tbuckley/cabot-search huggingface dataset:
Abstract 14181: Poor Long-Term Prognosis in Patients With Inflammatory Dilated Cardiomyopathy Diagnosed by Immunohistochemistry-Based Criteria
Authors: Yasuo Sugano, Takafumi Nakayama, Tetsuro Yokokawa, Toshiyuki Nagai, Keiko O Ogo, Yoshihiko Ikeda, Hatsue I Ueda, Takeshi Nakatani, Satoshi Yasuda, Hisao Ogawa, Toshihisa Anzai
Journal: Circulation (2015)

Background: Dilated cardiomyopathy (DCM) is highly heterogeneous and the future clinical course is almost unpredictable due to its diversity in each individual patient. Inflammatory DCM (DCMi) is defined by World Heart Federation (WHF) criteria as 14/mm 2 or more infiltrating T-lymphocytes or activated T-cells (including up to 4 macrophages) in the endomyocardial biopsy of a dilated heart. However, detail characteristics and long-term prognosis in patients with DCMi have not been fully understood. Methods: One hundred and sixteen consecutive patients between 2005 and 2007, who were finally diagnosed as DCM after right ventricular endomyocardial biopsy, were studied. Stored biopsy samples were immunohistochemically stained with antibodies specific for CD3 (T-lymphocytes) and CD68 (macrophages) to count the number of infiltrating cells into myocardium. We also collected each patient’s clinical characteristics, as well as prognostic data up to 9 years (mean 6.7 years) from diagnosis. Results: In total, 66 patients (57%) met the criteria for DCMi. Those patients showed no different baseline characteristics at diagnosis including age, sex, medications, past history, serum Na, creatinine, plasma BNP level, LV dimension, LV ejection fraction, and LV end-diastolic pressure compared to non-DCMi patients. During the observation period, 17 patients had poor clinical outcome of death or heart transplantation. Fifteen out of 66 patients with DCMi, despite only 2 out of 50 patients with non-DCMi, showed poor clinical outcome (23% vs 4%, p=0.007). Kaplan-Meier analysis revealed that DCMi patients had poorer long-term transplantation-free survival than non-DCMi patients (log-rank p=0.009, Figure). Conclusions: In our study, 57% of DCM patients fulfilled the immunohistochemistry-based criteria for DCMi defined by WHF. Patients who met the DCMi criteria had remarkably poor long-term prognosis regardless of similar baseline characteristics at diagnosis.
Case 25-2018: A 63-Year-Old Man with Syncope
Authors: Rory B. Weiner, William J. Hucker, Nandini M. Meyersohn, David M. Dudzinski, James R. Stone
Journal: New England Journal of Medicine (2018)

A 63-year-old man who had a history of coronary artery disease and coronary-artery bypass grafting presented with syncope. Echocardiography revealed two masses external to the right atrioventricular groove. Additional diagnostic tests were performed.
Abstract 527: Identification of novel target mRNAs of microRNA-143 in glioblastoma cells
Authors: Eunice Lozada-Delgado, Fatma Valiyeva, Maria Marcos, Pablo Vivas
Journal: Cancer Research (2018)

