tbuckley/cabot-search huggingface dataset:
Sulphate and osteoarthritis: decrease of serum sulphate levels by an additional 3-h fast and a 3-h glucose tolerance test after an overnight fast
Authors: C M Blinn, B A Biggee, T E McAlindon, M Nuite, J E Silbert
Journal: Annals of the Rheumatic Diseases (2006)

<b>Background:</b> Low sulphate levels in blood may contribute to osteoarthritis by decreasing cartilage chondroitin sulphation. <b>Objective:</b> To measure serum levels of sulphate during 3 h of fasting or glucose ingestion after overnight fasts to determine how much sulphate lowering may occur during this period. <b>Methods:</b> Sera from 14 patients with osteoarthritis who fasted overnight were obtained every 15–30 min during 3 h of continued fasting and during 3 h after ingestion of 75 g of glucose. Sulphate was assayed by high-performance liquid chromatography with a Metrohm-Peak 761 Compact IC and simultaneously assayed for glucose by high-performance liquid chromatography with a Metrohm-Peak 817 Bioscan. <b>Results:</b> Continuation of overnight fasting for 3 h resulted in a near-linear 3-h decrease in levels for all 14 patients ranging from 3% to 20% with a mean drop of 9.3%, whereas the 3-h decrease after glucose ingestion ranged from 10% to 33% with a mean drop of 18.9%. <b>Conclusion:</b> A 3-h continuation of fasting caused a marked reduction in serum sulphate levels, whereas ingestion of 75 g of glucose in the absence of protein resulted in doubling the reduction. This suggests that fasting and ingestion of protein-free calories may produce periods of chondroitin undersulphation that could affect osteoarthritis.
Gastro-oesophageal reflux related cough and its response to laparoscopic fundoplication
Authors: C. J Allen, M. Anvari
Journal: Thorax (1998)

<h3>BACKGROUND</h3> This study was designed to determine prospectively the rate of cough before and after laparoscopic Nissen fundoplication performed for the control of gastro-oesophageal reflux disease. <h3>METHODS</h3> One hundred and ninety five consecutive patients (76 men) of mean (SD) age 46.9 (14.1) years with proven gastro-oesophageal reflux disease, who were either on long term omeprazole (n = 187) or who had not responded to a trial of omeprazole (n = 8), took part in the study which was carried out in a university teaching hospital that included a regional respiratory referral centre. Patients underwent oesophageal manometry, 24 hour oesophageal pH testing, and symptom score evaluation by an independent observer before and six months after laparoscopic Nissen fundoplication. <h3>RESULTS</h3> One hundred and thirty three patients presented with reflux symptoms and 62 with respiratory symptoms; 68% of patients complained of cough before surgery (86% with respiratory symptoms, 60% with gastrointestinal symptoms). The percentage reflux time in 24 hours fell significantly (p&lt;0.0001) from a mean (SD) of 9.38 (10.99)% to 1.22 (2.92)%, lower oesophageal sphincter tone rose significantly (p&lt;0.0001) from a mean (SD) of 7.71 (5.90) mm Hg to 21.74 (10.84) mm Hg, and the cough score fell from a median value of 8.0 (IQR 12.0) to 0 (IQR 3) following surgery. Of the patients with cough, 51% were cough free after surgery and 31% improved. The patients with respiratory symptoms had a higher cough score before (median 12.0 (IQR 5.5) versus 4.0 (IQR 8.75), p&lt;0.0001) and after surgery (median 1 (7.5) versus 0.0 (IQR 1.0), p = 0.0045) than those with gastrointestinal symptoms. <h3>CONCLUSIONS</h3> Patients who present to gastroenterologists with severe reflux commonly complain of cough. Laparoscopic Nissen fundoplication is effective in the control of cough in patients with gastro-oesophageal reflux disease, with or without primary respiratory disease.
Industasis, a Promotion of Tumor Formation by Nontumorigenic Stray Cells
Authors: Petr Pajer, Vít Karafiát, Vladimír Pec̆enka, Dana Pru̇ková, Jana Dudlová, Jiří Plachý, Petra Kašparová, Michal Dvořák
Journal: Cancer Research (2009)

