tbuckley/cabot-search huggingface dataset:
Health Risks of Accidents at Nuclear Power Plants
Journal: New England Journal of Medicine (2011)

1. Falini B, Tiacci E. Hairy cell leukemia. In: Magrath IT, Boffetta P, Potter M, et al., eds. The lymphoid neoplasms. 3rd ed. New York: Oxford University Press, 2010:471-81. 2. Falini B, Tiacci E, Liso A, et al. Simple diagnostic assay for hairy cell leukaemia by immunocytochemical detection of annexin A1 (ANXA1). Lancet 2004;363:1869-70. [Erratum, Lancet 2004;363:2194.] 3. Matutes E, Morilla R, Owusu-Ankomah K, Houliham A, Meeus P, Catovsky D. The immunophenotype of hairy cell leukemia (HCL): proposal for a scoring system to distinguish HCL from B-cell disorders with hairy or villous lymphocytes. Leuk Lymphoma 1994;14:Suppl 1:57-61. 4. Foucar K, Falini B, Catovsky D, Stein H. Hairy cell leukaemia. In: Swerdlow S, Campo E, Harris NL, et al., eds. WHO classification of tumours of haematopoietic and lymphoid tissues. 4th ed. Lyon, France: International Agency for Research on Cancer, 2008:188-90. 5. Hoyer JD, Li CY, Yam LT, Hanson CA, Kurtin PJ. Immunohistochemical demonstration of acid phosphatase isoenzyme 5 (tartrate-resistant) in paraffin sections of hairy cell leukemia and other hematologic disorders. Am J Clin Pathol 1997;108:308-15.
PWE-118 Diagnostic and therapeutic outcomes in goblet cell appendiceal neuroendcorine tumours
Authors: M Pericleous, A Baneke, C Toumpanakis, T Meyer, M E Caplin
Journal: Gut (2012)

<h3>Introduction</h3> Goblet cell appendiceal neuroendocrine tumours (GCA-NETs), comprise approximately 6% of appendiceal neuroendocrine tumours (NETs) and share histologic features of both adenocarcinomas and NETs. We are presenting our data from 37 patients, focusing on diagnostic features, prognostic markers, treatment and survival. <h3>Methods</h3> A retrospective analysis included 18 male and 19 female patients (mean age: 48.8; range: 19–73 years). Follow-up was complete (mean follow-up: 4.1 years). <h3>Results</h3> Although majority of patients (69%) presented with appendicitis, 15.5% had bowel obstruction and 15.5% atypical abdominal pain. 27% had metastases at presentation (one in lungs). Chromogranin-A, CEA and CA-125 were not significantly raised in these patients. Initial treatment was appendicectomy (26 patients) and 24/26 had a subsequent prophylactic right hemicolectomy. Additional hysterectomy and bilateral oophorectomy was performed in six patients and four patients just underwent either single or bilateral oophorectomy. 12% had recurrence and all had Ki67 proliferation index ≥20%. Octreoscan was negative, but FDG-PET was positive in all these patients, and in patients with distal metastases at presentation. FOLFOX chemotherapy was given prophylactically in two patients with local lymph nodes resulting in no evidence of recurrence (Median=8 months) and in two patients with distal metastases resulting in only temporary disease stabilisation. 19% have died with disease and again all had Ki67 ≥20%. <h3>Conclusion</h3> GCA-NETs may metastasise to the lungs (first report in literature). Ki67 ≥20% seems to be related with a worse prognosis. FDG-PET is the molecular imaging of choice. No optimal biomarkers or chemotherapy regimens are available to date. <h3>Competing interests</h3> None declared.
A memorable patient: A communication headache
Authors: N. Fox
Journal: BMJ (1999)

