tbuckley/cabot-search huggingface dataset:
Comparison of the incidence, nature and cause of injuries sustained on grass and new generation artificial turf by male and female football players. Part 1: match injuries
Authors: Colin W Fuller, Randall W Dick, Jill Corlette, Rosemary Schmalz
Journal: British Journal of Sports Medicine (2007)

Objective: To compare the incidence, nature, severity and cause of match injuries sustained on grass and new generation artificial turf by male and female footballers. Methods: The National Collegiate Athletic Association Injury Surveillance System was used for a two-season (August to December) prospective study of American college and university football teams (2005 season: men 52 teams, women 64 teams; 2006 season: men 54 teams, women 72 teams). Injury definitions and recording procedures were compliant with the international consensus statement for epidemiological studies of injuries in football. Athletic trainers recorded details of the playing surface and the location, diagnosis, severity and cause of all match injuries. The number of days lost from training and match play was used to define the severity of an injury. Match exposures (player hours) were recorded on a team basis. Results: The overall incidence of match injuries for men was 25.43 injuries/1000 player hours on artificial turf and 23.92 on grass (incidence ratio 1.06; p = 0.46) and for women was 19.15 injuries/1000 player hours on artificial turf and 21.79 on grass (incidence ratio = 0.88; p = 0.16). For men, the mean severity of non-season ending injuries was 7.1 days (median 5) on artificial turf and 8.4 days (median 5) on grass and, for women, 11.2 days (median 5) on artificial turf and 8.9 days (median 5) on grass. Joint (non-bone)/ligament/cartilage and contusion injuries to the lower limbs were the most common general categories of match injury on artificial turf and grass for both male and female players. Most injuries were acute (men: artificial turf 24.60, grass 22.91; p = 0.40; women: artificial turf 18.29, grass 20.64; p = 0.21) and resulted from player-to-player contact (men: artificial turf 14.73, grass 13.34; p = 0.37; women: artificial turf 10.72; grass 11.68; p = 0.50). Conclusions: There were no major differences in the incidence, severity, nature or cause of match injuries sustained on new generation artificial turf and grass by either male or female players.
Trastuzumab induces antibody-dependent cell-mediated cytotoxicity (ADCC) in HER-2-non-amplified breast cancer cell lines
Authors: D.M. Collins, N. O'Donovan, P.M. McGowan, F. O'Sullivan, M.J. Duffy, J. Crown
Journal: Annals of Oncology (2011)

Antibody-dependent cell-mediated cytotoxicity (ADCC) mediated by CD56+natural killer (NK) cells may contribute to the activity of trastuzumab in HER-2-amplified tumours. In this study, we investigated the possibility that trastuzumab might induce ADCC against HER-2-non-amplified breast cancer cells.Induction of NK cell-mediated ADCC was examined in trastuzumab-treated HER-2-non-amplified breast cancer cell lines. HER-2 protein levels were also determined in tumour and autologous normal tissue samples from patients with HER-2 negative breast cancer.Trastuzumab induced a significant ADCC response in the HER-2-amplified HCC1954 and SKBR3 cell lines, and in all five of the non-amplified cell lines, which had low levels of detectable HER-2 by western blot (CAL-51, CAMA-1, MCF-7, T47D, and EFM19). Trastuzumab did not induce ADCC in the K562 control cell line or MDA-MB-468, which has very low levels of HER-2 detectable by enzyme-linked immunosorbent assay (ELISA) only. HER-2 protein was detected by ELISA in 14/15 patient tumour samples classified as HER-2-non-amplified. Significantly lower levels of HER-2 were detected in normal autologous tissue compared with tumour samples from the same patients.Our results suggest that HER-2-non-amplified breast cancer cells, with low but detectable levels of HER-2 protein, can bind trastuzumab and initiate ADCC.
Matuzumab plus epirubicin, cisplatin and capecitabine (ECX) compared with epirubicin, cisplatin and capecitabine alone as first-line treatment in patients with advanced oesophago-gastric cancer: a randomised, multicentre open-label phase II study
Authors: S. Rao, N. Starling, D. Cunningham, K. Sumpter, D. Gilligan, T. Ruhstaller, M. Valladares-Ayerbes, H. Wilke, C. Archer, R. Kurek, C. Beadman, J. Oates
Journal: Annals of Oncology (2010)
Immunonutrition enhances the expression and secretion of mouse intestinal defensins
Authors: O Froy
Journal: Gut (2006)

