tbuckley/cabot-search huggingface dataset:
Kystoskopischer Atlas. Ein Lehrbuch für Studierende und Aerzte.
Journal: JAMA (1921)

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 2874: <i>De novo</i> acquisition of RD3 loss with intensive multi-modal therapy harmonize neuroblastoma relapse
Authors: Dinesh Babu Somasundaram, Karthikeyan Subramanian, Sheeja Aravindan, Zhongxin Yu, Mohan Natarajan, Terence S. Herman, Natarajan Aravindan
Journal: Cancer Research (2019)

Abstract The majority of high-risk neuroblastoma that initially responds to therapy will ultimately relapse. Acquired genetic/molecular rearrangement contributes to tumor relapse and currently, no salvage treatment regimens are known to be curative. Our studies identified the loss of retinal-degeneration-protein-3 (RD3) in progressive disease (PD) and its association with poor clinical outcomes. Herein we investigated the acquisition of RD3-loss after current standard of care (SOC, intensive multimodal therapy) in neuroblastoma. Acquired transcriptional (RNA in situ hybridization, QPCR) and translational (IHC on a custom archived cell micro array, immunoblotting) loss of RD3 with SOC was investigated with bed-to-bench approach utilizing a panel of 15 stage-4 patient derived cell-lines with known therapy status, diagnosis [DX] vs. PD after SOC). Further, RD3-loss in progressive disease, its direct role in the pathogenesis disease progression (cell migration, invasion, tumorosphere formation and metastatic potential) was investigated using mouse model of progressive neuroblastoma and in experimental in vitro and ex vivo settings coupled with gene manipulation strategies. In addition, RD3 status in response to therapy were also affirmed by in silico analysis of independent studies on bed-to-bench and experimental models. Results demonstrated RD3-loss (transcriptional/translational) acquisition with SOC in human PD. Experimental in vitro, in vivo, ex vivo studies affirmed RD3 loss in PD and, further forced RD3-rearrangements in these models defined its functional role in PD pathogenesis. Data-mining experimental studies with salvage therapeutic agents affirmed the acquisition of RD3-loss in resistant cells and in residual tumors. For the first time, these results demonstrate the de novo acquisition of RD3 loss in PD after intensive multi-modal therapy. Defining the criticality of RD3-loss in PD and the defined role of RD3 loss in PD pathogenesis, benefit of targeted reinforcement could lead to improved salvage therapy for high-risk neuroblastoma. Citation Format: Dinesh Babu Somasundaram, Karthikeyan Subramanian, Sheeja Aravindan, Zhongxin Yu, Mohan Natarajan, Terence S. Herman, Natarajan Aravindan. De novo acquisition of RD3 loss with intensive multi-modal therapy harmonize neuroblastoma relapse [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2874.
Tamoxifen Flare
Authors: Johannes D. Veldhuis
Journal: JAMA (1979)

<h3>To the Editor.—</h3> The recent article by Plotkin et al, which describes tamoxifen flare in patients with advanced breast cancer, confirms observations by other investigators, including ourselves.<sup>1,2</sup>However, these authors regard the mechanism of flare as obscure. Recognizing that a precise mechanism remains to be proved critically, we offer the following testable hypothesis drawn from current concepts of hormone action. First, although not noted in patients defined in the group of Plotkin et al, transient hypercalcemia of an occasionally marked degree has been reported in association with bonepain flare.<sup>2</sup>Cutaneous metastases have also exhibited transient worsening. Collectively, these observations may be explained by transient stimulation of certain tumor cells, whether in bone or soft tissue. Second, under certain circumstances, tamoxifen citrate, like related antiestrogens, exerts an estrogen agonist rather than an antagonistic effect. This phenomenon has been observed in a variety of experimental models using hormonally responsive tissue.
Where to Find Information on Influenza and Influenza Vaccine
Journal: JAMA (2005)

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
Identification of patients with compensated cirrhosis who can safely use protease inhibitor-based therapy for HCV infection
Authors: Lisette Krassenburg, Raoel Maan, Alnoor Ramji, Michael P. Manns, Markus Cornberg, Heiner Wedemeyer, Robert De Knegt, Robert De Man, Harry Janssen, Bettina Hansen, Adriaan Van der Meer, Jordan Feld
Journal: Journal of Hepatology (2020)
Persistence of Decreased T-Helper Cell Function in Industrial Workers 20 Years after Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin
Authors: Torsten Tonn, Charlotte Esser, E. Marion Schneider, Wolfgang Steinmann-Steiner-Haldenstatt, Ernst Gleichmann
Journal: Environmental Health Perspectives (1996)

