tbuckley/cabot-search huggingface dataset:
Decreased breath excretion of redox active iron in COPD: a protective failure?
Authors: Sharon Mumby, Junpei Saito, Ian M. Adcock, Kian Fan Chung, Gregory J. Quinlan
Journal: European Respiratory Journal (2015)

Recent observational and genetic studies have highlighted a potential role for disrupted iron homeostasis in stable and exacerbating chronic obstructive pulmonary disease (COPD). Thus iron deficiency that is not limited to anaemia [1] and single nucleotide polymorphism in the gene encoding iron regulatory protein-2 [2], a key regulatory factor involved in cellular iron turnover and control, have been identified in this population. Disrupted systemic iron homeostasis is likely to limit iron availability for metabolic purposes due to overriding effects on tissue storage rather than on mobilisation and limitation of uptake from the gut. A specific pro-oxidant pool of iron (free or loosely bound ions, which are redox active/catalytic for damaging oxidant production) is measurable in exhaled breath condensate (EBC) [3]. While iron is essential for life, particularly for aerobes, poor or altered iron handling results in adverse effects related to oxidant production, microbial virulence, altered redox signalling events and altered cellular fate, including remodelling. This study was therefore undertaken to gain insight into iron handling in lungs and airways, and the extent to which these processes may be altered in COPD. Studies were undertaken to measure this specific iron pool by the bleomycin method [4] utilising EBC samples collected as previously described [3] and obtained from normal healthy individuals, healthy smokers and patients with COPD (current and ex-smokers). Serum levels of hepcidin and interleukin (IL)-6, known regulators of iron homeostasis, were also measured. Decreased redox active iron in exhaled breath condensate from COPD smokers may indicate an excretion failure <http://ow.ly/VA4vM>
Abstract 5586: NK cell killer Ig-like receptor (KIR) genotype as a novel biomarker for neuroblastoma patients receiving Anti-GD2 monoclonal antibody 3F8
Authors: Jeffrey M. Venstrom, Junting Zheng, Brian H. Kushner, Shakeel Modak, Karen E. Danis, Irene Y. Cheung, Bo Dupont, Nai-Kong Cheung, Katharine C. Hsu
Journal: Cancer Research (2010)

Abstract Background: Natural killer (NK) cells are regulated by inhibitory killer Ig-like receptors (KIRs) that recognize specific HLA class I ligands. KIR-HLA genotypes are tightly linked to NK cell function and clinical outcomes in allogeneic and autologous hematopoietic stem cell transplantation (HSCT). Because NK cells contribute to antibody-dependent cellular cytotoxicity, we hypothesized that specific KIR-HLA genotypes may predict NK cell responsiveness to mAb therapy, and thus, may be useful clinically to identify patients likely to respond to mAb therapy. Methods: 76 children with high risk neuroblastoma received cyclophosphamide-containing induction chemotherapy followed by murine IgG3 monoclonal antibody 3F8 against ganglioside GD2 between 1993 and 2007. HLA and KIR genotyping was performed, and patients were segregated into KIR-HLA groups based on known functional KIR-HLA ligand relationships: KIR2DL2/2DL3 with HLA-CAsn80(HLA-C1 group), KIR2DL1 with HLA-C Lys80(HLA-C2 group), and KIR3DL1 with HLA-Bw4. Overall survival and progression-free survival were estimated by Kaplan-Meier method and hazard ratios by Cox regression. No adjustments were made for multiple comparisons. Comparisons of each end point were based on the log-rank statistics. Results: 63% of the 76 children lacked at least 1 HLA ligand for his/her inhibitory KIR. At 3 years, 80% of patients lacking any KIR ligand (n=46) were alive compared with 69% of patients with all HLA ligands present (n=30) (HR 0.41; 95% CI 0.17-0.98; P=0.04). 23/23 (100%) patients specifically lacking the HLA-Bw4 ligand for KIR3DL1 were alive at 3 years compared with 34/52 (67%) patients exhibiting HLA-Bw4 for KIR 3DL1 (n=52) (HR 0.20; 95% CI 0.05-0.87; P=0.02). Conclusion: KIR-HLA immunogenetics may be a novel biomarker for neuroblastoma patients receiving chemo-immunotherapy. The milieu of HSCT may not be required for NK cells to behave according to “missing ligand,” and KIR-HLA combinations may be predictive of outcome for other malignancies similarly treated with mAb. 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 5586.
Trends in Invasive Breast Cancer Incidence Among American Women
Authors: B. A. Miller, E. J. Feuer, B. F. Hankey
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Trends in Invasive Breast Cancer Incidence Among American Women Get access Barry A. Miller, Barry A. Miller Search for other works by this author on: Oxford Academic PubMed Google Scholar Eric J. Feuer, Ph.D., Eric J. Feuer, Ph.D. Search for other works by this author on: Oxford Academic PubMed Google Scholar Benjamin F. Hankey, Sc.D. Benjamin F. Hankey, Sc.D. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 10, 15 May 1991, Page 678, https://doi.org/10.1093/jnci/83.10.678 Published: 15 May 1991
P343 IDENTIFICATION OF A NOVEL HEXOKINASE IN PATIENTS WITH ALCOHOLIC HEPATITIS
Authors: M. Moreno, M. García-Rocha, J. Altamirano, S. Affò, O. Morales-Ibanez, P. Sancho-Bru, C. Millan, V. Arroyo, J. Caballeria, P. Gines, J. Guinovart, R. Bataller
Journal: Journal of Hepatology (2014)
SP0138 Setting invividual treatment goals in complex cases
Authors: T.N. Dager
Journal: Annals of the Rheumatic Diseases (2013)

