tbuckley/cabot-search huggingface dataset:
Coexpression of CD163 and CD141 identifies human circulating IL-10-producing dendritic cells (DC-10)
Authors: Michela Comi, Daniele Avancini, Francesca Santoni de Sio, Matteo Villa, Molly Javier Uyeda, Matteo Floris, Daniela Tomasoni, Alessandro Bulfone, Maria Grazia Roncarolo, Silvia Gregori
Journal: Cellular and Molecular Immunology (2019)

Tolerogenic dendritic cells (DCs) are key players in maintaining immunological homeostasis, dampening immune responses, and promoting tolerance. DC-10, a tolerogenic population of human IL-10-producing DCs characterized by the expression of HLA-G and ILT4, play a pivotal role in promoting tolerance via T regulatory type 1 (Tr1) cells. Thus far, the absence of markers that uniquely identify DC-10 has limited in vivo studies. By in vitro gene expression profiling of differentiated human DCs, we identified CD141 and CD163 as surface markers for DC-10. The coexpression of CD141 and CD163 in combination with CD14 and CD16 enables the ex vivo isolation of DC-10 from the peripheral blood. CD14+CD16+CD141+CD163+ cells isolated from the peripheral blood of healthy subjects (ex vivo DC-10) produced spontaneously and upon activation of IL-10 and limited levels of IL-12. Moreover, in vitro stimulation of allogeneic naive CD4+ T cells with ex vivo DC-10 induced the differentiation of alloantigen-specific CD49b+LAG-3+ Tr1 cells. Finally, ex vivo DC-10 and in vitro generated DC-10 exhibited a similar transcriptional profile, which are characterized by an anti-inflammatory and pro-tolerogenic signature. These results provide new insights into the phenotype and molecular signature of DC-10 and highlight the tolerogenic properties of circulating DC-10. These findings open the opportunity to track DC-10 in vivo and to define their role in physiological and pathological settings.
NEGATIVE CHRONOTROPIC EFFECT AND ANGINA DUE TO THALIDOMIDE USE
Authors: Luis Olmos Dominguez, Milton Ernesto Guevara Valdivia, Jose Oscar Torres Jaimes, Karim Yarek Juarez Escobar, Yitzar Bañuelos Millan, Héctor Hugo Guevara Gasca, Jesus Bueno Campa, Pedro Gerardo Davila Flores
Journal: Journal of the American College of Cardiology (2019)
VESSEL PREPARATION IMPROVES DRUG ELUTING STENT (DES) EXPANSION PARAMETERS VERSUS DIRECT CORONARY STENTING IN NON-COMPLEX LESIONS AS ASSESSED BY HIGH-RESOLUTION OPTICAL COHERENCE TOMOGRAPHY (OCT)
Authors: Murtaza Ismail Bharmal, Alexandru Marginean, James Lloyd, Hitoshi Matsukage, Farah Hashim, Kent Brummel, Anthony Kanelidis, John Blair, Jonathan Paul, Atman Shah, Sandeep Nathan
Journal: Journal of the American College of Cardiology (2019)
A Prognostic Tool for the Identification of Patients with Early Stage Chronic Lymphocytic Leukemia at Risk of Progression
Authors: Adalgisa Condoluci, Lodovico Terzi di Bergamo, Lorenzo De Paoli, Julio Delgado, Massimo Gentile, Michael Doubek, Francesca Romana Mauro, Mattias Mattsson, Giovanna Cutrona, Jana Kotaskova, Clara Deambrogi, Bernhard Gerber, Valeria Spina, Alessio Bruscaggin, Emanuele Zucca, Franco Cavalli, Georg Stuessi, Antonino Neri, Manlio Ferrarini, Richard Rosenquist, Robin Foà, Sarka Pospisilova, Fortunato Morabito, Emili Montserrat, Gianluca Gaidano, William G. Wierda, Davide Rossi
Journal: Blood (2018)
DEFIBRILLATORS FOLLOWING RECENT ACUTE MYOCARDIAL INFARCTION: A META-ANALYSIS OF RANDOMIZED CLINICAL TRIALS
Authors: Yazan Zayed, Babikir Kheiri, Mahmoud Barbarawi, Laith Rashdan, Ghassan Bachuwa, Mustafa Hassan Mahmoud, Deepak L. Bhatt
Journal: Journal of the American College of Cardiology (2019)
ADHERENCE TO GUIDELINE-DIRECTED MEDICAL THERAPY OF ATRIAL FIBRILLATION: CAN WE IMPROVE QUALITY OF CARE IN PATIENTS ADMITTED WITH ATRIAL FIBRILLATION?
Authors: Sneha Arjun, Maya Ignaszewski, Rylie Pietrowicz, Krystal Hunter, Andrea M. Russo
Journal: Journal of the American College of Cardiology (2019)
TREND IN DEATH RATE OVERTIME FOLLOWING PERCUTANEOUS CORONARY INTERVENTION IN PATIENTS STRATIFIED BY PRESENTATION
Authors: Ron Waksman, Deepakraj Gajanana, Itsik Ben-Dor, Rebecca Torguson, Lowell Satler, Paul Kolm, Micaela Iantorno, Toby Rogers, Yuefeng Chen, Jaffar Khan, Evan Shlofmitz, Anees Musallam, Nauman Khalid, William Weintraub
Journal: Journal of the American College of Cardiology (2019)
Optical coherence tomography for diagnosis of BCC
Authors: N. Reddy, B.T. Nguyen
Journal: British Journal of Dermatology (2019)