The nutrient rich lumen of the small intestine provides a favourable environment for microbial cell growth. Secretion of defensins from Paneth cells constitutes a key source of antimicrobial peptide activity in the crypt lumen.1 In addition, defensins also recruit the adaptive immune system.2,3 Chronic disease, major surgery, trauma, or malnutrition results in immune compromise and can increase the risk of infection and sepsis.4 Several clinical studies have demonstrated that patients fed an immune enhancing formula had significantly fewer infectious complications, needed less antibiotics, and had a shorter hospital stay than patients fed standard diets.5 However, the mechanism by which these formulas bolster the immune system is unclear.

We hypothesised that a nutrient enriched diet bolsters the immune system by upregulating defensin expression in the jejunum and ileum, the two parts where cryptdins (mouse intestinal defensins) are highly expressed. To study the effect of an immune enhancing diet (Perative; Ross Products, Abbott Laboratories, USA) on intestinal defensin expression, …
A 3′-untranslated region KRAS variant and triple-negative breast cancer: a case-control and genetic analysis
Authors: Trupti Paranjape, Helen Heneghan, Robert Lindner, Florence K Keane, Aaron Hoffman, Antoinette Hollestelle, Jemima Dorairaj, Kimberly Geyda, Cory Pelletier, Sunitha Nallur, John WM Martens, Maartje J Hooning, Michael Kerin, Daniel Zelterman, Yong Zhu, David Tuck, Lyndsay Harris, Nicola Miller, Frank Slack, Joanne Weidhaas
Journal: The Lancet Oncology (2011)
Clonal dominance. I. Restricted nature of the IgM antibody response to group A streptococcal carbohydrate in mice.
Authors: D E Briles, J M Davie
Journal: The Journal of Experimental Medicine (1975)

The IgM antibody response of mice to the streptococcal group A carbohydrate (GAC) was measured. With most strains tested, large amounts of IgM antibody were produced; in AKR mice, over 1% of the total nucleated spleen cells secreted IgM anti-GAC antibody after hyperimmunization. The relative avidity of the antibody was extimated by a modification of the Jerne plaque assay where spleen cells from individual mice were tested against erythrocytes with varying GAC epitope densitymthese studies showed that the earliest, as well as latest, IgM antibodies produced were highly restricted in avidity heterogeneity. No evidence of affinity maturation was seen upon hyperimmunization. These data favor the conclusion that the restricted IgG response seen in mice hyperimmunized to GAC is not the result of affinity driven competition for antigen among precursor cells.
How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions*
Authors: Robert M. Sapolsky, L. Michael Romero, Allan U. Munck
Journal: Endocrine Reviews (2000)

The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole.
Syndecan-4 signalling inhibits apoptosis and controls NFAT activity during myocardial damage and remodelling
Authors: Frank Echtermeyer, Thomas Harendza, Svenja Hubrich, Anika Lorenz, Christine Herzog, Martin Mueller, Martina Schmitz, Andrea Grund, Jan Larmann, Jörg Stypmann, Bernhard Schieffer, Ralf Lichtinghagen, Denise Hilfiker-Kleiner, Kai C. Wollert, Jörg Heineke, Gregor Theilmeier
Journal: Cardiovascular Research (2011)

