tbuckley/cabot-search huggingface dataset:
AB0212 A study to determine the relationship between fatigue, physical activity and sitting time in patients with inflammatory arthritis.
Authors: D. Fitzpatrick, B. Mcgowan, A. McPartland, C. Silke, B. Whelan
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Fatigue is a common and debilitating symptom in inflammatory arthritis. Higher levels of physical activity are associated with better general health status and with better outcomes in inflammatory arthritis [1]. <h3>Objectives</h3> Our aim was to measure fatigue and physical activity in those with inflammatory arthritis and to examine the relationship between the two. <h3>Methods</h3> The study involved the use of two validated self-administered questionnaires 1) the FACIT-F questionnaire[2], to measure fatigue and wellbeing and 2)(the long version of the International Physical Activity Questionnaire (IPAQ)[3] in consecutive, unselected patients with a diagnosis of inflammatory arthritis (rheumatoid arthritis, psoriatic arthritis and juvenile idiopathic arthritis) attending the NWRU. The nonparametric results were analysed with Spearman correlation and Mann-Whitney U techniques. <h3>Results</h3> 63 patients were recruited. The mean age of the study cohort was 59.4 years with mean disease duration of 12 years. There was a positive correlation between sitting-time and fatigue score (R =.482, p&lt;.05) and a negative correlation between sitting-time and physical wellbeing score (R=.406, p&lt;.05). There is a weaker negative correlation between fatigue score and physical activity (R=.252, p&lt;.05). <h3>Conclusions</h3> As expected, fatigue is related negatively with physical activity. However, the positive relationship between fatigue and sitting-time is stronger and more significant. The utility of asking patients how much time they spend sitting to gauge physical activity and fatigue merits further investigation. <h3>References</h3> J. Cooney, R. Law, and V. Matschke, “Benefits of exercise in rheumatoid arthritis,” <i>Journal of aging</i>, 2011. “FACIT-F.” [Online]. Available: http://www.facit.org/FACITOrg/Questionnaires. [Accessed: 28-Jun-2012]. “International Physical Activity Questionnaire (Long Form).” [Online]. Available: http://www.ipaq.ki.se/. [Accessed: 28-Jun-2012]. <h3>Disclosure of Interest</h3> None Declared
Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography Correlated With Computed Tomographic Scan and Magnetic Resonance Imaging in a Case of Hematometrocolpos
Authors: SYLVAIN BEAULIEU, LUC BOUCHER, MARTIN LECOMPTE, FRANÇOIS BÉNARD
Journal: Clinical Nuclear Medicine (2000)

BEAULIEU, SYLVAIN M.D.; BOUCHER, LUC M.D.; LECOMPTE, MARTIN M.D.; BÉNARD, FRANÇOIS M.D. Author Information
P156 RIBAVIRIN PRETREATMENT IMPROVES THE IFN-γ RESPONSE OF NATURAL KILLER CELLS TO IFN-BASED THERAPY OF HEPATITIS C VIRUS INFECTION
Authors: J.M. Werner, E. Serti, X. Chepa-Lotrea, G. Ahlenstiel, J. Feld, T.J. Liang, B. Rehermann
Journal: Journal of Hepatology (2014)
Abstract 1740: Analogs of OSI-930 as potent ABCG2-mediated multidrug resistance reversal agents
Authors: Jay P. Patel, Ye-Hong Kuang, Kamlesh Sodani, Chun-Pu Wu, Li-Qiu Liao, Amit K. Tiwari, Chun-ling Dai, Xiang Chen, Li-Wu Fu, Suresh V. Ambudkar, Vijaya L. Korlipara, Zhe-Sheng Chen
Journal: Cancer Research (2011)