The argument taking place among the three people waiting to see me next in the headache clinic was not noisy because it was conducted in sign language. My next patient was deaf-mute and had been arguing with her husband, also deaf-mute, and with the hospital interpreter. My patient was refusing to use the interpreter except via her husband. Communication was virtually impossible. Each question took several minutes to go, via interpreter, to husband and to patient, back and forth between husband and wife, and then finally back via interpreter to me. The answers seemed to bear no relation to the questions I thought I had asked. “Her headache has been present for over 40 years, since the age of 10, is getting worse, is present all the time, and the treatments do not work, and no …
THU0212 Improved Remission Rates Acquired by Adding Adalimumab to Methotrexate and Intraarticular Glucocorticoid Cannot be Maintained after Withdrawal of Adalimumab. A 2-Year Investigator Initiated Randomised, Controlled Study on Early Rheumatoid Arthritis
Authors: K. Hørslev-Petersen, M. L. Hetland, P. Junker, J. Pødenphant, T. J. Ellingsen, P. Ahlqvist, H. M. Lindegaard, A. Linauskas, A. Schlemmer, M. Y. Dam, I. Hansen, T. Lottenburger, A. Jørgensen, S. B. Krintel, J. Raun, C. G. Ammitzbøll, J. S. Johansen, M. Østergaard, K. Stengaard-Pedersen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Recently we reported, that DAS28CRP&lt;3,2 was achieved in more than 75% of early (&lt; 6 months duration), treatment naïve rheumatoid arthritis (ERA) patients using methotrexate (MTX) + intraarticular (i.a.) triamcinolone (TRIAM) and in case of inadequate response after the 3<sup>rd</sup> month triple therapy with MTX, sulphasalazine (SZS) and hydroxychloroquine (HCQ)<sup>1</sup>. Addition of adalimumab (ADA) at baseline yielded even better clinical responses and remission rates after treatment for one year. <h3>Objectives</h3> The purpose of the present investigation was to study whether the improved clinical response obtained by adding ADA to MTX + i.a. TRIAM injections can be maintained after withdrawal of ADA. <h3>Methods</h3> Patients with ERA were randomized to receive i.a. TRIAM (40 mg/ml) in any swollen joint in combination with MTX (20 mg/wk) for two years and placebo-ADA (MTX+PLA) or MTX+ADA (40 mg eow) during the first year. Peroral glucocorticoid was not allowed. After 1 yr, ADA/PLA was withdrawn. If patients had swollen joints and DAS28(CRP)&gt;3.2 during yr 2, SZS and HCQ were added, and if active disease persisted, ADA (40 mg eow) replaced SZS and HCQ in both treatment arms. Clinical response was assessed by DAS28(CRP), CDAI, SDAI and ACR/EULAR remission criteria. Analysis was by ITT with last observation carried forward. Medians (5%/95% percentiles) or percentage. Mann-Whitney or Pearson's chi-square tests. <h3>Results</h3> Baseline characteristics were similar in the MTX+PLA and MTX+ADA groups (DAS28(CRP) 5.6 (3.8-7.3) vs. 5.5 (3.8-7.8), NS). Table shows 1 and 2 years results. Serious adverse events were seen in 10 MTX+PLA patients (malignancy: 2, infections: 5, other: 2) and in 16 MTX+ADA patients (malignancy: 3, infections: 5, other: 8). <h3>Conclusions</h3> Combined MTX and i.a. TRIAM provided excellent disease control at 2 years' follow-up of ERA patients. The improved clinical responses observed during additional ADA administration could not be maintained after withdrawal of ADA. Radiographic data are needed to evaluate the overall effect of 1 yr of ADA as induction therapy in combination with MTX and i.a. TRIAM in ERA <h3>References</h3> Hørslev-Petersen K et al. Ann Rheum Dis 2012: <h3>Disclosure of Interest</h3> None Declared
Arguments for a healthcare tax on migrants are politically motivated
Authors: F. Arnold
Journal: BMJ (2013)

Arie’s summary of the economic consequences of healthcare of migrants to and from Britain fails to capture important aspects.1 To analyse the situation in its totality, we must consider important factors that are difficult to quantify. For example, more than 30% of NHS staff were trained overseas, at substantial cost saving to the NHS and losses to their (largely underdeveloped) countries …
PWE-149 The Efficacy and Safety of Treating Hepatitis C in Patients with a Diagnosis of Schizophrenia
Authors: Z Mustafa, J Schofield, P R Mills, M Priest, R Fox, S Dutta, J Morris, E Forrest, R Gillespie, A J Stanley, S Barclay
Journal: Gut (2013)

