tbuckley/cabot-search huggingface dataset:
Exhaled breath profiling in diagnosing wheezy preschool children
Authors: Kim D.G. van de Kant, Joep J.B.N. van Berkel, Quirijn Jöbsis, Valéria Lima Passos, Ester M.M. Klaassen, Linda van der Sande, Onno C.P. van Schayck, Johan C. de Jongste, Frederik Jan van Schooten, Eduard Derks, Edward Dompeling, Jan W. Dallinga
Journal: European Respiratory Journal (2012)

Although wheeze is common in preschool children, the underlying pathophysiology has not yet been disentangled. Volatile organic compounds (VOCs) in exhaled breath may serve as noninvasive markers of early wheeze. We aimed to assess the feasibility of VOC collection in preschool children, and to study whether a VOC profile can differentiate between children with and without recurrent wheeze. We included children (mean (range) age 3.3 (1.9-4.5) yrs) with (n=202) and without (n=50) recurrent wheeze. Exhaled VOCs were analysed by gas chromatography-time-of-flight mass spectrometry. VOC profiles were generated by ANOVA simultaneous component analysis (ASCA) and sparse logistic regression (SLR). Exhaled breath collection was possible in 98% of the children. In total, 913 different VOCs were detected. The signal-to-noise ratio improved after correction for age, sex and season using ASCA pre-processing. An SLR model with 28 VOCs correctly classified 83% of the children (84% sensitivity, 80% specificity). After six-fold cross-validation, 73% were correctly classified (79% sensitivity, 50% specificity). Assessment of VOCs in exhaled breath is feasible in young children. VOC profiles are able to distinguish children with and without recurrent wheeze with a reasonable accuracy. This proof of principle paves the way for additional research on VOCs in preschool wheezing.
Prolonged low-dose corticosteroid therapy and osteoporosis in rheumatoid arthritis.
Authors: V J Hajiroussou, M Webley
Journal: Annals of the Rheumatic Diseases (1984)

Thirty-one patients with rheumatoid arthritis maintained on prednisolone 5 mg daily for an average period of 9.4 years were assessed radiologically to determine the degree of osteoporosis in their spine and peripheral skeleton. They were compared with a control group of 32 rheumatoid patients who had never received corticosteroids. The steroid-treated patients had more severe osteoporosis than the controls, though the difference was not statistically significant. In the female patients the spine appeared to be more sensitive than the peripheral skeleton to the osteoporotic effect of corticosteroids.
The human liver clears both asymmetric and symmetric dimethylarginine
Authors: Michiel P.C. Siroen, Joost R. M. van der Sijp, Tom Teerlink, Cors van Schaik, Robert J. Nijveldt, Paul A. M. van Leeuwen
Journal: Hepatology (2005)

Asymmetric (ADMA) and symmetric dimethylarginine (SDMA) inhibit production of nitric oxide. The concentration of both dimethylarginines is regulated by urinary excretion, although ADMA, but not SDMA, is also subject to degradation by dimethylarginine dimethylaminohydrolase, which is highly expressed in the liver but also present in the kidney. The exact roles of the human liver and kidney in the metabolism of dimethylarginines are currently unknown. Therefore, we aimed to investigate renal and hepatic handling of ADMA and SDMA in detail in 24 patients undergoing hepatic surgery. To calculate net organ fluxes and fractional extraction (FE) rates, blood was collected from an arterial line, the portal vein, hepatic vein, and renal vein, and blood flow of the hepatic artery, portal vein, and renal vein was determined using Doppler ultrasound techniques. Results showed a significant net uptake (median [IQR]) of ADMA in both the liver (9.6 nmol/min [5.6–13.2]) and the kidney (12.1 nmol/min [1.3–17.1]). SDMA uptake was present not only in the kidney (12.7 nmol/min [3.5–25.4]), but also in the liver (7.7 nmol/min [2.8–16.4]). FE rates of ADMA for the liver and kidney were 5.0% (3.5%–7.4%) and 8.4% (1.3%–13.9%), respectively. For SDMA, hepatic and renal FE rates were 3.4% (2.1%–7.5%) and 12.5% (3.6%–16.2%), respectively. In conclusion, this study gives a detailed description of the hepatic and renal elimination of dimethylarginines and shows that the clearing of SDMA is not only confined to the kidney, but the human liver also takes up substantial amounts of SDMA from the portal and systemic circulation. (HEPATOLOGY 200541:559–565.)
Decrease of histamine induced bronchoconstriction by caffeine in mild asthma.
Authors: J C Henderson, F O'Connell, R W Fuller
Journal: Thorax (1993)

