tbuckley/cabot-search huggingface dataset:
Birthplace and Classic Kaposi's Sarcoma in Italy
Authors: M. Geddes, S. Franceschi, D. Balzi, S. Arniani, L. Gafa, R. Zanetti
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Birthplace and Classic Kaposi's Sarcoma in Italy Get access Marco Geddes, Marco Geddes 1Servizio di Epidemiologia Descrittiva Valutativa e di Cancerogenesi Ambientale, Sezione Dell'ISTFirenze, Italy Search for other works by this author on: Oxford Academic PubMed Google Scholar Silvia Franceschi, Silvia Franceschi 2Servizio di Epidemiologia, Centro di Riferimento OncologicoAviano, Italy Search for other works by this author on: Oxford Academic PubMed Google Scholar Daniela Balzi, Daniela Balzi 3Unità Operativa di Epidemiologia, Servizio Multizonale di Prevenzione OncologicaFirenze Search for other works by this author on: Oxford Academic PubMed Google Scholar Stefania Arniani, Stefania Arniani 1Servizio di Epidemiologia Descrittiva Valutativa e di Cancerogenesi Ambientale, Sezione Dell'ISTFirenze, Italy Search for other works by this author on: Oxford Academic PubMed Google Scholar LOrenzo Gafà, LOrenzo Gafà 4Registro Tmori RagusaItaly Search for other works by this author on: Oxford Academic PubMed Google Scholar Roberto Zanetti Roberto Zanetti * 5Registro Tumori per il Piemonte e la Valle d' Aosta, Ospedale S. Giovanni Antica SedeTorino, Italy * Correspondence to: Silvia Franceschi, M.D., Servizio di Epidemiologia, Centro di Riferimento Oncologico, Via Pedemontana Occ., 33081 Aviano(PN), Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 13, 5 July 1995, Pages 1015–1017, https://doi.org/10.1093/jnci/87.13.1015 Published: 05 July 1995
S14 FVC as a surrogate marker for death and hospitalisation in IPF, sarcoid and bronchiectasis clinical trials
Authors: M Gimzewska, N Hirani, DA McAllister
Journal: Thorax (2013)

<h3>Introduction &amp; Objectives</h3> Decline in Forced Vital Capacity (FVC) is predictive of mortality in IPF and is commonly used as an end-point in IPF clinical trials. FVC has not, however, been formally validated as a surrogate end-point for death or hospitalisation, making it difficult to interpret the clinical importance of differences in decline in FVC, and its use controversial. Change in FVC has also been used in other chronic lung diseases as a clinical trial end-point. The aim of this project was to determine if FVC is a surrogate end-point for mortality and/or hospitalisation in IPF, sarcoidosis and bronchiectasis trials. We also aimed to comment on the reporting of FVC in chronic lung disease trials. <h3>Methods</h3> A systematic review was conducted. MEDLINE, EMBASE, LILACS and CENTRAL (1990-present) were searched on 25/03/2013. Reference lists and relevant journals (Jan-Apr 2013) were hand-searched, and experts in the field contacted to identify further studies. Only randomised controlled trials of drug interventions in adult participants with IPF, sarcoidosis and bronchiectasis were considered. <h3>Results</h3> 42 studies were identified, 37 of which were included in linear regression analysis. All studies reported mortality, and 17 studies reported hospitalisation. No association was found between difference in annual decline in FVC and annual mortality or hospitalisation rate (see graph). It was frequently difficult to combine results across studies due to variation in measures reported, or due to insufficient detail in reports. 32 studies reported change in FVC: 24 studies reported absolute changes (e.g. 7.2% decline from 67.6% to 60.4%), 4 reported relative change (e.g. 7.1% decline from 70.7% to 65.7%), and one study reported both. Clarification of change type from authors was required for 16 studies. <h3>Conclusions</h3> 1. Results of this analysis do not support the use of FVC as a surrogate end-point for mortality or hospitalisation in IPF, sarcoidosis or bronchiectasis trials. 2. Reporting of FVC in clinical trials is highly variable making synthesis of results for meta-analysis difficult. We suggest all trials make available baseline, final and change in FVC, both unadjusted and percent predicted, and as relative (% change), at least in an online appendix.
Attractive Option: Canine Clinical Trials
Authors: F. X. Mahaney
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Attractive Option: Canine Clinical Trials Get access Francis X. Mahaney, Jr Francis X. Mahaney, Jr Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 24, 20 December 1989, Pages 1860–1861, https://doi.org/10.1093/jnci/81.24.1860 Published: 20 December 1989
Perioperative Acute Kidney Injury—Reply
Authors: Charles Hobson, Matthew Huber, Azra Bihorac
Journal: JAMA Surgery (2016)

