tbuckley/cabot-search huggingface dataset:
Abstract 18854: Long-term Follow-up After Percutaneous Left Atrial Appendage Ligation With the Lariat Device
Authors: Carola Gianni, Luigi Di Biase, Sanghamitra Mohanty, Chintan Trivedi, Yalçin Gökoglan, Mahmut Günes, Rong Bai, J D Burkhardt, Rodney Horton, Andrew Krumerman, Eugene Palma, Douglas Gibson, Matthew J Price, Miguel Valderrabano, Dhanunjaya Lakkireddy, Andrea Natale
Journal: Circulation (2015)

Introduction: The objective of this retrospective multicenter study is to report the initial long-term performance results after percutaneous exclusion of the LAA with the endo-epicardial Lariat device to prevent AF-related thromboembolic events. Methods and results: Patients with successful LAA ligation and at least 1-year follow-up were analyzed (N=355). At 1 year, TEE follow-up was present in 172 patients. A leak was defined as presence of flow into the LAA as assessed by TEE. At 6 months, 19 (11%) patients had a leak; 2 strokes occurred: 1 in a patient without a leak and 1 associated with mesenteric ischemia in a patient without a known acute leak, who died before repeat TEE could be performed. At 12 months, 34 (20%) patients had a leak; 6 patients developed a neurological event (5 strokes and 1 TIA), 4 in patients with a leak, 2 in patients without a leak. 3% were followed-up for more than one 1 year (with a mean of 21±9 months). 1 additional thromboembolic event (TIA) occurred 14 months post-implant in a patient without anticoagulation and with a partially excluded LAA (stump), although no leak or thrombus were detected on standard TEE. Among patients with a leak (36% of those with long-term follow-up), 75% were on long-term anticoagulation and no additional TE events were detected. Out of 355 patients, 9 (2.5%) patients had a neurological event: 4 with a leak, 4 without a leak and 1 in a patient where TEE was not repeated. Considering those with known LAA status, thromboembolic events were more common in patients with a leak (4/34 vs 4/136; RR 4, 95% CI 1.1-15.4). Conclusion: In this multicenter experience with the Lariat device, the rate of leaks was high (20% of those with TEE follow-up at 1 year). Thromboembolic events were not rare (overall, 2.5%), and occurred more frequently in patients with a leak (RR 4).
Cotargeting Ephrin Receptor Tyrosine Kinases A2 and A3 in Cancer Stem Cells Reduces Growth of Recurrent Glioblastoma
Authors: Maleeha A. Qazi, Parvez Vora, Chitra Venugopal, Jarrett Adams, Mohini Singh, Amy Hu, Maryna Gorelik, Minomi K. Subapanditha, Neil Savage, Jiahe Yang, Chirayu Chokshi, Max London, Alexander Gont, David Bobrowski, Natalie Grinshtein, Kevin R. Brown, Naresh K. Murty, Johan Nilvebrant, David Kaplan, Jason Moffat, Sachdev Sidhu, Sheila K. Singh
Journal: Cancer Research (2018)

Abstract Glioblastoma (GBM) carries a dismal prognosis and inevitably relapses despite aggressive therapy. Many members of the Eph receptor tyrosine kinase (EphR) family are expressed by GBM stem cells (GSC), which have been implicated in resistance to GBM therapy. In this study, we identify several EphRs that mark a therapeutically targetable GSC population in treatment-refractory, recurrent GBM (rGBM). Using a highly specific EphR antibody panel and CyTOF (cytometry by time-of-flight), we characterized the expression of all 14 EphR in primary and recurrent patient-derived GSCs to identify putative rGBM-specific EphR. EPHA2 and EPHA3 coexpression marked a highly tumorigenic cell population in rGBM that was enriched in GSC marker expression. Knockdown of EPHA2 and EPHA3 together led to increased expression of differentiation marker GFAP and blocked clonogenic and tumorigenic potential, promoting significantly higher survival in vivo. Treatment of rGBM with a bispecific antibody against EPHA2/A3 reduced clonogenicity in vitro and tumorigenic potential of xenografted recurrent GBM in vivo via downregulation of AKT and ERK and increased cellular differentiation. In conclusion, we show that EPHA2 and EPHA3 together mark a GSC population in rGBM and that strategic cotargeting of EPHA2 and EPHA3 presents a novel and rational therapeutic approach for rGBM. Significance: Treatment of rGBM with a novel bispecific antibody against EPHA2 and EPHA3 reduces tumor burden, paving the way for the development of therapeutic approaches against biologically relevant targets in rGBM. Cancer Res; 78(17); 5023–37. ©2018 AACR.
Data Sharing—The Time Has (Not Yet?) Come
Authors: Clyde W. Yancy, Robert A. Harrington, Robert O. Bonow
Journal: JAMA Cardiology (2018)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Cardiology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Cardiology journal
Eosinophils suppress Th1 responses and restrict bacterially induced gastrointestinal inflammation
Authors: Isabelle C. Arnold, Mariela Artola-Borán, Paulino Tallón de Lara, Andreas Kyburz, Christian Taube, Karen Ottemann, Maries van den Broek, Shida Yousefi, Hans-Uwe Simon, Anne Müller
Journal: The Journal of Experimental Medicine (2018)

