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1. Anti‐Inflammatory HDL Function, Incident Cardiovascular Events, and Mortality: A Secondary Analysis of the JUPITER Randomized Clinical Trial

Author

Oluremi N. Ajala, Olga V. Demler, Yanyan Liu, Zareen Farukhi, Steven J. Adelman, Heidi L. Collins, Paul M Ridker, Daniel J. Rader, Robert J. Glynn, and Samia Mora

Subjects
cardiovascular disease risk factors, HDL function, HDL inflammatory index, HDL particle number, high‐density lipoprotein, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Background High‐density lipoprotein (HDL) cholesterol has inverse association with cardiovascular disease. HDL possesses anti‐inflammatory properties in vitro, but it is unknown whether this may be protective in individuals with inflammation. Methods and Results The functional capacity of HDL to inhibit oxidation of oxidized low‐density lipoprotein (ie, the HDL inflammatory index; HII) was measured at baseline and 12 months after random allocation to rosuvastatin or placebo in a nested case‐control study of the JUPITER (Justification for the Use of Statins in Prevention: An Intervention Evaluating Rosuvastatin) trial. There were 517 incident cases of cardiovascular disease and all‐cause mortality compared to 517 age‐ and sex‐matched controls. Multivariable conditional logistic regression was used to examine associations of HII with events. Median baseline HII was 0.54 (interquartile range, 0.50–0.59). Twelve months of rosuvastatin decreased HII by a mean of 5.3% (95% CI, −8.9% to −1.7%; P=0.005) versus 1.3% (95% CI, −6.5% to 4.0%; P=0.63) with placebo (P=0.22 for between‐group difference). HII had a nonlinear relationship with incident events. Compared with the reference group (HII 0.5–1.0) with the lowest event rates, participants with baseline HII ≤0.5 had significantly increased risk of cardiovascular disease/mortality (adjusted hazard ratio, 1.53; 95% CI, 1.06–2.21; P=0.02). Furthermore, there was significant (P=0.002) interaction for HDL particle number with HII, such that having more HDL particles was associated with decreased risk only when HDL was anti‐inflammatory. Conclusions In JUPITER participants recruited on the basis of chronic inflammation, HII was associated with incident cardiovascular disease/mortality, with an optimal anti‐inflammatory HII range between 0.5 and 1.0. This nonlinear relationship of anti‐inflammatory HDL function with risk may account in part for the HDL paradox. Registration URL: https://www.clini​caltr​ials.gov; Unique identifier: NCT00239681.

Published
2020
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2. Glucokinase mutation–a rare cause of recurrent hypoglycemia in adults: a case report and literature review

Author

Oluremi N. Ajala, David M. Huffman, and Ibrahim I. Ghobrial

Subjects
glucose, low plasma glucose, hypoglycemia, genetic, mutation, congenital hyperinsulinism, congenital, adult, care transition, care coordination, Internal medicine, RC31-1245
Abstract

Background: Hypoglycemia occurs frequently in patients both in the inpatient and outpatient settings. While most hypoglycemia unrelated to diabetes treatment results from excessive endogenous insulin action, rare cases involve functional and congenital mutations in glycolytic enzymes of insulin regulation. Case: A 21-year-old obese woman presented to the emergency department with complaints of repeated episodes of lethargy, syncope, dizziness, and sweating. She was referred from an outside facility on suspicion of insulinoma, with severe hypoglycemia unresponsive to repeated dextrose infusions. Her plasma glucose was 20 mg/dl at presentation, 44 mg/dl on arrival at our facility, and remained low in spite of multiple dextrose infusions. The patient had been treated for persistent hyperinsulinemic hypoglycemia of infancy at our neonatal facility and 4 years ago was diagnosed as having an activating glucokinase (GCK) mutation. She was then treated with octreotide and diazoxide with improvement in symptoms and blood glucose levels. Conclusion: Improved diagnostication and management of uncommon genetic mutations as typified in this patient with an activating mutation of the GCK gene has expanded the spectrum of disease in adult medicine. This calls for improved patient information dissemination across different levels and aspects of the health care delivery system to ensure cost-effective and timely health care.

Published
2016
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3. Abstract 16278: Discordant Lipid Phenotype and Other Determinants of Statin Response in the Pravastatin Inflammation/crp Evaluation (PRINCE) Trial

Author

Paul M. Ridker, Olga Demler, Oluremi N Ajala, Robert J. Glynn, Daniel I. Chasman, Yanyan Liu, and Samia Mora

Subjects
Oncology, medicine.medical_specialty, Statin, medicine.drug_class, business.industry, Inflammation, Phenotype, Physiology (medical), Primary prevention, Internal medicine, Cohort, medicine, lipids (amino acids, peptides, and proteins), medicine.symptom, Cardiology and Cardiovascular Medicine, business, Pravastatin, medicine.drug
Abstract

Introduction: Wide variability in LDL-C change is observed with statins, yet determinants of statin response are uncertain. Methods: Participants were selected from the primary prevention cohort of the Pravastatin Inflammation/CRP Evaluation double-blind trial that randomized participants to pravastatin 40 mg/d or placebo over 24 weeks. Baseline and 24-week levels of LDL-C and 15 other biomarkers were measured in 495 participants. We defined optimal statin response as >=30% LDL-C reduction and suboptimal response as =median (14%) decline in hs-CRP from baseline to 24 weeks and non-response as no decrease or an increase in hs-CRP. χ 2 , t-tests and ANOVA were used to compare variables across optimal statin response (N=166) and suboptimal response (N=287). Multivariable logistic regression models evaluated associations of determinants of statin response. Forward selection identified variables that associated with response. Xgboost was used to train and validate the models using 2/3 and 1/3 of the data respectively. Results: Significant determinants of optimal statin response included older age, and higher baseline levels of LDL-C and triglyceride-rich lipoproteins. By contrast, female sex, alcohol intake >=1 drink/day, diabetes, higher baseline levels of apo B and lipoprotein(a) were associated with decreased response, as was hs-CRP non-response (Table). Race, baseline hs-CRP and sub-optimal hs-CRP response, smoking, HDL-C and BMI had no significant effect on statin LDL-C response. Training and validation of models predicted suboptimal LDL-C response with an AUC of 0.71. Similarly, training and validation of models using Xgboost yielded an AUC of 0.85. Conclusion: This study identified discordant lipid phenotype and other determinants of moderate-intensity statin response and suggests other pathways of CVD risk beyond those addressed by statin treatment that require further investigation.

