tbuckley/cabot-search huggingface dataset:
SAT0186 Trends and correlates of erythropoiesis-stimulating agent use among patients with lupus nephritis reaching end-stage renal disease:
Authors: J.A. Gόmez-Puerta, S. Waikar, J. Liu, W. Winkelmayer, K.H. Costenbader
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> Approximately 20% of lupus nephritis (LN) patients develop end-stage renal disease (ESRD) within 10 years. As LN progresses, anemia is common. Little is known, however, about utilization patterns of erythropoiesis-stimulating agents (ESA) among U.S. patients with LN initiating treatment for ESRD. <h3>Objectives</h3> To identify sociodemographic and clinical factors associated with ESA use among incident LN ESRD patients <h3>Methods</h3> Individuals age ≥18 with incident LN ESRD (ICD-9 code 710.0), were identified in the US Renal Data System, 1995-2008. ESA use was ascertained from the Medical Evidence Report. Year of ESRD onset, age, sex, race/ethnicity, medical insurance, employment status, residential region, clinical factors and comorbidities were considered potentially associated with ESA use in multivariable-adjusted logistic regression analyses <h3>Results</h3> Of 14,074 individuals with incident LN ESRD, 4,690 (33.3%) patients received an ESA at ESRD onset; use increased from 1995 to 2004 and then declined. In multivariable-adjusted models, several variables were independently related to ESA use (Table). ESA users had higher serum albumin and hemoglobin levels, were more likely women, Asian, living in the Northeast and underweight. Conversely, Medicaid beneficiaries, the uninsured, unemployed, Blacks, Hispanics, and those with IV drug use and obesity had lower ESA use. <h3>Conclusions</h3> Among U.S. patients with LN-associated ESRD, one third received ESAs at ESRD onset and the proportion increased substantially between 1995 and 2004. Race, type of medical insurance, region of residence, low BMI, hypertension, CAD, PVD, and higher serum levels of albumin and hemoglobin, were significantly associated with receipt of ESA therapy. <h3>Disclosure of Interest</h3> None Declared
THU0552 Artesunate Modulates Atherosclerosis Related Factors through the Inhibition of Type I Interferon in Patients with Systemic Lupus Erythematosus
Authors: F. Gu, X. Feng, W. Chen, B.P. Tsao, L. Sun
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The chronic inflammatory nature of systemic lupus erythematosus (SLE) is hypothesized to lead to many co-morbidities including premature accelerated atherosclerosis. <h3>Objectives</h3> In this study, we: 1) assessed levels of several classic atherosclerosis related factors in SLE patients, including macrophage migration inhibitory factor (MIF), vascular endothelial growth factor (VEGF) and numbers of peripheral endothelial progenitor cells (EPCs), 2) explored the mechanisms by which SLE causes premature accelerated atherosclerosis, 3) investigated the potential role of artesunate (ART) in ameliorating SLE-associated atherosclerosis. <h3>Methods</h3> SLE disease activity was assessed by the Systemic Lupus Erythematosus Disease Activity Index. VEGF and MIF levels in serum and cultured supernatant were determined by ELISA. Peripheral CD34<sup>+</sup>KDR<sup>+</sup> cells were measured by flow cytometry to represent EPCs. Human umbilical vein endothelial cells (HUVECs) and PBMCs were cultured with or without the presence of 1000 U/ml interferon (IFN)α-1b for 24 hours. To detect the effect of ART on these cells, ART at a dose of 5 or 20 μmol/L was added to the culture system for 12 and 24 hours. <h3>Results</h3> SLE patients had high levels of MIF, low levels of VEGF and reduced numbers of EPCs, which were correlated with disease activity and aberrant IFN-inducible gene expressions. <i>In vitro</i> experiments indicated that MIF levels significantly elevated after IFNα treatment, while VEGF levels varied at different time periods by showing a decline after 12 hours stimulation but an incline at 24 hours. ART significantly suppressed IFN-α promoted VEGF and MIF production at 24 hours. <h3>Conclusions</h3> ART could modulate atherosclerosis related factors through the inhibition of type I IFN in SLE patients, thus may have therapeutic potential for SLE-associated atherosclerosis. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3480
Imaging of Transplanted Parathyroid Tissue in a Patient With Recurrent Hyperparathyroidism
Authors: ERIK J. KILGORE, ELIZABETH L. TEIGEN, ROBERT J. COWAN
Journal: Clinical Nuclear Medicine (1996)

Parathyroid scintigraphy is useful in detecting residual hyperplastic parathyroid tissue in patients who continue to have hyperthyroidism after “total parathyroidectomy.” Typically, only the neck and mediastinum are imaged. The authors report a case in which images of the forearm were helpful in detecting hyperplastic autologous transplanted parathyroid tissue.
