tbuckley/cabot-search huggingface dataset:
Abstract 11005: Influence of High-Degree Atrioventricular Block on 30-Day Clinical Outcome Following Acute Myocardial Infarction in the Drug-Eluting Stent Era: Results From Nation-Wide Registry of Acute Myocardial Infarction
Authors: Hack-Lyoung Kim, Sang-Hyun Kim, Jae-Bin Seo, Woo-Young Chung, Joo-Hee Zo, Myung-A Kim, Kyung-Woo Park, Bon-Kwon Koo, Hyo-Soo Kim, In-Ho Chae, Dong-Ju Choi, Myeong-Chan Cho, Young-Jo Kim, Ju Han Kim, Youngkeun Ahn, Myung Ho Jeong
Journal: Circulation (2014)

Introduction: This study was conducted to investigate the prognostic value of high-degree atrioventricular block (HDAVB) among patients with acute myocardial infarction (AMI) treated with DES. Methods: A total of 13,862 patients with AMI, registered in the nation-wide AMI database between January 2005 and June 2013, were analyzed. Second- (Mobitz type I or II) and third-degree atrioventricular block (AVB) were considered as HDAVB in this study. Thirty-day major adverse cardiac events (MACE) including all causes of death, recurrent myocardial infarction, and revascularization were evaluated. Results: Percutaneous coronary intervention with implantation of DES was performed in 89.8% of the patients. HDAVB occurred in 378 patients (2.7%). Thirty-day MACE occurred in 1,144 patients (8.2%). Patients with HDAVB showed worse clinical parameters at initial admission, and the presence of HDAVB was associated with 30-day MACE in univariate analyses. However, the prognostic impact of HDAVB was not significant after adjustment of potential confounders (p = 0.489). Among patients with HDAVB, patients with a culprit in the left anterior descending (LAD) coronary artery had worse clinical outcomes than those of patients with a culprit in the left circumflex or right coronary artery. LAD culprit was a significant risk factor for 30-day MACE even after controlling for confounders (odds ratio, 5.28; 95% confidence interval, 1.22-22.81; p = 0.026). Conclusions: Despite differences in clinical parameters at the initial admission, HDAVB was not an independent risk factor for 30-day MACE in adjusted analyses. However, a LAD culprit was an independent risk factor for 30-day MACE among patients with HDAVB.
Bronchodilation of Terbutaline in Small Doses from a 750 ml Spacer
Authors: Erik P. Munch, K.‐G. Hidinger, Bent Weeke
Journal: Allergy (1983)

The influence on lung function of small cumulative doses (31+31 + 63 + 125 + 250 μg) of terbutaline inhalations from a pressurized aerosol with a 750 ml spacer was evaluated in 12 stable asthmatics. The trial was douhle‐blind and cross‐over, using the double‐dummy method. Lung functions was recorded 5, 30, and 60 min after each inhalation. No significant differences in FEV 1 , FVC and FMI 25–75% were found between the two devices. A very marked response, which was not a placebo effect, was noted after the subjects had inhaled the first 31 μg dose. The results suggest that the number of inhalations is more important for the response in lung function than the dose administered. The addition of a 750 ml spacer to the pressurized aerosol is not likely to be beneficial for adults who an able to handle an ordinary aerosol properly.
Vitamin E and the risk of prostate cancer: Updated results of the Selenium and Vitamin E Cancer Prevention Trial (SELECT).
Authors: Eric A. Klein, Ian Thompson, Catherine M. Tangen, M. Scott Lucia, Phyllis Goodman, Lori M. Minasian, Leslie G. Ford, Howard L. Parnes, J. Michael Gaziano, Daniel D. Karp, Michael M. Lieber, Philip John Walther, J Kellogg Parsons, Joseph Chin, Amy K Darke, Scott Michael Lippman, Gary E. Goodman, Frank L. Meyskens, Laurence H. Baker
Journal: Journal of Clinical Oncology (2012)

