tbuckley/cabot-search huggingface dataset:
Muscle power predicts freestyle swimming performance.
Authors: J A Hawley, M M Williams, M M Vickovic, P J Handcock
Journal: British Journal of Sports Medicine (1992)

The purpose of this study was to determine the relationship between non-invasive laboratory measures of 'muscle power' and swim performance over sprint (50 m) and middle-distance (400 m) events. Twenty-two swimmers performed an upper and lower body Wingate Anaerobic Test (WAT) and a maximal sustained power output test (MPO) for the upper body. Peak power (PP) and mean power (MP) were determined for the WAT, while peak sustained workload (WLpeak) was determined for the MPO. Timed swims over 50 m and 400 m were undertaken by all swimmers during which the number of arm strokes per length was recorded. Highly significant relationships were found between sprint-swim speed (S50) and mean power of the arms (MP(arms)) (r = 0.63, P less than 0.01), between S50 and mean power of the legs (MP(legs)) (r = 0.76, P less than 0.001) and between S50 and the distance covered with each arm stroke (DS) (r = 0.91, P less than 0.001). Multiple regression analyses revealed that WAT power indices for the legs did not significantly increase explained variance in S50 above that of the arms. The relationship between WL(peak) and S400 was highly significant (r = 0.70, P less than 0.001) and indicates the importance of arm power in the longer distance swim events.
TYPE I INTERFERONS (α/β) IN IMMUNITY AND AUTOIMMUNITY
Authors: Argyrios N. Theofilopoulos, Roberto Baccala, Bruce Beutler, Dwight H. Kono
Journal: Annual Review of Immunology (2004)

▪ Abstract The significance of type I interferons (IFN-α/β) in biology and medicine renders research on their activities continuously relevant to our understanding of normal and abnormal (auto) immune responses. This relevance is bolstered by discoveries that unambiguously establish IFN-α/β, among the multitude of cytokines, as dominant in defining qualitative and quantitative characteristics of innate and adaptive immune processes. Recent advances elucidating the biology of these key cytokines include better definition of their complex signaling pathways, determination of their importance in modifying the effects of other cytokines, the role of Toll-like receptors in their induction, their major cellular producers, and their broad and diverse impact on both cellular and humoral immune responses. Consequently, the role of IFN-α/β in the pathogenesis of autoimmunity remains at the forefront of scientific inquiry and has begun to illuminate the mechanisms by which these molecules promote or inhibit systemic and organ-specific autoimmune diseases.
Alterations of the preproenkephalin system in cardiac hypertrophy and its role in atrioventricular conduction
Authors: J WEIL, O ZOLK, J GRIEPENTROG, U WENZEL, W ZIMMERMANN, T ESCHENHAGEN
Journal: Cardiovascular Research (2005)

The goal of this study was to investigate alterations of the endogenous opioid system in cardiac hypertrophy, to elucidate mechanisms of preproenkephalin (ppENK) gene expression, and to assess effects of endogenous opioids on myocardial contractility and atrioventricular conduction.Hypertrophy was induced by ligation of a renal artery (2K1C) or chronic isoprenaline infusion (ISO). ppENK and opioid receptor (mu-, delta-, kappa-OR) mRNA expression was quantified by Northern blot and quantitative RT-PCR, respectively. Isolated cardiac myocytes and non-myocytes from neonatal rat heart were used for cell culture experiments.Overall expression of OR in the heart was markedly lower than in brain tissue, with kappa-OR being the most abundant isoform in the heart. We did not observe differences in kappa-OR expression in ventricular and atrial myocardium. In contrast, delta-OR expression was markedly higher in atria than in ventricles. Mu-OR expression in the heart was below the detection limit of the developed qRT-PCR assay. In left ventricular myocardium, ppENK mRNA levels were significantly increased in 2K1C rats but decreased in ISO rats. Cell culture experiments from neonatal rat hearts revealed that myocytes and non-myocytes express ppENK mRNA. In these cells, receptor-dependent and -independent stimulation of the beta-adrenergic signalling pathway caused an increase in ppENK mRNA. Furthermore, inactivation of inhibitory G-proteins by pertussis toxin increased basal and noradrenaline-stimulated ppENK mRNA expression. The physiological significance of myocardial opioids was investigated in isolated perfused rat hearts. Opioid receptor antagonists (nor-BNI, naltrindol) and the enkephalinase inhibitor CPL had no effect on contractility but significantly altered atrioventricular conduction.These observations suggest that the cardiac opioid system is activated in cardiac hypertrophy. Pressure overload and stimulation of the beta-adrenergic signalling pathway have been identified as a possible mechanism leading to increased ppENK expression, which may contribute to opioid system activation. Finally, endogenous opioids modulate the dromotropic response to catecholamine stimulation. The latter finding raises the possibility that endogenous opioids may contribute to the pathogenesis of arrhythmias.
Arrested rotation of the outflow tract may explain double-outlet right ventricle.
Authors: M P Bostrom, G M Hutchins
Journal: Circulation (1988)

