tbuckley/cabot-search huggingface dataset:
AB0091 The Concentration of Serum Interleukin-6 before Biologic Treatment Are Related to Clinical Response in the Patients of Rheumatoid Arthritis
Authors: Y. Takakubo, H. Ohki, S. Yang, A. Sasaki, K. Sasaki, T. Hirayama, Y. Tamaki, Y. Naganuma, H. Orui, M. Takagi
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Biologics (BIO) have been developed the treatment of rheumatoid arthritis represent a remarkable advance over and beyond the conventional disease-modifying antirheumatic drugs (cDMARDs)<sup>1</sup>. However, 20–30% of rheumatoid arthritis (RA) patients using biologics are nonresponders or show only minor improvement. <h3>Objectives</h3> Recently it was reported the concentration of serum cytokine was related the response of treatment for RA<sup>2,3</sup>. We investigate the relationships of it before taking first BIO and the change of disease activity in our series. <h3>Methods</h3> One hundred nighty-nine RA patients have received BIO in our institutes from 2004 to 2013. Forty-one patients in BIO naive cases (infliximab 16 cases, etanercept 13, tocilizumab 9, adalimumab 3) were examined the concentration of serum tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 before receiving first BIO by ELISA. They are estimated the transition of disease activity score (DAS)28/C-reactive protein (CRP) score (4) and clinical disease activity index (CDAI) one year after first BIO. They are 7 men and thirty-four women. Their mean age is 55 years (range 32-74), mean duration of RA affliction was 7.8 years (1-22). <h3>Results</h3> The mean concentration of serum TNF-alpha and IL-beta, IL-6 was 16.2 (0.6-238) pg/ml,; 10 (10-11); 34.1 (0.5-303) before first BIO, respectively. The mean CRP levels, DAS28-CRP (4) and CDAI were 29 g/dl (range, 1–82), 4.9 (1.0-7.2) and 24.8 (0-67) before first BIO, which improved as 7 (0-34) g/dl, 3.1 (10-64) and 10.3 (0-30) one year after first BIO, respectively. EULAR response criteria were used, and there was a good response in twenty-eight patients (68%), a moderate response in eight (20%) and no response in five (12%), respectively, during the treatment period starting at the commencement of the BIO and one year after. Only the value of serum IL-6 was significantly related to the results of EULAR response and CRP before first BIO (p&lt;0.05, Fig. 1). Four case in good response group was satisfied of criteria of remission using CDAI scoring (&lt;2.8). <h3>Conclusions</h3> The value of serum IL-6 before receiving BIO seems to have the potential marker for predicting the response of BIO treatment in RA patients. <h3>References</h3> Klareskog L, et al: Lancet 2004; 363:675-681. Takeuchi T, et al: ARD 2012; 71: 1583-1585. Shimamoto K, et al: J Rheumatol 2013; 40:1074-1081. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3522
PMO-243 Faecal calprotectin analysis: does the method matter?
Authors: C Tomkins, Z Zeino, C Nwokolo, S C Smith, R Arasaradnam
Journal: Gut (2012)

