tbuckley/cabot-search huggingface dataset:
Downloadable Software Algorithm Reduces Inappropriate Shocks Caused by Implantable Cardioverter-Defibrillator Lead Fractures
Authors: Charles D. Swerdlow, Bruce D. Gunderson, Kevin T. Ousdigian, Athula Abeyratne, Haresh Sachanandani, Kenneth A. Ellenbogen
Journal: Circulation (2010)

Background— Downloadable software upgrades are common in consumer electronics but not in implantable medical devices. Fractures of implantable cardioverter-defibrillator (ICD) leads present commonly as inappropriate shocks. A lead-integrity alert (LIA) designed to reduce inappropriate shocks is the first software download approved to enhance nominally functioning, previously implanted ICDs. Methods and Results— We performed a prospective study to determine whether an LIA could reduce inappropriate shocks. Patients were included if they had ICD lead fractures confirmed by analysis of explanted leads. The LIA group included the first 213 patients who met the inclusion criteria after the LIA was approved who had the LIA downloaded. The LIA is triggered either by high impedance or rapid oversensing. It responds by delaying detection of ventricular fibrillation and initiating a patient alert every 4 hours. The control group included the first 213 patients who did not have the LIA downloaded. They were monitored by conventional daily impedance measurements that respond with a daily alert. The LIA group had a 46% relative reduction (95% confidence interval 34% to 55%) in the percentage of patients with ≥1 inappropriate shock (LIA 38% versus control 70%, P &lt;0.001) and a 50% relative reduction (95% confidence interval 33% to 61%) in the percentage with ≥5 shocks (25% versus 50%, P &lt;0.001). The LIA group also had a higher percentage of patients who either did not receive a shock or had ≥3 days of warning before the shock (72% versus 50%, P &lt;0.001). Conclusions— A software download that upgrades previously implanted ICDs without surgical revision reduces inappropriate shocks caused by lead fractures.
a Feasibility Study of the Full Outpatient Conduction of Hematopoietic Transplants in Persons with Multiple Sclerosis Employing Autologous Non-Cryopreserved Peripheral Blood Stem Cells
Authors: Guillermo J. Ruiz-Arguelles, Andrés A. León-Peña, Mónica León-Gonzalez, Ana Karen Núñez-Cortés, Merari Starlight Torres-Priego, Jocelyn Vargas-Espinosa, Emilio Medina-Ceballos, Alejandro Ruiz-Arguelles, Manuel Alejandro Ruiz-Delgado, Rodrigo J Ruiz-Delgado, Guillermo Ruiz-Reyes, Manuel Priesca-Marin, David Blumenkron-Marroquin, Guillermo J Ruiz-Delgado
Journal: Blood (2016)
Cold-induced conversion of cholesterol to bile acids in mice shapes the gut microbiome and promotes adaptive thermogenesis
Authors: Anna Worthmann, Clara John, Malte C Rühlemann, Miriam Baguhl, Femke-Anouska Heinsen, Nicola Schaltenberg, Markus Heine, Christian Schlein, Ioannis Evangelakos, Chieko Mineo, Markus Fischer, Maura Dandri, Claus Kremoser, Ludger Scheja, Andre Franke, Philip W Shaul, Joerg Heeren
Journal: Nature Medicine (2017)
Inhibition of MicroRNA-146a and Overexpression of Its Target Dihydrolipoyl Succinyltransferase Protect Against Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction
Authors: Ward A. Heggermont, Anna-Pia Papageorgiou, Annelies Quaegebeur, Sophie Deckx, Paolo Carai, Wouter Verhesen, Guy Eelen, Sandra Schoors, Rick van Leeuwen, Sergey Alekseev, Ies Elzenaar, Stefan Vinckier, Peter Pokreisz, Ann-Sophie Walravens, Rik Gijsbers, Chris Van Den Haute, Alexander Nickel, Blanche Schroen, Marc van Bilsen, Stefan Janssens, Christoph Maack, Yigal Pinto, Peter Carmeliet, Stephane Heymans
Journal: Circulation (2017)