In a previous study the possibility that tetralogy of Fallot and transposition of the great arteries may result of embryonic arrests in the normal rotation of the junction of the outflow tract and the great arteries was investigated. The results suggested that the development of other transposition complexes such as double-outlet right ventricle might also be related to arrests in this process of rotation. To further study this question 20 normal hearts and 15 hearts with double-outlet right ventricle obtained at autopsy were studied. The angle of the aortic-to-pulmonary valve axis relative to the inferior surface of the heart, as viewed from apex to base, was measured from postmortem radiographs. For normal hearts the mean angle was 81 +/- 7(SE) degrees. For 13 of the 15 hearts with double-outlet right ventricle the mean angle was 4 +/- 7(SE) degrees. Two hearts with double-outlet right ventricle showed markedly divergent aortic-to-pulmonary valve angles, with a mean of 228 +/- 11(SE) degrees, and were therefore grouped separately. Although direct comparison of hearts and embryos is difficult because of the differences in methods of determining angles, the valve positions in normal hearts was most similar to Carnegie stage 19, as found in an earlier study. The majority of the hearts with double-outlet right ventricle resembled stage 16 embryos. The results of this study, as well as those of the earlier studies, support the hypothesis that a spectrum of cardiac anomalies with anomalous origin of great vessels arises as arrests in the normal rotation of the semilunar valve region during embryogenesis.
Utility of Cardiac Monitoring in Fetuses at Risk for Congenital Heart Block
Authors: Deborah M. Friedman, Mimi Y. Kim, Joshua A. Copel, Claudine Davis, Colin K.L. Phoon, Julie S. Glickstein, Jill P. Buyon
Journal: Circulation (2008)

Background— Anti-SSA/Ro–associated third-degree congenital heart block is irreversible, prompting a search for early markers and effective therapy. Methods and Results— One hundred twenty-seven pregnant women with anti-SSA/Ro antibodies were enrolled; 95 completed an evaluable course in 98 pregnancies. The protocol included fetal echocardiograms performed weekly from 16 to 26 weeks’ gestation and biweekly from 26 to 34 weeks. PR intervals &gt;150 ms were considered prolonged, consistent with first-degree block. Ninety-two fetuses had normal PR intervals. Neonatal lupus developed in 10 cases; 4 were neonatal lupus rash only. Three fetuses had third-degree block; none had a preceding abnormal PR interval, although in 2 fetuses &gt;1 week elapsed between echocardiographic evaluations. Tricuspid regurgitation preceded third-degree block in 1 fetus, and an atrial echodensity preceded block in a second. Two fetuses had PR intervals &gt;150 ms. Both were detected at or before 22 weeks, and each reversed within 1 week with 4 mg dexamethasone. The ECG of 1 additional newborn revealed a prolonged PR interval persistent at 3 years despite normal intervals throughout gestation. No first-degree block developed after a normal ECG at birth. Heart block occurred in 3 of 16 pregnancies (19%) in mothers with a previous child with congenital heart block and in 3 of 74 pregnancies (4%) in mothers without a previous child with congenital heart block or rash ( P =0.067). Conclusions— Prolongation of the PR interval was uncommon and did not precede more advanced block. There was a trend toward more congenital heart block in fetuses of women with previously affected offspring than those without previously affected offspring. Advanced block and cardiomyopathy can occur within 1 week of a normal echocardiogram without initial first-degree block. Echodensities and moderate/severe tricuspid regurgitation merit attention as early signs of injury.
Ethnicity, Income, and Education as Potential Modifiers of the Effects of Shared Treatment Decision-Making (SDM) Between Asthma Care Manager and Patient on Asthma Controller Medication Adherence: The Better Outcomes of Asthma Treatment (BOAT) Trial
Authors: S.R. Wilson, P. Strub, S.B. Knowles, A.S. Buist, Q. Huang, M. Nguyen
Journal: Journal of Allergy and Clinical Immunology (2009)
Ultrastructural examination of bronchial specimens from children with moderate asthma
Authors: A Bush
Journal: Thorax (2003)

