tbuckley/cabot-search huggingface dataset:
Abstract C3: Gene expression profiling supports the hypothesis that human ovarian surface epithelia are pluripotent and capable of serving as ovarian cancer initiating cells
Authors: Nathan J. Bowen, L. DeEtte Walker, Lilya V. Matyunina, Sanjay Logani, Kimberly A. Totten, Benedict B. Benigno, John F. McDonald
Journal: Cancer Research (2009)

Abstract Accumulating evidence suggests that somatic stem cells undergo mutagenic transformation into cancer initiating cells. The serous subtype of ovarian adenocarcinoma in humans has been hypothesized to arise from at least two possible classes of progenitor cells: the ovarian surface epithelia (OSE) and/or an as yet undefined class of progenitor cells residing in the distal end of the fallopian tube. Comparative gene expression profiling analyses were carried out on OSE removed from the surface of normal human ovaries and ovarian cancer epithelial cells (CEPI) isolated by laser capture microdissection (LCM) from human serous papillary ovarian adenocarcinomas. Differentially expressed genes were analyzed using gene ontology, molecular pathway, and gene set enrichment analysis algorithms. Consistent with pluripotent capacity, genes in pathways previously associated with adult stem cell maintenance are highly expressed in ovarian surface epithelia and are not expressed or expressed at very low levels in serous ovarian adenomcarcinoma. The results of the gene expression analyses were selectively confirmed using immunohistochemistry. Among the over 2000 genes that are significantly differentially expressed, a number of pathways and novel pathway interactions are identified that may contribute to ovarian adenocarcinoma development. Our results are consistent with the hypothesis that human ovarian surface epithelia are pluripotent and capable of serving as the origin of ovarian adenocarcinoma. While our findings do not rule out the possibility that ovarian cancers may also arise from other sources, they are inconsistent with claims that ovarian surface epithelia cannot serve as the origin of ovarian cancer initiating cells. Citation Information: Cancer Res 2009;69(23 Suppl):C3.
OP0259-PARE Multi–lingual touch screen page on arthritis in children (DINFO)
Authors: J.S. Sagen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> <i>General:</i> The Norwegian organization for children and youth with rheumatism (BURG) is part of The Norwegian rheumatism Association (NRF). BURG is an organization working for children and youths with rheumatisms, and their families. With one national office and regional branches BURG focuses on activities information about diagnoses and rights for children and youths with rheumatism. <i>Specific:</i> BURG was in May 2011 granted the funds (150 000 NOK) by The South–Eastern Norway Regional Health Authority to publish multi–lingual information on arthritis in children. NRF has worked together with the Hospital IT unit, which is a unit that provides learning and mastery tools for children and youths (Dinfo), to produce quality assured information and include it in the Dinfo training tool. Dinfo is easy and can be used both on touch screen and ordinary PCs. <h3>Objectives</h3> NRF's main goal is that young people with rheumatism takes part in activities that give them tools to manage everyday life in the best way possible. Dinfo is a tool to help us reach this goal. Dinfo's primary meaning is to be an information guide for patients, but it's also make sure that families and health care easily receive the same information as the patients. <h3>Methods</h3> By using DINFO we reach a broader segment around the target group – which includes the patient's family and the health professionals working for the patient. Today's society is multicultural and it may be difficult to communicate in a foreign language, to a patient who has another language and another culture. The knowledge that is communicated may be inadequate. To solve this problem dinfo is multilingual. This in turn leads to increased efficiency and qualifiedtreatment of patients. <h3>Results</h3> Dinfo do not replace interpersonal communication between health professionals and patient, but complements and supports it, and contribute to increased confidence and motivation. In this way patients and their families gets personalized information that gives greater meaning than general information. <h3>References</h3> http://hospitality.no/dinfo_burg/ WWW.burg.no http://hospitality.no/ <h3>Disclosure of Interest</h3> None Declared
False-Negative Tc-99m MIBI Scintigraphy in Histopathologically Proved Recurrent High-Grade Oligodendroglioma
Authors: Ingeborg Goethals, Oliver De Winter, Rudi Dierckx, Allessio Annovazzi, Alberto Signore, Christophe van de Wiele
Journal: Clinical Nuclear Medicine (2003)