AB0331 Performance of various criteria sets in evaluating disease activity and remission in RA. An algerian multicenter study:
Authors: S. Slimani, A. Abbas, A. Ben Ammar, D. Kebaili, E.H. Ali, F. Rahal, C. Dahou-Makhloufi, N. Brahimi, S. Abtroun-Benmadi, A. Ladjouze-Rezig
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Composite indexes in RA are widely validated in clinical trials and have been adapted to everyday practice for therapeutic judgment, monitoring and determining remission. Our aim was to investigate the accuracy of the main composite scores (DAS28, SDAI, CDAI) in evaluating disease activity and remission in RA, in real life conditions. <h3>Methods</h3> Data from a nationwide observational cohort of RA patients, recruited from October 2010 to March 2011, in 11 centers. We investigated agreement between DAS28, SDAI and CDAI in different disease states using κ statistics, and agreement between DAS28, SDAI, CDAI and ACR/EULAR Boolean-based definition for remission. ROC curves were constructed to determine cut-off points for treatment interventions (DMARD changing or dosage increasing) and assess discriminative ability for every index. All statistic computation was done using SPSS ver 17.0. <h3>Results</h3> The mean age of the 249 patients was 50.1±14.5 years, mean disease duration 8.4±7.8 years, 85.5% were female. At inclusion, the mean DAS28 was 3.9±4.8, mean SDAI 22.5±21,7 and mean CDAI 11.1±10,2. Agreement between various activity states was good between DAS28, modified DAS28 and SDAI cut-offs (κ =0.41 to 0.67), but moderate with CDAI (κ =0.20 to 0.37) (see table). With the ACR/EULAR remission criteria set as a gold standard, the best performance was with the SDAI and modified DAS28. The optimal cut-off for treatment change was 4.25 for DAS28 (sensitivity 73.4%; specificity 69.8%), 16 for SDAI (sensitivity 76.8%; specificity 68.9%) and 8.75 for CDAI (sensitivity 72.7%; specificity 68.0%); areas under the curve were roughly the same with a slightly better discriminative ability with DAS28 (0.76 Vs 0.74 for SDAI and 0.73 for CDAI). <h3>Conclusions</h3> According to the various indices performed on an Algerian population, good agreement is noted between different states, except for CDAI. For remission, SDAI shows the best agreement with the ACR/EULAR remission criteria. Finally, DAS28 has the best ability for treatment changes. <h3>Disclosure of Interest</h3> None Declared
Abstract 1347: A human-mouse xenograft model to study the role of TSLP in CRLF2d B-ALL
Authors: Kimberly J. Payne, Rui-Jun Su, Olivia L. Francis, Shannalee R. Martinez, Terrence Bennett, Keshav Arogyaswamy, Christopher L. Morris, Sinisa Dovat
Journal: Cancer Research (2012)

Abstract B-cell precursor ALL where genetic defects lead to overexpression of CRLF2 (CRLF2d B-ALL) are high-risk with poor prognosis. CRLFd B-ALL occurs 5 times more frequently among children of Hispanic/Latino ethnicity and is a major contributor to the health disparity in survival of Hispanic children with ALL. CRLF2, together with the IL-7Rα, forms a receptor complex that is activated by the cytokine, TSLP. The JAK-STAT5 pathway is phosphorylated downstream of receptor activation. The activating JAK mutations found in some CRLF2 B-ALL have led to speculation that TSLP stimulation is not a factor in CRLF B-ALL. In preliminary studies to address this question we evaluated the effect of TSLP on two CRLF2d B-ALL cell lines with JAK defects and which have been reported to exhibit constitutive JAK-STAT5 activation. Our data show that TSLP increases STAT5 phosphorylation in both of these cell lines and in primary B-ALL cells that overexpress CRLF2. Our next step was to evaluate the role of TSLP-CRLF2 interaction in vivo in the human-mouse xenograft model. However, mouse TSLP is different from most other cytokines produced in the xenograft in that it is species-specific and does not activate the human TSLP receptor complex that contains CRLF2. Thus, traditional