tbuckley/cabot-search huggingface dataset:
Abstract 230: Repair of Aortic Coarctation in Neonates Less than Two Kilogram
Authors: Qiang Chen, Thomas Fleming, Massimo Caputo, Serban Stoica, Andrew Tometzki, Andrew Parry
Journal: Circulation Research (2018)

Objective: Though a significant number of low birth weight and premature neonates are born with aortic coarctation, waiting for the child to grow before intervening rarely permits significant useful weight gain and puts the child at risk of interim complications. Previous studies of early operation on these patients have shown a high hospital mortality up to 25% (25 out of 100) and 30% (30 out of 100) recurrence in one year. We reviewed our data to ascertain whether modern approaches allow better outcomes for these children. Methods: All patients weighing less than 2 kg with isolated coarctation between August 2008 and November 2015 were studied by retrospective chart review to ensure greater than 24 months follow-up. Eleven patients underwent extended end-to side surgical repair. In-hospital and medium term follow-up data were collected. Data are expressed as median (range). Results: Weight at time of surgery was 1.8kg (1.6-1.9). There were no deaths, in-hospital or during follow-up. One patient developed postoperative chylothorax. In-hospital stay was 18 days (4-47). At follow-up of 68 months (28-115) echocardiographic velocity across the repair was 1.6m/sec (1.4-4.5). One patient with William’s syndrome had evidence of recoarctation and required balloon coarctoplasty followed by stenting. This patient had grossly abnormal vessels at the time of initial surgery with aortic wall thickness greater than 3mm. Conclusions: Neonates below 2kg can undergo coarctation repair safely with low incidence of recurrence. Waiting for growth in this cohort of patients cannot therefore be justified.
IMPROVING ARRHYTHMIC RISK STRATIFICATION AND IMPIANTABLE CARDIOVERTER DEFIBRILLATOR PATIENT SELECTION: A PROSPECTIC STUDY COMPARING OLD AND NEW ECHOCARDIOGRAPHY PARAMETERS
Authors: Marco Previtero, Danila Azzolina, Chiara Palermo, Rosaria M. Tenaglia, Giuseppe Sammarco, Niccolò Ruozi, Patrizia Aruta, Sabino Iliceto, Denisa Muraru, Luigi Badano
Journal: Journal of the American College of Cardiology (2019)
Abstract 410: Prostaglandin E2 Reduces Carnitine Palmitoyltransferase 2 in Adult Mouse Cardiomyocytes
Authors: Pamela Harding, Timothy D Bryson, Indrani Datta, Yun Wang, Albert M Levin
Journal: Circulation Research (2018)

Prostaglandin E2 (PGE2) signals differently through its 4 receptor subtypes (EP1-EP4) to elicit diverse physiologic/pathologic effects. We previously reported that PGE2 via its EP3 receptor reduces cardiac contractility and male mice with cardiomyocyte-specific deletion of the EP4 receptor develop dilated cardiomyopathy. To determine pathway(s) responsible for the phenotype, we performed gene array on left ventricles from these mice followed by Ingenuity Pathway Analysis (IPA) which demonstrated that genes differentiating WT mice and EP4 KO mice were significantly overrepresented in mitochondrial (p=2.51x10 -28 ) and oxidative phosphorylation (p=3.16 x10 -30 ) pathways. Importantly, carnitine palmitoyltransferase 2 (cpt 2), an enzyme that transports fatty acids across the inner mitochondrial membrane was down-regulated in EP4 KO mice. We therefore hypothesized that PGE2 via EP3 decreases cpt 2 to impair mitochondrial function. To test this hypothesis, we used isolated mouse cardiomyocytes (AVM) from 16-18 week old male C57Bl/6 mice and treated them with either 1 μM of the EP3 agonist sulprostone (sulp), or PGE2. Treatment of AVM with sulp for 24 hrs. decreased cpt 2 levels from a control level of 1.0 to 0.57 ± 0.15, p &lt; 0.05 and treatment with PGE2 decreased cpt 2 levels to 0.74 ± 0.27. Since cpt 2 is regulated by the transcription factor NR4A2 in other cell types, we investigated whether NR4A2 was regulated by PGE2 or sulp. NR4A2 levels were reduced after 4 hr. treatment with either PGE2 or by treatment with sulp; from a control value of 1.0 to 0.70 ± 0.16 and to 0.86 ± 0.01 respectively, p&lt; 0.05 for sulp, n = 3. To associate these changes with mitochondrial function, we measured complex I activity with a spectrophotometric assay. Complex I activity was reduced by 50% (p &lt; 0.05) by 4 hr. treatment with PGE2, from 1.32 ± 0.36 to 0.66 ± 0.08 mOD/min, and this was associated with reduced expression of multiple genes from mitochondrial pathways including sub units of mitochondrial NADH dehydrogenase ubiquinone flavoprotein (Nduf), a component of complex I. In conclusion, these results suggest that increased PGE2 and its EP3 receptor in heart disease may contribute to impaired mitochondrial function and provide yet another link between inflammation and cardiac dysfunction.
