tbuckley/cabot-search huggingface dataset:
Detection of HSV-specific DNA in biopsy tissue of patients with erythema multiforme by polymerase chain reaction
Authors: J. ASLANZADEH, K. F. HELM, M. J. ESPY, S. A. MULLER, T. F. SMITH
Journal: British Journal of Dermatology (1992)

Formalin-fixed paraffin-embedded skin biopsies of lesions of erythema multiforme (EM) from 32 patients and 13 controls were examined for the presence of herpes simplex virus (HSV) by polymerase chain reaction (PCR) and for histological findings by direct immunofluorescence and staining with haematoxylin and eosin. HSV-specific DNA was detected in 23 (72%) patients. A history of recurrent skin rash was present in 59% of the PCR-positive cases, while 55% had had suspected HSV infections. Only two PCR-positive specimens were found in patients without a history of recurrent rash and/or previous oral lesions. One biopsy was positive for HSV by conventional cell cultures. There was no significant difference in histology between HSV-related and HSV-negative cases of EM. In the 13 control specimens [bullous pemphigoid (3), dermatitis herpetiformis (2), lichen planus (1), aphthous ulcer (1), fixed-drug eruption (1), varicella-zoster (1), hypereosinophilic syndrome (1), photocontact dermatitis (1), contact dermatitis (1), and cellulitis (1)], no HSV-DNA was detected.
Statins being prescribed for those "least in need"
Authors: B. Christie
Journal: BMJ (1999)

A lack of resources is hampering attempts to implement an effective strategy to combat the problem of coronary heart disease in the United Kingdom, which has some of the highest rates of the disease in the world, a consensus conference held last week has concluded.

The conference, organised by the Royal College of Physicians of Edinburgh, examined the issue of lowering lipids to prevent vascular events and called for a clear commitment by the government to implement preventive policies of proved value.

The conference agreed that a joint approach needs …
Pulmonary Resection for Metastatic Osteosarcoma
Authors: J. Judson McNamara
Journal: JAMA (1968)

<h3>To the Editor:—</h3> Pulmonary resection for isolated metastatic tumor has now been established as potentially curative.<sup>1-4</sup>The chances for cure appear to depend principally on the type of primary tumor and the interval between resection of the primary tumor and resection of the metastatic lesion. We have recently resected a second pulmonary metastasis of an osteogenic sarcoma 35 years after extremity amputation for the primary tumor and 17 years after thoractomy and resection of the first metastasis. The remarkable behavior of this usually highly malignant tumor has prompted the present report. <h3>Report of a Case:—</h3> A 68-year-old white woman entered the hospital with a three-week history of chest pain on the right side and hemoptysis. X-ray films of the chest revealed an 8-cm mass in the upper lobe of the right lung which appeared to contain calcium (Fig 1). In 1933, at age 33 the patient underwent amputation of
Frequency-dependent effects of quinidine on the ventricular action potential and QRS duration in humans.
Authors: K Nademanee, W G Stevenson, J N Weiss, V B Frame, M G Antimisiaris, T Suithichaiyakul, C M Pruitt
Journal: Circulation (1990)

We studied the frequency-dependent effects of quinidine on the right ventricular action potential and QRS duration in 10 patients (nine men and one woman; mean age, 57 +/- 14 years) undergoing electrophysiologic studies for clinical indications. The right ventricular monophasic action potential, electrocardiographic, and conventional intracardiac electrical signals from various sites were recorded at different pacing cycle lengths from 30 seconds to 1 minute before and after a 10-mg/kg i.v. quinidine infusion. We used the extrastimulus technique to determine the effects of quinidine on ventricular refractory periods at different pacing cycle lengths and on the abrupt changes of the action potential duration. The action potential duration progressively decreased as the ventricular pacing rate increased at baseline and after quinidine infusion. Quinidine significantly increased the action potential duration from that of control by 25 msec (p less than 0.02) at the relatively slow pacing cycle lengths of 600, 500, and 400 msec. Quinidine's effect on the action potential duration was attenuated at the pacing cycle length of 350 msec and became negligible at 300 msec. In contrast, quinidine progressively lengthened the QRS duration as the pacing rate increased (20, 18, 37, 46, and 34 msec at pacing cycle lengths of 600, 500, 400, 350, and 300 msec, respectively; p less than 0.05). There were no rate-dependent changes in the QRS duration during the control period. The relation between the ventricular refractory periods and the action potential duration at different pacing cycle lengths was also determined before and after quinidine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Proteomics analysis of mitochondrial proteins reveals overexpression of a mitochondrial protein chaperon, prohibitin, in cells expressing hepatitis C virus core protein
Authors: Takeya Tsutsumi, Mami Matsuda, Hideki Aizaki, Kyoji Moriya, Hideyuki Miyoshi, Hajime Fujie, Yoshizumi Shintani, Hiroshi Yotsuyanagi, Tatsuo Miyamura, Tetsuro Suzuki, Kazuhiko Koike
Journal: Hepatology (2009)