Published
2020
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4. Abstract 16471: Lipoprotein(a) Cholesterol and Cardiovascular Events in the VITamin D and OmegA 3 TriaL (Vital)

Author

Julie E. Buring, JoAnn E. Manson, Jacqueline S. Danik, Zareen Farukhi, Samia Mora, Heike Gibson, Krishnaji R. Kulkarni, Nancy R. Cook, Olga Demler, and Oluremi N Ajala

Subjects
medicine.medical_specialty, biology, Cholesterol, business.industry, Lipoprotein(a), Vitamin D and Omega-3 Trial, chemistry.chemical_compound, Endocrinology, chemistry, Physiology (medical), Internal medicine, medicine, biology.protein, Cardiology and Cardiovascular Medicine, business
Abstract

Background: It is unclear if lipoprotein(a) cholesterol (LpaC), the cholesterol carried by Lpa, is associated with CVD similar to Lpa mass, and if omega-3 fatty acids (n-3 FA) modify risk. Methods: 13,175 participants of the VITAL trial (NCT01169259) had baseline LpaC measured by density-gradient ultracentrifugation and were examined for incident CVD (n=416) by Cox models adjusted for risk factors. In a subset of participants (N=1639) with baseline and 1 year samples, we also analyzed randomized n-3 FA effects (1 g/d EPA+DHA) vs. placebo. Results: In unadjusted models, LpaC was associated with increased CVD risk (Table). After adjustment, risk was somewhat attenuated, with borderline significant association for LpaC >30 mg/dL (HR 1.37 [0.99, 1.90), p=0.056). N-3 FA increased median LpaC from 7 mg/dL (IQR, 5-10) at baseline to 8 mg/dL [IQR, 5-10] at 1 year (mean increase of 4.05% vs placebo, p=0.006 using natural logarithmic transformation for mean LpaC percent change). There was no effect modification (P interaction>0.05) by n-3 FA, race, sex or LDL-C. Conclusion: Very high LpaC had borderline significant increased risk for incident CVD, without diminution of levels or associated risk by n-3 FA treatment.

Published
2020
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5. Targeting Inflammation to Reduce Residual Cardiovascular Risk

Author

Oluremi N Ajala and Brendan M. Everett

Subjects
Vasculitis, Relative risk reduction, medicine.medical_specialty, Acute coronary syndrome, Interleukin-1beta, Anti-Inflammatory Agents, 030204 cardiovascular system & hematology, Antibodies, Monoclonal, Humanized, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, 030212 general & internal medicine, Myocardial infarction, Metabolic Syndrome, business.industry, medicine.disease, Residual risk, Canakinumab, C-Reactive Protein, Treatment Outcome, Diabetes Mellitus, Type 2, Cardiovascular Diseases, Heart Disease Risk Factors, Cardiology, Metabolic syndrome, Colchicine, Cardiology and Cardiovascular Medicine, business, Mace, medicine.drug
Abstract

Patients with established cardiovascular disease are at high risk for recurrent myocardial infarction, stroke, and cardiovascular death. The term residual risk refers to this risk that persists, even after optimal treatment. Considerable progress has been made to understand the biological basis of residual risk and to devise therapies that can safely and effectively reduce risk. The presence of ongoing subclinical vascular inflammation is known to be a marker of elevated residual risk, and reductions in measures of vascular inflammation predict improved outcome in these patients. Recent trials of anti-inflammatory agents have specifically tested the hypothesis that inflammation reduction reduces residual cardiovascular risk. Most prominent among these are the CANTOS, COLCOT, and CIRT trials. CANTOS enrolled patients with prior myocardial infarction (MI) and a high-sensitivity C-reactive protein ≥ 2 mg/L and reported a 15% reduction in major adverse cardiovascular events (MACE; HR 0.85, 95% CI 0.74–0.98) with the interleukin-1β inhibitor canakinumab. In COLCOT, colchicine 0.5 mg daily led to a 23% relative risk reduction (HR 0.77, 95% CI 0.61–0.96) in major vascular events in patients with recent acute coronary syndrome. By contrast, CIRT was stopped early for lack of benefit of low-dose methotrexate in preventing MACE in patients with coronary artery disease and either type 2 diabetes or the metabolic syndrome. Ongoing subclinical inflammation is an important marker of risk in patients with established cardiovascular disease, and novel therapies targeted at specific inflammatory pathways now demonstrate efficacy for the prevention of major adverse cardiovascular events.

Published
2020
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6. Anti‐Inflammatory HDL Function, Incident Cardiovascular Events, and Mortality: A Secondary Analysis of the JUPITER Randomized Clinical Trial

Author

Olga Demler, Daniel J. Rader, Yanyan Liu, Zareen M Farukhi, Robert J. Glynn, Samia Mora, Heidi L. Collins, Steven J. Adelman, Paul M. Ridker, and Oluremi N Ajala

Subjects
Male, medicine.medical_specialty, Inverse Association, HDL function, cardiovascular disease risk factors, medicine.drug_class, Anti-Inflammatory Agents, Disease, 030204 cardiovascular system & hematology, Gastroenterology, Anti-inflammatory, law.invention, Placebos, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, High-density lipoprotein, Randomized controlled trial, Risk Factors, law, HDL inflammatory index, Cardiovascular Disease, Internal medicine, Secondary analysis, medicine, Humans, 030212 general & internal medicine, Preventive Cardiology, Rosuvastatin Calcium, Original Research, Aged, Lipids and Cholesterol, business.industry, Cholesterol, Cholesterol, HDL, Middle Aged, Primary Prevention, Lipoproteins, LDL, chemistry, HDL particle number, Cardiovascular Diseases, Case-Control Studies, high‐density lipoprotein, Female, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, business, Lipoprotein
Abstract

BackgroundHigh‐density lipoprotein (HDL) cholesterol has inverse association with cardiovascular disease. HDL possesses anti‐inflammatory properties in vitro, but it is unknown whether this may be protective in individuals with inflammation.Methods and ResultsThe functional capacity of HDL to inhibit oxidation of oxidized low‐density lipoprotein (ie, the HDL inflammatory index; HII) was measured at baseline and 12 months after random allocation to rosuvastatin or placebo in a nested case‐control study of the JUPITER (Justification for the Use of Statins in Prevention: An Intervention Evaluating Rosuvastatin) trial. There were 517 incident cases of cardiovascular disease and all‐cause mortality compared to 517 age‐ and sex‐matched controls. Multivariable conditional logistic regression was used to examine associations of HII with events. Median baseline HII was 0.54 (interquartile range, 0.50–0.59). Twelve months of rosuvastatin decreased HII by a mean of 5.3% (95% CI, −8.9% to −1.7%;P=0.005) versus 1.3% (95% CI, −6.5% to 4.0%;P=0.63) with placebo (P=0.22 for between‐group difference). HII had a nonlinear relationship with incident events. Compared with the reference group (HII 0.5–1.0) with the lowest event rates, participants with baseline HII ≤0.5 had significantly increased risk of cardiovascular disease/mortality (adjusted hazard ratio, 1.53; 95% CI, 1.06–2.21;P=0.02). Furthermore, there was significant (P=0.002) interaction for HDL particle number with HII, such that having more HDL particles was associated with decreased risk only when HDL was anti‐inflammatory.ConclusionsIn JUPITER participants recruited on the basis of chronic inflammation, HII was associated with incident cardiovascular disease/mortality, with an optimal anti‐inflammatory HII range between 0.5 and 1.0. This nonlinear relationship of anti‐inflammatory HDL function with risk may account in part for the HDL paradox.RegistrationURL:https://www.clini​caltr​ials.gov; Unique identifier: NCT00239681.

