tbuckley/cabot-search huggingface dataset:
Abstract P107: Differences In Hypercholesterolemia Prevalence Between African Americans And Whites: A Cross-sectional Study Using 2017-2018 National Health And Nutrition Examination Surveys Data
Authors: Omar Sajdeya, Ruba Sajdeya, Mohamad B Taha, Mohammad As Sayaideh, Osama Dasa
Journal: Circulation (2021)

Importance: African Americans (AA) have a 20% higher risk of CVD death than Whites. Treating hypercholesterolemia (HC) is paramount in CVD primary prevention. Some evidence showed that AA have a lower risk of HC compared to whites. Methods: A cross-sectional study using the 2017-18 National Health and Nutrition Examination Surveys data. Logistic regression analysis was used to compare the prevalence of diagnosed HC in AA and whites aged 18-80 years old. Serum total cholesterol (TC) and high-density lipoprotein (HDL) levels were compared by multiple linear regression. Results: Among 2549 participants, 51.7% were females, and 63.4% were white. The mean (SD) age was 51.6 (19.1) years. AA had a 24 % reduced risk of HC diagnosis than whites after adjusting for age, Body Mass Index (BMI), diabetes, hypertension, and smoking; OR [95%CI]= 0.767 [0.621, 0.923]. There was no difference in TC level (p=0.7242), while HDL was higher among AA (p&lt;0.0001, β=3.83), adjusting for age, gender, BMI, smoking, diabetes, education level, and use of cholesterol medications. Conclusion: Consistent with some evidence, AA had a lower prevalence of HC diagnosis and higher HDL levels.
Abstract 16179: Concordance Between Machine Learning-based Methods of Atrial Fibrillation Subtyping in 49,905 Individuals and Relationship to Genetically Predicted Af Risk and Inflammation
Authors: Giovanni E Davogustto, Eric Farber-Eger, Katherine T MURRAY, Gregory F Michaud, Ben B Shoemaker, Jonathan Mosley, Dan M Roden, Quinn Wells
Journal: Circulation (2020)

Introduction: Atrial Fibrillation (AF) is a heterogeneous arrythmia. Identification of subgroups of patients with shared mechanisms, such as genetic predisposition to AF and inflammation, could facilitate precision care. Machine learning (ML) is increasingly applied to define disease subtypes in an unbiased fashion, but the extent to which purported subgroups are robust across ML methods and whether they align with underlying AF mechanisms is unclear. Objective: Compare AF subtypes identified using 2 ML methods, and assess the extent to which subtypes relate to genetically-predicted AF and inflammatory state. Methods: We identified individuals with AF in a large electronic health record and linked DNA biobank. Using 86 curated clinical features, 5 clusters were found using affinity propagation, which provided K for a complementary K-means clustering. Shared cluster membership was assessed with the Adjusted Rand Index (ARI). Polygenic risk scores (PRS) for AF and 5 inflammatory biomarkers (IL-1b, IL-6, TNF-α, IFN-γ, IL-10, and IL-17) were used to interrogate genetic mechanisms underlying clustering. Results: We identified 49,905 patients with AF, including 5,532 with genotyping. There was moderate agreement in subgroup membership between the two ML methods (ARI 0.53). Subgroups were distinguished by presence/absence of structural heart disease, comorbidities, mortality, AF ablation, bleeding events, and dialysis (Figure 1). All subgroups had greater mean AF PRS than non-AF controls. Among AF subgroups, the “high comorbidities” group had the lowest AF PRS values (Figure 2). PRS of inflammatory biomarkers were similar between clusters. Conclusion: In this real-world AF cohort, there was moderate agreement between 2 clustering methods. The genetically-predicted levels of inflammatory biomarkers were not different among clusters. Clusters have features comparable to clinically recognized AF subgroups, and differ in genetic liability toward AF.
