tbuckley/cabot-search huggingface dataset:
PTH-088 A faecal calprotectin level of &gt;100 μg/g in patients with negative bi-directional endoscopies is associated with high yield of pathology detection by capsule endoscopy
Authors: A Koulaouzidis, S Douglas, I Arnott, J N Plevris
Journal: Gut (2010)

<h3>Introduction</h3> Faecal calprotectin (FC) is a non-invasive marker of gastrointestinal inflammation with diagnostic precision in distinguishing inflammatory bowel disease (IBD) from non-IBD diagnoses; the higher precision is reported at a cut-off level of 100 μg/g. FC correlates with abnormalities seen on radiology of the small bowel, but little data exist in relation with capsule Endoscopy (SBCE). <h3>Aims</h3> We aim to correlate the findings of SBCE with FC values in patients with clinical suspicion of Crohn9s disease and negative bi-directional endoscopies. <h3>Methods</h3> Patients who underwent SBCE due to suspicion of small bowel Crohn9s were identified from the Rapid database. FC status was established for all review patients. Only patients with FC measured any time prior to the SBCE were included in the final review; in cases of multiple FC measurements, the value closest to the SBCE date was selected. Patients with prior known Crohn9s or NSAIDs use were excluded. <h3>Results</h3> A total of 45 patients were identified (32 females and 13 males). Two were excluded from further analysis as the capsules were retained in the upper GI tract. The remaining 43 cases, exhibited one or more of the following indications: Abdominal pain: 34, Loss of weight: 7, Diarrhoea: 21, High inflammation indices: 8 and anaemia/blood loss: 7. 18 patients had normal FC and 25 abnormal FC results. All those with FC&lt;50 μg/g (normal reference range &lt;50) and 7 patients who had FC between 50 and 100 μg/g, had normal SBCE. 18 patients had a FC &gt;100 μg/g; of those 8 (44.5%) had findings suggestive of Crohn9s disease. The patients (n=8) with SBCE indicative of Crohn9s, had a mean FC levels of 367.12, range 115–1430 μg/g. <h3>Conclusion</h3> FC&gt;100 μg/g is a useful predictor of small bowel Crohn9s findings by SBCE. FC levels &lt;100 μg/g seem to have an excellent NPV. FC is a useful tool in prioritising patients with suspected Crohn9s and increases the diagnostic yield of SBCE.
A Phase 1b/2a Study of Birinapant in Combination with 5-Azacitadine in Patients with Myelodysplastic Syndrome Who Are Naïve, Refractory to or Have Relapsed on 5-Azacitadine: a Preliminary Analysis
Authors: Gautam Borthakur, James M. Foran, Eunice S. Wang, Amol Rakkar, Steven Hager, Noelle V. Frey, Michael Andreeff, Guillermo Garcia-Manero, Tapan M. Kadia, Bing Z Carter, Hans Minderman, Lesley Russell, Raoul Tibes
Journal: Blood (2014)
A Circulating T Cell Clone in Early Mycosis Fungoides Is Not a Negative Prognostic Factor When the Disease Is Treated by a Combination of PUVA + Interferon α.
Authors: Serena Rupoli, Gaia Goteri, Renzo Ranaldi, Capretti Roberta, Anna Rita Scortechini, Alessandra Filosa, Stefano Pulini, Angela Tassetti, Donatella Brancorsini, Mirella Giangiacomi, Maria Cristiana Masia, Pietro Leoni
Journal: Blood (2004)
The Histopathogenesis of Pulmonary Tumors Induced in Strain a Mice by Urethan&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: F. K. Mostofi, M. D., C. D. Larsen, Ph. D.
Journal: JNCI Journal of the National Cancer Institute (1951)