Abstract 364: Metabolic Syndrome Induced by High Fat/high Fructose Diet in C57bl/6 Mice Impaired Cardiac Remodeling During Pregnancy
Authors: Yijun Yang, Yunichel Joo, Tao Wang, Giulia Borghetti, Shavonn Harper, Christopher Bryan, Sadia Mohsin, Steven R Houser
Journal: Circulation Research (2018)

Rationale: Due to the change of life style in the past decades, the incidence of metabolic syndrome (MetS) and obesity in women of childbearing age has been increased. Evidences have shown that complications during pregnancy, such as obesity and gestational diabetes, strongly link to future heart diseases. During pregnancy, the heart undergoes a physiological remodeling with mild ventricular dilation and hypertrophy. However, the effects of MetS on cardiac phenotype during pregnancy are not well understood. Moreover, animal models for MetS so far are not well established, which are usually species limited, gender limited and lack of translational significance. Thus, it’s important to develop an animal model which resembles the etiology of MetS in human beings. Objective: Establish a model of MetS in female C57BL/6J mice and determine the effects of MetS on cardiac remodeling during pregnancy. Methods and Results: To establish a mouse model of MetS, high fat (49% kcal)/high fructose (35.6% kcal) diet are given to C57BL/6J mice at the age of 8-week. Mice fed with normal diet (10% kcal fat) served as control. To better characterize the model within different genders, male mice are also subjected to the high fat/ high fructose (HFHF diet) and control diet. After 12 weeks feeding, mice fed with HFHF diet showed significantly higher body weight and gonadal fat weight compared with control mice in both genders. Also, mice fed with HFHF diet showed impaired glucose tolerance and higher serum total cholesterol level. However, the blood pressure showed no difference between groups in both genders. Overall, the symptoms of obesity, impaired glucose tolerance and dyslipidemia suggest the development of MetS. Female mice after 12-week special diet feeding will be subjected to breeding. Cardiac function is then evaluated by echocardiography before and during pregnancy. Female mice that developed MetS showed impaired cardiac function and pathological remodeling during pregnancy. Conclusion: We’ve developed a mouse model of MetS in both female and male C57BL/6J mice strain with 12 weeks feeding of HFHF diet, which resemble the western diet that affects human beings nowadays. Females that have MetS showed impaired cardiac function and pathological remodeling during pregnancy.
RIGHT VENTRICULAR STRAIN PREDICTS PULMONARY HYPERTENSION IN END STAGE LIVER DISEASE PATIENTS
Authors: Neeraja Yedlapati, Addis Asfaw, Arindam Sharma, Pradeep Podila, Uchenna Agbim, Benedict Maliakkal, West James, Timothy Woods
Journal: Journal of the American College of Cardiology (2019)
Abstract 516: Pharmacological Inhibition of Phosphatase and Tensin Homolog Ameliorates Adipose Tissue Inflammation and Increases Splenic Regulatory B and T Cells in Rats With Metabolic Syndrome
Authors: Ayako Uchinaka, Yumeno Kawai, Kanako Komuro, Aoi Fujieda, Minami Wataya, Mamoru Yoneda, Yuki Komatsu, Kiyoshi Aoyama, Toyoaki Murohara, Kohzo Nagata
Journal: Circulation Research (2018)

Objectives: B cells have emerged as a critical player in innate and adaptive immune responses. However, little is known about the role of B cells in obesity- and/or stress-induced immune responses. We previously reported that restraint stress exacerbates cardiac and adipose tissue pathology via β-adrenergic signaling in rats with metabolic syndrome (MetS). Phosphatidylinositol 3’-kinase (PI3K)/Akt pathway regulates interleukin-10 production by B cells. Phosphatase and tensin homolog (PTEN) is a lipid/protein phosphatase that can negatively regulate PI3K/Akt pathway. To identify the possible role of PI3K signaling in stress-induced immune responses in metabolic disorders, we now examined the effects of restraint stress and PTEN inhibition on B and T cell subsets in rats with MetS. Methods: We used DahlS.Z- Lepr fa / Lepr fa (DS/obese) rats, derived from a cross between Dahl salt-sensitive and Zucker rats, as an animal model of MetS. Rats were exposed to restraint stress (restraint cage, 2 h/day) for 2 wk from 9 wk of age with or without daily administration of the PTEN inhibitor bisperoxovanadium-pic [bpV(pic), 0.2 mg/kg, i.p.]