tbuckley/cabot-search huggingface dataset:
Epidemiologic study of myelodysplastic syndromes in a racially diverse inner-city population.
Authors: Rishi Jain, Ashwin Sridharan, Yiting Yu, K H Ramesh, Krishna Gundabolu, Ellen Friedman, Amit Verma
Journal: Journal of Clinical Oncology (2013)

7125 Background: The International Prognostic Scoring System (IPSS) and the revised IPSS (IPSS-R) are used to assess prognosis after diagnosis of myelodysplastic syndromes (MDS). They are based on cytogenetics, bone marrow (BM) blasts, and number and degree of cytopenias. This retrospective analysis examined racial disparities in the presentation and survival of MDS patients (pts) in Bronx, NY. Methods: MDS pts treated at the Einstein/Montefiore system between 1997-2011 were included. Diagnosis was confirmed by review of BM biopsy. Demographics, cytogenetics (for 135/161 pts), blood counts, and BM blasts at diagnosis were collected. The Kaplan-Meier method was used for median survival estimates. The two-sample t-test and chi-square analysis were used to compare clinical variables between groups. Results: 161 pts with MDS were identified. Mean length of follow-up was 3.66 years (yrs). There were significant differences between mean age at diagnosis between Hispanics and African-Americans (66.5 vs 72.3 yrs, p&lt;0.05) and Hispanics and whites (66.5 vs 73.1 yrs, p&lt;0.05). There was also significantly increased thrombocytopenia at diagnosis in Hispanics (p&lt;0.05, when compared to non-Hispanics). Median survival decreased with higher risk among IPSS groups, however, the intermediate risk group in IPSS-R had a longer median survival (9 yrs) than all other risk groups. Conclusions: The cohort used to validate prognostic risk with IPSS and IPSS-R was primarily Caucasian. In our minority rich inner-city population, Hispanics presented with MDS earlier and with more thrombocytopenia. IPSS was a stronger predictor of survival than IPSS-R as the IPSS-R intermediate risk group had better survival than lower risk groups. Larger studies should be conducted to assess the applicability of IPSS-R in minority rich populations. [Table: see text]
EFFECTS OF EXPOSURE TO POLYCYCLIC AROMATIC HYDROCARBONS ON INFLAMMATION AND ENDOTELIAL DYSFUNCTION MARKERS IN A MURINE MODEL
Authors: Nicolas Saavedra, Gabriel Rojas, Montserrat Hevia, Katherine Andara, Camilo Rebolledo, Fernando Tomas Lanas, Luis Salazar
Journal: Journal of the American College of Cardiology (2020)
TIMING OF IMPELLA USE IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION WITH CARDIOGENIC SHOCK: A META-ANALYSIS
Authors: Sharan Sharma, Angela Ghuneim, Kelsey Patel, William Harder, Crystal Marsh, Keith Frank, Pravalika Rudraraju, Adam Chornoby, Elias Kassab, Ashok Kondur
Journal: Journal of the American College of Cardiology (2020)
EFFECTS OF DYSLIPIDEMIA ON CAV AND GRAFT LOSS IN PEDIATRIC HEART TRANSPLANT RECIPIENTS: A PHTS MULTI-INSTITUTIONAL ANALYSIS
Authors: Carmel Bogle, Ryan Cantor, Devin Koehl, Jillien Lochridge, James K. Kirklin, Aliessa P. Barnes, Gonzalo Wallis, Shahnawaz Amdani, Rebecca Ameduri, Elfriede Pahl, Kathleen Simpson, Elizabeth Blume
Journal: Journal of the American College of Cardiology (2020)