Abstract OSI-930 {N-(4-trifluoromethoxyphenyl) 3-((quinolin-4-ylmethyl) amino) thiophene-2-carboxamide}, a dual c-Kit and KDR tyrosine kinase inhibitor, has been reported to be undergoing Phase I dose escalation study in cancer patients. A series of sixteen pyridyl and phenyl analogs (JP compounds) of OSI-930 was designed and synthesized. Extensive screening of these compounds led to the discovery that nitropyridyl and nitrophenyl analogs of OSI-930, JP1 and JP3, were effective in reversing ABC subfamily G member 2 (ABCG2/BCRP/MXR) transporter-mediated multidrug resistance (MDR). In the present study, JP1 and JP3 significantly sensitized ABCG2-expressing cells to established substrates of ABCG2 including mitoxantrone, SN-38 and doxorubicin in a concentration-dependent manner, but not to the non-ABCG2 substrate cisplatin. Furthermore, JP1 and JP3 were unable to reverse ABCB1- or ABCC1-mediated MDR indicating their selectivity for ABCG2. Western blot analysis was used to evaluate ABCG2 expression and it was found that neither JP1 nor JP3 significantly altered ABCG2 protein expression during the course of our experiment. Accumulation study with an ABCG2 substrate [3H]-mitoxantrone demonstrated that JP1 and JP3 increased the intracellular accumulation of [3H]-mitoxantrone. JP1 and JP3 also significantly inhibited the transport of [3H]-methotrexate by ABCG2 in the in vitro transport assays using membrane vesicles. Importantly, both JP1 and JP3 efficaciously stimulated the activity of ATPase of ABCG2 and inhibited the photoaffinity labeling of this transporter with its substrate [125I]-iodoarylazidoprazosin. Results from the present study suggest that analogs of OSI-930, JP1 and JP3, specifically inhibit the function of ABCG2 through direct interaction with its substrate binding site(s). Thus the OSI-930 analogs represent a new class of potential reversal compounds for the treatment of MDR in ABCG2 over-expressing tumors. 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 1740. doi:10.1158/1538-7445.AM2011-1740
Abstract 889: An analysis of single nucleotide polymorphisms of 125 DNA repair genes in the Texas genome-wide association study of lung cancer with a replication for the <i>XRCC4</i> SNPs
Authors: Hongping Yu, Hui Zhao, Li-E Wang, Younghun Han, Chen Wei V., Christopher I. Amos, Thorunn Rafnar, Patrick Sulem, Kari Stefansson, Maria Teresa Landi, Neil Caporaso, Demetrius Albanes, Michael Thun, James D. McKay, Paul Brennan, Yufei Wang, Richard S Houlston, Margaret R. Spitz, Qingyi Wei
Journal: Cancer Research (2011)

Abstract DNA repair genes are important for maintaining genomic stability and limiting carcinogenesis. We analyzed all single nucleotide polymorphisms (SNPs) of 125 DNA repair genes covered by the Illumina HumamHap300 (v1.1) BeadChips in a previously conducted genome-wide association study (GWAS) of 1,154 lung cancer cases and 1,137 controls and replicated the top-hits of XRCC4 SNPs in an independent set of 597 cases and 611 controls in Texas populations. We found that six of 20 XRCC4 SNPs were associated with a decreased risk of lung cancer with a P value of 0.01 or lower in the discovery dataset, of which the most significant SNP was rs10040363 (P for allelic test = 4.89 ×10−4). Moreover, the data in this region allowed us to impute a potentially functional SNP rs2075685 (imputed P for allelic test = 1.3 ×10−3). A luciferase reporter assay demonstrated that the rs2075685G&amp;gt;T change in the XRCC4 promoter increased expression of the gene. In the replication study of rs10040363, rs1478486, rs9293329, and rs2075685, however, only rs10040363 achieved a borderline association with a decreased risk of lung cancer in a dominant model (adjusted OR = 0.80, 95% CI = 0.62-1.03, P = 0.079). In the final combined analysis of both the Texas GWAS discovery and replication datasets, the strength of the association was increased for rs10040363 (adjusted OR = 0.77, 95% CI = 0.66-0.89, Pdominant = 5×10−4 and P for trend = 5×10−4) and rs1478486 (adjusted OR = 0.82, 95% CI = 0.71 -0.94, Pdominant = 6×10−3 and P for trend = 3.5×10−3). Finally, we conducted a meta-analysis of these XRCC4 SNPs with available data from published GWA studies of lung cancer with a total of 12,312 cases and 47,921 controls, in which none of these XRCC4 SNPs was associated with lung cancer risk. It appeared that rs2075685, although associated with increased expression of a reporter gene and lung cancer risk in the Texas populations, did not have an effect on lung cancer risk in other populations. This study underscores the importance of replication using published data in larger populations. 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 889. doi:10.1158/1538-7445.AM2011-889
456 PRETREATMENT OF HUMANIZED UPA/SCID MICE WITH INTERFERON ALPHA STRONGLY INHIBITS THE ESTABLISHMENT OF HEPATITIS B VIRUS INFECTION
Authors: T. Volz, J.-L. Braunschmidt, T. Bornscheuer, L. Allweiss, A.W. Lohse, J. Petersen, M. Lütgehetmann, M. Dandri
Journal: Journal of Hepatology (2012)
Reply to Fan et al.
Authors: Ryan Law, Todd Baron
Journal: Endoscopy (2014)