Ultrastructural examination of bronchial specimens from children with moderate asthmaWe have read the paper by Çokug ˘ras ¸and colleagues on bronchial biopsies in asthmatic children with great concern. 1 These authors performed a study in asthmatic children in which prophylactic medication was discontinued for 1 month before a bronchoscopic examination which was performed solely as a research procedure.The Royal College of Paediatricians and Child Health states that "High risk procedures such as lung or liver biopsy, arterial puncture, and cardiac catheterization are not justified for research purposes alone.They should be carried out only when research is combined with diagnosis or treatment intended to benefit the child concerned". 2 Other authorities state that "Non-therapeutic research is particularly difficult to defend in moral terms when undertaken on children". 3 The risks of rigid bronchoscopy are surely no less than an arterial puncture, and discontinuing presumably necessary medication could only increase those risks.How can such a study possibly be justified by the authors or their ethics committee, and how can the Editors of a reputable journal possibly justify the publication of such a study?That the science is valuable is unquestionable, even though the use of more sophisticated pathological techniques would have enhanced it; but the scientific value by no means justifies the disregard of ethical principles.A journal such as Thorax should know better, particularly in the light of the scholarly and ethical review in the very same issue.
Reduction of intrapulmonary shunt and resolution of digital clubbing associated with primary biliary cirrhosis after liver transplantation
Authors: James K. Stoller, Douglas Moodie, William A. Schiavone, David Vogt, Thomas Broughan, Eugene Winkelman, Patrice K. Rehm, William D. Carey
Journal: Hepatology (1990)

This report describes a patient with marked hypoxemia caused by intrapulmonary shunt associated with primary biliary cirrhosis. Liver transplantation resulted in resolution of digital clubbing and reduction of intrapulmonary shunt as demonstrated by normalization of room air arterial blood gases, reduction in shunt fraction and normalization of the indocyanine-enhanced echocardiogram and perfusion lung scan. This patient's course challenges the conventional notion that intrapulmonary shunting associated with chronic liver disease does not reverse after liver transplantation.
EGFR signalling and oncogenic pathway signature in colorectal cancer
Authors: Ibrahim Halil Sahin, Ahmet Afsin Oktay
Journal: Gut (2013)

Sun et al 1 reported a novel stratification model for classifying patients with colorectal cancer by characterising the gene expression profile of the tumours with wild type and mutant KRAS, BRAF and PIK3CA. The authors claimed that the combined transcription signature of these mutant signal molecules might help clinicians identify patients, whose tumour could have similar transcription signature without any mutation and who …
Clinical Characteristics, Management, and Outcomes of Patients Diagnosed With Acute Pulmonary Embolism in the Emergency Department
Authors: Charles V. Pollack, Donald Schreiber, Samuel Z. Goldhaber, David Slattery, John Fanikos, Brian J. O'Neil, James R. Thompson, Brian Hiestand, Beau A. Briese, Robert C. Pendleton, Chadwick D. Miller, Jeffrey A. Kline
Journal: Journal of the American College of Cardiology (2011)
Long-term mortality assessment of multidrug-resistant tuberculosis patients treated with delamanid
Authors: Charles D. Wells, Rajesh Gupta, Norbert Hittel, Lawrence J. Geiter
Journal: European Respiratory Journal (2015)

Multidrug-resistant tuberculosis (MDR-TB) is a serious obstacle to TB control [1]. The disproportionately negative outcomes among patients with drug resistance reflect a strong global need to develop new anti-TB drugs [2, 3]. Delamanid is a novel anti-TB agent that has recently been approved for the management of MDR-TB patients [4]. Treatment of MDR-TB patients with delamanid in combination with an optimised background regimen for 2 months significantly improved 2-month sputum culture conversion (SCC) by ∼50%, in comparison to treatment with placebo plus an optimised background regimen [5]. Additionally, compared to ≤2 months of treatment, ≥6 months of treatment with delamanid plus an optimised background regimen was associated with higher favourable treatment outcomes (55.0% versus 74.5%) and significantly lower mortality (8.3% versus 1.0%, p<0.001) [6]. While early SCC is recognised as a biomarker in the development of anti-TB drugs [7–9], the impact of early SCC on long-term mortality in MDR-TB patients has only been assessed in retrospective cohort analyses [10–13]. Using updated prospective data from the delamanid development programme, we assessed the association between 2-month SCC and mortality in MDR-TB patients and expanded a previous analysis on the impact of long-term treatment with delamanid on mortality. MDR-TB patients treated with 6 months or more of delamanid had significantly lower likelihood of mortality <http://ow.ly/HOv1d>
Treatment of thyroid cancer with the new oral agents
Authors: J.C. Galofré, J.M. Gómez-Sáez, C.A. Escola, E. Anda, A. Calleja, S. Donnay, A. Lucas-Martin, E. Menéndez-Torre, V. Pereg, B. Pérez-Corral, J. Santamaría, G. Riesco-Eizaguirre, C. Zafon
Journal: Annals of Oncology (2011)
Cellular localization of gastric inhibitory polypeptide in the duodenum and jejunum
Authors: J. M. Polak, S. R. Bloom, M. Kuzio, J. C. Brown, A. G. E. Pearse
Journal: Gut (1973)

