tbuckley/cabot-search huggingface dataset:
Real world effectiveness of primary implantable cardioverter defibrillators implanted during hospital admissions for exacerbation of heart failure or other acute co-morbidities: cohort study of older patients with heart failure
Authors: Chih-Ying Chen, Lynne Warner Stevenson, Garrick C Stewart, Deepak L Bhatt, Manisha Desai, John D Seeger, Lauren Williams, Jessica J Jalbert, Soko Setoguchi
Journal: BMJ (2015)

<b>Objectives</b> To examine the effectiveness of primary implantable cardioverter defibrillators (ICDs) in elderly patients receiving the device during a hospital admission for exacerbation of heart failure or other acute co-morbidities, with an emphasis on adjustment for early mortality and other factors reflecting healthy candidate bias rather than the effect of the ICD. <b>Design</b> Retrospective cohort study. <b>Setting</b> Linked data from the Centers for Medicare and Medicaid Services and American College of Cardiology-National Cardiovascular Data Registry ICD registry, nationwide heart failure registry, and Medicare claims data 2004-09. <b>Population</b> 23 111 patients aged ≥66 who were admitted to hospital for exacerbation of heart failure or other acute co-morbidities and eligible for primary ICDs. <b>Main outcome measures</b> All cause mortality and sudden cardiac death. Latency analyses with Cox regression were used to derive crude hazard ratios and hazard ratios adjusted for high dimension propensity score for outcomes after 180 days from index implantation or discharge. <b>Results </b>Patients who received an ICD during a hospital admission had lower crude mortality risk than patients who did not receive an ICD (40% <i>v</i> 60% at three years); however, with conditioning on 180 day survival and with adjustment for high dimension propensity score, the apparent benefit with ICD was no longer evident for sudden cardiac death (adjusted hazard ratio 0.95, 95% confidence interval 0.78 to 1.17) and had a diminished impact on total mortality (0.91, 0.82 to 1.00). There were trends towards a benefit with ICD in reducing mortality or sudden cardiac death in patients who had had a myocardial infarction more than 40 days previously, left bundle branch block, or low serum B type natriuretic peptide; however, these trends did not reach significance. <b>Conclusion </b>After adjustment for healthy candidate bias and confounding, the benefits of primary ICD therapy seen in pivotal trials were not apparent in patients aged 66 or over who received ICDs during a hospital admission for exacerbation of heart failure or other acute co-morbidities. Future research is warranted to further identify subgroups of elderly patients who are more likely to benefit from ICDs. Recognition of those patients whose dominant risk factors are from decompensated heart failure and non-cardiac co-morbidities will allow better focus on ICDs in those patients for whom the device offers the most benefit and provides meaningful prolonging of life.
Abstract 15096: Plgf Acts as a Master Regulator of Cardiac Inflammation Upon Pressure Overload, by Controlling TIMP-3/TACE Axis.
Authors: Daniela Carnevale, Giuseppe Cifelli, Giada Mascio, Fatima Campopiano, Valentina Fardella, Stefania Fardella, Fabio Pallante, Giuseppe Lembo
Journal: Circulation (2011)

Heart failure is the final stage of several overload cardiomyopathies, preceded by an early adaptive hypertrophic response, characterized by coordinated cardiomyocyte growth, angiogenesis and infla...
Abstract 18106: Short- and Long-Term Outcomes of Patients With Type A Acute Aortic Dissection and Cardiogenic Shock: Contemporary Results From the International Registry of Acute Aortic Dissection (IRAD)
Authors: Eduardo Bossone, Reed E Pyeritz, Alan C Braverman, Mark D Peterson, Marek P Ehrlich, Patrick O’Gara, Toru Suzuki, Santi Trimarchi, Dan Gilon, Kevin Greason, Nimesh D Desai, Daniel G Montgomery, Eric M Isselbacher, Christoph A Nienaber, Kim A Eagle
Journal: Circulation (2013)