Cardiovascular diseases remain the predominant cause of death worldwide, with the prevalence of heart failure continuing to increase. Despite increased knowledge of the metabolic alterations that occur in heart failure, novel therapies to treat the observed metabolic disturbances are still lacking.Mice were subjected to pressure overload by means of angiotensin-II infusion or transversal aortic constriction. MicroRNA-146a was either genetically or pharmacologically knocked out or genetically overexpressed in cardiomyocytes. Furthermore, overexpression of dihydrolipoyl succinyltransferase (DLST) in the murine heart was performed by means of an adeno-associated virus.MicroRNA-146a was upregulated in whole heart tissue in multiple murine pressure overload models. Also, microRNA-146a levels were moderately increased in left ventricular biopsies of patients with aortic stenosis. Overexpression of microRNA-146a in cardiomyocytes provoked cardiac hypertrophy and left ventricular dysfunction in vivo, whereas genetic knockdown or pharmacological blockade of microRNA-146a blunted the hypertrophic response and attenuated cardiac dysfunction in vivo. Mechanistically, microRNA-146a reduced its target DLST-the E2 subcomponent of the α-ketoglutarate dehydrogenase complex, a rate-controlling tricarboxylic acid cycle enzyme. DLST protein levels significantly decreased on pressure overload in wild-type mice, paralleling a decreased oxidative metabolism, whereas DLST protein levels and hence oxidative metabolism were partially maintained in microRNA-146a knockout mice. Moreover, overexpression of DLST in wild-type mice protected against cardiac hypertrophy and dysfunction in vivo.Altogether we show that the microRNA-146a and its target DLST are important metabolic players in left ventricular dysfunction.
Home Monitoring of Patients with Cystic Fibrosis to Identify and Treat Acute Pulmonary Exacerbations. eICE Study Results
Authors: Noah Lechtzin, Nicole Mayer-Hamblett, Natalie E. West, Sarah Allgood, Ellen Wilhelm, Umer Khan, Moira L. Aitken, Bonnie W. Ramsey, Michael P. Boyle, Peter J. Mogayzel, Ronald L. Gibson, David Orenstein, Carlos Milla, John P. Clancy, Veena Antony, Christopher H. Goss, Lynne Quittell, Patrick A. Flume, Shannon S. Carson, John Conlon, Susan Banks-Schlegel, Kelli Joubran, Elena Mullin, Kathy Seidel, Dionne Howe, Noah Lechtzin, Veena Antony, Scott Donaldson, Susanna McColley, John Clancy, Elliott Dasenbrook, Karen McCoy, Jerry Nick, Frank Accurso, Richard Ahrens, Joanne Billings, Carlos Milla, David Orenstein, Ronald L. Gibson, Christopher H. Goss
Journal: American Journal of Respiratory and Critical Care Medicine (2017)

Individuals with cystic fibrosis (CF) experience frequent acute pulmonary exacerbations, which lead to decreased lung function and reduced quality of life.The goal of this study was to determine if an intervention directed toward early detection of pulmonary exacerbations using home spirometry and symptom monitoring would result in slower decline in lung function than in control subjects.We conducted a multicenter, randomized trial at 14 CF centers with subjects at least 14 years old. The early intervention arm subjects measured home spirometry and symptoms electronically twice per week. Sites were notified if a participant met criteria for an exacerbation and contacted participants to determine if treatment for acute exacerbation was required. Participants in the usual care arm were seen every 3 months and were asked to contact the site if they were concerned about worsening pulmonary symptoms.The primary outcome was the 52-week change in FEV1. Secondary outcomes included time to first exacerbation and subsequent exacerbation, quality of life, and change in weight. A total of 267 patients were randomized, and the study arms were well matched at baseline. There was no significant difference between study arms in 52-week mean change in FEV1 slope (mean slope difference, 0.00 L, 95% confidence interval, -0.07 to 0.07; P = 0.99). The early intervention arm subjects detected exacerbations more frequently than usual care arm subjects (time to first exacerbation hazard ratio, 1.45; 95% confidence interval, 1.09 to 1.93; P = 0.01). Adverse events were not significantly different between treatment arms.An intervention of home monitoring among patients with CF was able to detect more exacerbations than usual care, but this did not result in slower decline in lung function. Clinical trial registered with www.clinicaltrials.gov (NCT01104402).
Use of Adjuvant Chemotherapy After Surgery in Patients With Colon Cancer—Reply
Authors: Kangmin Zhu, Janna Manjelievskaia, Craig D. Shriver
Journal: JAMA Surgery (2017)

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 Surgery 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 Surgery journal
CHAPTER XI: Morbidity and Mortality
Journal: Circulation (1973)

