tbuckley/cabot-search huggingface dataset:
Abstract P102: Risk of Incident Hypertension and Diabetes Mellitus in Habitual Snorers and Sleep Apneic Individuals; The Multiethnic Study of Atherosclerosis
Authors: WaqasQureshi, JosephYeboah, AlainBertoni, GregoryBurke, DavidHerrington, CapriFoy, SusanRedline
Journal: Circulation (2014)

Background: Data regarding temporal association of sleep apnea and snoring with incident hypertension (HTN) and diabetes mellitus(DM) are limited. Hypothesis: We hypothesized that sleep apnea and snoring are associated with incident HTN and DM. Methods: Participants of age 45 - 65 years from 4 ethnicities (Asian, Hispanic, African American and Caucasian) without known cardiovascular disease from Multi Ethnic Study of Atherosclerosis (MESA) were administered a sleep questionnaire. HTN was defined as being on antihypertensive medication or blood pressure ≥140/90 mmHg. DM was defined as fasting blood glucose ≥126 mg/dL or use of antidiabetic medications. Participants with baseline HTN and DM were excluded. Cox proportional hazard models were constructed to evaluate the association of habitual snoring (defined as snoring on ≥3 days of week) and sleep apnea (self-report of diagnosis by doctor) with hypertension or diabetes. The analysis was adjusted for age, gender, race, body mass index (BMI), exercise, educa...
Abstract 18319: The Impact of Low Grade Urinary Albumin on the Risk of Cardiovascular Disease in the Nonhypertensive and Nondiabetic Population
Authors: FumitakaTanaka, ShinjiMakita, ToshiyukiOnoda, KozoTanno, MasakiOhsawa, KazuyoshiItai, KiyomiSakata, Shin-ichiOmama, KuniakiOgasawara, YasuhiroIshibashi, AkiraOkayama, MotoyukiNakamura
Journal: Circulation (2014)

Background: The guidelines recommend screening for microalbuminuria in patients with hypertension and diabetes. Recent cohort studies document a continuous association between low grade urinary albumin (UA) and increased risk of cardiovascular disease (CVD) in these patient groups. However, it is unclear whether this association is present in individuals without hypertension and diabetes. Hypothesis: Even in the nonhypertensive and nondiabetic population, UA from low levels may be related to future CVD risk. Methods: A population-based prospective cohort study was performed in 13,451 nonhypertensive, nondiabetic individuals aged 40 to 89 years (mean age = 60.4±10.2 years) with no cardiovascular history. A multivariate Cox regression analysis was performed to examine the relationship between quartile of urinary albumin/creatinine ratios (UACRs) and the incidence of CVD which was defined as stroke or acute myocardial infarction/sudden cardiac death. Results: During a mean follow-up period of 5.6 years, 213 ...
Abstract 3179: TORC1/2 inhibition sensitizes MYC-driven medulloblastoma cells to carboplatin chemotherapy
Authors: Rachael E. Maynard
Journal: Cancer Research (2018)