Tc-99m MIBI is a small lipophilic radioligand that enters cells by diffusion and is preferentially trapped in mitochondria. As a result of the high mitochondrial activity in tumors, Tc-99m MIBI accumulates significantly more in tumor tissue compared with normal tissues. Accordingly, Tc-99m MIBI has been used successfully to visualize primary, metastatic, and recurrent tumor. In brain tumors, Tc-99m MIBI SPECT has been shown to identify tumor recurrence after treatment in high-grade gliomas. In this report, early (30 minutes after injection) and delayed (4 hours after injection) Tc-99m MIBI SPECT did not visualize a histopathologically proved recurrent high-grade oligodendroglioma. Increased vascular supply, disruption of the blood-brain barrier, high-grade cancer, and viability of tumor cells are decisive factors related to increased Tc-99m MIBI uptake in brain tumors. However, the authors' results suggest that still other mechanisms may be involved in Tc-99m MIBI accumulation, which may account for false-negative imaging in brain tumors.
Four treatment failures of pharyngeal gonorrhoea with ceftriaxone (500 mg) or cefotaxime (500 mg), Sweden, 2013 and 2014
Authors: D Golparian, A K Ohlsson, H Janson, P Lidbrink, T Richtner, O Ekelund, H Fredlund, M Unemo
Journal: Eurosurveillance (2014)

We describe four cases in Sweden of verified treatment failures of pharyngeal gonorrhoea with ceftriaxone (500 mg; n=3) or cefotaxime (500 mg; n=1) monotherapy. All the ceftriaxone treatment failures were caused by the internationally spreading multidrug-resistant gonococcal NG-MAST genogroup 1407 clone. Increased awareness of treatment failures is crucial particularly when antimicrobial monotherapy is used. Frequent test of cure and appropriate verification/falsification of suspected treatment failures, as well as implementation of recommended dual antimicrobial therapy are imperative.
Hazard of Overwhelming Infection after Splenectomy in Childhood
Authors: A. J. Eraklis, S. V. Kevy, L. K. Diamond, R. E. Gross
Journal: New England Journal of Medicine (1967)

THE exact role of the spleen in preventing or suppressing bacterial infections in human beings is unknown. The spleen, an important part of the reticuloendothelial system, acts as a filter for circulating debris including bacteria and as an important source of lymphoid cells and antibody production. There should therefore be little doubt that splenectomy may alter the ability to prevent or to suppress some infections. However, in a child, the extent to which this change is clinically significant has been a source of continuing controversy.Since the initial report by King and Shumacker in 19521 a number of articles have . . .
Positive Tc-99m MIBI Breast Study Related to a Psoriatic Lesion
Authors: Q T Islam, M K Karimeddini, R P Spencer, S H Kurtzman, J A Vento
Journal: Clinical Nuclear Medicine (2000)

A woman was examined because of a painful left breast accompanied by excoriation and ulceration of the areola and nipple and some deformity. Because of the pagetoid changes in the nipple, a Tc-99m Miraluma (Tc-99m sestamibi) imaging study was performed. This revealed uptake in the areola and a small area near the chest wall. Biopsy of the areola revealed psoriasis. She was treated with an antipsoriatic cream, which healed the skin lesion. Two months after the initial Tc-99m Miraluma image, the results of another study were negative in both the areola and deep regions.
OUTCOMES OF PATIENTS WITH ≥3+ AORTIC REGURGITATION AND PRESERVED LEFT VENTRICULAR EJECTION FRACTION: A SINGLE TERTIARY CARE CENTER EXPERIENCE
Authors: Amgad G. Mentias, Ke Feng, Alaa Alashi, L. Leonardo Rodriguez, A. Gillinov, Joseph Sabik, Lars Svensson, Brian Griffin, Milind Desai
Journal: Journal of the American College of Cardiology (2016)
P1004 COMPARISON OF THE ACCURACY OF SHEAR WAVE ELASTOGRAPHY AND ACOUSTIC RADIATION FORCE IMPULSE IN DETERMINING LIVER FIBROSIS AMONG PATIENTS WITH CHRONIC LIVER DISEASE
Authors: J.-A.V. Bisnar, J.L. Gopez-Cervantes, J.C. Bocobo, I.H.Y. Cua, W. Polido
Journal: Journal of Hepatology (2014)
Abstract 4054: Prognostic value of microRNAs expression in diffuse large B cell lymphoma
Authors: Michal Kushnir, Meir Lahav, Ron Ram, Shlomit Gilad, Meirav Zepeniuk, Lahav Cohen, Meital Ezagouri, Osnat Baery, Ofer Spilberg, Meora Feinmesser, Ranit Aharonov, Gila Lithwick Yanai
Journal: Cancer Research (2010)