A comparison of morbidity and mortality following urokinase and heparin infusions showed few differences between the two treatment groups, other than an increased incidence of bleeding at cutdown sites during urokinase infusion. The incidence of recurrent pulmonary embolism among patients in both treatment groups was greater if they received inadequate anticoagulant therapy.
Outcome of neoadjuvant-treated young patients with hormone receptor-positive breast cancer.
Authors: Cynthia Mayte Villarreal-Garza, Claudia Arce-Salinas, Federico Lasa, Nancy Reynoso, Juan Antonio Matus, Fernando Lara-Medina, Enrique Bargallo-Rocha, Diana Fabiola Flores Diaz, Robin J. Shaw, Alberto Alvarado-Miranda, Noel Jaime Castañeda, Bertha Alejandra Martinez-Cannon, Alejandro Mohar
Journal: Journal of Clinical Oncology (2015)

e11577 Background: Although late-stage at diagnosis and aggressive histologic subtypes partially explain the poor prognosis in young women with breast cancer (BC), other biological differences may dictate patients’ outcomes. The purpose of our study was to compare the recurrence-free survival (RFS) among neoadjuvant-treated patients according to age and histologic subtypes. Methods: All consecutive patients with BC diagnosed at the National Cancer Institute in Mexico between 2007-2013 were included. BC was classified as Hormone-receptor (HR)+ and HER2-, HER2+ and triple-negative (TN). The Chi-square test was used for comparison between groups according to age, [≤40 (young) vs. >40] and the association of clinical and histologic factors with RFS was assessed with Cox proportional hazard analysis. Results: Of the 3,110 included patients, 40% received neoadjuvant treatment and 18% were young. For neoadjuvant-treated patients there was no distribution difference in histologic subtypes between age groups. Although young patients achieved higher pathologic complete response (PCR) rates, the RFS interval was shorter at the expense of the HR+/HER2- subgroup. For patients with residual disease, young age remained a significant independent predictor of recurrence in patients with HR+/HER2- tumors, but not in the HER2+ and TN subtypes. Conclusions: The results of our present study suggest that the poor survival associated with young age in neoadjuvant-treated patients may be explained by the poor prognosis in the most prevalent HR+/HER2- subgroup. Possible explanations for this finding are a greater proportion of Luminal B BC, tamoxifen resistance or poor adherence to treatment. Further characterization of HR+ BC should be pursued and aggressive therapeutic strategies must be considered for treatment of young women with high-risk features. Neoadjuvant treated-patients ≤40 >40 HR p Total 228 (18%) 1013 (82%) % % Histologic subtype HR+/HER2- 46 51 0.29 HER2+ 29 28 TN 25 21 PCR 37 25 <0.001 PCR by subtype HR+/HER2- 26 28 0.12 HER2+ 35 46 TN 39 26 RFS 1.49 0.006 RFS by subtype HR+/HER2- 2.36 <0.001 HER2+ 1.00 0.98 TN 0.84 0.54 RFS with residual disease by subtype HR+/HER2- 1.94 0.01 HER2+ 0.87 0.76 TN 1.30 0.45
Relationship of the Breast Ductal Carcinoma <i>In Situ</i> Immune Microenvironment with Clinicopathological and Genetic Features
Authors: Shona Hendry, Jia-Min B. Pang, David J. Byrne, Sunil R. Lakhani, Margaret C. Cummings, Ian G. Campbell, G. Bruce Mann, Kylie L. Gorringe, Stephen B. Fox
Journal: Clinical Cancer Research (2017)

Abstract Purpose: The immune microenvironment of breast ductal carcinoma in situ (DCIS) has yet to be fully explored, and the relationship of immune cells to genetic features of DCIS is unknown. Experimental Design: We quantified tumor associated lymphocytes (TIL) and evaluated PD-L1 protein levels by immunohistochemistry in a cohort of pure DCIS (138 and 79 cases, respectively), some of which had copy number (n = 55) and mutation data (n = 20). Results: TILs were identified in the stroma surrounding DCIS (119/138, 86%) and present at a median TIL score of 5% (range, 0%–90%). Most DCIS were negative for tumor cell PD-L1 staining (89%), but 25% of cases were positive for immune cell staining. We observed that, as in invasive breast cancer, TILs and PD-L1 positivity were significantly greater in high-grade (P = 0.002/0.035), ER-negative (P = 0.02/0.02), and ERBB2-amplified tumors (P &amp;lt; 0.001/0.048). Comedo necrosis was significantly positively associated with TILs (P &amp;lt; 0.0001) but not with PD-L1. The TILs score was significantly higher in cases with TP53 mutation (P = 0.03) but not with PIK3CA or GATA3 mutation. In the cases with copy number data, both the fraction of the genome altered and the number of telomeric imbalances were significantly positively correlated with TILs (both P &amp;lt; 0.001). This result strongly contrasted with invasive breast cancer data, where aneuploidy was not correlated to TIL levels. Conclusions: Although a small cohort, our data suggest a preliminary model by which the progression of DCIS to invasive carcinoma may involve an altered relationship of tumor copy number with the immune microenvironment, possibly by the immunoediting of the tumor. Clin Cancer Res; 23(17); 5210–7. ©2017 AACR.
The Transcription Factor T-bet Limits Amplification of Type I IFN Transcriptome and Circuitry in T Helper 1 Cells
Authors: Shigeru Iwata, Yohei Mikami, Hong-Wei Sun, Stephen R. Brooks, Dragana Jankovic, Kiyoshi Hirahara, Atsushi Onodera, Han-Yu Shih, Takeshi Kawabe, Kan Jiang, Toshinori Nakayama, Alan Sher, John J. O’Shea, Fred P. Davis, Yuka Kanno
Journal: Immunity (2017)
Hepatitis B virus X protein–elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis
Authors: Yuen Gao, Jinyan Feng, Guang Yang, Shuqin Zhang, Yunxia Liu, Yanan Bu, Mingming Sun, Man Zhao, Fuquan Chen, Weiying Zhang, Lihong Ye, Xiaodong Zhang
Journal: Hepatology (2017)

