tbuckley/cabot-search huggingface dataset:
Effect of inhaled procaterol on cough receptor sensitivity to capsaicin in patients with asthma or chronic bronchitis and in normal subjects.
Authors: M Fujimura, S Sakamoto, Y Kamio, T Bando, K Kurashima, T Matsuda
Journal: Thorax (1993)

BACKGROUND--To evaluate the effect of inhaled beta 2 adrenergic agonists on the sensitivity of airway cough receptors, the effect of inhaled procaterol on cough induced by aerosolised capsaicin, a stimulant of C fibres, was studied in patients with asthma or chronic bronchitis and in normal subjects. METHOD--Eleven patients with asthma and 10 with chronic bronchitis and 14 normal subjects participated. Increasing concentrations of capsaicin solution were inhaled for 15 seconds by tidal breathing through the mouth at one minute intervals until five or more coughs were elicited, before and 30 minutes after inhalation of 20 micrograms procaterol or placebo (freon gas alone) through a metered dose inhaler. Cough threshold was defined as the lowest concentration of capsaicin that elicited five or more coughs. To evaluate the bronchodilator effect of procaterol and the bronchoconstrictor effect of inhaled capsaicin, forced expiratory volume in one second (FEV1) was measured before and one minute after a capsaicin provocation test. This test was carried out both before and 30 minutes after treatment with procaterol or placebo. RESULTS--The geometric mean value of cough threshold to capsaicin was significantly increased by procaterol and placebo in both groups of patients but not in the control subjects. The increment in the cough threshold was not significantly different between the treatments with procaterol and placebo in each group. FEV1 was significantly increased by procaterol but not by placebo in all three groups. CONCLUSIONS--Inhaled procaterol has no effect on airway cough receptor sensitivity to capsaicin. The attenuation of the cough sensitivity seen after inhalation of procaterol in patients with asthma and bronchitis may result from tachyphylaxis to capsaicin.
Tc-99m-Labeled Red Blood Cell Scan Showing Gastrointestinal Bleeding Point, and Also Showing an Incidental Hepatic Hemangioma
Authors: R.E Russell Taylor
Journal: Clinical Nuclear Medicine (2004)

Tc-99m-labeled red blood cell (RBC) scans can be used to characterize hepatic hemangiomas and to localize gastrointestinal bleeding points. A case is described of a patient who underwent a Tc-99m-labeled RBC scan for melena. The scan showed a bleeding point, and also an incidental hepatic hemangioma.
Modulation of Thin Filament Activation by Breakdown or Isoform Switching of Thin Filament Proteins
Authors: Steven B. Marston, Charles S. Redwood
Journal: Circulation Research (2003)

In the heart, the contractile apparatus is adapted to the specific demands of the organ for continuous rhythmic contraction. The specialized contractile properties of heart muscle are attributable to the expression of cardiac-specific isoforms of contractile proteins. This review describes the isoforms of the thin filament proteins actin and tropomyosin and the three troponin subunits found in human heart muscle, how the isoform profiles of these proteins change during development and disease, and the possible functional consequences of these changes. During development of the heart, there is a distinctive switch of isoform expression at or shortly after birth; however, during adult life, thin filament protein isoform composition seems to be stable despite protein turnover rates of 3 to 10 days. The pattern of isoforms of actin, tropomyosin, troponin I, troponin C, and troponin T is not affected by aging or heart disease (ischemia and dilated cardiomyopathy). The evidence for proteolysis of thin filament proteins in situ during ischemia and stunning is evaluated, and it is concluded that C-terminal cleavage of troponin I is a feature of irreversibly injured myocardium but may not play a role in reversible stunning.
Giant Lymph Node Hyperplasia Resembling Abdominal Abscess on Gallium Scan
Authors: H W WAHNER, J R GOELLNER, H C HOAGLAND
Journal: Clinical Nuclear Medicine (1978)

A case of giant lymph node hyperplasia with systemic symptoms resembling chronic infection is described which showed intense gallium uptake indistinguishable from uptake seen in an abscess. This rare syndrome may mimic an abdominal abscess and should be considered in the differential diagnosis of patients without prior history of abdominal surgery and in whom an abdominal abscess is suspected. The condition is relatively benign.
Effects of calcium mediated secretagogues on the growth of pancreatic acinar cells in vitro.
Authors: C D Logsdon
Journal: Gut (1987)

Caerulein, CCK8, and gastrin, hormones which interact with the cholecystokinin receptor increased the growth of mouse pancreatic acinar cells in vitro. In contrast, bombesin, substance P, and carbachol, factors which interact with separate receptors, and stimulate pancreatic secretion similarly to CCK by mobilising intracellular Ca2+, did not have any effect on the growth of pancreatic acinar cells in vitro. These results suggest both a unique role for cholecystokinin in the physiological regulation of the pancreas and that the mechanisms that mediate the trophic effects of cholecystokinin are different from those that mediate secretion.
Functional Upregulation of the Vascular Endothelial Growth Factor Receptor KDR by Hypoxia
Authors: Johannes Waltenberger, Ulrike Mayr, Siegwald Pentz, Vinzenz Hombach
Journal: Circulation (1996)