Myocardial infarction (MI) results in acute impairment of left ventricular (LV) function through the initial development of cardiomyocyte death and subsequent progression of LV remodelling. The expression of syndecan-4 (Sdc4), a transmembrane proteoglycan, is up-regulated after MI, but its function in the heart remains unknown. Here, we characterize the effects of Sdc4 deficiency in murine myocardial ischaemia and permanent infarction. Targeted deletion of Sdc4 (Sdc4–/–) leads to increased myocardial damage after ischaemic–reperfusion injury due to enhanced cardiomyocyte apoptosis associated with reduced activation of extracellular signal-regulated kinase in cardiomyocytes in vitro and in vivo. After ischaemic–reperfusion injury and permanent infarction, we observed an increase in cardiomyocyte area, nuclear translocation of nuclear factor of activated T cells (NFAT), and transcription of the NFAT target rcan1.4 in wild-type mice. NFAT pathway activation was enhanced in Sdc4–/– mice. In line with the in vivo data, NFAT activation and hypertrophy occurs in isolated cardiomyocytes with reduced Sdc4 expression during phenylephrine stimulation in vitro. Despite the initially increased myocardial damage, echocardiography revealed improved LV geometry and function in Sdc4–/– mice 7 days after MI. Interception of the Sdc4 pathway enhances infarct expansion and hypertrophic remodelling during early infarct healing in ischaemic–reperfusion injury and permanent infarction mouse models and exerts net beneficial effects on LV function.
LUX-Lung 4: A Phase II Trial of Afatinib in Patients With Advanced Non–Small-Cell Lung Cancer Who Progressed During Prior Treatment With Erlotinib, Gefitinib, or Both
Authors: Nobuyuki Katakami, Shinji Atagi, Koichi Goto, Toyoaki Hida, Takeshi Horai, Akira Inoue, Yukito Ichinose, Kunihiko Koboyashi, Koji Takeda, Katsuyuki Kiura, Kazuto Nishio, Yoko Seki, Ryuichi Ebisawa, Mehdi Shahidi, Nobuyuki Yamamoto
Journal: Journal of Clinical Oncology (2013)

New molecular targeted agents are needed for patients with non-small-cell lung cancer (NSCLC) who progress while receiving erlotinib, gefitinib, or both. Afatinib, an oral irreversible ErbB family blocker, has preclinical activity in epidermal growth factor receptor (EGFR [ErbB1]) mutant models with EGFR-activating mutations, including T790M.This was a Japanese single-arm phase II trial conducted in patients with stage IIIB to IV pulmonary adenocarcinoma who progressed after ≥ 12 weeks of prior erlotinib and/or gefitinib. Patients received afatinib 50 mg per day. The primary end point was objective response rate (complete response or partial response) by independent review. Secondary end points included progression-free survival (PFS), overall survival (OS), and safety.Of 62 treated patients, 45 (72.6%) were EGFR mutation positive in their primary tumor according to local and/or central laboratory analyses. Fifty-one patients (82.3%) fulfilled the criteria of acquired resistance to erlotinib and/or gefitinib. Of 61 evaluable patients, five (8.2%; 95% CI, 2.7% to 18.1%) had a confirmed objective response rate (partial response). Median PFS was 4.4 months (95% CI, 2.8 to 4.6 months), and median OS was 19.0 months (95% CI, 14.9 months to not achieved). Two patients had acquired T790M mutations: L858R + T790M, and deletion in exon 19 + T790M; they had stable disease for 9 months and 1 month, respectively. The most common afatinib-related adverse events (AEs) were diarrhea (100%) and rash/acne (91.9%). Treatment-related AEs leading to afatinib discontinuation were experienced by 18 patients (29%), of whom four also had progressive disease.Afatinib demonstrated modest but noteworthy efficacy in patients with NSCLC who had received third- or fourth-line treatment and who progressed while receiving erlotinib and/or gefitinib, including those with acquired resistance to erlotinib, gefitinib, or both.
Novel, Bedside, Tissue Factor–Dependent Clotting Assay Permits Improved Assessment of Combination Antithrombotic and Antiplatelet Therapy
Authors: Michael B. Holmes, David J. Schneider, Michael G. Hayes, Burton E. Sobel, Kenneth G. Mann
Journal: Circulation (2000)

Background —Because optimal use of combinations of antiplatelet and antithrombotic drugs requires improved methods for assessment of therapeutic efficacy, we developed an assay designed to increase sensitivity that is based on initiation of clotting by tissue factor in minimally altered whole blood. Methods and Results —Blood samples were obtained from healthy subjects, and the contact pathway of coagulation was inhibited with corn trypsin inhibitor (a specific factor XIIa inhibitor without effect on other coagulation factors). Clotting was initiated with relipidated tissue factor and detected with a Hemochron ACT instrument. Results were reproducible with samples from 25 healthy volunteers (mean time to clot, 125±17 seconds). Blood was also exposed to pharmacological concentrations of antithrombotic and antiplatelet agents in vitro. Heparin (0.25 anti-IIa/Xa U/mL) prolonged the time to clot by 2.4-fold (172 seconds, P &lt;0.05); hirudin (1.0 anti-IIa U/mL), by 3-fold (250 seconds P &lt;0.05); and enoxaparin (0.6 anti-Xa U/mL), by 2 -fold (123 seconds, P &lt;0.05). Additive effects of antiplatelet agents were readily detectable with both heparin and hirudin. Thus, addition of 3 μg/mL abciximab to 1.0 anti-IIa/Xa U/mL heparin and to 1.0 anti-IIa U/mL hirudin further prolonged the times to clot by 140 and 67 seconds, respectively ( P &lt;0.05 for each). Addition of abciximab to enoxaparin did not further prolong the time to clot (increment, 13 seconds; P =NS). Conclusions —The assay developed should facilitate improved dose selection, titration, and monitoring of combination antithrombotic and antiplatelet treatment regimens.
Never-Smokers With Lung Cancer: Epidemiologic Evidence of a Distinct Disease Entity
Authors: Chee-Keong Toh, Fei Gao, Wan-Teck Lim, Swan-Swan Leong, Kam-Weng Fong, Swee-Peng Yap, Anne A.L. Hsu, Philip Eng, Heng-Nung Koong, Agasthian Thirugnanam, Eng-Huat Tan
Journal: Journal of Clinical Oncology (2006)

