tbuckley/cabot-search huggingface dataset:
Abstract 405: Antioxidant Treatment Prevents Profibrotic Changes And Cardiac Dysfunction In Prenatal Alcohol Exposure
Authors: Van K Ninh, Elia C El Hajj, Jason D Gardner
Journal: Circulation Research (2018)

Prenatal ethanol exposure is often associated with cardiac defects. Our studies focus on the role of cardiac fibroblasts in the developing heart, and how they are affected by prenatal ethanol exposure. There have been numerous studies demonstrating the protective effects of antioxidant treatment against alcohol-induced injury during cardiac development. Thus, we hypothesize that in utero ethanol (EtOH) exposure creates oxidative stress and activates neonatal cardiac fibroblasts, leading to a profibrotic phenotype and cardiac dysfunction. Further, we hypothesize that these effects are prevented by antioxidant treatment. We performed in utero EtOH administration to C57/BL6 mice on gestation days 6.75 and 7.5. Dams were intraperitoneally injected with 2.9 g EtOH/kg body weight to produce a blood EtOH content of ~0.26 g/dL each time. Controls were injected with vehicle saline. Randomly selected dams in both groups were treated with 100 gram/kg body weight of the antioxidant N-acetylcysteine (NAC) immediately after EtOH or vehicle administration. Left ventricular (LV) chamber dimension and function were assessed in sedated animals on neonatal day 5 using echocardiography. Eccentric index was calculated as a ratio of LV interior diameter and LV posterior wall thickness*2 at diastole. Eccentric index increased in EtOH-exposed animals (2.2±0.1 EtOH vs 1.8±0.1 saline, p&lt;0.05). There were no changes in EtOH animals treated with NAC (1.9±0.1, NS). Additionally, ejection fraction decreased in the EtOH group (60±2% EtOH vs 68±2% saline). NAC treatment prevented this depression of systolic function in EtOH-exposed neonates (72±2%). Hearts were analyzed for expression of profibrotic proteins. In EtOH-exposed pups, collagen I decreased (0.02±.01 vs 0.04±.01 au), but collagen III expression increased (0.21±.02 vs 0.13±.01 au) compared to saline animals; the overall collagen I/III ratio significantly decreased (0.47±0.07 vs 1.0±0.17). When EtOH-exposed mice were treated with NAC, collagen I/III ratio did not change (0.83±0.11). Overall, our data demonstrate that in utero EtOH exposure produces a profibrotic phenotype in neonatal hearts and a decline in both diastolic and systolic function. These adverse effects were prevented by antioxidant treatment.
AGING AGGRAVATES LEFT VENTRICULAR DYSFUNCTION IN OBESITY THROUGH THE IMPAIRMENT OF MITOCHONDRIAL FUNCTION, AUTOPHAGY, AND INCREASED APOPTOSIS IN OBESE RATS
Authors: Cherry Bo-Htay, Thazin Shwe, Krekwit Shinlapawittayatorn, Siripong Palee, Siriporn Chattipakorn, Nipon Chattipakorn
Journal: Journal of the American College of Cardiology (2019)
Targeting slug-mediated non-canonical activation of c-Met to overcome chemo-resistance in metastatic ovarian cancer cells
Authors: Linlin Chang, Yan Hu, Yingying Fu, Tianyi Zhou, Jun You, Jiamin Du, Lin Zheng, Ji Cao, Meidan Ying, Xiaoyang Dai, Dan Su, Qiaojun He, Hong Zhu, Bo Yang
Journal: Acta Pharmaceutica Sinica B (2019)

Metastasis-associated drug resistance accounts for high mortality in ovarian cancer and remains to be a major barrier for effective treatment. In this study, SKOV3/T4, a metastatic subpopulation of ovarian cancer SKOV3 cells, was enriched to explore potential interventions against metastatic-associated drug resistance. Quantitative genomic and functional analyses were performed and found that slug was significantly increased in the SKOV3/T4 subpopulation and contributed to the high resistance of SKOV3/T4. Further studies showed that slug activated c-Met in a ligand-independent manner due to elevated levels of fibronectin and provoked integrin α V function, which was confirmed by the significant correlation of slug and p-Met levels in 121 ovarian cancer patient samples. Intriguingly, c-Met inhibitor(s) exhibited greatly enhanced anti-cancer effects in slug-positive ovarian cancer models both in vitro and in vivo. Additionally, IHC analyses revealed that slug levels were highly correlated with reduced survival of ovarian cancer patients. Taken together, this study not only uncovers the critical roles of slug in drug resistance in ovarian cancer but also highlights a promising therapeutic strategy by targeting the noncanonical activation of c-Met in slug-positive ovarian cancer patients with poor prognosis.
