tbuckley/cabot-search huggingface dataset:
Abstract 346: Essential Role of Extracellular SOD in Reparative Neovascularization Induced by Hindlimb Ischemia
Authors: Ha Won Kim, Angela Lin, Robert E Guldberg, Masuko Ushio-Fukai, Tohru Fukai
Journal: Circulation (2007)

Neovascularization is important physiological repair mechanism in response to ischemic injury and its process is dependent on reactive oxygen species (ROS). Overproduction of superoxide anion (O2· −) rather contributes to various cardiovascular diseases. The extracellular superoxide dismutase (ecSOD) is the major antioxidant enzymes against O2· − in vascular extracellular space; however, its role in neovascularization induced by tissue ischemia is unknown. Here we show that hindlimb ischemia of mice stimulates a significant increase in ecSOD activity in ischemic tissues where ecSOD protein is highly expressed at arterioles. In mice lacking ecSOD, ischemia-induced increase in blood flow recovery, collateral vessel formation and capillary density are significantly inhibited as compared to wild-type (WT) mice (37.6 %, 36.5%, and 26.4% decrease, respectively). Impaired neovascularization in ecSOD knockout (KO) mice is associated with enhanced ischemia induced O2· − production by 1.5 fold, TUNEL-positive apopt...
A General Cutoff Level Combined With Personalized Dynamic Change of Serum Carcinoembryonic Antigen Can Suggest Timely Use of FDG PET for Early Detection of Recurrent Colorectal Cancer
Authors: Yu-Yi Huang, Pei-Ing Lee, Mei-Ching Liu, Chien-Chih Chen, Kuo-Cheng Huang, Andrew T. Huang
Journal: Clinical Nuclear Medicine (2015)

FDG PET that has been used is good for diagnosing asymptomatic colorectal cancer (CRC) recurrence in patients with elevated serum carcinoembryonic antigen (CEA) level. However, there is no reference level of CEA rise that would universally suggest the necessity of a PET study. The purpose of this retrospective study was to identify the high-risk group of CRC recurrence through an examination of the dynamics of the CEA level rise as a recurrence indicator.Between July 2002 and May 2010, 112 patients (59 men, 53 women; age, 18-87 years) had FDG PET for suspicious CRC recurrence indicated by elevated CEA level. We reviewed the PET results and the medical records for recurrence verification and calculated the ratio of increase and the velocity of change in CEA levels for risk stratification.The patient-based sensitivity, specificity, and accuracy of PET are 96.6%, 91.3%, and 95.5%, respectively. The probability of recurrence positively correlated with the CEA level rise and the newly diagnosed disease stage. Carcinoembryonic antigen level greater than 13 ng/mL indicated significantly higher risks of recurrence. In patients with CEA level rise of 13 ng/mL or less, an increase over 3.34 times the individualized baseline also indicated high risks of recurrence.A posttreatment CEA level rise to greater than 13 ng/mL is suggestive of the optimal use of FDG PET, and so is a mild increase below 13 ng/mL at an increase rate over 3.34.
Abstract 2240: How Does Load Affect Diastolic Mitral Annular (E’) Velocity in Humans?
Authors: Barry A Borlaug, Vojtech Melenovsky, Kristy Kessler, Ela Chamera, Theodore Abraham
Journal: Circulation (2006)