Tobacco smoke is a definite causative agent for lung cancer. It is increasingly being recognized that never-smokers can be afflicted with non-small-cell lung cancer (NSCLC). We aim to assess survival differences between smokers and never-smokers with NSCLC.We analyzed 975 NSCLC patients who presented from January 1999 to December 2002. Clinical characteristics among current-, former- and never-smokers were tested using chi2 or Kruskal-Wallis test. The hazard ratio (HR) for death and its 95% CI were calculated by Cox regression.Of 975 patients, 59 had no smoking history and 33 had no quit time recorded. Of 883 patients analyzed, 286 patients (32.4%) were never-smokers. One hundred ninety-six never-smokers (68.5%) were females compared with 12% among current- and 13% among former-smokers (P < .001). There was a significant difference in histologic subtype between never-smokers and smokers: 69.9% with adenocarcinoma versus 39.9% (current-smokers) versus 47.3% (former-smokers); 5.9% with squamous cell carcinoma versus 35.7% (current-smokers) versus 28% (former-smokers; P < .001). Smokers had significantly poorer performance status (P = .002) and higher median age at diagnosis (P < .001) while more never-smokers presented with advanced disease (P = .002). Eight hundred and five patients (82.6%) died by May 30, 2005. The HR for smokers was significantly higher on both univariate and multivariate analysis (HR, 1.297; 95% CI, 1.040 to 1.619).Never-smokers comprised a high proportion of NSCLC patients in Singapore. Definite epidemiologic differences exist between never-smokers and smokers. Differences in survival outcome further suggest that the biology underlying the pathogenesis and behavior of the disease may be different for never-smokers.
Untangling Practice Redesign from Disease Management: How Do We Best Care for the Chronically Ill?
Authors: Katie Coleman, Soeren Mattke, Patrick J. Perrault, Edward H. Wagner
Journal: Annual Review of Public Health (2008)

In the past 10 years, a wide spectrum of chronic care improvement interventions has been tried and evaluated to improve health outcomes and reduce costs for chronically ill individuals. On one end of the spectrum are disease-management interventions--often organized by commercial vendors--that work with patients but do little to engage medical practice. On the other end are quality-improvement efforts aimed at redesigning the organization and delivery of primary care and better supporting patient self-management. This qualitative review finds that carve-out disease management interventions that target only patients may be less effective than those that also work to redesign care delivery. Imprecise nomenclature and poor study design methodology limit quantitative analysis. More innovation and research are needed to understand how disease-management components can be more meaningfully embedded within practice to improve patient care.
Galectin-9 as a Prognostic Factor with Antimetastatic Potential in Breast Cancer
Authors: Akemi Irie, Akira Yamauchi, Keiichi Kontani, Minoru Kihara, Dage Liu, Yukako Shirato, Masako Seki, Nozomu Nishi, Takanori Nakamura, Hiroyasu Yokomise, Mitsuomi Hirashima
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Galectin-9, a member of the β-galactoside–binding galectin family, induces aggregation of certain cell types. We assessed the contribution of galectin-9 to the aggregation of breast cancer cells as well as the relation between galectin-9 expression in tumor tissue and distant metastasis in patients with breast cancer. Experimental Design: Subclones of MCF-7 breast cancer cells with high or low levels of galectin-9 expression were established and either cultured on plastic dishes or transplanted into nude mice. The tumors of 84 patients with breast cancer were tested for galectin-9 expression by immunohistochemistry. The patients were followed up for 14 years. Results: MCF-7 subclones with a high level of galectin-9 expression formed tight clusters during proliferation in vitro, whereas a subclone (K10) with the lowest level of galectin-9 expression did not. However, K10 cells stably transfected with a galectin-9 expression vector aggregated in culture and in nude mice. Ectopic expression of galectin-9 also reduced MCF-7 cell adhesion to extracellular matrix proteins. Tumors of 42 of the 84 patients were galectin-9 positive, and those of 19 of the 21 patients with distant metastasis were galectin-9 negative. None of the 13 patients with galectin-9–positive tumors and lymph node metastasis up to level II manifested distant metastasis. The cumulative disease-free survival ratio for galectin-9–positive patients was more favorable than that for the galectin-9–negative group (P &amp;lt; 0.0001). Multivariate analysis revealed that galectin-9 status influenced distant metastasis independently of and to a greater extent than lymph node metastasis. Conclusions: Galectin-9 is a possible prognostic factor with antimetastatic potential in breast cancer.
Inhibition of Na-Ca exchange by general anesthetics.
Authors: R A Haworth, A B Goknur, H A Berkoff
Journal: Circulation Research (1989)