Goal planning is considered an essential part of rehabilitation practice and is a collaborative process between the patient and the rehabilitation team directed at setting goals at various levels of function, within different life areas, and in various time frames (Wade et al. 2000)&amp; Key components of goal setting comprise ggal identification and negotiation, action planning, and appraisal and feedback of performance (Holliday et al 2005, Scobbie et al. 2011). Goal setting further involves behavioural, cognitive and psychological elements. In a systematic review, Levack et al.(2006)found limited evidence that goal planning can influence patient adherence to treatment regimes and strong evidence that prescribed, specific, challenging goals can improve immediate patient performance in some specific clinical contexts. The process of sorting and giving priority to some areas can be personally challenging and affect psychological themes and ambivalence. Personal rehabilitation goals therefore benefits from well funded decisions. An individual rehabilitation goal funded on personal values and conscious commitment is more robust when challenged by competing considerations. The National Center for Rehabilitation in Rheumatology at Diakonhjemmet Hospital offer rehabilitatiof to patients with complex and multiple illness-related challenges, who are in need of a broad multidisciplinary approach. Based on a thorough assessment by all members of the interdisciplanarq team, individual goals are defined through a structured goal setting approach. The goals are documented in an individual rehabilitation plan which is adjusted throughout the rehabilitation stay, and evaluated at discharge (Kjeken et al. 2008). Results from a recent qualitative study (Dager et al 2011) of rehabilitation outcomes emanating from the rehabilitation center emphasizes the need to understand and take into account the patients' own understanding of challenges when formulating individual rehabilitation goals. At the work-shop, the goal-setting process will be illustrated through patient cases, and factors facilitating or hampering the goal setting process will be discussed. <h3>Disclosure of Interest</h3> None Declared
THE ASSOCIATION OF FRAILTY WITH MORTALITY IN HIGH RISK PATIENTS UNDERGOING TRANSCATHETER AORTIC VALVE REPLACEMENT: AN ANALYSIS OF THE PARTNER II ALTERNATIVE ACCESS COHORTS
Authors: Hersh Maniar, Alan Zajarias, Nishath Quader, Suzanne Arnold, David Cohen, Michael Mack, Spencer Melby, Maria Alu, Girma Ayele, Brian Lindman, John Lasala, Augusto Pichard, Stephen Ramee, Vinod Thourani, Wilson Szeto, Martin Leon, Philip Green
Journal: Journal of the American College of Cardiology (2016)
PREDICTORS OF SURVIVAL FOLLOWING AORTIC VALVE REPLACEMENT AND CAUSE OF DEATH IN LOW FLOW VERSUS NORMAL FLOW SEVERE AORTIC STENOSIS WITH PRESERVED EJECTION FRACTION
Authors: Mackram F. Eleid, Hector Michelena, Vuyisile Nkomo, Rick Nishimura, Youssef Maalouf, Christopher Scott, Patricia Pellikka
Journal: Journal of the American College of Cardiology (2015)
PWE-179 A Survey On Patient Wellbeing And Patient Comfort During Oesophageal Intubations. A Multicentre Study: Abstract PWE-179 Table 1
Authors: M Brennan, T Moran, P Lawlor, L Barry, M Treacy, JV Reynolds, R Narayanasamy
Journal: Gut (2014)