As pointed out by Fan et al., endoscopic retrograde cholangiopancreatography (ERCP) can be performed using a variety of techniques in patients with Roux-en-Y gastric bypass (RYGB) anatomy. However, we believe each technique has substantial limitations. ERCP performed after laparoscopic [1] or radiologic [2] access to the gastric remnant requires schedule coordination, which may further delay a needed procedure. We do acknowledge that ERCP with laparoscopic assistance may be feasible in centers where surgeons also perform ERCP. It should be noted that our technique does not require gastrostomy tract maturation, as gastropexy is performed prior to gastrostomy creation. This allows immediate use of the gastrostomy tract.
727 HEPATIC ARTERIAL CHEMOEMBOLIZATION FOR THE METASTATIC LIVER CARCINOID
Authors: D.V. Komov, E.M. Roschin, E.R. Virshke, E.V. Poddubskaya, O.M. Sergeeva, B.I. Dolgushin, S.B. Polikarpova, I.V. Kolyadina, H.I. Borovskaya
Journal: Journal of Hepatology (2012)
Abstract 2840: A functional nonsynonymous single nucleotide polymorphism in the migration and invasion inhibitory protein (<i>MIIP)</i> gene confers differential risk of breast cancer
Authors: Kexin Chen, Fangfang Song, Ping Ji, Hong Zheng, Fengju Song, Yingmei Wang, Xishan Hao, Qingyi Wei, Wei Zhang
Journal: Cancer Research (2010)

Abstract The migration and invasion inhibitory protein (MIIP) gene encodes an inhibitor of cancer cell migration and invasion. Our previous studies using the colony formation assay have demonstrated that MIIP also inhibits tumorigenesis in breast cancer cells. Therefore, we hypothesized that genetic variations in MIIP may affect breast cancer development and prognosis. In this case-control study, we genotyped the MIIP single nucleotide polymorphism (SNP) rs2295283 (codon 167, A&amp;gt;G, K&amp;gt;E) from 1524 breast cancer patients and 1592 age-matched controls for its association with breast cancer risk. The SNP analysis was next performed on a validation set (736 cases and 760 controls). Colony formation and cell migration assays were then conducted to functionally interrogate the difference between the A and G variants. Compared with the AA genotype in both the test and validation sets, the combined AG+GG genotypes (167E) were associated with a significantly lower risk of breast cancer. Among the test set, the protective effect of the AG+GG genotypes was more evident among participants with a family history of cancer. Further case series analysis revealed that the GG genotype was less susceptible to breast cancer with tumor size &amp;gt;2 cm and late clinical stage (II+III+IV). Colony formation assays showed that MIIP 167E (the G variant) was a more potent inhibitor of colony formation but not cell migration. These results suggest that MIIP K167E SNP may be a genetic predictor of breast cancer development and prognosis, as supported by differential abilities of the two isoforms in inhibiting breast cancer colony formation in vitro. 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 2840.
PD-1 blockade: a therapeutic option for treatment of metastatic Merkel cell carcinoma
Authors: J.K. Winkler, C. Bender, C. Kratochwil, A. Enk, J.C. Hassel
Journal: British Journal of Dermatology (2016)

The immune system is extremely important in the development and progression of Merkel cell carcinoma (MCC). Immune checkpoint blockade has recently been shown to enable efficacious treatment of a variety of tumours. We report the use of an anti-programmed death receptor 1 (PD-1) antibody for treatment of a patient with metastatic MCC. An 80-year-old patient with metastatic MCC received off-label treatment with the anti-PD-1 antibody pembrolizumab after the disease had progressed during therapy with oral etoposide. A positron emission tomography (PET) computed tomography scan performed after three cycles of pembrolizumab revealed responses to therapy with reduced size of the adrenal gland metastases and less PET activity in the adrenal gland and lymph node metastases. Treatment was resumed owing to disease progression after a treatment-free interval of > 4 months. During subsequent months of treatment, the size of the metastases stabilized and uptake of nuclide by all tumour sites once again decreased. These results reveal the potential efficacy of an anti-PD-1 antibody for treatment of metastatic MCC. Thus, they contribute to currently limited data on the use of anti-PD-1 antibodies for the treatment of MCC. Moreover, this is the first report of successful resumption of treatment of metastatic MCC with an anti-PD-1 antibody. Results from ongoing trials will contribute to determination of the relevance of PD-1 blockade in metastatic MCC.
Abstract 1194: p53 negatively regulates the hepatoma growth factor HDGF
Authors: Takashi Tokino, Masashi Idogawa, Yasushi Sasaki
Journal: Cancer Research (2012)