Chronic hepatitis B virus (HBV) infection is a leading cause in the occurrence of hepatitis B, liver cirrhosis, and liver cancer, in which nuclear HBV covalently closed circular DNA (cccDNA), the genomic form that templates viral transcription and sustains viral persistence, plays crucial roles. In the present study, we explored the hypothesis that HBV X protein (HBx)‐elevated male‐specific lethal 2 (MSL2) activated HBV replication by modulating cccDNA in hepatoma cells, leading to hepatocarcinogenesis. Immunohistochemical analysis revealed that the expression of MSL2 was positively associated with that of HBV and was increased in the liver tissues of HBV‐transgenic mice and clinical HCC patients. Interestingly, microarray profiling identified that MSL2 was associated with those genes responding to the virus. Mechanistically, MSL2 could maintain HBV cccDNA stability through degradation of APOBEC3B by ubiquitylation in hepatoma cells. Above all, HBx accounted for the up‐regulation of MSL2 in stably HBx‐transfected hepatoma cell lines and liver tissues of HBx‐transgenic mice. Luciferase reporter gene assays revealed that the promoter region of MSL2 regulated by HBx was located at nucleotide −1317/−1167 containing FoxA1 binding element. Chromatin immunoprecipitation assay validated that HBx could enhance the binding property of FoxA1 to MSL2 promoter region. HBx up‐regulated MSL2 by activating YAP/FoxA1 signaling. Functionally, silencing MSL2 was able to block the growth of hepatoma cells in vitro and in vivo . Conclusion : HBx‐elevated MSL2 modulates HBV cccDNA in hepatoma cells to promote hepatocarcinogenesis, forming a positive feedback loop of HBx/MSL2/cccDNA/HBV. Our finding uncovers insights into the mechanism by which MSL2 as a promotion factor in host cells selectively activates extrachromosomal DNA. (H epatology 2017;66:1413–1429).
Епідеміологічні особливості запальних захворювань кишечника за даними ДУ «Інститут гастроентерології НАМНУ»
Authors: T.Y. Boyko
Journal: GASTROENTEROLOGY (2013)

Проведений ретроспективний аналіз історій хвороби 843 пацієнтів із неспецифічним виразковим колітом та 222 — із хворобою Крона, які знаходились на стаціонарному лікуванні в ДУ «Інститут гастроентерології НАМН України» із 2001 по 2011 р. Отримані дані свідчать про загальну тенденцію зростання числа запальних захворювань кишечника за останнє десятиріччя. Установлено вікові та гендерні особливості запальних захворювань кишечника в обстеженого контингенту хворих. Показано вплив урбанізації та соціального статусу на розвиток хвороби. Для визначення обсягу відповідної медичної допомоги цій категорії хворих та створення програми профілактики, ранньої діагностики, адекватної індукційної та підтримуючої терапії необхідне проведення повномасштабних епідеміологічних досліджень в усіх регіонах України.
Abstract P005: Direct Differentiation of Atrial and Ventricular Myocytes from Human Embryonic Stem Cells
Authors: Yue Ma
Journal: Circulation Research (2011)

