tbuckley/cabot-search huggingface dataset:
Factors influencing post-transfusional platelet increment in pediatric patients given hematopoietic stem cell transplantation
Authors: CL Balduini, L Salvaneschi, C Klersy, P Noris, M Mazzucco, F Rizzuto, G Giorgiani, C Perotti, P Stroppa, MDi Pumpo, B Nobili, F Locatelli
Journal: Leukemia (2001)
Clinical Experience With Tc-99m Nofetumomab Merpentan (Verluma) Radioimmunoscintigraphy
Authors: H B Breitz, A Tyler, M J Bjorn, T Lesley, P L Weiden
Journal: Clinical Nuclear Medicine (1997)

Tc-99m nofetumomab merpentan (Verluma), consisting of a Fab fragment of the pancarcinoma murine antibody NR-LU-10, has been previously evaluated as a diagnostic imaging agent in staging patients with lung cancer. The authors have taken advantage of the pancarcinoma reactivity of this antibody to select patients with a variety of carcinomas for radioimmunotherapy trials. These have included gastrointestinal, breast, ovary, pancreas, kidney, cervix, and bladder carcinoma. This article documents the range of tumor types and locations that can be identified by gamma camera imaging with this radioimmunoconjugate. Tumor was positively identified in 92% of 107 patients studied. In 15 patients, the images led to suspicion of previously unknown disease. The authors conclude that this radioimmunoconjugate is useful in assessing patients with advanced disease. Additional studies may be warranted to explore further the potential benefit of this diagnostic imaging agent in evaluating the extent of disease in patients with a variety of carcinomas.
The impact of the 2014–15 Ebola virus disease epidemic on emergency care attendance and capacity at a tertiary referral hospital in Freetown, Sierra Leone: a retrospective observational study
Authors: Daniel Youkee, Nathaniel Williams, Michael Laggah, Patrick Howlett, Marta Lado, Leanne Brady, Samuel B Seisay, Hooi-Ling Harrison
Journal: The Lancet (2016)
Case 42-1994
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, Eric L. Logigian, Megan B. Murray
Journal: New England Journal of Medicine (1994)

Presentation of CaseA 19-year-old man was admitted to the hospital on New Year's Day because of ascending paresthesias, progressive weakness of the legs, and a rash.He had been well until 10 days earlier, when a sore throat, productive cough, sweats, fever with a rise in the temperature to 39.4 °C, and dizziness developed. A physician found pharyngeal injection with questionable tonsillar exudates, and amoxicillin was prescribed. A rapid test for group A streptococcal antigen was negative. Five days before admission, the patient felt better, discontinued the amoxicillin, and returned to work. Three days later he began to have . . .
Abstract 5517: Pre-existing medical conditions and risk of breast cancer in Korea: A hospital based case-control study
Authors: Sun Jae Jung, Ji-Yeob Choi, Keun-Young Yoo, Daehee Kang
Journal: Cancer Research (2012)