Indirect immunofluorescence studies using an antiserum to purified porcine gastric inhibitory polypeptide indicate, in the gastrointestinal tract of dog and man, that this polypeptide is present in cells situated predominantly in the mid-zone of the glands in the duodenum and, to a lesser extent, in the jejunum. Absolute correlation of the gastric inhibitory polypeptide cell with one or other of the known endocrine-like cells identified by electron microscopy awaits confirmation by electron immunocytochemistry. It is here identified as an endocrine polypeptide cell of the APUD series and, provisionally, as the D(1) cell. While the hormonal status of a given polypeptide depends ultimately on physiological experiments the present results strengthen the view that gastric inhibitory polypeptide is indeed a hormone.
Modulation of Proliferating Renal Epithelial Cell Affinity for Calcium Oxalate Monohydrate Crystals
Authors: Gerard Farell, Erick Huang, Soo Y. Kim, Rüdiger Horstkorte, John C. Lieske
Journal: Journal of the American Society of Nephrology (2004)

Adhesion of urinary crystals to distal tubular cells could be a critical event that triggers a cascade of responses ending in kidney stone formation. Monolayer cultures of distal nephron-derived MDCKI cells were used as a model to study crystal–cell interactions. COM crystal adhesion reached a peak 2 d after plating and progressively fell thereafter. The decline in crystal binding was accelerated by prostaglandin E2 (PGE2) supplementation and delayed by blockade of PG production. Crystals avidly adhered to cells that migrated in to repair a scrape wound made in the monolayer and after a transient hypoglycemic insult. Exposure of MDCKI cells to uric acid crystals and soluble uric acid was also associated with increased crystal adhesion. Treatment of physically or hypoglycemically injured cells with trypsin or neuraminidase reduced crystal binding to baseline levels, suggesting that increased exposure of cell surface glycoproteins mediated the effect, whereas PGE2 treatment blunted crystal binding to regenerating cells. Furthermore, when cells were grown in the presence of synthetic D-mannosamine analogues that can modify the conformation of cell surface sialoglycoconjugates, crystal binding to proliferating cells was decreased, whereas blockade of N-glycosylation with tunicamycin increased crystal adhesion to these cells. Therefore, COM crystal binding is enhanced to growing renal cells, synthesis of N-glycosylated cell surface proteins is essential to downregulate crystal binding to cells, and this response is modulated by physiologic signals such as PGE2. Sialic acid residues seem to mediate crystal adhesion to growing cells, either directly or via linkage to other crystal-binding molecules. Subtle renal injury and subsequent nephron repair could be a factor promoting crystal adhesion and favoring calculus formation.
Recent Major Progress in Long-Term Cancer Patient Survival Disclosed by Modeled Period Analysis
Authors: Hermann Brenner, Adam Gondos, Volker Arndt
Journal: Journal of Clinical Oncology (2007)

To disclose most recent trends in long-term cancer patient survival.We estimated trends in 5- and 10-year relative survival of cancer patients in the United States in 1998 to 2003 from the 1973 to 2003 database of the Surveillance, Epidemiology, and End Results Program using recently introduced period-analysis modeling techniques that provide the most up-to-date and precise survival estimates.Statistically significant and partly very substantial improvement in 5- and 10-year relative survival in the 1998 to 2003 period was seen for 14 of 24 of the assessed common forms of cancer, including breast and colorectal cancer. For example, by 2003, 5-year relative survival exceeded 90% for patients with breast cancer and reached levels of about two thirds for patients with colorectal cancer and kidney cancer and patients with non-Hodgkin's lymphoma. Unfortunately, 5-year relative survival remained essentially unchanged at approximately 16% for lung cancer patients, and, despite statistically significant improvement, as low as 7% for pancreatic cancer patients. Overall, improvement was most pronounced for patients with regional tumor spread and somewhat less so for patients with localized tumors, whereas hardly any improvement was achieved for patients with distant tumor spread.Our analysis discloses further major improvement in prognosis for most, but not all forms of cancer in recent years. The largest contribution to this improvement comes from improved prognosis of patients with regional tumor spread.
Monoclonal antibody characterization of a unique immune response control locus between H-2S and D.
Authors: L H Shapiro, E S Dugan, J E Neiderhuber
Journal: The Journal of Experimental Medicine (1985)