The Histopathogenesis of Pulmonary Tumors Induced in Strain a Mice by Urethan Get access F. K. Mostofi, M. D., F. K. Mostofi, M. D. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. D. Larsen, Ph. D. C. D. Larsen, Ph. D. Pathology Biochemistry Sections, National Cancer Institute, National Institutes of Health, U. S. Public Health Service, Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 11, Issue 6, June 1951, Pages 1187–1221, https://doi.org/10.1093/jnci/11.6.1187 Published: 01 June 1951 Article history Received: 31 January 1951 Published: 01 June 1951
Selection bias in trials of transplantation for metastatic breast cancer: have we picked the apple before it was ripe?
Authors: G P Canellos
Journal: Journal of Clinical Oncology (1997)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1997.15.10.3169 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 9336351 Selection bias in trials of transplantation for metastatic breast cancer: have we picked the apple before it was ripe? G P CanellosxG P CanellosSearch for articles by this author https://doi.org/10.1200/JCO.1997.15.10.3169 PDF "Selection bias in trials of transplantation for metastatic breast cancer: have we picked the apple before it was ripe?." Journal of Clinical Oncology, 15(10), pp. 3169–3170© 1997 by American Society of Clinical Oncology
P-072 Pattern of recurrence and efficacy of salvage therapy after relapse in locally advanced esophageal carcinoma treated with preoperative chemoradiotherapy plus surgery
Authors: M. Oliva, M. Saigí, L. Aliste, G. Hormigo, M. Calvo, Ò. Serra, H. Aranda, C. Bettonica, N. Virgili, J. Robles, N. Romero, M. Boladeras Ana, J. Paúles Maria, B. Gornals Joan, L. Farran, M. Galán
Journal: Annals of Oncology (2016)
Sulfhydryl Groups in the Cathepsin of Rat Lymphosarcoma
Authors: Mary E. Maver, J. W. Thompson, Antoinette Greco
Journal: JNCI Journal of the National Cancer Institute (1946)

Journal Article Sulfhydryl Groups in the Cathepsin of Rat Lymphosarcoma Get access Mary E. Maver, Mary E. Maver senior biochemist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar J. W. Thompson, J. W. Thompson pharmacologist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar Antoinette Greco Antoinette Greco technical assistance National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 6, Issue 6, June 1946, Pages 355–362, https://doi.org/10.1093/jnci/6.6.355 Published: 01 June 1946
Abstract 2362: Myonecrosis is Predicted by Lack of Platelet Inhibition Measured in Response to Multiple Agonists in Patients Undergoing Elective Stenting:The Risk of A Global High Platelet Reactivity Phenotype
Authors: Kevin Bliden, Joseph DiChiara, Udaya Tantry, Paul Gurbel
Journal: Circulation (2007)

Background: Small studies have demonstrated the relation of clopidogrel nonresponsiveness to adverse clinical events. We sought to determine: the relation between inhibition of ADP-induced platelet aggregation and inhibition of aggregation induced by other agonists and the relation of clopidogrel responsiveness to periprocedural myonecrosis in patients undergoing stenting treated with a 600mg clopidogrel loading dose and bivalirudin. Methods: Platelet inhibition by low and high dose ADP, collagen and TRAP by conventional aggregometry (LTA) was determined at 2 hr and 24 hr post-stenting in 50 patients treated with aspirin, bivalirudin and 600 mg clopidogrel. Patients were stratified into low clopidogrel responders (LR)[≤10% relative platelet inhibition (RPI)], moderate responders (&gt;10 – &lt;30% RPI) and high responders (&gt;30% RPI)]. Results: Inhibition measured by 5uM ADP correlated with inhibition by 20uM ADP, collagen and TRAP (r =0.98, 0.91, and 0,83, respectively, p &lt; 0.001 for all). Myocardial marker release occurred in the LR and MR groups only. (Table ) Conclusions: 600 mg clopidogrel markedly inhibits platelet reactivity to multiple agonists in selected patients who are in turn protected from periprocedural MI during elective stenting. These data suggest that low and high risk patients can be identified by platelet function testing that may enhance decision making for adjunctive antithrombotic therapy in elective stenting.
P291 Relationship of<i>in vitro</i>particle size to<i>in vivo</i>lung deposition and exhaled fraction
Authors: G Poli, B Lipworth
Journal: Thorax (2015)