Abstract Medulloblastoma is the most common malignant pediatric brain tumor. Tumors having high levels of c-MYC have the worst clinical prognosis, with only a minority of patients surviving. To address this unmet clinical need, we generated a human neural stem cell model of high medulloblastoma that recapitulated the most aggressive subtype phenotypically and by mRNA expression profiling. We performed an in silico analysis of these cells, which predicted that mTOR inhibitors would be potential therapeutic agents. The dual TORC1/2 inhibitor TAK228 (also known as MLN128 and INK128) is orally bioavailable and penetrates the brain. TAK228 is currently in early clinical trials for adults with glioblastoma. We hypothesized that TAK228 would have activity against MYC-driven medulloblastoma. We tested this hypothesis using the MYC amplified medulloblastoma cell lines D425 and D283 as well as our human neural stem cell models. We determined that TAK228 was effective in inhibiting both mTORC1/2 as measured by western blots showing decreased p-S6 and p-AKT473 expression. P-S6 expression is decreased by 90% and p-AKT expression is decreased by 70% in D425 cell lines treated with 20nM TAK228. We found that treatment with TAK228 decreases cell growth in D425 and D283 high-MYC medulloblatoma cell lines at concentrations of 20nM (D425 p&amp;lt;0.005 vs vehicle, D283 p&amp;lt;0.0005 vs vehicle). We also found that TAK228 induces apoptosis as measured by cleaved caspase 3 staining and an increased expression of cleaved PARP (D425 p&amp;lt;0.05 vs vehicle, D283 p&amp;lt;0.0005 vs vehicle). Because mTOR inhibition can suppress glutathione production, and glutathione is required to detoxify platinum containing chemotherapy, we hypothesized that TAK228 would cooperate with carboplatin, which is part of the current standard treatment for high-risk medulloblastoma. TAK228 in combination with carboplatin inhibits cell growth as measured by MTS assay (D425 p&amp;lt;0.05 vs vehicle, D283 p&amp;lt;0.05 vs vehicle) and induces apoptosis as measured by cleaved PARP expression. Combination therapy of TAK228 and carboplatin treatment leads to a 7-fold increase in cleaved PARP compared to cells treated with the vehicle. In vivo testing in orthotopic xenografts is currently underway to determine the survival benefit of TAK228 in combination with carboplatin. TAK228 is effective at inhibiting growth and inducing apoptosis in high-MYC medulloblastoma cell lines and shows strong combinatorial efficacy with carboplatin. Citation Format: Rachael E. Maynard. TORC1/2 inhibition sensitizes MYC-driven medulloblastoma cells to carboplatin chemotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3179.
A Severe Restrictive Aortic Regurgitation Resulting From Valve Tenting by Unusual Aortic Chordae Tendineae Strands
Authors: Ahmed-AmirBouchachi, ThierryFolliguet, Jean-LouisHébert, BoutheinaZeghidi, AnneLegendre, LamyaDrissi, NadiaIannino, PatrickAssayag
Journal: Circulation (2012)
Levels of Circulating Progenitor Cells, Cardiovascular Outcomes and Death
Authors: MauroRigato, AngeloAvogaro, Gian PaoloFadini
Journal: Circulation Research (2016)

Rationale:Circulating progenitor cells (CPCs), including endothelial progenitor cells (EPCs) are biologically related to many aspects of cardiovascular disease, as they promote angiogenesis and vascular repair. Objective:We herein aimed to meta-analyze studies reporting the prognostic role of the CPC/EPC measure on cardiovascular outcomes and death. Methods and Results:We screened the English-language literature for longitudinal studies reporting the association between baseline CPC/EPC levels, future cardiovascular events, and death. We retrieved 28 studies, 21 of which contained poolable data and entered the meta-analysis, for a total of 4155 patients, mostly with a high baseline cardiovascular risk. Sixty percent of the studies met at least 11 of 16 items of quality assessment. Overall, reduced CPC/EPC levels were associated with a ≈2-fold increased risk of future cardiovascular events and cardiovascular death. The most predictive phenotype was CD34+CD133+: low versus high levels predicted cardiovascul...
Myocardial Perfusion, Fibrosis, and Contractility in Children With Kawasaki Disease
Authors: Prakash Muthusami, Wietske Luining, Brian McCrindle, Rob van der Geest, Eugenie Riesenkampff, Shi-Joon Yoo, Michael Seed, Cedric Manlhiot, Lars Grosse-Wortmann
Journal: JACC. Cardiovascular imaging (2018)
Very Late Stent Thrombosis and Late Target Lesion Revascularization After Sirolimus-Eluting Stent Implantation
Authors: TakeshiKimura, TakeshiMorimoto, YoshihisaNakagawa, KazuyaKawai, ShunichiMiyazaki, ToshiyaMuramatsu, NobuoShiode, MasanobuNamura, TakahitoSone, ShigeruOshima, HideoNishikawa, YoshikazuHiasa, YasuhikoHayashi, MasakiyoNobuyoshi, KazuakiMitudo
Journal: Circulation (2012)

