tbuckley/cabot-search huggingface dataset:
NATIONAL AGE RELATED OUTCOMES IN PATIENTS WITH ST ELEVATION MYOCARDIAL INFARCTION AND CARDIOGENIC SHOCK THAT UNDERWENT PERCUTANEOUS LEFT VENTRICULAR ASSIST DEVICE PLACEMENT
Authors: Sumeet Lall, Ryan Wilson, Tariq Ali Ahmad, Brent Dembo, James Kogut, Jovan Plamenac, Chad Zack
Journal: Journal of the American College of Cardiology (2019)
Extracting Prognostic Molecular Information from PET-CT Imaging of Multiple Myeloma Using Radiomic Approaches
Authors: Christopher Wardell, Terri Lynn Alpe, Phil Farmer, Michael W Rutherford, Yan Wang, Niels Weinhold, Ruslana G. Tytarenko, Purvi Patel, Michael A Bauer, Cody Ashby, Eileen M Boyle, Carolina D. Schinke, Sharmilan Thanendrarajan, Frits van Rhee, Maurizio Zangari, Brian A Walker, Gareth Morgan, Faith E. Davies
Journal: Blood (2018)
OUTCOMES FOR NON-TRAUMATIC INTRACEREBRAL HEMORRHAGE IN PATIENTS WITH ATRIAL FIBRILLATION ON ANTICOAGULATION AND POSSIBLE/PROBABLE CEREBRAL AMYLOID ANGIOPATHY
Authors: Shiva Ponamgi, Robert Ward, Stephen English, Christopher DeSimone, Jonathan Graff-Radford, Alejandro Rabinstein, Samuel Asirvatham, David Holmes
Journal: Journal of the American College of Cardiology (2019)
ABLATION OUTCOME IN OCTOGENARIAN WOMEN UNDERGOING CATHETER ABLATION FOR RECURRENT PAROXYSMAL ATRIAL FIBRILLATION
Authors: Sanghamitra Mohanty, Chintan Trivedi, Domenico Della Rocca, Qiong Chen, Omer Gedikli, Alfredo C. Tapia, Sharan Sharma, John Burkhardt, Javier Sanchez, Gerald Gallinghouse, Amin Al-Ahmad, Rodney Horton, Dhanunjaya Lakkireddy, Luigi di Biase, Andrea Natale
Journal: Journal of the American College of Cardiology (2019)
First-Year Report Cards From the Merit-Based Incentive Payment System (MIPS)
Authors: Vinay K. Rathi, J. Michael McWilliams
Journal: JAMA (2019)

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REVASCULARIZATION OF COMPLEX CORONARY ARTERY DISEASE BY THE PRESENCE OF HEART TEAMS IN THE UNITED STATES: RESULTS FROM THE TRANSLATING OUTSTANDING PERFORMANCE IN PERCUTANEOUS CORONARY INTERVENTION (TOP PCI) STUDY
Authors: Mohammed S. Al-Damluji, Karl Minges, Paul Fiorilli, Craig Parzynski, Jeptha Curtis
Journal: Journal of the American College of Cardiology (2019)
Abstract 262: GRK5 is a Novel Regulator of Fibroblast Activation
Authors: Akito Eguchi, Walter J Koch
Journal: Circulation Research (2018)