xenograft models do not provide the TSLP-CRLF2 interactions that we believe to be a major factor in CRLF2 B-ALL. To overcome this obstacle we have engineered immune deficient NOD/SCID IL-2Rγ null (NSG) mice to express human TSLP (hTSLP+ mice) as well as control mice that lack the TSLP cytokine (hTSLP- mice). ELISA assays show plasma hTSLP levels in the hTSLP+ mice that approximate the normal range in human plasma. We have used this hTSLP+/− system to expand a sample of primary pre-B ALL cells from a patient that includes clones of CRLF2-HI and CRLF2- B-ALL cells. Preliminary data indicate that the pre-B ALL cells expanded in hTSLP+ mice show higher expression levels of the TSLPR components (CRLF2 and IL-7Rα) than cells expanded in the hTSLP- mice. This data provide evidence that the TSLP produced in this model is active and that it impacts primary pre-B ALL cells. The hTSLP+ mice that we produce will allow for the first time the study of normal and malignant B lymphopoiesis in a model that provides the complex bone marrow architecture of the xenograft while providing the full range of cytokines that are known to act on early B lineage cells (IL-7, FL and TSLP). This model will be particularly important for identifying therapies that can effectively target CRLF2-d B-ALL and reduce cancer health disparities in Hispanic childhood B-ALL. 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 1347. doi:1538-7445.AM2012-1347
Hepatitis B in an Oncology Unit
Authors: Jack R. Wands, John A. Walker, Thomas T. Davis, Lawrence A. Waterbury, Albert H. Owens, C. C. J. Carpenter
Journal: New England Journal of Medicine (1974)

In nine of 91 personnel working in an oncology unit serious hepatitis-B infection developed. Eight others with pre-existing hepatitis-B surface antibody (anti-HBs) before the epidemic showed a fourfold or greater rise in anti-HBs titer during the epidemic and appeared protected from the hepatitis-B illness. Asymptomatic hepatitis-B surface antigen (HBs Ag) exposure became apparent when seroconversion from anti-HBs negative to positive was noted in 11 employees. A 19.5 per cent frequency of HBs Ag was detected in 87 patients with tumor before, during and after the epidemic. In five asymptomatic patients with pre-existing HBs Ag, unusually high HBs Ag titers (mean, 1:128,000) developed on high dose antitumor chemotherapy, and one of these patients may have served as a common source exposure for eight personnel. Asymptomatic and anicteric HBs Ag-positive patients with tumor represent a great risk to oncology-unit personnel, and prophylactic measures should be instituted. (N Engl J Med 291:1371–1375, 1974)
Abstract 3552: Cancer immunoediting: Profile of cytokines in a mammary adenocarcinoma tumor model
Authors: Lucas Pagura, Juan M. Caceres, Albertina Cardinale, Olga G. Scharovsky, Ricardo J. Di Masso, María J. Rico, Viviana R. Rozados
Journal: Cancer Research (2012)

Abstract Cancer immunoediting is a dynamic process composed of three phases: elimination (EL), equilibrium (EQ), and escape (ES), that encompasses the potential host-protective and tumor-sculpting functions of the immune system throughout tumor development. Inbred mice models provide an interesting tool for identifying genes that control susceptibility to breast cancer. Inbred CBi/L FS mice were artificially selected by body conformation from CBi mice. The M-406 mammary adenocarcinoma appeared spontaneously in CBi female mouse and it is maintained in vivo in mice of the same line. When CBi/L FS mice are s.c. challenged with M-406 they show the three phases: 51.6% in ES, 18.5% in EQ en 29.8% in EL. The aim of this study was to evaluate in CBi/L FS mice in the three phases of M-406 tumor growth: 1) the profile of cytokines Th1(IL-2; INF-γ); Th2(IL-4; IL-10) in serum and 2) the effect of conditioned media (CM) from CBi/L FS mononuclear cells on tumor cells proliferation. The serum and CM cytokines were evaluated by ELISA. CMs were obtained after 24h