Abstract 15519: The Prognostic Impact of Transcardiac Gradient of Follistatin-like 1 in Patients With Non-ischemic Dilated Cardiomyopathy
Authors: Hideo Oishi, TAKAHIRO OKUMURA, Koji Ohashi, Yuki Kimura, Shingo Kazama, Naoki Shibata, Yoshihito Arao, Hiroo Kato, Tasuku Kuwayama, Shogo Yamaguchi, Toru Kondo, Hiroaki Hiraiwa, Ryota Morimoto, Noriyuki Ouchi, Toyoaki Murohara
Journal: Circulation (2020)

Introduction: Follistatin-like 1 (FSTL1) is secreted from various tissues including myocardium and could play a cardioprotective role against harmful stimuli. It has been shown that the expression of FSTL1 protein in patients with heart failure is higher than that in healthy subjects. However, little is known about the association between serum FSTL1 levels and the cardiac prognosis. Hypothesis: We hypothesized that the transcardiac gradient of FSTL1 reflect myocardial FSTL1 and is useful for predicting prognosis in patients with non-ischemic dilated cardiomyopathy (NIDCM). Methods: Thirty-two NIDCM patients were enrolled. Blood samples were simultaneously collected from the aortic root (Ao), coronary sinus (CS) as well as peripheral vein during cardiac catheterization. The transcardiac gradient of FSTL1 was calculated by the difference between serum FSTL1 levels of CS and Ao (FSTL1 CS-Ao ). Patients were divided into two groups at the median of FSTL1 CS-Ao : Low FSTL1 CS-Ao group, &lt;0 ng/mL; High- FSTL1 CS-Ao group, &gt; 0 ng/mL. The primary endpoint of this study was the occurrence of a cardiac event, which was defined as a composite of cardiac deaths and unexpected hospitalizations for worsening heart failure. Results: The median plasma B type natriuretic levels and mean left ventricular ejection fraction in the Low and High FSTL1 CS-Ao groups were 91.9 (21.7 - 277.5) vs. 94.1 (59.1 - 236.5) pg/mL (P = 1.000) and 31.4 ± 6.5 vs. 30.5 ± 7.3 % (P = 0.714), respectively. FSTL1 CS-Ao was negatively correlated with pulmonary capillary wedge pressure (R = -0.400, P = 0.023), mean pulmonary artery pressure (R = -0.40, P = 0.023) and right atrial pressure (R = -0.41, P = 0.019). Kaplan-Meier analysis showed that event-free survival rate was significantly lower in the Low FSTL1 CS-Ao group (p=0.0126). Conclusions: Transcardiac gradient of FSTL1 is associated with hemodynamics and low transcardiac gradient of FSTL1 might be associated with poor prognosis in NIDCM patients.
Anticoagulant Use for Atrial Fibrillation Among Persons With Advanced Dementia at the End of Life
Authors: Gregory M. Ouellet, Terri R. Fried, Lauren G. Gilstrap, John R. O’Leary, Andrea M. Austin, Jonathan S. Skinner, Andrew B. Cohen
Journal: JAMA Internal Medicine (2021)

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Diabetes-Related Factors and the Effects of Ticagrelor Plus Aspirin in the THEMIS and THEMIS-PCI Trials
Authors: Lawrence A. Leiter, Deepak L. Bhatt, Darren K. McGuire, Hwee Teoh, Kim Fox, Tabassome Simon, Shamir R. Mehta, Eli I. Lev, Róbert G. Kiss, Anthony J. Dalby, Héctor Bueno, Wilhelm Ridderstråle, Anders Himmelmann, Jayne Prats, Yuyin Liu, Jane J. Lee, John Amerena, Mikhail N. Kosiborod, Philippe Gabriel Steg
Journal: Journal of the American College of Cardiology (2021)

THEMIS (The Effect of Ticagrelor on Health Outcomes in Diabetes Mellitus Patients Intervention Study) (n = 19,220) and its pre-specified THEMIS-PCI (The Effect of Ticagrelor on Health Outcomes in Diabetes Mellitus Patients Intervention Study-Percutaneous Coronary Intervention) (n = 11,154) subanalysis showed, in individuals with type 2 diabetes mellitus (median duration 10.0 years; HbA1c 7.1%) and stable coronary artery disease without prior myocardial infarction (MI) or stroke, that ticagrelor plus aspirin (compared with placebo plus aspirin) produced a favorable net clinical benefit (composite of all-cause mortality, MI, stroke, fatal