7 Background: The initial report of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) found no reduction in risk of prostate cancer with either selenium or vitamin E supplements but a non-statistically significant increase in prostate cancer risk with vitamin E. Longer follow-up and more prostate cancer events provide further insight into the relationship of vitamin E and prostate cancer. Methods: SELECT randomized 35,533 men from 427 study sites in the United States, Canada and Puerto Rico in a double-blind manner between August 22, 2001 and June 24, 2004. Eligible men were 50 years or older (African Americans) or 55 years or older (all others) with a PSA &lt;4.0 ng/mL and a digital rectal examination not suspicious for prostate cancer. Included in the analysis are 34,887 men randomly assigned to one of four treatment groups: selenium (n=8752), vitamin E (n=8737), both agents (n=8702), or placebo (n=8696). Data reflect the final data collected by the study sites on their participants through July 5, 2011. Results: This report includes 54,464 additional person-years of follow-up since the primary report. Hazard ratios (99% confidence intervals [CI]) and numbers of prostate cancers were 1.17 (99% CI 1.004-1.36, p=.008, n=620) for vitamin E, 1.09 (99% CI 0.93-1.27, p=.18, n=575) for selenium, 1.05 (99%CI 0.89-1.22, p=.46, n=555) for selenium + vitamin E vs. 1.00 (n=529) for placebo. The absolute increase in risk compared with placebo for vitamin E, selenium and the combination were 1.6, 0.9 and 0.4 cases of prostate cancer per 1,000 person-years. Conclusions: Dietary supplementation with Vitamin E significantly increases the risk of prostate cancer among healthy men.
Relationship of Sedentary Behavior and Physical Activity to Incident Cardiovascular Disease
Authors: Andrea K. Chomistek, JoAnn E. Manson, Marcia L. Stefanick, Bing Lu, Megan Sands-Lincoln, Scott B. Going, Lorena Garcia, Matthew A. Allison, Stacy T. Sims, Michael J. LaMonte, Karen C. Johnson, Charles B. Eaton
Journal: Journal of the American College of Cardiology (2013)
Thrombocytopenia after bone marrow transplantation caused by a recipient origin Br(a) allo-antibody: presence of mixed chimerism 3 years after the graft without hematologic relapse
Authors: P Bierling, JM Pignon, M Kuentz, MT Mitjavila, P Fromont, V Barbu, M Goossens, N Duedari, W Vainchenker, JP Vernant
Journal: Blood (1994)
Abstract #LB-162: Blockade of PD-L1 in combination with adoptive T cell therapy and DC vaccination enhances survival of lymphopenic mice bearing melanoma
Authors: Shari Pilon-Thomas, Nasreen Vohra, Amy Mackay, James Mule
Journal: Cancer Research (2009)

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO

Inhibition of anti-tumor T cell responses may be mediated by the interaction between the programmed death-1 (PD-1) receptor on T cells and its ligand PD-L1. The purpose of this study was to examine the effect of blocking PD-L1 signaling on the induction of anti-tumor immunity in a murine model of melanoma. PD-L1 is highly expressed on the murine melanoma cell line, B16 (mean fluorescent intensity of 487 compared to 36 for isotype antibody control). Treatment of C57BL/6 mice with bi-weekly injections of anti-PD-L1 antibody alone was insufficient to delay the growth of established B16 tumor and by day 35 all mice had succumbed to disease. Combination therapy with gp100 peptide-pulsed DC alone or in combination with anti-PD-L1 antibody was unable to improve survival of B16 melanoma-bearing mice and by day 40 all mice had succumbed to disease. We next examined whether treatment with anti-PD-L1 antibody in combination with total body irradiation (TBI) could enhance anti-tumor immunity. Mice bearing B16 melanoma were treated with 600 rad TBI, then received anti-PD-L1 antibody. Again, no anti-tumor effect was noted and all mice treated with 600 rad in combination with either anti-NrIgG control antibody or anti-PD-L1 antibody succumbed to disease by day 35. In contrast, a significant increase in survival could be achieved following a combination treatment with TBI, anti-PD-L1 antibody and gp100 peptide-pulsed DC (mean survival time of 54 days; p<0.05 compared to NrIgG treated mice). Further addition of the adoptive transfer of gp100-specific CD8+ T cells resulted in long-term survival of 50% of the treated mice (mean survival time of 105 days; p<0.05). Since it has been shown that PD-1 is highly expressed on CD8+ T cells during homeostatic proliferation, it is possible that blocking PD-1/PD-L1 interactions after induction of lymphopenia leads to the expansion of anti-tumor specific T cells. Additional studies to determine the expansion and long-term survival of adoptively transferred T cells in combination with anti-PD-L1 antibody treatment are ongoing.