Published
2020
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7. Abstract P260: Determinants of Statin Response: A Secondary Analysis of the Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER)

Author

Samia Mora, Paul M. Ridker, Daniel I. Chasman, Olga Demler, Yanyan Liu, Oluremi N Ajala, and Robert J. Glynn

Subjects
medicine.medical_specialty, Statin, business.industry, medicine.drug_class, Jupiter, Physiology (medical), Internal medicine, Secondary analysis, medicine, Rosuvastatin, Intervention trial, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract

Introduction: Wide variability in LDLC change is observed with statins, yet determinants of statin response are uncertain. Hypotheses: Some markers of inflammation are associated with decreased statin response. Components of metabolic syndrome and older age are associated with better response. Methods: JUPITER (NCT00239681) randomized participants with LDLC2 , t-tests and ANOVA were used to compare variables across optimal (N=3,801), suboptimal (N=3,235) and non-responders (N=868). Multinomial regression models evaluated associations of determinants of statin response after adjusting for risk factors including compliance. Backward selection identified variables that associated with response. t-distributed Stochastic Neighbor Embedding (t-SNE) suggested predictor clusters for statin response. Results: Compliance was the strongest determinant of statin response (Table). On multivariable analyses, blacks and Hispanics were at higher risk for suboptimal/non-response compared with whites as were greater alcohol use and HbA1c. Higher baseline levels of lipids [lipoprotein(a), apolipoprotein (apo) AI and B], inflammatory biomarkers, and lower branched-chain amino acids associated with decreased statin response (Table). By contrast, determinants of better response included older age, female sex, and higher waist circumference and baseline levels of LDLC, triglycerides, and blood pressure. We observed systematic patterns in t-SNE clustering for statin response by LDLC, LDL particle number, and apo B. Conclusions: This study identified determinants for high-intensity statin response and suggests other pathways of CVD risk beyond those addressed by statin treatment that require further investigation.

Published
2020
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8. Decreased serum TRAIL is associated with increased mortality in smokers with comorbid emphysema and coronary artery disease

Author

Divay Chandra, Yingze Zhang, Jessica Bon, Oluremi N Ajala, Aman Gupta, and Frank C. Sciurba

Subjects
Male, Pulmonary and Respiratory Medicine, medicine.medical_specialty, medicine.medical_treatment, Comorbidity, Coronary Artery Disease, Disease, 030204 cardiovascular system & hematology, Article, TNF-Related Apoptosis-Inducing Ligand, Angina, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Angioplasty, medicine, Humans, Myocardial infarction, Biosimilar Pharmaceuticals, Coronary atherosclerosis, Aged, Emphysema, COPD, Smokers, Lung, business.industry, Smoking, Middle Aged, medicine.disease, respiratory tract diseases, Survival Rate, medicine.anatomical_structure, 030228 respiratory system, Cardiology, Female, business, Biomarkers
Abstract

Background Smokers are highly susceptible to lung and cardiovascular disease that can reduce their survival. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a protein in the circulation that may suppress vascular and pulmonary inflammation. Therefore, we hypothesized that diminished circulating TRAIL levels would be associated with poor survival in smokers with lung and cardiovascular disease. Methods Serum TRAIL level was measured by immunoassay in 474 smokers. Coronary atherosclerosis was assessed by coronary artery calcium scoring along with emphysema, lung function, and survival. Results The 474 smokers were 65.7 ± 6.3 years old and 52.2% male with 55.3 ± 31.5 pack-years of tobacco-exposure. 83 of them died during 3588.2 person-years of follow up. At baseline, lower TRAIL level was associated with more coronary artery calcium (OR = 1.2 per SD, 95%CI 1.1–1.5, p = 0.02), and with history of myocardial infarction (OR = 2.3 per SD, 95%CI 1.2–4.5, p = 0.02), angina (OR = 1.6 per SD, 95%CI 1.1–2.6, p = 0.03), and angioplasty (OR = 1.8 per SD, 95%CI 1.0–3.1, p = 0.04) in models adjusted for cardiovascular risk-factors, FEV1, and emphysema. Also, lower TRAIL level was associated with emphysema severity independent of demographics and tobacco exposure (β = 0.11 sq. root units, 95% CI 0.01–0.22, p = 0.03). Further, TRAIL level was lowest in smokers with comorbid emphysema and coronary artery calcification rather than either condition alone. Finally, lower TRAIL level was independently associated with increased mortality in smokers particularly in those with comorbid emphysema and coronary artery calcification (HR = 1.38, 95% CI 1.01–1.90). Conclusions TRAIL level is reduced in smokers with comorbid emphysema and coronary artery disease, and is associated with reduced survival.

Published
2018
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9. Association of obstructive sleep apnea with microvascular endothelial dysfunction and subclinical coronary artery disease in a community-based population

Author

Kevin E. Kip, Steven E. Reis, Sebhat Erqou, Daniel Shpilsky, Oluremi N Ajala, Patrick J. Strollo, Oladipupo Olafiranye, Aryan Aiyer, and Sanjay R. Patel

Subjects
Male, medicine.medical_specialty, Population, Hyperemia, Coronary Artery Disease, 030204 cardiovascular system & hematology, Coronary Angiography, Severity of Illness Index, White People, Fingers, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Internal medicine, Prevalence, medicine, Humans, Prospective Studies, Endothelial dysfunction, Vascular Calcification, education, Prospective cohort study, Lung, Reactive hyperemia, Aged, Subclinical infection, Sleep Apnea, Obstructive, education.field_of_study, Framingham Risk Score, business.industry, Microcirculation, Middle Aged, Pennsylvania, medicine.disease, respiratory tract diseases, Black or African American, Obstructive sleep apnea, Cross-Sectional Studies, Asymptomatic Diseases, Microvessels, Cardiology, Female, Endothelium, Vascular, Sleep, Tomography, X-Ray Computed, Cardiology and Cardiovascular Medicine, business, 030217 neurology & neurosurgery
Abstract