<h3>Introduction and objectives</h3> <i>The particle size distribution and the median mass aerodynamic diameter (MMAD) of an inhaled product are</i> important characteristics which may influence the deposition of the drug in the lung and as a consequence may also affect its therapeutic index. We evaluated the relationship between <i>in vitro</i> MMAD and <i>in vivo</i> lung deposition (LD, expressed as fraction of the delivered dose) and the exhaled fraction (EF), using relevant literature from scintigraphic studies conducted in healthy volunteers and asthmatic patients. Moreover the relationship between the ratio of EF to LD and MMAD has been further assessed. <h3>Methods</h3> Data from 21 studies in healthy volunteers (15 with pressurised metered dose inhalers (pMDI) and 6 with dry powder inhalers (DPI)) and 11 studies in asthmatic patients (8 pMDI and 3 DPI) have been evaluated. Asthmatic patients had a FEV1 &gt;70% predicted, supporting pooling of the data with that of healthy volunteers. <h3>Results</h3> LD increased when MMAD decreased, so that when MMAD is about 1 µm the LD is more than 50%of the delivered dose and becomes markedly lower when MMAD approach 4 µm. EF is low and did not change markedly. On the contrary, the ratio EF/LD is independent of the MMAD, suggesting that the EF is proportional to the LD and not affected by MMAD. <h3>Conclusion</h3> These data demonstrate that the EF/LD ratio is independent from the MMAD providing reassurance that a smaller particle size will not be associated with a higher exhaled fraction.
Daratumumab in Combination with Lenalidomide and Dexamethasone in Patients with Relapsed or Relapsed and Refractory Multiple Myeloma: Updated Results of a Phase 1/2 Study (GEN503)
Authors: Torben Plesner, Hendrik-Tobias Arkenau, Peter Gimsing, Jakub Krejcik, Charlotte Lemech, Monique C. Minnema, Ulrik Lassen, Jacob P. Laubach, Antonio Palumbo, Steen Lisby, Linda Basse, Jianping Wang, A Kate Sasser, Mary E Guckert, Howard Yeh, Tahamtan Ahmadi, Henk M. Lokhorst, Paul G. Richardson
Journal: Blood (2015)
Inhibition of mast cell‐secreted histamine decreases biliary proliferation and fibrosis in primary sclerosing cholangitis Mdr2−/− mice
Authors: Hannah Jones, Laura Hargrove, Lindsey Kennedy, Fanyin Meng, Allyson Graf‐Eaton, Jennifer Owens, Gianfranco Alpini, Christopher Johnson, Francesca Bernuzzi, Jennifer Demieville, Sharon DeMorrow, Pietro Invernizzi, Heather Francis
Journal: Hepatology (2016)

Hepatic fibrosis is marked by activation of hepatic stellate cells (HSCs). Cholestatic injury precedes liver fibrosis, and cholangiocytes interact with HSCs promoting fibrosis. Mast cells (MCs) infiltrate following liver injury and release histamine, increasing biliary proliferation. We evaluated if inhibition of MC-derived histamine decreases biliary proliferation and fibrosis. Wild-type and multidrug resistance 2 knockout mice (9-11 weeks) were treated with cromolyn sodium for 1 week to block MC-derived histamine. Biliary mass and proliferation were evaluated by immunohistochemistry for cytokeratin 19 and Ki-67. Bile flow, bicarbonate excretion, and total bile acids were measured in all mice. Fibrosis was evaluated by sirius red/fast green staining and by quantitative polymerase chain reaction for alpha-smooth muscle actin, fibronectin, collagen type 1a, and transforming growth factor-beta 1. HSC activation was evaluated by quantitative polymerase chain reaction in total liver and immunofluorescent staining in tissues for synaptophysin 9. Histamine serum secretion was measured by enzymatic immunoassay. Mouse liver and human liver samples from control or primary sclerosing cholangitis patients were evaluated for MC markers by quantitative polymerase chain reaction and immunohistochemistry. In vitro, cultured MCs were transfected with histidine decarboxylase short hairpin RNA to decrease histamine secretion and subsequently cocultured with cholangiocytes or HSCs prior to measuring fibrosis markers, proliferation, and transforming growth factor-beta 1 secretion. Treatment with cromolyn sodium decreased biliary proliferation, fibrosis, histamine secretion, and bile flow in multidrug resistance 2 knockout mice. Primary sclerosing cholangitis mice and patients have increased MCs. Knockdown of MC histidine decarboxylase decreased cholangiocyte and HSC proliferation/activation.MCs are recruited to proliferating cholangiocytes and promote fibrosis. Inhibition of MC-derived histamine decreases fibrosis, and regulation of MC mediators may be therapeutic for primary sclerosing cholangitis. (Hepatology 2016;64:1202-1216).
BMA Annual Representative Meeting, Manchester, 27 June to 30 June: BMA condemns competition and payment by results in NHS
Authors: Annabel Ferriman
Journal: BMJ (2005)

The competitive market in the NHS and the policy of “payment by results” were both condemned by representatives at the BMA's annual meeting in Manchester this week. George Rae, a BMA Council member, said that the government seemed to be “obsessed with the private sector.” Payment by results, whereby hospitals are paid for operations according to a set national tariff, could only work if all parties, both public and private, were treated equally, he said.

“There must be no preferential treatment for the private sector. We must not have a competitive market that works against the NHS.” Dr Rae asked the government not to dilute or fragment the health service and not to engage in superficially attractive policies with potentially damaging results.

Jacky Davis, a consultant radiologist in London and a member of the BMA's consultants committee, pointed out that this government had once described the internal market as a cancer, but now favoured having a rigged market, in which independent treatment centres were given a guaranteed income.