. Age-matched homozygous lean littermates of DS/obese rats (DahlS.Z- Lepr + / Lepr + rats) served as controls. Results: Treatment with bpV (pic) attenuated hypertension in DS/obese rats under restraint stress. This agent also reduced subcutaneous fat mass and alleviated adipocyte hypertrophy and inflammation in subcutaneous adipose tissue as well as tended to suppress epididymal adipose tissue inflammation in such rats. Flow cytometric analysis showed that regulatory B (Breg) cells were increased and B-1 cells, which attenuate inflammation and insulin resistance, tended to be increased by bpV (pic) in the spleen of DS/obese rats subjected to restrain stress. In addition, bpV (pic) treatment led to an increase in splenic regulatory T (Treg) cells and downregulation of CD8 + T cells in epididymal adipose tissue of stressed rats. Conclusions: PTEN inhibition with bpV (pic) attenuated subcutaneous adipose tissue inflammation as well as increased splenic Breg and Treg cells in DS/obese rats under restraint stress. Pharmacological inhibition of negative regulator of PI3K may represent a therapeutic approach for the treatment of MetS.
PATIENTS WITH TAKOTSUBO CARDIOMYOPATHY HAVE HIGHER PREVALENCE OF DEPRESSION AND ANXIETY THAN PATIENTS WITH ACUTE CORONARY SYNDROME: FROM THE NATIONAL INPATIENT SAMPLE
Authors: Ashraf Abugroun, Fady Iskander, Osama Hallak, Mina Iskander, Lloyd W. Klein
Journal: Journal of the American College of Cardiology (2019)
Abnormal Distribution and Function of NK Cells Subsets May Lead to Impaired Tumor Surveillance in a JAK2V617F Myeloproliferative Neoplasm Model
Authors: Thiago Mantello Bianco, Diego Antonio Pereira-Martins, Patrícia Vianna Bonini Palma, Josiane Lilian Schiavinato, Cleide Araújo Silva, Ann Mullally, Susumu S Kobayashi, Eduardo Magalhães Rego, Lorena Lobo Figueiredo-Pontes
Journal: Blood (2018)
Abstract 426: Stress-induced Kinase Targets of Cardioprotective 3’,4’-dihydroxyflavonol in Injured Myocardium
Authors: Dominic Richards, Yvonne Yeap, Melissa Reichelt, Phillip van der Peet, Spencer J Williams, Owen L Woodman, Grant McLachlan, Dominic Ng
Journal: Circulation Research (2018)

3’,4’-dihydroxyflavonol (DiOHF) is a synthetic flavonol in a class of phytochemicals known as flavonoids can have beneficial biological properties. Previous studies revealed that intravenous administration of DiOHF immediately preceding myocardial reperfusion potently reduced infarct size in anaesthetised sheep that was comparable to ischemic preconditioning and the protective effects of DiOHF were recapitulated ex vivo during ischemia/reperfusion (I/R) of Langendorff-perfused rat hearts and in vitro on isolated cardiac myocytes. These studies highlight the therapeutic potential of DiOHF, with derivatives recently entering Phase II trials for the reduction of ventricular injury and contractile dysfunction following myocardial infarction (NCT02557217). In our current study, we confirmed potent cytoprotective effects of DiOHF in preventing apoptotic and necrotic death of primary rat cardiomyocytes. In addition, we revealed potent anti-hypertrophic effects in cardiomyocytes stimulated with alpha and beta-adrenergic agonists. In comparison with structurally similar compounds, fisetin, quercetin and dihydroxyflavone, DiOHF exhibited enhanced anti-hypertrophic and protective properties. The molecular targets of DiOHF that underpin it’s beneficial effects are of immense interest as they aid clinical development of derivative compounds, rational design of new compounds with biological activity and provide novel insights into the regulatory mechanisms that define the protected myocardium. In exploring the DiOHF mechanisms of action, we had previously reported DiOHF inhibited Ca2+/calmodulin dependent protein kinase II (CaMKII) activity in in vitro kinase assays and in cultured myoblasts. Here, we used resin-immobilized DiOHF for affinity purification from heart tissue lysates and confirmed direct drug-interaction with CaMKII/p-CaMKII from injured rat myocardium (I/R). In addition, we revealed DiOHF interaction and direct inhibition of apoptosis-signal regulated kinase (ASK1) from I/R rat hearts. Our ongoing studies will define whether flavonol inhibition of CaMKII and ASK1 defines protective benefits of DiOHF in the injured myocardium.