Abstract Tumor suppressor genes may exert a significant part of their activity by regulating autocrine and paracrine growth factor pathways. This study reveals how the transcriptional repression function of p53 mediates cancer cell growth and migration. Hepatoma-derived growth factor (HDGF) is a secreted heparin-binding growth factor that has been implicated in cancer development and progression. Here we report that HDGF is a critical target for transcriptional repression by the tumor suppressor p53. Endogenous HDGF expression was decreased in cancer cells with introduction of wild-type p53, which also downregulated HDGF expression after DNA damage. In support of the likelihood that HDGF is a critical driver of cancer cell growth, addition of neutralizing HDGF antibodies to culture media was sufficient to block cell growth, migration and invasion. Similarly, these effects were elicited by conditioned culture medium from p53-expressing cells and they could be reversed by the addition of recombinant human HDGF. Interestingly, we found that HDGF was overexpressed also in primary gastric, breast and lung cancer tissues harboring mutant p53 genes. Mechanistic investigations revealed that p53 repressed HDGF transcription by altering HDAC-dependent chromatin remodeling. Taken together, our results reveal a new pathway in which loss of p53 function contributes to the aggressive pathobiological potential of human cancers by elevating HDGF expression. 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 1194. doi:1538-7445.AM2012-1194
A three-legged stool needs a stronger third leg
Authors: Ramon Greenberg
Journal: Behavioral and Brain Sciences (2013)

Abstract Whereas the target article stresses the neurobiology and psychology of dreams, this commentary emphasizes that the role of dreams in emotional integration and adaptation contributes to a fuller understanding of dreaming and memory. The dream presented in the target article is used, within the constraints of space, as a possible example of a broader approach to dream material.
A6.38 Toll-like receptor 7 and 9 in the pathogenesis of inflammatory autoimmune arthritis
Authors: A Fischer, S Herman, C Böhm, V Saferding, E Goncalves-Alves, G Steiner
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background and objectives</h3> There is evidence that release and insufficient removal of endogenous nucleic acids may be involved in triggering harmful autoimmune reactions important in the initiation of systemic autoimmune diseases including rheumatoid arthritis (RA). Nucleic acid sensing molecules, such as the endosomal Toll-like receptors (TLRs) 7 and 9, have been linked to pathogenetic autoimmune processes, particularly in systemic lupus erythematosus, but their role in RA is less clear. We aimed to study the role of TLR7 and TLR9 in the pathogenesis of inflammatory arthritis by antagonising or stimulating them in rats with pristane-induced arthritis (PIA). <h3>Materials and methods</h3> Arthritis was induced in Dark Agouti rats with the mineral oil pristane. Antagonists or agonists, respectively, for TLR7 and TLR9, a non-inhibitory control sequence or PBS as placebo were applied every other day. Treatment was started before disease induction. Arthritis was scored using established scoring systems, inflammation and bone erosion were quantified by histological analysis. Serum cytokine levels were measured by ELISA. <h3>Results</h3> While the control sequence showed no effect on arthritis development and severity, the TLR9 antagonist reduced arthritis severity significantly in PIA. In contrast, a slight aggravation of disease severity was observed in animals treated with the TLR7 antagonist. Inhibition of TLR9 led to strongly reduced bone erosion, whereas it appeared moderately aggravated in animals treated with the TLR7 inhibitor. Furthermore, IL-6 serum levels were reduced in animals treated with the TLR9 antagonist. However, these effects were only seen when the inhibitor was applied before disease onset. When treatment with the antagonists was started at disease-onset neither disease severity nor bone erosion were affected. Treatment with agonists for TLR9 or TLR7 showed no significant effect on disease severity in animals treated with the TLR9 agonist. In contrast, disease was significantly aggravated in animals treated with the TLR7 agonist and this effect was more pronounced than that observed in previous experiments with the TLR7 antagonist. <h3>Conclusions</h3> Inhibition of TLR9 in rats with PIA significantly reduced inflammation and bone erosion whereas stimulation of TLR7 aggravated disease severity. Therefore, these results suggest different roles for TLR7 and TLR9 in the T cell-dependent initiation phase of PIA and thus an important involvement of the DNA (CpG) recognising TLR9 and the RNA recognising TLR7 in the initiation of autoimmune arthritis which needs to be further elucidated in ongoing and future experiments.
The Effect of Diabetic Control on the Width of Skeletal-Muscle Capillary Basement Membrane in Patients with Type I Diabetes Mellitus
Authors: Philip Raskin, Angel O. Pietri, Roger Unger, W. Allen Shannon
Journal: New England Journal of Medicine (1983)