Basal cell carcinoma (BCC) is the most common form of skin cancer in the world. Its incidence in Europe has increased at an alarming rate of 5.5% per year over the past four decades. In the U.K., the incidence of BCC has risen at a rate six times higher than in the rest of Europe. The diagnosis of BCC typically requires a biopsy of the skin and careful analysis under a microscope. Optical coherence tomography (OCT) is an imaging tool that uses light to visualize the layers underneath the skin surface in real‐time without the need to perform a skin biopsy. It has been proposed as a non‐invasive, alternative tool to diagnose BCC. This study, from the U.S., investigated current medical literature to comprehensively assess the accuracy of OCT technology in evaluating BCCs. The authors reviewed 901 BCCs collected from 31 studies that utilized OCT for diagnosing BCC. The authors found that OCT was able to diagnose BCC with a sensitivity of 89.3%, meaning that it correctly identified 9 out of 10 BCCs. Of the different types of OCT, the most advanced, Fourier‐Domain OCT, obtained the highest accuracy. OCT was able to detect features of BCC that are normally seen under the microscope in up to 80% of tumours. In addition, the authors noted that OCT was best at predicting the depth of shallow BCC tumors less than 1mm deep. Based on these results, the authors envision OCT to be a valuable, non‐invasive tool for diagnosing BCC.
A SAFE AND STANDARDIZED PROTOCOL TO PREDICT SUCCESSFUL EXPLANTATION OF LEFT VENTRICULAR ASSIST DEVICES
Authors: Jan Knierim, Felix Schoenrath, Sajjad Soltani, Philipp Stawowy, Stephan Dreysse, Julia Stein, Marcus Müller, Johanna Mulzer, Michael Dandel, Christoph Knosalla, Volkmar Falk, Thomas Krabatsch, Evgenij Potapov
Journal: Journal of the American College of Cardiology (2019)
Treatment Free Remission (TFR) in Chronic Myeloid Leukaemia (CML): The Tawam Hospital Experience
Authors: Arif Alam, Imran Mirza, Khaled al Qawasmeh, Ali Rababa'H, Hani Osman, Sabir Hussain, Amar Lal, Jorgen Kristensen
Journal: Blood (2017)
OPTICAL COHERENCE TOMOGRAPHY GUIDANCE WAS NOT ASSOCIATED WITH SMALLER MINIMAL LUMEN DIAMETER AT FOLLOW-UP IN CHRONIC TOTAL OCCLUSION LESION
Authors: Kohki Ishida, Yoshiyasu Minami, Toshimitsu Sato, Yusuke Muramatsu, Ryota Kakizaki, Teruyoshi Nemoto, Takuya Hashimoto, Kazuhiro Fujiyoshi, Kentaro Meguro, Takao Shimohama, Taiki Tojo, Junya Ako
Journal: Journal of the American College of Cardiology (2019)
Abstract 242: Drug Repurpose Using Human Stem Cell Models of Cardiac Arrhythmias
Authors: Masayuki Yazawa, LouJin Song, Kumi Morikawa
Journal: Circulation Research (2018)