In experimentally exposed animals 2,3,7,8-tetrachlorodibenzo-n-dioxin (TCDD) causes severe immunosuppression. However, the overall susceptibility of humans for the different pathological effects of TCDD has remained unclear. We examined the long-term effects of TCDD in 11 industrial workers who were exposed to high doses of TCDD for several years 20 years ago. Current TCDD body burdens were still at least 10 times higher (between 43 and 874 pg/g blood far) in these exposed persons than in the average German population. To evaluate possible TCDD-induced changes in the percentage of different lymphocyte subsets, we determined a large panel of lymphocyte subsets in the blood by flow cytometric analysis. Immunocompetence of T-and B-lymphocytes was tested by nitrogen (phytohemagglutinin, pokeweed mitogen)- induced lymphoproliferation assays and by assays using sensitive mixed-lymphocyte cultures. No significant differences could be detected between the individuals tested and controls for surface marker distribution or mitogen-induced lymphoproliferation TCDD-exposed subjects showed a reduced response to human lymphocyte antigen-allogeneic lymphocytes and interleukin-2-boosted proliferation. Responder cells of the dioxin-exposed persons proliferated less in response to irradiated stimulator cells (p &lt; or = 0.05), and the third-party mixed lymphocyte reaction against unirradiated stimulator cells revealed suppressive activity in the responder cell fraction compared to the controls (p &lt; or = 0.01). Furthermore, the capacity of a pool of T cells isolated from TCDD-exposed subjects to proliferate upon interleukin-2 stimulation was significantly diminished (p &lt; or = 0.05). TCDD has a long-term immunosuppressive-effect on T-helper cell function, which is mediated more likely by a reduced functionality of individual cells rather than by a reduction in absolute cell numbers in the peripheral blood.
Defining scientific misconduct. The relevance of mental state
Authors: R. Dresser
Journal: JAMA (1993)

HARDLY a month goes by without word from the science journalists of another alleged "research scandal." The reports are a product of the increased awareness that scientists, subject to normal human frailties, sometimes place self-interest and convenience above the painstaking disinterestedness good research demands. They also reflect the growing acknowledgment that traditional safeguards of replication and peer review are insufficient in the contemporary research climate. Today, scientists, institutional administrators, and government officials subject the research process to unprecedented scrutiny in an effort to detect, For editorial comment see p 915. investigate, penalize, and prevent behavior that unacceptably departs from scientific standards. After over a decade of extensive debate and analysis, however, an adequate definition of the targeted behavior has yet to emerge. There is a disturbing lack of clarity regarding the specific conduct that ought to be the focus of professional, institutional, and government attention. This lack of clarity has
Expression and hypoxic regulation of angiopoietins in human astrocytomas
Authors: Hao Ding, Luba Roncari, Xiaoli Wu, Nelson Lau, Patrick Shannon, Andras Nagy, Abhijit Guha
Journal: Neuro-Oncology (2001)

Vascular endothelial growth factor (VEGF) is a major inducer of tumor angiogenesis and edema in human astrocytomas by its interaction with cognate endothelial-speci c receptors (VEGFR1/R2).Tie1 and Tie2/Tek are more recently identi ed endothelial-speci c receptors, with angiopoietins being ligands for the latter.These angiogenic factors and receptors are crucial for the maturation of the vascular system, but their role in tumor angiogenesis, particularly in astrocytomas, is unknown.In this study, we demonstrate that the angiopoietin family member Ang1 is expressed by some of the astrocytoma cell lines.In contrast to VEGF, Ang1 is down regulated by hypoxia.Ang2 was not overexpressed.Expression proles of low-grade astrocytoma specimens were similar to those of normal brain, with low levels of Ang1, Ang2, and VEGF expression.Glioblastoma multiforme expressed higher levels of Ang1, but not to the same degree as pseudopalisading astrocytoma cells around necrotic and hypoxic zones expressed VEGF, as shown in previous studies.Ang2 expression in the highly proliferative tumor vascular endothelium was also increased, as was phosphorylated Tie2/Tek.The expression pro le of these angiogenic factors and their endothelial cell receptors in human glioblastomas multiforme was similar to that in a transgenic mouse model of glioblastoma multiforme.These data suggest that both VEGF and angiopoietins are involved in regulating tumor angiogenesis in human astrocytomas.
Medical Education, Registration and Hospital Service
Journal: JAMA (1922)

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
Circulatory Factors Governing the Viability of the Human Placenta, Based on a Morphologic Study
Journal: JAMA (1963)