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr LB-162.
Gadolinium-induced nephrogenic systemic fibrosis in a patient with an acute and transient kidney injury
Authors: R.E. Kalb, T.N. Helm, H. Sperry, C. Thakral, J.L. Abraham, E. Kanal
Journal: British Journal of Dermatology (2007)

Journal Article Gadolinium‐induced nephrogenic systemic fibrosis in a patient with an acute and transient kidney injury Get access R.E. Kalb, R.E. Kalb Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Correspondence: Robert E. Kalb. E‐mail: kalb@buffalo.edu Search for other works by this author on: Oxford Academic Google Scholar T.N. Helm, T.N. Helm Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar H. Sperry, H. Sperry Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar C. Thakral, C. Thakral Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar J.L. Abraham, J.L. Abraham Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar E. Kanal E. Kanal Departments of Dermatology and *Internal Medicine, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Williamsville, NY 14221, U.S.A. †Department of Pathology, SUNY Upstate Medical University, Syracuse, NY, U.S.A. ‡University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 158, Issue 3, 1 March 2008, Pages 607–610, https://doi.org/10.1111/j.1365-2133.2007.08369.x Published: 01 March 2008
Serum levels of visfatin and omentin-1 in patients with psoriasis and their relation to disease severity
Authors: S.A. Ismail, S.A. Mohamed
Journal: British Journal of Dermatology (2012)

The association of the novel adipokines visfatin and omentin-1 with psoriasis is still obscure. Data concerning other inflammatory diseases suggest a possible role of these adipokines in the pathophysiology of psoriasis.To investigate serum levels of visfatin and omentin-1 in patients with psoriasis compared with healthy controls, and to consider their relation to disease duration, disease severity and obesity markers.Visfatin and omentin-1 concentrations were measured in 46 patients with plaque-type psoriasis and 42 healthy controls by using specific enzyme-linked immunosorbent assays.Patients with psoriasis showed considerably higher serum levels of visfatin than healthy controls with significant positive correlation with disease severity and duration. They also showed lower levels of ominten-1 compared with healthy controls with significant inverse correlation with body mass index and waist circumference.Coordinated roles for visfatin and omentin-1 are suggested in the modulation of the inflammatory environment in patients with psoriasis. Given the significant relations of omentin-1 with obesity markers, the health consequences of excessive weight should be better communicated to patients with psoriasis.
Myocardial Infarction After Dog Bite
Authors: Edward G. Abinader
Journal: Circulation (2001)