Abstract Background: Diffuse large cell lymphoma (DLBCL) is heterogeneous in its clinical sequel. Approximately 50% of patients relapse after treatment and many succumb to the disease. Risk stratification of these patients is based mainly on the International Prognostic Index (IPI), while molecular profiling is not widely used for prognostication. Thus, there exists a need for identification of additional biomarkers that can be used as prognostic indicators for patients with DLBCL. Here we propose microRNAs, a family of small non-coding regulatory RNAs involved in cancer development, as an emerging class of potential biomarkers for risk stratification of DLBCL. Methods: Expression profiling of microRNAs was performed on RNA extracted from biopsy specimens of 83 DLBCL patients diagnosed and treated at Rabin Medical Center, using custom microRNAs microarrays. All patients were treated with CHOP or CHOP like therapy and were dichotomized into a “good prognosis” group (patients that achieved complete remission and no relapse within 5 years) and a “bad prognosis” group (patients that were either resistant to treatment or relapsed within 9 months). Expression levels were compared between the two groups of samples and statistically analyzed. The expression of differential microRNAs was verified using a microRNA qRT-PCR platform. Results: We found that several microRNAs are significantly differentially expressed in tumors from patients with bad prognosis compared with patients with good prognosis. Proprietary microRNA qRT-PCR showed a high correlation to microarrays and similar separation into prognosis groups based on miR expression. Conclusion: In summary, according to the results of this study, miRNA expression can serve as a novel tool for risk stratification and prognosis prediction of DLBCL patients. This approach can potentially be used to tailor treatment and further management to specific patient needs. 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 4054.
Abstract 4530: Pralatrexate-induced apoptosis in multiple myeloma cells correlates with RFC-1 and DHFR expression
Authors: Michael Mangone, Enrica Marchi, Luigi Scotto, Owen A. O'Connor, Hearn J. Cho
Journal: Cancer Research (2011)

Abstract Pralatrexate (PDX, 10-propargyl 10-deazaaminopterin) is a novel anti-folate agent that is approved for use in relapsed peripheral T cell lymphoma (PTCL). It is distinguished from the parent drug methotrexate (MTX) by having significantly greater affinity for the reduced folate carrier (RFC)-1, the principle transporter that internalize anti-folates, as well as broader efficacy, which strongly suggests that PDX has mechanisms of action beyond inhibition of nucleotide synthesis. Given the activity of PDX in aggressive lymphoid malignancies such as PTCL, we examined the activity of this agent in preclinical models of multiple myeloma (MM), a plasma cell malignancy that is currently incurable. We examined the cytotoxic activity of anti-folates in vitro against a panel of human multiple myeloma cell lines (HMCL) and showed that PDX induced dose-dependent apoptotic cell death in a subset of these. In sensitive cell lines (MM.1s and ARH-77) PDX demonstrated significantly greater potency at 48 hours compared to MTX (LD50 PDX = 2-3 nM vs. LD50 MTX = 25-30 nM). PDX also induced apoptosis in a polyclonal population of primary myeloma cells isolated from a patient specimen, whereas MTX had no effect on viability in these cells. PDX-induced apoptosis in sensitive HMCL was characterized by cleavage and activation of caspase-3 and -9, accompanied by the loss of the anti-apoptotic Bcl-2 family protein Mcl-1. Quantitative RT-PCR analysis of a panel of folate metabolism genes, including RFC-1, folyl polyglutamate synthetase (FPGS), gamma-glutamyl hydrolase (GGH), thymidylate synthase (TS), and dihydrofolate reductase (DHFR) revealed that RFC-1 expression was significantly higher in sensitive HMCL compared to resistant. Dose-dependent up-regulation of DHFR protein expression was observed by western blot in PDX-resistant cell lines, but not in PDX-sensitive ones. Incubation of HMCL with the proteasome inhibitor bortezomib or the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA), both of which demonstrate activity in MM, did not affect expression of RFC-1 in PDX-resistant HMCL and did not synergize with PDX to induce apoptosis in vitro. These results demonstrate that PDX induces apoptosis in sensitive HMCL, and that RFC-1 expression and DHFR up-regulation are functional biomarkers for susceptibility to this anti-folate. These data support further exploration of PDX therapy in MM, including combination therapy with agents that can increase expression of RFC-1 and/or block up-regulation of DHFR. 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 4530. doi:10.1158/1538-7445.AM2011-4530
Therapy Related Leukemia During Adjuvant Chemotherapy for Pancreatic Cancer Developed After Adjuvant for Breast Cancer
Authors: Tsuyoshi Muta, Goichi Yoshimoto, Kentaro Kohno, Fumiaki Jinnouchi, Takahiro Shima, Kenjiro Kamezaki, Koji Kato, Katsuto Takenaka, Toshihiro Miyamoto, Koichi Akashi
Journal: Annals of Oncology (2014)
Abstract 1982: Turmeric oil inhibits hepatocellular carcinoma through abolishing EpCAM expression
Authors: Yan Li, Erik Dunki-Jacobs, Suping Li, Robert C.G Martin
Journal: Cancer Research (2012)