The predictive factors and patient-selection associated with the survival benefits of gefitinib in patients with advanced non-small cell lung cancer (NSCLC)
Authors: Y. Funada, M. Satouchi, T. Miyagawa, Y. Urata, T. Shimada, S. Yoshimura, Y. Watanabe, T. Kurata, S. Adachi, Y. Takada, S. Negoro
Journal: Journal of Clinical Oncology (2006)

17020 Background: Gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase, has shown meaningful antitumor activity for advanced NSCLC. Survival benefit of treatment with gefitinib has not been shown in unselected patients, however heterogeneity in survival outcomes between sub-group (histological types, gender, smoking status and ethnicity) of patients has been observed. The aim of this study was to identify the potential predictive features associated with the survival benefit of treatment with gefitinib. Methods: All NSCLC patients who began taking gefitinib during the period from July 2002 until July 2005 in our institute were retrospectively reviewed. Potential factors analyzed included age, gender, smoking history, performance status (PS), histology, stage, and prior chemotherapy. Results: Overall 221 patients were analyzed. The overall response rate of gefitinib was 26.7%. Median survival time (MST) was 8.0 months. MST of patients whose tumor response was partial response (PR) was 34.5 months. Univariate analysis revealed that the predictive factors of favorable survival were female (p = 0.001), never-smoker (p &lt; 0.0001), good PS (p &lt; 0.0001) and adenocarcinoma (p &lt; 0.0001). Multivariate analysis showed that never-smoking history (p = 0.005), adenocarcinoma (p = 0.004), and better PS (P &lt; 0.001) were significant independent predictors of long survival. The Brinkman index (BI), number of cigarettes per day multiplied by number of years smoked, was associated with survival benefit. MST was 17.6 months in the BI = 0 group (never-smokers), 9.7 months in 1 ≤BI &lt;500, 6.9 months in 500 ≤BI &lt;1000, 4.4 months in 1000 ≤BI &lt;1500, and 4.0 months in BI ≥1500. Conclusion: Never-smokers and adenocarcinoma are predictive factors for prolonged survival. As for smoking status, lower BI is associated with better prognosis after treatment with gefitinib. Therefore, histological factors and smoking status must be considered when treating with gefitinib. No significant financial relationships to disclose.
GenomegaMap: Within-Species Genome-Wide dN/dS Estimation from over 10,000 Genomes
Authors: Daniel J Wilson, Derrick W Crook, Timothy E A Peto, A Sarah Walker, Sarah J Hoosdally, Ana L Gibertoni Cruz, Joshua Carter, Clara Grazian, Sarah G Earle, Samaneh Kouchaki, Alexander Lachapelle, Yang Yang, David A Clifton, Philip W Fowler, Zamin Iqbal, Martin Hunt, Jeffrey Knaggs, E Grace Smith, Priti Rathod, Lisa Jarrett, Daniela Matias, Daniela M Cirillo, Emanuele Borroni, Simone Battaglia, Arash Ghodousi, Andrea Spitaleri, Andrea Cabibbe, Sabira Tahseen, Kayzad Nilgiriwala, Sanchi Shah, Camilla Rodrigues, Priti Kambli, Utkarsha Surve, Rukhsar Khot, Stefan Niemann, Thomas A Kohl, Matthias Merker, Harald Hoffmann, Katharina Todt, Sara Plesnik, Nazir Ismail, Shaheed Vally Omar, Lavania Joseph, Guy Thwaites, Thuong Nguyen Thuy Thuong, Nhung Hoang Ngoc, Vijay Srinivasan, Timothy M Walker, David Moore, Jorge Coronel, Walter