lives of pilots with diabetes. This achievement follows the ADA’s accomplishments for commercial drivers with diabetes and demonstrates that the ADA’s interdisciplinary collaboration model is successful in overcoming barriers to employment for people with diabetes.

Disclosure
D. Lorber: None. S. Fech-Baughman: None.
1162-P: Coverage, Formulary Restrictions, and Average Retail Prices of SGLT2 Inhibitors and GLP-1 Receptor Agonists across Medicare Part D Plans in 2019
Authors: LUO JING , FELDMAN ROBERT , ROTHENBERGER SCOTT D. , GELLAD WALID F. 
Published: June 2020

Access to SGLT2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP-1RA) may be limited by high drug prices and insurance related barriers including prior authorization or step therapy requirements. These barriers are particularly challenging for seniors covered under Medicare’s prescription drug benefit (Part D). We used Q1 2019 national Part D Formulary files to examine: 1) the proportion of plans (weighted by enrollment) that cover a SGLT2i or GLP-1RA without prior authorization or step therapy and 2) the average retail price [IQR] for a 30-day supply of each medication. Among 3,992 plans (enrolling at least 37,980,936 beneficiaries), weighted coverage without prior authorization or step therapy for canagliflozin, dapagliflozin and empagliflozin was 53.2% (95% CI: 49.1 to 57.4), 63.7% (95% CI: 60.1 to 67.3) and 95.4% (95% CI: 94.3 to 96.4), respectively. Coverage without prior authorization or step therapy for GLP-1RA of ranged from 3.2% (95% CI: 1.8 to 4.6) for lixisenatide to a high of 87.4% (95% CI: 85.5 to 89.3) for dulaglutide. The mean retail price [IQR] for a 30-day supply of a SGLT2i or a GLP-1RA ranged from $295 [$285-$303] (ertugliflozin) to $512 [$501-$527] (canagliflozin) and $641.38 [$629-$657] (lixisenatide) to $946.17 [$930-$968] (liraglutide), respectively. In 2019, coverage without prior authorization and step therapy for SGLT2i and GLP-1RA were mixed across Part D plans. Most beneficiaries enrolled in plans that covered at least one SGLT2i and one GLP-1RA without restrictions. Cost sharing (i.e., high out-of-pocket payments) may be more problematic for patients than either prior authorization or step therapy.

Disclosure
J. Luo: Consultant; Self; Alosa Health. R. Feldman: None. S.D. Rothenberger: None. W.F. Gellad: None.

Funding
National Center for Advancing Translational Sciences (KL2TR001856)