For translational approach toward drug development, we has investigated the molecular mechanisms underlying various inherited cardiac diseases and identified lead compounds to test the derivatives in iPSC and mouse models. In this study, we focus on a lethal disease, Timothy syndrome (TS), which is characterized as a developmental disorder containing multiple organ dysfunctions including autism and cardiac arrhythmia such as long QT syndrome (type 8, LQTS8) and ventricular tachycardia. TS is caused by de novo gain-of-function mutations in a voltage-gated calcium channel Ca V 1.2, which is essential for cardiac excitation-contraction coupling. Previous reports demonstrated that beta blockers and calcium channel blockers were not sufficient to prevent the lethal arrhythmias in TS patients. In fact, some TS infants died shortly after birth. Therefore, new drug development or FDA drug repurposing is really crucial for the patients. We generated and characterized human iPSC and mouse models of TS. Also, we have used familial LQTS8 and LQTS1 iPSC lines to generate more LQTS iPSC models. Interestingly, our chemical tests identified that an FDA-approved drug, fluvoxamine, rescued cardiac phenotypes in TS (de novo LQTS8), familial LQTS8 and LQTS1 iPSC models. Fluvoxamine has been clinically used for depression and anxiety disorder as a selective serotonin reuptake inhibitor (SSRI). Fluvoxamine is also known to activate Sigma 1 receptor (Sigma-1R). To explore the mechanisms underlying the beneficial effects of fluvoxamine, we tested several Sigma-1R agonists (ex. PRE-084 as a non-SSRI) and antagonists (ex. NE-100) and other SSRIs which do not have any effect on Sigma-1R function (ex. peroxetine) on TS iPSC-derived cardiomyocytes. The results demonstrate that Sigma-1R activation using PRE-084 could rescue the phenotypes in TS models. The molecular mechanism in which Sigma-1R activation rescues cardiac arrhythmic phenotypes is novel. Furthermore, we share our next strategy of chemical synthesis for the development of novel Sigma-1R agonists, which are less permeable to the brain through the blood-brain barrier (BBB), as new therapeutic compounds for LQTS.
Abstract 118: NLRP3 Inflammasome Mediates the Obesity-induced Pathogenesis of Atrial Fibrillation
Authors: Larry Scott, Changqun Yao, Na Li
Journal: Circulation Research (2018)

Background: Obesity increases the risk of atrial fibrillation (AF), the most common cardiac arrhythmia; but it is unknown what molecular pathway(s) underlying obesity promotes AF pathophysiology. ‘NACHT, LRR &amp; PYD Domains-containing Protein 3’ (NLRP3) inflammasome can activate Caspase-1 (Casp1) and mediate inflammatory response associated with obesity. Prior studies revealed that NLRP3 activity is enhanced in atrial tissues of AF patients, and our preliminary studies demonstrated a positive correlation between obesity and NLRP3 activation. Thus, we hypothesized that diet-induced obesity promotes AF pathogenesis via activation of the NLRP3 inflammasome. Methods and Results: Wildtype (WT) and NLRP3 knockout (KO) mice were fed high fat diet (HFD, 60% kcal) or normal chow (NC, as control) for 10 weeks to establish the obese but non-diabetic phenotype. At 10 weeks, WT+HFD and KO+HFD mice showed a significant increase in body weight, compared to WT+NC and KO+NC mice (P&lt;0.001). Echocardiography showed ventricular function were similar among all groups at 10 weeks. Western blotting revealed increased levels of mature Casp1 in atria of WT+HFD mice (P&lt;0.05 vs WT+NC mice), suggesting activity of NLRP3 is enhanced by HFD. Programmed intracardiac stimulation was performed to assess the inducibility of AF. While only 3 of 14 (21.3%) WT+NC mice showed AF evoked by atrial pacing, 7 of 8 (87.5%) WT+HFD mice developed pacing-induced AF (P&lt;0.05). Atrial effective refractory period (AERP) was reduced in WT+HFD mice (P&lt;0.05 vs WT+NC), suggesting that HFD promotes an electrical remodeling substrate for AF development. In contrast, AF incidence was reduced to 33.3% (3 of 9; P&lt;0.05 vs WT+HFD) and AERP was normalized in KO+HFD mice, suggesting NLRP3 is required for AF development in obese mice. Compared to WT+NC mice, Ca 2+ sparks were increased in atrial myocytes of WT+HFD mice (4.5±0.6 vs 6.4±0.7 sparks/100μm/s, P&lt;0.05), which was normalized in KO+HFD mice (4.4 ±0.4 sparks/100μm/s, P&lt;0.05). Conclusion: Our data suggests that obesity promotes NLRP3 activation and inhibition of NLRP3 can prevent the development of substrate for AF development. Our study potentially establishes a mechanistic link between obesity-induced inflammatory signaling and AF pathogenesis.
THE ASSOCIATION BETWEEN MEASUREMENTS OF BODY COMPOSITION AND LONG-TERM CARDIOVASCULAR EVENTS IN PATIENTS WITHOUT CORONARY ARTERY DISEASE
Authors: Jose Medina-Inojosa, Hannah Perez, Andrea De Leon Tejada, John Batsis, Farzane Saeidifard, Manlio Vinviguerra, Andrea Maugeri, Jennifer Zundel, Lynne Johnson, Francisco Lopez-Jimenez
Journal: Journal of the American College of Cardiology (2019)
Abstract 486: Role of the Adenine Nucleotide Translocator Family in the Mitochondrial Permeability Transition Pore
Authors: Jason Karch, Michael J Bround, Randi J Parks, Naohiro Terada, Douglas C Wallace, Elizabeth Murphy, Jeffery D Molkentin
Journal: Circulation Research (2018)