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 Surgery HomeNew OnlineCurrent IssueFor Authors Podcast 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 Surgery journal
Seeing in the Dark
Authors: Eric Manheimer
Journal: New England Journal of Medicine (2012)

In a dark time, the eye begins to see. — Theodore RoethkeThe clouds were heavier, the air thicker. The wind picked up. The news that the subways would be shut down at 7 p.m. spread quickly by word of mouth. The streets in our Greenwich Village neighborhood were filled with people carrying food and water to their apartments. From my home, I could see the lights of LaGuardia and Kennedy airports and the imposing red-brick power station with its four smokestacks on 14th Street and the East River. We spent the weekend filling our bathtub with water and . . .
Abstract 701: A mechanistic study of mdr1a gene regulation in vivo using bioimaging
Authors: Long Gu, Min Lin, Kathleen Higgins, Barry Forman, Susan E. Kane
Journal: Cancer Research (2011)

Abstract The human P-glycoprotein (Pgp) encoded by the MDR1 gene is as a transmembrane drug transporter that mediates the efflux of drugs from cells. It confers multidrug resistance in cancer cells that overexpress MDR1. In addition, basal expression of MDR1 in organs such as liver, kidney, and colon affects the pharmacokinetics of drug uptake and excretion for agents that are substrates for Pgp transport. Nuclear receptors such as SXR and CAR have been suggested as possible master regulators of xenobiotic- and drug-inducible expression of MDR1 and of other genes involved in drug metabolism in drug processing organs. However, the mechanism of MDR1 regulation in tumors or in normal, non-malignant tissue, particularly in response to xenobiotics, has yet to be demonstrated in vivo. To facilitate the mechanistic study of MDR1 gene regulation in vivo, we previously reported a mouse model that allows non-invasive bioimaging of the mdr1 gene expression in vivo and in real time by inserting a firefly luciferase (fLUC) gene into the murine mdr1a genetic locus by homologous recombination.1 To determine the role of PXR, the murine homologue of SXR, in drug-mediated induction of mdr1a, we crossed mdr1a.fLUC mice with PXR knockout mice. Pregnenolone-16α-carbonitrile (PCN), a known SXR substrate, induced intestinal mdr1a.fLUC expression in the PXR wild type background but not the PXR knockout background. Notably, mdr1a.fLUC was re-inducible over three rounds of drug dosing, which could be measured longitudinally in our real-time assessment of gene expression. TCPOBOP, a known CAR ligand, induced mdr1a.fLUC in both the wild type and knockout background, consistent with the idea that mdr1a is also regulated by the CAR nuclear receptor. The chemotherapeutic agent docetaxel induced mdr1a.fLUC in the PXR wild type background but induction was dramatically reduced in the PXR KO background; paclitaxel gave only low-level induction in both genetic backgrounds. This result is consistent with the reported ligand specificity of mouse PXR. Future studies in a CAR-null background will determine if the observed effect of paclitaxel on mdr1a expression is mediated through CAR. These studies demonstrate the utility of our murine imaging model for the in vivo study of mdr1 gene regulation in real time. Studies with additional chemotherapeutic drugs and genetic backgrounds will establish the variety of agents capable of inducing mdr1a at the transcriptional level and the trans-acting factors that are involved in such induction. 1Gu et al. Proc Natl Acad Sci 106:5394-5399 (2009) 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 701. doi:10.1158/1538-7445.AM2011-701
Abstract P1-05-07: Prognostic relevance of Claudin-2 expression in metastatic breast cancer
Authors: I Hedenfalk, S Kimbung, A Kovacs, L Skoog, Z Einbeigi, T Walz, M Malmberg, N Loman, M Fernö, T Hatschek
Journal: Cancer Research (2012)