Background—There is a scarcity of long-term data from large-scale drug-eluting stent registries with a large enough sample to evaluate low-frequency events such as stent thrombosis (ST). Methods and Results—Five-year outcomes were evaluated in 12 812 consecutive patients undergoing sirolimus-eluting stent (SES) implantation in the j-Cypher registry. Cumulative incidence of definite ST was low (30 day, 0.3%; 1 year, 0.6%; and 5 years, 1.6%). However, late and very late ST continued to occur without attenuation up to 5 years after sirolimus-eluting stent implantation (0.26%/y). Cumulative incidence of target lesion revascularization within the first year was low (7.3%). However, late target lesion revascularization beyond 1 year also continued to occur without attenuation up to 5 years (2.2%/y). Independent risk factors of ST were completely different according to the timing of ST onset, suggesting the presence of different pathophysiological mechanisms of ST according to the timing of ST onset: acute coron...
Abstract 16803: Subclinical Atherosclerosis is Associated With Loss Of CXCR4 Surface Marker Expression on Non-classical Monocytes in HIV-infected Women
Authors: Karin A Mueller, David B Hanna, Erik Ehinger, Xiaonan Xue, Livia Baas, Kathryn Anastos, Mardge H Cohen, Stephen J Gange, Sonya L Heath, Jason M Lazar, Chenglong Liu, Wendy J Mack, Igho Ofotokun, Phyllis C Tien, Howard N Hodis, Alan L Landay, Robert C Kaplan, Klaus Ley
Journal: Circulation (2016)

Introduction: HIV infection is associated with increased risk of cardiovascular disease (CVD). Identification of immunologic mechanisms associated with subclinical CVD (sCVD) among HIV-positive ind...
Electrophysiological Effects of Dofetilide in an In Vitro Model of “Border Zone” Between Normal and Ischemic/Reperfused Myocardium
Authors: RenéRouet, SandraPicard, ChristianLibersa, MathieuGhadanfar, ColinAlabaster, Jean-LouisGérard
Journal: Circulation (2000)

Background—To evaluate both class III activity and antiarrhythmic action of dofetilide at the level of the “border zone,” we investigated its electrophysiological effects on guinea pig ventricular strips submitted partly to normoxia (normal zone, NZ) and partly to simulated severe ischemia, then reperfusion (altered zone, AZ). Methods and Results—Because of the differential class III effects of dofetilide in normal and ischemic regions, the dispersion of the action potential duration at 90% repolarization (APD90) between NZ and AZ was reduced by 5 nmol/L of drug during early ischemia (at 10 minutes, APD90 NZ/APD90 AZ was 1.68±0.22 versus 2.82±0.17 in control, P<0.05), whereas 50 nmol/L dofetilide worsened it during late ischemia (at 30 minutes, APD90 NZ/APD90 AZ was 4.62±0.76 versus 2.57±0.21 in control, P<0.05). Concomitantly, dofetilide at 5, 10, and 50 nmol/L abolished the early extrastimulus (ES)-induced arrhythmias, and at 10 and 50 nmol/L, it significantly enhanced the incidence of late spontaneous ...
Abstract 4690: FoxP3+T cells program/re-program the prostatic tumor microenvironment
Authors: Sanjay Kumar, James Stoke III, Shalie Malik, Udai P. Singh, Selvarangan Ponnazhagan, Upender Manne, Manoj K. Mishra
Journal: Cancer Research (2018)

Abstract Foxp3+ T cells play a critical role in maintaining immunological tolerance by regulating functions of other immune cells, thus preventing autoimmunity. Previous studies have demonstrated the importance of Foxp3+ T cells in the tumor, however, the role increasingly recruited FoxP3+ T cells in the programming of prostatic tumor microenvironment is not well illustrated. Therefore, in this study, we have investigated the role of Foxp3+ T cells in the prostatic tumor microenvironment with the notion that increased Foxp3+ T cells facilitate tumor growth. To accomplish this, we carried out tumor induction studies in C57/BL-6 mice using transgenic adenocarcinoma of mouse prostate (TRAMP cell lines: -C1, -C2 and -C3) as tumor models. Mice were administered with TRAMP (C1-3) cells using the Matrigel system. TRAMP-C3 cells are non-tumorigenic while TRAMP-C1 and TRAMP-C2 cells form tumors. Mice were sacrificed by cervical dislocation when tumor sizes reached ~18-20mm in diameter. To prepare single cell suspension, spleen and tumor were dissected out and cells were stained with various cell surface as well as intracellular immune markers to determine the number of Foxp3+ T cells and other immune cells in the prostatic tumor microenvironment. Our findings suggest that the high number of Foxp3+ T cells was found in the spleen and tumor of TRAMP-C1 and TRAMP-C2 mice than the spleen and tiny tumor of TRAMP-C3 mice. Furthermore, the number of cytotoxic T lymphocytes and NK cells were also observed to be low in the tumorigenic TRAMP-C1 and -C2 mice as compared to non-tumorigenic mice (TRAMP-C3). Therefore, our findings suggest that the number of Foxp3+ T cells may play a critical role in shaping the prostatic tumor microenvironment. Citation Format: Sanjay Kumar, James Stoke III, Shalie Malik, Udai P. Singh, Selvarangan Ponnazhagan, Upender Manne, Manoj K. Mishra. FoxP3+T cells program/re-program the prostatic tumor microenvironment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4690.
Abstract 16087: Vigorous Exercise and Risk of Sudden Cardiac Death in Healthy Men
Authors: Patricia Tung, Shuang Hu, I-Min Lee, J M Gaziano, Christine M Albert
Journal: Circulation (2013)