Background:  Increased afterload prolongs relaxation in invasive studies, but the effects of altered load and loading sequence on commonly-measured indexes of diastolic function, such early diastolic mitral annular velocity (E’), remains unresolved.   Methods:  48 healthy volunteers (age 19 – 84, 48% female, 54% hypertensive) underwent comprehensive echo-Doppler and 2-D tissue Doppler exam with noninvasive BP measurement and carotid tonometry at rest, during sympathetic stimulation (isometric handgrip, HG; cold pressor test, CPT), and with pharmacologic preload reduction (sublingual nitroglycerin, GTN).   Results:  At rest, there was an inverse relationship between E’ and afterload, whether measured as mean resistance (SVRI, r=0.44, p=0.003), effective arterial elastance (Ea, r=0.44, p=0.003), characteristic impedance (Z 0 , r=0.47, p=0.001), or by the amplitude of late-systolic reflected waves (augmentation index, AI, r=0.64, p 0 , r=0.53, p=0.0002; AI, r=0.57, p   Conclusions:  Early diastolic mitral annular velocity (E’) is diminished with increasing afterload, but varies directly with preload volume. Acute, balanced increases in afterload and preload (as with CPT and HG) are thus associated with neutral effects on E’, whereas isolated preload reduction (GTN) reduces E’.
Cladribine and cytarabine in refractory multisystem Langerhans cell histiocytosis: results of an international phase 2 study
Authors: Jean Donadieu, Frederic Bernard, Max van Noesel, Mohamed Barkaoui, Odile Bardet, Rosella Mura, Maurizio Arico, Christophe Piguet, Virginie Gandemer, Corinne Armari Alla, Niels Clausen, Eric Jeziorski, Anne Lambilliote, Sheila Weitzman, Jan Inge Henter, Cor Van Den Bos
Journal: Blood (2015)
Abstract 16273: Cardiospheres Recapitulate a Niche-Like Microenvironment Rich in Stemness and Cell-Matrix Interactions, Rationalizing Their Enhanced Functional Potency for Myocardial Repair
Authors: Tao-Sheng Li, Shuo-Tsan Lee, Ke Cheng, Satoshi Matsushita, Darryl Davis, Konstantinos Malliaras, Yiqiang Zhang, Noriko Matsushita, Rachel R Smith, Eduardo Marban
Journal: Circulation (2010)

Aims: Cardiac stem cells are promising candidates for use in myocardial regenerative therapy. We compared the functional effects and phenotypes of cardiac-derived cells cultured as three-dimensiona...
Abstract 4778: Postoperative ST2 Blood Concentrations Predict One Year Mortality in Coronary Artery Bypass Patients
Authors: Michael C Grant, Robert Christenson, Jeffrey Gray, Jeremy S Pollock, Eric Christenson, Ashish Joshi, Robert S Poston
Journal: Circulation (2008)

Soluble ST2 (sST2) is released from myocytes in response to mechanical overload and predicts poor outcome in heart failure and myocardial infarction. We evaluated the capability of early sST2 release after coronary artery bypass surgery (CABG) to predict mortality during the first postoperative year. We prospectively evaluated sST2 baseline prior to CABG (BL), immediately after CABG (post), and 24h and 72h. The primary endpoint of the study was all-cause mortality at 1 year. Of the 210 patients enrolled, death occurred in 3 (1.5%) within 30 days and 20 (9.5%) by 1 year. sST2 levels did not change immediately post-CABG (BL: 0.32±0.42, post: 0.42±0.46) but became significantly elevated at 24h and 72h (3.39±3.08, 0.95±1.04 ng/ml; P&lt;0.001). Compared to survivors, sST2 was significantly elevated in decedents at 24h (7.68±3.15 vs. 2.78±2.56, P&lt;0.001) and 72h (1.56±1.62 vs. 0.88±0.44, P&lt;0.03). On ROC analysis, sST2 at 24h strongly predicted death at 1 yr (AUC 0.868, 95% CI=0.77– 0.96). In multivariate analysis, sST2 level was a more powerful predictor of death (OR 17.0, P&lt;0.0001) than traditional predictors (STS risk score, age, left ventricular ejection fraction) or other biomarkers (OR 1.59, P&lt;0.0001) including troponin I, CPK-MB, and NT-pBNP. Although operative mortality was better than predicted by STS score, the 9.5% risk of death over 1yr highlights the need to better stratify mortality risk in order to guide appropriate follow-up after hospital discharge. As a strong predictor of 1yr mortality, independent of traditional laboratory or clinical variables, the sST2 level at 24 hrs may help advance this goal.
Cancers of the Nasopharynx and Oropharynx and Formaldehyde Exposure
Authors: Aaron Blair, Patricia A. Stewart, Robert N. Hoover, Joseph F. Fraumeni, Judy Walrath, Maureen O'Berg, William Gaffey
Journal: JNCI Journal of the National Cancer Institute (1987)