Myocardial Infarction After Dog BiteTo the Editor:We do not agree with the diagnosis of myocardial infarction in the case of a 36-year-old man 2 days after a dog bite 1 .For several reasons, we believe that the patient had myopericarditis rather than myocardial infarction.First, the patient had symptoms, signs, and laboratory findings consistent with sepsis, and blood cultures yielded Capnocytophaga canimorsus.Myocardial infarction occurs occasionally in patients with bacteremia, and it usually results from sepsisassociated hypotension or from endocarditis with septic embolism to the coronary arteries.However, viral and bacterial infections are more commonly the cause of pericarditis and myocarditis. 2,3ECG patterns of acute myopericarditis are known to resemble those seen with acute myocardial infarction. 4 The presented ECG demonstrated ST elevations in both anterior and inferior leads in a manner consistent with the pattern found in acute myopericarditis. 4,5 Second, the absence of regional wall motion abnormalities and the documentation of diffuse hypokinesia with left ventricular systolic dysfunction are typically seen in myopericarditis.Abnormal regional wall motion is nearly universally present in acute myocardial infarction.Presentation with chest discomfort and laboratory examinations with elevated levels of creatine kinase and raised troponin-I concentrations are consistent with myopericarditis as well as with myocardial infarction.Third, coronary angiography demonstrating normal vessels without signs of atherosclerosis is also consistent with the diagnosis of myopericarditis.This finding makes acute myocardial infarction less likely but does not definitely rule out previous coronary artery occlusion.In summary, we think that the diagnosis of acute myopericarditis is more likely than acute myocardial infarction in the reported case.
Abstract 14642: Do Diuretics, Beta-Blockers, and Statins Increase the Risk of Diabetes in Patients with Impaired Glucose Tolerance? Insights from the NAVIGATOR Study
Authors: Lan Shen, Bimal Shah, Eric Reyes, Laine Thomas, Peter Diem, Lawrence Leiter, Bernard Charbonnel, Viacheslav Mareev, Edward Horton, Steven Haffner, Vladimir Soska, Rury Holman, M. Angelyn Bethel, Frank Schaper, Jie-Lena Sun, John McMurray, Robert Califf, Henry Krum
Journal: Circulation (2012)
Adenosine kinase is a key determinant for the anti-HCV activity of ribavirin
Authors: Kyoko Mori, Osamu Hiraoka, Masanori Ikeda, Yasuo Ariumi, Akiko Hiramoto, Yusuke Wataya, Nobuyuki Kato
Journal: Hepatology (2013)

Ribavirin (RBV) is often used in conjunction with interferon-based therapy for patients with chronic hepatitis C. There is a drastic difference in the anti-hepatitis C virus (HCV) activity of RBV between the HuH-7-derived assay system, OR6, possessing the RBV-resistant phenotype (50% effective concentration [EC50 ]: >100 µM) and the recently discovered Li23-derived assay system, ORL8, possessing the RBV-sensitive phenotype (EC50 : 8 µM; clinically achievable concentration). This is because the anti-HCV activity of RBV was mediated by the inhibition of inosine monophosphate dehydrogenase in RBV-sensitive ORL8 cells harboring HCV RNA. By means of comparative analyses using RBV-resistant OR6 cells and RBV-sensitive ORL8 cells, we tried to identify host factor(s) determining the anti-HCV activity of RBV. We found that the expression of adenosine kinase (ADK) in ORL8 cells was significantly higher than that in RBV-resistant OR6 cells harboring HCV RNA. Ectopic ADK expression in OR6 cells converted them from an RBV-resistant to an RBV-sensitive phenotype, and inhibition of ADK abolished the activity of RBV. We showed that the differential ADK expression between ORL8 and OR6 cells was not the result of genetic polymorphisms in the ADK gene promoter region and was not mediated by a microRNA control mechanism. We found that the 5' untranslated region (UTR) of ADK messenger RNA in ORL8 cells was longer than that in OR6 cells, and that only a long 5' UTR possessed internal ribosome entry site (IRES) activity. Finally, we demonstrated that the long 5' UTR functioned as an IRES in primary human hepatocytes.These results indicate that ADK acts as a determinant for the activity of RBV and provide new insight into the molecular mechanism underlying differential drug sensitivity.
IL-25 prevents and cures fulminant hepatitis in mice through a myeloid-derived suppressor cell-dependent mechanism
Authors: Massimiliano Sarra, Maria Laura Cupi, Roberta Bernardini, Giulia Ronchetti, Ivan Monteleone, Marco Ranalli, Eleonora Franzè, Angelamaria Rizzo, Alfredo Colantoni, Flavio Caprioli, Marco Maggioni, Alessandra Gambacurta, Maurizio Mattei, Thomas T. Macdonald, Francesco Pallone, Giovanni Monteleone
Journal: Hepatology (2013)