The hepatitis C virus (HCV) core protein is involved in viral pathogenesis such as oxidative stress induction and lipid metabolism disturbance, and is primarily located in the cytoplasm and endoplasmic reticulum in association with lipid droplets as well as in the mitochondria. To clarify the impact of the core protein on mitochondria, we analyzed the expression pattern of mitochondrial proteins in core protein-expressing cells by two-dimensional polyacrylamide gel electrophoresis. Several proteins related to the mitochondrial respiratory chain or protein chaperons were identified by mass spectrometry. Among the identified proteins with consistently different expressions, prohibitin, a mitochondrial protein chaperon, was up-regulated not only in core-expressing cells but also in full-genomic replicon cells and livers of core-gene transgenic mice. The stability of prohibitin was increased through interaction with the core protein. Further analysis demonstrated that interaction of prohibitin with mitochondrial DNA-encoded subunits of cytochrome c oxidase (COX) was disturbed by the core protein, resulting in a significant decrease in COX activity. Conclusion: The HCV core protein affects the steady-state levels of a subset of mitochondrial proteins including prohibitin, which may lead to an impaired function of the mitochondrial respiratory chain with the overproduction of oxidative stress. (HEPATOLOGY 2009.)
Metabolism of aromatic amines by prostaglandin H synthase.
Authors: J A Boyd, T E Eling
Journal: Environmental Health Perspectives (1985)

The metabolism of aromatic amines by the peroxidase activity of prostaglandin H synthase (PHS) has been studied in this laboratory by use of two model compounds, the carcinogenic primary amine 2-aminofluorene (2-AF) and the substituted amine aminopyrine (AP). 2-AF is oxidized by PHS to 2, 2-azobisfluorene, 2-aminodifluorenylamine, 2-nitrofluorene, polymeric material, and products covalently bound to macromolecules. In the presence of phenolic compounds, 2-AF oxidation results in the formation of amine/phenol adducts. The data are consistent with a one-electron mechanism of 2-AF oxidation by PHS; furthermore, an N-hydroxy intermediate is not involved in 2-AF metabolism by PHS. PHS also catalyzes the binding of 2-AF to DNA in vitro. Unique 2-AF/DNA adducts were isolated and are distinct from the N-(deoxyguanosin-8-yl)-2-AF adduct formed from the reaction of N-hydroxy-2-AF with DNA. These new adducts represent a marker unique to peroxidative activation of 2-AF. AP is oxidized by the peroxidase activity of PHS to the cation radical, with one molecule of hydroperoxy fatty acid reduced for every two molecules of AP free radical formed. The decay of the AP radical follows second order kinetics, supporting the proposed mechanism in which the AP radical disproportionates to an iminium cation, followed by hydrolysis of this species to the demethylated amine and formaldehyde. In the presence of glutathione, the cation radical is reduced to the parent amine, resulting in the formation of the glutathione thiyl radical. It thus appears that both primary and substituted aromatic amines may undergo one-electron oxidation by PHS.
Abstract 4414: Clinical significance of CHD1L in hepatocellular carcinoma and therapeutic potentials of virus-mediated CHD1L depletion
Authors: Leilei Chen, Hon Man Chan, Xin-Yuan Guan
Journal: Cancer Research (2011)