Solano, George F Gao, Guangxue He, Yanlin Zhao, Chunfa Liu, Aijing Ma, Baoli Zhu, Ian Laurenson, Pauline Claxton, Anastasia Koch, Robert Wilkinson, Ajit Lalvani, James Posey, Jennifer Gardy, Jim Werngren, Nicholas Paton, Ruwen Jou, Mei-Hua Wu, Wan-Hsuan Lin, Lucilaine Ferrazoli, Rosangela Siqueira de Oliveira, Irena Arandjelovic, Angkana Chaiprasert, Iñaki Comas, Calle Jaime Roig, Francis A Drobniewski, Maha R Farhat, Qian Gao, Rick Ong Twee Hee, Vitali Sintchenko, Philip Supply, Dick van Soolingen
Journal: Molecular Biology and Evolution (2020)

The dN/dS ratio provides evidence of adaptation or functional constraint in protein-coding genes by quantifying the relative excess or deficit of amino acid-replacing versus silent nucleotide variation. Inexpensive sequencing promises a better understanding of parameters, such as dN/dS, but analyzing very large data sets poses a major statistical challenge. Here, I introduce genomegaMap for estimating within-species genome-wide variation in dN/dS, and I apply it to 3,979 genes across 10,209 tuberculosis genomes to characterize the selection pressures shaping this global pathogen. GenomegaMap is a phylogeny-free method that addresses two major problems with existing approaches: 1) It is fast no matter how large the sample size and 2) it is robust to recombination, which causes phylogenetic methods to report artefactual signals of adaptation. GenomegaMap uses population genetics theory to approximate the distribution of allele frequencies under general, parent-dependent mutation models. Coalescent simulations show that substitution parameters are well estimated even when genomegaMap's simplifying assumption of independence among sites is violated. I demonstrate the ability of genomegaMap to detect genuine signatures of selection at antimicrobial resistance-conferring substitutions in Mycobacterium tuberculosis and describe a novel signature of selection in the cold-shock DEAD-box protein A gene deaD/csdA. The genomegaMap approach helps accelerate the exploitation of big data for gaining new insights into evolution within species.
CHEST PAIN CENTER ACCREDITATION IS ASSOCIATED WITH BETTER IN-HOSPITAL OUTCOMES FOR ACUTE PULMONARY EMBOLISM PATIENTS
Authors: Yan Zhang, Pengfei Sun, Jianping Li, Xingang Wang, Yuxi Li, Bin Zhang, Ying Shi, Haibo Wang, Hu Chen, Yong Huo
Journal: Journal of the American College of Cardiology (2020)
SAFETY AND EFFICACY OF ANTICOAGULANT MONO-THERAPY IN STABLE CORONARY ARTERY DISEASE AND ATRIAL FIBRILLATION: A META-ANALYSIS
Authors: Waqas Ullah, Yasar Sattar, Sohaib Roomi, Wajahat Humayun, Mishal Shaukat, Donald Haas
Journal: Journal of the American College of Cardiology (2020)
NATURAL LANGUAGE PROCESSING CAN ACCURATELY IDENTIFY HOSPITALIZATIONS FOR WORSENING HEART FAILURE USING ELECTRONIC HEALTH RECORDS
Authors: Rishi Parikh, Andrew Ambrosy, Sue Hee Sung, Anand Narayanan, Rajeev Masson, Phuong-Quang Lam, Kevin Kheder, Alan Iwahashi, Alexander Hardwick, Jesse Fitzpatrick, Alan Go
Journal: Journal of the American College of Cardiology (2020)
The effect of continuous exposure to serotonin receptor antagonism on delayed emesis: An analysis of 1,535 patients in two randomized clinical trials with granisetron (G), APF530, and palonosetron (palo).