Studies have reported an association between obstructive sleep apnea (OSA) and cardiovascular disease (CVD) morbidity and mortality. Proposed mechanisms include endothelial dysfunction and atherosclerosis. We aimed to investigate the associations of OSA with endothelial dysfunction and subclinical atherosclerotic coronary artery disease (CAD), and assess the impact of race on these associations. We used data from the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) study, a community-based prospective cohort with approximately equal representation of black and white participants. OSA severity was measured in 765 individuals using the apnea-hypopnea index (AHI). Endothelial dysfunction was measured using the Endo-PAT device, expressed as Framingham reactive hyperemia index (F_RHI). Coronary artery calcium (CAC), a marker of subclinical CAD, was quantified by electron beam computed tomography. There were 498 (65%) female participants, 282 (37%) black individuals, and 204 (26%) participants with moderate/severe OSA (AHI ≥15). In univariate models, moderate/severe OSA was associated with lower F_RHI and higher CAC, as well as several traditional CVD risk factors including older age, male sex, hypertension, diabetes, higher body mass index, and lower high-density lipoprotein cholesterol levels. In a multivariable model, individuals with moderate/severe OSA had 10% lower F_RHI and 35% higher CAC, which did not reach statistical significance ( p=0.08 for both comparisons). There was no significant interaction of race on the association of OSA with F_RHI or CAC ( p-value >0.1 for all comparisons). In a community-based cohort comprised of black and white participants, moderate/severe OSA was modestly associated with endothelial dysfunction and subclinical atherosclerotic CAD. These associations did not vary by race.

Published
2018
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10. Effect of Vitamin D3 Supplements on Development of Advanced Cancer

Author

Paulette D. Chandler, Aditi Hazra, Edward Giovannucci, Nancy R. Cook, JoAnn E. Manson, Vadim Bubes, I-Min Lee, Walter C. Willett, Wendy Y. Chen, Julie E. Buring, and Oluremi N Ajala

Subjects
Male, Vitamin, medicine.medical_specialty, Comorbidity, law.invention, chemistry.chemical_compound, Double-Blind Method, Randomized controlled trial, law, Neoplasms, Internal medicine, Vitamin D and neurology, Humans, Medicine, Obesity, Neoplasm Metastasis, Aged, Cholecalciferol, Proportional Hazards Models, Original Investigation, business.industry, Research, Incidence (epidemiology), Cancer, Vitamins, General Medicine, Middle Aged, Overweight, medicine.disease, Featured, Clinical trial, Online Only, Oncology, chemistry, Dietary Supplements, Disease Progression, Female, business, Body mass index
Abstract

Key Points Question Does vitamin D3 supplementation reduce the risk of developing advanced (metastatic or fatal) cancer among adults without a diagnosis of cancer at baseline? Findings In this secondary analysis of a randomized clinical trial with 25 871 patients, supplementation with vitamin D3 reduced the incidence of advanced (metastatic or fatal) cancer in the overall cohort, with strongest risk reduction in individuals with normal weight and no reduction among individuals with overweight or obesity. Meaning These findings suggest that vitamin D3 may reduce the risk of developing advanced cancer among adults without a diagnosis of cancer at baseline; this protective effect is apparent for those who have normal but not elevated body mass index., This secondary analysis of a randomized clinical trial evaluates the effect vitamin D on the incidence of advanced (metastatic or fatal) cancer among adults without cancer at baseline and examines possible effect modification by body mass index., Importance Epidemiologic and trial data suggest that vitamin D supplementation may reduce metastatic cancer and cancer mortality, reflecting shared biological pathways. Objective To follow up on the possible reduction in cancer death in the Vitamin D and Omega-3 Trial (VITAL) with an evaluation of whether vitamin D reduces the incidence of advanced (metastatic or fatal) cancer and an examination possible effect modification by body mass index. Design, Setting, and Participants VITAL is a randomized, double-blind, placebo-controlled, 2 × 2 factorial clinical trial of vitamin D3 (cholecalciferol, 2000 IU/d) and marine omega-3 fatty acids (1 g/d). This multicenter clinical trial was conducted in the United States; participants included men aged 50 years or older and women aged 55 years or older who were free of cancer and cardiovascular disease at baseline. Randomization took place from November 2011 through March 2014, and study medication ended on December 31, 2017. Data for this secondary analysis were analyzed from November 1, 2011, to December 31, 2017. Interventions Vitamin D3 (cholecalciferol, 2000 IU/d) and marine omega-3 fatty acids (1 g/d) supplements. Main Outcomes and Measures For the present analysis, the primary outcome was a composite incidence of metastatic and fatal invasive total cancer, because the main VITAL study showed a possible reduction in fatal cancer with vitamin D supplementation and effect modification by body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) for total cancer incidence reduction for individuals with normal BMI, but not for individuals with overweight or obesity. Secondary analyses included examination of BMI (

Published
2020
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11. Vitamin D supplements and marine omega-3 fatty acids and development of advanced cancer

Author

Edward Giovannucci, JoAnn E. Manson, Nancy R. Cook, Wendy Y. Chen, Oluremi N Ajala, Paulette D. Chandler, Vadim Bubes, Aditi Hazra, Julie E. Buring, and I-Min Lee

Subjects
Cancer mortality, Cancer Research, medicine.medical_specialty, Vitamin d supplementation, business.industry, Incidence (epidemiology), Advanced cancer, Gastroenterology, Oncology, Internal medicine, Vitamin D and neurology, Medicine, Epidemiologic data, business
Abstract