Abstract A tumor cell is formed when a critical amount of endogenous and/or exogenous tumorigenic stimuli is exceeded. We have shown that the transient presence of nontumorigenic stray cells in tissues of experimental animals that contain cells with a subcritical set of genetic mutations can act as a tumor-promoting stimulus. To induce somatic mutations in all chicken tissues, we have used the MAV-2 retroviral insertion system that almost exclusively generates nephroblastomas. MAV-2 mutagenized animals i.v. inoculated with nonmalignant cells developed early clonal lung tumors before nephroblastomas. Importantly, the injected cells did not become a component of resultant tumors. Lung tumors displayed specific mutational signature characterized by an insertion of MAV-2 provirus into the fyn-related kinase (frk) promoter that results in the overexpression of the frk gene. In contrast, plag1, foxP, and twist genes were most often mutagenized in nephroblastomas. Based on such observations, we propose the mechanism termed industasis, a promotion of fully malignant phenotype of incipient tumor cell by stray cells, and hypothesize that it might be the underlying cause of human multiple primary tumors. [Cancer Res 2009;69(11):4605–12]
Statin Use Is Associated with Improved Function and Survival of Lung Allografts
Authors: Bruce A. Johnson, Aldo T. Iacono, Adriana Zeevi, Kenneth R. McCurry, Steven R. Duncan
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are widely used antilipidemic agents that are also immunomodulatory. We evaluated possible effects of these agents after lung transplantation by comparing outcomes of 39 allograft recipients, who were prescribed statins for hyperlipidemia, with those of 161 contemporaneous control recipients who did not receive these drugs. Acute rejection (>or= Grade II) was less frequently found in the statin group (15.1 versus 25.6% of biopsies, p < 0.01). None of 15 recipients started on statins during postoperative Year 1 developed obliterative bronchiolitis, whereas the cumulative incidence of this complication among control subjects was 37% (p < 0.01). Total cellularity, as well as proportions of inflammatory neutrophils and lymphocytes, were significantly lower in bronchoalveolar lavages of statin recipients. Among double lung recipients, those taking statins had significantly better spirometry: FVC (80 +/- 2 versus 70 +/- 1%) and FEV1 (87 +/- 2 versus 70 +/- 1%), as percentages of predicted values, and absolute FEV1/FVC (83.4 +/- 1.2 versus 78.6 +/- 0.5) (all p < 0.01). The 6-year survival of recipients taking statins (91%) was much greater than that of control subjects (54%) (p < 0.01). These data suggest statin use may have substantial clinical benefits after pulmonary transplantation.
Disruption of Hemoglobin Oxygen Transport Does Not Impact Oxygen-Dependent Physiological Processes in Developing Embryos of Zebra Fish ( <i>Danio rerio</i> )
Authors: Bernd Pelster, Warren W. Burggren
Journal: Circulation Research (1996)

Embryonic hemoglobin circulated by the developing heart in the early vertebrate embryo is widely assumed (without substantiation) to perform the same vital role of O 2 carriage that it does in fetuses and adults. In order to challenge this assumption, we measured highly O 2 -dependent physiological variables like O 2 consumption, cardiac performance, and initial swim bladder filling in the presence and absence of functional hemoglobin in the embryos and early larvae of the zebra fish, Danio (= Brachydanio ) rerio . Functional ablation of hemoglobin by carbon monoxide or phenylhydrazine did not reduce whole-animal O 2 consumption, which was ≈85 to 90 μmol·g −1 ·h −1 . Similarly, no differences in heart variables like ventricular pressure development or heart rate, which increased from 135 to 175 bpm between stages 36h and 96h (indicating developmental stages 36 and 96 hours after fertilization, respectively), were observed in these experiments. Initial opening of the swim bladder was not influenced in the presence of CO-occupied hemoglobin but was significantly impaired when the embryonic hemoglobin was chemically modified by incubation with phenylhydrazine. That aerobic processes continue without hemoglobin O 2 transport indicates the adequacy in the embryo of simple O 2 diffusion alone even in developmental stages with extensive convective blood circulation generated by the heart.
STUDIES ON THE METABOLISM OF PLASMA PROTEINS IN THE NEPHROTIC SYNDROME. I. ALBUMIN, γ-GLOBULIN AND IRON-BINDING GLOBULIN 1
Authors: David Gitlin, Charles A. Janeway, Lee E. Farr
Journal: Journal of Clinical Investigation (1956)