Authors: Harry Raftopoulos, Erin Oboyle, Richard J. Gralla, Martin Rosenberg, John Barr
Journal: Journal of Clinical Oncology (2012)

e19635 Background: Serotonin-type 3 receptor antagonists (5HT3RA) are recommended by all evidence-based guideline groups. Controversies remain over the role of 5HT3RA in delayed emesis and in dosages. This analysis was conducted to examine if: 1) serotonin antagonism helps prevent delayed emesis, 2) length of continuous exposure to a 5HT3RA impacts efficacy, and 3) higher doses of a 5HT3RA influence results. Palo, a 5HT3RA with a long half life, was superior to older 5HT3RA agents in single agent trials and to G + dexamethasone (dex) in a combination trial in untreated patients (pts) (Saito et al, Lancet Oncol 2009 – Trial 1). APF530 is an extended release formulation of 2% G (500mg = 10 mg of G) in a biodegradable polymer, which with dex showed non-inferiority with palo + dex in a mix of untreated and treated pts (Grous et al, ASCO 2009 – Trial 2). Methods: We analyzed results of only untreated pts from Trial 2 so that the population was similar to those in Trial 1 (previously untreated, highly or moderately emetic chemo and received dex + single administration of a 5HT3RA). This allows comparison, over 2 trials, of G, APF530, palo at 0.25 mg and 0.75 mg. Results: See table. All three groups treated with the long acting 5HT3RA (palo at 0.25 mg or 0.75 mg) or the extended release 5HT3RA (APF530) had similar efficacy in complete control of acute, delayed, or overall 5-day emesis. Only the short acting G was associated with poorer results, in delayed and overall 5-day control. Conclusions: This analysis indicates that 1) continuous exposure to 5HT3RA as a long acting agent or as an extended release formulation provide better emetic control than the standard 5HT3RA granisetron, even with added dex, and 2) similar results were found with palo at 0.25 mg and 0.75 mg. These results indicate a role for serotonin antagonism in delayed emesis provided the patient receives continuous exposure of a 5HT3RA agent. [Table: see text]
BURDEN OF RELAPSES AND ITS ASSOCIATION WITH ETIOLOGY IN PATIENTS WITH RECURRENT PERICARDITIS
Authors: Bryce Montane, Muhammad Furqan, Ray Tabucanon, Tom Kai Ming Wang, Jain Vardhmann, Jarmanjeet Singh, Christine Louise Jellis, Deborah Kwon, Chadi Ayoub, Allan Klein
Journal: Journal of the American College of Cardiology (2020)
Disappointing Early Results From Opioid Prescribing Limits for Acute Pain
Authors: Kao-Ping Chua, Lauren Kimmel, Chad M. Brummett
Journal: JAMA Surgery (2020)

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PERIPHERAL ARTERY DISEASE, ABNORMAL ANKLE-BRACHIAL INDEX AND PROGNOSIS AFTER ACUTE CORONARY SYNDROME
Authors: Anat Berkovitch, Zaza Iakobishvili, Shmuel Fuchs, Shaul Atar, Omri Braver, Katia Orvin, Michael Glikson, Roy Beigel, Shlomi Matetzky
Journal: Journal of the American College of Cardiology (2020)
Combined targeting of LSD1 (KDM1A) and histone deacetylases exerts superior efficacy against human AML.
Authors: Warren Fiskus, Sunil Sharma, Rekha Rao, Ramesh Balusu, Sreedhar Venkannagari, Siddhartha Ganguly, David Bearss, Kapil N. Bhalla
Journal: Journal of Clinical Oncology (2012)

10549 Background: LSD1 (KDM1A) is FAD-dependent histone H3K4Me2 demethylase. Inhibition of LSD1 increases H3K4Me3-a permissive mark for gene expression, and inhibits growth of pluripotent cancer cells. We have previously noted that treatment with the histone deacetylase (HDAC) inhibitor panobinostat (PS) depletes EZH2 (the catalytic subunit of the polycomb repressive complex 2, PRC2) and disrupts its interaction with the other PRC2 proteins, attenuates LSD1, and de-represses growth inhibitory and pro-apoptosis genes. Methods: In the present studies, we determined the chromatin effects and the pre-clinical in vitro and in vivo anti-AML activity of the novel, non-monoamine oxidase, reversible inhibitor of LSD1, HCI2509 (100 to 500 nM), alone and in combination with PS, utilizing cultured (OCI-AML3 and HL-60) and primary human AML blast progenitor cells. Results: Treatment with HCI2509 dose-dependently increased the levels of H3K4Me3, p16, p27, and CEBPα in cultured AML cells. This correlated with inhibition of cell growth and induction of morphologic differentiation in AML cells. Exposure to HCI2509 disrupted the binding of LSD1 with the co-repressor CoREST and HDAC1. Treatment with PS (10 to 50 nM) dose-dependently depleted not only LSD1 but also EZH2, SUZ12 and BMI1 in AML cells. Co-treatment with PS enhanced the chromatin modifying effects of HCI2509. The combination also synergistically induced loss of viability of cultured and primary AML cells (combination indices, CI &lt;1.0). Following tail vein infusion and establishment of AML by OCI-AML3 cells in NOD-SCID mice, treatment with HCI2509 (25 mg/kg, b.i.w, IP, for 3 weeks) improved survival, as compared to the control mice (p &lt;0.001). HCI2509 treatment (15 mg/kg IP) also dramatically improved survival of NSG mice with established human AML following tail-vein injection of primary AML blasts expressing FLT3-ITD. Survival was further improved upon co-treatment with HCI2509 and PS (5 mg/kg IP, MWF). Mice did not experience any toxicity or weight loss. Conclusions: Combined epigenetic therapy with HCI2509 and PS exerts superior pre-clinical activity, warranting further in vivo development and testing of HCI2509 against human AML.