Pathological remodeling of the heart is a hallmark of heart failure (HF) and these structural changes of the heart further perpetuates the disease. Cardiac fibroblasts are the critical cell type that is responsible for maintaining the structural integrity of the heart. Stress conditions, such as a myocardial infarction, can activate and induce the transdifferentiation of quiescent fibroblasts into synthetic and contractile myofibroblasts. G protein-coupled receptor (GPCR) kinases (GRKs) are important mediators of cardiovascular homeostasis through dampening of GPCR signaling. Recently, non-canonical activities of these GRKs have been elucidated. GRK5 is one isoform of these kinases that is expressed in the heart and has been shown to be up-regulated in human HF. Of note, GRK5 has been demonstrated to translocate to the nucleus in cardiomyocytes, promoting hypertrophic gene transcription through activation of nuclear factor of activated T-cells (NFAT) and nuclear factor κB (NFκB). Interestingly, these transcription factors are also involved in fibroblast activation and transdifferentiation. GRK5 is highly expressed and active in cardiac fibroblasts, however its physiological and pathological role in these crucial cardiac cells is unknown. Utilizing adult mouse cardiac fibroblasts in vitro , our preliminary data suggests a relevant role for GRK5 in the activation and function of fibroblasts. We observed that genetic deletion of GRK5 in cardiac fibroblasts attenuated α smooth muscle actin (α-SMA) expression, a classical myofibroblast marker, after stimulation with Transforming Growth Factor β (TGFβ) and Angiotensin II (AngII). In addition, deletion of GRK5 diminished the expression of myofibroblast specific genes and proteins such as Collagen I and II after AngII stimulation and were refractory to TGFβ and AngII mediated collagen gel contraction. Conversely, GRK5 overexpression led to an increase in differentiation markers such as α-SMA. These data support the hypothesis that GRK5 is an essential regulator of fibroblast activation. GRK5 fibroblast knockout mice are currently being examined to determine if GRK5 regulates fibroblast transdifferentiation in vivo .
SAFETY AND EFFICACY OF TRANSRADIAL VERSUS TRANSFEMORAL ACCESS FOR PERCUTANEOUS CORONARY INTERVENTION OF UNPROTECTED LEFT MAIN DISEASE: A META- ANALYSIS
Authors: Aravdeep Jhand, Muhammad Ahsan, Abhishek Thandra, Dinesh Reddy Apala, Toufik Mahfood Haddad, Venkata Alla
Journal: Journal of the American College of Cardiology (2019)
INTERINDIVIDUAL VARIABILITY IN WEIGHT LOSS WITH LORCASERIN: AN ANALYSIS FROM THE CAMELLIA-TIMI 61 STUDY
Authors: Arman Qamar, Benjamin M. Scirica, Stephen Wiviott, Christina Fanola, KyungAh Im, Silvio Inzucchi, Darren McGuire, Anthony Keech, Steven Smith, Sabina Murphy, Carlos Perdomo, Wenfeng Miao, Tushar Patel, Marc Sabatine, Erin Bohula
Journal: Journal of the American College of Cardiology (2019)
Characteristics and prevalence of plaque psoriasis in patients with palmoplantar pustulosis
Authors: Y.M.F. Andersen, M. Augustin, J. Petersen, K. Hagenström, L. Mallbris, R. Burge, A. Egeberg
Journal: British Journal of Dermatology (2019)

Palmoplantar pustulosis (PPP) is a chronic pustular skin condition on the palms and soles. The disease is often seen in combination with plaque psoriasis, and whether PPP is a variant of psoriasis has been debated. The disease prevalence of PPP and co‐occurring psoriasis is not yet established and the patient group remains understudied. To estimate the prevalence of PPP and co‐occurring psoriasis in three population‐based cohorts and to provide information on patient demographics and characteristics. Administrative healthcare registries and insurance databases from the U.S.A., Denmark and Germany were used as data sources. Patients with PPP were defined by a single International Classification of Diseases 10th Revision code for PPP during a 1‐year period. Information regarding co‐occurring plaque psoriasis and other comorbidities was extracted. Furthermore, use of antipsoriatic medication was identified. In total 1435, 751 and 1832 patients with PPP were identified in the U.S., Danish and German populations, with estimated 1‐year prevalences of 0·009%, 0·005% and 0·08%, respectively. Plaque psoriasis was present in 14·2–61·3% of patients with PPP. Patients with co‐occurring psoriasis had an overall higher prevalence of psoriatic arthritis. Similarly, medication use was more prevalent in patients with PPP with co‐occurring psoriasis, and especially pronounced was the use of biologic therapies. This large observational study on patients with PPP provides detailed information regarding patient demographics, comorbidities and medication use. The 1‐year prevalence of PPP varied in the three studied populations, possibly due to differences in diagnostics and recording practices. Psoriasis frequently co‐occurred in patients with PPP. What's already known about this topic? Palmoplantar pustulosis (PPP) is a skin disease of the palms of the hands and soles of the feet and is known to be related to psoriasis. Whether PPP is a distinct disease or a variant of psoriasis is not yet established. The condition is understudied in terms of disease prevalence, disease predictors, patient characteristics and comorbidity. What does this study add? In this study using data from three large population‐based cohorts we found low prevalence rates (< 0·1%) of PPP. The prevalence of psoriasis was estimated at between 14·2% and 61·3% in patients with psoriasis. Patients with PPP with co‐occurring psoriasis have a higher prevalence of psoriatic arthritis and use of antipsoriatic drugs.
Biodegradable Polymers as a Noncoding miRNA Nanocarrier for Multiple Targeting Therapy of Human Hepatocellular Carcinoma
Authors: Chengbin Yang, Mingjie Yin, Gaixia Xu, Wei‐Jen Lin, Jiajie Chen, Yinling Zhang, Tao Feng, Peng Huang, Chih‐Kuang Chen, Ken‐Tye Yong
Journal: Advanced Healthcare Materials (2019)