Abstract The site of relapse is known to be a strong prognostic factor of survival from metastatic breast cancer. The liver is the third most frequent site affected and patients with hepatic metastases have an inferior prognosis relative to patients with bone and lung metastases. Predicting the likelihood of liver metastasis after adjuvant therapy of primary breast cancer is challenging. The aim of this study was to identify and characterize genes associated with breast cancer liver metastases. We thus performed global transcriptional profiling of 120 metastatic lesions from different anatomical sites from breast cancer patients enrolled in a randomized clinical trial1 and found that while the expression of other matrix remodelling and tight-junction molecules was down-regulated in liver metastases, Claudin-2 (CLDN2) was significantly up-regulated (p = 0.001). Furthermore, high expression of CLDN2 was also observed amongst patients diagnosed with a liver metastasis, irrespective of the specific site of the metastasis that was profiled, compared to patients without hepatic metastases (p = 0.001). We further investigated the prognostic significance of CLDN2 protein expression by immunohistochemical staining of primary tumours and matched lymph node metastases from a larger cohort of patients (n∼200) with metastatic breast cancer. We found CLDN2 to be significantly more frequently expressed in lymph node metastases compared to primary tumours (p = 0.013). Also, consistent with mRNA expression levels, more frequent expression of CLDN2 protein was observed in the primary tumours of patients who eventually developed a liver metastasis (p = 0.027). Interestingly, high expression of CLDN2 in the primary tumour was associated with a shorter time to recurrence (p = 0.032). Specifically, high expression of CLDN2 in the primary tumour was associated with a shorter progression to liver metastasis (p = 0.002). These data highlight a potential role of CLDN2 in the development and prognosis of breast cancer liver metastases. 1. Hatschek, T., et al. Individually tailored treatment with epirubicin and paclitaxel with or without capecitabine as first-line chemotherapy in metastatic breast cancer: a randomized multicenter trial. Breast Cancer Res Treat. 2012, 131(3):939–47. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-05-07.
Abstract 3421: Twist1 and clusterin regulate epithelial-mesenchymal transition
Authors: Masaki Shiota, Amina Zoubeidi, Masafumi Kumano, Seiji Naito, Colleen C. Nelson, Martin E. Gleave
Journal: Cancer Research (2011)

Abstract INTRODUCTION AND OBJECTIVE: Clusterin (CLU) is a stress-activated, cytoprotective molecular chaperone, and is highly expressed in cells surviving apoptotic stimuli and in advanced and treatment-resistant cancers. In addition, CLU has recently been reported to be implicated in epithelial-mesenchymal transition (EMT). Similarly, oncogenic transcription factor Twist1 which binds to E-box (core sequence, 5’-CANNTG-3’) is known to be a master regulator of EMT. Although CLU is known to be transcriptionally activated by heat-shock factor 1, the mechanism CLU expression in EMT is not fully elucidated. This study begins to define mechanism of CLU expression and relevance in EMT of prostate cancer. METHODS: Human prostate cancer PC-3 and LNCaP cells were used to examine whether the manipulation of Twist1 expression affected CLU expression using quantitative real-time PCR, Western blotting and luciferase reporter assay using CLU promoter region. Chromatin-immunoprecipitation (ChIP) assays were used to determine whether Twist1 binds to CLU promoter region. We also examined markers of EMT after treatment with TGF-β1 and manipulation of Twist1/CLU expression. RESULTS: Twist1 overexpression was shown to upregulate CLU expression whereas Twist1 knockdown reduced CLU expression. ChIP assay and luciferase reporter assay revealed that Twist1 was bound to CLU promoter region and regulated CLU transcription. Treatment with TGF-β1, which is known to be an EMT-inducing cytokine, upregulated Twist1 expression followed by CLU expression. Furthermore, CLU knockdown ameliorated EMT induced by TGF-β1 and Twist1. CONCLUSIONS: This study indicates that CLU regulates EMT induced by TGF-β1 and Twist1 in prostate cancer cells. Modulation of CLU expression may be a useful strategy for developing novel therapeutics regulating EMT. 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 3421. doi:10.1158/1538-7445.AM2011-3421
Acyclovir Treatment of the Chronic Fatigue Syndrome
Journal: New England Journal of Medicine (1989)