<h3>Introduction</h3> Treating hepatitis C with pegylated interferon alpha may induce or exacerbate psychiatric illness including depression, mania and aggressive behaviour. There is limited data regarding treatment in the context of chronic schizophrenia. We sought to establish the safety and efficacy of treatment of patients with a diagnosis of schizophrenia amongst patients attending treatment centres in Greater Glasgow <h3>Methods</h3> Patient and treatment data collected on the Scottish hepatitis C database were retrospectively analysed according to the presence or absence of a diagnosis of schizophrenia. Combination antiviral therapy was defined as Interferon (pegylated or standard) and Ribavirin. Treatment outcomes including sustained viral response (SVR) rates, reasons for treatment termination and adverse events were documented <h3>Results</h3> 5497 patients were recorded on the database, of whom 64 (1.2%) had a diagnosis of schizophrenia. Patients with and without schizophrenia were of similar age at diagnosis [median 34 (IQR 31–40) vs 36 (IQR 29–41) years, p = 0.85]. Patients with schizophrenia had higher rates of current or previous intravenous drug use [50/64 (78.1%) vs 3015/5433 (55.5%), p &lt; 0.01] and prior alcohol excess &gt; 21 units/week [25/64 (39%) vs 1211/5433 (22.2%), p = 0.02)]. More patients with schizophrenia had a diagnosis of cirrhosis [13/64 (20.3%) vs 589/5419 (10.86%), p = 0.02]. Of those patients who had attended at least one clinic appointment 1639/4415 (37.1%) of patients without schizophrenia commenced treatment versus 26/61 (42.6%) of patients with schizophrenia (p = 0.21). Patients with schizophrenia took almost three times as long to commence treatment after initial referral [median 1123 (IQR 531–2130) vs 421 (IQR 209–1086) days, p &lt; 0.01], despite similar times from referral to first attendance [median 65 (IQR 36–141) vs 62 (IQR 35–130) days, p = 0.92] The treatment outcomes were as follows: <h3>Conclusion</h3> Patients with stable schizophrenia are good candidates for hepatitis C treatment <h3>Disclosure of Interest</h3> None Declared.
Phase I evaluation of telatinib, a VEGF receptor tyrosine kinase inhibitor, in combination with irinotecan and capecitabine in patients with advanced solid tumors
Authors: P. Witteveen, M. Langenberg, H. M. Verheul, J. Roodhart, M. Roelvink, J. van der Sar, E. Brendel, N. Laferriere, J. H. Schellens, E. E. Voest
Journal: Journal of Clinical Oncology (2008)

2530 Background: Telatinib is an orally available, small molecule tyrosine kinase domain inhibitor of the VEGFR-2, VEGFR-3, PDGFR-β and c-Kit. We studied the feasibility of telatinib in combination with capecitabine and irinotecan in a phase I study. Methods: Telatinib (cohort 1 and 2: 300 mg bid; cohort 3: 600 mg bid; cohort 4; 900 mg bid continuously, day 1–21), irinotecan (cohort 1; 125 mg/m2 iv and cohort 2,3 and 4; 180 mg/m2 iv on day 1) and capecitabine (1,000 mg/m2 oral twice daily, day 1–14, all cohorts) were administered every three weeks in cohorts of at least 3 patients. Pharmacokinetic measurements were performed. Results: 17 patients (median age 60, range 40–71) with colon (6), gastric (2), pancreatic (1), small cell lung cancer (1) or other solid tumors (7) were included. The most frequently reported adverse events were (CTC grade I/II/III/all %) vomiting (29/18/6/53%), nausea (29/6/12/47%), fatigue (18/17/6/41%), diarhea (24/11/6/41%) and hand foot syndrome (18/23/0/41%). A silent myocardial infarction and a decreased LVEF CTC grade 3 were reported 9 weeks and 16 weeks after start of study treatment. The MTD was not reached at telatinib 900 mg bid, irinotecan 180 mg/m2, capecitabine 1000 mg/m2. The study was terminated when the advised dose of telatinib (900 mg bid), obtained in phase I single agent studies, was reached. Pharmacokinetic (PK) profiles of telatinib, irinotecan/SN 38, and capecitabine/5-FU were obtained on Day 1 of Cycle 1 (chemotherapy, without telatinib), Day 21 of Cycle 1 (telatinib without chemotherapy), and on Day 1 of Cycle 2 (telatinib with concomitant chemotherapy). No clinically relevant changes in exposure to telatinib, irinotecan, SN-38, capecitabine and 5-FU were observed upon coadministration of the 3 drugs. 3 out of 12 patients developed a PR and 6 out of 12 patients showed SD for at least 3 months. Conclusions: Preliminary data show that daily bid telatinib 900 mg can be safely combined with irinotecan (180 mg/m2 ) and capecitabine (1,000 mg/m2 oral twice daily, day 1–14). The observed tumor shrinkage and disease stabilization in various patients indicate preliminary activity of this combination. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration Bayer
ESTIMATING THE LIFETIME CLINICAL BENEFITS OF APIXABAN VERSUS ASPIRIN IN THE LOW RISK NON-VALVULAR ATRIAL FIBRILLATION PATIENTS IN THE US: HOW MAY RESULTS FROM AVERROES HELP IMPROVE PATIENT CARE?
Authors: Gregory Y.H. Lip, Tereza Lanitis, Jack Mardekian, Thitima Kongnakorn, Hemant Phatak, Paul Dorian
Journal: Journal of the American College of Cardiology (2015)
Modulation of Serum and Breast Ductal Fluid Lipids by a Very-Low-Fat, High-Fiber Diet in Premenopausal Women
Authors: D. Bagga, J. M. Ashley, S. Geffrey, H.-J. Wang, J. Barnard, R. Elashoff, D. Heber
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Modulation of Serum and Breast Ductal Fluid Lipids by a Very-Low-Fat, High-Fiber Diet in Premenopausal Women Get access D. Bagga, D. Bagga Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. M. Ashley, J. M. Ashley Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Geffrey, S. Geffrey Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar Hei-Jing Wang, Hei-Jing Wang Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Barnard, J. Barnard Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar R. Elashoff, R. Elashoff Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar D. Heber D. Heber Division of Clinical Nutrition and the UCLA Clinical Nutrition Research Unit, Department of Medicine, University of California, Los Angeles, School of MedicineLos Angeles, Calif. Correspondence to : David Heber, M.D., Ph.D., Division of Clinical Nutrition, Department of Medicine, UCLA School of Medicine, 1000 Veteran Ave., Rm. A1–57, Los Angeles, CA 90024–1742. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 18, 21 September 1994, Pages 1419–1421, https://doi.org/10.1093/jnci/86.18.1419 Published: 21 September 1994 Article history Received: 16 February 1994 Revision received: 07 June 1994 Accepted: 29 June 1994 Published: 21 September 1994
Abstract C60: IGF-1 signaling enhances mitochondrial activity and biogenesis in cancer cells independently of the glycolytic phenotype
Authors: Cedric Favre, Alexander Zhdanov, Dmitri Papkovsky, Rosemary O'Connor
Journal: Cancer Research (2011)

