tbuckley/cabot-search huggingface dataset:
Utility of an electronic nose in discriminating obstructive sleep apnea and COPD by breath fingerprints analysis
Authors: Simone Scarlata, Giorgio Pennazza, Marco Santonico, Anna Zito, Livio Cortese, Davide Fontana, Mariangela Calabrese, Simona Santangelo, Domenica Chiurco, Claudio Pedone, Arnaldo D'Amico, Raffaele Antonelli Incalzi
Journal: European Respiratory Journal (2013)

Introduction: the diagnosis of two major respiratory causes of sleep disturbances, Obstructive Sleep Apnea Syndrome (OSAS) and Chronic Obstructive Pulmonary Disease (COPD),is technically demanding,cost-intensive and time consuming.The measurement of volatile organic compounds(VOCs) by an electronic nose device is an innovative method to determine distinct molecular patterns of exhaled breath in different patient groups,and its potential use in OSAS and COPD,distinctly,has recently been evaluated (1,2).We assessed whether breath fingerprints analysis can effectively distinguish OSAS from COPD.  Methods:we included 19 OSAS patients and 20 COPD(6 hypoxemic).Exhaled breath of all participants was analyzed using an e-Nose,based on an array of eight Quartz Micro Balance covered with biomaterial as non-selective sensing materials.Partial Discriminant Analysis was employed to test our hypothesis.  Results:we identified a discriminant function separating OSAS from COPD.The electronic nose percentage of correct classification was 93% (36/39).  Conclusions: the electronic nose is highly efficient in distinguish OSAS from COPD.This technology could be employed in large screenings to address,in a simply and not expensive way,patients with suspected respiratory disorders to the adequate test without delays and waste of resources.  References  Incalzi RA,Pennazza G,Scarlata S,et al.Reproducibility and respiratory function correlates of exhaled breath fingerprint in chronic obstructive pulmonary disease. PLoS One.2012;7:e45396.doi:10.1371  Greulich T,Hattesohl A,Grabisch A et al.Detection of obstructive sleep apnoea by an electronic nose. Eur Respir J 2012[Epub Ahead of print].PMID: 23100503.
Biomarkers to discriminate bacterial, viral and mixed community acquired pneumonia (CAP)
Authors: Elisa Mincholé, Ana Lasierra, Ana Lilian Simόn, Sergio Fandos, Maria Angeles Ruiz, Virginia Moya, Francisco De Pablo, Salvador Bello
Journal: European Respiratory Journal (2011)

To find out if C Reactive Protein (CRP), Procalcitonin (PCT) and Proadrenomedullin (Pro-ADM) are able to discriminate different CAP etiologies, we collected biological samples from 228 patients admitted in our hospital with CAP in the first 24 hours. Average age: 73 years, 61% males. We performed a complete microbiological searching, and found at least one pathogen in 155 (67.98%) patients. Fifty seven were typical bacterial CAP, 57 viral or atypical and 41 were mixed (virus + bacteria).   Results:   PCT was the only biomarker that showed significant differences (p  PCT and CRP levels in viral CAP showed significant differences (p  A PCT cut-off of 0.255 ng/mL identified typical bacterial involved CAP (bacterial and mixed) from viral/atypical ones, with a sensitivity of 74.23% and a specificity of 50%.   Conclusion:  CRP, and especially PCT, seem to be useful in early identification of typical bacteria-involved CAP, including those in association with viruses.
Superiority of second over first generation chemotherapy in a randomized trial for stage III-IV intermediate and high-grade Non-Hodgkin's Lymphoma (NHL): The 1980–1985 EORTC trial
Authors: P. Carde, J.H. Meerwaldt, M. van Glabbeke, R. Somers, M. Monconduit, J. Thomas, C. de Wolf-Peeters, B. de Pauw, A. Tanguy, J.C. Kluin-Nelemans, E.M. Noordijk, R. Regnier, D. Bron, J. Lustinan-Marechal, B. Caillou, J. Bosq, P. van Heerde, J.A.M. van Unnik, J.M.V. Burgers, M. Hayat, J.M. Cosset, E. van der Schueren, J. Wagener, A. Hagenbeek, A. Cattan, N. Duez, M. Tubiana
Journal: Annals of Oncology (1991)
Abstract 2453: Reversible Left Ventricular Dysfunction in the Presence of Frequent of Idiopathic Premature Ventricular Complexes - Is There a Critical PVC Burden?
Authors: Timir S Baman, David C Lange, Karl J Ilg, Sanjaya K Gupta, Eric Good, Aman Chugh, Krit Jongnarangsin, Frank Pelosi, Thomas Crawford, Hakan Oral, Fred Morady, Frank Bogun
Journal: Circulation (2009)
Differential dropout may affect exacerbation risk estimates differently in moderate-to-very severe COPD
Authors: Peter Calverley, Göran Eriksson, Dirkje Postma, Christine Jenkins, Antonio Anzueto, Barry Make, Anders Persson, Malin Fagerås, Thomas Similowski
Journal: European Respiratory Journal (2012)