Abstract Twenty-seven adults with a diagnosis of the chronic fatigue syndrome were enrolled in a double-blind, placebo-controlled study of acyclovir therapy. The patients had had debilitating fatigue for an average of 6.8 years, accompanied by persisting antibodies to Epstein–Barr virus early antigens (titers ≥1:40) or undetectable levels of antibodies to Epstein–Barr virus nuclear antigens (titers <1:2) or both. Each course of treatment consisted of intravenous placebo or acyclovir (500 mg per square meter of body-surface area) administered every eight hours for seven days. The same drug was then given orally for 30 days (acyclovir, 800 mg four times daily). There were six-week observation periods before, between, and after the treatments. Three patients had acyclovir-induced nephrotoxicity and were withdrawn from the study. Of the 24 patients who completed the trial, similar numbers improved with acyclovir therapy and with placebo (11 and 10, respectively). Neither acyclovir treatment nor clinical impro...
Framework launched for GP fundholding BMA publishes code on hepatitis B NHS trust boards are on Nolan agenda GPs organise commissioning conference
Authors: L. Beecham
Journal: BMJ (1994)

# Framework launched for GP fundholding {#article-title-2}

A new accountability framework has been launched for general practice fundholding. It identifies four main areas of fundholders' responsibilities—management accountability, accountability to patients and the wider public, financial accountability, and professional accountability.

Under management accountability it is proposed that practices should set out in an annual plan how it proposes to use the fund and management allowances and submit the plan to the health authority for approval. Fundholders should announce major shifts in their purchasing intentions; should submit a brief annual report to the health authority setting out performance against plan; and should hold regular meetings with the health authority.

To make them more accountable to the public fundholders are expected to publish key documents such as annual practice plans and primary health care charters and send them to the community health council as well as making them available for consultation by patients. There should be appropriate …
Case 48-1990
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, Powel A. Kazanjian, Eugene J. Mark
Journal: New England Journal of Medicine (1990)

Presentation of CaseA 65-year-old man was admitted to the hospital because of a persistent cough, increasing dyspnea, and bilateral pulmonary infiltrates.There was a history of Wegener's granulomatosis 11 months earlier, with involvement of the kidneys, lungs, and paranasal sinuses; a test for antineutrophil cytoplasm antibodies (ANCA) was positive. Prednisone and cyclophosphamide were administered, and plasmapheresis was performed. The ANCA test became negative, but renal function worsened progressively, with the development of hypertension, and long-term hemodialysis was required twice weekly. Microscopical examination of a stained specimen of sputum early in the hospital course showed acid-fast bacilli, and isoniazid and . . .
Abstract 820: Molecular markers for head and neck cancer detection
Authors: Lutecia Pereira, Isildinha Reis, Robert Duncan, Jarrard Goodwin, Elizabeth Franzmann
Journal: Cancer Research (2010)