BACKGROUND--While high doses of caffeine may affect pulmonary function and bronchial challenge tests in patients with mild asthma, the effects of lower doses (&lt; or = 5 mg/kg) are less well documented. Specific recommendations exist for withholding theophylline, but not caffeine, before bronchoprovocation and pulmonary function testing. METHODS--To assess the effect of a single oral dose of caffeine (5 mg/kg) on FEV1 and bronchial responsiveness to histamine a double blind, placebo controlled study was performed in eight patients with mild stable asthma. RESULTS--While caffeine had no effect on FEV1, mean (95% confidence interval) log PC20 histamine was significantly higher 150 minutes [caffeine = 0.99 (0.2) mg/ml, placebo = 0.53 (0.29)] and 240 minutes [caffeine = 0.89 (0.24), placebo = 0.44 (0.26)] after administration of caffeine than after placebo. CONCLUSIONS--Caffeine should be excluded from the diet for a period of more than four hours before bronchial provocation testing. The exact length of time for which it must be excluded requires further study.
Pulmonary necrobiotic nodules as a presenting feature of rheumatoid arthritis.
Authors: S Hull, J A Mathews
Journal: Annals of the Rheumatic Diseases (1982)

In rheumatoid disease only 4 cases have been reported in which lung nodules preceded arthritis. Two further cases are presented in which intrapulmonary nodules were noted at the onset of the disease, thus provoking a diagnostic dilemma. In the first patient rheumatoid factor tests were initially negative, and diagnostic thoracotomy was performed. In the second patient serological tests were positive, and biopsy was avoided. It therefore seems that detection of circulating rheumatoid factor in patients with lung shadows can be a useful aid to diagnosis and management.
P681 HBsAg MUTATIONS WITH ENHANCED CAPABILITY TO EVADE IMMUNE RESPONSE ARE ASSOCIATED WITH HBV REACTIVATION DURING IMMUNOSUPPRESSION
Authors: R. Salpini, C. Alteri, L. Colagrossi, M.-C. Bellocchi, D. Armenia, F. Di Santo, L. Carioti, F. Continenza, A. Bertoli, Y. Louzoun, M. Pollicita, A. Ricciardi, C. Mastroianni, M. Paoloni, A. Marrone, L. Sarmati, C. Sarrecchia, M. Andreoni, M. Angelico, C.-F. Perno, V. Svicher
Journal: Journal of Hepatology (2014)
Clinical Notes upon the Rectal Contour and Consistence of a Thousand Prostate Glands
Authors: E. H. Fenwick
Journal: BMJ (1899)

THE CONTOUR OP PROSTA'2E.'_L__________I__its_ tures If' -eurgeyi mde-many operations feasible which had previouslybeen c6ndemned, andc has'proved a help of extreme value in the diagnosis of disease.Furthermore, one of the scientific descendants of Hunter, deeply imbued with his spirit, transcendently patient and painstaking in detail as was his master, as minute an observer of Nature's ways, and as careful an experimenter, after much trying and much thinking, has realised, in the discovery of the methods of antiseptic surgery, a benefit to mankind which only surgeons can to the full appreciate.What was hazardous before is now rendered safe, what was .atcomplishedwith pain and suffering is now free from both.There is scarcely a limit to what might be said in praise of -this great work.The name of Lister, like that of John Hunter, will stand forth in the records of scientific progress as one who has immeasurably benefited humanity, and as the author of the means whereby surgery has been mainly enabled to make that marvellous progress of which we are all so proud.This is recognised throughout the world, and were I not con- vinced that our science has fresh achievements in store, I 4hould say that Lister had finally crowned the edifice whose corner-stone Hunter laid.Of all the great minds which have illuminated the scientific world and guided its destinies, John Hunter's is the one which first directed surgery into the pathways of science, and, dying, left to surgeons a future in the memory of his past.He is the one great man without whose aid it is impossible to imagine surgery all that it now is; we cannot take his influence away and yet retain all that we now possess.Our science might have spared some other workers, but it could not have become the science we know without John Hunter.
Reduction in rotavirus disease due to the infant immunisation programme in England; evidence from national surveillance
Authors: Christina Atchison, Sarah Collins, David Brown, Mary E. Ramsay, Shamez Ladhani, Rohini Manuel, Duncan Clark, John Magee, Husam Osman, Anthony D. Hale, Hamid Jalal, Mark Farrington, Martin L’Estrange, Ed Kaczmarski, Andrew Turner, Emanuela Pelosi, Peter Hawtin, David Carrington, Adam Finn
Journal: Journal of Infection (2015)
Suppression of Constitutive and Tumor Necrosis Factor α-Induced Nuclear Factor (NF)-κB Activation and Induction of Apoptosis by Apigenin in Human Prostate Carcinoma PC-3 Cells: Correlation with Down-Regulation of NF-κB-Responsive Genes
Authors: Sanjeev Shukla, Sanjay Gupta
Journal: Clinical Cancer Research (2004)