Journal Article Cancers of the Nasopharynx and Oropharynx and Formaldehyde Exposure Get access Aaron Blair, Aaron Blair Search for other works by this author on: Oxford Academic PubMed Google Scholar Patricia A. Stewart, Patricia A. Stewart Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert N. Hoover, Robert N. Hoover Search for other works by this author on: Oxford Academic PubMed Google Scholar Joseph F. Fraumeni, Joseph F. Fraumeni Search for other works by this author on: Oxford Academic PubMed Google Scholar Judy Walrath, Judy Walrath Search for other works by this author on: Oxford Academic PubMed Google Scholar Maureen O'Berg, Maureen O'Berg Search for other works by this author on: Oxford Academic PubMed Google Scholar William Gaffey William Gaffey Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 78, Issue 1, January 1987, Pages 191–193, https://doi.org/10.1093/jnci/78.1.191 Published: 01 January 1987
Abstract 16189: Developing a Realistic in vitro Arrhythmia Model: Fibroblast Content Determines Conduction Velocity and Refractory Properties on 3-D Engineered Tissue Constructs
Authors: Stephane Masse, Nimalan Thavandiran, Patrick F Lai, Hannah Song, Talha Farid, Peter Zandstra, Milica Radisic, Kumaraswamy Nanthakumar
Journal: Circulation (2011)

Background: We have used cardiac monolayers as in-vitro model for electrophysiology studies in fibrillation. However their 2-D structure cannot sustain scrolls, which have been shown as an importan...
Psychiatric illness in the mothers of anxious children
Authors: C G Last, M Hersen, A E Kazdin, G Francis, H J Grubb
Journal: American Journal of Psychiatry (1987)

The authors compared maternal lifetime psychiatric illness for children with separation anxiety disorder and/or overanxious disorder (N = 58) and for children who were psychiatrically disturbed but did not manifest an anxiety or affective disorder (N = 15). The vast majority (83%) of mothers of children with separation anxiety disorder and/or overanxious disorder had a lifetime history of an anxiety disorder. Moreover, over one-half (57%) of the mothers presented with an anxiety disorder at the same time at which their children were seen for similar problems. Both of these rates significantly differed from those obtained for control subjects.
Abstract 5405: Real Time High-Resolution Dynamic Imaging Provides New Insights for Understanding Cardiac Function
Authors: Muhammad Ashraf, Xiaokui Li, Aman Mahajan, David J Sahn
Journal: Circulation (2008)

We used high frame rate echocardiography to define the relationship of strain and rotation parameters with dynamic cardiac function. We studied 15 open chest pigs scanned with a 10S probe on a GE Vivid 7 ultrasound system directly from the surface of heart to allow acquisition of high-resolution apical and basal short axis views (&gt;150 frames/sec). Images were analyzed offline in EchoPac PC using a speckle tracking based strain and motion calculation program. We divided the cardiac cycle into 3 phases to describe results. Phase 1 (37% ± 4.5% of RR’ interval; red in figure ) ended when septal and global circumferential strain reached peak. After initial clockwise motion, the LV showed counterclockwise rotation and 55% ± 5.5% decrease in short axis area during this phase. Phase 2 (marked blue; 18% ± 3.75% of RR’ interval) ended when lateral wall strain reached peak. Global circumferential strain (1–3% decrease) and short axis area (4–6% increase) showed minimal changes. The septum showed 4–7% decrease and lateral wall showed 3–5% increase in strain. All segments continued to twist and reached peak twist coinciding with peak strain in the LV lateral wall. During Phase 3 (33% ± 2.65% of the RR’ interval; red), all segments showed untwisting, 16–18% reduction in circumferential strain, and 52–59% increase in short axis area. Coordinated and sequential contraction results in LV twisting that continues into very early diastole. The isovolumic phase demonstrates minimal contraction in the lateral wall and relaxation in the septum, resulting in continued early isovolumic twisting (torsion), which is then rapidly released.
Abstract 1810: Metabolic Homeostasis is Maintained in Myocardial Hibernation by Adaptive Changes in the Transcriptome and Proteome
Authors: Manuel Mayr, Dalit May, Basetti Madhu, John Griffiths, Anton Horrevoets, Eli Keshet
Journal: Circulation (2009)

Background: Hibernation is a cardioprotective response that preserves myocardial viability under hypoxia. We have recently established a transgenic mouse model for conditional induction of long-ter...
Abstract 4570: Association Between Intra-operative and Early Postoperative Glucose Levels and Adverse Outcomes Following Complex Congenital Heart Surgery
Authors: Angelo Polito, Ravi R Thigarajan, Peter C Laussen, Kimberlee Gauvreau, Michael S Agus, Mark A Scheurer, Frank A Pigula, John M Costello
Journal: Circulation (2008)