incubation of mononuclear cells from CBi/L FS seeded at 4x105 cells/well, in RPMI + 10% BFS. Tumor cells (5x104 cells/well) were incubated 24h with different CMs and proliferation evaluated (WST-1). In serum we observed the presence of high levels of INF-γ in the ES condition, compared with EQ and EL (p&amp;lt;0.0001). Also, we found that IL-10 was increased in EL (p&amp;lt;0.049), and IL-4 presented high levels in ES followed by EQ and then EL (p&amp;lt;0.001). On the other hand, IL-2 did not show significant variations between conditions. The percentage of proliferation of M-406 cells was significantly higher with CM prepared from naive mice than with RPMI control medium (p=0.0048). No significant differences were found in proliferation between control medium and CM prepared from EL or ES mononuclear cells. Detectable levels of IL-4 and IL-10 were found in CMs. Interestingly, CM IL-10 level correlated negatively (p=0.0016, r=−0.8252) with M-406 proliferation. In conclusion we observed that while IL-4 concentration varied as expected in the three tumor phases, IL-10 and IFN-γ did the opposite. Furthermore, both in vivo and in vitro experiments would indicate that IL-10 might act as an inhibitor of tumor growth.These results are supported by new findings that endow immune inhibitory and stimulatory functions to IFN- γ and IL-10, respectively. 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 3552. doi:1538-7445.AM2012-3552
Abstract 3979: In vitro modeling of pharmacodynamics of resveratrol-induced anti-proliferation in breast cancer cells
Authors: Hongyu Li, Elliot Melaney, Sharon Lin, Noah Rubin, Charles Bender, Ran Meng, David London, Heng-Yuan Tang, Hung-Yun Lin
Journal: Cancer Research (2010)

Abstract We and others have shown that resveratrol, a naturally-occurring stilbene, induces p53-dependent apoptosis in human and animal cancer cell lines. The molecular basis of induction of apoptosis by resveratrol includes activation and nuclear translocation of mitogen-activated protein kinase (MAPK; ERK1/2) and MAPK-mediated Ser-15 phosphorylation of p53 (pSer15-p53). In this study, we used a newly developing perfusion bellows cell culture system to investigate resveratrol-induced apoptosis in the human estrogen receptor (ER)-negative breast cancer MDA-MB-231 cells. The cell culture system is a disposable bioreactor capable of high density cell culture for studies of anti-cancer drugs. Bellows-induced alternate flow of culture medium and air through porous matrices where cells are grown provides a relatively low shear, high aeration, foam-free culture environment. Medium level is raised and lowered to submerge and expose matrices to create a dynamic interface between air and media on the cell surface. Anchorage-dependent cells are grown on plastic flakes in the system; the flakes facilitate harvesting of whole cells for analysis. After 6 days incubation, the IC50 of resveratrol-induced apoptosis was 0.1 μM. Short term incubation with 10 μM resveratrol for 6 days inhibited cell proliferation by 75%. Using an injection system to pump media with different concentrations of resveratrol (0.5 μM to 100 μM), we were able to reproduce the resveratrol-induced anti-proliferation effect in the perfusion bellows culture system. Incubating the cells in either acidic or alkaline condition did not affect anti-proliferation induced by resveratrol. The effect of resveratrol-induced apoptosis is based on increasing transcription of pro-apoptotic p53-dependent genes such as PIG3, c-fos, c-jun and BAD. The aim of the present study is to establish the pharmacodynamics of resveratrol in the suppression or elimination of human breast cancer cells. With the use of the perfusion bellows cell culture system we will provide an efficient, convenient and financially beneficial method for determining optimal regimens for the effective suppression and elimination of these cancer cells. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 3979.