<h3>Introduction</h3> Faecal calprotectin (FC) is a sensitive marker of intestinal inflammation and is useful to help distinguish between organic and non-organic (functional) disease. The increasing popularity of this test, with various analytical methods available, potentially leads to confusion in interpreting results. The aim of this study was to technically evaluate FC measured by different ELISA methods in secondary/tertiary care. <h3>Methods</h3> 62 stool samples were collected from sequential out-patients presenting with chronic diarrhoea. All participants had a colonoscopy with biopsy, to which FC results were compared. FC was measured by ELISA assays: Immundiagnostik PhiCal (version 1) and Buhlmann EK-CAL. A subset were also measured by PhiCal (version 2). Stool was weighed and extracted, and ELISAs performed manually. <h3>Results</h3> 38 patients with IBD/other organic bowel disease (mean 36 yrs, range 15–49) and 24 patients with IBS (mean 36 yrs, range 20–48) were sampled. Sensitivity and specificity for active IBD vs IBS using manufacturers9 cut-offs of 50 μg/g were: Buhlmann EK-CAL 86% (95% CI 42 to 99) and 60% (95% CI 33% to 83%), PPV 50% (95% CI 22% to 78%), NPV 90% (95% CI 54% to 99%); PhiCal1 78% (95% CI 40% to 96%) and 92% (95% CI 60% to 100%), PPV 88% (95% CI 47% to 99%) and NPV 86% (95% CI 56% to 97%). Correlation across full range of results were PhiCal1 vs EK-CAL, R<sup>2</sup>=0.45; PhiCal2 vs PhiCal1, R<sup>2</sup>=0.54. However for results &lt;100 μg/g by PhiCal1, correlations improved that is, R<sup>2</sup>=0.64 and R<sup>2</sup>=0.83 respectively. Intra-batch imprecision of the whole process, including extraction of native stool, was assessed at a range of clinically relevant concentrations: Buhlmann EK-CAL 17% (10 μg/g), 12% (47 μg/g), 19% (62 μg/g); PhiCal1 21% (8 μg/g), 24% (10 μg/g), 18% (27 μg/g); PhiCal2 19.5% (18.9 μg/g). Inter-batch imprecision of ELISA analysis was lower: Buhlmann EK-CAL 8.6% (30 μg/g), 5.8% (129 μg/g); PhiCal1 6.2% (39 μg/g), 10.8% (135 μg/g); PhiCal2 8.9% (33 μg/g). Functional sensitivity: Buhlmann EK-CAL 10 μg/g; both PhiCal 20 μg/g. Assays were found to be linear (without further sample dilution) up to 600 μg/g for EK-CAL, PhiCal1 400 μg/g, PhiCal2 800 μg/g. Mean recovery in spiked stool samples: Buhlmann EK-CAL 98%, PhiCal1 83%, PhiCal2 79%. <h3>Conclusion</h3> All three ELISA assays evaluated have relatively high coefficients of variation compared to other laboratory tests, due to heterogeneity of stool material and manual extraction/analysis. Results from different FC methods are not directly comparable, despite widespread adoption of single cut-offs. Using 50 μg/g cut-off, PhiCal1 performed better than Buhlmann EK-CAL in distinguishing IBD from IBS in our study. There is improved assay linearity using PhiCal2. Clinicians should be aware of type of ELISA methods employed when interpreting FC results, and cut-offs used should be fully evaluated. <h3>Competing interests</h3> None declared.
Abstract 2463: Side population cells have some stem-like properties in hepatocellular carcinoma
Authors: Hirohisa okabe, Toru Beppu, Takatoshi Ishiko, Akira Chikamoto, Toshiro Masuda, Ryu Otao, Horlad Hasita, Kosuke Mima, Hiroshi Takamori, Hideo Baba
Journal: Cancer Research (2011)

Abstract Background: There are many problems to be solved in cancer stem cells (CSCs) in digestive organs. Liver cancer stem cells also have a major problem that we have to determine the cancer stem cell markers and clarify the function of CSCs. In this study, we tried to validate CSC markers that are previously reported using side population (SP) cells in hepatocellular carcinoma cell lines. Methods: Side population cells in seven hepatocellular carcinoma (HCC) cell lines (PLC/PRF/5, HuH1, HuH7, HLE, HepG2, HLF, and SK-Hep1) were analyzed using Flow cytometry (FACS AriaII). The differences between SP cells and Non-SP cells in several markers relating to epithelial-mesenchymal transition and in several liver CSC markers were investigated using quantitative RT-PCR. The difference about intracellular signals between them was also studied using Western blot analysis. Using HuH7 cell, the ability of spheroid formation of SP cells and the difference between spheroid forming cells and 2-dimensional cultured cells were investigated. Results: The range of percentage of SP cells was from 0 % to 4.1 %. We sorted SP cells from four HCC cell lines (PLC/PRF/5, HuH1, HuH7, and HLE). There were no remarkable difference of CDH1 and vimentin between SP cells and Non-SP cells. Previously reported liver cancer stem cell markers such as EpCAM, CD90, and CD44 were significantly increased in SP cells. However, the expression of CD133 and Bmi1 in SP cells was unexpectedly decreased or similar to non-SP cells. The ability of spheroid formation of SP cells was significantly higher than that of non-SP cells. Spheroid forming cells showed remarkably higher expression of EpCAM, CD90, and CD44 than 2-dimensional cultured cells. These were considered to be important markers regulating CSCs. The expression of cell cycle marker MIB1 in the SP cells was remarkably decreased compared to that of non-SP cells. This fact supports to the theory that normal or cancer stem cells maintain their cell cycle arrest. SP cells maintained specific signals activated such as sonic hedgehog and MAPK signals. Conclusions: Liver cancer stem cell markers such as EpCAM, CD90, and CD44 were considered to be important for the maintenance of SP cells in hepatocellular carcinoma. The activation of specific intracellular signals was also seen in SP cells. We are now challenging to confirm the importance of those signals using HCC cells extracted from human liver tissues. The current study may be help of understanding the regulation of liver cancer stem cells. 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 2463. doi:10.1158/1538-7445.AM2011-2463
P195 HEPATITIS C VIRUS CELL–CELL TRANSMISSION AND RESISTANCE TO DIRECT-ACTING ANTIVIRAL AGENTS
Authors: F. Xiao, I. Fofana, L. Heydmann, H. Barth, E. Soulier, F. Habersetzer, M. Doffoël, J. Bukh, A.H. Patel, M.B. Zeisel, T.F. Baumert
Journal: Journal of Hepatology (2014)
Endoscopic ultrasound fine-needle aspiration of peritoneal deposits for diagnosis of tubercular peritonitis in a cirrhotic patient with ascites
Authors: S. Rana, D. Bhasin, R. Srinivisan, K. Singh
Journal: Endoscopy (2010)