BACKGROUND: Differential withdrawal of patients from clinical trials (dropout) complicates interpretation of the effect of intervention on the exacerbation frequency in COPD studies. We examined the impact of differential dropout on exacerbations in moderate-to-very severe COPD (GOLD grades 2–4).   METHODS: Patients in 3 pooled COPD studies 1,2,3  were randomised to budesonide/formoterol (B/F 320/9µg bid) or placebo (P) via Turbuhaler®. Exacerbations, dropouts and a composite of the two outcomes were examined over the first 3 months of treatment.   RESULTS: 1583 COPD patients were studied (24% moderate; 61% severe, 14% very severe). B/F improved time to first exacerbation in moderate and severe but not very severe COPD (HR B/F / P : 0.43 [95% CI 0.25–0.72], 0.45 [0.33–0.63] and 0.58 [0.32–1.05]) vs. P.  Time to dropout was improved by B/F vs. P, the differences being larger with increasing COPD severity (HR B/F / P : 0.62 [0.34–1.11], 0.56 [0.39–0.81] and 0.38 [0.18–0.80]). A composite measure of time to first exacerbation or dropout showed a significant effect of B/F in all severities.   CONCLUSIONS: Differential study dropout (greater with P than B/F) increased as the severity of COPD worsened. This should be considered when interpreting clinical COPD trial data.  1.Calverley et al. ERJ 2003;22:912–9  2.Szafranski et al. ERJ 2003;21:74–81  3.Welte et al. AJRCCM 2009;180:741–50.
Transfusion-associated TT virus co-infection in patients with hepatitis C virus is associated with type II mixed cryoglobulinemia but not with B-cell non-Hodgkin lymphoma
Authors: P. Cacoub, E. Rosenthal, V. Gerolami, P. Hausfater, P. Ghillani, Y. Sterkers, V. Thibault, H. Khiri, J.C. Piette, P. Halfon
Journal: Clinical Microbiology and Infection (2003)
Continuous Noninvasive Monitoring of pH and Temperature in Rat Walker 256 Carcinoma During Normoglycemia and Hyperglycemia23
Authors: Rakesh K. Jain, Sudhir A. Shah, Pamela L. Finney
Journal: JNCI Journal of the National Cancer Institute (1984)