1510 Background: Epidemiologic data suggest that vitamin D supplementation may reduce cancer mortality. We tested whether vitamin D and/or omega-3 supplementation reduces the incidence of advanced stage cancer at diagnosis or lethal cancer, and whether body mass index (BMI) modifies these associations. Methods: The VITamin D and OmegA-3 TriaL (VITAL) is a randomized, placebo-controlled, 2x2 factorial trial of vitamin D3 (cholecalciferol, 2000 IU/day) and marine omega-3 fatty acids (1 g/day) that enrolled men aged ≥50 years and women aged ≥55 years free of cancer and cardiovascular disease at baseline. For this particular analysis, the primary outcome is a composite of metastatic and fatal invasive total cancer. Secondary analyses included examination of BMI (= 30 kg/m2) as effect modifiers of the observed associations. Results: VITAL randomized 25,871 participants, among whom 1,617 were diagnosed with invasive cancer over a median 5.3 year intervention period. No significant differences by treatment arm (vitamin D vs placebo: hazard ratio [HR]=0.96; 95% confidence interval, 0.88-1.06; p=0.47; omega-3 vs placebo; HR 1.03 [0.93-1.13]; p=0.56) were observed. However, a significant reduction in advanced cancers (metastatic or fatal) was found for those randomized to vitamin D, compared to placebo (226 assigned to vitamin D and 274 to placebo; HR 0.83 [0.69-0.99]; p=0.036). There was no difference by omega-3 assignment (246 assigned to omega-3 and 254 to placebo: HR 0.97 [0.81-1.15], p=0.72). When stratified by BMI, there was a significant reduction for the vitamin D arm in incident metastatic or fatal cancer among those with normal BMI (BMI=30: HR 1.05 [0.74-1.49]); p for interaction by BMI =0.03. There was no effect modification by BMI noted for the omega 3 arm. Conclusions: In a randomized clinical trial, supplementation with vitamin D, but not omega-3s, reduced incidence of advanced (metastatic or fatal) cancer in the overall cohort, with strongest risk reduction in normal weight individuals. Further research is needed to understand these findings. Clinical trial information: NCT01169259.

Published
2020
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12. Global, regional, national, and selected subnational levels of stillbirths, neonatal, infant, and under-5 mortality, 1980-2015 : a systematic analysis for the Global Burden of Disease Study 2015

Author

Vasiliki Stathopoulou, Kiran Thapa, Vesper Hichilombwe Chisumpa, Azeem Majeed, Hjalte Holm Andersen, Devasahayam J. Christopher, Alireza Mohammadi, John J. McGrath, Konstantin Kazanjan, Naohiro Yonemoto, Guoqing Hu, Yousef Khader, Suzanne Barker-Collo, Frida Namnyak Ngalesoni, Jennifer O Lam, Laetitia Huiart, Xiaofeng Liang, Amanuel Tesfay Gebremedhin, Lalit Dandona, Felix Masiye, Joseph R Fitchett, Derrick A Bennett, Rosana E. Norman, Theo Vos, Tuomo J. Meretoja, Rahman Shiri, Melvin Barrientos Marzan, Charles R. Newton, Kelly Cercy, Masoud Vaezghasemi, Elena Alvarez Martin, Christopher Troeger, Ismael R. Campos-Nonato, Amany H Refaat, Ruben Castro, Amiran Gamkrelidze, Michael R. Phillips, Samath D Dharmaratne, Reed J D Sorensen, Roderick J. Hay, Johan Ärnlöv, Ivo Rakovac, Alexandra Brazinova, Nancy Fullman, Sara Sheikhbahaei, Liliana G Ciobanu, Nader Jahanmehr, Yuming Guo, Luigi Naldi, Rana Jawad Asghar, Tsegaye Tewelde Gebrehiwot, Corine Karema, Biju Abraham, Rynaz H S Rabiee, Emerito Jose A. Faraon, Philimon Gona, Jonathan I. Silverberg, Alexandria Brown, Kovin Naidoo, Suleman Atique, Yun Jin Kim, Benn Sartorius, Hwashin Hyun Shin, George Mugambage Ruhago, Adugnaw Berhane, Tesfaye Tekle, Abdur Rahman Khan, Vipin Gupta, Nima Hafezi-Nejad, Héctor Gómez-Dantés, Jun She, Ted R. Miller, Tolesa Bekele, Yohannes Kinfu, Srinivas Murthy, Alaa Badawi, Mahfuzar Rahman, Raghib Ali, Robert G. Weintraub, Nicholas Steel, Khalid A Altirkawi, Muhammad Imran Nisar, Man Mohan Mehndiratta, Thomas N. Williams, Adrian Davis, Usha Ram, Nobuyuki Horita, Qingyang Xiao, Bishal Gyawali, Burcu Kucuk Bicer, Eun-Kee Park, Subas Neupane, Mohammad Tavakkoli, Lorenzo Monasta, Roman Topor-Madry, Marc-Alain Widdowson, James Leigh, Padukudru Anand Mahesh, Stephen M. Amrock, Stefan Ma, Virendra Singh, Amir Kasaeian, Mahdi Mahdavi, Shahrzad Bazargan-Hejazi, Kim Moesgaard Iburg, Vafa Rahimi-Movaghar, Julio Cesar Campuzano, Maria Dolores Sanchez-Niño, Jean B. Nachega, Hamid Asayesh, Pratik Pinal Doshi, Charles Shey Wiysonge, Peter J. Hotez, Ying Jiang, Girma Temam Shifa, Warren D. Lo, Francis Apolinary Mhimbira, Joan B. Soriano, Ritul Kamal, Young-Ho Khang, Isaac Akinkunmi Adedeji, Daniel C Casey, Adeladza Kofi Amegah, Demewoz Haile, Tomi Akinyemiju, Andrew L. Thorne-Lyman, Achala Upendra Jayatilleke, Rajeev Gupta, Rosario Cárdenas, Peter W. Gething, Ami R. 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Subjects
Pediatrics, Nutrition and Disease, Global Health, Communicable Disease, 0302 clinical medicine, Voeding en Ziekte, Infant Mortality, Compensation law of mortality, Global health, Medicine, LIFE EXPECTANCY, 030212 general & internal medicine, DEVELOPING-COUNTRIES, 10. No inequality, Medicine(all), NEWBORN BABIES, Medicine (all), Mortality rate, 1. No poverty, DEATH, Public Health, Global Health, Social Medicine and Epidemiology, General Medicine, 11 Medical And Health Sciences, Stillbirth, 3. Good health, Child Mortality, SURVIVAL, CHILD-MORTALITY, HEALTH, Life Sciences & Biomedicine, DEVELOPMENT GOAL 4, Human, INTERVENTIONS, medicine.medical_specialty, RJ, INTEGRATED APPROACH, Developing country, Communicable Diseases, neonatal, 03 medical and health sciences, Medicine, General & Internal, 030225 pediatrics, General & Internal Medicine, Life Science, Humans, Global Burden of Disease Study, VLAG, Estimation, Science & Technology, business.industry, Klinisk medicin, Infant, GBD 2015 Child Mortality Collaborators, Infant mortality, Malaria, Child mortality, Folkhälsovetenskap, global hälsa, socialmedicin och epidemiologi, Life expectancy, Clinical Medicine, RG, business, Demography
Abstract