Abstract 333: FISH markers in oral tongue squamous cell carcinoma
Authors: Darawalee Wangsa, Michael Ryott, Göran Elmberger, Alejandro A. Schäffer, Gert Auer, Elisabeth Åvall Lundqvist, Eva Munck-Wikland, Thomas Ried, Kerstin Heselmeyer-Haddad
Journal: Cancer Research (2010)

Abstract Oral tongue squamous cell carcinoma (OTSCC) is a continued health problem worldwide, and is associated with poor prognosis. Genetic alterations in head and neck cancers have frequently been shown, however, reports about alterations in OTSCC and their correlation with clinical and histopathological parameters are limited. We investigated OTSCC by analyzing five probe markers (TERC, CCND1, EGFR, P53 and CEP®4) by means of fluorescence in situ hybridization (FISH) in sixty-five patients (Stage I, n=15; Stage II, n=30; Stage III, n=7; Stage IV, n=13). Higher copy number gains in all five markers was found to be significantly (P=0.002) correlated to non-smoking habits while low-level copy number gains corresponded to smokers in OTSCC patients. Of the five markers, CCND1 was found to have the highest mean copy number gain in comparison to all other markers used in this study. The percentage of cells with elevated (&amp;gt;3 signals) CCND1 copy number gain increased with stage. In Stage II OTSCC, CCND1 copy number gain correlated significantly (P=0.03) with a better prognosis in patients. Of the patients with increased CCND1 copy number gains (&amp;gt;3 signals in at least 5% of cells), all were non-smokers. In conclusion, high copy number gain using FISH correlated with non-smoking habits, making it particularly interesting to explore the mechanism of how these patients develop cancer. 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 333.
669 RANDOM SPOT URINE SODIUM/POTASIUM RATIO IS ASSOCIATED WITH RENAL DYSFUNCTION AND OUTCOME IN PATIENTS WITH DECOMPENSATED CIRRHOSIS AND ASCITES
Authors: E. Cholongitas, J. Goulis, G. Arsos, T. Nakouti, J. Kouvelis, C. Birtsou, S. Papadopoulou, K. Karakatsanis, E. Akriviadis
Journal: Journal of Hepatology (2012)
Hepatitis B e Antigen and the Risk of Hepatocellular Carcinoma
Authors: Hwai-I Yang, Sheng-Nan Lu, Yun-Fan Liaw, San-Lin You, Chien-An Sun, Li-Yu Wang, Chuhsing K. Hsiao, Pei-Jer Chen, Ding-Shinn Chen, Chien-Jen Chen
Journal: New England Journal of Medicine (2002)

The presence of hepatitis B e antigen (HBeAg) in serum indicates active viral replication in hepatocytes. HBeAg is thus a surrogate marker for the presence of hepatitis B virus DNA. We conducted a prospective study to determine the relation between positivity for hepatitis B surface antigen (HBsAg) and HBeAg and the development of hepatocellular carcinoma.
Abstract 1281: POLD3 is required for DNA damage response to endogenous and exogenous DNA damage in human cells.
Authors: Xu Tian, James Swenberg, Jun Nakamura
Journal: Cancer Research (2013)

Abstract Methyl methanesulfonate (MMS) induces mutations in a nonlinear (hockey-stick-shaped) dose-response curve in DT40 cells, about 55% of which are located at A:T sites with a high frequency of A to T mutations. We hypothesized that these transversion mutations are due to base excision repair (BER) intermediates, such as abasic sites and single strand breaks derived from N3-methyladenine. One candidate polymerase to bypass abasic sites is polymerase delta (POLD). POLD is responsible for the lagging strand during DNA replication. POLD is referred to as a high fidelity DNA polymerase because of its ability to discriminate deoxynucleotides and its 3’-&amp;gt;5’ exo-nuclease activity. One of the POLD subunits, POLD3, is important to recruit PCNA binding to the POLD core enzyme and is implied to have critical roles for translesion DNA synthesis. In yeast, cells deficient in POLD3 homologous gene POL32 are sensitive to DNA damaging agents and resistant to mutations caused by mutagens, such as MMS and UV. Here we generated POLD3 knock-down (KD) cells via lentivirus based shRNA in three different human cell lines. All POLD3 KD cells grow slower than the control cells, suggesting POLD3 function tolerates endogenous DNA lesions. Furthermore, we found that POLD3 KD cells were sensitive to various genotoxic agents including MMS and potassium chromate. To further investigate the role of POLD3 in the DNA damage response, we introduced a series of deletion mutations of POLD3 in POLD3 deficient cells. We found that both the POLD2 binding domain and the middle linker domain are critical for the activity of POLD3 while the C-terminal PCNA binding domain is dispensable. While there is little homology between human POLD3 and yeast POL32, function of these two proteins appears to be quite similar in structure biology analysis. Our results also suggest that POLD3 plays important roles to bypass DNA lesions caused by endogenous and various exogenous genotoxic agents. Citation Format: Xu Tian, James Swenberg, Jun Nakamura. POLD3 is required for DNA damage response to endogenous and exogenous DNA damage in human cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1281. doi:10.1158/1538-7445.AM2013-1281