Abstract Background: In previous study, we found that turmeric oil, a volatile oil from turmeric, can prevent hepatocellular carcinoma (HCC) in an orthotopic HCC mouse model. Epithelial cell adhesion molecule (EpCAM), a marker of cancer stem cells (CSC), is correlated with HCC initiation, progression, and prognosis. Our resent data showed that turmeric oil can decrease EpCAM expression in esophageal cancer and HCC cell lines. Since the role of EpCAM in HCC carcinogenesis is becoming clarified, it is likely that turmeric oil prevents HCC through EpCAM signaling. Aim: To investigate the mechanism of turmeric oil for HCC prevention. Method: EpCAM expression in the specimens from HCC patients (n=25) was evaluated by immunohistochemical staining. Red fluorescent protein (RFP)-labeled H4IIE cells were inoculated into liver lobe of ACI rats. The rat HCC tumor tissues from RFP-H4IIE cell inoculation were evaluated for the subpopulation cells, which co-expressed RFP and EpCAM. The HCC rats by H4IIE cell inoculation were treated with turmeric oil (100mg/kg, i.p, every 2 days) for 2 weeks. The H4IIE cells treated with turmeric oil as well as with EpCAM siRNA, and then inoculated at 106 into the right flank of nude BALB/c mice for 1 week. Three HCC cell lines from human (HepG-2), mouse (hepal-6), and rat (H4IIE) cells, were treated with turmeric oil to evaluate the cell viability EpCAM expression, and β-catenin in vitro. Results: In human samples, a strong EpCAM expression was found HCC tissues, while EpCAM was barely detected in the healthy controls. In HCC animal models, RFP+ EpCAM+ cells were detected in the formed tumor tissue and in circulation. The incidence of HCC by H4IIE cells inoculation was significantly decreased in rats treated with turmeric oil. Abolishing of EpCAM by turmeric oil caused the H4IIE cells unable to form tumor in nude mice. In cell culture study, turmeric oil significantly decreased EpCAM expression in all three HCC cell lines. Turmeric oil caused relocalization of β-catenin, a component in Wnt/β-catenin pathway, in nuclear and cytosol (Figure 1). Conclusion: 1) EpCAM-positive HCC cells contribute to HCC initiation in animal models; 2) The inhibition of HCC by turmeric oil is through decreasing EpCAM expression; 3). The regulation of EpCAM expression by turmeric oil is associated with Wnt/β-catenin pathway. 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 1982. doi:1538-7445.AM2012-1982
AB1328 Characterizing norwegian rheumatoid arthritis patients using the quest-ra protocol for comparison with other european countries:
Authors: G. Haugeberg, E.R. Wilberg, H.K. Gjelberg, E. Rødevand, T.S. Isler
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The QUEST-RA project (Quantitative Standard Monitoring of Patients with Rheumatoid Arthritis) a multi centre and multinational project has revealed significant differences in disease severity and treatment in RA patients in European countries (1,2). Norway joined QUEST-RA in 2009. <h3>Objectives</h3> To compare Norwegian RA patients with other European countries using the QUEST-RA protocol. <h3>Methods</h3> From two ordinary rheumatology outpatient clinics in Norway (Kristiansand and Trondheim) 200 consecutive RA patients 100 from each centre using the QUEST-RA protocol was included. Data on demographics, disease severity and treatment was collected. Data collection was finished spring 2010. Continuous variables are presented as mean (SD) or median [range]. <h3>Results</h3> Demographic: age 58 (13) years, females 65.5%, BMI 25.7 kg/m<sup>2</sup>, Caucasian 98.5%, current smoker 26.6%, education 11.0 [4-20] years, full time employed 17.1%, full time employed age &lt;65 years 25.0%, disease duration 13.3 (10.9) years. Disease activity: DAS28 3.6 (1.4), 28 joint count swollen 1.0 [0-21] and tender 3.0 [0-28], doctors global 1.8 [0-7.7] mm, ESR 14 [2-78] mm/hr. Patient reported outcomes measures (PROMs): HAQ 0.88 [0-2.63], pain 3.5 [0-9.3] cm, fatigue 3.8 [0-10] cm, patient global 3.8 [0-9.8] cm, morning stiffness 45.0 [0-301] min. Disease markers: RF+ 73.1%, erosive status 61.5%. Treatment: biologics 27.0%, methotrexate 59.5%, other DMARDs 14.0%, prednisolone 52.0%. Significant (p&lt;0.05) gender differences (men/women) were found for the following variables: full time employed &lt;65 years (47.7%/14.1%), DAS28 (3.1/3.9), HAQ (0.50/0.88). No significant gender differences were found for e.g. swollen joints, ESR, RF and erosions and treatment. In comparison with other European QUEST-RA countries disease activity and health status in Norwegian RA patients were comparable with countries that had reported the lowest disease activity (DAS28) and the best health status in their RA patients (see table below). The proportion of RA patients treated with biologics in Norway is among the highest in Europe. <h3>Conclusions</h3> Norway is among European countries reporting the lowest level of disease activity in their RA patients and is also among countries with the highest proportion of patients on biologics. This however cannot be explained by use of biologics alone as e.g. Finland (1) using significant less biologics than Norway is reporting even a lower disease activity in their RA patients. <h3>References</h3> Sokka T et al. Ann Rheum Dis. 2007;66:1491-6. Sokka T et al. Ann Rheum Dis. 2009;68:1666-72. <h3>Disclosure of Interest</h3> G. Haugeberg Grant/Research support from: Abbott Norway, E. Wilberg: None Declared, H. Gjelberg: None Declared, E. Rødevand: None Declared, T. Isler Grant/Research support from: Abbott International
SP0120 Innate Lymphoid Cells and TH2 Immunity
Authors: A. Mckenzie
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> Innate lymphoid cells (ILC) are members of the lymphoid lineage with roles in immunity, regulating tissue homeostasis and inflammation. ILC2, in addition to the classical Th2 cells, produce the type-2 cytokines IL-4, IL-5, IL-9, and IL-13, and play critical roles in the initiation of the type-2 response. ILC subsets are particularly prevalent at mucosal surfaces, which are constantly exposed to infectious agents in the external environment. ILC2 rapidly secrete high levels of IL-5 and IL-13, resulting in eosinophilia and mucus hyper-secretion, and provide a potent innate effector response to combat intestinal parasitic helminth infections and inappropriately during asthma and allergy. In recent studies we have demonstrated that ILC2 increase in human skin from AD patients and shown that ILC2 can be induced in human skin by challenge with the common allergen house dust mite. These skin ILC2 were highly responsive to prostaglandin D2 that bound to the CRTH2 to induce high levels of IL-5 and IL-13 production, highlighting the opportunity for potential therapeutic intervention with CRTH2 or PGD2 inhibitors. Ongoing studies using new reagents, including ILC2-deficient mice, are aimed at dissecting the roles of ILC2 in their interactions with innate and adaptive immune responses. Notably we have demonstrated that ILC2 can potentiate the adaptive Th2 response. Intranasal administration of protease allergen papain was used to stimulate ILC2 and Th2 cells, causing allergic lung inflammation. This activation of Th2 cells was severely impaired in ILC2-deficient mice. Notably, ILC2-derived IL-13 was critical for the induction of inflammation due to IL-13 promoting migration of activated lung dendritic cells into the draining lymph node to prime Th2 cell differentiation. <h3>Disclosure of Interest</h3> A. Mckenzie Grant/Research support from: Funding from Janssen <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6250
A Dual-Energy X-ray Absorptiometry Artifact and Potential Pitfall
Authors: Paul J Bohdiewicz, Abdul-Majid Khan
Journal: Clinical Nuclear Medicine (2002)

From the Departments of Nuclear Medicine* and Diagnostic Radiology†, William Beaumont Hospital, Royal Oak, Michigan Received for publication February 20, 2002. Revision accepted June 11, 2002. Reprint requests: Paul J. Bohdiewicz, Department of Nuclear Medicine, William Beaumont Hospital, 3601 W. 13 Mile Road, Royal Oak, Michigan 48073. E-mail: [email protected]