bleeding, and intracranial bleeding) if the patients had a previous percutaneous coronary intervention.In these post hoc analyses, the authors examined whether the primary efficacy outcome (cardiovascular death, MI, stroke: 3-point major adverse cardiovascular events [MACE]), primary safety outcome (Thrombolysis In Myocardial Infarction-defined major bleeding) and net clinical benefit varied with diabetes-related factors.Outcomes were analyzed across baseline diabetes duration, HbA1c, and antihyperglycemic medications.In THEMIS, the incidence of 3-point MACE increased with diabetes duration (6.7% for ≤5 years, 11.1% for >20 years) and HbA1c (6.4% for ≤6.0%, 11.8% for >10.0%). The relative benefits of ticagrelor plus aspirin on 3-point MACE reduction (hazard ratio [HR]: 0.90; p = 0.04) were generally consistent across subgroups. Major bleeding event rate (overall: 1.6%) did not vary by diabetes duration or HbA1c and was increased similarly by ticagrelor across all subgroups (HR: 2.32; p < 0.001). These findings were mirrored in THEMIS-PCI. The efficacy and safety of ticagrelor plus aspirin did not differ by baseline antihyperglycemic therapy. In THEMIS-PCI, but not THEMIS, ticagrelor generally produced favorable net clinical benefit across diabetes duration, HbA1c, and antihyperglycemic medications.Ticagrelor plus aspirin yielded generally consistent and favorable net clinical benefit across the diabetes-related factors in THEMIS-PCI but not in the overall THEMIS population.
Abstract 13152: Do Survivors of Acute Coronary Syndrome Due to Unprotected Left Main Coronary Artery Occlusion Treated With Extracorporeal Membrane Oxygenation Have Higher Mortality in Chronic Phase?
Authors: Haruko Shiota, Eisuke Kagawa, Masaya Kato, Noboru Oda, Eiji Kunita, Michiaki NAGAI, Keigo Dote
Journal: Circulation (2020)

Introduction: Mortality in patients with acute coronary syndrome (ACS) due to unprotected left main coronary artery (LMA) occlusion is high. Extracorporeal membrane oxygenation (ECMO) could rapidly provide circulatory support. Hypothesis: This study aimed to verify the hypotheses that the patient who required circulatory support with ECMO in acute phase of LMA-ACS had greater cardiac function deterioration and had higher mortality in the chronic phase than those who did not require ECMO. Methods: Patients with LMA-ACS who underwent percutaneous coronary revascularization between 2000 and 2020 were enrolled in this study. The patients were divided into two groups based on whether or not they received ECMO. Thirty-day (acute phase) and 30-day to 6-year (chronic phase) survival curves were constructed by Kaplan-Meier method. The cause of death in acute and chronic phase were examined. Results: Among the 85 study patients, 23 (27%) were in the ECMO-group. Median age was younger in the ECMO-group (65 y [57 - 72] vs. 73 y [69 - 83], p &amp;lt; 0.01), and male sex (67% vs. 63%) were similar in ECMO group and non-ECMO groups respectively. The prevalence of ST elevation myocardial infarction (STEMI), non-STEMI, unstable angina were 52%, 48%, and 0% vs. 15%, 42%, and 44% in the ECMO group and non-ECMO group, respectively. The 30-day mortality was significantly higher in ECMO group (61% vs. 15%, p &amp;lt; 0.01); however, the 30-day to 6-year mortality was similar between the two groups (41% vs. 33%, p = 0.59) (Figure). The cause of death in the acute phase were cardiac failure (79% and 67%) and those in chronic phase were cardiac failure (50% and 25%), malignancy (0% and 13%), and infection (50% and 36%). Conclusions: The mortality in chronic phase in LMA-ACS patients who survived up to 30 days were similar in ECMO group and non-ECMO group. Moreover the patients whose cardiac function deteriorated severely and required ECMO in acute phase had similar prognosis to those that did not require ECMO.