Background Vascular endothelial growth factor (VEGF) is a specific endothelial mitogen and chemoattractant that has been shown to be useful for inducing therapeutic angiogenesis in ischemic myocardium and found to stimulate mitogenicity and chemotaxis of endothelial cells through the receptor tyrosine kinase KDR. Although VEGF expression is upregulated by hypoxic stimuli, regulation of KDR remained unknown under these conditions. Methods and Results With the use of human umbilical vein endothelial cells and transfected porcine aortic endothelial cells, KDR protein was found to be upregulated under hypoxic conditions (2% O 2 ) in both cell types. This process of KDR upregulation was found to be reversible, was maximal after 24 hours of hypoxia, and was regulated on a posttranscriptional level. Furthermore, the susceptibility for VEGF-induced mitogenicity was enhanced under hypoxic conditions as shown by [ 3 H]-thymidine incorporation assay. The activated state of increased VEGF function in hypoxic endothelial cells was associated with elevated tyrosine phosphorylation of KDR as demonstrated by anti-phosphotyrosine blot. Conclusions These data indicate that hypoxia stimulates VEGF-dependent signaling not only by upregulation of VEGF ligand but also by functional upregulation of a specific signaling receptor. Therefore, these data provide evidence that the endothelium plays an active role in hypoxia-induced angiogenesis.
Serum IgG, IgM, and IgA levels in ankylosing spondylitis.
Authors: E M Veys, M van Leare
Journal: Annals of the Rheumatic Diseases (1973)

Using immunoelectrophoresis, Mackiewicz and Fenrych (1961) found broader and more intense IgM precipitation lines in sera from patients with ankylosing spondylitis (AS).Kriegel, Burger, Kapp, and Alexopulos (1969) determined Ig levels in AS by single-radial immuno- diffusion (Mancini, Vaerman, Carbonara, and Heremans, 1964) and reported a rise of the IgA level.Using the same technique, Langness, Banavsky, Alexopulos, Kriegel, and Burger (1971) found increased IgG and IgA serum levels in patients with AS.These authors did not consider the frequency distribution of the results nor the age distribution of the groups investigated.We have determined the IgG, IgM, and IgA con- centration in AS with the linear plate immuno- diffusion technique (Wieme and Veys, 1970; Veys, 1971), and have compared the results with the Ig levels found in a normal population (Veys, Wieme, and Vuylsteek, in press) and in patients with rheuma- toid arthritis (Veys, 1971).The patients with AS were then subdivided into groups to look for correlations between Ig levels and duration and activity of the disease.
Abstract 1732: DNA methylation profiling defines clinically relevant biological subsets of non-small cell lung cancer
Authors: Kim Walter, Thomas Holcomb, Tom Januario, Pan Du, Garret M. Hampton, Lukas C. Amler, Robert L. Yauch, Richard Bourgon, David S. Shames
Journal: Cancer Research (2012)

Abstract Purpose: Non-small cell lung cancers (NSCLC) comprise multiple distinct biological groups with different prognoses. For example, patients with epithelial-like (EL) tumors have a better prognosis and exhibit greater sensitivity to inhibitors of the epidermal growth factor receptor (EGFR) pathway than patients with mesenchymal-like (ML) tumors. Here we test the hypothesis that EL NSCLCs can be distinguished from ML NSCLCs on the basis of global DNA methylation patterns. Experimental Design: To determine whether phenotypic subsets of NSCLC can be defined based on their DNA methylation patterns, we combined microfluidics-based gene expression analysis and genome-wide methylation profiling. We derived robust classifiers for both gene expression and methylation in cell lines and tested these classifiers in surgically resected NSCLC tumors. We validate our approach using quantitative RT-PCR and methylation specific PCR in formalin-fixed biopsies from NSCLC patients who went on to fail front-line chemotherapy. Results: We show that patterns of methylation divide NSCLCs into EL and ML subsets as defined by gene expression and that these signatures are similarly correlated in NSCLC cell lines and tumors. We show that DNA methylation differences predict EL or ML phenotypes NSCLC cell lines, surgically resected tumors, and formalin-fixed biopsies from NSCLC patients who went on to fail front-line chemotherapy. Conclusions: Our data demonstrate that patterns of DNA methylation can divide non-small lung cancers into two phenotypically distinct subtypes of tumors and provide proof of principle that differences in DNA methylation can be used as a platform for predictive biomarker discovery and development. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1732. doi:1538-7445.AM2012-1732
IMPROVEMENT OF LONGITUDINAL LEFT VENTRICULAR STRAIN IS ASSOCIATED WITH LEFT ATRIAL STRAIN ENHANCEMENT AFTER PULMONARY-VEIN ISOLATION FOR ATRIAL FIBRILLATION
Authors: Jun Koyama, Hirohiko Motoki, Kazunori Aizawa, Megumi Koshikawa, Hiroki Kasai, Atsushi Izawa, Takeshi Tomita, Yusuke Miyashita, Setsuo Kumazaki, Uichi Ikeda
Journal: Journal of the American College of Cardiology (2010)
Rifampin-Amphotericin B Synergism?
Authors: L. FRED AYVAZIAN
Journal: Annals of Internal Medicine (1976)