Although hyperglycemia is associated with increased mortality in critically ill adults, studies in children undergoing cardiac surgery are limited and have reached conflicting conclusions. We sought to determine whether associations exist between perioperative glucose exposure, prolonged hospitalization and morbid events following complex congenital heart surgery. Metrics of glucose control including average, peak, minimum and standard deviation of glucose levels, and duration of hyperglycemia (hours &gt;126 mg/dL and 200 mg/dL) were determined intraoperatively and for 72 hours following surgery for 378 consecutive children who had a Risk Adjustment in Congenital Heart Surgery-1 category ≥3. Regression analyses were used to determine relationships between glucose variables, hospital length of stay and a composite morbidity-mortality outcome (death, ECMO, infection, hepatic injury, renal failure, and/or brain injury) after controlling for multiple variables known to influence early outcomes. Intraoperatively, a minimum glucose ≤75 mg/dL was associated with greater adjusted odds of reaching the composite morbidity-mortality endpoint (odds ratio [OR], 3.10; 95% confidence interval [CI], 1.49 – 6.48), but other metrics of glucose control were not associated with the composite endpoint or length of stay. Greater duration of hyperglycemia (glucose &gt;126 mg/dl) during the first 72 postoperative hours was associated with longer duration of hospitalization (p&lt;0.001). In the 72 hours after surgery, average glucose &lt;110 mg/dl (OR, 7.30; 95% CI, 1.95–27.25) or &gt;143 mg/dl (OR, 5.21, 95% CI, 1.37–19.89), minimum glucose ≤75 mg/dL (OR, 2.85, 95% CI, 1.38 –5.88), and peak glucose level ≥250 mg/dl (OR, 2.55, 95% CI, 1.20 –5.43) were all associated with greater adjusted odds of reaching the composite morbidity-mortality endpoint. In children undergoing complex congenital heart surgery, intraoperative hyperglycemia was not associated with adverse outcomes. When considering analyses of several metrics of glucose control, the optimal postoperative glucose range may be 110 –126 mg/dl. A randomized trial of strict glycemic control achieved with insulin infusions in this patient population is needed.
Abstract 3612: Apelin Prevents Aortic Aneurysm Formation by Inhibiting Macrophage Inflammation and Infiltration
Authors: Nicholas J Leeper, Maureen M Tedesco, Yoko Kojima, Geoff Schultz, Michael Y Ho, Ramendra K Kundu, Joshua P Anderson, Philip S Tsao, Ronald L Dalman, Thomas Quertermous
Journal: Circulation (2008)

To investigate the hypothesis that Apelin treatment would attenuate aortic injury in a murine model of elastase-induced abdominal aortic aneurysm (AAA) disease, by limiting disease-related vascular wall inflammatory. Male C57BL/6 mice were implanted with osmotic mini-pumps filled with Apelin (2 mg/kg/day) or saline (Control), and subsequently treated with intra-aortic porcine pancreatic elastase to create infrarenal AAA’s. Mice were sacrificed at day 3 for aortic PCR analysis or followed ultrasonographically until day 7 and then sacrificed for histological analysis (Elastic Masson, VCAM, ICAM-1, E-Selectin, and Mac-2 semi-quantitative analysis). The cellular expression of inflammatory cytokines and chemokines in response to Apelin was assessed by TaqMan analysis of both macrophages (J774, RAW, and harvested intraperitoneal cells) and rat aortic smooth muscle cells (A7R5) and compared to other stimuli. Apelin treatment resulted in diminished AAA formation, with a 30% reduction in in vivo aortic diameter by ultrasound (1.04 mm vs 1.48 mm, p &lt; 0.05), and a 59% reduction in maximal aortic cross-sectional area by histology (0.59 mm2 vs 1.43 mm2, p &lt; 0.05) relative to the saline-treated group. The macrophage infiltrate also was significantly reduced in the Apelin-treated mice compared to the Control group (68.6 cells/hpf vs 285.4 cells/hpf, p &lt; 0.001). Apelin treatment was associated with reduced mean aortic MCP-1, MIP 1-alpha, IL-6 and TNF-alpha mRNA levels, although these did not reach statistical significance. Apelin stimulation of cultured macrophage models significantly reduced MCP-1 and TNF-alpha mRNA levels compared to basal conditions (−1.12 and −1.49 fold expression change, p &lt; 0.05, respectively). No difference in endothelial cell adhesion molecule expression or smooth muscle cell cytokine production was found in response to Apelin. Apelin significantly reduces AAA formation in this accepted model of human AAA disease. The mechanism appears to be decreased macrophage infiltration, perhaps related to an apelin-mediated decrease in pro-inflammatory cytokine and chemokine activation. This research has received full or partial funding support from the American Heart Association, AHA Western States Affiliate (California, Nevada &amp; Utah).
Abstract 3363: Anti-Ischemic and Antianginal Efficacy of Ivabradine, a Selective and Specific If Current Inhibitor, in Elderly Patients with Stable Angina
Authors: Michal Tendera, Klinika Kardiologii, K Fox, J.c. Tardif, I Ford
Journal: Circulation (2006)