The extracellular pH and temperature of Walker 256 carcinoma and of normal subcutaneous tissue were measured continuously in unanesthetized female Sprague-Dawley rats for up to 20 hours following glucose or galactose administration. The pH was monitored with flexible glass electrodes contained in micropore chambers implanted in the flank of a rat. Temperature was measured with miniature thermistor probes incorporated in the tumor or in subcutaneous tissue. The pH in the untreated Walker 256 carcinoma decreased linearly from approximately 7.3 to 6.2 with increasing tumor mass up to 50 g. Administration of glucose (6 g/kg body wt, ip) in tumor-bearing rats increased glucose concentrations in blood and tumor, as well as lactic acid concentration in tumor, and had no significant effect on lactic acid concentration in blood. Plasma volume was not affected by either glucose or galactose loading as compared to that in rats given saline alone. However, the blood viscosity increased by up to 30% within 30 minutes after galactose injection, but not after glucose injection, and this significant difference in viscosities persisted for approximately 6 hours after glucose and galactose injections. In small tumors (less than 10 g), a decrease of up to 1 pH unit was observed within 6 hours after glucose administration, and the return of pH to pretreatment values began about 10 hours after glucose injection. Response of large ulcerated tumors (greater than 20 g) was not as uniform; the pH decreased by about 0.5 to 1 pH unit for only a brief period. After galactose injection, pH in some tumors remained unchanged, whereas in others an average decrease of about 0.2 pH units was observed. The pH in normal tissue was not affected by glucose or galactose administration. Both glucose and galactose decreased tumor temperature by about 7 degrees C.
Regimen-related toxicity in patients undergoing bone marrow transplantation.
Authors: S I Bearman, F R Appelbaum, C D Buckner, F B Petersen, L D Fisher, R A Clift, E D Thomas
Journal: Journal of Clinical Oncology (1988)

Bone marrow transplantation is associated with significant morbidity and mortality, some of which is due to high-dose chemoradiotherapy. In order to quantitate toxicity that was felt to be due to the preparative regimen (termed regimen-related toxicity [RRT]), a system was developed in which toxicities were graded from 0 (none) to 4 (fatal). One hundred ninety-five patients who underwent marrow transplantation for leukemia were studied retrospectively to determine whether toxicities that were clinically felt to be due to the preparative regimen were influenced by other factors such as disease status, graft-versus-host disease (GVHD) prophylaxis, and allogenicity. All patients developed grade I toxicity in at least one organ, and 30 developed grades III-IV (life-threatening or fatal) RRT. RRT was more common in relapsed patients v remission patients (P = .04), in those receiving 15.75 Gy total body irradiation (TBI) v 12.0 Gy TBI (P = .028), and in those receiving allogeneic marrow v autologous marrow (P = .0029). Autologous marrow recipients did not develop grades III-IV toxicity in this study. A multivariate analysis controlling for autologous marrow grafting showed that the dose of TBI was the only statistically significant predictor of grades III-IV RRT. Those patients who developed grade III RRT were unlikely to survive 100 days from transplant, though not all deaths could be attributed to RRT. Patients who developed grade II toxicity in three or more organs were more likely to die within 100 days than those developing grade II toxicity in two or less organs (P = .0027). This system was generally able to distinguish RRT from other toxicities observed in marrow recipients.
A controlled trial of the effect of 4-hydroxypyrazolopyrimidine (allopurinol) on the toxicity of a single bolus dose of 5-fluorouracil.
Authors: P V Woolley, M J Ayoob, F P Smith, J L Lokey, P DeGreen, A Marantz, P S Schein
Journal: Journal of Clinical Oncology (1985)