Abstract The purpose of this study is to assess the biological role of microRNA-143 (miR-143) in Glioblastoma multiforme (GBM). In the United States, the incidence of GBM is about 17% of all primary brain tumors and about 60-75% of all Astrocytomas. Many patients recur even after therapy with a median survival rate of 15 months. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression post-transcriptionally. Deregulated miRNAs have been identified in cancer including GBM. In this study, we aim to thoroughly uncover the role of miR-143 by using GBM cell lines, mouse models, and patient samples. Previous qPCR data from FFPE samples of Puerto Rican GBM patients showed a higher relative expression of miR-143 in GBM patients compared to control individuals and paired surrounding non-cancerous tissue suggesting an oncogenic role. Moreover, in vitro data of transient transfections of a miR-143 oligonucleotide inhibitor in GBM cells showed reduced cell proliferation (clonogenic assay), increased apoptosis and cell cycle arrest in the G0/G1-S phase (flow cytometry and western blot analysis). Furthermore, we want to identify novel target mRNAs of miR-143 in GBM cells that may explain these results. Using in silico analysis tools and a qPCR analysis we identified 5 candidate genes as potential miR-143 targets. Western blot analysis of the proteins encoded by these genes using miR-143 overexpressing cells showed that the Integral membrane protein 2B (ITM2B) and Zinc transporter 8 (SLC30A8) protein levels were reduced and when miR-143 was transiently inhibited their protein levels where increased. These results suggest that miR-143 targets these mRNAs. Ongoing luciferase reporter assays will determine direct binding of miR-143 to the 3'UTR of these mRNAs in GBM cells. Citation Format: Eunice Lozada-Delgado, Fatma Valiyeva, Maria Marcos, Pablo Vivas. Identification of novel target mRNAs of microRNA-143 in glioblastoma cells [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 527.
Clinical Practice Guidelines
Authors: Paul G. Shekelle
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Pedunculated Morphology of T1 Colorectal Tumors Associates With Reduced Risk of Adverse Outcome
Authors: Koen Kessels, Yara Backes, Sjoerd G. Elias, Aneya van den Blink, G. Johan A. Offerhaus, Jeroen D. van Bergeijk, John N. Groen, Tom C.J. Seerden, Matthijs P. Schwartz, Wouter H. de Vos tot Nederveen Cappel, Bernhard W.M. Spanier, Joost M.J. Geesing, Marjon Kerkhof, Peter D. Siersema, Paul Didden, Jurjen J. Boonstra, Lorenza Alvarez Herrero, Frank H.J. Wolfhagen, Frank ter Borg, Anja U. van Lent, Jochim S. Terhaar sive Droste, Wouter L. Hazen, Ruud W.M. Schrauwen, Frank P. Vleggaar, Miangela M. Laclé, Leon M.G. Moons
Journal: Clinical Gastroenterology and Hepatology (2018)
High-Affinity Arginine Transport of Bovine Aortic Endothelial Cells Is Impaired by Lysophosphatidylcholine
Authors: Ken-ichiroKikuta, TatsuyaSawamura, SoichiMiwa, NobuoHashimoto, TomohMasaki
Journal: Circulation Research (1998)

Abstract—The mechanisms of endothelial dysfunction characterized by the impaired nitric oxide (NO) release have not yet been clarified. Because the phenomenon is mimicked in vitro by the application of oxidized LDL and its major lipid constituent, lysophosphatidylcholine (LPC), we analyzed their effects on the arginine-NO system, especially on the arginine transport system. LPC inhibited NO release induced by ADP in cultured bovine aortic endothelial cells. The inhibition was attenuated by the excess amount of extracellular arginine. LPC was found to inhibit the arginine transport in bovine aortic endothelial cells, which is mediated by high- and low-affinity components. LPC predominantly impaired the high-affinity component. In the presence of a high concentration of arginine, LPC showed apparently no inhibition of arginine transport, because the low-affinity transporter compensated for the activity. Taken together, the impairment of the high-affinity transport system might account for the inhibition of ...
Abstract CT090: Neoadjuvant chemotherapy of FOLFIRI with or without radiotherapy in the treatment of marginally resectable recurrent rectal cancer exposed to oxaliplatin: A cohort study
Authors: Jian Xiao, Zerong Cai, Yingxin Tan, Yufeng Chen, Yanhong Deng, Yifeng Zou, Xiaojian Wu, Ping Lan
Journal: Cancer Research (2018)