BACKGROUND: Established in 2000, Millennium Development Goal 4 (MDG4) catalysed extraordinary political, financial, and social commitments to reduce under-5 mortality by two-thirds between 1990 and 2015. At the country level, the pace of progress in improving child survival has varied markedly, highlighting a crucial need to further examine potential drivers of accelerated or slowed decreases in child mortality. The Global Burden of Disease 2015 Study (GBD 2015) provides an analytical framework to comprehensively assess these trends for under-5 mortality, age-specific and cause-specific mortality among children under 5 years, and stillbirths by geography over time. METHODS: Drawing from analytical approaches developed and refined in previous iterations of the GBD study, we generated updated estimates of child mortality by age group (neonatal, post-neonatal, ages 1-4 years, and under 5) for 195 countries and territories and selected subnational geographies, from 1980-2015. We also estimated numbers and rates of stillbirths for these geographies and years. Gaussian process regression with data source adjustments for sampling and non-sampling bias was applied to synthesise input data for under-5 mortality for each geography. Age-specific mortality estimates were generated through a two-stage age-sex splitting process, and stillbirth estimates were produced with a mixed-effects model, which accounted for variable stillbirth definitions and data source-specific biases. For GBD 2015, we did a series of novel analyses to systematically quantify the drivers of trends in child mortality across geographies. First, we assessed observed and expected levels and annualised rates of decrease for under-5 mortality and stillbirths as they related to the Soci-demographic Index (SDI). Second, we examined the ratio of recorded and expected levels of child mortality, on the basis of SDI, across geographies, as well as differences in recorded and expected annualised rates of change for under-5 mortality. Third, we analysed levels and cause compositions of under-5 mortality, across time and geographies, as they related to rising SDI. Finally, we decomposed the changes in under-5 mortality to changes in SDI at the global level, as well as changes in leading causes of under-5 deaths for countries and territories. We documented each step of the GBD 2015 child mortality estimation process, as well as data sources, in accordance with the Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). FINDINGS: Globally, 5·8 million (95% uncertainty interval [UI] 5·7-6·0) children younger than 5 years died in 2015, representing a 52·0% (95% UI 50·7-53·3) decrease in the number of under-5 deaths since 1990. Neonatal deaths and stillbirths fell at a slower pace since 1990, decreasing by 42·4% (41·3-43·6) to 2·6 million (2·6-2·7) neonatal deaths and 47·0% (35·1-57·0) to 2·1 million (1·8-2·5) stillbirths in 2015. Between 1990 and 2015, global under-5 mortality decreased at an annualised rate of decrease of 3·0% (2·6-3·3), falling short of the 4·4% annualised rate of decrease required to achieve MDG4. During this time, 58 countries met or exceeded the pace of progress required to meet MDG4. Between 2000, the year MDG4 was formally enacted, and 2015, 28 additional countries that did not achieve the 4·4% rate of decrease from 1990 met the MDG4 pace of decrease. However, absolute levels of under-5 mortality remained high in many countries, with 11 countries still recording rates exceeding 100 per 1000 livebirths in 2015. Marked decreases in under-5 deaths due to a number of communicable diseases, including lower respiratory infections, diarrhoeal diseases, measles, and malaria, accounted for much of the progress in lowering overall under-5 mortality in low-income countries. Compared with gains achieved for infectious diseases and nutritional deficiencies, the persisting toll of neonatal conditions and congenital anomalies on child survival became evident, especially in low-income and low-middle-income countries. We found sizeable heterogeneities in comparing observed and expected rates of under-5 mortality, as well as differences in observed and expected rates of change for under-5 mortality. At the global level, we recorded a divergence in observed and expected levels of under-5 mortality starting in 2000, with the observed trend falling much faster than what was expected based on SDI through 2015. Between 2000 and 2015, the world recorded 10·3 million fewer under-5 deaths than expected on the basis of improving SDI alone. INTERPRETATION: Gains in child survival have been large, widespread, and in many places in the world, faster than what was anticipated based on improving levels of development. Yet some countries, particularly in sub-Saharan Africa, still had high rates of under-5 mortality in 2015. Unless these countries are able to accelerate reductions in child deaths at an extraordinary pace, their achievement of proposed SDG targets is unlikely. Improving the evidence base on drivers that might hasten the pace of progress for child survival, ranging from cost-effective intervention packages to innovative financing mechanisms, is vital to charting the pathways for ultimately ending preventable child deaths by 2030. FUNDING: Bill & Melinda Gates Foundation. Erratum: Department of Error, The Lancet,Volume 389, Issue 10064, 2017, Page e1. DOI: 10.1016/S0140-6736(16)32608-3

Published
2016
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13. IDEAL CARDIOVASCULAR HEALTH METRICS IN COUPLES: A COMMUNITY-BASED POPULATION STUDY

Author

Andrew D. Althouse, Michael S. Sharbaugh, Claudia Bambs, Oluremi N Ajala, Aryan Aiyer, Kevin E. Kip, Sebhat Erqou, and Steven E. Reis

Subjects
Community based, Ideal (set theory), Cvd risk, business.industry, Cardiovascular health, Environmental health, Population study, Medicine, social sciences, cardiovascular diseases, Disease, Cardiology and Cardiovascular Medicine, business
Abstract

Background: Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality. Better understanding of CVD determinants is needed to decrease CVD risk. We hypothesized that ideal CVD health metrics are mostly concordant among heterosexual spousal or cohabitating couples. Methods: We

Published
2017
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14. Correction to Lancet HIV 2016; 3: e361–87