Abstract 335: Introducing a Multiwell Cardiac μGMEA Platform for Action Potential Recordings From Human iPSC Derived Cardiomyocyte Constructs
Authors: Stacie L Edwards, Viviana Zlochiver, Donald M Conrad, Ravi Vaidyanathan, Rosy Joshi-Mukherjee
Journal: Circulation Research (2018)

Multielectrode array technology utilizing iPSC derived cardiomyocytes has proven useful for drug screening and arrhythmia studies. However, its application for direct action potential (AP) measurements from multicellular preparations remains limiting. We report a novel platform for high temporal resolution AP recordings from human iPSC-derived cardiomyocyte (hiPSC-CM) constructs. Derivation of high purity hiPSC-CMs yielded syncytial monolayers when cultured on a PEDOT-coated micro-gold multielectrode array (μGMEA). We gained intracellular access via 30 seconds of localized electroporation causing a revertible transition of extracellular field potential signals to quasi-APs to APs. We recorded a total of 492 AP waveforms within and across 9 constructs simultaneously and classified their morphologies based on action potential duration ratio (APD 50 /APD 90 ) and difference (APD 90 –APD 50 ). The vast majority of the waveforms (90.8%) were found to be ventricular-like with APD 50 /APD 90 and APD 90 –APD 50 of 0.75-0.95 and 52-166ms respectively. APD 30 displayed a wider variability within individual constructs when compared to the APD 80 distribution. The variability in fractional repolarization (APD 80 – APD 30 /APD 80 ) and triangulation (APD 80 – APD 30 ), parameters widely used for drug screening and arrhythmogenesis, ranged from 0.1- 0.8 and 100- 550ms respectively. The Gaussian distribution produced a single peak across these parameters confirming the ventricular-like properties of all the constructs. We confirmed the reliability of the system by recapitulating known drug induced responses on APs. Norepinephrine and isoproterenol associated with β-adrenergic stimulation produced a dose dependent increase in beating rate and shortening of APD. E4031, a hERG channel blocker, elicited a dose dependent prolongation of the APD and produced arrhythmic early afterdepolarizations (EADs) thus modulating AP waveforms via external factors. Our cardiac μGMEA model has the capability to distinguish subtle differences in AP morphology for identifying novel cardio-factors and for drug screening.