Abstract Therapeutic strategy based on the restoration of tumor suppressor‐microRNAs (miRNAs) is a promising approach for cancer therapy, but the low delivery efficiency of miRNA remains a huge hurdle due to the lack of safe and efficient nonviral carriers. In this work, with the use of newly developed PEGylated biodegradable charged polyester‐based vectors (PEG‐BCPVs) as the carrier, the miR26a and miR122 codelivering therapeutic strategy (PEG‐BCPVs/miR26a/miR122 as the delivery formulation) is successfully developed for efficient treatment of human hepatocellular carcinoma (HCC). In vitro study results show that PEG‐BCPVs are capable of effectively facilitating miRNA cellular uptake via a cell endocytosis pathway. Consequently, the restoration of miR26a and miR122 remarkably inhibit the cell growth, migration, invasion, colony formation, and induced apoptosis of HepG2 cells. More importantly, the chemosensitivity of HepG2 to anticancer drug is also considerably enhanced. After treatment with the PEG‐BCPV‐based miRNA delivery system, the expression of the multiple targeted genes corresponding to miR26a and miR122 in HepG2 cells is greatly downregulated. Accordingly, the newly developed miRNA restoration therapeutic strategy via biodegradable PEG‐BCPVs as the carrier should be a promising modality for combating HCC.
Abstract 571: <i>MYBPC3</i> Mutations Cause Hypertrophic Cardiomyopathy by Dysregulating Myosin: Implications for Therapy
Authors: Christopher N Toepfer, Hiroko Wakimoto, Amanda C Garfinkel, Barbara McDonough, Dan Liao, Jianming Jiang, Angela Tai, Josh Gorham, Ida G Lund, Ida G Lund, Mingyue Lun, Thomas L Lynch, Sakthivel Sadayappan, Charles S Redwood, Hugh Watkins, Jonathan Seidman, Christine Seidman
Journal: Circulation Research (2018)

The mechanisms by which truncating mutations in MYBPC3 (encoding cardiac myosin binding protein-C; cMyBPC) or myosin missense mutations cause hyper-contractility and poor relaxation in hypertrophic cardiomyopathy (HCM) are incompletely understood. Using genetic and biochemical approaches we explored how depletion of cMyBPC altered sarcomere function. We demonstrate that stepwise loss of cMyBPC resulted in reciprocal augmentation of myosin contractility. Direct attenuation of myosin function, via a damaging missense variant (F764L) that causes dilated cardiomyopathy (DCM) normalized the increased contractility from cMyBPC depletion. Depletion of cMyBPC also altered dynamic myosin conformations during relaxation - enhancing the myosin state that enables ATP hydrolysis and thin filament interactions while reducing the super relaxed conformation associated with energy conservation. MYK-461, a pharmacologic inhibitor of myosin ATPase, rescued relaxation deficits and restored normal contractility in mouse and human cardiomyocytes with MYBPC3 mutations. These data define dosage-dependent effects of cMyBPC on myosin that occur across all phases of the cardiac cycle as the pathophysiologic mechanisms by which MYBPC3 truncations cause HCM. Therapeutic strategies to attenuate cMyBPC activity may rescue depressed cardiac contractility in DCM patients, while inhibiting myosin by MYK-461 should benefit the substantial proportion of HCM patients with MYBPC3 mutations.
Abstract 387: Lymphatic Endothelial Cells Derived Exosomes Promote Neolymphangiogenesis After Injury
Authors: Maria Cimini, Giulia Borghetti, Steven Houser, Raj Kishore
Journal: Circulation Research (2018)