We studied the relation between the control of blood glucose and the width of skeletal-muscle capillary basement membrane in 23 insulin-dependent (Type I) diabetic patients. After initial measurement of levels of glycosylated hemoglobin and width of skeletal-muscle capillary basement membrane, the patients were divided into two groups: an experimental group of 13 patients who were treated with continuous subcutaneous insulin infusion, and a control group of 10 patients who continued to receive conventional treatment--usually two injections of insulin daily. After two years, the experimental group had a significant decrease in glycosylated hemoglobin levels as compared with base-line values (mean +/- S.E.M., 7.6 +/- 0.4 vs 10.2 +/- 0.7 per cent; P less than 0.001), reflecting improved control of blood glucose, and a significant reduction in the width of skeletal-muscle capillary basement membrane (1293 +/- 68 vs. 1717 +/- 182 A; P less than 0.05). The control group of patients had no significant change in their levels of glycosylated hemoglobin or in the width of their skeletal-muscle capillary basement membranes. If changes in the capillaries in skeletal muscle parallel those in the capillaries in retinal or renal tissue, then meticulous control of blood glucose may be beneficial over time in preventing the microvascular complications of diabetes.
FRI0399 Improved survival in patients with systemic sclerosis (SSC)-related pulmonary arterial hypertension (PAH) and interstitial lung disease (ILD) treated with aggressive use of pah therapy.
Authors: E. Volkmann, R. Saggar, N. Borazan, B. Torres, H. Agrawal, M. Flora, R. Saggar, P. Maranian, D. E. Furst
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The two leading causes of death in SSc are PAH and ILD. Historically, survival is worse in patients with combined PAH-ILD compared with isolated PAH (1), and there may not be any survival benefit with using PAH-medications in patients with PAH-ILD (2). <h3>Objectives</h3> To investigate the effects of aggressive PAH therapy on survival in SSc-PAH patients with and without ILD, and to determine which factors predict mortality. <h3>Methods</h3> All UCLA SSc patients who had a right heart catheterization diagnostic for PAH (mean pulmonary artery pressure (mPAP) ≥25 mm Hg, pulmonary capillary wedge pressure ≤15 mm Hg, pulmonary vascular resistance ≥240 dynesxsecond/cm<sup>5</sup>), between 2001-2012 were enrolled. ILD was defined as a forced vital capacity &lt;70%. Kaplan-Meier and Cox proportional hazards models were used to analyze survival and to identify prognostic variables. Mortality was defined as death (due to any cause) or lung transplantation. <h3>Results</h3> At baseline, patients with isolated PAH (n=41) and combined PAH-ILD (n=59) were similar for ethnicity, comorbidities, SSc type and duration, mean mPAP (PAH: 42; PAH-ILD: 39; p=NS). Patients with isolated PAH were older (mean 60 vs. 54 yrs in PAH-ILD, p=0.03), and had a greater percentage of women (93% vs. 68% in PAH-ILD, p=0.003). Mean follow up time was 30 and 27 months for the PAH and PAH-ILD groups, respectively, p=NS. There were no significant group differences in use of a systemic prostacyclin (PAH: 29%, PAH-ILD: 32%), use of a second PAH agent (61% in each group), or use of third PAH agent (PAH: 35%, PAH-ILD: 34%) during the study period. The 1-, 2-, 3-year survival estimates were 80%, 64%, 54%, and 74%, 64%, 56%, for the PAH and PAH-ILD groups, respectively, p=NS. In a multivariate model of the entire cohort (with the following covariates: mPAP, ILD, age, gender, ethnicity, body mass index, SSc type and duration, use of immunosuppression, hemoglobin T≤11 gm/dL), age was the only significant risk factor for mortality. <h3>Conclusions</h3> Compared with historical series (1, 2), long-term survival in SSc patients with both isolated PAH and PAH-ILD has improved, perhaps partly due to aggressive use of PAH therapy. <h3>References</h3> Condliffe R, et al. Am J Respir Crit Care Med 2009;179:151. Le Pavec J, et al. Arthritis Rheum 2011;63:2456. <h3>Disclosure of Interest</h3> None Declared