Abstract Cancer cells exhibit increases glycolytic rates and glucose transport to facilitate adaptation to the high energy demand imposed by increased proliferation rates and their often hypoxic environment. Moreover, this is often accompanied by reduced mitochondrial activity due to the accumulation of mtDNA mutations. Since there is close coordination of glycolysis and mitochondrial respiration, cancer cells may be particularly sensitive to pharmacological agents that increase mitochondrial activity. We recently identified a mitochondrial UTP transporter, PNC1, whose expression is induced by IGF-1 in an Akt-mTOR-dependant manner in transformed cells. PNC1 is a conserved orthologue of a yeast UTP carrier that is essential for maintenance of mtDNA replication and transcription and thereby mitochondrial biogenesis and activity. Suppression of PNC1 leads to increased mitochondrial ROS production, acquisition of an invasive phenotype, and mitochondrial biogenesis in cancer cells. Overexpression of PNC1 suppresses ROS production, mitochondrial biogenesis and protects from TGF-beta-induced epithelial-mesenchymal transition (EMT). The function of IGF-1-regulated PNC1 in cancer cells lead us to hypothesize that the IGF-1 signaling pathway may directly influence mitochondrial activity in cancer cells even in the presence of a switch to the glycolytic phenotype. Here we show that IGF-I stimulation increases mitochondrial mass in both normal cells and several cancer cell lines. The increased mitochondrial mass correlates with an increase in both mitochondrial protein and mRNA levels. This increase in mitochondrial biogenesis is also accompanied by increased oxygen consumption and ATP production. Furthermore, we show that the increase in both mitochondrial biogenesis and mitochondrial activity is due to IGF-1-mediated activation of a ROS-AMPK-PGC1 alpha signaling pathway. We conclude that mitochondrial activity and biogenesis in cancer cells is enhanced by the IGF-1 signaling pathway. Thus, attenuation of growth factor signaling may lead to accumulation of mtDNA damage and the consequent effects of increased ROS production on cancer cell phenotype. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr C60.
825 ANALYSIS OF THE OPTIMAL TVR DOSE PER WEIGHT JUDGING FROM ANEMIA DURING PEG-IFN/RBV/TVR COMBINATION THERAPY
Authors: Y. Karino, I. Ozeki, S. Hige, J. Toyota, M. Imamura, M. Tsuge, K. Chayama, N. Akuta, F. Suzuki, H. Kumada
Journal: Journal of Hepatology (2013)
Diaphragmatic hernia: a rare adverse event of colonoscopy
Authors: Yongqiang Li, Qingning Li
Journal: Endoscopy (2013)