Abstract 254: Mitochondrial Permeability Transition Pore, Calcium Uniporter, and Iron Overload in the Heart
Authors: Richard Gordan, Suwakon Wongjaikam, Nadezhda Fefelova, Natthaphat Siri-Angkul, Judith K Gwathmey, Nipon Chattipakorn, Siriporn C Chattipakorn, Lai-Hua Xie
Journal: Circulation Research (2018)

Although iron (Fe) overload-induced cardiomyopathy/arrhythmias remain a significant clinical challenge, the underlying mechanism is not well defined. In the present study, we assessed the involvement of mitochondrial permeability transition pore (mPTP) and Ca uniporter (mCU) in Fe overload-induced mitochondrial Ca mishandling and cardiac contractile dysfunction. Firstly, we tested the hypothesis that Fe overload promotes reactive oxygen species (ROS) production and mitochondrial membrane potential (Δ Ψ m ) depolarization that may open the mPTP and promote intracellular Ca dysfunction. In isolated mouse ventricular myocytes, both cytosolic and mitochondrial Fe levels (monitored by using specific Fe dyes) were elevated following acute perfusion with Fe 3+ /8-Hydroxyquinoline (8-HQ) (1-100 μM). Mitochondrial superoxide generation (by MitoSOX Red) and cytosolic ROS levels (by DCF) were significantly enhanced by Fe overload. Furthermore, Fe overload induced Δ Ψ m depolarization as measured by TMRM. The mitochondrial maximal respiration rate and reserve capacity (using the Seahorse XF e 96 analyzer) were significantly reduced by Fe overload. Fe overload significantly increased the rate of Ca waves as imaged with Fluo-4. Fe overload-promoted Ca waves were significantly reduced by the mPTP inhibitor cyclosporine A (CsA). In Langendorff-perfused hearts subjected to programmed S 1 -S 2 stimulation, Fe significantly increased arrhythmia scores compared to the hearts pretreated with CsA, indicating mPTP inhibition can ameliorate the proarrhythmic effects of Fe-overload. These observations were confirmed in cyclophilin D knockout mice, in which mPTP opening is impaired. Furthermore, the involvement of the mCU was evaluated in a chronic Fe overload model (Fe dextran injection, i.p. ) by using conditional mCU knockout (mCU KO) mice. We observed that mCU KO prevented mitochondrial Fe uptake and conferred a significantly higher resistance to Fe-induced mitochondrial ROS generation, Ca mishandling and cardiac contractile dysfunction. In conclusion, mitochondrial Fe uptake and mitochondrial Ca dysregulation, presumably mediated by both mCU and mPTP, account for the molecular/cellular mechanism for Fe-induced cardiomyopathy and arrhythmias.