Abstract Introduction: Fifty thousand new cases of HNSCC are diagnosed in the United States each year. Unfortunately, most of these cases are advanced and only cured about 40% of the time. Cure rates could reach over 80% if diagnosed in earlier stages. We are developing a simple and inexpensive molecular screening test for the early detection of HNSCC. The markers under investigation are detectable in oral rinses and include soluble CD44 (solCD44), hyaluronic acid (HA) and total protein. Materials and Methods: To study the population most likely to benefit from this early detection test, high-risk controls were identified by their smoking and/or drinking behavior from primary care clinics. They received a complete head and neck exam and had no clinical evidence of malignancy or premalignancy. Low-risk controls were normal volunteers. All subjects completed a detailed questionnaire including demographic, socioeconomic, risk factor and general health information. Oral samples were collected using a previously described swish and gargle method. We performed the solCD44, HA and protein assays in blinded fashion on oral rinses from 18 HNSCC cases, 18 frequency-matched high-risk controls and 21 low-risk controls using previously reported ELISA and ELISA-like assays. Results: We statistically assessed the adequacy of matching between the cases and high-risk controls with respect to age, gender, race, socioeconomic status, tobacco and alcohol exposure and oral health. There were no significant differences between cases and controls for any of these variables except for a borderline significant difference in race. Log2solCD44 levels were significantly higher in cancer cases (2.42 ng/ml) and high-risk controls (2.12 ng/ml) compared to low risk controls (0.64 ng/ml, p&amp;lt;0.05). Log2protein levels were also higher in cancer cases (0.88 mg/ml) and high-risk controls (0.97 mg/ml) compared to low-risk controls (0.52, p&amp;lt;0.05). Following receiver operating curve analysis, the AUC for distinguishing high-risk controls from low-risk controls was 0.94 for solCD44 and 0.82 for protein. The AUC for distinguishing cancer from low-risk controls was 0.95 for solCD44 and 0.77 for protein. After adjusting for race, the AUC for distinguishing cancer from high-risk controls was 0.76 for solCD44 and 0.68 for protein. Both of these were better for the nonwhite group (0.84 for solCD44 and 0.83 for protein). Conclusions: In this preliminary data set, the solCD44 and protein test appear to effectively distinguish HNSCC cases from high and low-risk controls. Race may have an impact on results. Further work including more subjects with longer follow-up must be done to confirm or refute these findings. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 820.
Abstract 1430: Automation of both sample preparation and analysis of a cell migration assay
Authors: Sarah E. Burroughs, Keren I. Hulkower, Simone Schicktanz, Jennifer A. Fronczak, Karin Boettcher, Timothy E. Cloutier
Journal: Cancer Research (2011)

Abstract Cell migration is a critical event in the process of angiogenesis. Aberrant cell migration can contribute to metastatic cancer and other diseases. Understanding the signaling pathways involved in regulating migration is crucial for discovering new targets to develop drugs that inhibit migration and angiogenesis. Because cell migration is a phenotypic or whole-cell event, it can be challenging to conduct and quantitatively analyze such cell-based assays in a consistent and efficient manner. Automation of such assays allows researchers to analyze more conditions than would be feasible with manual methods. With advances in migration plate technology and automated liquid handling, it is now possible to increase one's capacity to run these important assays. However, liquid handling automation parameters are critical and must be optimized so as not to interfere with the biology or its analysis. Here we demonstrate a successful automation of the sample preparation the Platypus Oris® Pro 384-Well Cell Migration Assay on a PerkinElmer JANUS® Automated Liquid Handling Workstation. In addition, quantitation of such assays is now possible with multi-mode detection and High Content Screening (HCS) technologies. Analysis of cell migration using the Operetta® / Harmony® HCS platform and the EnSpire™ multilabel plate reader shows the assay to be a robust and reproducible quantification of cell motility. Using these methods the authors demonstrate statistically significant inhibition of this phenotypic cellular process by a variety of compounds, including cytochalasin D and the MEK inhibitor U0126. 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 1430. doi:10.1158/1538-7445.AM2011-1430
New Project Helps Ballplayers Quit Smokeless Tobacco
Authors: Tom Reynolds
Journal: JNCI Journal of the National Cancer Institute (1991)

New Project Helps Ballplayers Quit Smokeless Tobacco Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 17, 4 September 1991, Page 1215, https://doi.org/10.1093/jnci/83.17.1215 Published: 04 September 1991