Abstract Background: Hepatocellular carcinoma (HCC) is among the most lethal of human malignancies. It is difficult to detect early, has a high recurrence rate and is refractory to chemotherapies. Amplification of 1q21 is one of the most frequent genetic alterations in HCC. CHD1L is a newly identified oncogene responsible for 1q21 amplicon. This study aims to investigate the role of CHD1L in predicting prognosis and chemotherapy response of HCC patients, its chemo-resistant mechanism and whether virus-mediated CHD1L silencing has therapeutic potentials for HCC treatment. Methods: We assessed the clinical significance of CHD1L in a cohort of 109 HCC cases including 50 cases who received transarterial chemoembolization (TACE) treatment by clinical correlation and Kaplan-Meier analyses. CHD1L-overexpressing cell model was generated and the mechanism of CHD1L-involved chemo-resistance was investigated. Adenovirus-mediated silencing method was used to knockdown CHD1L and its effects on tumorigenicity as well as chemo-resistance were investigated in vivo and in vitro. Results: Overexpression of CHD1L was significantly associated with tumor microsatellite formation (p=0.045), advanced tumor stage (p=0.018), overall survival (OS) time (p=0.002), OS time of patients who received TACE treatment (p=0.028) and chemo-resistance (p=0.020) in HCC. Interestingly, CHD1L could inhibit apoptosis induced by 5-fluorourail (5-FU) but not doxorubicin (DOX). The mechanistic study revealed that the involvement of Nur77-mediated pathway in chemotherapeutic agent-induced apoptosis can dictate if CHD1L could confer resistance to chemotherapy. Furthermore, adenoviral vector containing shRNAs against CHD1L (CHD1L-shRNAs) could suppress cell growth, clonogenicity and chemo-resistance to 5-FU. In vivo study found that CHD1L-shRNAs could inhibit xenograft tumor growth and increase the sensitivity of tumor cells to 5-FU in nude mice. Conclusions: Our study highlighted for the first time the prognostic value of CHD1L in HCC and the potential application of virus-mediated CHD1L silencing in HCC therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4414. doi:10.1158/1538-7445.AM2011-4414
Prevention and the Reforming U.S. Health Care System: Changing Roles and Responsibilities for Public Health
Authors: Randolph L. Gordon, Edward L. Baker, William L. Roper, Gilbert S. Omenn
Journal: Annual Review of Public Health (1996)

This review presents historical and cost-effectiveness perspectives of prevention in health care; discusses the nature, extent, and determinants of health system change, particularly the transition to managed care with large integrated health care corporations; and identifies implications for public health agencies and opportunities for prevention within the reforming health system.
Radical Prostatectomy for Incidental (Stage T1a–T1b) Prostate Cancer: Analysis of Predictors for Residual Disease and Biochemical Recurrence
Authors: Umberto Capitanio, Vincenzo Scattoni, Massimo Freschi, Alberto Briganti, Andrea Salonia, Andrea Gallina, Renzo Colombo, Pierre I. Karakiewicz, Patrizio Rigatti, Francesco Montorsi
Journal: European Urology (2008)
Abstract 359: Systematic manipulation of brain tumor diversity using piggybac transposon mediated transgenesis approach in rat.
Authors: Fuyi Chen, Albert Becker, Joseph LoTurco
Journal: Cancer Research (2013)