Background: Shock is a highly dreaded complication of type A acute aortic dissection (TAAAD). However, few data exist on its incidence and association with prognosis. Methods: We evaluated 2704 TAAAD patients [mean age 61.4 ± 14.5, (67.6%) male] from the International Registry of Acute Aortic Dissection. Results: Shock was present at arrival in 407 (15.1%) TAAAD patients. These patients demonstrated no difference in age (61.5 ± 15.2 with shock vs. 61.4 ± 14.4 years without; p=0.873), but were more likely to have history of hypertension (83.1% vs. 73.0%; p&lt;0.001), atherosclerosis (36.5% vs. 21.7%, p&lt;0.001) and diabetes (12.3% vs. 7.0%, p=0.001) than patients without shock. They had more surgical management (90.9% vs. 86.0%; p=0.007). In-hospital complications such as hypotension (49.8% vs. 28.6%; p&lt;0.001), coma (11.4% vs. 5.8%; p&lt;0.001), tamponade (33.6% vs. 18.2%; p&lt;0.001) and myocardial ischemia/infarction (19.7% vs. 13.7%; p=0.006) were more common among shock patients. Overall in-hospital mortality (30.2% vs. 23.9%; p=0.007) and mortality by management (surgical: 24.6% vs. 19.1%; p=0.015; medical: 88.9% vs. 53.3%, p&lt;0.001) were higher among shock patients. Independent predictors of in-hospital mortality in shock patients are displayed in Table 1. Among hospital survivors, Kaplan-Meier estimates of follow-up mortality were similar between groups (p=0.609). Conclusions: Shock occurred in 15.1% of patients with TAAAD and was associated with increased in-hospital morbidity and mortality, but not long-term mortality.
Abstract A106: BRCA mutation sensitizes pancreatic tumors to treatment with cisplatin
Authors: Ines Lohse, Pinjian Cao, Emin Ibrahimov, Ming-Sound Tsao, David W. Hedley
Journal: Cancer Research (2015)

Abstract Rationale: Recent clinical observations in pancreatic cancer suggest that cancers arising in germline BRCA1/2 mutation carriers are highly sensitive to Cisplatin chemotherapy. Both BRCA1 and BRCA2 are required for DNA double-strand break repair by homologous recombination (HR). Platinum chemotherapy generates interstrand cross-links that can only be adequately repaired by HR-based DNA repair, and consequently BRCA1/2-deficient cells are highly sensitive to platinum chemotherapy both in vitro and in vivo. With a strong biological rationale and favourable clinical observations, we aim to investigate whether BRCA mutation indeed sensitize to Cisplatin treatment and if the addition of the PARP inhibitor ABT-888 further reduces tumor growth in patient-derived pancreatic xenografts Methods: Primary xenografts were derived from three patients with known BRCA2 germline mutations (2 from surgical resections, 1 from ascites fluid). All 3 patients experienced a major response when treated with cisplatin. These models were used to assess the in vivo sensitivity to the drugs Cisplatin, Gemcitabine and the PARP inhibitor ABT-888, all of which are being used in the clinic. Treatment sensitivities were compared to 2 primary xenografts that were BRCA w/t. For single treatments, animals were treated with 4mg/kg Cisplatin weekly, 100mg/kg Gemcitabine biweekly or 12.5mg/kg ABT-888 daily for 30 days. For the combination treatment, animals were treated with a single dose of 4mg/kg Cisplatin followed by 30 days of 12.5mg/kg ABT-888 daily. Results: Preliminary results show no difference in tumor growth between BRCA2 wt and mt models was observed in response to treatment with ABT-888 alone. Treatment with cisplatin or gemcitabine on the other hand significantly reduced tumor growth and increased survival in all 3 BRCA2 mutated xenograft models, while being mostly ineffective in BRCA w/t tumors. The combination of Cisplatin and ABT-888 significantly reduced tumor growth when compared to ABT-888 alone. Conclusions: The results suggest that BRCA1/2 mt pancreatic xenograft models are highly sensitive to cisplatin. The availability of these models facilitates “near-clinical” testing of alternative strategies for optimizing the individualized treatment of patients carrying these rare mutations, and for the exploration of protocols incorporating novel agents. Citation Format: Ines Lohse, Pinjian Cao, Emin Ibrahimov, Ming-Sound Tsao, David W. Hedley. BRCA mutation sensitizes pancreatic tumors to treatment with cisplatin. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A106.
Abstract 8390: Contrast-Induced Nephropathy Independently Predicts Mortality After Cardiac Surgery
Authors: Santiago Garcia, Byungsoo Ko, Selcuk Adabag
Journal: Circulation (2011)