Chromosome segregation errors generate a diverse spectrum of simple and complex genomic rearrangements
Authors: Peter Ly, Simon F. Brunner, Ofer Shoshani, Dong Hyun Kim, Weijie Lan, Tatyana Pyntikova, Adrienne M. Flanagan, Sam Behjati, David C. Page, Peter J. Campbell, Don W. Cleveland
Journal: Nature Genetics (2019)
A DIAGNOSIS OF SCHIZOPHRENIA IS ASSOCIATED WITH LOWER UTILIZATION OF STENTS AND CORONARY ARTERY BYPASS GRAFTS AMONG PATIENTS WITH ACUTE MYOCARDIAL INFARCTION: A NATIONWIDE ANALYSIS USING THE NATIONAL INPATIENT SAMPLE DATABASE OF 2014
Authors: Wojciech Rzechorzek, Mario Rodriguez, Ruchit Shah, Scott Kaplin, Swiri Konje, Jacqueline Tamis-Holland
Journal: Journal of the American College of Cardiology (2019)
International Initiative for Outcomes for vitiligo trials (INFO)
Authors: V. Eleftheriadou, I. Hamzavi, A.G. Pandya, P. Grimes, J.E. Harris, R.H. Huggins, H.W. Lim, N. Elbuluk, B. Bhatia, A. Tovar‐Garza, A.F. Nahhas, T. Braunberger, K. Ezzedine
Journal: British Journal of Dermatology (2019)

In order to develop and test a treatment, researchers measure an ‘outcome’. For example the ‘outcome’ might include a measure of how fast a white patch gets its color back (repigmentation) in vitiligo. Vitiligo is a skin condition, which causes white patches of the skin and sometimes hair. Currently, there is no cure nor firm clinical recommendations for the treatment of vitiligo. One of the main reasons behind this is that different studies measure different outcomes; therefore the studies can't be combined and compared. Recently, the International INitiative for Outcomes for vitiligo (INFO for vitiligo), which includes patients, their caregivers, medical journal editors and doctors from over 24 countries worldwide, have come to an agreement over a set of outcomes for vitiligo, which should be measured in every trial: repigmentation of skin lesions, side effects/harms of treatment and how long the colour stays after repigmentation of vitiligo lesions has occurred. Still, there was no agreement amongst patients and clinicians on which scale (outcome measure) should be used to measure repigmentation. This means that even if all the future trials measure repigmentation, but use different scales to do so, study results still can't be combined and compared. This international study was conducted with an aim to define successful repigmentation from patients’ point of view and propose how and when repigmentation should be evaluated in clinical trials in vitiligo. The authors conducted 3 workshops with vitiligo patients and their parents/care givers in the U.S.A. 73 participants were recruited. “Successful repigmentation” from patients’ perspective means achieving over 80% of repigmentation in a vitiligo patch. Both percentage of repigmentation quartiles (0‐25%, 26‐50%, 51‐79%, 80‐100%) and cosmetic acceptability of the results from patients’ point of view, should be measured in every trial. In conclusion, this was the largest patients’ outcomes workshop. Unity among the researchers on using the same scales to measure repigmentation in future trials will bring richer data and therefore clearer clinical recommendations.
PERI-VALVE THROMBUS AFTER VALVE IN VALVE TRANSCATHETER AORTIC VALVE REPLACEMENT FOR BIOPROSTHETIC AORTIC VALVE STENOSIS
Authors: Apurva Patel, Razvan Dadu, Mohammed Chamsi-Pasha, John Mahmarian, Alpesh Shah, Ross Reul, Michael Reardon, Neal Kleiman, Colin Barker
Journal: Journal of the American College of Cardiology (2019)
Abstract 240: Predictive and Experimental Modeling of Bag3-associated Cardiomyocyte Dysfunction
Authors: Christopher McDermott-Roe, Wenjian Lv, Amarda Shehu, Ivor Benjamin, Aron Geurts, Kiran Musunuru
Journal: Circulation Research (2018)

High throughput sequencing continues to uncover novel potentially pathogenic variants in cases of familial cardiomyopathy. Clinical interpretation of such variants is challenging, and hence definitive assignment of causality frequently remains unestablished. A case in point is provided by BAG3, a critical regulator of protein quality control in cardiomyocytes, which has been recurrently linked to dilated cardiomyopathy (DCM). Using theoretical and experimental approaches, we assessed the impact of a functionally-uncharacterized DCM-associated variant in BAG3 (c.1430G&gt;A; p.Arg477His). Molecular dynamics simulations of wildtype and mutant forms of BAG3 suggested the residue substitution perturbs a crucial interaction between BAG3 and HSC70 by altering electrostatic field distribution, conformational rigidity and side-chain orientation. Acute and stable expression of the mutant BAG3 protein led to reduced HSC70 engagement and protein aggregation in HEK293 and HL1 cells. Using the CRISPR-Cas9 system, we then introduced the variant into a healthy induced pluripotent stem cell line line and upon differentiation into cardiomyocytes, observed protein aggregation and a sensitivity to pro-apoptotic stressors. In conclusion, disease-in-a-dish modeling was used to study the molecular and cellular consequences of a potentially pathogenic BAG3 variant. We define what we believe is the primary molecular lesion and propose ectopic protein quality control and potentiated stress sensitivity as possible pathogenic drivers and potential therapeutic entry points.
