tbuckley/cabot-search huggingface dataset:
Abstract 5338: Universal Definition of Myocardial Infarction Classification and the Risk of Cardiovascular Death: Observations From the TRITON-TIMI 38 Trial
Authors: Marc P Bonaca, Steven D Wiviott, Eugene Braunwald, Sabina A Murphy, Christian T Ruff, Carolyn H McCabe, Elliott M Antman, David A Morrow
Journal: Circulation (2009)

The prognostic implications of new or recurrent MI after an acute coronary syndrome have not been completely defined in the era of the Universal Definition of Myocardial Infarction and newer more sensitive biomarker assays. Therefore, we investigated the association between new or recurrent MI by MI Type and the risk of cardiovascular death among 13,608 patients with ACS undergoing coronary intervention in the TRITON-TIMI 38 Trial. METHODS : MI events were categorized on the basis of subtypes as defined by the AHA/ACC/ESC/WHF Task Force for the Redefinition of MI. The risk of CV death was evaluated by landmark analysis starting at the time of the new MI through the end of follow-up and adjusted for important clinical covariates. Outcomes were adjudicated by a blinded CEC. RESULTS : Pts who experienced a MI during follow up were at higher risk of CV death at 6 months than patients who did not experience a MI (6.5% vs 1.3% vs, p&lt;0.001). This association was present across all subtypes of MI with the highest rate among Type 4b (stent thrombosis, 15.4%) and the lowest among Type 4a (non-stent thrombosis PCI related) (figure ). After adjusting for important clinical covariates, the occurrence of any MI was associated with a 4 fold higher risk of death at 6 months (95% CI 3.3–5.6) with similar increased risk across subtype (figure ). CONCLUSIONS : New or recurrent MI after ACS is associated with a significantly increased risk of CV death. This pattern is consistent across all types as defined by the Universal Classification System, including peri-procedural MI. These findings underscore the clinical relevance of these events and therapies aimed at attenuating this risk.
Abstract 4244: Inhibition of HER2 and IGF2 triggers cell death in trastuzumab-resistant HER2 positive JIMT1 cells
Authors: Xousaen M. Helu, Daisy De Leon
Journal: Cancer Research (2014)

Abstract Breast cancer is the second leading cause of death in women. Overexpression of Human Epidermal Growth Factor Receptor 2 (HER2) is detected in 20-30% of breast cancers. Increased levels of HER2 are linked to poor prognosis, more aggressive phenotype, and resistance to chemotherapy and hormonal treatment. HER2 is part of a four member family of cell surface receptors that are implicated in transmission of signals controlling cell growth and differentiation. HER2 has an intracellular domain with tyrosine kinase catalytic activity and dimerization of HER2 activates the MAP kinase and AKT pathways. HER2 receptor also heterodimerizes with the IGF1 receptor(IGF1R) in trastuzumab-resistant cell lines. The insulin-like growth factor 2 (IGF2) has an important role in fetal and cancer development signaling through the IGF1R, insulin receptor (InsR), and cross-talk with the estrogen receptor alpha and beta (ERα, ERß). Previous findings in our lab demonstrate an increased expression of IGF2 in trastuzumab-resistance cell line JIMT1 when compared to trastuzumab-sensitive cell lines BT474, SKBR3, and ZR75-30. We hypothesis that to overcome trastuzumab-resistance in JIMT1 cell lines, dual inhibition of HER2 and IGF2 is necessary to induce cell death. When JIMT1 cells were treated with resveratrol, both HER2 and IGF2 mRNA and protein levels were reduced and a decrease in cell viability was observed. We also analyzed the phosphorylation levels of HER2 and IGF1R. Our studies suggest that blocking both HER2 and IGF2 is necessary to decrease cell viability in trastuzumab-resistant JIMT1 cells. Citation Format: Xousaen M. Helu, Daisy De Leon. Inhibition of HER2 and IGF2 triggers cell death in trastuzumab-resistant HER2 positive JIMT1 cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4244. doi:10.1158/1538-7445.AM2014-4244
Abstract 26: MUC1 enhances neuropilin-1 signaling in pancreatic ductal adenocarcinoma
Authors: Ru Zhou, Jennifer Curry, Priyanka Grover, Lopamudra Das Roy, TinChung Leung, Pinku Mukherjee
Journal: Cancer Research (2014)