Author

Kerrie E. Doyle, Olalekan A. Uthman, Laxmikant Chavan, Azmeraw T. Amare, Rasmus Havmoeller, Maryam S. Farvid, Louisa Degenhardt, Mohamed Hsairi, Kimani M Harun, Zoubida Zaidi, Hassan Magdy Abd El Razek, Masako Horino, Rajesh Sagar, Bradford D. Gessner, Bongani M. Mayosi, Konrad Pesudovs, Man Mohan Mehndiratta, Sadaf G. Sepanlou, Akindele Olupelumi Adebiyi, Hye Youn Park, Alexandria Brown, Charles Shey Wiysonge, Bach Xuan Tran, Haidong Kan, Ajit Kumar Yadav, Arsène Kouablan Adou, Karzan Abdulmuhsin Mohammad, In-Hwan Oh, Juan Jesus Carrero, Pratik Pinal Doshi, Panniyammakal Jeemon, Teshome Gebre, Abdullah Sulieman Terkawi, Vasiliki Stathopoulou, Hsing-Yi Chang, Bulat Idrisov, Azeem Majeed, Yoshihiro Kokubo, Zahid A Butt, Yuichiro Yano, Nataliya Foigt, Naris Silpakit, Rajesh Kumar Rai, Rajaa Mohammad, Alireza Esteghamati, Seok Jun Yoon, Kathryn H. Jacobsen, Carl Abelardo T. Antonio, Sibhatu Biadgilign, Ruoyan Tobe-Gai, Balem Demtsu Betsu, Haidong Wang, Samir Soneji, Devasahayam J. Christopher, Ileana Heredia-Pi, Boris Bikbov, John Q. Wong, Yun Jin Kim, Giancarlo Logroscino, Raimundas Lunevicius, Eesh Bhatia, Kazem Rahimi, Sajjad Ur Rahman, Henock Yebyo, Mehdi Yaseri, Rodrigo Sarmiento-Suarez, Yong Zhao, Joseph Friedman, André Faro, Nelson Alvis-Guzman, Yongmei Li, Bemnet Amare Tedla, Wanqing Chen, Shafiu Mohammed, Vivekanand Jha, Achala Upendra Jayatilleke, Guoqing Hu, Yousef Khader, Rafael Alfonso-Cristancho, Girma Temam Shifa, Suzanne Polinder, Bryan L. Sykes, Kaja Abbas, Nadia Akseer, Rakhi Dandona, Aleksandra Barac, Simon I. Hay, Scott B. Patten, Jiabin Shen, Donal Bisanzio, Hilda L Harb, Gizachew Assefa Tessema, Wagner Marcenes, Chabila C Mapoma, Miia Kivipelto, Hsiang Huang, Jung-Chen Chang, P. V. Rao, Amanda J. Mason-Jones, Bolajoko O. Olusanya, Hilton Lam, Amare Deribew, Saleem M Rana, Mohammad Taghi Hedayati, Khurshid Alam, Reza Malekzadeh, Mohamed Magdy Abd El Razek, Mojde Mirarefin, Juan Sanabria, Umar Bacha, Rashmi Gupta, Laith J. Abu-Raddad, Amanuel Tesfay Gebremedhin, Felix Masiye, Maurice Giroud, Palwasha Anwari, Sergey Petrovich Ermakov, Ole Frithjof Norheim, Zulfiqar A Bhutta, Rosario Cárdenas, John J Huang, Alaa Badawi, Edward J Mills, Guohong Jiang, Matthew M Coates, Martin McKee, Jacqueline Castillo Rivas, Norito Kawakami, Chandrashekhar T Sreeramareddy, Mohammad Tavakkoli, Pieter de Jager, Hajo Zeeb, Tim Driscoll, James Leigh, Mohammad Yahya Saeedi, Gelin Xu, Rana J. Asghar, Koranteng Adofo, Sivadasanpillai Harikrishnan, Zewdie Aderaw Alemu, Roberto Tchio Talongwa, Jeanne Françoise Kayibanda, Tuomo J. Meretoja, Alemseged Aregay Gebru, Yuantao Hao, Bereket Yakob, Melvin Barrientos Marzan, Jose Martinez-Raga, Rosana E. Norman, Gebre Yitayih Abyu, Anders Larsson, Dayane Gabriele Alves Silveira, Sasa Rajsic, Elena Alvarez, Nikolaos Tsilimparis, Kenji Shibuya, Alexandra Brazinova, Nader Jahanmehr, Solomon Abreha Damtew, Ambuj Roy, Elisabete Weiderpass, Derrick A Bennett, Holly Hagan, Julio Cesar Campuzano, Shifalika Goenka, Gudlavalleti V S Murthy, Mirriam Chibalabala, Mostafa Qorbani, Peter Njenga Keiyoro, Stein Emil Vollset, Andrea Werdecker, Sanjay Zodpey, Alemayehu B. Mekonnen, Addisu Shunu Beyene, Stephen M. Amrock, Soewarta Kosen, Haseeb Nawaz, Tukur Dahiru, Gessessew Bugssa Hailu, Atsushi Goto, Abdur Rahman Khan, Vipin Gupta, Nima Hafezi-Nejad, Parvaiz A Koul, John Nelson Opio, Jun She, Michael Brainin, Luke Nyakarahuka, Edson Serván-Mori, Dimitris Karletsos, Chandrasekharan Nair Kesavachandran, Van C. Lansingh, Ala'a Alkerwi, Elizabeth Glaser, Ziad A. Memish, Sinead Langan, Usha Ram, Alicia Aleman, Brighton Murimira, Jae-Hyun Park, Foluke Adetola Ojelabi, Anil Kaul, Foad Abd-Allah, Aman Yesuf Endries, Erika Ota, Mark Drew Crosland Guimarães, Rajesh Sharma, Mahdi Mahdavi, Andre Pascal Kengne, Joan B. Soriano, Soumya Swaminathan, Ritul Kamal, Quyen Nguyen, Felix Akpojene Ogbo, Alan J Thomson, Don C. Des Jarlais, Sara Sheikhbahaei, Al Artaman, Chigozie Jesse Uneke, Tsegaye Tewelde Ghiwot, Maya S Fraser, Veena S. Kulkarni, Corine Karema, Samer Hamidi, Randah R. Hamadeh, Marek Majdan, Sait Mentes Birlik, Mihajlo Jakovljevic, Kingsley N. Ukwaja, Jeffrey A. Towbin, Tariku Jibat, Julian David Pillay, Suleman Atique, Raghib Ali, Shicheng Yu, Carlos A. Castañeda-Orjuela, Nobuyuki Horita, Graeme J. Hankey, Prashant Singh, Mouhanad Hammami, Nicholas Steel, Yohannes Kinfu, Hao Zhang, Niveen M E Abu-Rmeileh, François Alla, Johanna M. Geleijnse, Nancy Fullman, Rintaro Mori, Ying Jiang, Semaw Ferede Abera, Atte Meretoja, Katherine Pearson, Robert G. Weintraub, Zubair Kabir, Juanita A. Haagsma, Muhammad Imran Nisar, Benn Sartorius, Lalit Dandona, Amir Kasaeian, Andrew H. Kemp, Melkamu Dedefo Gishu, Ferrán Catalá-López, Deena Alasfoor, Isaac Akinkunmi Adedeji, Hwashin Hyun Shin, Peter Memiah, Muhammad Muhammad Saleh, Mahfuzar Rahman, Yohannes Adama Melaku, Barthelemy Kuate Defo, Alan D. Lopez, Meghan D. Mooney, Inga Dora Sigfusdottir, Walid Ammar, Vegard Skirbekk, David M. Prokop, Edgar P. Simard, Jagdish Khubchandani, Fortuné Gbètoho Gankpé, Arindam Basu, Roman Topor-Madry, Walter Mendoza, Amador Goodridge, G Anil Kumar, Jean de Dieu Ngirabega, Amanuel Alemu Abajobir, João C. Fernandes, Michael Burch, Gholamreza Roshandel, Leo Zoeckler, Ai Koyanagi, Emmanuel Peprah, Maysaa El Sayed Zaki, Shiwei Liu, Shireen Sindi, Adam Trickey, Ali H. Mokdad, William Msemburi, James D. Wilkinson, Rafael Tabarés-Seisdedos, Sungho Won, Abdishakur M. Abdulle, Ted R. Miller, Oluremi N Ajala, Karen Sliwa, Linhong Wang, Awoke Misganaw Temesgen, Jasvinder A. Singh, Kaire Innos, Fisaha Haile Tesfay, Steven E. Lipshultz, Belinda Lloyd, Burcu Kucuk Bicer, Vasiliy Victorovich Vlassov, Maziar Moradi-Lakeh, Abera Kenay Tura, Adeladza Kofi Amegah, Peggy Pei-Chia Chiang, Charles D.A. Wolfe, Ulrich O Mueller, Francis Apolinary Mhimbira, Nicholas J K Breitborde, Monika Sawhney, Eyal Oren, Kim Moesgaard Iburg, Vafa Rahimi-Movaghar, Tomi Akinyemiju, Tissa Wijeratne, Giuseppe Remuzzi, Alemayehu Amberbir, Itamar S. Santos, Ibrahim A Khalil, Aliya Naheed, Anwar Rafay, Beatriz Paulina Ayala Quintanilla, Saleh F. Aldhahri, Jacob Olusegun Olusanya, André Karch, Harish Chander Gugnani, Mohammad Hifz Ur Rahman, Ronny Westerman, Vinod K. Paul, Dietrich Plass, David Rojas-Rueda, Reza Assadi, Tigist Assefa Bayou, Vinay Nangia, Ayalnesh Zemene Yalew, Eric L. Ding, Justin Beardsley, Veena R. Iyer, Stephen S Lim, Bineyam Taye, Till Bärnighausen, Ademola Lukman Adelekan, Joshua A. Salomon, Chakib Nejjari, Josep Maria Haro, Diego De Leo, Faris Lami, Sameer Vali Gopalani, Om P. Singh, Farshad Farzadfar, Kalkidan Hassen Abate, Ejaz Ahmad Khan, Yibeltal Tebekaw Bayou, Norberto Perico, Bruno F. Sunguya, Narayanaswamy Venketasubramanian, Ashish Awasthi, Lorenzo Monasta, David O Soti, Hamid Asayesh, Young-Ho Khang, Thomas Fürst, Hmwe H Kyu, Heidi J. Larson, Amber Sligar, Mahesh Anand Padukudru, Ricky Leung, Reed J D Sorensen, Farshad Pourmalek, Liliana G Ciobanu, Luigi Naldi, Kiran Thapa, Vesper Hichilombwe Chisumpa, Yousef M. Elshrek, Naohiro Yonemoto, Frida Namnyak Ngalesoni, Jennifer O Lam, Neeraj Bedi, Masood Ali Shaikh, Iqbal R. F. Elyazar, Soraya Seedat, Mehdi Javanbakht, Paul S. F. Yip, Grant Nguyen, Peter A. Meaney, Joseph Mikesell, Kebede Deribe, Johan Ärnlöv, Emmanuela Gakidou, Robert W Aldridge, Joseph Robert Ander Fitchett, José das Neves, Ubai Alsharif, Diego Augusto Santos Silva, Cyrus Cooper, H. Dean Hosgood, Seyed-Mohammad Fereshtehnejad, Liesl Zühlke, Dharmesh Kumar Lal, Tim M. Wolock, David M. Pereira, Carla Sofia e Sa Farinha, Miguel Angel Alegretti, Babak Eshrati, Paulo A. Lotufo, Salem Al-Raddadi, Christopher J L Murray, Austin Carter, Rajeev Gupta, Jee-Young Jasmine Choi, Mustafa Z. Younis, Michael R. Phillips, Snehal Patil, Samath D Dharmaratne, Robert P. Dellavalle, George Mugambage Ruhago, Tesfaye Tekle, Shahrzad Bazargan-Hejazi, Peter W. Gething, Isabela M. Benseñor, Zacharie Tsala Dimbuene, Max Petzold, Chuanhua Yu, Ziyad Al-Aly, Ibrahim Abubakar, Noore Alam, Aletta E. Schutte, Andrew L. Thorne-Lyman, Denis Nash, Luca Ronfani, Manisha Dubey, Lydia S. Atkins, Hans W. Hoek, David C. Schwebel, Jost B. Jonas, Carla Makhlouf, Sergey K Vladimirov, Damian G Hoy, Euripide Frinel G Arthur Avokpaho, Florian Fischer, and Imad D A Faghmous