Role of angiopoietin-2 in venous thrombus resolution and chronic thromboembolic disease
Authors: Lukas Hobohm, Sebastian Kölmel, Caroline Niemann, Philipp Kümpers, Valentin J. Krieg, Magdalena L. Bochenek, Alexander H. Lukasz, Yvonne Reiss, Karl-Heinz Plate, Christoph Liebetrau, Christoph B. Wiedenroth, Stefan Guth, Thomas Münzel, Gerd Hasenfuß, Philip Wenzel, Eckhard Mayer, Stavros V. Konstantinides, Katrin Schäfer, Mareike Lankeit
Journal: European Respiratory Journal (2021)

Defective angiogenesis, incomplete thrombus revascularisation and fibrosis are considered critical pathomechanisms of chronic thromboembolic pulmonary hypertension (CTEPH) after pulmonary embolism. Angiopoietin-2 (ANGPT2) has been shown to regulate angiogenesis, but its importance for thrombus resolution and remodelling is unknown.ANGPT2 plasma concentrations were measured in patients with CTEPH (n=68) and acute pulmonary embolism (n=84). Tissue removed during pulmonary endarterectomy (PEA) for CTEPH was analysed (immuno)histologically. A mouse model of inferior vena cava ligation was used to study the kinetics of venous thrombus resolution in wild-type mice receiving recombinant ANGPT2 via osmotic pumps, and in transgenic mice overexpressing ANGPT2 in endothelial cells.Circulating ANGPT2 levels were higher in CTEPH patients compared to patients with idiopathic pulmonary arterial hypertension and healthy controls, and decreased after PEA. Plasma ANGPT2 levels were elevated in patients with pulmonary embolism and diagnosis of CTEPH during follow-up. Histological analysis of PEA specimens confirmed increased ANGPT2 expression, and low levels of phosphorylated TIE2 were observed in regions with early-organised pulmonary thrombi, myofibroblasts and fibrosis. Microarray and high-resolution microscopy analysis could localise ANGPT2 overexpression to endothelial cells, and hypoxia and transforming growth factor-β1 were identified as potential stimuli. Gain-of-function experiments in mice demonstrated that exogenous ANGPT2 administration and transgenic endothelial ANGPT2 overexpression resulted in delayed venous thrombus resolution, and thrombi were characterised by lower TIE2 phosphorylation and fewer microvessels.Our findings suggest that ANGPT2 delays venous thrombus resolution and that overexpression of ANGPT2 contributes to thrombofibrosis and may thus support the transition from pulmonary embolism to CTEPH.