Background: Ivabradine, a novel heart rate-reducing agent acting on the sinus node If current, was found to be as effective as atenolol in a 4-month, randomized, double-blind noninferiority trial c...
Effectiveness and Safety of Sirolimus Stent Implantation for Coronary In-Stent Restenosis
Authors: Francesco Liistro, Massimo Fineschi, Paolo Angioli, Giuseppe Sinicropi, Giovanni Falsini, Tommaso Gori, Kenneth Ducci, Achille Bravi, Leonardo Bolognese
Journal: Journal of the American College of Cardiology (2006)
Abstract 541: Dyxin/Lmcd1, A Novel LIM Protein, Is Both Necessary And Sufficient For The Induction Of Cardiomyocyte Hypertrophy
Authors: Derk Frank, Christiane Hanselmann, Rainer Will, Hugo A Katus, Norbert Frey
Journal: Circulation (2007)

Sustained cardiac hypertrophy may lead to heart failure and sudden death. While significant progress has been made in elucidating the underlying molecular mechanisms, it is believed that several molecules that modulate cardiomyocyte growth remain elusive. To identify novel candidates involved in hypertrophic signalling, we conducted a genome-wide screening experiment by subjecting neonatal rat cardiomyocytes (NRCM) to either biomechanical stretch or phenylephrine (PE) stimulation followed by microarray analyses. Among several other molecules (stretch: n=164; PE: n=238), the new LIM protein Dyxin/Lmcd1 was significantly upregulated both by stretch (5.6fold, p&lt;0.001) and PE (2.5 fold, p&lt;0.01). Moreover, Dyxin was markedly induced in hypertrophic hearts of transgenic mice overexpressing the phosphatase calcineurin (3.8fold on mRNA- and 2.9fold on protein level (both p&lt;0.01)). To dissect the putative function of this novel molecule, we adenovirally overexpressed Dyxin in NRCM, which led to marked cellular hypertrophy (1.5fold increase in cell surface area, p&lt;0.001) and induction of ANF (3.8fold, p&lt;0.05). In addition, the calcineurin-responsive gene MCIP1.4 was found upregulated (3.2fold, p&lt;0.001), suggesting that Dyxin activates the calcineurin pathway. In order to test whether Dyxin is also required for cardiomyocyte hypertrophy, we stimulated NRCVM with either PE or stretch and utilized adenovirus-encoded microRNAs to knock down Dyxin (−75% on protein, −85% on mRNA level). While both PE and stretch induced significant hypertrophy (+41% and +48%, p&lt;0.001), the inhibition of Dyxin expression completely blunted the hypertrophic response to both stimuli (p&lt;0.001). Consistently, induction of the “hypertrophic gene program” (including ANF, BNP, and alpha-skeletal actin) was abrogated. Likewise, PE-mediated upregulation of MCIP1.4 expression (7.3fold; p&lt;0.001), was entirely prevented by the knockdown of Dyxin (0.8fold, p=n.s.). We show here that Dyxin, which has not been implicated in hypertrophy before, is significantly upregulated in cardiac hypertrophy. Moreover, it is both necessary and sufficient for cardiomyocyte hypertrophy, and this effect is mediated, at least in part by modulation of calcineurin signalling.
Ischemia Detected on Continuous Electrocardiography After Acute Coronary Syndrome
Authors: Benjamin M. Scirica, David A. Morrow, Andrzej Budaj, Anthony J. Dalby, Satishkumar Mohanavelu, Jie Qin, Julian Aroesty, Chester M. Hedgepeth, Peter H. Stone, Eugene Braunwald
Journal: Journal of the American College of Cardiology (2009)
Randomized Phase IIIb Study Of Rapid Vitamin K Antagonist Reversal In Patients Requiring An Urgent Surgical Procedure: Four-Factor Prothrombin Complex Concentrate Is Superior To Plasma
Authors: Majed A. Refaai, Joshua N. Goldstein, Truman J. Milling, Brandon Lewis, Robert Goldberg-Alberts, Bruce A. Hug, Ravi Sarode
Journal: Blood (2013)
Abstract 154: Hydrogen Peroxide-Induced Contractile Dysfunction is Mediated Through Oxidation of SERCA on Cysteine-674
Authors: Steve Lancel, Jingmei Zhang, Gabriela M Kuster, Jia Ying, David R Pimentel, Mario P Trucillo, Ellen O Weinberg, Deborah A Siwik, Richard A Cohen, Wilson S Colucci
Journal: Circulation (2007)