Background: Contrast induced nephropathy (CIN) is a predictor of poor outcome and long-term mortality. Coronary angiography is usually performed in close proximity to cardiac surgery. The goal of this investigation is to assess whether CIN also predicts post-surgical morbidity and mortality. Methods: We evaluated 949 patients undergoing cardiac surgery at the Minneapolis VA Medical Center from 2004 to 2010. The cohort was divided in 3 groups according to change in serum creatinine 48 hours post-angiography (no increase, Δ &lt;0.5 mg/dl, and Δ ≥0.5 mg/dl). Outcomes were operative mortality and post-operative acute kidney injury (AKI) using the AKI network and RIFLE (Risk, Injury, Failure, Loss, End-stage) definitions. Multivariable logistic-regression analysis adjusting for the VA mortality risk score was performed. Estimated glomerular filtration rate (eGFR) was calculated with the Modification of Diet in Renal Disease (MDRD) method. Results: Mean age of the patients was 67 (±9.6) and 36% were diabetics. The mean (±SD) serum creatinine pre and post-angiogram were 1.18 (±0.39) and 1.11 (±0.41) mg/dl, with corresponding eGFR of 71.71 (±21) and 77.75 (±23) ml/m/1.73 m2. The incidence of post-operative outcomes in relation to Δ creatinine are presented in the table. In multivariable analysis, a rise in creatinine &gt;0.5 mg after coronary angiogram was associated with a 5.6 fold increase in operative mortality after cardiac surgery (OR 5.6, 95% CI 1.3-23.7, p=0.02). Conclusions: The development of CIN during diagnostic angiography is an independent predictor of post-operative kidney injury and mortality after cardiac surgery. Strategy-based studies to modify this risk are warranted.
Abstract 16056: Pulmonary Oxidative Stress Contributes to Ambient Fine Particulate Matter (PM2.5)-Induced Vascular VEGF Resistance and Endothelial Progenitor Cell Retention
Authors: Petra Haberzettl, James McCracken, Rodney Folz, Igor Zelko, Aruni Bhatnagar, Daniel J Conklin
Journal: Circulation (2014)

Background and Rationale:  Epidemiological evidence suggests that exposure to ambient fine particulate matter (PM2.5) is associated with increased cardiovascular disease (CVD) risk. Previous studies in our laboratory have shown that in both humans and mice, endothelial progenitor cells (EPCs) are early and sensitive targets of air pollution. EPC depletion has been suggested to be a significant contributor to cardiovascular injury and disease and circulating EPC levels predict CVD risk and mortality. Nevertheless the mechanisms by which PM2.5 exposure decreases EPC levels remain unknown. We tested the hypothesis that PM2.5 exposure decreases EPC levels by inducing pulmonary oxidative stress.   Methods and Results:  Exposure to concentrated air PM2.5 particulate matter (CAP) for 9 days induced vascular hypercontractility and impaired aortic VEGF signaling in young adult mice. Flow cytometry analysis showed that CAP exposure decreased circulating EPC (Flk-1+/Sca-1+-cells) levels (52±7% of control; p=0.002) and increased in bone marrow EPCs (141±9% of control; p=0.007). Glutathione levels, measured by flow cytometry in the Flk-1+/Sca-1+-cell-populations, were decreased upon CAP exposure. CAP exposure also enhanced the abundance of protein-acrolein adducts in the lung, indicating increased oxidative stress. To test the role of pulmonary oxidative stress, we exposed mice transgenic for lung-specific extracellular superoxide dismutase (ecSOD) to CAP. In contrast with WT mice no increase in protein acrolein adducts was observed in the lung of CAP-exposed ecSOD-transgenic mice. No differences in EPC abundance or GSH levels were found in the blood or the bone marrow isolated from air- or CAP-exposed ecSOD transgenic mice. Pulmonary overexpression of ecSOD also preserved aortic VEGF-stimulated Akt phosphorylation after CAP exposure.   Conclusions:  Exposure to PM2.5 depletes circulating EPC levels by inducing oxidative stress in the lungs, which also impairs VEGF signaling. These findings suggest that the antioxidant capacity of the lung may be an important determinant of PM2.5-induced cardiovascular injury and that increasing pulmonary antioxidant defense could attenuate cardiovascular injury induced by exposure to fine air pollution.
Abstract 16419: Deletion of Low-Density Lipoprotein Receptor in Rats Induces Hyperlipidemia and Atherosclerotic Lesion Formation
Authors: Srinivas D Sithu, Krista A Riggs, Millicent A Gornek, Daniel W Riggs, Abhinav Agarwal, Aruni Bhatnagar, Sanjay Srivastava
Journal: Circulation (2012)