Abstract Background FOLFIRI is the standard second-line chemotherapy for recurrent rectal cancer previously exposed to oxaliplatin. For resectable recurrent rectal cancer, the optimal sequence of chemotherapy and resection is still unknown. We carried out a cohort study to evaluate the efficacy and feasibility of neoadjuvant chemotherapy of FOLFIRI in this setting. Patients and Methods Patients aged from 18 to 80 year-old with histologically confirmed and resectable recurrent rectal adenocarcinoma previously exposed to oxaliplatin were recruited. Resectability was decided by three colorectal surgeons. Eligible patients received six preoperative and six more postoperative FOFIRI regimens (irinotecan 180mg/m2 , folinic acid 400mg/m2 and fluorouracil 2800mg/m2, repeated every 14 days). Tumor response was assessed after 3 and 6 cycles. The primary end point was R0 resection rate and the second end points were grade 3 or 4 toxicity and tumor regression grade (Ryan). All the patients signed written informed consent. Result 65 eligible patients were enrolled in this trial. According to RECIST criteria, 22 ( 33.8%) cases had partial remission, 18 ( 27.7%) cases had stable disease, 24 ( 36.9%) cases had progression disease and 1 patient refused to evaluate and quit study. 21 ( 32.8%) patients achieved R0 resection with 5 cases of TRG 1, 11 cases of TRG 2 and 5 cases of TRG 3. 25 patients received concurrent radiotherapy. Grade 3 or 4 toxicity was seen in 4 (6%) patients. One patient had intestinal perforation and one had bowel obstruction during chemotherapy. No one died during treatment. Conclusion Neoadjuvant chemotherapy of FOLFIRI in resectable recurrent rectal cancer can be well tolerated. But more active regimen is still needed for this setting to accomplish better outcome. Funding: This study was supported by 5010 Project of Clinical Research of Sun Yat-sen University (2010012) Citation Format: Jian Xiao, Zerong Cai, Yingxin Tan, Yufeng Chen, Yanhong Deng, Yifeng Zou, Xiaojian Wu, Ping Lan. Neoadjuvant chemotherapy of FOLFIRI with or without radiotherapy in the treatment of marginally resectable recurrent rectal cancer exposed to oxaliplatin: A cohort study [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 CT090.
Abstract 19350: The Decline of the Montreal Cognitive Test Can Detect Post-stroke Cognitive Decline Determined by a Formal Neuropsychological Evaluation
Authors: KennyXu, CatherineDong, ChristopherChen
Journal: Circulation (2015)

Objective: We aimed to establish the association of decline in cognitive screening tests scores, the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE), with the decline in neuropsychological diagnostic status from 3-6 months to a year later. Method: Patients with ischemic stroke/ Transient Ischemic Attack (TIA) received the MoCA and MMSE within 14 days after stroke, then 3-6 months and 1 year later. The decline in MoCA and MMSE scores were defined by reduction of 2 points or more in total scores, while stable/improved MoCA scores referred to reduction of MoCA scores less than 2 or improved scores. The decline in neuropsychological diagnostic status was defined by category transition from no cognitive impairment to any cognitive impairment (≥1 domain), from mild cognitive impairment (impairment in 1-2 domains) to moderate cognitive impairment (impairment >2 domains) and dementia (i.e., functional loss associated with cognitive impairment, DSM-IV criteria), as well as from modera...
Oxygen-Enhanced and Dynamic Contrast-Enhanced Optoacoustic Tomography Provide Surrogate Biomarkers of Tumor Vascular Function, Hypoxia, and Necrosis
Authors: Michal R. Tomaszewski, Marcel Gehrung, James Joseph, Isabel Quiros-Gonzalez, Jonathan A. Disselhorst, Sarah E. Bohndiek
Journal: Cancer Research (2018)

Measuring the functional status of tumor vasculature, including blood flow fluctuations and changes in oxygenation, is important in cancer staging and therapy monitoring. Current clinically approved imaging modalities suffer long procedure times and limited spatiotemporal resolution. Optoacoustic tomography (OT) is an emerging clinical imaging modality that may overcome these challenges. By acquiring data at multiple wavelengths, OT can interrogate hemoglobin concentration and oxygenation directly and resolve contributions from injected contrast agents. In this study, we tested whether two dynamic OT techniques, oxygen-enhanced (OE) and dynamic contrast-enhanced (DCE)-OT, could provide surrogate biomarkers of tumor vascular function, hypoxia, and necrosis. We found that vascular maturity led to changes in vascular function that affected tumor perfusion, modulating the DCE-OT signal. Perfusion in turn regulated oxygen availability, driving the OE-OT signal. In particular, we demonstrate for the first time a strong per-tumor and spatial correlation between imaging biomarkers derived from these
Lack of Insulin Receptor Substrate-2 Causes Progressive Neointima Formation in Response to Vessel Injury
Authors: TetsuyaKubota, NaotoKubota, MasaoMoroi, YasuoTerauchi, TsuneoKobayashi, KatsuoKamata, RyoSuzuki, KazuyukiTobe, AtsushiNamiki, ShinichiAizawa, RyozoNagai, TakashiKadowaki, TetsuYamaguchi
Journal: Circulation (2003)