Eosinophils are predominantly known for their contribution to allergy. Here, we have examined the function and regulation of gastrointestinal eosinophils in the steady-state and during infection with Helicobacter pylori or Citrobacter rodentium We find that eosinophils are recruited to sites of infection, directly encounter live bacteria, and activate a signature transcriptional program; this applies also to human gastrointestinal eosinophils in humanized mice. The genetic or anti-IL-5-mediated depletion of eosinophils results in improved control of the infection, increased inflammation, and more pronounced Th1 responses. Eosinophils control Th1 responses via the IFN-γ-dependent up-regulation of PD-L1. Furthermore, we find that the conditional loss of IFN-γR in eosinophils phenocopies the effects of eosinophil depletion. Eosinophils further possess bactericidal properties that require their degranulation and the deployment of extracellular traps. Our results highlight two novel functions of this elusive cell type and link it to gastrointestinal homeostasis and anti-bacterial defense.
Coronary Atherosclerosis and Myocardial Infarction in Autopsied Patients in Gondar, Ethiopia
Authors: M Maru
Journal: Journal of the Royal Society of Medicine (1989)

Autopsy study of 124 Ethiopian patients for atherosclerotic lesions and myocardial infarction revealed aortic lesions in 58 (47%), coronary lesions in 26 (21%) and myocardial infarction in 8 (6.5%) cases. Fatty streaks in the coronary arteries were detected after the age of 19 years. Thereafter the frequency increased gradually with age reaching a peak of 33.3% by the age group of 50-59 years. Fibrous plaque appeared at the age of 40 years and progressed with age reaching a maximum of 44.4% by the age of 60-69 years. Myocardial infarction was the cause of sudden death in two cases. Six of the patients with myocardial infarction had moderate to severe lesions. Calcification with narrowing of the left anterior descending coronary artery was found in a 60-year-old female. The significance of the increasing incidence of CHD in black Africans and particularly in Ethiopians is discussed.
Baseline Characteristics of the Vitamin D and Type 2 Diabetes (D2d) Study: A Contemporary Prediabetes Cohort That Will Inform Diabetes Prevention Efforts
Authors: Erin S. LeBlanc, Richard E. Pratley, Bess Dawson-Hughes, Myrlene A. Staten, Patricia R. Sheehan, Michael R. Lewis, Anne Peters, Sun H. Kim, Ranee Chatterjee, Vanita R. Aroda, Chhavi Chadha, Lisa M. Neff, Irwin G. Brodsky, Clifford Rosen, Cyrus V. Desouza, John P. Foreyt, Daniel S. Hsia, Karen C. Johnson, Philip Raskin, Sangeeta R. Kashyap, Patrick O’Neil, Lawrence S. Phillips, Neda Rasouli, Emilia P. Liao, David C. Robbins, Anastassios G. Pittas, Erin S. LeBlanc, Richard E. Pratley, Bess Dawson-Hughes, Myrlene A. Staten, Patricia R. Sheehan, Michael R. Lewis, Anne Peters, Sun H. Kim, Ranee Chatterjee, Vanita R. Aroda, Chhavi Chadha, Lisa M. Neff, Irwin G. Brodsky, Clifford Rosen, Cyrus V. Desouza, John P. Foreyt, Daniel S. Hsia, Karen C. Johnson, Philip Raskin, Sangeeta R. Kashyap, Patrick O’Neil, Lawrence S. Phillips, Neda Rasouli, Emilia P. Liao, David C. Robbins, Anastassios G. Pittas
Journal: Diabetes Care (2018)

To describe baseline characteristics of the Vitamin D and Type 2 Diabetes (D2d) study, the first large U.S. diabetes prevention clinical trial to apply current American Diabetes Association (ADA) criteria for prediabetes.
The NHS at 70: many happy returns?
Authors: Sophie Cook
Journal: BMJ (2018)

It is right to celebrate the NHS’s 70th anniversary. It is admired beyond the UK and has weathered many restructures, adapted to medical advances, and managed a growing population with longer life expectancy, all while coping with increasing financial strain. On 5 July we can light the candles, raise a glass, cut the cake, or otherwise mark this historic occasion.