Cardiomyocyte necrosis is dependent on the prolonged opening of the mitochondrial permeability transition pore (MPTP) which has escaped molecular identification for decades. Once thought to be comprised of the adenine nucleotide translocator (ANT) family, this hypothesis has fell by the way side when it was shown that liver mitochondria devoid of ANT 1 and 2 still display MPTP opening, even though these mitochondria were desensitized to MPTP opening and required a greater calcium bolus for it to engage. Thus, the ANT family has been labeled as a critical regulator of the MPTP and not the pore forming component. However, mice express three isoforms of ANT and only two of the three isoforms where deleted when ANTs were deemed to be non-essential. We hypothesize that the third ANT isoform may have compensated for the loss of the other two ANT family members during this analysis. Here, we have generated mice lacking all isoforms of ANT in a heart-, liver-, or cell-specific manner. Surprisingly, mice lacking all isoforms of ANT specifically in the liver are viable and are highly resistant to MPTP opening. Indeed, the amount of calcium required to engage the MPTP in mitochondria lacking all ANTs is 11 fold higher than wild type mitochondria and greater than 2 fold higher than wild type mitochondria treated with the MPTP inhibitor cyclosporine A (CsA). Furthermore, the treatment of CsA on ANT null liver mitochondria completely blocks MPTP opening suggesting that the ANT family is the primary pore in the liver. However, when subjected to extreme levels of calcium, a cyclophilin D (CypD) dependent pore engages. CypD is the MPTP trigger located in the matrix of the mitochondria which is inhibited by CsA and in wild type mitochondria high levels of calcium are enough to overcome the inhibition of CypD to open the pore. But, in ANT depleted liver mitochondria, extremely high levels of calcium do not override CypD inhibition which is suggestive of the presence of an additional pore. Further experimentation is underway to determine if MPTP-conductance is detectable by patch clamping mitoplasts lacking all isoforms of ANT.
Enhanced Recovery After Surgery in the United States
Authors: Stavros G. Memtsoudis, Jashvant Poeran, Henrik Kehlet
Journal: JAMA (2019)

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COMMUNITY HEALTH WORKERS REDUCE REHOSPITALIZATIONS AND EMERGENCY DEPARTMENT VISITS FOR LOW-SOCIOECONOMIC URBAN PATIENTS WITH HEART FAILURE
Authors: Adam Vohra, Rhys Chua, Stephanie A. Besser, Charina Alcain, Sweta Basnet, Brenda Battle, Mitchell J. Coplan, Kirk T. Spencer, James Liao, Corey Tabit
Journal: Journal of the American College of Cardiology (2019)
Embryonal cancer initiation: MYCN-mediated mechanisms of resistance to cell death causing embryonal cell persistence
Authors: Wayne Thomas, Eric Sekyere, Joanna Keating, Anna Raif, Bellamy Cheung, Murray Norris, Michelle Haber, Patricia Armatai, David Kaplan, Freda Miller, William Weiss, Glenn Marshall
Journal: Cancer Research (2007)