PROGNOSIS OF DRUG-COATING BALLOON ANGIOPLASTY FOR TREATMENT OF IN-STENT RESTENOSIS AFTER PERCUTANEOUS CORONARY INTERVENTION TO CORONARY ARTERY CALCIUM LESION
Authors: Yasushi Akutsu, Kosuke Nomura, Teruo Sekimoto, Hiroki Tanisawa, Kyouichi Kaneko, Yusuke Kodama, Hiroaki Tsujita, Toshiro Shinke
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF MEAN PLATELET VOLUME ON ST RESOLUTION FOLLOWING THROMBOLYSIS IN ACUTE ST ELEVATION MYOCARDIAL INFARCTION: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Wasawat Vutthikraivit, Pavida Pachariyanon, Pattara Rattanawong, Saranapoom Klomjit, Pakpoom Tantrachoti, Mohammad Ansari, Scott Shurmur, Pablo Paz, Sofia Prieto, Mohamed Elmassry
Journal: Journal of the American College of Cardiology (2019)
SEX AND RACE DIFFERENCES IN CIRCULATING LEVELS OF NATRIURETIC PEPTIDE CONCENTRATIONS AND THE ASSOCIATION WITH INCIDENT HEART FAILURE IN THE COMMUNITY: THE ATHEROSCLEROSIS RISK IN COMMUNITIES STUDY
Authors: Peder L. Myhre, Brian Claggett, Christie Ballantyne, Elizabeth Selvin, Helge Rosjo, Torbjorn Omland, Scott Solomon, Hicham Skali, Amil Shah
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE ON TRANSCATHETER AND SURGICAL AORTIC VALVE REPLACEMENT: FROM THE PARTNER 2 COHORT A TRIAL
Authors: Tomo Ando, Danny Dvir, Tamim Nazif, Shmuel Chen, Alexandros Briasoulis, Ajay Kirtane, Luis Afonso, Hisato Takagi, Aaron Crowley, Maria Alu, Martin Leon, Susheel Kodali
Journal: Journal of the American College of Cardiology (2019)
Abstract 249: Cortical-bone Derived Stem Cells Improve Cardiac Outcomes After Myocardial Infarction by Modulating the Inflammatory Response
Authors: Alexander R Hobby, Thomas E Sharp, Eric Feldsott, Sadia Mohsin, Hajime Kubo, Remus Berretta, Steven R Houser
Journal: Circulation Research (2018)

Rationale: Cortical-bone derived stem cells (CBSCs) improve cardiac pump function and reduce scar size after myocardial infarction (MI) compared to Cardiac-Derived and Mesenchymal Stem Cells. However, the mechanism for these improved outcomes is not known. Recent data in a swine model of MI has demonstrated acute changes to the immune response elicited by MI in CBSC treated animals compared to vehicle controls, suggesting that CBSCs may improve post-MI remodeling by modulation of the immune response. Objective: Identify the changes in the immune response of CBSC-treated animals and determine the role of these changes in cardiac healing and wound repair. Methods and Results: Using multi-color flow cytometry, we found that murine bone marrow-derived macrophages (BMDMs) cultured and exposed to CBSC conditioned culture medium in vitro express higher levels of the mannose receptor CD206 than controls, indicating alternative “M2” activation. In addition, CD86 expression on BMDMs exposed to the classical (M1) activators interferon-γ (INF-γ) and lipopolysaccharide (LPS) in conditioned CBSC media was significantly lower than cells treated only with INF-γ and LPS. Blocking the IL-4 receptor on the BMDMs with a monoclonal antibody in conditioned media decreased CD206 expression, increased CD86 expression, and failed to mitigate the activation elicited by INF-γ and LPS. Exposing the BMDMs to conditioned media also increased the amount of the anti-inflammatory cytokine IL-1 receptor antagonist (IL1-RA) released compared to controls, matching previous data from a swine-model of MI that showed increased IL-1RA blood levels in CBSC-treated swine 72 hours post-MI. Together these data implicate IL-4 as a possible mechanism through which CBSCs influence the inflammatory response raised to MI. Conclusion: Soluble factors secreted by CBSCs change the phenotype of immune cells in vitro and in vivo . A possible mechanism for the beneficial effects of CBSCs on cardiac wound healing after MI may come from their ability to modulate the monocyte/macrophage response to preserve cardiac structure and function.
Evaluation of the Inclusion of Studies Identified by the FDA as Having Falsified Data in the Results of Meta-analyses
Authors: Craig A. Garmendia, Liliana Nassar Gorra, Ana Lucia Rodriguez, Mary Jo Trepka, Emir Veledar, Purnima Madhivanan
Journal: JAMA Internal Medicine (2019)

Discussion | Discharge instructions were translated by the new GT algorithm with higher accuracy and fewer seriously harmful inaccuracies than previously, 2 yet 2% of Spanish and 8% of Chinese sentence translations had potential for significant harm.While GT can supplement (not replace) written English instructions, machine-translated instructions should include a warning about potentially inaccurate translations.Clinicians using GT can reduce potential harm by having patients read translations while receiving verbal instructions; being vigilant about spelling and grammar; and avoiding complicated grammar, medical jargon (eg, fingerstick), and colloquial English.Study limitations include assessment of only 2 languages (though our inclusion of Chinese is a strength, since non-European languages are often less accurately translated by machines); no assessment of translation readability; and no comparison to human translators.Google Translate can be used to translate clinicianentered, patient-specific ED instructions for Spanish-and Chinese-speaking patients.Potential for harm can be minimized by using clear communication practices.