Although there is unanimity of opinion that the nephrotic syndrome is characterized by proteinuria, hypoproteinemia, edema and hyperlipemia, there is considerably less agreement as to the mechanisms which result in these findings.It is now generally held that the proteinuria found in this disease is related directly to the renal lesion (1) and is not attributable to the excretion of ab- normal plasma proteins (2).The cause of the severe hypoproteinemia in this disease, however, is a more controversial subject.The association of proteinuria and hypoproteinemia as cause and ef- fect has been postulated by a number of investigators (1-4) and the occasionally prodigious amounts of plasma protein excreted by children with the nephrotic syndrome makes the relation- ship attractive.This concept, however, is not universally accepted (5), and it has long been sug- gested that the degree of hypoproteinemia may not depend upon the severity of proteinuria alone (6).This study was undertaken in an effort to de- termine the factors responsible for hypoproteinemia in children with the nephrotic syndrome.Since the concentration of a given plasma protein in the circulation is dependent upon its rate of syn- thesis, its rate of loss from the body whether by catabolism or excretion or both, and its distribu- tion within the body, an attempt was made to esti- mate these quantities for albumin, y-globulin and iron-binding globulin during various stages of this disease. METHODSPatients: Six children with the nephrotic syndrome were selected for study.The pertinent medical data are summarized in Table I.
The changing face of familial colorectal cancer
Authors: Ayan Banerjea, Sue Clark, Sina Dorudi
Journal: BMJ (2004)

Young patients with colorectal cancer should be assessed for genetic predispositions 

C olorectal cancer is predominantly a disease of elderly people in the developed world. The annual incidence of more than 35 000 cases in the United Kingdom means that many people have at least one affected relative. Colorectal cancer in elderly relatives may be due to shared environmental exposure rather than a true genetic predisposition, although the risk of developing colorectal cancer rises with the number of relatives affected. Genetic factors may have a role in up to 30% of cases,1 but only a small proportion (less than 5%) of colorectal cancers arise in families with strong histories in which tumours develop at a young age (less than 50 years) and represent truly high risk inherited predispositions. Even so, more than 1500 families per year need to be counselled and screened.

Most hereditary colorectal cancers are attributable to two recognised syndromes. Familial adenomatous polyposis usually has a clear phenotype, characterised by numerous (more than 100) adenomatous polyps in the large bowel by the second to third decades of life, which inevitably progress into cancers. This autosomal dominant condition, caused by APC gene mutations, has been a paradigm for the …
Vascular prostaglandin and thromboxane production in a canine model of myocardial ischemia.
Authors: J M Schmitz, P G Apprill, L M Buja, J T Willerson, W B Campbell
Journal: Circulation Research (1985)

Whereas numerous studies have investigated the role of prostacyclin and thromboxane A2 in the maintenance of coronary blood flow, most of these have focused on normal vessels. In the present investigation, we examined the prostaglandin- and thromboxane-synthesizing capacity of isolated coronary artery segments obtained from the site of a critical coronary artery stenosis. Cyclic flow variations were produced by placing a hard cylindrical constrictor on the proximal left anterior descending coronary artery in open-chest, anesthetized dogs. Cyclic flow variations are characterized by progressive declines in coronary blood flow, interrupted by sudden spontaneous restorations of flow. After cyclic flow variations had been induced, the hearts were removed, and the left anterior descending and circumflex coronary arteries were dissected. The vessels were cut into segments and incubated in the presence of increasing concentrations of arachidonic acid (10(-4)-10(-6) M). The synthesis of prostaglandin E2, thromboxane B2, and 6-keto prostaglandin F1 alpha by the coronary segments was measured by radioimmunoassay. When incubated in the presence of 10(-5) M arachidonic acid, coronary artery segments obtained from the left anterior descending coronary artery undergoing cyclic flow variations produced substantially more thromboxane B2 (142 +/- 27 vs. 29 +/- 3 pg/mg P less than 0.01) and less 6-keto prostaglandin F1alpha (125 +/- 12 vs. 350 +/- 30 pg/mg, P less than 0.01) than control circumflex coronary artery segments. Circumflex coronary vessels in which the endothelium was removed ex vivo produced 6-keto prostaglandin F1alpha levels comparable to those found in the left anterior descending coronary artery (147 +/- 17 pg/mg), but did not synthesize thromboxane B2 (23 +/- 2.6 pg/mg).(ABSTRACT TRUNCATED AT 250 WORDS)
2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease
Authors: Stephan D. Fihn, Julius M. Gardin, Jonathan Abrams, Kathleen Berra, James C. Blankenship, Apostolos P. Dallas, Pamela S. Douglas, JoAnne M. Foody, Thomas C. Gerber, Alan L. Hinderliter, Spencer B. King, Paul D. Kligfield, Harlan M. Krumholz, Raymond Y.K. Kwong, Michael J. Lim, Jane A. Linderbaum, Michael J. Mack, Mark A. Munger, Richard L. Prager, Joseph F. Sabik, Leslee J. Shaw, Joanna D. Sikkema, Craig R. Smith, Sidney C. Smith, John A. Spertus, Sankey V. Williams
Journal: Circulation (2012)
Quantitative Assessment of Pulmonary Edema
Authors: O. ROBERT LEVINE, ROBERT B. MELLINS, ALFRED P. FISHMAN
Journal: Circulation Research (1965)