<h3>Introduction</h3> A Multicentre survey was undertaken from November 2013 until January 2014 on 80 patients (45f Vs 35m) undergoing oesophageal manometry and/or oesophageal 24 hr pH/impedance study. The aim of this study was to determine the overall wellbeing of the patient during their investigation. Oesophageal intubations are invasive techniques which many patients find quite distressing. These studies require the patient to be alert and to be able to swallow liquid boluses. In order to retain their normal oesophageal function, sedation or oral anaesthetic spray is not routinely administered. This study was compiled to obtain specific patient data from Gastrointestinal (GI) Units throughout Ireland by conducting a survey post patient procedure. <h3>Methods</h3> A survey containing short answer questions was devised and GI units providing a service in GI Physiology testing were asked to participate. The patient was asked to answer either ‘Yes’ or ‘No’ to the questions or score the answers to the questions with a value from 0–10 with 10 being the most severe scale of discomfort/anxiety and 0 being the least. <h3>Results</h3> Table 1 below shows the results obtained from the multicentre survey. The reasons given for failed intubations included patient anxiety, nasal sensitivity and previous traumatic Endoscopy experience. With regards to patient anxiety prior to investigation; no option for general anaesthetic, sedation, nasal spray, throat spray, and the fear of the unknown were the main reasons for the high patient anxiety scores. <h3>Conclusion</h3> Appropriately trained GI Physiologists achieved a 96.3% rate of successful oesophageal intubations. Despite this, patient anxiety in anticipation of their procedure is relatively high. With the option of a nasal spray, this survey suggests that patient anxiety levels prior to their investigation would be reduced, thus making the intubation a more pleasant, tolerable and less traumatic experience. <h3>Disclosure of Interest</h3> None Declared.
Abstract SY12-01: Stem cell approaches dissect lung cancer biology
Authors: Carla F. Kim
Journal: Cancer Research (2011)

Abstract Lung cancer is the major cause of death from cancer worldwide. The five-year survival rate for the majority of lung cancer patients is only 16% because their tumors are refractory to chemotherapeutics or quickly become resistant to therapeutic response. Also contributing to morbidity, most lung cancer patients already have advanced, metastatic disease at the time of diagnosis or develop metastases after surgical removal of early-stage primary lung tumors. The cancer stem cell (CSC) hypothesis is an attractive explanation for tumor growth, recurrence after treatment, and metastasis in some cancers, yet the precise role of CSCs in lung tumors has not been established. Since successful cancer therapy requires the elimination or incapacitation of all tumor cells capable of regenerating a tumor, it is crucial to characterize the cells that are able to propagate a tumor in vivo. We refer to these functionally important cancer cells as tumor-propagating cells (TPCs). Importantly, understanding the identity and molecular nature of TPCs will provide new opportunities for early detection, treatment and prevention of metastatic disease, whether or not they fit the CSC model in each type of cancer. My laboratory recently showed that murine lung adenocarcinomas, the most prevalent lung cancer subtype, contain a TPC population. In mice bearing tumors initiated with oncogenic Kras and deletion of p53, the cell surface marker Sca1 identifies cancer cells with stem cell properties. In contrast, TPCs are Sca1-negative in lung tumors that express a mutant EGFR. Thus, the predominant driving oncogenotype is an important determinant in the identification of TPC phenotype in lung cancer. This finding suggests that treatments directed against cancer stem cells should be targeted to subsets of patients grouped according to their oncogenotype. We have recently obtained global gene expression data from the Sca1-sorted populations of murine lung tumor cells, as well as their normal wild-type counterparts, to uncover the molecular pathways responsible for tumor propagation in lung adenocarcinoma. I will also discuss new avenues we have taken to understand the connections between TPCs and metastasis in mouse models as well as translating the importance of our findings in human lung cancer cells and patient samples. 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 SY12-01. doi:10.1158/1538-7445.AM2011-SY12-01
Abstract 776: Therapeutic immunity against melanoma by IL-12 cDNA electroporation: a possible therapeutic mechanism
Authors: Jeong-Im Sin, Hun Mo Ryoo
Journal: Cancer Research (2011)