Abstract Objective: To estimate the effect of highly prevalent medical conditions in Korean population on breast cancer risk in a large case-control study conducted in Korea. Methods: Cases were 3,358 women with incident, histologically confirmed breast cancer in two major hospitals interviewed between 2000 and 2007. Controls were 1820 women admitted to the same hospital and one another hospital for a variety of non-neoplastic conditions. Information of each disease was obtained from standardized questionnaire by trained personnel. Odds ratio(OR) for each disease were derived from multiple logistic regression adjusted for age, hospital, enrollment year, body mass index, age of menarche, age of first pregnancy and family history of breast or other cancer. Results: Among all incident breast cancer patients, pre-existing gastroduodenal diseases and asthma reduced the risk of breast cancer (OR=0.48; 95% confidence interval (C.I.)=0.35-0.67 and OR=0.39; 95% C.I.=0.24-0.64), whereas pre-existing ovarian disease increased the risk(OR=1.63; 95% C.I.=1.12-2.36) when other factors adjusted. Among premenopausal and postmenopausal women, the results of pre-existing gastroduodenal diseases and asthma were similar to those in all cases. But only among postmenopausal women, pre-existing diabetes and hypertension increased the risk of breast cancer significantly (OR=1.66; 95% C.I.=1.01-2.70, OR=1.41; 95% C.I.=1.03-1.92). Conclusion: There had been many studies indicating the association between diabetes and breast cancer development, and our results present the possibility of other disease to effect breast cancer development which can be differed by the menopausal status of women. Also, our study indicates other possible correlation for pre-existing diseases such as asthma, gastroduodenal disease and hypertension with altered breast cancer risk. 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 5517. doi:1538-7445.AM2012-5517
P47 AXL SIGNALING VIA 14-3-3 ZETA IS CENTRAL FOR THE PROGRESSION OF HEPATOCELLULAR CARCINOMA
Authors: P. Reichl, M. Dengler, F. van Zijl, C. Reichel, H. Huber, W. Sieghart, M. Peck-Radosavljevic, M. Grubinger, W. Mikulits
Journal: Journal of Hepatology (2014)
Treatment of Pain in Dying Patients
Authors: Kathryn L. Tucker
Journal: New England Journal of Medicine (1998)

To the Editor: A disturbingly large percentage of dying patients experience unrelieved pain.1 This percentage is far higher than it should be, given the availability of pain medications and the knowledge of how to use them. Many physicians believe that they could risk disciplinary action if they use high doses of narcotics or other controlled substances to manage pain at the end of life.2 They also believe that if they undertreat pain, they risk no professional consequences. Dying patients clearly have the right to adequate pain medication; this was recently recognized by the Supreme Court.3,4 Physicians have not been . . .
AB0059 Chromatin Modifying Mechanisms in Macrophages Differ between Healthy Controls and Patients Wih Rheumatoid Arthritis
Authors: K. Rooke, L. Kruidenier, H. Che, P. Mander, C. Swales, R. Prinjha, U. Oppermann
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Macrophages are central players in the pathogenesis of rheumatoid arthritis, and targeted inhibition of their principal cytokine products, TNFα and IL-6, are effective treatments. However, a significant proportion of patients still fail to respond to current therapies, and there is a continuing need for new therapeutic targets. Epigenetic modifications are increasingly recognised as key pathogenic features of RA and therefore inhibition of epigenetic anomalies has been identified as a potential future therapeutic strategy. <h3>Objectives</h3> This study used small molecule inhibitors to identify epigenetic factors that mediate macrophage-derived pro-inflammatory cytokine production from healthy donors and patients with RA. <h3>Methods</h3> Peripheral blood monocytes (PBMCs) were isolated from 10 healthy donors and 3 patients with rheumatoid arthritis; synovial fluid (SF) macrophages were also derived from the RA patients following therapeutic arthrocentesis. All patients were recruited from the Nuffield Orthopaedic Centre and gave written informed consent. PBMCs were differentiated into macrophages and stimulated with lipopolysaccharide (LPS) as a model of inflammation. PBMC and SF-derived macrophages were then treated with a panel of small molecule bromodomain, demethylase and deacetylase inhibitors to assess the impact of chromatin modification on macrophage pro-inflammatory cytokine production, including TNFα and IL-6. Cytokine production was detected by multiplex ELISA and supported by q-PCR data. Cell viability was determined using a WST-1 assay. <h3>Results</h3> Macrophages from healthy volunteers and patients with RA responded differently to the tested epigenetic inhibitors. Bromodomain (PFI-1, (+)-JQ1 and I-BET), demethylase (GSK-J4) and deacetylase (SAHA and CXD101) inhibitors all significantly reduced the production of TNFα and IL-6 from healthy donor PBMC-derived macrophages. The bromodomain and demethylase inhibitors effectively inhibited cytokine production from the PBMCs of patients with RA, but of the deacetylase inhibitors tested, only SAHA had significant effect. In addition, cytokine production from RA SF-derived macrophages was significantly reduced by the bromodomain inhibitors and SAHA-mediated deacetylase inhibition, but there was no significant effect with demethylase inhibition. <h3>Conclusions</h3> Differential responses to epigenetic inhibitors may represent differences in epigenetic modifications or mechanisms between healthy and RA macrophages. Further investigation into these differences, as well as specific mechanistic effects of epigenetic inhibitors, could lead to a clearer understanding of disease pathogenesis and help to identify novel therapeutic targets. <h3>Acknowledgements</h3> This work was generously funded by BBSRC and GSK <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4218
397 THE PRO-INFLAMMATORY RESPONSE INDUCED BY TOLL-LIKE RECEPTOR ACTIVATION IN VIVO IS NOT IMPAIRED IN THE LIVER OF HBV-TRANSGENIC MICE LACKING HBsAg
Authors: C.I. Real, R. Broering, K. Kleinehr, S. Driftmann, R. Schirmbeck, M. Lu, G. Gerken, J.F. Schlaak
Journal: Journal of Hepatology (2013)
Effect of Hydroxyurea on the Frequency of Painful Crises in Sickle Cell Anemia
Authors: Samuel Charache, Michael L. Terrin, Richard D. Moore, George J. Dover, Franca B. Barton, Susan V. Eckert, Robert P. McMahon, Duane R. Bonds
Journal: New England Journal of Medicine (1995)