Abstract Pancreatic ductal adenocarcinoma (PDA) has the worst prognosis of all cancers and is the 4th leading cause of cancer-related deaths in the United States. Mucin1 (MUC1) is a transmembrane glycoprotein over-expressed in more than 60% of PDA and its expression correlates with high metastases and poor prognosis. In PDA, there is a correlation between blood vessel density, tumor levels of VEGF, and disease progression. We have recently discovered a novel association between MUC1 and neuropilin-1 (NRP-1) expression. Neuropilin-1 (NRP-1) is a co-receptor for VEGF165 and blockade of NRP-1-VEGF165 interaction has been shown to inhibit angiogenesis and tumor growth in several other cancer types. Thus, we hypothesize that MUC1 induces a pro-angiogenic tumor microenvironment by increasing levels of VEGF and NRP-1, thus enhancing disease progression and metastases. We have generated Muc1-expressing KC and Muc1-null KCKO mouse PDA cell lines for this study. Compared to KCKO, KC cells secrete more VEGF and express higher levels of NRP-1 as well as VEGF receptors (1/2/3). Although the cell culture supernatants from KC do not alter the NRP-1 level on the endothelial line 2H11 cells, they significantly promote the 2H11 cell tube formation. Consistent with the in vitro results, tumor lysates from KC-bearing mice have higher levels of NRP-1 and VEGFR2 and its phosphorylations at Tyr residues 951, 996, and 1175. In human PDA cell lines, inhibition of MUC1 expression by specific siRNA reduced NRP-1 level while overexpression of full-length MUC1 increases NRP-1 expression. This suggests a direct regulation of NRP-1 by MUC1. Furthermore, the over-expression of MUC1 in BxPC3 human PDA cell line induces strong angiogenesis and promotes tumor metastasis in a zebrafish tumor xenograft model. Finally, we report that inhibition of NRP-1 by its specific blocking peptide suppresses BxPC3.MUC1 tumor growth in vivo. Taking together, MUC1 in PDA cells can enhance their own NRP-1 levels and promote the VEGF-VEGFR-NRP-1 signaling, which may favor the creation of a pro-angiogenic microenvironment for tumor growth and metastases. Our findings highlight the potential for MUC1 targeted blockade of VEGF-NRP-1 interaction in PDA by conjugating the NRP-1 inhibitory agents to a MUC1 targeting antibody. Citation Format: Ru Zhou, Jennifer Curry, Priyanka Grover, Lopamudra Das Roy, TinChung Leung, Pinku Mukherjee. MUC1 enhances neuropilin-1 signaling in pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 26. doi:10.1158/1538-7445.AM2014-26
Risk Management of Accutane
Authors: Bernard A. Schwetz
Journal: JAMA (2002)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Abstract 13943: Alterations in Left Ventricular Twist Mechanics and Regional Strain by Speckle Tracking Echocardiography During Cardiac Sympathetic Stimulation
Authors: Wei Zhou, Sunny Patel, Rafael Ramirez, Olujimi Ajijola, Shivkumar Kalyanam, Aman Mahajan
Journal: Circulation (2011)

Background— Left ventricular (LV) twist mechanics and regional strain during cardiac sympathetic efferent activation are poorly understood. The purpose of this study was to compare the effects of s...
Expression of aberrant O-glycans attached to leukosialin in differentiation-deficient HL-60 cells.
Authors: Osamu Saitoh, Robert E. Gallagher, Minoru Fukuda
Journal: Cancer Research (1991)