ASSOCIATION OF TRICUSPID REGURGITATION WITH LONG-TERM OUTCOMES IN PATIENTS WITH PULMONARY HYPERTENSION
Authors: Jun Mukai, Hidekazu Tanaka, Hiroyuki Sano, Kentaro Yamashita, Yusuke Tanaka, Ayu Shono, Makiko Suzuki, Sachiko Yoshikawa, Keiko Sumimoto, Nao Shibata, Shun Yokota, Makiko Suto, Fumitaka Soga, Hiroki Takada, Kumiko Dokuni, Keiko Hatazawa, Eriko Hisamatsu, Kensuke Matsumoto, Kazuhiko Nakayama, Noriaki Emoto, Ken-Ichi Hirata
Journal: Journal of the American College of Cardiology (2019)
COST OF HOSPITALIZATION TRENDS FOLLOWING PERCUTANEOUS CORONARY INTERVENTION IN THE UNITED STATES
Authors: Mohamed M. Gad, Keerat Rai Ahuja, Najdat Bazarbashi, Antonette Karrthik, Yasser Sammour, Manpreet Kaur, Kamalpreet Dhaliwal, Amer Kadri, Samir Kapadia
Journal: Journal of the American College of Cardiology (2019)
METABOLOMIC INVESTIGATION OF LONG-TERM RISK OF MAJOR ADVERSE CARDIOVASCULAR EVENTS IN A COMMUNITY-BASED COHORT (HEART SCORE) STUDY
Authors: Nnadozie Emechebe, Anh Thy Nguyen, Linh Duong, Kevin Kip, Ahmad Masri, Sebhat Erqou, Steven Reis
Journal: Journal of the American College of Cardiology (2019)
Clinical Outcomes of Weekly Prophylaxis with rFVIIIFc: Longitudinal Analysis of the A-LONG and ASPIRE Study Population
Authors: Amy D. Shapiro, Alok Srivastava, Margaret V. Ragni, Ingrid Pabinger, Stefan Lethagen, Elisa Tsao, Desilu Glazebrook, Doris Quon
Journal: Blood (2017)
TREATMENT OF MORBID OBESITY IS ASSOCIATED WITH WEIGHT-DEPENDENT 1-YEAR CHANGES IN BIOMARKERS OF INFLAMMATION AND SUBCLINICAL MYOCARDIAL INJURY
Authors: Kristin Moberg Aakre, Torbjorn Omland, Njord Nordstrand, Espen S. Gjevestad, Eirik Ikdahl, Jøran Hjelmesæth
Journal: Journal of the American College of Cardiology (2019)
VERY LOW PREVALENCE OF NORMAL GLUCOSE METABOLISM IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION IN THE CURRENT ERA
Authors: Kazuoki Dai, Kazuki Suruga, Takayuki Nakano, Hajime Takemoto, Yu Hashimoto, Syunsuke Tomomori, Tadanao Higaki, Kuniomi Oi, Tomoharu Kawase, Yasuharu Nakama, Kazuyoshi Suenari, Kenji Nishioka, Masaya Otsuka, Yoshiko Masaoka, Nobuo Shiode, Yasuki Kihara
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF ULTRA-CONSERVATIVE IMPLANTABLE CARDIOVERTER DEFIBRILLATOR PROGRAMMING IN PATIENTS WITH LEFT VENTRICULAR ASSIST DEVICES: AVOIDING UNNECESSARY TACHY-THERAPIES
Authors: Alexander Robinson, Valay Parikh, Mohammad-Ali Jazayeri, Michael Pierpoline, Madhu Reddy, Martin Emert, Rhea Pimentel, Raghuveer Dendi, Loren Berenbom, Katie Christensen, Andrew Sauer, Zubair Shah, Nicholas Haglund, Travis Abicht, Seth Sheldon
Journal: Journal of the American College of Cardiology (2019)
Exploring the Mechanisms of Thalassemic Erythropoiesis Improvement Caused By Bone Marrow Tfr2 Deletion
Authors: Antonella Nai, Irene Artuso, Maria Rosa Lidonnici, Sandro Altamura, Giacomo Mandelli, Mariateresa Pettinato, Martina U. Muckenthaler, Laura Silvestri, Giuliana Ferrari, Clara Camaschella
Journal: Blood (2018)