Abstract Purpose: Development of androgen independence and resistance to apoptosis in prostate cancer are often correlated with high levels of serum tumor necrosis factor (TNF)-α in these patients. The loss of sensitivity to TNF-α-induced apoptosis in androgen-insensitive prostate carcinoma cells is due in part to constitutive activation of Rel/nuclear factor (NF)-κB transcription factors that regulate several cell survival and antiapoptotic genes. Our previous studies have demonstrated growth inhibitory and apoptotic effects of apigenin, a common plant flavonoid, in a variety of human prostate carcinoma cells. Here we examined whether apigenin is effective in inhibiting NF-κB expression in androgen-insensitive human prostate carcinoma cells exhibiting high constitutive levels of NF-κB. Experimental Design: Using androgen-insensitive human prostate carcinoma PC-3 cells, the effect of apigenin was assessed on NF-κB activation by electrophoretic mobility shift assay and reporter gene assay. Expression of NF-κB subunits p65 and p50, IκBα, p-IκBα, in-beads kinase assay and NF-κB-regulated genes were determined by Western blot analysis. Apoptosis was determined by annexin V/propidium iodide staining after fluorescence-activated cell-sorting analysis. Results: Treatment of cells with 10–40-μm doses of apigenin inhibited DNA binding and reduced nuclear levels of the p65 and p50 subunits of NF-κB. Apigenin inhibited IκBα degradation and IκBα phosphorylation and significantly decreased IKKα kinase activity. Apigenin also inhibited TNF-α-induced activation of NF-κB via the IκBα pathway, thereby sensitizing the cells to TNF-α-induced apoptosis. The inhibition of NF-κB activation correlated with a decreased expression of NF-κB-dependent reporter gene and suppressed expression of NF-κB-regulated genes [specifically, Bcl2, cyclin D1, cyclooxygenase-2, matrix metalloproteinase 9, nitric oxide synthase-2 (NOS-2), and vascular endothelial growth factor]. Conclusions: Our results indicate that inhibition of NF-κB by apigenin may lead to prostate cancer suppression by transcriptional repression of NF-κB-responsive genes as well as selective sensitization of prostate carcinoma cells to TNF-α-induced apoptosis.
Analysis of Nitric Oxide Synthase and Nitrotyrosine Expression in Human Pulmonary Tuberculosis
Authors: Hyung-Seok Choi, Pradeep R. Rai, Hong Wei Chu, Carlyne Cool, Edward D. Chan
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

The role of nitric oxide (NO) in the host-defense against human tuberculosis (TB) is controversial. Although experimental evidence indicates that NO may play an important role in controlling TB, its expression in human tuberculous lungs has not been systematically characterized. We therefore investigated the expression of NO synthases (NOS) and of nitrotyrosine, the latter a marker of NO expression, in surgically resected lungs of eight patients with TB. Immunohistochemical and morphometric analyses revealed that, compared with control subjects, inducible NOS, endothelial NOS, and nitrotyrosine, but not neuronal NOS, were significantly elevated in the inflammatory zone of the tuberculous granulomas, and in the nongranulomatous pneumonitis zone. Tumor necrosis factor-α (TNF-α) was also significantly increased in tuberculous lungs and was principally localized to the necrotic, and to a lesser extent, the inflammatory and fibrotic areas of the granulomas. The NOS isoforms, nitrotyrosine, and TNF-α were expressed by the epithelioid macrophages and giant cells within the granulomas and in alveolar macrophages and epithelial cells in pneumonitis areas. This descriptive study provides evidence that in human TB, NOS isoenzymes and NO are present in specialized areas of the tuberculous granulomas; their precise role in human TB remains to be determined.
Novel Interaction of MUC4 and Galectin: Potential Pathobiological Implications for Metastasis in Lethal Pancreatic Cancer
Authors: Shantibhusan Senapati, Pallavi Chaturvedi, William G. Chaney, Subhankar Chakraborty, Vinayaga S. Gnanapragassam, Aaron R. Sasson, Surinder K. Batra
Journal: Clinical Cancer Research (2010)