Clinical pharmacokinetics of the Smac-mimetic birinapant (TL32711) as a single agent and in combination with multiple chemotherapy regimens.
Authors: Gerald J. Fetterly, Biao Liu, Neil N. Senzer, Ravi K. Amaravadi, Russell J. Schilder, Lainie P. Martin, Patricia LoRusso, Kyriakos P. Papadopoulos, Alex A. Adjei, Patricia D. Zagst, Mark A McKinlay, David Edward Weng, Martin Graham
Journal: Journal of Clinical Oncology (2012)

3029 Background: Birinapant is a novel small molecule Smac-mimetic that targets members of the inhibitor of apoptosis proteins (cIAP1, cIAP2 and XIAP) involved in the blockade of apoptosis. A population PK model was developed to characterize the interpatient variability in birinapant PK and to evaluate the effect of multiple combination regimens on birinapant disposition and safety. Methods: Birinapant was administered alone or in combination to 114 patients (55M/59F; 89% Caucasian) with advanced malignancies. Birinapant was administrated by a 30 min IV infusion QW alone (30 pats), or approx. 30 min. after chemotherapy with irinotecan (19 pats), docetaxel (20 pats), gemcitabine (17 pats), liposomal doxorubicin (13 pats), or paclitaxel/carboplatin (15 pats). Birinapant dose levels ranged from 0.18 to 35 mg/m 2 . Population PK modeling was performed to investigate the effect of the following patient covariates: [BW (38.5-127.5 kg), age (27.5-86.0 yrs), CrCL (36.4-219.2 ml/min), ALT (6-121 IU/L), and TBIL (0.1-1.7 mg/dL)]. Results: A 3-compartment PK model described the time course of birinapant disposition with predicted values for T1/2, CL, and Vd of 40 h, 21 L/h and 10.2 L, respectively. Birinapant displayed linear PK across the dose range with no significant accumulation in plasma following weekly dosing. Goodness of fit plots supported the model fit, with residual variability of 23%. The PK of birinapant remained unchanged when combined with irinotecan, docetaxel, gemcitabine and liposomal doxorubicin. Concomitant administration with paclitaxel/carboplatin resulted in a 2-fold increase in birinapant AUC possibly due to reduced OATP1B3 mediated tissue uptake. Conclusions: These data show that birinapant possesses an excellent PK profile with dose proportional kinetics, a long terminal half-life for target coverage, low/moderate interpatient variability in CL and no significant accumulation following weekly dosing. Importantly, the PK of birinapant remained unchanged when combined with multiple chemotherapy regimens and the increased exposure with paclitaxel/carboplatin was not associated with any change in birinapant tolerability.
Verification of EZH2 as a druggable target in metastatic uveal melanoma
Authors: Bei Jin, Ping Zhang, Hailin Zou, Huijing Ye, Yun Wang, Jing Zhang, Huasheng Yang, Jingxuan Pan
Journal: Molecular Cancer (2020)

Hepatic metastasis develops in ~ 50% of uveal melanoma (UM) patients with no effective treatments. Although GNAQ/GNA11 mutations are believed to confer pathogenesis of UM, the underlying mechanism of liver metastasis remains poorly understood. Given that profound epigenetic evolution may occur in the long journey of circulating tumor cells (CTCs) to distant organs, we hypothesized that EZH2 endowed tumor cells with enhanced malignant features (e.g., stemness and motility) during hepatic metastasis in UM. We aimed to test this hypothesis and explore whether EZH2 was a therapeutic target for hepatic metastatic UM patients.