Background— Insulin resistance is associated with atherosclerosis, but its mechanism is unknown. It has been reported that insulin receptor substrate (IRS)-1 deficient (IRS-1−/−) mice showed insulin resistance without type 2 diabetes, whereas the IRS-2 deficient (IRS-2−/−) mice showed insulin resistance with type 2 diabetes. Methods and Results— We investigated neointima formation in the IRS-1−/− and IRS-2−/− mice at 8 and 20 weeks. The IRS-2−/− mice showed much greater neointima formation than the IRS-1−/− and wild-type mice at 8 weeks. At 20 weeks, the IRS-2−/− mice had greater neointima formation than the IRS-1−/− mice, which showed more enhanced neointima formation than the wild-type mice. The IRS-1−/− and IRS-2−/− mice had dyslipidemia, hypertension, and insulin resistance. The IRS-2−/− mice had more metabolic abnormalities than the IRS-1−/− mice at 8 and 20 weeks. IRS-2 expression was detected, but IRS-1 expression was not detected in the vessels. Conclusions— The neointima formation in the IRS-1−/−...
Metabolism of Atherosclerotic Tissue of Rabbit and Dog, with Special Reference to Esterase and Lipase
Authors: Neliciamaier, Henryhaimovici
Journal: Circulation Research (1965)

Esterase and lipase were studied in the aorta, liver, and serum of dogs and rabbits on an atherogenic diet. With the exception of dog serum, lipase was not present in any of the tissues studied. At a relatively early stage the atherosclerotic intima-media layer, separated at the cleavage plane, showed increased esterase activity in both animals. At later stages, a reverse trend was noted in the rabbit, whereas in the dog, the esterase activity remained markedly increased. No pre-atherosclerotic enzymatic changes were noted. The liver of both species showed increased esterase activity first and reversal to normal values later. In contrast, rabbit serum displayed no change for several months and decreased activity subsequently whereas in the dog, decreased esterase activity was noted throughout the administration of the atherogenic diet. Lipase activity in dog serum, which was unaffected for several months, decreased later. Our results expand previous findings with other arterial enzymes and indicate furthe...
Abstract 12324: Sestrin2 is an Essential Regulator of Cardiac AMPK Signaling During Ischemia
Authors: Alex Morrison, Yina Ma, Linda Wang, Yanqing Wang, Ji Li
Journal: Circulation (2013)

Background: A novel stress-inducible protein, sestrin2, has emerged as a mediator of AMP-activated Protein Kinase (AMPK) signaling pathway. AMPK is a pertinent stress-activated kinase shown to have substantial cardioprotective capabilities against myocardial ischemia/reperfusion (I/R) injury. The regulation of AMPK in the ischemic heart remains elusive and is critical to the development of new therapeutic strategies. We hypothesized that sestrin2 mediating cardiac AMPK activation and protecting heart from ischemic damage. Methods and Results: C57BL/6 mice were subjected to left anterior descending coronary artery occlusion for different time points of ischemia and I/R in order to detect the signaling activity in the left ventricle. The kinetics of AMPK phosphorylation at Thr172 of the α catalytic subunit appears brief and bell-shaped, peaking between 10 and 15 min (3.6-fold vs. sham, p≤0.01), decreasing with prolonged ischemia (30 min, 2-fold vs. sham, p≤0.05), and leveling off to basal levels upon reperf...
T-Type Ca2+ Channel Blockade Prevents Sudden Death in Mice With Heart Failure
Authors: HideyukiKinoshita, KoichiroKuwahara, MakotoTakano, YujiArai, YoshihiroKuwabara, ShinjiYasuno, YasuakiNakagawa, MichioNakanishi, MasakiHarada, MasatakaFujiwara, MasaoMurakami, KenjiUeshima, KazuwaNakao
Journal: Circulation (2009)

Background— Pharmacological interventions for prevention of sudden arrhythmic death in patients with chronic heart failure remain limited. Accumulating evidence suggests increased ventricular expression of T-type Ca2+ channels contributes to the progression of heart failure. The ability of T-type Ca2+ channel blockade to prevent lethal arrhythmias associated with heart failure has never been tested, however. Methods and Results— We compared the effects of efonidipine and mibefradil, dual T- and L-type Ca2+ channel blockers, with those of nitrendipine, a selective L-type Ca2+ channel blocker, on survival and arrhythmogenicity in a cardiac-specific, dominant-negative form of neuron-restrictive silencer factor transgenic mice (dnNRSF-Tg), which is a useful mouse model of dilated cardiomyopathy leading to sudden death. Efonidipine, but not nitrendipine, substantially improved survival among dnNRSF-Tg mice. Arrhythmogenicity was dramatically reduced in dnNRSF-Tg mice treated with efonidipine or mibefradil. Efo...
Impact of Salusin-α and -β on Human Macrophage Foam Cell Formation and Coronary Atherosclerosis
Authors: TakuyaWatanabe, KaeNishio, TomokoKanome, Taka-akiMatsuyama, ShinjiKoba, TetsuoSakai, KengoSato, ShigekiHongo, KiyoshiNose, HidekazuOta, YouichiKobayashi, TakashiKatagiri, MasayoshiShichiri, AkiraMiyazaki
Journal: Circulation (2008)