A 30-year-old man, known to have alcohol-related cirrhosis, presented with tiredness and loss of appetite. He had stopped drinking alcohol 1 year ago when he was diagnosed with cirrhosis and was prescribed diuretics. An ultrasound performed 6 months later did not show ascites and the diuretics were stopped. However, the ascites reaccumulated 1 month prior to presentation. Laboratory investigations revealed serum albumin of 3.1 g/dL. An ultrasound of the abdomen revealed features of chronic liver disease with ascites. Ascitic fluid analysis revealed high gradient, lymphocytic nonmalignant ascites with an adenosine deaminase level of 28 IU/L. An ascitic fluid culture as well as polymerase chain reaction (PCR) for Mycobacterium tuberculosis were negative. Computed tomography (CT) of the abdomen revealed findings similar to the ultrasound findings, and the lung parenchyma was normal on CT chest. Endoscopic ultrasound (EUS) of the stomach revealed ascites and peritoneal deposits, visualized as hyperechoic rounded lesions ([Fig. 1]).
IN VIVO VERIFICATION OF LIPID DETECTION BY NEAR-INFRARED SPECTROSCOPY IN CALCIFIED LESIONS - COMPARISON WITH OPTICAL COHERENCE TOMOGRAPHY
Authors: Sadako Motoyama, Yuliya Vengrenyuk, Jacobo Pena, Anitha Rajamanickam, Joseph Sweeny, Samin Sharma, Jagat Narula, Annapoorna Kini
Journal: Journal of the American College of Cardiology (2015)
AACR President Assesses State of Cancer Research
Authors: Elaine Blume
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article AACR President Assesses State of Cancer Research Get access Elaine Blume Elaine Blume Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 7, 6 April 1994, Pages 483–485, https://doi.org/10.1093/jnci/86.7.483 Published: 06 April 1994
Blocking internalization of pBP1, a secreted homeoprotein, kills breast cancer cells but not normal breast epithelial cells.
Authors: J Rheey, L Bivona, P Berg
Journal: Cancer Research (2009)