Novel Measure of Ventricular Repolarization Instability and Ventricular Tachyarrhythmias in Patients with Early Phase of Acute Coronary Syndrome-TWIST Study-
Authors: Ichikawa Tomohide, Watanabe Eiichi, Yoshioka Koichiro, Tomita Takeshi, Amino Mari, Nakamura Mari, Yamamoto Mayumi, Harigaya Hiroto, Okuda Kentaro, Sobue Yoshihiro, Ozaki Yukio
Journal: Circulation (2013)
Abstract 16665: Intracoronary Administration of Neonatal Cardiac Mesenchymal Cells Promotes Cardiac Functional Recovery in a Porcine Model of Acute Myocardial Infarction
Authors: Mohamed Abdullah, David Morales, Aakash M Shah, Lauren Levy, Progyaparamita Saha, Rachana Mishra, Sudhish Sharma, Sunjay Kaushal
Journal: Circulation (2020)

Background: The strong regenerative potential of neonatal mesenchymal stem cells (nMSCs) in animal MI models when compared to adult MSCs have been attributed to their paracrine secretions. This study determines the therapeutic potential of nMSC-based therapies in a translationally relevant animal large model. Methods: Yorkshire Pigs underwent a 60-minute coronary occlusion followed by reperfusion. Pigs were randomized for intracoronary administration of 10 million nMSCs (n=4), 20 million nMSCs (n=4), 2 mg/kg of TCM (n=4), 10 million nMSCs plus 2 mg/kg TCM (n=5), or placebo (n=4). The infarct size was quantified 48 hours post-infarction. Separate (10 million nMSCs plus 2 mg TCM treated and control) groups were allowed to survive for 28 days, and cardiac MRI (cMR) was performed on post- operative days 7 and 28. Results: After 48hrs, increasing the dose of nMSCs (20 million vs 10 million nMSCs) showed more decrease in infarct size (74+0.03% vs 83.2+0.05%, p =0.25). 2 mg TCM reduced the infarct size in comparison to control (60.8+ 0.09% vs 91+0.03%, p= 0.02). Combination of 10 million nMSCs plus 2 mg TCM achieved the greater reduction of infarct size from 91+ 0.03% to 56+0.02% ( p =0.0002). At 28 days, infarct percent mass to the left ventricle mass was significantly smaller in the combination of 10 million nMSCs and 2mg TCM than control group (3.98+1.7 % vs 13.63 + 3.9%, p =0.003). These combination treated animals showed an increase in stroke volume (+ 10 mL vs - 1.7 mL, p= 0.002) and preserved LV dimensions and ejection fraction by day 28 as compared to day 7. None of the treatment groups showed any end-organ damage. The infarct zone for treated animals showed enhanced angiogenesis and reduced fibrosis, inflammation and apoptosis. Anti-apoptotic signaling molecules related to MAPK pathway are being investigated. Conclusions: Intracoronary infusion of nMSCs-TCM is safe, promotes the strongest cardiac and vascular regeneration by decreasing scar and improving LV function in pigs after AMI. These results provide the rationale for a subsequent translation of a combination allogenic product of nMSCs-TCM to clinical trials.
FLT3 Positivity Is a Predictor of Early Relapse Post-Transplantation — Allo-HCT Is an Ineffective Salvage Strategy in Active AML
Authors: Pavan Kumar Bhamidipati, Han Se-Young, Shivaprasad Manjappa, Feng Gao, Mark A. Schroeder, Ravi Vij, Amanda F. Cashen, Camille N. Abboud, John F DiPersio
Journal: Blood (2017)
Questioning the Value of High-Deductible Health Plans for Children With Chronic Conditions
Authors: Jennifer Kusma, Matthew M. Davis
Journal: JAMA Pediatrics (2021)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Molecular Characterization of Waldenström's Macroglobulinemia Patients Using Peripheral Blood Cell-Free Tumor DNA
Authors: Tina Bagratuni, Ioannis Ntanasis-Stathopoulos, Nefeli Mavrianou-Koutsoukou, Christine Liacos, Nikolaos Kanellias, Magdalini Migkou, Dimitrios C. Ziogas, Evangelos Eleutherakis-Papaiakovou, Maria Roussou, Despina Fotiou, Maria Gavriatopoulou, Evangelos Terpos, Eftathios Kastritis, Meletios A. Dimopoulos
Journal: Blood (2017)
ハワイの日本人・日本の日本人・米国の白人における第二次世界大戦後の出生コホートの男性の脳卒中死亡率
Authors: Sekikawa A, Horiucha By, Curb Dj, Sutton-Tyrell K, Edmundowicz D, Ueshima H, Kadowaki T, Kuller Lh
Journal: Circulation (2002)
Alteration of MDM2 by the Small Molecule YF438 Exerts Antitumor Effects in Triple-Negative Breast Cancer
Authors: Peipei Shan, Feifei Yang, Hongzhao Qi, Yunjie Hu, Sujie Zhu, Zhenqing Sun, Zhe Zhang, Chuanxiao Wang, Caixia Hou, Jie Yu, Lirong Wang, Zhixia Zhou, Peifeng Li, Hua Zhang, Kun Wang