The primary in vitro antibody response to the type 2 antigen, trinitrophenyl (TNP)-Ficoll, is controlled by two complementing loci in the H-2 region of the mouse major histocompatibility complex (MHC). High responder alleles at both loci are necessary for a high responder phenotype. Previous studies mapped one locus of control to the I-A subregion. In this report we demonstrate by recombinant analysis that the second locus of control is located between the H-2S and D regions. A comparison of responses in the B10.BAR6, B10.BAR10, and B10.BAR11 strains defined a locus controlling the response to TNP-Ficoll in a single haplotype, bounded on the left by the crossover event in the B10.BAR10 and on the right by the crossover event in the B10.BAR6 strain. A monoclonal antibody directed against this right-hand region of control has been produced (48.21.7) that blocks the response to TNP-Ficoll at the level of the antigen-presenting cell. The monoclonal antibody 48-21.7 is specific for the high responder b allele at the right-hand locus and did not inhibit responses to other protein antigens tested. The immune response to TNP-Ficoll was not inhibited by monoclonal antibodies that react with H-2Db or Qa-2 specificities, suggesting that the TNP-Ficoll response is controlled by a unique locus located between H-2S and D. Finally, 48-21.7 recognizes and precipitates a unique product of approximately 40,000 mol wt that is distinct from the H-2D region product recognized by the monoclonal antibody B22/249.
Right Ventricular Hypertrophy in Guinea Pigs Exposed to Simulated High Altitude
Authors: ENRIQUE VALDIVIA
Journal: Circulation Research (1957)

Guinea pigs exposed to simulated altitudes of 18,000 feet developed right heart dilatation followed by hypertrophy, more conspicuous in the infundibular area of the right ventricle. Under the described experimental conditions, pulmonary artery hypertension may be the etiologic factor.
Massively parallel sequencing reveals maternal somatic IL2RG mosaicism in an X-linked severe combined immunodeficiency family
Authors: Laia Alsina, Eva González-Roca, María Teresa Giner, Mónica Piquer, Irene Puga, Mariona Pascal, Estibaliz Ruiz-Ortiz, Isabel Badell, María Anunciación Martín-Mateos, Andrea Cerutti, Manel Juan, Jordi Yagüe, Ana M. Plaza, Juan I. Aróstegui
Journal: Journal of Allergy and Clinical Immunology (2013)
Recombinant Human Hexamer-Dominant IgM Monoclonal Antibody to Ganglioside GM3 for Treatment of Melanoma
Authors: Yumiko Azuma, Yuji Ishikawa, Shigeto Kawai, Toshiaki Tsunenari, Hiroyuki Tsunoda, Tomoyuki Igawa, Shin-ichiro Iida, Masahiko Nanami, Masami Suzuki, Reiko F. Irie, Masayuki Tsuchiya, Hisafumi Yamada-Okabe
Journal: Clinical Cancer Research (2007)

Abstract Purpose: L612, a human IgM monoclonal antibody produced by an EBV-transformed human B-cell line, binds to ganglioside GM3 and kills GM3-positive human melanoma cells in the presence of complement. It has been shown to be effective in some patients with late-stage melanoma. L612 consists of hexameric IgM (about 20%), pentameric IgM (about 74%), and other minor IgM molecules. Because hexameric IgM activates complement more effectively than pentameric IgM, we developed and evaluated a hexamer-dominant recombinant IgM for clinical applications. Experimental Design: Chinese hamster ovary (CHO) cells were transfected with heavy- and light-chain genes of L612, with or without the joining-chain gene. Antitumor effects of the recombinant IgM secreted from CHO cells were evaluated in vitro and in vivo. Results: Recombinant IgM secreted from CHO cells without the joining chain (designated CA19) was ∼80% hexameric, whereas recombinant IgM from CHO cells transfected with heavy-, light-, and joining-chain genes (designated CJ45) was about 90% pentameric. Both CA19 and CJ45 recombinant IgMs caused complement-dependent cytotoxicity against human and mouse melanoma cell lines, but the amount of CA19 required for 50% specific cytotoxicity was 5 to 10 times smaller. I.v. injection of CA19 compared with CJ45 or native L612 elicited more profound antitumor activity in nude rats bearing a GM3-positive mouse melanoma xenograft. Conclusions: A hexamer-dominant human IgM against GM3 may provide a more potent treatment option for patients with GM3-positive melanoma.