Abstract Abstract #3068 Background: BP1 is a member of the homeobox gene family, a highly conserved family of transcription factor genes. pBP1 is a homeotic protein that is upregulated in 80% of invasive ductal breast tumors. We have previously shown that the percentage of pBP1 positive breast cancer cases increases with the extent of cellular proliferation and carcinogenesis. BP1 expression is associated with aggressive tumors: 100% of ER negative tumors were BP1 positive, compared with 73% of ER positive tumors. pBP1 is secreted by MCF-7 cells, T47D cells, and MDA-MB-231 breast cancer cells, but not by MCF10A or H16N2 normal breast epithelial cells. In all cell lines tested, secreted pBP1 is internalized, resulting in stimulation of growth. Moreover, incubation of MCF-7 or MCF10A cells in recombinant pBP1 results in stimulation of several oncogenes, including bcl-2, Twist, and Met. These results led us to ask whether we could abrogate mitogenic stimulation by addition of anti-pBP1 antibody.&amp;#x2028; Materials and Methods. Cells were incubated in 10 µg/ml anti-BP1 Ab (Novus) or 10 µg/ml IgG for three days. Growth was measured using MTT assays and apoptosis was assessed by flow cytometry after staining with Annexin V (Trevigen).&amp;#x2028; Results. Addition of anti-BP1 Ab to the growth medium of MCF-7 cells, T47D cells, and MDA-MB-231 cells caused significant growth inhibition and apoptosis. In contrast, addition of anti-BP1 Ab to the growth medium of MCF10A and H16N2 cells did not lead to significant growth inhibition or apoptosis.&amp;#x2028; Discussion. Our novel finding that pBP1 is secreted by breast cancer cells but not normal breast epithelial cells was the impetus to test the effect of adding anti-BP1 Ab to the growth media of both types of cells. Remarkably, anti-BP1 Ab kills only the breast cancer cells, suggesting they may be BP1-dependent. Our data indicate it may be possible to specifically target BP1 positive breast cancer cells in the 80% of women with BP1 positive tumors. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 3068.
Abstract 3446: Stat3 is a potential molecular target for chemoradiosensitization of colorectal cancer cells
Authors: Melanie Spitzner, Birte Roesler, Christian Bielfeld, Jochen Gaedcke, Margret Rave-Fränk, Tim Beißbarth, Thomas Ried, B. Michael Ghadimi, Marian Grade
Journal: Cancer Research (2012)

Abstract Introductory sentence: Resistance to preoperative chemoradiotherapy represents a major clinical problem in the treatment of patients with locally advanced rectal cancer. Therefore, the identification of novel molecular targets that are differently expressed in responsive and resistant tumors is exceedingly important. Furthermore, modulating target gene expression may sensitize a priori resistant tumors to multimodal therapy. Experimental procedures: Previously, we established an in vitro model for chemoradiotherapy in 12 colorectal cancer cell lines, and correlated differences in treatment sensitivity with pretherapeutic gene expression profiles. Within our signature we identified the signal transducer and activator of transcription 3 (STAT3), which was significantly correlated with treatment resistance. To test the functional relevance of the observed over-expression of STAT3, we first determined STAT3 mRNA and protein expression levels in all 12 cell lines. Subsequently, we established doxycycline-inducible stable shRNA single cell populations and a non-silencing shRNA (shNEG) in SW480. The induced single cell clones and shNEG were treated with 3µM 5-FU and exposed to 1, 2, 4, 6, and 8 Gy of X-rays. In addition, STAT3 was inhibited using two different siRNAs and a small-molecular inhibitor (STATTIC). Successful RNAi-mediated silencing of STAT3 and inhibitor treatment was detected by Western blot. Data: STAT3 was significantly overexpressed in resistant cells at mRNA and protein level. In stable STAT3 knockdown single cell clones and transiently siRNA transfected SW480 and SW837 cells, successful silencing of the STAT3 protein was detected after 72 hours, and STATTIC-induced inhibition of STAT3-phosphorylation after 1 hour. The silencing/inhibition resulted in a significantly increased chemoradiosensitivity with dose-reduction factors of 1.8 to 2. Conclusions: STAT3 is highly overexpressed in resistant colorectal cancer cells, and silencing of STAT3 leads to a significantly increased chemoradiosensitivity. This highlights the potential relevance of STAT3 as a novel molecular target in rectal cancer to sensitize a priori resistant colorectal tumor cells to chemoradiotherapy. 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 3446. doi:1538-7445.AM2012-3446
US Supreme Court is asked to rule on validity of patents on BRCA1 and BRCA2 genes
Authors: C. Dyer
Journal: BMJ (2012)

The US Supreme Court has been asked to review the validity of patents on isolated human genes associated with breast and ovarian cancer, which campaigners and medical groups said stifle research and hamper women’s access to care.

The American Civil Liberties Union (ACLU) and the Public Patent Foundation have filed a brief with the court asking it to look at whether patents held on BRCA1 and BRCA2 by a Utah company, Myriad Genetics, are valid.