The meeting unanimously passed a motion that said that “more emphasis should be placed on collaboration as opposed to competition,” and that the new competitive market must not prejudice the NHS through any guaranteed flow of income to the private sector. But it threw out a proposal that the BMA should join with other unions to campaign for the restoration of public and planned provision of the NHS as the only way to maintain a universal equitable healthcare system.
Systematic Review of Tumor Necrosis Factor Antagonists in Extraintestinal Manifestations in Inflammatory Bowel Disease
Authors: Laurent Peyrin-Biroulet, Gert Van Assche, David Gómez-Ulloa, Laura García-Álvarez, Núria Lara, Chris M. Black, Sumesh Kachroo
Journal: Clinical Gastroenterology and Hepatology (2016)
The &lt;italic&gt;In Vitro&lt;/italic&gt; Initiation of Pulmonary Adenomas in Mouse Lung Tissue with Nitrogen Mustard. I. The Influences of Concentration of Agent, Duration of Exposure, and Mitotic State of the Tissue at the Time of Exposure&lt;xref ref-type="fn" rid="fn1"&gt;2&lt;/xref&gt;
Authors: Stanfield Rogers
Journal: JNCI Journal of the National Cancer Institute (1955)

The In Vitro Initiation of Pulmonary Adenomas in Mouse Lung Tissue with Nitrogen Mustard. I. The Influences of Concentration of Agent, Duration of Exposure, and Mitotic State of the Tissue at the Time of Exposure Get access Stanfield Rogers Stanfield Rogers Department of Pathology, Duke University School of Medicine, Durham, N. C. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 5, April 1955, Pages 1379–1390, https://doi.org/10.1093/jnci/15.5.1379 Published: 01 April 1955 Article history Received: 10 September 1954 Published: 01 April 1955
Afatinib (A) vs erlotinib (E) as second-line therapy of patients (pts) with advanced squamous cell carcinoma (SCC) of the lung following platinum-based chemotherapy: Overall survival (OS) analysis from the global phase III trial LUX-Lung 8 (LL8).
Authors: Jean-Charles Soria, Enriqueta Felip, Manuel Cobo, Shun Lu, Konstantinos N. Syrigos, Ki Hyeong Lee, Erdem Goker, Vassilis Georgoulias, Wei Li, Dolores Isla, Salih Zeki Guclu, Alessandro Morabito, Young Joo Min, Andrea Ardizzoni, Shirish M. Gadgeel, Bushi Wang, Vikram K. Chand, Glenwood D. Goss
Journal: Journal of Clinical Oncology (2015)

8002 Background: Treatment options for pts with advanced SCC of the lung progressing after platinum-based chemotherapy are limited. Overexpression of EGFR, ErbB receptors and the dysregulation of their downstream pathways are implicated in SCC pathobiology. Primary analysis of LL8 (2nd line A, an irreversible ErbB family blocker vs E, a reversible EGFR tyrosine kinase inhibitor [TKI; only TKI approved in this setting], in pts with SCC of the lung) showed significantly better progression-free survival (PFS) with A. OS and updated PFS are reported here. Methods: Pts with stage IIIB/IV disease were randomized 1:1 to receive A (40 mg/day) or E (150 mg/day) until disease progression. Primary endpoint: PFS; key secondary endpoint: OS. Other endpoints: objective response (ORR), disease control (DCR), patient reported outcomes and safety. 632 events and a sample size of 800 pts was needed to detect a HR of 0.8 with 80% power for OS. Results: OS was significantly better with A (n = 398) vs E (n = 397), with a 19% reduced risk of death (median 7.9 vs 6.8 mos; HR [95% CI] 0.81 [0.69–0.95]; p = 0.008). Significant differences in OS were seen at 6 (63.6 vs 54.6%; p = 0.010), 12 (36.4 vs 28.2%; p = 0.016) and 18 (22.0 vs 14.4%; p = 0.013) mos. PFS (median 2.6 vs 1.9 mos; HR [95% CI] 0.81 [0.69–0.96]; p = 0.010), ORR (5.5 vs 2.8%; p = 0.055) and DCR (50.5 vs 39.5%; p = 0.002) were all better for A vs E. More pts had improved global health status/quality of life (35.7 vs 28.3%; p = 0.041), cough (43.4 vs 35.2%; p = 0.029) and dyspnea (51.3 vs 44.1%; p = 0.061) with A vs E. Adverse event (AE) profiles were comparable (G ≥ 3 AEs: 57.1 and 57.5% for A vs E) with a higher incidence of drug-related G3/4 diarrhea (9.9/0.5 vs 2.3/0.3%), G3 stomatitis (4.1 vs 0%) with A and a higher incidence of G3 rash/acne with E (5.9 vs 10.4%). Preliminary data from FoundationOne analysis of tumor blocks will be shown. Conclusions: A significantly improved OS vs E in pts with SCC of the lung in a 2nd line setting. PFS and DCR were also significantly better. With a manageable AE profile, added QoL benefit, and symptom control seen in LL8, A should be preferred over E for these pts. Clinical trial information: NCT01523587.
EU governments commit to tackle antimicrobial resistance
Authors: Rory Watson
Journal: BMJ (2016)