Neolymphangiogenesis after myocardial infarction (MI) has been extensively documented; however the source of new lymphatic vessels (LVs) is still unknown. It has been described that new LVs may derive from resident lymphatic endothelial cells (LECs) or from trans-differentiation of endothelial cells (ECs) and pericytes from veins into LECs. Which signals activate both the spreading and the trans-differentiation needs to be investigated. LECs are known to release transcytotic vesicles and exosomes, thus, we hypnotized that the enriched protein and RNA cargo of LECs derived exosomes may promote the new LVs formation after injury. Exosomes derived from LECs were isolated from LECs cultured conditioned medium and HUVECs were treated with different concentration of exosomes cargo for 10 days. After treatment, q-PCR for the major endothelial and lymphatic endothelial markers was performed on treated HUVECs. In a dose dependent manner we observed a decreased expression of KDR and CD31, endothelial markers that are not expressed by LECs and an increased expression of Prox-1 and VEGFR3. Prox-1 is the major lymphatic endothelial transcription factor that is not activated in ECs and is responsible for the transcription of LYVE-1 and podoplanin. VEGFR3 is the only known vascular endothelial growth factor receptor expressed on LECs which is not displayed by ECs. Next, we evaluated the effect of LECs derived exosomes on in vitro lymphangiogenesis assay by measuring the ability of LECs to organize into capillary-like structures on matrigel. LECs treated with LECs derived exosomes are able to form tubes and branches as early as within 1 hour compared to untreated cells. Our preliminary results show cargo of exosomes from LECs activates the signal transduction and metabolism of LECs and HUVECs promoting the new LVs formation through spreading and trans-differentiation of the targeted cells.
TIMING OF ELECTRONIC HEALTH RECORD INTEGRATED DECISION AID (IDEA) FOR STROKE PREVENTION IN ATRIAL FIBRILLATION MATTERS
Authors: Stacey L. Schott, Keren Xu, Julia Berkowitz, Curtis Petersen, Catherine Saunders, Navjot Sobti, Megan Coylewright
Journal: Journal of the American College of Cardiology (2019)
SAFETY OF INOTERSEN TREATMENT IN PATIENTS WITH TRANSTHYRETIN AMYLOID CARDIOMYOPATHY
Authors: Noel R. Dasgupta, Rodney H. Falk, Brian M. Drachman, Mathew S. Maurer, Carol J. Whelan, Thomas Brannagan, Teresa Coelho, Marcia Waddington Cruz, Thibaud Damy, Mazen Hanna, John L. Berk, Giampaolo Merlini, Isabel Conceição, Steven G. Hughes, Jesse Kwoh, Shiangtung W. Jung, Spencer Guthrie, Michael Pollock, Morie Gertz, Merrill D. Benson, Stephen Heitner
Journal: Journal of the American College of Cardiology (2019)
BLOOD-BIOMARKER-BASED ACOUSTICAL FEATURE SELECTION IMPROVES OVERALL CLASSIFICATION ACCURACY FOR PUMP THROMBOSIS IN LEFT VENTRICULAR ASSIST DEVICES
Authors: Beren Semiz, Sinan Hersek, Cynthia Partida, Leticia B. Arroyo, Van Selby, Georg Wieselthaler, Omer Inan, Liviu Klein
Journal: Journal of the American College of Cardiology (2019)
Structure and function of the immune system in the spleen
Authors: Steven M. Lewis, Adam Williams, Stephanie C. Eisenbarth
Journal: Science Immunology (2019)

The spleen is the largest secondary lymphoid organ in the body and, as such, hosts a wide range of immunologic functions alongside its roles in hematopoiesis and red blood cell clearance. The physical organization of the spleen allows it to filter blood of pathogens and abnormal cells and facilitate low-probability interactions between antigen-presenting cells (APCs) and cognate lymphocytes. APCs specific to the spleen regulate the T and B cell response to these antigenic targets in the blood. This review will focus on cell types, cell organization, and immunologic functions specific to the spleen and how these affect initiation of adaptive immunity to systemic blood-borne antigens. Potential differences in structure and function between mouse and human spleen will also be discussed.
Risk of bullous pemphigoid in patients with cancer
Authors: C.T. Chen, H.Y. Hu, Y.T. Chang, C.P. Li, C.Y. Wu
Journal: British Journal of Dermatology (2019)