Several studies have reported aberrant expression of MUC4 in pancreatic cancer (PC), which is associated with tumorigenicity and metastasis. Mechanisms through which MUC4 promote metastasis of PC cells to distant organs are poorly defined.Identification of MUC4-galectin-3 interaction and its effect on the adhesion of cancer cells to endothelial cells were done by immunoprecipitation and cell-cell adhesion assays, respectively. Serum galectin-3 level for normal and PC patients were evaluated through ELISA.In the present study, we have provided clinical evidence that the level of galectin-3 is significantly elevated in the sera of PC patients with metastatic disease compared with patients without metastasis (P = 0.04) and healthy controls (P = 0.00001). Importantly, for the first time, we demonstrate that MUC4 present on the surface of circulating PC cells plays a significant role in the transient and reversible attachment (docking) of circulating tumor cells to the surface of endothelial cells. Further, exogenous galectin-3 at concentrations similar to that found in the sera of PC patients interacts with MUC4 via surface glycans such as T antigens, which results in the clustering of MUC4 on the cell surface and a stronger attachment (locking) of circulating tumor cells to the endothelium.Altogether, these findings suggest that PC cell-associated MUC4 helps in the docking of tumor cells on the endothelial surface. During cancer progression, MUC4-galectin-3 interaction-mediated clustering of MUC4 may expose the surface adhesion molecules, which in turn promotes a stronger attachment (locking) of tumor cells to the endothelial surface.
Aldosterone Stimulates Reactive Oxygen Species Production through Activation of NADPH Oxidase in Rat Mesangial Cells
Authors: Kayoko Miyata, Matlubur Rahman, Takatomi Shokoji, Yukiko Nagai, Guo-Xing Zhang, Guang-Ping Sun, Shoji Kimura, Tokihito Yukimura, Hideyasu Kiyomoto, Masakazu Kohno, Youichi Abe, Akira Nishiyama
Journal: Journal of the American Society of Nephrology (2005)

It has recently been shown that glomerular mesangial injury is associated with increases in renal cortical reactive oxygen species (ROS) levels in rats treated chronically with aldosterone and salt. This study was conducted to determine the mechanisms responsible for aldosterone-induced ROS production in cultured rat mesangial cells (RMC). Oxidative fluorescent dihydroethidium was used to evaluate intracellular production of superoxide anion (O(2)(-)) in intact cells. The lucigenin-derived chemiluminescence assay was used to determine NADPH oxidase activity. The staining of dihydroethidium was increased in a dose-dependent manner by aldosterone (1 to 100 nmol/L) with a peak at 3 h in RMC. Aldosterone (100 nmol/L for 3 h) also significantly increased NADPH oxidase activity from 232 +/- 18 to 346 +/- 30 cpm/5 x 10(4) cells. Immunoblotting data showed that aldosterone (100 nmol/L for 3 h) increased p47phox and p67phox protein levels in the membrane fraction by approximately 2.1- and 2.3-fold, respectively. On the other hand, mRNA expression of NADPH oxidase membrane components, p22phox, Nox-1, and Nox-4, were not altered by aldosterone (for 3 to 12 h) in RMC. Pre-incubation with the selective mineralocorticoid receptor (MR) antagonist, eplerenone (10 micromol/L), significantly attenuated aldosterone-induced O(2)(-) production, NADPH oxidase activation and membranous translocation of p47phox and p67phox. These results suggest that aldosterone-induced ROS generation is associated with NAPDH oxidase activation through MR-mediated membranous translocation of p47phox and p67phox in RMC. These cellular actions of aldosterone may play a role in the pathogenesis of glomerular mesangial injury.
Use of a fenestrated silicone drain to stent a malignant tracheobronchial stenosis.
Authors: R L Insall, G N Morritt
Journal: Thorax (1990)

An innovative use of a fenestrated silicone drainage tube as an endobronchial stent is reported. The patient had respiratory obstruction due to a carinal tumour and laser photoresection had failed to restore airway patency.
Imatinib mesylate is effective in children with chronic myelogenous leukemia in late chronic and advanced phase and in relapse after stem cell transplantation
Authors: F Millot, J Guilhot, B Nelken, T Leblanc, E S De Bont, A N Békassy, H Gadner, S Sufliarska, J Stary, H Gschaidmeier, F Guilhot, M Suttorp
Journal: Leukemia (2005)
Pulmonary morphofunctional effects of acute myocardial infarction
Authors: D.S. Faffe, P.S.C. Chagas, A.S. Medeiros, E.A. Saad, P.H.N. Saldiva, P.R.M. Rocco, W.A. Zin
Journal: European Respiratory Journal (1999)