Although cell transplantation studies have suggested promising therapeutic potentials for myocardial infarction, the leading cause of death worldwide, the incapability to obtain relatively homogeneous ventricular myocytes for transplantation is one major obstacle to the development of clinical therapies for myocardial repair1. Human embryonic stem cell (hESC) is a promising source of cardiomyocytes. Here we show that both Noggin and pan-retinoic acid receptor antagonist BMS-1894532 (RAi) significantly increase the cardiac differentiation efficiency of hESCs. Investigating retinoid function by comparing Noggin+RAi-treated cultures with Noggin+RA-treated cultures, we found that with 64±0.88% (mean ±s.e.m) cardiac differentiation efficiency, 83% of the cardiomyocytes in Noggin+RAi-treated cultures had embryonic ventricular-like action potentials (AP); while, with 50±1.76% cardiac differentiation efficiency, 94% of those in Noggin+RA-treated cultures had embryonic atrial-like APs. These findings demonstrating that relatively homogeneous embryonic atrial and ventricular myocyte populations can be efficiently derived from hESCs by specifically influencing signaling cascades.
Imaging the Biliary Tract: Comparable Roles of Ultrasonagraphy and Magnetic Resonance
Authors: HJ Khan, M Towers, FO Cunningham, JP McGrath
Journal: Endoscopy (2004)

The Role of Magnetic Resonance Imaging (MRI) in the diagnosis of pancreatico-biliary pathology is well recognized, Ultrasonography (US) continues to play a pivotal role however. With escalating health costs the expense incurred in obtaining MRI requires justification. The aim of this study was to examine the comparable roles of US and MRI in a group of patients with suspected biliary tract disease over a twelve month period.
The thrombopoietin/MPL axis is activated in the Gata1low mouse model of myelofibrosis and is associated with a defective RPS14 signature
Authors: M Zingariello, L Sancillo, F Martelli, F Ciaffoni, M Marra, L Varricchio, R A Rana, C Zhao, J D Crispino, A R Migliaccio
Journal: Blood Cancer Journal (2017)

Myelofibrosis (MF) is characterized by hyperactivation of thrombopoietin (TPO) signaling, which induces a RPS14 deficiency that de-regulates GATA1 in megakaryocytes by hampering its mRNA translation. As mice carrying the hypomorphic Gata1low mutation, which reduces the levels of Gata1 mRNA in megakaryocytes, develop MF, we investigated whether the TPO axis is hyperactive in this model. Gata1low mice contained two times more Tpo mRNA in liver and TPO in plasma than wild-type littermates. Furthermore, Gata1low LSKs expressed levels of Mpl mRNA (five times greater than normal) and protein (two times lower than normal) similar to those expressed by LSKs from TPO-treated wild-type mice. Gata1low marrow and spleen contained more JAK2/STAT5 than wild-type tissues, an indication that these organs were reach of TPO-responsive cells. Moreover, treatment of Gata1low mice with the JAK inhibitor ruxolitinib reduced their splenomegaly. Also in Gata1low mice activation of the TPO/MPL axis was associated with a RSP14 deficiency and a discordant microarray ribosome signature (reduced RPS24, RPS26 and SBDS expression). Finally, electron microscopy revealed that Gata1low megakaryocytes contained poorly developed endoplasmic reticulum with rare polysomes. In summary, Gata1low mice are a bona fide model of MF, which recapitulates the hyperactivation of the TPO/MPL/JAK2 axis observed in megakaryocytes from myelofibrotic patients.
Prevalence Of Lumbar And Femoral Osteoporosis (Op) In A Cohort Of Post-Menopausal Women Affected With Rheumatoid Arthritis (Ra): An Observational Study
Authors: A. Del Rosso, M. Bassetti, M. Matucci Cerinic, S. Maddali-Bongi
Journal: Annals of the Rheumatic Diseases (2008)
In the Mind of the Market: Theory of Mind Biases Value Computation during Financial Bubbles
Authors: Benedetto De Martino, John P. O’Doherty, Debajyoti Ray, Peter Bossaerts, Colin Camerer
Journal: Neuron (2013)

(Neuron 79, 1222–1231; September 18, 2013) On page 1226, Equation 1 contained an error. In the originally published version of this article, xi was added to 3 and the result was divided by 8. Instead, xi should be added to 3/8. The equation has been corrected online and is shown here.yi=(xi+38)1/2(Equation 1) In the Mind of the Market: Theory of Mind Biases Value Computation during Financial BubblesDe Martino et al.NeuronSeptember 18, 2013In BriefDe Martino demonstrates that the ability to infer the intentions and mental states of other individuals (“theory of mind”) biases evaluation when people interact with complex modern institutions like financial markets, contributing to the formation of economics bubbles. Full-Text PDF Open Access