We have evaluated, in a controlled study, the modification of the toxicity of a single bolus dose of 5-fluorouracil (5-FU) by allopurinol. Patients first received a single dose of 5-FU and were monitored for toxicity. If a measurable nadir in WBC or platelet count occurred, then the same dose of 5-FU was repeated with concurrent allopurinol, given for four consecutive days at an initial dose of 300 mg twice daily, starting the day before the administration of 5-FU. With this schedule, each evaluable patient received courses of 5-FU with and without allopurinol that could be compared for toxicity. Twenty patients received initial 5-FU doses of either 1,200 mg/m2 or 1,500 mg/m2 and later had the same dose repeated with allopurinol. Nineteen of these patients had a higher WBC count with allopurinol than without it. In several patients who received a further course of 5-FU with 900-mg/d allopurinol, the WBC count was yet higher than with 600-mg/d allopurinol. The myelosuppression produced by 5-FU was characterized by a decrease in granulocyte levels that was much greater than the decrease in lymphocyte levels, and the result of allopurinol treatment was to attenuate this effort on granulocytes. In a second part of the trial, the goal was to establish the maximum tolerated dose of 5-FU given with concurrent allopurinol. In this part of the study, all patients entered were given 5-FU, usually 1,200 mg/m2, with allopurinol, usually 600 mg/d for four days. Escalations of one or the other drugs were made on subsequent treatments. The data for 22 patients showed that 1,800 mg/m2 of 5-FU was well tolerated if given with 600 to 1,200 mg of allopurinol per day, and that the WBC count nadirs were no more severe than those of 1,200-mg/m2 5-FU without allopurinol. Neurotoxicity became limiting in some patients treated at these higher doses. We conclude that allopurinol given in the proper dose and schedule can diminish the granulocytopenia produced by bolus doses of 5-FU, thereby allowing a 50% increase in the maximal tolerated dose of 5-FU.
Cell-Surface Antigens From Human Breast Tumor Cells 2
Authors: Michael P. Lerner, J Hill Anglin, Robert E. Nordquist
Journal: JNCI Journal of the National Cancer Institute (1978)

Journal Article Cell-Surface Antigens From Human Breast Tumor Cells Get access Michael P. Lerner, Michael P. Lerner 3Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Okla. 73190. Search for other works by this author on: Oxford Academic PubMed Google Scholar J Hill Anglin, J Hill Anglin 4Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center. Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert E. Nordquist Robert E. Nordquist 5Cancer Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Okla. 73104. 6Present address: Department of Anatomical Sciences, University of Oklahoma Health Sciences Center. 7We thank Richard Strecker, Peggy Riggs, Peggy Munson, and Lucy Durbin for excellent technical assistance. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 60, Issue 1, January 1978, Pages 39–44, https://doi.org/10.1093/jnci/60.1.39 Published: 01 January 1978 Article history Received: 15 March 1977 Accepted: 01 August 1977 Published: 01 January 1978
Spartan - a Randomized Double-Blind, Comparative Study of Arn-509 Plus Androgen Deprivation Therapy (Adt) Vs Adt Alone in Non-Metastatic Castration-Resistant Prostate Cancer (M0-Crpc)
Authors: B. Tombal, J. Jassem, S.M. Shreeve, G.C. Trudel, A. Sosa, T. Kheoh, M. Yu, M.R. Smith, E.J. Small, S. Oudard
Journal: Annals of Oncology (2014)
Abstract 8229: Layer Specific Strain-Encoded Magnetic Resonance Imaging for Evaluation of Left Ventricular Function and Infarct Transmurality in Patients With Chronic Coronary Artery Disease
Authors: Ralf Koos, Ertunc Altiok, Jochen Doetsch, Nikolaus Marx, Rainer Hoffmann
Journal: Circulation (2011)

Background: Strain-encoded imaging (SENC) is a new technique for myocardial deformation analysis in cardiac magnetic resonance imaging (MRI). The study aimed to evaluate whether myocardial deformation imaging performed by SENC allows quantification of regional left ventricular (LV) function and is related to scar transmurality defined by contrast-enhanced MRI (ceMRI). Methods: 50 patients (age 62 ± 10 years) with chronic ischemic LV dysfunction underwent ceMRI using a clinical 1.5T scanner (Achieva, Philips, Best, The Netherlands). Strain-encoded images were acquired using a commercially available software to calculate myocardial endocardial and epicardial strain (Diagnosoft SENC version 2.05, Diagnosoft Inc., Palo Alto, USA). Layer-specific peak circumferential strain was measured from long-axis views and peak longitudinal strain was evaluated from short-axis views in a 16-segment model. The extent of myocardial infarction was determined semiautomatically (CAAS MRV 3.3, Pie Medical, Netherlands) for each segment as relative amount of hyperenhancement by ceMRI (0%: no infarction; 1-50%: non-transmural infarction; 51-100%: transmural infarction). Results: A total of 589 of 600 segments (98%) were analyzed. Endocardial and epicardial circumferential as well as longitudinal strain showed significant differences between visually defined segmental function states and differed also significantly between the degree of infarct transmurality (all p&lt;0.001). A cutoff peak circumferential endocardial strain value of -15% differentiated nontransmural from transmural infarcted myocardium with a sensitivity of 100% and a specificity of 86% (area under the curve (AUC) 0.94). Distinction of nontransmural infarcted myocardium from transmural infarcted myocardium was done more accurately using circumferential endocardial strain compared to longitudinal endocardial strain (AUC 0.94 vs. AUC 0.76, p=0.003). Conclusions: Layer-specific SENC provides objective quantification of regional myocardial function and allows accurate discrimination between different transmurality states of myocardial infarction. Circumferential endocardial strain showed the best distinction between the different degrees of infarct transmurality.
Protective role for club cell secretory protein-16 (CC16) in the development of COPD
Authors: Maria E. Laucho-Contreras, Francesca Polverino, Kushagra Gupta, Katherine L. Taylor, Emer Kelly, Victor Pinto-Plata, Miguel Divo, Naveed Ashfaq, Hans Petersen, Barry Stripp, Aprile L. Pilon, Yohannes Tesfaigzi, Bartolome R. Celli, Caroline A. Owen
Journal: European Respiratory Journal (2015)