In a previous open-label study of hydroxyurea therapy, the synthesis of fetal hemoglobin increased in most patients with sickle cell anemia, with only mild myelotoxicity. By inhibiting sickling, increased levels of fetal hemoglobin might decrease the frequency of painful crises.
Abstract 5585: Phase I clinical trial of continuous infusion of tyroserleutide in patients with advanced hepatocellular carcinoma
Authors: Jia Jinbin, Xiao Zhen-Yu, Chen Xiao-Ping
Journal: Cancer Research (2012)

Abstract Hepatocellular carcinoma (HCC) is usually diagnosed in advanced stage, which causes difficulty of using surgical treatment. Previous studies demonstrated that tyroserleutide (YSL), an immunologically active tripeptide compound, could suppress the proliferation and tumor formation of some liver cancer cell lines. We aimed to investigate the feasibility and toxicity of continuous administration of YSL by a portable infusion pump to patients with advanced HCC and its biologically effective but non-toxic doses used in outpatient setting. Forty patients (12 in stage 1, 28 in stage 2, total 10 treated in each dose cohort) were treated with YSL 6, 12, 18 or 24 mg/d lasting for 5 days. No treatment-related mortality was observed. The overall response rates were 25% (3/12) and 7.2% (2/28) in stages 1 and 2 respectively. The median 6-month overall survival (OS) in stage 1 were 75, 64, and 41 days for 6, 18, and 24 mg/d groups respectively; all patients survived in the 12 mg/d group. The median OS in stage 2 were 68, 72, and 60 days for 12, 18, and 24 mg/d groups respectively; all survived in the 6 mg/d group. The most common adverse reactions were abnormal liver function (59/107) and hemogram (22/107). The dose limiting toxicities of 24 mg/d group contained abdominal distention (1/10), sicchasia (1/10), hyponatremia (1/10), myocardiac ischemia (1/10), and abnormal hemogram (6/10). We conclude that the continuous administration of YSL by portable infusion pump was well tolerated. Treatment responses of doses 6 and 12 mg/d were better than other two groups. Further studies of continuous infusion of YSL to determine its efficacy are warranted. Keywords tyroserleutide • hepatocellular carcinoma • clinical trial • portable infusion pump [Supported by China Postdoctoral Science Foundation-funded project (No. 20080440077 and 200902203)] 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 5585. doi:1538-7445.AM2012-5585
Abstract 247: A novel mPGES-1/EGR1/beta-catenin signaling axis in hepatocarcinogenesis
Authors: Dongdong Lu, Chang Han, Tong Wu
Journal: Cancer Research (2011)