Subjects
Burden of disease, medicine.medical_specialty, Operations research, Epidemiology, business.industry, Incidence (epidemiology), Immunology, Human immunodeficiency virus (HIV), medicine.disease, medicine.disease_cause, Infectious Diseases, Acquired immunodeficiency syndrome (AIDS), Virology, Family medicine, Medicine, business
Abstract

© 2016 Elsevier Ltd GBD 2015 HIV Collaborators. Estimates of global, regional, and national incidence, prevalence, and mortality of HIV, 1980–2015: the Global Burden of Disease Study 2015. Lancet HIV 2016; 3: e361–87—In this Article, Kerrie E Doyle and David M Pereira have been added to the list of collaborators and Claudia C Pereira has been removed. These corrections have been made as of Aug 22, 2016.

Published
2016
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15. LOWER CIRCULATING LEVELS OF TUMOR NECROSIS FACTOR RELATED APOPTOSIS-INDUCING LIGAND (TRAIL) ARE ASSOCIATED WITH INCREASED SUB-CLINICAL CORONARY ATHEROSCLEROSIS IN SMOKERS

Author

Yingze Zhang, Oluremi N Ajala, Divay Chandra, Frank C. Sciurba, Samir Saba, and Steven E. Reis

Subjects
business.industry, Ligand (biochemistry), medicine.disease, In vitro, Apoptosis, Immunology, Sub clinical, Cancer research, Medicine, In patient, Tumor necrosis factor alpha, Myocardial infarction, Cardiology and Cardiovascular Medicine, business, Coronary atherosclerosis
Abstract

There is significant in vitro evidence demonstrating anti-atherogenic effect of circulating Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). Also, decreased circulating TRAIL levels have been reported in patients with acute myocardial infarction and in those undergoing coronary

Published
2016
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