Abstract Animal models are important for interrogating the native biology of tumor formation, invasiveness, and may lead to novel therapeutic approaches. Here we describe the development of a rat glioma model which provides a fast and convenient approach to reproducibly induce brain tumors of different type in rat. We utilize a piggybac transposon system delivered by in utero electroporation (PB-IUE) to express oncogenic HRasV12 in different cell types in CNS. When expression of HRasV12 was driven by ubiquitous CAG promoter in radial glia cells, glioblastoma multiforme (GBM) was induced. When we specifically express HRasV12 in astrocytes using a mouse GFAP promoter, malignant astroglioma resembling GBM was induced in rat brains. In contrast, anaplastic oligoastrocytoma was induced when HRasV12 were expressed in oligodendrocytes under the control a rat MBP promoter. Surprisingly when co-expressing a basic helix loop helix protein Neurogenin2 (Ngn2) with HRasV12 both driven by CAG promoter, primitive neuroectodermal tumor (PNET) like tumors were generated. Molecular classification of tumors induced by CAG and GFAP HRasV12 matched mesenchymal GBM subtypes. Our data demonstrate the induction of different tumor types using a non-viral piggyBac transposon mediated transgenesis approach. The binary plasmid system we developed provides a method to direct different oncogenetic signals to different cell types. The models generated with this system should facilitate our understanding of the sources of tumor diversity. Citation Format: Fuyi Chen, Albert Becker, Joseph LoTurco. Systematic manipulation of brain tumor diversity using piggybac transposon mediated transgenesis approach in rat. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 359. doi:10.1158/1538-7445.AM2013-359
Pathology of the Heart and Blood Vessels
Authors: Henry C. McGill
Journal: JAMA (1969)

Dr. Gould has edited an updated and enlarged third edition of this cardiovascular pathology text that has been widely used since it first appeared in 1953. Ten new chapters increase its scope. The book, prepared by 34 writers and the editor, presents an encyclopedic assemblage of information. The 28 chapters range widely in style and approach. They include philosophical and historical broad-brush surveys such as the history of cardiac pathology and the relation of civilization to heart disease; detailed descriptions of the pathogenesis, morbid anatomy, and manifestations of major cardiac diseases; brief descriptions of cardiac lesions produced by systemic diseases; reviews of experimental cardiac lesions such as metabolic myocardial necroses; and introductions to diagnostic and therapeutic techniques such as electrocardiography, cardiac surgery, and angiography. Particularly helpful and convenient to have in the same volume are chapters on embryology, gross anatomy, conduction system structure, and gross examination of the heart. Discussions
A Comedy of Errors
Authors: J. J. Robbins
Journal: JAMA (1966)

<h3>To the Editor:—</h3> In assessing the controversy between Drs. Fontana and Lowell, the principal point of agreement seems to be that of the difficulty of measuring symptoms and therapeutic results, both by patient and by physician observer. No amount of objectivity by the most unbiased of observers has been able to circumvent the inherent differences between patients, or between symptoms, in this variable disease. When observations are inconsistent, are not of high degree of accuracy, or vary with different observers, the scientific method demands that other means of ascertaining the truth be employed. The first of these available to the investigator is that of reason. Do these observations make sense, and can some rational explanation be made? When hyposensitization is examined in this light, it is found that the originators of this form of therapy, Noon and Freeman, believed that allergens were synonymous with toxins and that they were immunizing
Detection and Management of Small Aortic Aneurysms
Authors: Robert W. Thompson
Journal: New England Journal of Medicine (2002)

Abdominal aortic aneurysms arise through a chronic degenerative process that produces localized weakening of the aortic wall. They have a natural history characterized by progressive expansion and eventual rupture.1 Population-based screening studies reveal that up to 9 percent of persons over 65 years of age have an unsuspected and asymptomatic abdominal aortic aneurysm, and it is estimated that ruptured abdominal aortic aneurysms cause at least 15,000 deaths each year in the United States.2 The principal goal of treatment for these aneurysms is to extend life by preventing the rupture of the aneurysm. There is long-standing evidence that elective surgical repair . . .
EFFECT ON MORTALITY OF METOPROLOL IN ACUTE MYOCARDIAL INFARCTION
Authors: Å. Hjalmarson, J. Herlitz, I. Málek, L. Rydén, A. Vedin, A. Waldenström, H. Wedel, D. Elmfeldt, S. Holmberg, G. Nyberg, K. Swedberg, F. Waagstein, J. Waldenström, L. Wilhelmsen, C. Wilhelmsson
Journal: The Lancet (1981)
IS CAROTID STENTING A DURABLE TECHNIQUE? ACUTE AND UP TO 7 YEARS LONG-TERM CLINICAL RESULTS FROM A SINGLE-CENTER CONSECUTIVE SERIES OF PATIENTS
Authors: Piero Montorsi, Costanza Boiti, Stefano Galli, Paolo Ravagnani, Marco Agrifoglio, Franco Fabbiocchi, Daniela Trabattoni, Giovanni Teruzzi, Antonio Bartorelli, Gianluca Pontone, Cesare Fiorentini
Journal: Journal of the American College of Cardiology (2010)
An elderly woman with recurrent episodes of confusion
Authors: A. Brooks, B. Vaidya
Journal: BMJ (2010)