Abstract Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme that couples with cyclooxygenase-2 (COX-2) for the production of PGE2. Although COX-2-derived PGE2 is known to participate in the development and progression of several human cancers including hepatocellular carcinoma (HCC), the role of mPGES-1 in carcinogenesis remains poorly understood. This study provides novel evidence for an important role of mPGES-1 in human HCC. Forced overexpression of mPGES-1 in two HCC cell lines (Hep3B and Huh7) promoted tumor cell growth and increased clonogenic formation capacity, in vitro. Conversely, mPGES-1 knockdown inhibited tumor cell growth and prevented clonogenic formation. Overexpression of mPGES-1 in Hep3B and Huh7 cells also increased cell invasion and migration/repair capacity, whereas knockdown of mPGES-1 reduced these parameters. Flowcytometric analysis revealed that mPGES-1 knockdown caused cell cycle arrest at G1/S checkpoint. In SCID mouse tumor xenograft model, mPGES-1 overexpressed cells formed palpable tumors at earlier time points and developed larger tumor nodules when compared to the control cells (p&amp;lt;0.01); in contrast, mPGES-1 knockdown delayed tumor development and reduced tumor growth in SCID mice (p&amp;lt;0.01). Mechanistically, mPGES-1-induced HCC cell proliferation, invasion and migration involve activation of EGR1 and beta-catenin. mPGES-1 induced the formation of EGR1-beta-catenin complex, which interacted with TCF4 transcription factors in HCC cells. Our findings depict a novel mPGES1/EGR1/beta-catenin signaling axis that is crucial in hepatocarcinogenesis. 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 247. doi:10.1158/1538-7445.AM2011-247
FRI0547 Improved work participation in early rheumatoid arthritis in the netherlands 1995-2011
Authors: K. Britsemmer, W. van der Weele, D. van Schaardenburg
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> During the past decades, major steps were made towards earlier diagnosis of rheumatoid arthritis (RA) and development of better therapies, leading to an improved prognosis of patients with early RA. Retaining work participation is increasingly accepted as an important outcome of RA treatment. <h3>Objectives</h3> To study whether the work participation in early RA has changed in the Netherlands in the years 1995-2011. <h3>Methods</h3> All incident patients with early RA according to the 2010 ACR/EULAR classification criteria and of working age (18-64 years), included from 1 January 1995 to 31 December 2009 in the Reade early arthritis cohort in Amsterdam, were selected. Patient cohorts were analysed in 5-year inclusion periods (1995-1999, 2000-2004, 2005-2009), corresponding to initial DMARD monotherapy, initial DMARD combination therapy and addition of biologics in case of non-response, respectively. The mean hours of paid work per week in the three subcohorts were analysed over time and compared to age and sex matched controls (data from the entire Dutch population [Statline database: www.cbs.nl]) <h3>Results</h3> The three subcohorts consisted of 138 (1995-1999), 206 (2000-2004) and 208 (2005-2009) patients at baseline. Five year follow-up data were available for 85, 122, and 62 patients, respectively. No significant differences in baseline age and DAS28 were found. Patients included in 1995-1999 had longer disease duration than patients included in the other sub-cohorts (median 5 months vs 4 and 3 months, respectively [p&lt;0.001]). The percentage with paid work was 49% (1995-1999), 52% (2000-2004) and 60% (2005-2009) at baseline in RA patients compared to 61%, 64% and 66% in the general population (p&lt;0.05, except for 2005-2009). After 5 years follow-up the percentages with paid work in early RA were 45%, 55% and 68%, respectively. Figure 1 shows the mean hours of paid work of early RA patients over 5 year follow-up compared to the mean hours of age and sex matched controls from the entire Dutch population. <h3>Image/graph</h3> <h3>Conclusions</h3> Work participation of early RA patients at their first visit was less than in the general population, but this difference declined in subsequent subcohorts. In working early RA patients, the mean hours of paid work were also lower than in the general population. Work participation rates and number of paid hours per week declined during follow-up in the patients included between 1995-1999, but remained at least stable in patients included in the later periods. A limitation is that no data were available on the timing of the presumed decline in work participation in the period before the diagnosis of RA. Although these data do not allow explanatory analysis, it is probable that the improved work participation after diagnosis is closely related to the earlier recognition and intensified treatment of early RA. <h3>Disclosure of Interest</h3> None Declared
Effect of Intramuscular Injections of Benzathine Penicillin G on Some Acute-Phase Reactants
Authors: Raymond C. Haas, Angelo Taranta, Harrison F. Wood
Journal: New England Journal of Medicine (1957)