Acute myocardial infarction (AMI) may yield several respiratory changes. Nevertheless, no comprehensive pulmonary morphological/physiological correlation has been performed under this condition. The aims of the present investigation were: 1) to determine the respiratory parameters in an experimental model of coronary artery occlusion, 2) to relate these results to findings from lung histopathology, and 3) to evaluate the effects of propranolol used prior to AMI. Twenty-eight rats were anaesthetized and mechanically ventilated. In the control group (C), a suture line was passed around the left anterior descending coronary artery (LADCA). The infarct group (I) was similarly prepared but the LADCA was ligated and infarct resulted. In the control/propranolol (CP) and infarct/propranolol (IP) groups, propranolol was intravenously injected 5 min before surgery as performed in groups C and I, respectively. Lung static (EL,st) and dynamic (EL,dyn) elastances, airway resistance (RL,int), and viscoelastic/inhomogeneous pressure (deltaP2L) were determined before and 30, 60 and 120 min after surgery. In group I, EL,st, EL,dyn, RL,int and deltaP2L increased progressively throughout the experiment, and were higher than those found in groups C, CP and IP. All respiratory parameters but EL,st remained unaltered in group IP. Lung histopathological examination demonstrated alveolar, interstitial and intrabronchial oedema in group I. Group IP showed only interstitial oedema. Acute myocardial infarction yields lung resistive, elastic and viscoelastic changes. The last two results from alveolar and interstitial oedema, respectively. The previous use of propranolol diminishes respiratory changes.
Tribbles homologue 3 stimulates canonical TGF-β signalling to regulate fibroblast activation and tissue fibrosis
Authors: Michal Tomcik, Katrin Palumbo-Zerr, Pawel Zerr, Barbora Sumova, Jerome Avouac, Clara Dees, Alfiya Distler, Radim Becvar, Oliver Distler, Georg Schett, Ladislav Senolt, Jörg H W Distler
Journal: Annals of the Rheumatic Diseases (2015)

Objectives Tribbles homologue 3 (TRB3) is a pseudokinase that modifies the activation of various intracellular signalling pathways to control fundamental processes extending from mitosis and cell activation to apoptosis and modulation of gene expression. Here, we aimed to analyse the role of TRB3 in fibroblast activation in systemic sclerosis (SSc). Methods The expression of TRB3 was quantified by quantitative PCR, western blot and immunohistochemistry. The role of TRB3 was analysed in cultured fibroblasts and in experimental fibrosis using small interfering RNA (siRNA)-mediated knockdown and overexpression of TRB3. Results TRB3 expression was increased in fibroblasts of patients with SSc and in murine models of SSc in a transforming growth factor-β (TGF-β)/Smad-dependent manner. Overexpression of TRB3 stimulated canonical TGF-β signalling and induced an activated phenotype in resting fibroblasts. In contrast, knockdown of TRB3 reduced the profibrotic effects of TGF-β and decreased the collagen synthesis. Moreover, siRNA-mediated knockdown of TRB3 exerted potent antifibrotic effects and ameliorated bleomycin as well as constitutively active TGF-β receptor I-induced fibrosis with reduced dermal thickening, decreased hydroxyproline content and impaired myofibroblast differentiation. Conclusions The present study characterises TRB3 as a novel profibrotic mediator in SSc. TGF-β induces TRB3, which in turn activates canonical TGF-β/Smad signalling and stimulates the release of collagen, thereby inducing a positive feedback loop that may contribute to aberrant TGF-β signalling in SSc.
Fibroblast Growth Factor 23 and Risks of Mortality and End-Stage Renal Disease in Patients With Chronic Kidney Disease
Authors: Tamara Isakova, Huiliang Xie, Wei Yang, Dawei Xie, Amanda Hyre Anderson, Julia Scialla, Patricia Wahl, Orlando M. Gutiérrez, Susan Steigerwalt, Jiang He, Stanley Schwartz, Joan Lo, Akinlolu Ojo, James Sondheimer, Chi Yuan Hsu, James Lash, Mary Leonard, John W. Kusek, Harold I. Feldman, Myles Wolf
Journal: JAMA (2011)

IBROBLAST GROWTH FACTOR 23 (FGF-23) is an endocrine hormone that regulates phosphorus metabolism.Circulating levels of FGF-23 increase progressively as kidney function declines, eventually reaching concentrations in patients with chronic kidney disease that are among the highest in any condition commonly encountered in clinical practice. 1Fibroblast growth factor 23 levels increase in chronic kidney disease as an appropriate physiological adaptation to maintain neutral phosphate balance and normal serum phosphate levels in the setting of reduced renal capacity for phosphate excretion.Preventing increases in serum phosphate is likely beneficial in chronic kidney disease given reports of greater risk of adverse renal and cardiovascular outcomes in association with overt hyperphosphatemia and even modest elevations in serum phosphate within