Journal: Cancer Research (2021)

Abstract Triple-negative breast cancer (TNBC) exhibits a high mortality rate and is the most aggressive subtype of breast cancer. As previous studies have shown that histone deacetylases (HDAC) may represent molecular targets for TNBC treatment, we screened a small library of synthetic molecules and identified a potent HDAC inhibitor (HDACi), YF438, which exerts effective anti-TNBC activity both in vitro and in vivo. Proteomic and biochemical studies revealed that YF438 significantly downregulated mouse double minute 2 homolog (MDM2) expression. In parallel, loss of MDM2 expression or blocking MDM2 E3 ligase activity rendered TNBC cells less sensitive to YF438 treatment, revealing an essential role of MDM2 E3 ligase activity in YF438-induced inhibition of TNBC. Mechanistically, YF438 disturbed the interaction between HDAC1 and MDM2, induced the dissociation of MDM2-MDMX, and subsequently increased MDM2 self-ubiquitination to accelerate its degradation, which ultimately inhibited growth and metastasis of TNBC cells. In addition, analysis of clinical tissue samples demonstrated high expression levels of MDM2 in TNBC, and MDM2 protein levels closely correlated with TNBC progression and metastasis. Collectively, these findings show that MDM2 plays an essential role in TNBC progression and targeting the HDAC1–MDM2–MDMX signaling axis with YF438 may provide a promising therapeutic option for TNBC. Furthermore, this novel underlying mechanism of a hydroxamate-based HDACi in altering MDM2 highlights the need for further development of HDACi for TNBC treatment. Significance: This study uncovers the essential role of MDM2 in TNBC progression and suggests that targeting the HDAC1–MDM2–MDMX axis with a hydroxamate-based HDACi could be a promising therapeutic strategy for TNBC.
Abstract 012: Association Between Premature Menopause And Lifetime Risk Of Coronary Heart Disease: Lifetime Risk Pooling Project
Authors: Priya M Freaney, Hongyan Ning, Mercedes R Carnethon, John T Wilkins, Norrina B Allen, Donald M Lloyd-Jones, Sadiya Khan
Journal: Circulation (2021)

Introduction: Menopause before the age of 40 years is recognized as a risk enhancer for coronary heart disease (CHD) by the 2019 AHA/ACC Primary Prevention guidelines. Race-specific prevalence of premature menopause and its association with lifetime risk of CHD morbidity and mortality have not been well described in Black and White women, and could inform risk stratification and intensity of prevention efforts. Hypothesis: We hypothesized that Black and White women who experience premature menopause (&lt;40 years) will have similarly elevated lifetime burden of CHD compared with women of the same race who do not have premature menopause. Methods: We pooled individual-level data from Black and White postmenopausal women aged 55-69 years from 6 US population-based cohorts. We included women without CHD at baseline and excluded women who reported surgical menopause. We defined premature menopause as age &lt;40 years. We performed (1) modified Kaplan Meier analysis and (2) competing Cox models to estimate joint cumulative risk for CHD or non-cardiovascular death adjusted for age, smoking, education, obesity, hypertension, and diabetes. Results: Of the 3522 Black women and 6514 White women, mean ages were 61.2 ± 4.3 and 60.0 ± 4.4 years, respectively. Premature menopause (&lt;40 years) occurred more commonly in Black (15.5%) compared with White (4.8%) women. Lifetime risk of CHD was higher in Black and White women with premature menopause ( Figure ). Hazard ratios adjusted for risk factors and accounting for competing risk of death were higher in Black (1.41 [1.04, 1.90]) and White (1.39 [1.03, 1.87]) women with premature menopause compared those Black and White women without premature menopause, respectively. Conclusions: Black women are three times more likely to experience premature natural menopause (&lt;40 years) than White women. Premature menopause is independently associated with 40% higher risk of CHD in both Black and White women and should be assessed as a risk-enhancing feature in clinical prevention decisions.