BENZATHINE penicillin (N,N′-dibenzylethylenediamine dipenicillin G) is a long-acting repository penicillin that provides low serum penicillin levels for three or four weeks after a single intramuscular injection of 1,200,000 units.1 It has been shown to be highly effective and safe in preventing recurrences of rheumatic fever in children2 and is being widely used for this purpose as well as for the treatment of streptococcal pharyngitis.It was observed that after the intramuscular injection of this compound, in addition to local inflammatory reaction and fever,1 , 2 elevation of the erythrocyte sedimentation rate and appearance of C-reactive protein were apt to occur. Since both . . .
Effect of policy, economics, and the changing alcohol marketplace on alcohol related deaths in England and Wales
Authors: Nick Sheron, Ian Gilmore
Journal: BMJ (2016)

The economic downturn and rises in alcohol taxation seem to have stemmed the persistent rise in alcohol related deaths in England and Wales, but <b>Nick Sheron</b> and <b>Ian Gilmore</b> caution that changes to fiscal policy could see mortality increase once more
Abstract 196: Functional role of death-associated protein 3 in high grade gliomas of childhood
Authors: Valentina A. Vladimirova, Niels Soerensen, Torsten Pietsch
Journal: Cancer Research (2011)

Abstract Background: High grade gliomas (HGG) are highly invasive tumors and respond poorly to conventional treatments. Although significant progress has been made in understanding the molecular pathways that lead to the development of HGG in adults, comparatively few data is available for gliomas of childhood. The death-associated protein 3 (DAP3) is localized on the chromosomal region 1q21-22 that has been previously described as a region of frequent chromosomal gain associated with poor outcome in HGG. Moreover, DAP3 has been reported to be overexpressed and to play anti-apoptotic role in invasive glioblastoma cells. Methods: In the current study to investigate the functional role of DAP3 in pediatric versus adult HGG, we suppressed the endogenous DAP3 protein using DAP3-specific short hairpin RNA (shRNA) or chemical inhibitors of protein kinase C, and analyzed the phenotypic effect on glioma cell proliferation, migration, mitochondrial morphology and apoptosis. Results: We found that knockdown of DAP3 by shRNA induced mitochondrial fragmentation and apoptosis in pediatric glioma cell lines while in adult glioma cell lines it suppressed cell proliferation and reduced mitochondrial potential without inducing mitochondrial fragmentation. Specific chemical inhibition of the two classical PKC isoforms (PKCα and PKCβ) significantly reduced the expression of DAP3 protein in both pediatric and adult glioma cell lines. The inhibition of PKCα changed cell morphology, mitochondrial status and significantly suppressed proliferation and migration of both pediatric and adult glioma cell lines without associated caspase activation indicating that DAP3 may mediate nonapoptotic form of cell death in HGG. The suppression of PKCβ rendered pediatric glioma cells more sensitive to the apoptotic effect of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) through a caspase-dependent process as compared with adult glioma cells suggesting a possible implication of DAP3 in intrinsic and extrinsic pathways for apoptosis in pediatric HGG. Conclusion: Our findings confirmed the anti-apoptotic role of DAP3 in glioma cell biology suggesting that specific PKC isoforms mediated the DAP3 suppression of apoptosis in HGG and pointed out the specific functional role of this protein in mitochondrial maintenance. DAP3 may represent a novel target for the treatment of gliomas. 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 196. doi:10.1158/1538-7445.AM2011-196