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
Systemic mastocytosis with associated clonal hematological non-mast cell lineage disease: Clinical significance and comparison of chomosomal abnormalities in SM and AHNMD components
Authors: Sa A. Wang, Lloyd Hutchinson, Guilin Tang, Su S. Chen, Patricia P. Miron, Yang O. Huh, Dan M. Jones, Carlos Bueso-Ramos, Srdan Verstovsek, L. Jeffrey Medeiros, Roberto N. Miranda
Journal: American Journal of Hematology (2013)
A Handbook for School Nurses.
Journal: JAMA (1918)

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
Preventive Medicine and Public Health
Authors: William H. Foege
Journal: JAMA (1993)

The two foundation stones of public health have not changed. The philosophical base continues to be social justice in the application of scientific knowledge. The science base for defining problems, developing interventions, and measuring results is still epidemiology. However, as preventive medicine and public health make contributions in areas that were beyond our comprehension a professional lifetime ago, it is now not only accepted, but expected, that state and local health departments will respond to problems such as lead exposure, occupational hazards, tobacco, dietary fat, suicide clusters, violence, birth defects, and alcohol and other drug abuse. While the logic is inescapable, public health was slow to accept and even seek out the expertise of the social and behavioral sciences. Whether dealing with acquired immunodeficiency syndrome (AIDS) and its prevention, the treatment of tuberculosis, smoking cessation, or child abuse, the major intervention strategies require understanding human behavior, motivations, incentives, and thought
Glosario de Semiologia.
Journal: JAMA (1924)

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
Ensuring Effectiveness of Communitywide Emergency Cardiac Care
Journal: JAMA (1992)

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
THE THEORY OF OXYGEN SECRETION BY THE LUNGS
Journal: JAMA (1920)

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
PTH-067 Incidental Diagnosis of Inflammatory Bowel Disease in A British Bowel Cancer Screening Cohort: 6-Year Clinical Outcome of The First Reported Cohort
Authors: J Scott, U Nosegbe, R Butcher, A Abbasi, R Prudham, R George, J Limdi
Journal: Gut (2016)

<h3>Introduction</h3> The UK Bowel Cancer Screening programme (BCSP) was launched in 2006 in England and Wales, screening individuals aged 60–69 years with a Faecal Occult Blood test (FOBt) followed by a screening colonoscopy if FOBt positive. We reported the first ever experience of incidental diagnosis of Inflammatory bowel disease (IBD) through screening in 2012. We present a 6 year follow-up of this cohort. <h3>Methods</h3> We conducted a retrospective case record review of clinical outcomes until 31<sup>st</sup> December 2015 for patients diagnosed with IBD from the BCSP from April 2008 until September 2011. We reviewed their symptoms at diagnosis, treatment course and compared stage of disease at initial presentation to that at last follow-up. <h3>Results</h3> Between April 2008 and September 2011, 136,811 patients were invited to the BCSP and 67,485 were screened with a 49.33% uptake and FOBt positivity of 2.02%. Colonoscopy was performed in 1401 patients and 13 patients (3 female) were diagnosed with IBD. Of these, 6 patients had Ulcerative colitis (UC), 5 had Crohn’s disease (CD), 2 had IBD-unclassified (IBDU). One IBDU patient was subsequently re-classified as UC during follow-up. At diagnosis 7 (53.8%) patients were asymptomatic. An asymptomatic patient died of an unrelated cause, with follow-up data available for 12 patients. Median follow-up time was 80 months (range 39–87 months). Using the Montreal classification the distribution for UC included E1 (2), E2 (2) and E3 (2) and in CD showed L2 (7). Four CD patients had B1 disease and 1 had B2. Disease progressed in 2 patients and all 6 (100%) asymptomatic patients developed symptoms during follow-up. Treatment included steroids (10), 5 ASA (12), Azathioprine (6); Methotrexate (1) and Anti-TNF (Infliximab (2); Adalimumab (1)). Median time to immunomodulator was 29.5 months and to anti-TNF, 28.0 months. Mean CRP at diagnosis for those who progressed to Immunomodulator was 10.4 compared to 5.5 in those that didn’t and 15.5 in those that required biologics. A patient with symptomatic IBDU underwent subtotal colectomy 54 months after diagnosis but died 7 days post-operatively. Another patient died at 39 months from an unrelated cause. <h3>Conclusion</h3> Incidental diagnosis of IBD presents an important model for the study of early disease. A proportion of initially asymptomatic patients demonstrate disease progression with a rapid requirement for treatment escalation. <h3>Disclosure of Interest</h3> None Declared