INTRODUCTION: Vigorous exercise is known to both trigger and protect against sudden cardiac death (SCD) at the time of exertion, and exertion-related SCD is more common among men. While habitual le...
Terminal Portion of Pulmonary Arterial Tree in People Native to High Altitudes
Journal: JAMA (1963)

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Abstract 4325: Cisplatin treatment of testicular cancer introduces long-term changes to the epigenome
Authors: Trine B. Rounge, Cecilie Bucher-Johannessen, Christian M. Page, Trine B. Haugen, Sophie D. Fosså, Hege S. Haugnes, Tom Grotmol
Journal: Cancer Research (2018)

Abstract Testicular cancer (TC) survival rates have increased substantially over the last decades, largely due to the introduction of cisplatin (CP) chemotherapy. This treatment is, however, associated with increased risk of developing metabolic syndrome (MetS), defined according to the National Cholesterol Education Program. We aimed to investigate if CP treatment were associated with epigenetic changes, and whether these changes render TC survivors susceptible for developing MetS later in life. We included 279 Norwegian TC survivors with and without CP treatment and MetS, matched on age at blood sampling (Table 1). The TC survivors were re-examined on average 16 years after the orchiectomy, and for some patients, CP treatment. Whole genome DNA methylation profiles were measured with MethylationEPIC BeadChip and analyzed with the R package minfi. We used a linear regression model adjusting for smoking, age and cell type composition to identify CP differentially methylated CpG sites and logistic regression adjusting for smoking and age to identify differentially methylated CpG sites associated with MetS. Gene enrichment analyses were based on Fisher's exact test using KEGG and Reactome pathways. 32 and 15 differentially methylated CpG sites were associated with CP treatment after adjusting for multiple testing with False Discovery Rate (FDR) and Bonferroni correction, respectively. The PTK6-RAS-MAPk pathway was significantly enriched with the FDR significant CpGs (p-value &amp;lt; 0.1). We could not identify FDR significant differentially methylated CpGs associated with MetS with our sample size. In conclusion, our results suggest that CP treatment has long-term effects on the epigenome. Genes involved in double-strand break repair, consistent with the cytotoxicity of CP treatment, are among the differentially methylated CpGs. Our top list of differentially methylated CpGs associated with MetS (lowest unadjusted p-values), should be further explored in a larger sample set of TC survivors. Table 1: Overview of sample characteristicsCP+ MetS+CP- MetS+CP+ MetS-CP- MetS-N613411569Mean age at surgery31312730Mean age at sample collection49484443Time between surgery and sample collection17181714 Citation Format: Trine B. Rounge, Cecilie Bucher-Johannessen, Christian M. Page, Trine B. Haugen, Sophie D. Fosså, Hege S. Haugnes, Tom Grotmol. Cisplatin treatment of testicular cancer introduces long-term changes to the epigenome [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4325.
Abstract 16981: Gender-specific Differences in High-sensitive Cardiac Troponin T and B-type Natriuretic Peptides Across the Spectrum of Aging in CVD-Free Adults: The Multi-Ethnic Study of Atherosclerosis (MESA)
Authors: Christopher deFilippi, James deLemos, Susie Hong-Zohlman, Lori B Daniels, Robert Christenson, Joao Lima, Alain Bertoni, Stephen Seliger
Journal: Circulation (2016)