Role of Deranged Energy Deprivation Signaling in the Pathogenesis of Cardiac and Renal Disease in States of Perceived Nutrient Overabundance
Authors: Milton Packer
Journal: Circulation (2020)

Sodium-glucose cotransporter 2 inhibitors reduce the risk of serious heart failure and adverse renal events, but the mechanisms that underlie this benefit are not understood. Treatment with SGLT2 inhibitors is distinguished by 2 intriguing features: ketogenesis and erythrocytosis. Both reflect the induction of a fasting-like and hypoxia-like transcriptional paradigm that is capable of restoring and maintaining cellular homeostasis and survival. In the face of perceived nutrient and oxygen deprivation, cells activate low-energy sensors, which include sirtuin-1 (SIRT1), AMP-activated protein kinase (AMPK), and hypoxia inducible factors (HIFs; especially HIF-2α); these enzymes and transcription factors are master regulators of hundreds of genes and proteins that maintain cellular homeostasis. The activation of SIRT1 (through its effects to promote gluconeogenesis and fatty acid oxidation) drives ketogenesis, and working in concert with AMPK, it can directly inhibit inflammasome activation and maintain mitochondrial capacity and stability. HIFs act to promote oxygen delivery (by stimulating erythropoietin and erythrocytosis) and decrease oxygen consumption. The activation of SIRT1, AMPK, and HIF-2α enhances autophagy, a lysosome-dependent degradative pathway that removes dangerous constituents, particularly damaged mitochondria and peroxisomes, which are major sources of oxidative stress and triggers of cellular dysfunction and death. SIRT1 and AMPK also act on sodium transport mechanisms to reduce intracellular sodium concentrations. It is interesting that type 2 diabetes mellitus, obesity, chronic heart failure, and chronic kidney failure are characterized by the accumulation of intracellular glucose and lipid intermediates that are perceived by cells as indicators of energy overabundance. The cells respond by downregulating SIRT1, AMPK, and HIF-2α, thus leading to an impairment of autophagic flux and acceleration of cardiomyopathy and nephropathy. SGLT2 inhibitors reverse this maladaptive signaling by triggering a state of fasting and hypoxia mimicry, which includes activation of SIRT1, AMPK, and HIF-2α, enhanced autophagic flux, reduced cellular stress, decreased sodium influx into cells, and restoration of mitochondrial homeostasis. This mechanistic framework clarifies the findings of large-scale randomized trials and the close association of ketogenesis and erythrocytosis with the cardioprotective and renoprotective benefits of these drugs.
LACK OF EARLY-RECURRENCE ATRIAL FIBRILLATION IN THE FOLLOW-UP PERIOD ASSOCIATED WITH PERIPROCEDURAL TNT AND CK-MB INCREASE IN CRYOABLATION AS COMPARED TO RADIOFREQUENCY ABLATION
Authors: Jan Budzianowski, Jarosław Hiczkiewicz, Katarzyna Korybalska, Konrad Pieszko, Janusz Rzeźniczak, Paweł Burchardt
Journal: Journal of the American College of Cardiology (2020)
THE IMPACT OF AIR POLLUTION ON ATHEROSCLEROSIS BURDEN IN PATIENTS WITH CORONARY ARTERY DISEASE
Authors: Evangelos Oikonomou, Vasiliki-Chara Mystakidi, Panagiotis Theofilis, Petros Fountoulakis, Margarita Asimakopoulou, Nikolaos Barbaresos, Ioannis Giannarakis, Georgia Vogiatzi, Margenti Papakonstantinou, Sotirios Tsalamandris, George Lazaros, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2020)
COMORBIDITY BURDEN AND ADVERSE OUTCOMES AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Daniel Feldman, Mikhail Romashko, Benjamin Koethe, Sonika Patel, Hassan Rastegar, Yong Zhan, Charles Resor, Carey Kimmelstiel, David Allen, Andrew R. Weintraub, Benjamin Wessler
Journal: Journal of the American College of Cardiology (2020)