Fulminant hepatitis (FH) is a disease characterized by massive destruction of hepatocytes with severe impairment of liver function. The pathogenesis of FH is not fully understood, but hyperactivity of T cells and macrophages with excessive production of cytokines are important hallmarks of the condition. In this study, we investigated the role of interleukin (IL)-25 in FH. IL-25 expression was evaluated in patients with FH and in livers of mice with FH induced by D-galactosamine (D-Gal) and lipopolysaccharide (LPS). Mice were treated with IL-25 before D-Gal/LPS-induced FH and before or after concanavalin A (ConA)-induced FH. Mononuclear cells were isolated from livers of mice treated with or without IL-25 and analyzed for GR1(+) CD11b(+) cells. CFSE-labeled T cells were cocultured with GR1(+) CD11b(+) cells and their proliferation was evaluated by flow cytometry. Mice were also treated with a depleting anti-GR1 antibody before IL-25 and D-Gal/LPS administration. IL-25 was constitutively expressed in mouse and human liver and down-regulated during FH. IL-25 prevented D-Gal/LPS-induced FH and this effect was associated with increased infiltration of the liver with cells coexpressing GR1 and CD11b. In vitro studies showed that GR1(+) CD11b(+) cells isolated from mice given IL-25 inhibited T-cell proliferation. Consistently, in vivo depletion of GR1(+) cells abrogated the protective effect of IL-25 in experimental D-Gal/LPS-induced FH. IL-25 was both preventive and therapeutic in ConA-induced FH.IL-25 expression is markedly reduced during human and experimental FH. IL-25 promotes liver accumulation of GR1(+) CD11b(+) cells with immunoregulatory properties.
Abstract IA22: Investigating breast cancer evolution and diversity with single-cell sequencing
Authors: Nicholas E. Navin
Journal: Clinical Cancer Research (2015)

Abstract Sequencing breast tumor cohorts has identified many prevalent mutations, but provides limited insight into the genomic diversity within tumors. Here, we developed a whole-genome and exome single-cell sequencing approach called Nuc-Seq that can achieve 83-97% coverage breadth with low error rates. We applied this method to sequence single normal and tumor cells from an estrogen-receptor positive breast cancer and a triple-negative ductal carcinoma, and performed copy number profiling in parallel. Our data shows that aneuploid rearrangements occurred early in tumor evolution and remained highly stable as the tumor masses expanded. In contrast, point mutations evolved gradually, generating extensive clonal diversity. Many of the diverse mutations were shown to occur at low frequencies (0.03 -10%) in the tumor mass by targeted single-molecule sequencing. Using mathematical modeling we found that the triple-negative tumor cells had an increased mutation rate (13.3X) while the ER+ tumor cells did not. These findings have important implications for the diagnosis, therapeutic treatment and evolution of chemoresistance in breast cancer. Citation Format: Nicholas E. Navin. Investigating breast cancer evolution and diversity with single-cell sequencing. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; Jun 18-21, 2014; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(4 Suppl): Abstract nr IA22.
ECG multiple lead systems.
Authors: R D Rifkin
Journal: Circulation (1978)

To the Editor:In the recent paper by Angelini et al. (Circulation 56: 1107, 1977), the authors described an electrocardiogram of a 5-year-old child with evidence of right ventricular hypertrophy.Figure 1 in this paper shows no R waves of V4R, V3R or V, and no S in V6V7, with a normal QRS axis.The only slight abnormal finding was an R/S complex from V2 to V5 which can suggest mild biventricular hypertrophy, but not "signs of right ventricular hypertrophy."In addition, the title of the paper, "Truncus Arteriosus Communis.Unusual Case Associated with Transposition" is confusing.I think that this case is a truncus arteriosus type I with biventricular origin and posterior pulmonary trunk.In transposition of the great arteries, the aorta takes origin from the right ventricle and the pulmonary trunk from the left ventricle.