A 25-year-old man underwent diagnostic colonoscopy because of mild upper abdominal pain. He had no history of trauma. The colonoscopy was completed without any significant difficulty. During the procedure, the patient did not complain of any pain or uncomfortable feelings. However, 24 hours after the procedure, the patient returned to the hospital with complaints of serious upper abdominal pain. On physical examination he had rebound tenderness in the upper abdomen and decreased breath sounds on the left chest. A chest radiograph ([Fig. 1]) indicated left diaphragmatic hernia. The chest and abdominal computed tomography (CT) scan ([Fig. 2]) confirmed a posterolateral diaphragmatic agenesis, with most of the stomach, the whole spleen, the tail of the pancreas, and the splenic flexure of the colon all appearing in the left chest. The patient underwent immediate left thoracotomy and diaphragmatic repair. He made an uneventful recovery and was discharged 15 days later. He is now asymptomatic.
Abstract SY05-03: microRNAs, EMT, and cancer stem cells
Authors: Thomas Brabletz
Journal: Cancer Research (2012)

Abstract We have shown, that in particular tumor cells at the invasive front undergo an epithelial-mesenchymal transition (EMT) and aberrantly express EMT-associated transcriptional repressors, like ZEB1. The amount of such cells strongly correlates with metastasis formation and poor clinical outcome. Strikingly, metastases show again a differentiated phenotype, indicating a mesenchymal-epithelial re-transition (MET) and a support a regulatory role of the tumor environment for malignant tumor progression. We described that the EMT-activator ZEB1 is a crucial promoter of metastasis and demonstrated that ZEB1 inhibits expression of cell polarity factors and the microRNA-200 family, whose members are strong inducers of epithelial differentiation. These results indicate that ZEB1 triggers a microRNA-mediated feedback-loop, which stabilizes EMT and promotes dissemination of cancer cells. Moreover we detected that in addition ZEB1 is necessary for the tumor initiating capacity of pancreatic and colorectal cancer cells. ZEB1 inhibits expression of miR-200c, miR-203 and miR-183, which cooperate to suppress expression of stem cell factors, as demonstrated for the polycomb repressor Bmi1. We propose that ZEB1 links EMT-activation and stemness-maintenance by suppressing stemness-inhibiting microRNAs and thereby is a promoter of mobile, migrating cancer stem cells. Notably, these cells also acquired a drug-resistance phenotype. Thus, targeting the ZEB1 - miR-200 feedback loop might be a promising treatment option for fatal tumors, such as pancreatic cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY05-03. doi:1538-7445.AM2012-SY05-03
DNA methylation within melatonin receptor 1A (MTNR1A) mediates paternally transmitted genetic variant effect on asthma plus rhinitis
Authors: Chloé Sarnowski, Catherine Laprise, Giovanni Malerba, Miriam F. Moffatt, Marie-Hélène Dizier, Andréanne Morin, Quentin B. Vincent, Klaus Rohde, Jorge Esparza-Gordillo, Patricia Margaritte-Jeannin, Liming Liang, Young-Ae Lee, Jean Bousquet, Valérie Siroux, Pier Franco Pignatti, William O. Cookson, Mark Lathrop, Tomi Pastinen, Florence Demenais, Emmanuelle Bouzigon
Journal: Journal of Allergy and Clinical Immunology (2016)
Glycemic Control and Peripheral Nerve Conduction in Children and Young Adults After 5–6 Mo of IDDM
Authors: Catherine Allen, Stephen C Duck, Sufit Robert L, Herbert M Swick, Donn J D'alessio
Journal: Diabetes Care (1992)

Objective A cohort of people (n = 86) was examined in the first few months after insulin-dependent diabetes mellitus (IDDM) diagnosis to evaluate the effect of hyperglycemia on nerve conduction velocities and latencies. Research Design and Methods Unselected cases with IDDM, who were 6–29 yr of age, were identified at diagnosis from a large, geographically defined area of southern Wisconsin. Peripheral nerve conduction was measured on a sample from this cohort. Results Peroneal nerve conduction velocity was significantly inversely related to glycosylated hemoglobin (P &amp;lt;0.05, age and height adjusted). All other nerve conduction velocities and latencies (median motor, median sensory, and sural) showed the same tendency, but the associations were not statistically significant. Twenty-four-hour urine C-peptide and duration of diabetes (3–11 mo) were not consistently related to nerve conduction parameters after controlling for age and height. Conclusions These findings suggest that as early as 5–6 mo after diabetes diagnosis, and at a time frequently characterized by partial remission of IDDM, hyperglycemia has a role in the acute slowing of nerve conduction velocity. Other factors such as residual endogenous insulin production do not appear to influence these early changes.