The present study has attempted to establish a reliable method for distinguishing quantitatively between pulmonary engorgement and engorgement plus edema. Pulmonary engorgement was produced in intact, anesthetized dogs by inflating a balloon in the left atrium followed by saline hemodilution. Hemodynamic events monitored included left atrial and pulmonary arterial pressures, and the colloid osmotic pressure. Clinical criteria, such as the rate and frequency of breathing, the chest roentgenogram, and the presence of audible rales, failed to distinguish reliably between engorgement and edema. The mechanics of breathing were more severely altered by engorgement and edema than by engorgement alone, but considerable overlap was present. Determination of the pulmonary blood volume and the extravascular water space of the lungs, by means of simultaneous T-1824 and tritiated water dilution curves, as described by Chinard and Enns, was a reliable method of detecting and quantifying pulmonary edema. The water space measured by this technique averaged 3.5 ml/kg body wt in normal, anesthetized dogs. It correlated well with the total lung water content determined at autopsy, measuring a constant fraction (approximately 50%) of the total lung water content, even in the presence of severe pulmonary edema. According to the results of the present study, pulmonary edema could be predicted reliably at autopsy when the extra-vascular water space was 6.0 ml/kg of body wt or greater.
Extensive and fatal basal cell carcinoma: a report of three cases
Authors: C.B. KO, S. WALTON, K. KECZKES
Journal: British Journal of Dermatology (1992)

Journal Article Extensive and fatal basal cell carcinoma: a report of three cases Get access C.B. KO, C.B. KO Department of Dermatology, Hull Royal Infirmary, Hull, U.K. Search for other works by this author on: Oxford Academic Google Scholar S. WALTON, S. WALTON Department of Dermatology, Hull Royal Infirmary, Hull, U.K. Search for other works by this author on: Oxford Academic Google Scholar K. KECZKES K. KECZKES Department of Dermatology, Hull Royal Infirmary, Hull, U.K. Dr. K.Keczkes, Hull Royal Infirmary, Anlaby Road, Hull HU3 2JZ, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 127, Issue 2, 1 August 1992, Pages 164–167, https://doi.org/10.1111/j.1365-2133.1992.tb08050.x Published: 01 August 1992
Microfluidic-Based Multiplex qRT-PCR Identifies Diagnostic and Prognostic microRNA Signatures in the Sera of Prostate Cancer Patients
Authors: Felix Moltzahn, Adam B. Olshen, Lauren Baehner, Andrew Peek, Lawrence Fong, Hubert Stöppler, Jeffry Simko, Joan F. Hilton, Peter Carroll, Robert Blelloch
Journal: Cancer Research (2010)

Abstract Recent prostate-specific antigen–based screening trials indicate an urgent need for novel and noninvasive biomarker identification strategies to improve the prediction of prostate cancer behavior. Noncoding microRNAs (miRNA) in the serum and plasma have been shown to have potential as noninvasive markers for physiologic and pathologic conditions. To identify serum miRNAs that diagnose and correlate with the prognosis of prostate cancer, we developed a multiplex quantitative reverse transcription PCR method involving the purification of multiplex PCR products followed by uniplex analysis on a microfluidics chip to evaluate 384 human miRNAs. Using Dgcr8 and Dicer knockout (small RNA-deficient) mouse ES cells as the benchmark, we confirmed the validity of our technique and uncovered a considerable lack of accuracy in previously published methods. Profiling 48 sera from healthy men and untreated prostate cancer patients with differing CAPRA scores, we identified miRNA signatures that allow us to diagnose cancer patients and correlate with a prognosis. These serum signatures include oncogenic and tumor-suppressive miRNAs, suggesting functional roles in prostate cancer progression. Cancer Res; 71(2); 550–60. ©2010 AACR.
Basic mechanisms of development of airway structural changes in asthma
Authors: E. D. Fixman, A. Stewart, J. G. Martin
Journal: European Respiratory Journal (2007)