Health ministers of European Union countries have given a strong political commitment to reducing the use of antibiotics in humans and animals. Meeting in Luxembourg on 17 June, they endorsed a call for all 28 countries to have national action plans against antimicrobial resistance in place by the middle of next year.

They agreed that national action plans should include measurable qualitative or quantitative goals to reduce infections and cut use of antimicrobials in humans and animals. They also agreed that there was a need to consider how legislation relevant to antimicrobial resistance …
Macrophages
Authors: R Swartz, C Holmes
Journal: New England Journal of Medicine (1995)

Figure 1. Scanning electron micrographs show macrophages on the surface of peritoneal-dialysis catheters after the devices had been removed because of infectious complications. Panel A shows a sessile macrophage (M) with pseudopodia (P) scavenging scattered clumps of coccal forms (C) (×3200). In Panel B another macrophage with pseudopodia is more actively “hugging” an unidentified object (×6400).
MicroRNA Profiling Reveals a Role for MicroRNA-218-5p in the Pathogenesis of Chronic Obstructive Pulmonary Disease
Authors: Griet Conickx, Pieter Mestdagh, Francisco Avila Cobos, Fien M. Verhamme, Tania Maes, Bart M. Vanaudenaerde, Leen J. M. Seys, Lies Lahousse, Richard Y. Kim, Alan C. Hsu, Peter A. Wark, Philip M. Hansbro, Guy F. Joos, Jo Vandesompele, Ken R. Bracke, Guy G. Brusselle
Journal: American Journal of Respiratory and Critical Care Medicine (2016)

Aberrant expression of microRNAs (miRNAs) can have a detrimental role in disease pathogenesis.To identify dysregulated miRNAs in lung tissue of patients with chronic obstructive pulmonary disease (COPD).We performed miRNA and mRNA profiling using high throughput stem-loop reverse-transcriptase quantitative polymerase chain reaction and mRNA microarray, respectively, on lung tissue of 30 patients (screening cohort) encompassing 8 never-smokers, 10 smokers without airflow limitation, and 12 smokers with COPD. Differential expression of miRNA-218-5p (miR-218-5p) was validated by reverse-transcriptase quantitative polymerase chain reaction in an independent cohort of 71 patients, an in vivo murine model of COPD, and primary human bronchial epithelial cells. Localization of miR-218-5p was assessed by in situ hybridization. In vitro and in vivo perturbation of miR-218-5p combined with RNA sequencing and gene set enrichment analysis was used to elucidate its functional role in COPD pathogenesis.Several miRNAs were differentially expressed among the different patient groups. Interestingly, miR-218-5p was significantly down-regulated in smokers without airflow limitation and in patients with COPD compared with never-smokers. Decreased pulmonary expression of miR-218-5p was validated in an independent validation cohort, in cigarette smoke-exposed mice, and in human bronchial epithelial cells. Importantly, expression of miR-218-5p strongly correlated with airway obstruction. Furthermore, cellular localization of miR-218-5p in human and murine lung revealed highest expression of miR-218-5p in the bronchial airway epithelium. Perturbation experiments with a miR-218-5p mimic or inhibitor demonstrated a protective role of miR-218-5p in cigarette smoke-induced inflammation and COPD.We highlight a role for miR-218-5p in the pathogenesis of COPD.
Développement d’un score pour mieux apprécier le niveau de risque des patients présentant des adénomes colo-rectaux
Authors: N. Musquer
Journal: Endoscopy (2016)

Chez les patients à risque élevé de cancer colo-rectal, l’intervalle entre deux coloscopies de surveillance est défini dans la plupart des pays, comme en France, à partir de caractéristiques endoscopiques et histologiques prises de façon indépendante comme la taille du polype, la présence d’une dysplasie de haut grade,… Plutôt que de les considérer indépendamment, cette équipe néerlandaise a cherché au contraire à combiner ces caractéristiques au sein d’un score de risque d’adénome avancé (dysplasie de haut grade, composante villeuse, taille ≥ 10 mm) à la coloscopie de surveillance. Dans un deuxième temps, cette stratégie de stratification des patients a été comparée à plusieurs stratégies actuellement en vigueur.