“Laws of nature” and “products of nature” are not patentable under US law, and the ACLU has …
THU0371 The Role of MEFV Mutations in the Concurrent Disorders Observed in Patients with Familial Mediterranean Fever
Authors: S. Güncan, N.S. Yaşar Bilge, D. Üsküdar Cansu, T. Kaşifoğlu, C. Korkmaz
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Familial Mediterranean Fever (FMF) is characterized by recurrent serositis and fever attacks, which may accompany such other rheumatic disorders as Henoch-Schonlein purpura (HSP), and Behcet9s disease (BD). MEFV mutation modifies not only the clinical presentation of FMF but it also modifies other inflammatory disorders. However, the role of MEFV mutations in the FMF co-existing with other inflammatory disorders remains to be ascertained. <h3>Objectives</h3> This study aims to investigate the frequency in which FMF coexists with other diseases, and determine whether MEFV mutations are involved in such simultaneity. <h3>Methods</h3> Consecutive 142 patients with FMF investigated for MEFV mutation were enrolled for this study (F:87; M:55, mean age 32±12 yrs (11-62). They were diagnosed based on the Tell-Hashomer diagnostic criteria. The presence of MEFV mutation was investigated by multiplex-PCR reverse hybridization method in exon 2, 3, 5 and 10. All the patients were questioned for the presence of concomitant disorders and the medical records of these patients were revised retrospectively. A previous diagnosis for a disorder was considered true if it met the relevant criteria. MEFV mutations were divided into 2 groups including M694V and its subgroup (Group I) and others (Group II). <h3>Results</h3> 129 of the 142 FMF patients had positive mutation for MEFV gene, but 13 of them showed no such mutation. M694V and its subgroup mutations (Group I) and other mutations (Group II) were found in 73 (56.6%) and 56 (43.4%) patients with FMF, respectively. Concomitant disorders were found in 16 FMF patients (21.9%) in Group I, 5 FMF (8.9%) patients in Group II (p=0.04). Concomitant disorders in Group I were as follows: 7 amyloidosis, 2 BD, 4 ankylosing spondylitis (AS), 1 antiphospholipid syndrome, 1 HSP, 1 combination of psoriatic arthritis, HSP and membranoproliferative glomerulonephritis. In group II, 1 amyloidosis, 1 BD, 1 AS, 1 ulcerative colitis, 1 vitiligo were found. No concurrent disorders could be found in FMF patients with negative MEFV mutation. The rate of the family history showed no significant difference for Groups I and II (63% vs 57%, p=0.5). <h3>Conclusions</h3> MEFV mutations can modify both clinical manifestations of the FMF itself and those of other inflammatory disorders. The presence of M694V mutation may predispose FMF patients to developing other inflammatory disorders. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5550
Mark Beresford McEvedy
Authors: B. Hilton
Journal: BMJ (2014)

The son of a distinguished Manchester surgeon, Mark Beresford McEvedy had a great interest in physics, which led him to train in radiotherapy under Ralston Paterson at the Christie Hospital in Manchester, a centre set up to treat new malignancies caused by industrial pollution. In 1959 Mark was appointed consultant radiotherapist at Pembury Hospital, near Tunbridge Wells, Kent. Guy’s Hospital had staffed a unit at Pembury …
Children's blood lead levels in New Haven: a population-based demographic profile.
Authors: R F Quah, A D Stark, J W Meigs, E R DeLouise
Journal: Environmental Health Perspectives (1982)

This report presents the geometric mean blood lead levels of an 80% cross-sectional sample of children aged 1-72 months in New Haven, Connecticut. Blood lead levels were related to age, sex and race. It was found that age and race were independently important sources of variation in blood lead levels. Sex of children in this age group was not related to differences in blood lead levels. The highest geometric mean blood lead levels occurred in children between 25 and 36 months of age. Black children had higher levels than white or Hispanic children.
When Molecules Tell Tales, Cancer Researchers Listen
Authors: E. Blume
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article When Molecules Tell Tales, Cancer Researchers Listen Get access Elaine Blume Elaine Blume Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 19, 5 October 1994, Pages 1440–1441, https://doi.org/10.1093/jnci/86.19.1440 Published: 05 October 1994