While celebrating the achievements we can’t ignore the widening cracks. Despite its overall top performance in an influential international comparison last year, in terms of outcomes the NHS has fallen in global rankings.1 And we shouldn’t take for granted …
Retrosigmoid Versus Traditional Ileal Conduit for Urinary Diversion After Radical Cystectomy
Authors: Vincenzo Ficarra, Gianluca Giannarini, Alessandro Crestani, Vito Palumbo, Marta Rossanese, Claudio Valotto, Antonino Inferrera, Vito Pansadoro
Journal: European Urology (2018)
Self-repopulating recipient bone marrow resident macrophages promote long-term hematopoietic stem cell engraftment
Authors: Simranpreet Kaur, Liza J. Raggatt, Susan M. Millard, Andy C. Wu, Lena Batoon, Rebecca N. Jacobsen, Ingrid G. Winkler, Kelli P. MacDonald, Andrew C. Perkins, David A. Hume, Jean-Pierre Levesque, Allison R. Pettit
Journal: Blood (2018)
Risk-stratified clinical management of superficially invasive esophageal squamous cell carcinoma after endoscopic resection: finding the sweet spot
Authors: Marnix Jansen, Jacques Bergman
Journal: Endoscopy (2018)

See also: Management decision based on lymphovascular involvement leads to favorable outcomes after endoscopic treatment of esophageal squamous cell carcinomaEndoscopy eFirstDOI: 10.1055/s-0043-124433
Targeting ERBB2 mutations in solid tumors: biological and clinical implications
Authors: Sophie Cousin, Emmanuel Khalifa, Amandine Crombe, Yech’an Laizet, Carlo Lucchesi, Maud Toulmonde, Sylvestre Le Moulec, Céline Auzanneau, Isabelle Soubeyran, Antoine Italiano
Journal: Journal of Hematology & Oncology (2018)

Preclinical data have shown that ERBB2 activating mutations are responsive to HER2 tyrosine kinase inhibitors. The aim of this study is to characterize the landscape of ERBB2 mutations in solid tumors and the potential efficacy of ERBB2 targeting.We analyzed the next-generation sequencing results from 17,878 patients with solid tumors and reported the outcome of 4 patients with advanced ERBB2-mutated tumors treated with a combination of trastuzumab and lapatinib.ERBB2 mutations occurred in 510 patients (2.85%). The tumor types with the highest incidence of ERBB2 mutations were the following: bladder (16.6%), small bowel (8.6%), ampullar (6.5%), skin non-melanoma (6.1%), and cervical cancer (5.5%). 49.4% (n = 282) were known as activating mutations. ERBB2 mutation was not mutually exclusive of ERBB2 amplification which occurred in up to 10% of cases. PI3KCA activating mutations were associated with ERBB2 mutations in 12.4% of cases mainly in breast and lung cancer. Four patients (endometrial, colorectal, cholangiocarcinoma, and adenosarcoma of the uterus) were treated with a combination of trastuzumab and lapatinib. All of them experienced tumor shrinkage resulting in stable disease in three cases and partial response in one case. One patient developed secondary resistance. Sequencing of the progressing metastasis allowed the identification of the ERBB2 L869R mutation previously associated with resistance to lapatinib in vitro.These results support further clinical investigation aiming to demonstrate that ERBB2-mutational driven therapy can improve patient care irrespective of histology.
Successful endoscopic removal of fractured guidewire fragments from a peripheral bile duct using a biliary stent delivery system and biopsy forceps
Authors: Yoshihiro Nishikawa, Norimitsu Uza, Yuki Yamauchi, Akihisa Fukuda, Yoshihide Ueda, Yuzo Kodama, Hiroshi Seno
Journal: Endoscopy (2018)