General anesthetics, typically octanol, were found to inhibit the influx of calcium in isolated sodium-loaded adult rat heart cells, using 45Ca, quin 2, or indo 1. Inhibition by octanol, like inhibition by sodium, was competitive with calcium. Octanol and sodium together inhibited calcium influx synergistically. At physiological levels of extracellular calcium and sodium, the EC50 was 177 +/- 37 microM for octanol and 48 +/- 5 microM for decanol. These values are threefold to fourfold larger than those reported to cause 50% loss of righting reflex in tadpoles, a measure of their anesthetic effectiveness. We conclude that general anesthetics inhibit Na-Ca exchange at the sarcolemma. We suggest that octanol inhibits like sodium, and the synergism stems from the cooperativity of sodium inhibition at the binding and regulatory sites of the exchanger. Insofar as Na-Ca exchange may regulate inotropy, the inhibition of Na-Ca exchange by general anesthetics could contribute to their negative inotropic effect.
42. HUMORAL CHANGES IN THE TREATMENT OF SCHIZOPHRENIA WITH PROLONGED NARCOSIS
Authors: A. E. Kulkow, W. J. Weiland, B. E. Kakusina
Journal: American Journal of Psychiatry (1938)

In our study of the humoral changes in our patients with prolonged narcosis (Cloetta's Mixture) we may provisionally point out the following results: 1. The morphological blood changes show most strikingly in the number of leukocytes and in the shift to the left in the leukocytic equilibrium, with esinopenia and neutrophilia. 2. The sedimentation reaction of erythrocytes showed a rise in all the cases but not always of the same degree. 3. The changes in the protein content and protein metabolism present themselves as follows: in most of the cases there was a decrease in the total protein, in the albumin content and the protein coefficient with a synchronous increase in the globulin fraction, the amino nitrogen and the polypeptides. These changes we ascribe primarily to the toxic effects of Cloetta's Mixture. 4. We did not succeed in establishing any correlation whatever between the effectiveness of the treatment and the changes in the proteins and protein metabolism; one can only point out that the changes in the protein content and protein metabolism were quite marked both in the cases where there was a therapeutic effect and in those where there was none. 5. The sugar values varied during the narcosis within the limits of normal, but in individual cases there were sporadically hyperglycemia and hypoglycemia. Upon the awakening the sugar values showed a definite rise, especially in the cases where the awakening was ushered in with confusion and excitement. 6. In most cases the potassium values fell during the first days of the narcosis but did not pass the lower limits of normal. The calcium showed a certain tendency to rise, but not an equal rise in all cases, nor on the same days of the narcosis. 7. The bromide content fell in most of the cases during the narcosis: near the end of the narcosis and especially after its ending the bromide rose to its original level. 8. The chloride content ran almost constantly parallel to the bromide content. These changes in the bromide and chloride contents we are inclined to think, are to be ascribed rather to a certain state of hunger of the organism (increased excretion of chlorides) than to the narcosis. 9. With reference to the iodide we could not see any regularity; in some of the cases there was a rise in the iodide content during the narcosis and in others there was a fall.