Abstract We observed that large-established melanoma was eradicated by intratumoral (IT)-electroporation (EP) of IL-12 cDNA in an animal model. In this study, we explored the mechanism(s) as to how this tumor eradication is mediated in vivo and evaluated if long-term memory responses to parental tumor cell re-challenge can be induced. Melanoma (B16) cells were subcutaneously inoculated. When tumor reached 6-8 mm in mean diameter, 50 μg of IL-12 cDNA was intratumorally injected and electroporated using Cellectra® of VGXI at 0.2A for 4 sec. To further determine the antitumor mechanism(s), IT-EP was performed in tumor-bearing wild type, IFN-γ knockout (KO), and perforin KO animals. Furthermore, immune cell infiltration was measured by histological analysis. In vitro and in vivo immune cell subset depletion assay was also performed to see an involvement of T and NK cell populations in tumor Ag-specific IFN-γ production and tumor control. IT-EP of IL-12 cDNA resulted in eradicating tumors established on the skin without any significant levels of long-term antitumor memory immunity. This effect required mainly CD8+ and to a lesser degree CD4+ T cells, but not NK cells. Both IFN-γ KO animal studies and IT-EP assay of IFN-γ cDNA confirmed that IFN-γ was indirectly involved in melanoma control. Furthermore, perforin was found to be essential for the tumor-eradicating activity. However, B16 melanoma cells expressed Fas, but failed to exhibit Fas-mediated cell lysis, suggesting that perforin/granzyme B-mediated killing pathway is associated with CD8+ T cell-mediated melanoma control. Taken together, these studies show that IT-EP of IL-12 cDNA is an important approach to control melanoma on the skin and this antitumor effect is mediated mainly by CD8+ T cells (as a killer T cell) through perforin/granzyme B-mediated killing pathway. This study also suggests that additional approaches are needed to induce long-term antitumor memory responses. 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 776. doi:10.1158/1538-7445.AM2011-776
Hereditary Deficiencies of Clotting Factors VII and X Associated with Carotid-Body Tumors
Authors: A. J. Kroll, B. Alexander, F. Cochios, L. Pechet
Journal: New England Journal of Medicine (1964)

AN elevated prothrombin time as determined by the Quick1 procedure may be due to many abnormalities, including deficiency of factors I (fibrinogen), II (prothrombin), V (achéal-globulin), VII (proconvertin) or X (Stuart). When acquired, these defects arise from hepatic disease, vitamin K deficiency or coumarin therapy. They may also be congenital or inherited.The present investigation was initiated by the incidental preoperative finding of a prolonged Quick prothrombin time in a woman with a carotid-body tumor. The demonstration of a similar clotting abnormality and tumors in a number of the patient's relatives led to a detailed study of all available members . . .
Abstract 5346: Tumor cell heterogeneity and chromosomal abnormality in malignant pleural effusion (MPE) samples of lung cancer
Authors: Saroj Kumar Basak, Nagesh P. Rao, Scott Oh, Veena S. Mysore, Eri S. Srivatsan, Raj K. Batra
Journal: Cancer Research (2012)