Club cell secretory protein-16 (CC16) is the major secreted product of airway club cells, but its role in the pathogenesis of chronic obstructive pulmonary disease (COPD) is unclear. We measured CC16 airway expression in humans with and without COPD and CC16 function in a cigarette smoke (CS)-induced COPD murine model. Airway CC16 expression was measured in COPD patients, smokers without COPD and non-smokers. We exposed wildtype (WT) and CC16(-/-)mice to CS or air for up to 6 months, and measured airway CC16 expression, pulmonary inflammation, alveolar septal cell apoptosis, airspace enlargement, airway mucin 5AC (MUC5AC) expression, small airway remodelling and pulmonary function. Smokers and COPD patients had reduced airway CC16 immunostaining that decreased with increasing COPD severity. Exposing mice to CS reduced airway CC16 expression. CC16(-/-) mice had greater CS-induced emphysema, airway remodelling, pulmonary inflammation, alveolar cell apoptosis, airway MUC5AC expression, and more compliant lungs than WT mice. These changes were associated with increased nuclear factor-κB (NF-κB) activation in CC16(-/-) lungs. CS-induced acute pulmonary changes were reversed by adenoviral-mediated over-expression of CC16. CC16 protects lungs from CS-induced injury by reducing lung NF-κB activation. CS-induced airway CC16 deficiency increases CS-induced pulmonary inflammation and injury and likely contributes to the pathogenesis of COPD.
A phase I study of trastuzumab-MCC-DM1 (T-DM1), a first-in-class HER2 antibody-drug conjugate (ADC), in patients (pts) with HER2+ metastatic breast cancer (BC)
Authors: M. Beeram, I. Krop, S. Modi, A. Tolcher, N. Rabbee, S. Girish, J. Tibbitts, S. Holden, S. Lutzker, H. Burris
Journal: Journal of Clinical Oncology (2007)