Abstract  Promyelocytic leukemia HL-60 cells can be induced to differentiate into granulocytic cells by various agents including retinoic acid (RA), dimethyl sulfoxide, and 6-thioguanine (6-TG). Although the induced cells are no longer capable of proliferation, a few cells continue to divide in the presence of inducers, and these cells are resistant to terminal differentiation by these inducers (R. E. Gallagher, D. A. Giangiulio, C-S. Chang, C. J. Glover, and R. L. Felsted, Blood, 68: 1402–1406, 1986).  The present study examined the structures of O-glycans attached to leukosialin, a major sialoglycoprotein in HL-60 cells, and the activities of glycosyltransferases involved in O-glycan synthesis. Leukosialin from RA-resistant and 6-TG-resistant HL-60 sublines migrated much more slowly than those from wild-type HL-60 cells when applied to sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The dimethyl sulfoxide-resistant HL-60 subline, on the other hand, expressed leukosialin with a molecular weight similar to wild-type HL-60 cells. RA-resistant and 6-TG-resistant HL-60 cells were found to express a significant amount of tetrasaccharides that contain no sialic acid residue, while wild-type HL-60 cells expressed mainly disialosyl hexasaccharides and contained no detectable amount of asialo-oligosaccharides. Furthermore, wild-type HL-60 cells treated with the inducers for 4 days were found to express the same saccharides present in untreated wild-type HL-60 cells, indicating that the altered O-glycans present in RA and 6-TG sublines were not caused by a direct effect of these agents but rather are intrinsically unique to these sublines.  To better understand the mechanisms underlying the differences in O-glycans, the activities of four sialyltransferases were measured: Galβ1→3GalNAcα2→3sialyltransferase, Galβ1→4(3)GlcNAcα2→3sialyltransferase, Galβ1→4GlcNAcα2→6sialyltransferase, and GalN-Acα2→6sialyltransferase. Among them, Galβ1→3GalNAcα2→3sialyltransferase and Galβ1→4(3)GlcNAcα2→3sialyltransferase were much lower in the RA- or 6-TG-resistant HL-60 subline than in wild-type HL-60 cells. These findings indicate that the differences in O-glycans are due to the differences in α2→3sialyltransferase activities. These results strongly suggest that O-glycans associated with leukosialin may play some role in HL-60 cell differentiation.
Involvement of the AML1 gene in the t(3;21) in therapy-related leukemia and in chronic myeloid leukemia in blast crisis
Authors: Giuseppina Nucifora, Debra J. Birn, Rafael Espinosa, Paul Erickson, Michelle M. LeBeau, Diane Roulston, Timothy W. McKeithan, Harry Drabkin, Janet D. Rowley
Journal: Blood (1993)
Optimizing Informed Decision Making for Basal Cell Carcinoma in Patients 85 Years or Older
Authors: Erica H. Lee, Jerry D. Brewer, Deborah F. MacFarlane
Journal: JAMA Dermatology (2015)

This viewpoint emphasizes the importance of elderly patients' involvement in their own BCC treatment decisions and the need for dermatologists and primary physicians together to adapt management plans to the patient's values, preferences, and social circumstances.
Skin Hazards in American Industry
Authors: L. Schwartz, L. Tulipan
Journal: JAMA (1935)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Abstract 14884: Patients with Renal Impairment Derive Long-Term Benefit from Cardiac Resynchronization Therapy: Results from the MADIT-CRT Long-Term Follow-Up
Authors: Usama Daimee, Arthur Moss, Ilan Goldenberg, Scott Solomon, Scott McNitt, Bronislava Polonsky, Helmut Klein, Wojciech Zareba, Valentina Kutyifa
Journal: Circulation (2014)

Background: Whether patients with renal impairment experience benefit from cardiac resynchronization therapy plus an implantable cardioverter-defibrillator (CRT-ICD) during long-term follow-up is unknown. Hypothesis: We assessed the hypothesis that baseline renal function affects long-term risk of all-cause mortality and heart-failure events (HFEs) as well as benefit derived from CRT-ICD. Methods: We evaluated the impact of renal function in 1274 patients with mild heart failure and left-bundle branch block enrolled in MADIT-CRT. Patients with BUN&gt;70 mg/dl or creatinine&gt;3.0 mg/dl were excluded from the trial. Two subgroups were created based on the estimated glomerular filtration rate (GFR): GFR&lt;60 and GFR≥60 ml/min/1.73 m2. Patients were studied over a follow-up period of 7 years for the end points of all-cause mortality and HFEs. Results: There were 413 patients with baseline GFR&lt;60 ml/min/1.73 m2 (mean 48.1±8.3). Relative to those with GFR≥60 ml/min/1.73 m2 (mean 79.6±16.0), the low-GFR patients experienced greater risk of death (HR=2.14, 95% CI: 1.57-2.91, p&lt;0.0001) and HFEs (HR= 1.31, 95% CI: 1.02-1.69, p=0.03). In both GFR groups, CRT-ICD relative to ICD alone was associated with significantly lower risk of death (GFR&lt;60: HR=0.63, 95% CI: 0.42-0.94, p=0.024, absolute risk reduction [ARR]=12%; GFR≥60: HR=0.65, 95% CI: 0.42-0.99, p=0.049, ARR=8%) [Figure]. Similarly, there was significant reduction in the risk of HFEs (GFR&lt;60: HR=0.36, 95% CI: 0.25-0.53, p&lt;0.0001, ARR=27%; GFR≥60: HR= 0.42, 95% CI: 0.31-0.57, p&lt;0.0001, ARR=17%). Conclusion: In conclusion, in mild heart failure patients, moderate renal dysfunction is associated with higher risk of all-cause mortality and HFEs relative to mildly impaired-to-normal renal function. While patients in both groups derive long-term benefit from CRT-ICD with similar relative reductions in all-cause mortality and HFEs, the greater absolute benefit occurs in patients with moderate renal disease.
Dynamism of a Soccer Player (Dinamismo di un footballer
Authors: M. Therese Southgate
Journal: JAMA (2003)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
A Diagnostic Triad in Syphilitic Aortitis
Authors: C. S. Danzer
Journal: Annals of Internal Medicine (1931)