<h3>Background and objective</h3> The impact of the COVID-19 pandemic on the quality of care for patients with acute myocardial infarction (AMI) is uncertain. We aimed to compare quality of AMI care in England and Wales during and before the COVID-19 pandemic using the 2020 European Society of Cardiology Association for Acute Cardiovascular Care quality indicators (QIs) for AMI. <h3>Methods</h3> Cohort study of linked data from the AMI and the percutaneous coronary intervention registries in England and Wales between 1 January 2017 and 27 May 2020 (representing 236 743 patients from 186 hospitals). At the patient level, the likelihood of attainment for each QI compared with pre COVID-19 was calculated using logistic regression. The date of the first national lockdown in England and Wales (23 March 2020) was chosen for time series comparisons. <h3>Results</h3> There were 10 749 admissions with AMI after 23 March 2020. Compared with before the lockdown, patients admitted with AMI during the first wave had similar age (mean 68.0 vs 69.0 years), with no major differences in baseline characteristics (history of diabetes (25% vs 26%), renal failure (6.4% vs 6.9%), heart failure (5.8% vs 6.4%) and previous myocardial infarction (22.9% vs 23.7%)), and less frequently had high Global Registry of Acute Coronary Events risk scores (43.6% vs 48.6%). There was an improvement in attainment for 10 (62.5%) of the 16 measured QIs including a composite QI (43.8% to 45.2%, OR 1.06, 95% CI 1.02 to 1.10) during, compared with before, the lockdown. <h3>Conclusion</h3> During the first wave of the COVID-19 pandemic in England and Wales, quality of care for AMI as measured against international standards did not worsen, but improved modestly.
Detecting Radiation Damage
Authors: Rebecca Voelker
Journal: JAMA (1998)

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
Hypoxia-inducible MicroRNA-210 augments the metastatic potential of tumor cells by targeting vacuole membrane protein 1 in hepatocellular carcinoma
Authors: Qiao Ying, Linhui Liang, Weijie Guo, Ruopeng Zha, Qi Tian, Shenglin Huang, Jian Yao, Jie Ding, Meiyan Bao, Chao Ge, Ming Yao, Jinjun Li, Xianghuo He
Journal: Hepatology (2010)

Abstract As the “master” microRNA that is induced by hypoxia, miR-210 is involved in multiple processes in the hypoxia pathway. However, whether miR-210 mediates hypoxia-induced tumor cell metastasis still remains unclear. Here, we demonstrate that miR-210 is frequently up-regulated in hepatocellular carcinoma (HCC) samples and promotes the migration and invasion of HCC cells. Furthermore, miR-210 can be induced by hypoxia in HCC cells and mediates hypoxia-induced HCC cell metastasis. We identify vacuole membrane protein 1 (VMP1) as the direct and functional downstream target of miR-210; in addition, we show that its expression is negatively correlated with the expression of miR-210 in HCC. Intriguingly, VMP1 is reduced by hypoxia, and down-regulation of VMP1 by miR-210 mediates hypoxia-induced HCC cell metastasis. Conclusion: These findings extend our understanding of the function of miR-210 in the hypoxia pathway, and this newly identified hypoxia/miR-210/VMP1 pathway should facilitate the development of novel therapeutics against hypoxic tumor cells. (Hepatology 2011)
CD4-mediated regulatory T-cell activation inhibits the development of disease in a humanized mouse model of allergic airway disease
Authors: Helen Martin, Sebastian Reuter, Nina Dehzad, Anke Heinz, Iris Bellinghausen, Joachim Saloga, Ina Haasler, Stephanie Korn, Helmut Jonuleit, Roland Buhl, Christian Becker, Christian Taube
Journal: Journal of Allergy and Clinical Immunology (2011)