A 61-year-old man with sclerosing cholangitis was referred to our hospital. Blood tests on admission suggested he had acute cholangitis. An abdominal radiograph revealed, in addition to two plastic biliary stents, a foreign body in the upper abdominal area, which appeared to be a fractured guidewire fragment in a peripheral bile duct that had remained after endoscopic retrograde cholangiopancreatography (ERCP) performed at the previous hospital ([Fig. 1]).
Genome Editing of Induced Pluripotent Stem Cells to Decipher Cardiac Channelopathy Variant
Authors: Priyanka Garg, Angelos Oikonomopoulos, Haodong Chen, Yingxin Li, Chi Keung Lam, Karim Sallam, Marco Perez, Robert L. Lux, Michael C. Sanguinetti, Joseph C. Wu
Journal: Journal of the American College of Cardiology (2018)
An Anti–CLL-1 Antibody–Drug Conjugate for the Treatment of Acute Myeloid Leukemia
Authors: Bing Zheng, Shang-Fan Yu, Geoffrey del Rosario, Steven R. Leong, Genee Y. Lee, Rajesh Vij, Cecilia Chiu, Wei-Ching Liang, Yan Wu, Cecile Chalouni, Jack Sadowsky, Vanessa Clark, Angela Hendricks, Kirsten Achilles Poon, Wayne Chu, Thomas Pillow, Melissa M. Schutten, John Flygare, Andrew G. Polson
Journal: Clinical Cancer Research (2018)

The treatment of acute myeloid leukemia (AML) has not significantly changed in 40 years. Cytarabine- and anthracycline-based chemotherapy induction regimens (7 + 3) remain the standard of care, and most patients have poor long-term survival. The reapproval of Mylotarg, an anti-CD33-calicheamicin antibody-drug conjugate (ADC), has demonstrated ADCs as a clinically validated option to enhance the effectiveness of induction therapy. We are interested in developing a next-generation ADC for AML to improve upon the initial success of Mylotarg.The expression pattern of CLL-1 and its hematopoietic potential were investigated. A novel anti-CLL-1-ADC, with a highly potent pyrrolobenzodiazepine (PBD) dimer conjugated through a self-immolative disulfide linker, was developed. The efficacy and safety profiles of this ADC were evaluated in mouse xenograft models and in cynomolgus monkeys.We demonstrate that CLL-1 shares similar prevalence and trafficking properties that make CD33 an excellent ADC target for AML, but lacks expression on hematopoietic stem cells that hampers current CD33-targeted ADCs. Our anti-CLL-1-ADC is highly effective at depleting tumor cells in AML xenograft models and lacks target independent toxicities at doses that depleted target monocytes and neutrophils in cynomolgus monkeys.Collectively, our data suggest that an anti-CLL-1-ADC has the potential to become an effective and safer treatment for AML in humans, by reducing and allowing for faster recovery from initial cytopenias than the current generation of ADCs for AML.
Abstract 18517: GCN2 Dysfunction at the Heart of Pulmonary Veno-Occlusive Disease Development
Authors: Fabrice Antigny, Esther J Nossent, Melanie Lambert, Benoit Ranchoux, David Montani, Barbara Girerd, Florent Soubrier, Florence Lecerf, Harm J Bogaard, Elie Fadel, Gérald Simonneau, Anton Vonk Noordegraaf, Katrien Grünberg, Marc Humbert, Peter Dorfmüller, Frederic Perros
Journal: Circulation (2016)

Background: We identified autosomal recessive bi-allelic mutations in the EIF2AK4 gene (coding for GCN2) as the major genetic cause of pulmonary veno-occlusive disease (PVOD). Recently, we created ...
Response to: ‘Infrapatellar fat pad resection during total knee replacement: yet another reason?’ by Ryan
Authors: Zhaohua Zhu, Weiyu Han, Guangfeng Ruan, Shuang Zheng, Changhai Ding
Journal: Annals of the Rheumatic Diseases (2018)

We thank Ryan1 for the interest in our original paper2 and response3 regarding to the associations between infrapatellar fat pad (IPFP) maximal area and knee osteoarthritic measures including symptoms and structural changes.

Our previous studies revealed that IPFP maximal area and volume were associated with reduced knee pain, decreased loss of cartilage volume and reduced risks of cartilage defect progression, indicating a beneficial effect of IPFP size.2 4 On the other hand, our further investigation demonstrated that IPFP signal intensity alteration was negatively associated with maximum area of IPFP and, moreover, associated with increased knee cartilage defects, subchondral bone marrow lesions and knee pain, suggesting IPFP with abnormal quality may play a detrimental role in knee osteoarthritis (OA).5 

Based on these findings, we proposed that IPFP with normal qualities, rather than abnormal …
Failing to encourage physical activity with wearable technology: what next?
Authors: David A Ellis, Lukasz Piwek
Journal: Journal of the Royal Society of Medicine (2018)