Article1 July 1931A Diagnostic Triad in Syphilitic AortitisC. S. DANZER, M.D., F.A.C.P.C. S. DANZER, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-5-1-29 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIt is superfluous to discuss the importance of recognizing aortic syphilis early. The contrasting results in properly treated and untreated cases speak for themselves. As far as I know, a clean-cut symptom-picture by which this disease may be diagnosed, is still lacking. I shall attempt this task in the present communication.The confusion in the past was due largely to two factors, the frequent association of this disease with aortic atherosclerosis, and the misinterpretation of the Wassermann reaction.How often have we seen on examining an aorta at autopsy, atheromatous, calcified placques with wrinkling of the intima and pink streaks...Bibliography1 BRAUN L: Herz u. Psyche, Wien-Deuticke, 1920. Google Scholar2 DANZER CS: Address before Amer. College of Physicians, Boston, Mass., April 11, 1929. Google Scholar3 CZERMAK IN: Gesammelte Schriften, Leipzig, 1878. I, 779. Google Scholar4 HERING HE: Die Karotissinusreflexe auf Herz u. Gefasse, Steinkopff, Leipzig, 1927. Google Scholar5 CHIARI : Verhandl. d. deutschen pathol. Gesellsch. 1905, IX, 326. Google Scholar6 MÖNCKEBERG JG: Handb. d. ärztlich. Erfahrungen im Weltkriege, 1921, VIII, 11-15. Google Scholar7 JOSLIN E: Annals of Int. Med., 1930, IV, 54. Google Scholar8 WOLFKOFF E: Virchows Archiv. Pathol. Anat. u. Physiol., 1923, CCLXI, 42. CrossrefGoogle Scholar9 WESTERGREN A: Am. Rev. Tuberc., 1926, XIV, 94-101. Google Scholar10 LEWIS T: The Blood Vessels of the Human Skin and their Responses, Shaw, London, 1927. Google Scholar11 EPPINGERPAPPSCHWARTZ HL: Über das Asthma Cardiale, Springer, Berlin, 1924. Google Scholar12 DANZER CB: Annals of Int. Med. 1928, II, 239. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Brooklyn, N. Y.*From the Medical Services of the Cumberland and Unity Hospitals, Brooklyn, N. Y.†Read before the Minneapolis Meeting of the American College of Physicians, February 14th, 1930. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySYPHILITIC AORTIC INCOMPETENCE 1 July 1931Volume 5, Issue 1Page: 29-39KeywordsAortaAtherosclerosisAutopsyMedical servicesSyphilis ePublished: 1 December 2008 Issue Published: 1 July 1931 PDF downloadLoading ...
Allergy-inducing nickel concentration is lowered by lipopolysaccharide at both the sensitization and elicitation steps in a murine model
Authors: M. Kinbara, N. Sato, T. Kuroishi, T. Takano-Yamamoto, S. Sugawara, Y. Endo
Journal: British Journal of Dermatology (2010)

Journal Article Allergy‐inducing nickel concentration is lowered by lipopolysaccharide at both the sensitization and elicitation steps in a murine model Get access M. Kinbara, M. Kinbara Department of Molecular RegulationDepartment of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University, 4‐1 Seiryo‐machi, Aoba‐ku, Sendai 980‐8575, Japan Masayuki Kinbara. E‐mail: kinbara@dent.tohuku.ac.jp Search for other works by this author on: Oxford Academic Google Scholar N. Sato, N. Sato Department of Molecular Regulation Search for other works by this author on: Oxford Academic Google Scholar T. Kuroishi, T. Kuroishi Department of Molecular Regulation Search for other works by this author on: Oxford Academic Google Scholar T. Takano‐Yamamoto, T. Takano‐Yamamoto Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University, 4‐1 Seiryo‐machi, Aoba‐ku, Sendai 980‐8575, Japan Search for other works by this author on: Oxford Academic Google Scholar S. Sugawara, S. Sugawara Department of Molecular Regulation Search for other works by this author on: Oxford Academic Google Scholar Y. Endo Y. Endo Department of Molecular Regulation Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 164, Issue 2, 1 February 2011, Pages 356–362, https://doi.org/10.1111/j.1365-2133.2010.10016.x Published: 01 February 2011
Blood Transfusion in Clinical Medicine.
Authors: Patrick Mollison
Journal: JAMA (1952)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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