Background: Reactive oxygen species (ROS) are critical mediators of cardiomyocyte contractile dysfunction. We previously reported that H 2 O 2 induces thiol oxidative post-translational modifications of the calcium handling protein sarco/endoplasmic reticulum calcium ATPase (SERCA), leading to a reduction of its activity and contractile dysfunction. Here, we tested the hypothesis that cysteine-674 of SERCA is critical for H 2 O 2 -induced contractile dysfunction in adult rat ventricular myocytes (ARVM). Methods: Overexpression of wild-type (WT) or mutant SERCA, in which cysteine-674 was mutated to serine (C674S), was accomplished by 36 hours of adenoviral infection. ARVM were paced at 5Hz and superfused with 100μM H 2 O 2 . Cell shortening and calcium transients were measured over 20 minutes using video-edge detection and fura-2 fluorescence. Thiol oxidation of SERCA was assessed using biotinylated iodoacet- amide (BIAM)-labeling. Results: After 14min of H 2 O 2 exposure, cell shortening was markedly reduced in WT-SERCA overexpressing ARVM (−43 ± 21%) but not in C674S-SERCA overex-pressing ARVM (−49% ± 31%, p&lt;0.05 vs WT-SERCA, n=21–24/group). Time of 50% cell relengthening was prolonged by 15 ± 5% in WT-SERCA ARVM (p&lt;0.05 vs time 0) but not in C674S-SERCA cells (+1 ± 4%, NS vs time 0). Compared with WT-SERCA ARVM, expression of C674S-SERCA attenuated the H 2 O 2 -induced reduction in calcium transient amplitude (−51 ± 11% vs −87 ± 6%, p&lt;0.05 C674S-SERCA vs WT-SERCA). The 50% calcium reuptake time was prolonged in WT-SERCA compared with C674S-SERCA ARVM (60 ± 3ms vs 46 ± 3ms, p&lt;0.05), reflecting a decrease in SERCA activity in WT-SERCA but not in C674S-SERCA ARVM. H 2 O 2 decreased BIAM-labeling in ARVM overexpressing WT-SERCA by 40% ± 7% (p&lt;0.01,n=3) but failed to decrease BIAM-labeling in ARVM overexpressing C674S-SERCA. Conclusion: Increased thiol oxidative post-translational modification was correlated with a reduced SERCA activity and calcium handling abnormalities, and these effects were attenuated in ARVM overexpressing mutated SERCA modified at Cys674. These findings suggest that oxidation on Cys674 of SERCA is responsible for H 2 O 2 -induced reduction in its activity leading to contractile dysfunction.
肺癌患者における副腎腫瘍の評価における18F-FDG PET/CT
Authors: Goya T, Abe Y, Koshiishi Y, Nagashima Y, Masui K, Nakazato Y, Karita S, Kawachi R, Tachibana K, Takei H
Journal: Journal of Thoracic Oncology (2009)