Introduction: High sensitive cardiac troponin T (hs-cTnT) and amino-terminal proBNP (NT-proBNP) as measures of myocyte injury and neurohormonal activation can predict risk of heart failure and card...
Abstract 11806: High-Mobility Group Box 1 Aggravates Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure
Authors: Lei Zhang, Ming Liu, Hong Jiang, Ying Yu, Shuning Zhang, Jian Wu, Quan Cao, Peng Yu, Aijun Sun, Yunzeng Zou, Junbo Ge
Journal: Circulation (2014)

Introduction: Inflammatory response is involved in pressure overload-induced cardiac remodeling, but the mechanisms have not yet been fully elucidated. Hypothesis: High-mobility group box 1 (HMGB1), which is of crucial importance in inflammatory response, may participate in pressure overload-induced cardiac hypertrophy and heart failure. Methods: Pressure overload was imposed on the heart of adult male wild-type C57BL/6J mice by transverse aortic constriction (TAC), while 200ng recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the left ventricular wall. Transthoracic echocardiography, detection of proteins and genes expression in myocardium were performed at 2 and 4 weeks after the operation. Sections for histological analyses were generated from paraffin embedded hearts. Moreover, cardiac myocytes were cultured and given sustained mechanical stress and/or HMGB1 treatment before signaling pathways detection under the blockage of receptor for advanced glycation end...
Abstract 15948: Frequency and Prognosis of Recurrent In-hospital Cardiac Arrest
Authors: Maya L Chan, Yuanyuan Tang, Monique Anderson, Paul S Chan
Journal: Circulation (2016)

Introduction: Nearly 200,000 patients experience an in-hospital cardiac arrest (IHCA) annually in the U.S. However, the proportion of patients who experience a recurrent IHCA and the associated prognosis with a recurrent cardiac arrest is unknown. Methods: Within Get With The Guidelines-Resuscitation, we identified 192,250 patients with an IHCA between 2000 to 2014. Patients were categorized as having no recurrent IHCA (only 1 event), a recurrent IHCA (2 or more events), and a recurrent out-of-hospital cardiac arrest (OHCA), defined as an IHCA after being hospitalized for an index OHCA. Using multivariable hierarchical logistic regression models, rates of survival to discharge and favorable neurological survival (discharge CPC score of 1) between patients with recurrent IHCA and those with no recurrent IHCA and recurrent OHCA were compared. Results: Overall, 165,446 (86.1%) had no recurrent IHCA, 23,643 (12.3%) had recurrent IHCA, and 3162 (1.6%) had recurrent OHCA. Patients with no recurrent IHCA were ol...
Abstract 5427: Inhibition of hypoxia-inducible factor 1 (HIF-1) transcriptional activity and cell mobility via G9a/GLP-mediated methylation of HIF-1α
Authors: Lei Bao, Yan Chen, Hsien-Tsung Lai, Cheng-Ming Chiang, Gregg L. Semenza, Yingfei Wang, Weibo Luo
Journal: Cancer Research (2018)

Abstract Hypoxia-inducible factor 1 (HIF-1) is a main regulator of cellular response to hypoxia and its transcriptional activity is crucial for cancer cell migration and invasion. Post-translational modifications of the α subunit of HIF-1 (HIF-1α) play dominant roles in regulating its function. In this study, we demonstrated that the lysine methyltransferases G9a and GLP catalyzed mono- and di-methylation of HIF-1α at lysine (K) 674 in vitro and in vivo. Functionally, K674 methylation suppressed HIF-1 transcriptional activity as well as expression of the HIF-1 target genes including PTGS1, NDNF, SLC6A3, and Linc01132 in human glioblastoma U251MG cells. Moreover, mutation of K674 of HIF-1α significantly enhanced U251MG cell migration under hypoxia. Importantly, we found that G9a level was downregulated by hypoxia in glioblastoma, which was negatively correlated with PTGS1 expression and survival rate in glioblastoma patients. These findings reveal a novel naturally existing negative feedback mechanism that maintains high activity of HIF-1 and cell mobility in human glioblastoma. Citation Format: Lei Bao, Yan Chen, Hsien-Tsung Lai, Cheng-Ming Chiang, Gregg L. Semenza, Yingfei Wang, Weibo Luo. Inhibition of hypoxia-inducible factor 1 (HIF-1) transcriptional activity and cell mobility via G9a/GLP-mediated methylation of HIF-1α [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5427.