Abstract Tumor heterogeneity is a hallmark of cancer and different types and stages of cancer express various cell surface markers and gene expression profiles. To understand tumor cell heterogeneity in lung cancer, we have developed a model using primary cells from malignant plural effusion (MPE) from lung cancer patients. Using this system we have identified CD44high expressing primary tumor cells within the MPE that form colonies in soft agar in vitro, and tumors in SCID/NOD mice. RT-PCR analysis revealed higher expression of cancer stem cell markers, Bmi-1, hTERT, EZH2, and OCT-4 in CD44high cells than the CD44low cells. Thus, our results indicate that primary tumor cells of MPE derived from lung cancer patients show heterogeneity with respect to their tumorigenic potential. To determine whether we could detect cytogenetic abnormalities in these samples, we performed karyotypic analysis of the MPE samples. Fibroblast cell line GM 05399 served as a control for these studies. Hyperdiploidy was observed in all three MPE samples and in the control cell line H 2122. Abnormalities of chromosome 1p were observed seen in all the samples that led us to perform FISH (fluorescence in situ hybridization) studies using a dual color 1p36 and 1q25 probe (control). We found LOH (loss of heterozygosity) at 1p36 in two MPE samples and rearrangements of both 1p/1q regions in the third MPE sample. Cell line H 2122 contained one normal chromosome 1 and an unbalanced translocation of unknown origin at 1p36 consistent with deletion of 1p. Our studies therefore suggest that this 1p36 deletion could result in the inactivation of a tumor suppressor gene and other sequences that include miRNA 34a also mapped to this locus. Chromosomal rearrangements further indicate that cells with multiple phenotypes including those related to metastasis, and chemo-radiation resistance might be present in the MPE samples. These studies provide a good basis suggesting that MPE would serve as a useful model system for the identification of genes related to the progression of lung cancer. 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 5346. doi:1538-7445.AM2012-5346
PWE-076 Dendritic Cell Characteristics in Pouchitis
Authors: J Landy, H O Al-Hassi, E R Mann, S T Peake, P J Ciclitira, J Nicholls, S K Clark, S C Knight, A L Hart
Journal: Gut (2013)

<h3>Introduction</h3> The role of dendritic cells (DC) in inflammatory bowel disease is increasingly recognised for their function in regulating intestinal immune responses. To our knowledge there are no previous studies of DC in pouchitis. We aimed to characterise changes in DC in pouchitis that may underlie the dysregulated immune response to the pouch microbiota. <h3>Methods</h3> Mucosal biopsy samples were taken from patients with pouchitis (n = 14) and ulcerative colitis patients without pouchitis (n = 10). Lamina propria DC were isolated by collagenase digestion. DC were identified as an HLA DR+, lineage -(CD3-, CD14-, CD16-, CD19-, CD34-) population. DC expression of TLR 2 and 4, CCR9, β7 and CD40 were measured by multicolour flow cytometry. The t-test was used for statistical analysis. <h3>Results</h3> DC expression of TLR 2 and 4 were both significantly elevated in patients with pouchitis compared with non-pouchitis patients (p = 0.007 and 0.008). In pouchitis patients, DC expression of β7 was increased (p = 0.02) and expression of CCR 9 was decreased (p = 0.02). DC expression of CD40 was increased in patients with pouchitis (p ≤ 0.0001). <h3>Conclusion</h3> In pouchitis, DC are activated and upregulate expression of microbial recognition receptors. In addition, DC expression of gut homing markers is elevated in pouchitis with a more colonic homing marker profile. Similarly to other IBD, DC are likely to be key in the initation and perpetuation of the inflammatory response to the dysbiosis of the pouch microbiota <h3>Disclosure of Interest</h3> J. Landy Grant/Research Support from: The Broad Foundation, H. Al-Hassi: None Declared, E. Mann: None Declared, S. Peake: None Declared, P. Ciclitira: None Declared, J. Nicholls: None Declared, S. Clark: None Declared, S. Knight: None Declared, A. Hart: None Declared