Wearable devices and associated systems that provide real-time feedback aim to encourage healthy behaviours. However, while the research base has grown considerably, results continue to paint a mixed picture when demonstrating wearables’ ability to increase levels of physical activity. Given these recent developments, this commentary explores the key reasons why wearable devices and other mobile technologies often fail to change behaviour. We also provide several suggestions that could feed into future research designs and maximise the success of subsequent interventions. These recommendations aim to stimulate interdisciplinary discussions by encouraging clinicians and researchers to consider how these technological advances can be effectively leveraged, and become a core component of preventative medicine in the 21st century.
Inosine Monophosphate Dehydrogenase Dependence in a Subset of Small Cell Lung Cancers
Authors: Fang Huang, Min Ni, Milind D. Chalishazar, Kenneth E. Huffman, Jiyeon Kim, Ling Cai, Xiaolei Shi, Feng Cai, Lauren G. Zacharias, Abbie S. Ireland, Kailong Li, Wen Gu, Akash K. Kaushik, Xin Liu, Adi F. Gazdar, Trudy G. Oliver, John D. Minna, Zeping Hu, Ralph J. DeBerardinis
Journal: Cell Metabolism (2018)
Abstract 12145: Remote Ischemic Preconditioning Regulates Post-resuscitation Microcirculation via A KAtp Channel-dependent Mechanism in a Rat Model of Cardiac Arrest
Authors: Shen Zhao, Ziren Tang, Jiangang Wang, Zhengfei Yang, Feng Chen, Mary A Peberdy, Joseph P Ornato, Wanchun Tang
Journal: Circulation (2016)

Introduction: Remote ischemic preconditioning (RIPC) provides potent protection to tissue microcirculation against ischemic-reperfusion injury. However, the underlying microvascular mechanism of RI...
Abstract 3099: Hydrocarbon carcinogenicity reexamined: An extremly potent direct-acting mutagen is common to smoke, soot and ash from a variety of combustion sources, including cigarette tobacco
Authors: Gary R. Blackburn
Journal: Cancer Research (2018)

Abstract Percivall Pott (1714-1788), an English surgeon, is generally credited with being the first to suggest that cancer may be induced by exposure to environmental carcinogens – in his case, cancer of the scrotum in London chimney sweeps occupationally exposed to soot. It is perhaps not surprising, therefore, that combustion products became a primary focus of later research into the mechanisms of chemical carcinogenesis. Early on, those studies pointed toward a particular class of compounds as being primarily responsible for cancer induction by such materials, a group of environmentally ubiquitous compounds called polycyclic aromatic hydrocarbons, or PAHs. One such PAH, benzo[a]pyrene (BaP), is perhaps the most studied compound in all of cancer research. While there is little doubt that BaP and its congeners are the primary carcinogens in incomplete combustion products like coal tar, their concentrations in other hydrocarbon mixtures are too low to fully account for their overall carcinogenic potency. It is possible that other factors such as tumor promotion contribute to the additional potency, but it might also be expected that there are significant contributions from nitro-PAH derivatives, in particular the isomers of dinitropyrene (DNP) found in carbon black, diesel exhaust and other combustion products. One such isomer, 1,6-dinitropyrene was shown by Iwagawa et al. to have three-times the carcinogenic potency of BaP when injected directly into the lungs of rats. In order to indirectly test nitroaromatic contribution to combustion product carcinogenicity, extracts of smoke soot, ash and food products exposed to smoke during processing were fractionated by HPLC, and the fractions tested in the Ames Test without metabolic activation. All showed a common peak of extremely potent direct-acting mutagenicity at a retention time similar to that of dinitropyrene. Efforts are currently underway to fully characterize the mutagen by a combination of standard analytical means. Citation Format: Gary R. Blackburn. Hydrocarbon carcinogenicity reexamined: An extremly potent direct-acting mutagen is common to smoke, soot and ash from a variety of combustion sources, including cigarette tobacco [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3099.
Association Between Population Density and Genetic Risk for Schizophrenia
Authors: Lucía Colodro-Conde, Baptiste Couvy-Duchesne, John B. Whitfield, Fabian Streit, Scott Gordon, Kathryn E. Kemper, Loic Yengo, Zhili Zheng, Maciej Trzaskowski, Eveline L. de Zeeuw, Michel G. Nivard, Marjolijn Das, Rachel E. Neale, Stuart MacGregor, Catherine M. Olsen, David C. Whiteman, Dorret I. Boomsma, Jian Yang, Marcella Rietschel, John J. McGrath, Sarah E. Medland, Nicholas G. Martin
Journal: JAMA Psychiatry (2018)

Urban life has been proposed as an environmental risk factor accounting for the increased prevalence of schizophrenia in urban areas. An alternative hypothesis is that individuals with increased genetic risk tend to live in urban/dense areas.