Airway remodelling is a complex process that involves all of the component tissues of the airway from the epithelium to the adventitia. Each of the changes has the potential to alter airway physiology so as to promote airway narrowing, hyperresponsiveness and inflammation. Structural changes, such as epithelial metaplasia, airway fibrosis and airway smooth muscle hyperplasia, have been successfully modelled in animals. These models are being extensively characterised and are providing valuable insights into mechanisms that are likely to be quite relevant to human asthma. Remodelling is induced by factors synthesised and secreted both by inflammatory cells and by structural cells, the latter frequently under the influence of the former. While information concerning the genesis of inflammation is abundant, the precise factors responsible for cellular hyperplasia, hypertrophy and altered matrix deposition are far from resolved. Elucidation of these factors will no doubt lead to novel therapies designed to prevent or reverse these changes.
Canakinumab Reduces The Risk Of Acute Gouty Arthritis Flares During Initiation Of Allopurinol Therapy: Results Of A Double-blind, Randomised Study
Authors: N. Schlesinger, E. Mysler, H. Lin, M. DeMeulenmeester, J. Rovensky, U. Arulmani, A. Balfour, G. Krammer, P. Sallstig, A. So
Journal: Journal of Allergy and Clinical Immunology (2011)
Can immunotherapy by gene transfer tip the balance against colorectal cancer?
Authors: S M TODRYK, H CHONG, R G VILE, H PANDHA, N R LEMOINE
Journal: Gut (1998)

Can immunotherapy by gene transfer tip the balance against colorectal cancer?Summary Gene therapy, in particular the transfer of genes encoding immunostimulatory molecules (cytokines and costimulatory molecules) as well as selectively cytotoxic enzymes and DNA vaccination, has the potential of enhancing cell mediated immune responses against tumours including those of colorectal origin.Genes can be transferred using viral vectors either to cultured tumour cells in vitro that can be returned to the patient as a "cancer vaccine", or directly to tumour cells in vivo.Vaccination with DNA constructs expressing specific tumour antigens characteristic of colorectal neoplasia can trigger immune recognition and destruction of tumour cells.The aim is to tip the balance from protumour to antitumour mechanisms by generating a local immune response and systemic antitumour immune memory to destroy metastases.Studies in murine models, combined with human studies, show that such approaches could become an adjunct to current treatments for human colorectal cancer in the near future.
Coxsackievirus B3 Induces T Regulatory Cells, Which Inhibit Cardiomyopathy in Tumor Necrosis Factor-α Transgenic Mice
Authors: Sally A. Huber, Arthur M. Feldman, Danielle Sartini
Journal: Circulation Research (2006)

Innate immunity promotes both the generation of autoimmunity and immunoregulation of adaptive immunity. Transgenic mice expressing the tumor necrosis factor-α (TNF-α) gene under the cardiac myosin promoter (TNF1.6 mice) develop dilated cardiomyopathy. Transgenic mice show extensive cardiac inflammation, suggesting that immunopathogenic mechanisms may promote cardiomyopathy. Two coxsackievirus B3 (CVB3) variants infect and replicate in the heart. H3 variant is highly myocarditic, but H310A1 variant activates CD4 + T regulatory cells, which protect against viral myocarditis. T-cell depletion of TNF1.6 mice using monoclonal anti-CD3 or anti-CD4 antibody significantly reduced heart size and plasma troponin I concentrations compared with control TNF1.6 mice. Cardiomyopathy in TNF1.6 mice correlates to a CD4 + Th1 response and autoimmune IgG2a antibodies. TNF1.6 mice infected with H310A1 virus reduced heart size and cardiac inflammation corresponding to the activation of CD4 + CD25 + FoxP3 + (T regulatory cells). Immunosuppression is dependent on IL-10 but not TGFβ. Adoptive transfer of the CD4 + CD25 + cells from H310A1-infected mice into uninfected TNF1.6 recipients abrogated cardiomyopathy. Exogenous administration of recombinant TNF-α to H310A1-infected mice for 4 days abrogated immunosuppression. Cardiac enlargement in TNF1.6 mice is partly attributable to T-cell activation and humoral autoimmunity caused by cytokine expression. T regulatory cells induced by H310A1 virus abrogate autoimmunity caused by TNF-α overexpression. H3 virus infection induces high levels of systemic TNF-α, whereas H310A1 virus does not. The low TNF-α response during H310A1 infections is likely responsible for the T regulatory cell response in these animals.