The LDL-receptor (LDLR) plays a major role in removing circulating LDL. Deletion of the receptor in mice results in profound dyslipidemia and atherosclerotic lesion formation. Although LDL-R null m...
Abstract 2132: Mutant Kras associated protein oxidation in pancreatic neoplasia
Authors: Michelle Schultz, Brian DeCant, Andrew Diaz, Sharon Solman, Rital Shah, David Bentrem, Paul J. Grippo
Journal: Cancer Research (2015)

Abstract Recent studies have suggested that mutant Kras associated activation of the Nrf2 pathway may have a significant role in pancreatic cancer (PaCa) tumorigenesis. Nrf2 regulates a battery of antioxidant genes, including peroxiredoxin-1 (Prdx-1), thioredoxin (Txn), and sulfiredoxin (Srxn), which are responsible for maintaining redox homeostasis in the cell. While ROS detoxification may have significant roles in cancer, several non-classical mechanisms of redox signaling associated with protein oxidation and phosphorylation are also important in tumorigenesis. Prdx-1 can regulate transcription as a cofactor in multiple oxidation states, represses tumorigenesis in its reduced state, and can act as a nuclear chaperone in elevated states of oxidation and when phosphorylated. Txn and Srxn prevent Prdx-1 overoxidation. We are therefore investigating the role of Prdx-1 oxidation and Txn and Srxn regulation in oncogenic signaling pathways in mutant Kras models of pancreatic tumorigenesis and neoplasia. Our data suggest that throughout tumor progression, Prdx-1 expression and localization are differentially regulated. These changes also correlated with reduced Txn and Srxn expression in lesions. In vitro, neoplastic and tumorigenic pancreatic cell lines have more total prdx-1 expression and oxidized Prdx-1 expression than non-tumorigenic cell lines. Moreover, cells that have mutant Kras were associated with higher levels of protein oxidation than those with wildtype Kras expression. Interestingly, mutant Kras was also associated with differences in pERK interaction with Prdx-1, which was also differentially regulated by NOX inhibitors and omega-3 fatty acids that control pancreatic neoplasia. ERK inhibitors also differentially affected Prdx1 expression in pancreatic cells in vitro. In addition, AKT, ERK, and FOXO3a phosphorylation were also modified by DPI treatment (NOX inhibitor) and omega-3 fatty acid treatment in wildtype and mutant Kras normal, neoplastic, and tumorigenic cell lines. We therefore conclude that mutant Kras is associated with elevated levels of Prdx-1 oxidation and that Kras-mediated activation of ERK could be associated with changes in Prdx-1 signaling in pancreatic neoplasia. Citation Format: Michelle Schultz, Brian DeCant, Andrew Diaz, Sharon Solman, Rital Shah, David Bentrem, Paul J. Grippo. Mutant Kras associated protein oxidation in pancreatic neoplasia. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2132. doi:10.1158/1538-7445.AM2015-2132
妊娠剧吐的跨代复发：母亲患病，其女儿患病风险将增加3倍
Authors: Catherine, Nelson, Piercy, 沈洁, 杨孜
Journal: BMJ (2010)

妊娠剧吐是孕妇反复入院的重要原因，常常引起心理困扰，与母胎发病率增加相关，并具有潜在的致命性。在对挪威出生注册处人群的队列研究中，Vikanes等发现若母亲患有妊娠剧吐，其女儿患该病的风险将比未患病母亲所生女儿的患病风险增加3倍（见本期第236页）。
Cascade system for getting urgent information to doctors
Authors: R. Sullivan
Journal: BMJ (1996)

and community controls we published both sets of results.The component of the study that looked at acute myocardial infarction was not powerful enough for analysis of subgroups (except perhaps the community controls).In the British dataset for the component that looked at venous thromboembolic disease there were no differences in the estimates of risk between the hospital and community controls.Table 1-Use of oral contraceptives by controls in component oftransnational study looking at venous thromboembolic disease No Third Second current generation generation use pills pills Hospital controls 470 103 180 Community controls
Abstract 11425: Prevalence of Kawasaki Disease in Young Adults with Suspected Myocardial Ischemia
Authors: Lori B Daniels, Matthew S Tjajadi, Hannah H Walford, Daryl B Fick, Hoang-Anh L Phan, Peter E Linz, Keshav Nayak, Andrew M Khan, Jane C Burns, John B Gordon
Journal: Circulation (2011)