IMPACT OF PERCUTANEOUS CORONARY INTERVENTION COMPLEXITY IN REAL-WORLD PRACTICE
Authors: Tomoya Timothy Hinohara, Gennaro Giustino, Usman Baber, Anton Camaj, Melissa Aquino, Bimmer Claessen, Serdar Farhan, Srushti Shah, Nitin Barman, Pooja Vijay, Jason Kovacic, Joseph Sweeny, George Dangas, Annapoorna Kini, Roxana Mehran, Samin Sharma
Journal: Journal of the American College of Cardiology (2019)
SEPTAL MYECTOMY IN PATIENTS WITH PREVIOUS CORONARY REVASCULARIZATION: OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY MASQUERADING AS ISCHEMIC HEART DISEASE
Authors: Jessey Mathew, Anita Nguyen, Rick Nishimura, Jeffrey Geske, Joseph Dearani, Steve Ommen, Brian Lahr, Hartzell Schaff
Journal: Journal of the American College of Cardiology (2019)
Abstract 407: Defective Branched Chain Amino Acid Catabolism Impairs Exercise Endurance
Authors: Lauren E Abell
Journal: Circulation Research (2018)

The branched chain amino acids (BCAA), leucine, isoleucine and valine, are essential for mammals, and they play a positive role in exercise capacity, muscle development, and a lean body phenotype. BCAA supplementation is commonly paired with exercise in order to promote muscle growth, increase resistance to fatigue and reduce muscle soreness. Conversely, elevated serum BCAA is strongly and positively correlated with the development of insulin resistance, coronary heart disease, and type II diabetes, and is predictive of patient response to therapeutics and intervention outcomes. We have previously shown that defective BCAA catabolism in mice impaired glucose metabolism in the heart and increased susceptibility to stress-induced cardiac damage. In this study we sought to determine the effects of elevated BCAA levels on skeletal muscle performance and response to exercise training using mouse models with systemically elevated BCAA levels. Here we assess the hypothesis that defective BCAA catabolism negatively impacts exercise capacity and endurance through deregulation of substrate utilization in the skeletal muscle using a mouse model with systemically elevated BCAA levels. Impairment of BCAA catabolism due to the deletion of mitochondrial-localized protein phosphatase 2C (PP2Cm), a key enzyme in activating BCAA catabolism, leads to elevated BCAA levels in mice. To study this, PP2Cm-knock out (KO) mice and their littermate controls were subjected to high-intensity and low-intensity exercise capacity tests via forced treadmill running. PP2Cm-KO mouse has a 20% reduction in exercise capacity. Reduced exercise capacity positively correlated with elevated serum BCAA levels. Additionally, KO animals supplemented with BCAAs demonstrated elevated serum succinate, alanine and glutamate levels, which are metabolic markers of physiological stress. We conclude that the inability to catabolize BCAAs has a negative effect on exercise capacity and endurance.