1042 Background: ADCs utilize tumor-specific and/or over-expressed surface antigens that undergo internalization to deliver highly potent anti-tumor agents via linkage to antigen-specific monoclonal antibodies (MoAbs). T-DM1 contains the humanized anti-HER2 MoAb trastuzumab (T) previously demonstrated to prolong survival in HER2+ BC to which a highly potent antimicrotubule drug (DM1) derived from maytansine has been chemically linked. Maytansine has been studied as a free drug with responses noted in breast and lung cancer pts; principal adverse events (AEs) were nausea, vomiting, diarrhea, and neuropathy. The MCC linker employed in T-DM1 provides a stable bond between T and DM1 that is designed to prolong exposure and reduce the toxicity of T-DM1 while maintaining activity; T-DM1 is the first ADC with an MCC linker in clinical trials. T-DM1 has activity in T-resistant HER2+ BC xenografts; its principal preclinical toxicities were reversible transaminase elevations, reversible decreases in platelets, and neuropathy. Methods: This ongoing first-in-human phase I study is evaluating the safety and pharmacokinetics (PK) of T-DM1 given IV q3 weeks to pts with HER2+ metastatic BC who have progressed on a T-containing regimen. Results: Seven pts (median age 58 (range 47–70); all PS 0–1; median number prior chemo regimens 6 (range 5–11)) have received 24 doses of T-DM1 at 5 dose levels (0.3–4.8 mg/kg). Related grade (gr) 1–2 AEs include elevations in hepatic transaminases (2 pts), fatigue (2 pts), anemia (1 pt), and thrombocytopenia (TCP, 1 pt). Related gr 3–4 AEs have been limited to rapidly reversible gr 4 TCP at 4.8 mg/kg (1 pt). There has been no cardiac toxicity. Consistent with preclinical modeling, dose dependent decrease in clearance was observed for T-DM1 across dose levels. One pt at 2.4 mg/kg has maintained an ongoing partial response for 6 cycles. Conclusions: At these initial doses, gr =2 AEs related to T-DM1 have been infrequent and manageable; gr 4 (dose-limiting) rapidly reversible TCP was seen at 4.8 mg/kg. T-DM1 PK is consistent with q3-week dosing. Objective tumor response has been observed. Enrollment is ongoing to determine the maximum tolerated dose of q3-week T-DM1. No significant financial relationships to disclose.
Selective Estrogen Receptor Modulators: Structure, Function, and Clinical Use
Authors: C. Kent Osborne, Hong (Holly) Zhao, Suzanne A. W. Fuqua
Journal: Journal of Clinical Oncology (2000)

ABSTRACT: The sex hormone estrogen is important for many physiologic processes. Prolonged stimulation of breast ductal epithelium by estrogen, however, can contribute to the development and progression of breast cancer, and treatments designed to block estrogen’s effects are important options in the clinic. Tamoxifen and other similar drugs are effective in breast cancer prevention and treatment by inhibiting the proliferative effects of estrogen that are mediated through the estrogen receptor (ER). However, these drugs also have many estrogenic effects depending on the tissue and gene, and they are more appropriately called selective estrogen receptor modulators (SERMs). SERMs bind ER, alter receptor conformation, and facilitate binding of coregulatory proteins that activate or repress transcriptional activation of estrogen target genes. Theoretically, SERMs could be synthesized that would exhibit nearly complete agonist activity on the one hand or pure antiestrogenic activity on the other. Depending on their functional activities, SERMs could then be developed for a variety of clinical uses, including prevention and treatment of osteoporosis, treatment and prevention of estrogen-regulated malignancies, and even for hormone replacement therapy. Tamoxifen is effective in patients with ER-positive metastatic breast cancer and in the adjuvant setting. The promising role for tamoxifen in ductal carcinoma-in-situ or for breast cancer prevention is evolving, and its use can be considered in certain patient groups. Other SERMs are in development, with the goal of reducing toxicity and/or improving efficacy, and future agents have the potential of providing a new paradigm for maintaining the health of women.
Variations in Carcinoembryonic Antigen Localization in Tumors of the Colon
Authors: V. Y. Rogalsky
Journal: JNCI Journal of the National Cancer Institute (1975)

The localization of carcinoembryonic antigen (CEA) in 78 tumors of the human colon was studied with the use of antibody to CEA in an indirect Coons test. The neoplasms differed morphologically and could be divided into two types: a) tissues in which CEA was localized in cells, and b) tissues in which malignant cells secreted CEA in greater or lesser quantity. In the first type of tissue, five forms of cells were observed: goblet-like, small vacuolar, limbic, those with intracellular accumulation of antigen, and diffuse. Tumor tissue secreting CEA could also be divided into five forms: holocrine-like, aprocrinelike, intraglandular, apical-basal, and lacunar-infiltrative. The change in CEA localization in pathologically altered cells was designated “antigenic translocation”.