Background: Up to 25% of patients with untreated Kawasaki Disease (KD) and 5% of those treated will develop coronary artery aneurysms. Missed diagnosis may occur when the clinical signs of KD go un...
Clinical Evaluation of the Resolute Zotarolimus-Eluting Coronary Stent System in the Treatment of De Novo Lesions in Native Coronary Arteries
Authors: Alan C. Yeung, Martin B. Leon, Ash Jain, Thaddeus R. Tolleson, Douglas J. Spriggs, Brent T. Mc Laurin, Jeffrey J. Popma, Peter J. Fitzgerald, Donald E. Cutlip, Joseph M. Massaro, Laura Mauri
Journal: Journal of the American College of Cardiology (2011)
Epidemic Encephalitis (Encephalitis Lethargica).
Authors: C K Russell
Journal: JAMA (1920)

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Abstract A76: Loss of GLI1 accelerates pancreatic cancer progression in the KPC mouse model
Authors: Lisa D. Mills, Lizhi Zhang, Ronald J. Marler, Phyllis A. Svingen, Maite Fernandez-Barena, Maneesh Dave, William Bamlet, Robert McWilliams, William A. Faubion, Martin E. Fernandez-Zapico
Journal: Cancer Research (2015)

Abstract The role of the transcription factor GLI1 in pancreatic tumor initiation promoting the progression of preneoplastic lesions into tumors is well established. However, its function at later stages of pancreatic carcinogenesis remains poorly understood. To address this issue, we crossed the GLI1 knockout animal (GKO) with cre-dependent pancreatic activation of oncogenic KRAS concomitant with loss of the tumor suppressor TP53 (KPC). Interestingly, in this model, GLI1 played a tumor protective function, where survival of GKO/KPC mice was reduced compared to KPC littermates. Both cohorts developed pancreatic cancer without significant histopathological differences in survival studies. However, analysis of mice using ultrasound-based imaging at earlier time-points showed increased tumor burden in GKO/KPC mice. These animals have larger tumors, decreased body weight, increased lactate dehydrogenase production, and leukopenia. Expression studies identified FAS and FAS ligand as potential mediators of this phenomenon. The FAS /FASL axis, an apoptotic inducer, plays a role in the progression of pancreatic cancer, where its expression is usually lost or significantly reduced in advanced stages of the disease. Chromatin immunoprecipitation assays identified FAS and FASL as direct targets of GLI1 where GKO/KPC mice showed lower levels of this ligand compared to KPC animals. Furthermore, GLI1 overexpression and knockdown studies demonstrate a key regulatory role for GLI1 in both FAS and FASL expression. Finally, decreased levels of apoptosis were detected in the tumor tissue in the absence of GLI1 by TUNEL staining. Together, these findings define a novel pathway regulated by GLI1 controlling pancreatic tumor progression and provide a new theoretical framework to help the design and analysis of trials targeting GLI1-related pathways. Citation Format: Lisa D. Mills, Lizhi Zhang, Ronald J. Marler, Phyllis A. Svingen, Maite Fernandez-Barena, Maneesh Dave, William Bamlet, Robert McWilliams, William A. Faubion, Martin E. Fernandez-Zapico. Loss of GLI1 accelerates pancreatic cancer progression in the KPC mouse model. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A76.
Highlights of the 2007 Scientific Sessions of the European Society of Cardiology
Authors: Steen D. Kristensen, Helmut Baumgartner, Helmut Drexler, Eric Eeckhout, Gerasimos Filippatos, Anselm K. Gitt, Cecilia Linde, Luc A. Pierard, Don Poldermans, Heribert Schunkert, Karin R. Sipido, Ernst E. van der Wall, Kim Fox, Jeroen J. Bax
Journal: Journal of the American College of Cardiology (2007)
Survival Implication of Left Ventricular End-Systolic Diameter in Mitral Regurgitation Due to Flail Leaflets
Authors: Christophe Tribouilloy, Francesco Grigioni, Jean François Avierinos, Andrea Barbieri, Dan Rusinaru, Catherine Szymanski, Marinella Ferlito, Laurence Tafanelli, Francesca Bursi, Faouzi Trojette, Angelo Branzi, Gilbert Habib, Maria G. Modena, Maurice Enriquez-Sarano
Journal: Journal of the American College of Cardiology (2009)
Pharmacokinetic Analysis Of Response In Hairy Cell Leukemia Treated By Anti-CD22 Recombinant Immunotoxin Moxetumomab Pasudotox
Authors: Robert J. Kreitman, Evgeny Arons, Maryalice Stetler-Stevenson, Wyndham H Wilson, David J. P. FitzGerald, Ira Pastan
Journal: Blood (2013)