RELATIONSHIP BETWEEN THE PRESENCE OF LIPID DETECTED BY NEAR-INFRARED SPECTROSCOPY AND STENOSIS SEVERITY IN TERMS OF ANATOMY AND FUNCTION
Authors: Masahiro Hada, Masahiro Hoshino, Tomoki Horie, Haruhito Yuki, Hidenori Hirano, Yoshinori Kanno, Hiroaki Ohya, Yohei Sumino, Masao Yamaguchi, Yoshihisa Kanaji, Akinori Sugano, Taishi Yonetsu, Tsunekazu Kakuta
Journal: Journal of the American College of Cardiology (2019)
18F-FLOURIDE UPTAKE IN PENILE ARTERIES: DOES IT REPRESENT ATHEROSCLEROTIC BASIS OF ERECTILE DYSFUNCTION IN PATIENTS WITH PROSTATE CANCER
Authors: Takehiro Nakahara, Jagat Narula, Jan Tijssen, Sunil Agarwal, Mohammed Chowdhury, Patrick A. Coughlin, Marc Dweck, James Rudd, Masahiro Jinzaki, John Mulhall, Harry Strauss
Journal: Journal of the American College of Cardiology (2019)
Clarifications Needed on Study of Association Between Physician Burnout and Patient Safety
Authors: Nicholas A. Jansen
Journal: JAMA Internal Medicine (2019)

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An aluminum adjuvant-integrated nano-MOF as antigen delivery system to induce strong humoral and cellular immune responses
Authors: Xiaofang Zhong, Yunting Zhang, Lu Tan, Tao Zheng, Yingying Hou, Xiaoyu Hong, Guangsheng Du, Xiaoyan Chen, Yuandong Zhang, Xun Sun
Journal: Journal of Controlled Release (2019)
LONG-TERM CLINICAL OUTCOME OF INTENSIVE VERSUS USUAL BLOOD PRESSURE CONTROL IN PATIENTS WITH CORONARY ARTERY DISEASE RECEIVED DRUG-ELUTING STENT
Authors: Jung-Hee Lee, Jung-Lee Kim, Chan Sunwoo, Jung-Bin Park, Jong-Ho Nam, Chan-Hee Lee, Jang-Won Son, Ung Kim, Jong-Seon Park, Dong-Gu Shin
Journal: Journal of the American College of Cardiology (2019)
Abstract 318: MicroRNA Regulation of G Protein-Coupled Receptor Kinase 2 After Cardiac Injury
Authors: Melissa Lieu, Kurt Chuprun, Erhe Gao, Walter J Koch
Journal: Circulation Research (2018)

The increase in myocardial expression and activity of G Protein-Coupled Receptor (GPCR) Kinase 2 (GRK2) during the development and progression of heart failure (HF) has been documented to be pathological. Upregulation of GRK2 that is involved with deactivating agonist-activated β-adrenergic receptors (βARs) results in weakened contractile responsiveness through decreases in βAR density, coupling, and sensitivity. Non-GPCR activity of GRK2 has also been shown to be involved in cardiac dysfunction. Studies with knockout or blockade of GRK2 are able to significantly reduce and/or prevent HF phenotypes. Conversely, models with over-expressed GRK2 produce increased injury and accelerated HF development. Being such an important kinase in cardiac disease, regulation of GRK2 expression and activity is critical. Of interest, there is not much known about how GRK2 is regulated (mRNA or protein) in the heart and mechanisms for its up-regulation after cardiac injury are not well understood. There is evidence of GRK2 being regulated by microRNAs (miRNAs) in endothelial and blood cells. We believe cardiac GRK2 may also be regulated in a similar miRNA-mediated fashion. MiRNA profiles become dysregulated with the onset of stress/injury and contribute to orchestrating many classical HF phenotypes, including βAR aberrations. We hypothesize that the expression of a GRK2-regulating miRNA is altered in HF, which contributes to changes in GRK2 regulation resulting in its pathological increase. MiRNA microarray analysis was done on 2-week post-myocardial infarction (MI) murine hearts to examine miRNA profiles compared to sham-operated. Cardiac miRNA species were examined for their expression levels, seed sequence, and TargetScan prediction and alignment to mouse and human GRK2 3’UTR. Candidate miRNAs underwent 3’UTR analysis against GRK2 3’UTR and transfection into AC16 cardiac cells. Two miRNAs were identified to significantly reduce GRK2 protein and/or RNA levels as well directly bind to the 3’UTR of GRK2. Further studies will be done to elucidate the mechanism these miRNAs are able to regulate GRK2 levels. Results from these studies can be applied towards GRK2 inhibition via miRNA-based therapeutics.