516  The majority of child cancer arises in embryonal cells which have persisted beyond birth, having failed to undergo cell death following normal organogenesis in utero. The mechanism of embryonal cell persistence, and thus, tumour initiation are unknown. Resistance to spontaneous regression by neuroblasts is an important early step in human neuroblastoma tumorigenesis. We have previously shown that perinatal expression of a MYCN transgene in paravertebral murine neuroblasts mediates transient neuroblast proliferation and resistance to apoptotic cell death, as the first step in neuroblastoma tumorigenesis (Hansford et al., PNAS 2004). Here we analysed the mechanism of resistance to apoptotic cell death in primary ganglion cells from MYCN transgenic, compared with normal mice.  MYCN-mediated resistance to cell death was seen in ganglion cells following a variety of different death stimuli: nerve growth factor (NGF) withdrawal, hypoxia, nutrient deprivation and doxorubicin. The mRNA expression levels of known MycN transcriptional target genes in 2-week old primary ganglion tissue from normal and MYCN transgenic mice was then assessed. We found only induction of telomerase, α-prothymosin, multidrug resistance protein-1, MCM7 minichromosome maintenance deficient-7 and ornithine decarboxylase in MYCN mouse tissues. We next used an adenoviral gene transfer system to express deletion mutant MycN proteins in normal primary ganglion cells, and showed that only the Myc Box II domain of the full-length MycN protein was necessary for MycN-mediated resistance to NGF withdrawal. Following NGF withdrawal, ganglion cells from MYCN mice demonstrated markedly reduced nuclear translocation of both apoptosis-inducing factor and caspase-activated DNAse. The response of regulatory and effector proteins in the known apoptosis pathway activated by NGF withdrawal was then studied. Following NGF withdrawal, MYCN transgenic and normal ganglion cells did not differ for the phosphorylation responses of Jun kinase, ATF2, or c-Jun, or nuclear translocation of FOXO3a and consequent Bim transcription. In contrast, translocation of Bax to mitochondria was significantly reduced in MYCN, compared with normal, ganglion cells.  Taken together our data indicate a MycN-driven mechanism for death resistance in neuroblasts involving the Myc Box II domain of the MycN protein and Bax translocation, which may represent a general mechanism for embryonal cancer initiation.
Abstract 18949: Associations of Physical Activity Levels, Body Mass Index, and Risks of Heart Failure With Preserved Ejection Fraction vs. Reduced Ejection Fraction: An Individual-Level Pooled Analysis
Authors: Ambarish Pandey, Michael LaMonte, Liviu Klein, Colby Ayers, Bruce Psaty, Charles Eaton, Norrina Allen, James De Lemos, Mercedes Carnethon, Philip Greenland, Jarett Berry
Journal: Circulation (2016)

Introduction: Low levels of physical activity (PA) and higher BMI have each been associated independently with risk of HF. However, it is unclear if this relationship is consistent for the two HF s...
BET PROTEIN INHIBITION AND COGNITION: A PRE-SPECIFIED SUBSTUDY OF THE BETONMACE PHASE 3 TRIAL EVALUATING APABETALONE IN PATIENTS WITH DIABETES AND ACUTE CORONARY SYNDROME
Authors: Kausik K. Ray, Stephen Nicholls, Michael Sweeney, Jan Johansson, Norman Wong, Ewelina Kulikowski, Kenneth Lebioda, Peter Toth, Henry Ginsberg, Kamyar Kalantar-Zadeh, Mathias L. Haarhaus, Bengt Winblad, Jeffrey L. Cummings, Gregory Schwartz
Journal: Journal of the American College of Cardiology (2019)
Long-term Association of Depression Symptoms and Antidepressant Medication Use With Incident Cardiovascular Events in the Look AHEAD (Action for Health in Diabetes) Clinical Trial of Weight Loss in Type 2 Diabetes
Authors: Helen P. Hazuda, Sarah A. Gaussoin, Rena R. Wing, Susan Z. Yanovski, Karen C. Johnson, Mace Coday, Thomas A. Wadden, Edward S. Horton, Brent Van Dorsten, William C. Knowler
Journal: Diabetes Care (2019)

To examine whether depression symptoms or antidepressant medication (ADM) use predicts the probability of cardiovascular events in overweight/obese individuals with type 2 diabetes.Preplanned analyses of depression and incident cardiovascular disease (CVD) were performed in the Look AHEAD (Action for Health in Diabetes) weight loss trial after a median follow-up of 9.6 years. Depression symptoms, assessed with the Beck Depression Inventory (BDI), were analyzed both as a continuous and dichotomized variable (BDI score <10 or ≥10). ADM use was coded from participants' prescription medications. Four composite CVD outcomes were defined in the study protocol. Sex-stratified Cox proportional hazards models were adjusted for a range of baseline covariates.Depression symptoms were only significantly associated with a composite secondary outcome comprising CVD death, nonfatal myocardial infarction, nonfatal stroke, hospitalized angina, congestive heart failure, peripheral vascular disease, coronary artery bypass graft, and carotid endarterectomy. Significant sex interactions were observed for BDI score and BDI score ≥10. BDI score was significantly associated with higher probability of this composite outcome in men but was not associated with the outcome in women. BDI score ≥10 was positively associated with this composite outcome in men but was negatively associated in women. Exploratory analysis identified a significant BDI ≥10 × ADM use interaction for this composite outcome that differed in men versus women. Men with both BDI score ≥10 and ADM use compared with those with neither had 60% higher probability of the outcome, whereas women with both compared with those with neither had 50% lower probability.Sex differences in the association of depression symptoms and ADM use with incident CVD warrant further investigation.