Background— Human salusins, related bioactive polypeptides with mitogenic effects on vascular smooth muscle cells and fibroblasts and roles in hemodynamic homeostasis, may be involved in the origin of coronary atherosclerosis. Macrophage foam cell formation, characterized by cholesterol ester accumulation, is modulated by scavenger receptor (cholesterol influx), acyl-coenzyme A:cholesterol acyltransferase-1 (ACAT-1; storage cholesterol ester converted from free cholesterol), and ATP-binding cassette transporter A1 (cholesterol efflux). Methods and Results— Serum salusin-α levels were decreased in 173 patients with angiographically proven coronary artery disease compared with 40 patients with mild hypertension and 55 healthy volunteers (4.9±0.6 versus 15.4±1.1 and 20.7±1.5 pmol/L, respectively; P<0.0001). Immunoreactive salusin-α and -β were detected in human coronary atherosclerotic plaques, with dominance of salusin-β in vascular smooth muscle cells and fibroblasts. After 7 days in primary culture, acety...
Identification of Patients Most Likely to Benefit From Implantable Cardioverter-Defibrillator Therapy
Authors: RobertSheldon, StuartConnolly, AndrewKrahn, RobinRoberts, MichaelGent, MartinGardner
Journal: Circulation (2000)

Background—Patients with resuscitated ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation) benefit from implantable cardioverter-defibrillators (ICDs) compared with medical therapy. We hypothesized that the patients who benefit most from an ICD are those at greatest risk of death. Methods and Results—In the Canadian Implantable Defibrillator Study (CIDS), 659 patients with resuscitated ventricular tachyarrhythmias were randomly assigned to receive an ICD or amiodarone and were then followed for a mean of 3 years. There were 98 and 83 deaths in the amiodarone and ICD groups, respectively. We used multivariate Cox analysis to assess the impact of baseline parameters on the mortality in the amiodarone group. Reduced left ventricular ejection fraction, advanced age, and poor NYHA status identified high-risk patients (P=0.0001 to 0.0009). Quartiles of risk were constructed, and the mortality reduction associated with ICD treatment in each quartile was assessed. There was a significan...
Abstract LB-384: A-to-I miR-378a-3p editing prevents melanoma progression via regulation ofPARVA expression
Authors: Einav Shoshan, Guermarie Velazquez-Torres, Enrique Fuentes-Mattei, Cristina Ivan, Menashe Bar-Eli
Journal: Cancer Research (2018)

Abstract Although recent studies have shown that adenosine-to-inosine (A-to-I) RNA editing occurs in microRNAs (miRNAs), the effects of A-to-I miRNAs editing on melanoma growth and metastasis are yet to be determined. Previously we have reported that metastatic melanoma cell lines and tumor specimens have reduced expression of ADAR1 and consequently are impaired in their ability to perform A-to-I microRNA (miRNA) editing. Here we report that miR-378a-3p is undergoing A-to-I editing only in the non-metastatic but not in metastatic melanoma cells. The function of the edited form is different from its wild-type counterpart. The edited form of miR-378a-3p preferentially binds to the 3'UTR of the PARVA oncogene and inhibits its expression, thus preventing the progression of melanoma towards the malignant phenotype. Indeed, edited miR- 378a-3p but not its WT form inhibits melanoma metastasis in vivo. These results further emphasize the role of RNA editing in melanoma progression. Citation Format: Einav Shoshan, Guermarie Velazquez-Torres, Enrique Fuentes-Mattei, Cristina Ivan, Menashe Bar-Eli. A-to-I miR-378a-3p editing prevents melanoma progression via regulation ofPARVA expression [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 LB-384.