APPLICATION OF THE H2FPEF-SCORE TO A GLOBAL CLINICAL TRIAL OF PATIENTS WITH HEART FAILURE WITH PRESERVED EJECTION FRACTION: THE TOPCAT TRIAL
Authors: Peder Myhre, Muthiah Vaduganathan, Brian Claggett, Carolyn Lam, Akshay Desai, Inderjit Anand, Nancy K. Sweitzer, James Fang, Eileen O'Meara, Sanjiv Shah, Amil Shah, Eldrin Lewis, Jean Rouleau, Bertram Pitt, Scott Solomon
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF INITIAL EVOLUT TAVR DEPLOYMENT ORIENTATION ON FINAL VALVE ORIENTATION AND CORONARY REACCESS: A PILOT STUDY
Authors: Gilbert Hin-Lung Tang, Syed Zaid, Nish Patel, Eisha Gupta, Hasan Ahmad, Asaad Khan, Jason Kovacic, Cenap Undemir, Joshua B. Goldberg, Muhammad Khan, Steven Lansman, George Dangas, Samin Sharma, Annapoorna Kini
Journal: Journal of the American College of Cardiology (2019)
SURVIVAL FOLLOWING IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR IMPLANTATION IN PATIENTS WITH CARDIAC SARCOIDOSIS
Authors: Angela Higgins, Amarnath Annapureddy, Yongfei Wang, Karl Minges, Rachel Lampert, Lynda Rosenfeld, Daniel Jacoby, Jeptha Curtis, Edward Miller, James Freeman
Journal: Journal of the American College of Cardiology (2019)
Use of Low-Dose Aspirin and Mortality After Prostate Cancer Diagnosis
Authors: Charlotte Skriver, Christian Dehlendorff, Michael Borre, Klaus Brasso, Signe Benzon Larsen, Susanne Oksbjerg Dalton, Mette Nørgaard, Anton Pottegård, Jesper Hallas, Henrik Toft Sørensen, Søren Friis
Journal: Annals of Internal Medicine (2019)

Recent studies suggest that aspirin use may improve survival in patients with prostate cancer.To assess the association between postdiagnosis use of low-dose aspirin and prostate cancer mortality.Nationwide cohort study.Denmark.Men with incident prostate adenocarcinoma between 2000 and 2011.Nationwide registry data on tumor characteristics, drug use, primary prostate cancer therapy, comorbidity, and socioeconomic parameters. Postdiagnosis use of low-dose aspirin (75 to 150 mg) was defined as 2 or more prescriptions filled within 1 year after prostate cancer diagnosis. Follow-up started 1 year after prostate cancer diagnosis. In secondary analyses, low-dose aspirin use was assessed within exposure periods of 5 or 7.5 years after prostate cancer diagnosis.Of 29 136 patients (median age, 70 years), 7633 died of prostate cancer and 5575 died of other causes during a median follow-up of 4.9 years (interquartile range, 3.1 to 7.2 years), through 2015. Postdiagnosis low-dose aspirin use was associated with adjusted hazard ratios (HRs) of 0.95 (95% CI, 0.89 to 1.01) for prostate cancer-specific mortality and 1.12 (CI, 1.05 to 1.20) for other-cause mortality. The secondary analyses showed that prostate cancer mortality was slightly reduced with low-dose aspirin use after the 5-year (HR, 0.91 [CI, 0.83 to 1.01]) and 7.5-year (HR, 0.84 [CI, 0.72 to 0.97]) postdiagnosis exposure periods, notably among patients filling prescriptions for a large quantity of low-dose aspirin tablets during the 7.5-year period.Data on over-the-counter aspirin use were unavailable. Some residual confounding was possible as a result of incomplete data on some prognostic factors.The study did not support an overall effect of postdiagnosis low-dose aspirin use on prostate cancer mortality. However, results for extended exposure periods suggest that low-dose aspirin use might be inversely associated with prostate cancer mortality after 5 years from cancer diagnosis.Danish Cancer Society.
Osteogenesis depends on commissioning of a network of stem cell transcription factors that act as repressors of adipogenesis
Authors: Alexander Rauch, Anders K. Haakonsson, Jesper G. S. Madsen, Mette Larsen, Isabel Forss, Martin R. Madsen, Elvira L. Van Hauwaert, Christian Wiwie, Naja Z. Jespersen, Michaela Tencerova, Ronni Nielsen, Bjørk D. Larsen, Richard Röttger, Jan Baumbach, Camilla Scheele, Moustapha Kassem, Susanne Mandrup
Journal: Nature Genetics (2019)