Bullous pemphigoid (BP) is a skin condition that causes rashes and itchy blistering in the skin. It is caused by the individual developing antibodies against their own skin – known as autoimmunity. Disease flare‐ups cause extreme discomfort, requiring effort from dermatologists and the family to care for the patients. People diagnosed with BP tend to be suffering already from other medical conditions such as diabetes, neurological diseases including Parkinson's and Alzheimer's and cardiovascular disease, and these are known risk factors for BP. However, the relationship between cancer and BP remains controversial. This study, from Taiwan, aimed to find out if there is an increased risk for subsequent BP among cancer patients. It also aimed to find out which type of cancer might have the strongest relationship. The authors used the Taiwan National Health Insurance Database, which includes one million randomly sampled beneficiaries, to perform this study. A total of 36,838 cancer patients and 147,352 people without cancer were chosen (the latter as a control group). To calculate incidence, broadly meaning rates of new cases of a disease, scientists calculate the incidence in ‘person years’ which takes into account both the number of people in the study and the amount of time each person spends in the study, and then how many of these develop the disease during the study time. Using this method, between 2002 and 2011, 22 people developed BP among the cancer patients (17.2 per 100,000 person‐years) and 171 among the control group (19.8 per 100,000 person‐years). The incidence of BP in the cancer patients was not higher than in the controls. Age, diabetes mellitus, and cerebrovascular disease were observed to be risk factors for BP. The study also observed that patients with brain and other nervous system cancers had a relatively higher incidence of subsequent BP (128.3 per 100,000 person‐years) than those with other types of cancer. The findings of this study provide solid evidence that cancer is not a risk factor for BP.
Drifting into unconsciousness: Jason Zirganos and the mystery of undetected hypothermia
Authors: Mike Tipton
Journal: British Journal of Sports Medicine (2019)

Swimming authorities must enforce minimum temperature rules in open water swimming because some open water swimmers—particularly those who are well acclimatised to cold—are unable to judge how cold they are. This potential problem was confirmed in the study of Saycell et al in this issue of British Journal of Sports Medicine .1 

Cold habituation from repeated exposure to cold water can produce a ‘hypothermic’ adaptation to cold in which the acclimated individuals lose their perceptual and physiological responses to cooling. They do not shiver as much and paradoxically feel more comfortable as their deep body temperature falls. This was clearly demonstrated in the classic studies of Channel swimmers published in 1955 …
Abstract 307: Focal Adhesion Kinase Activity and Nuclear Localization Controls Vascular Smooth Muscle Cell Proliferation and Intimal Hyperplasia Through a GATA4-Cyclin D1 Axis
Authors: Kyuho Jeong, Jung-Hyun Kim, James Murphy, Hyeonsoo Park, Erin Ahn, Steve Lim
Journal: Circulation Research (2018)

Neointimal formation is a hallmark of occlusive disorders such as atherosclerosis, post-angioplasty restenosis, vein graft, and allograft vasculopathy. Upon vessel injury, increased growth factor secretion augments focal adhesion kinase (FAK) activity to promote vascular smooth muscle cell (VSMC) proliferation. However, the molecular mechanism of how FAK contributes to intimal hyperplasia remains unknown. To test the role of FAK activity in VSMC proliferative diseases, we performed femoral arterial wire injury and orally administered a FAK inhibitor (VS-4718) twice daily. FAK inhibition significantly reduced intimal hyperplasia compared to vehicle-treated mice 4 weeks after injury. We found that platelet-derived growth factor (PDGF) activated FAK and increased GATA-binding protein 4 (GATA4) expression which is correlated with VSMC proliferation, whereas FAK inhibition abolished the PDGF-induced GATA4 upregulation. Further, chromatin immunoprecipitation (ChIP) revealed that GATA4 binds the mouse cyclin D1 promoter to enhance cyclin D1 transcription, leading to VSMC proliferation via G1 to S cell cycle progression. Importantly, GATA4 and cyclin D1 expression were increased upon vascular injury parallel with increased FAK activity in vehicle-treated mice, but not changed in FAK inhibitor-treated mice. Mechanistically, FAK inhibition reduces VSMC proliferation through increased nuclear FAK, which can bind and turnover GATA4. Genetic FAK kinase-dead (KD) mice (ERT2-Myh11-Cre) developed less intimal thickening following wire injury, implicating VSMC-specific FAK activity is critical for VSMC proliferation. FAK KD VSMCs also showed increased nuclear FAK, decreased GATA4 and cyclin D1 levels compared to FAK WT. This study has uncovered the importance of GATA4 and nuclear FAK in VSMC hyperplasia.
Abstract 18290: Heterozygous Deletion of KCNH2 Models Long QT Type 2 in Human Pluripotent Stem Cell-derived Cardiomyocytes
Authors: Vincenzo S Macri, Adam Hirst, Jessica Norberg, Melanie Kardel, Arthur Sampaio, Wing Chang, Terry Thomas, Allen Eaves, Stephen Szilvassy, Sharon Louis
Journal: Circulation (2017)

Introduction: Heterozygous variants are most frequently associated with cardiac arrhythmias, including long QT syndrome, in the general population and within families. Genome-editing of human induc...