Comments1 October 1976Rifampin-Amphotericin B Synergism?L. FRED AYVAZIAN, M.D., F.A.C.P.L. FRED AYVAZIAN, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-85-4-539_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I have read with interest the "Drugs Five Years Later" paper on rifampin by Dr. Sanders in the July 1976 issue (Ann Intern Med 85:82-86, 1976). With reference to his perhaps incomplete statements regarding the use of rifampin with amphotericin B in the treatment of fungal diseases in man, I wish to call attention to a paper from our group. The point made in the last sentence of the abstract (excerpted below) of that paper may be pertinent to use of rifampin:A case of disseminated histoplasmosis resembling miliary tuberculosis is reported from a geographic area in... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: L. FRED AYVAZIAN, M.D., F.A.C.P. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byClinical Use of Rifampicin in Combination for Non-Mycobacterial Infections: A Survey of Published Evidence 1 October 1976Volume 85, Issue 4Page: 539-539KeywordsAmphotericinDrugsFungal diseasesGeographic areasHistoplasmosisMiliary tuberculosis ePublished: 1 December 2008 Issue Published: 1 October 1976 PDF downloadLoading ...
Blood Pressure Response During Treadmill Testing as a Risk Factor for New-Onset Hypertension
Authors: Jagmeet P. Singh, Martin G. Larson, Teri A. Manolio, Christopher J. O’Donnell, Michael Lauer, Jane C. Evans, Daniel Levy
Journal: Circulation (1999)

Although systolic blood pressure (SBP) response to exercise has been shown to predict subsequent hypertension in small samples of men, this association has not been studied in a large population-based sample of middle-aged men and women. The purpose of this study was to examine, in normotensive subjects, the relations of SBP and diastolic blood pressure (DBP) during the exercise and recovery periods of a graded treadmill test to the risk of developing new-onset hypertension.BP data from exercise testing in 1026 men and 1284 women (mean age, 42+/-10 years; range, 20 to 69 years) from the Framingham Offspring Study who were normotensive at baseline were related to the incidence of hypertension 8 years later. New-onset hypertension, defined as an SBP >/=140 mm Hg or DBP >/=90 mm Hg or the initiation of antihypertensive drug treatment, occurred in 228 men (22%) and 207 women (16%). Exaggerated SBP (Ex-SBP 2) and DBP (Ex-DBP 2) response and delayed recovery of SBP (R-SBP 3) and DBP (R-DBP 3) were defined as an age-adjusted BP greater than the 95th percentile during the second stage of exercise and third minute of recovery, respectively. After multivariable adjustment, Ex-DBP 2 was highly predictive of incident hypertension in both men (OR, 4.16; 95% CI, 2.15, 8.05) and women (OR, 2.17; CI, 1.19, 3.96). R-SBP 3 was predictive of hypertension in men in a multivariable model that included exercise duration and peak exercise BP (OR, 1.92; CI, 1.00, 3.69). Baseline resting SBP (chi2, 23.4 in men and 34.7 in women) and DBP (chi2, 11.3 in men and 13.1 in women) had stronger associations with new-onset hypertension than exercise DBP (chi2, 16.4 in men and 6.1 in women) and recovery SBP (chi2, 6.5 in men and 2.1 in women) responses.An exaggerated DBP response to exercise was predictive of risk for new-onset hypertension in normotensive men and women. An elevated recovery SBP was predictive of hypertension in men. These findings may reflect subtle pathophysiological features in the preclinical stage of hypertension.
Diuretic Therapy and Response of Essential Hypertension to Saralasin
Authors: GUNNAR H. ANDERSON
Journal: Annals of Internal Medicine (1977)

Thirty-four patients, most with a low-renin "essential" hypertension, and seven normal subjects were placed on diuretic therapy for 4 to 5 weeks. In the normal subjects, infusion of a highly specific, competitive angiotensin II analogue (1-sar-8-ala-angiotensin II, saralasin) did not significantly change recumbent blood pressure either before or after diuretic administration. In contrast, the hypertensive patients as a group had a low stimulated plasma renin activity before diuretic therapy and a rise in blood pressure during saralasin infusion. After therapy, the stimulated plasma renin activity was higher and saralasin produced a fall in blood pressure in some patients who were still hypertensive. The results suggest that short-term diuretic therapy, which is thought to act through its natriuretic effects, can convert some patients with essential hypertension, many with a low or a low-normal stimulated plasma renin activity, to individuals whose hypertension is supported by angiotensin II. The fall in blood pressure to saralasin infusion after diuretic therapy was directly proportional to the height to which diuretics elevated the stimulated plasma renin activity.
Effect of Amphotericin B on the Permeability of the Toad Bladder*
Authors: Norman S. Lichtenstein, Alexander Leaf
Journal: Journal of Clinical Investigation (1965)

Neurohypophyseal hormones have been found to induce large net transfers of water across various transporting epithelia from anurans while the low permeability of these tissues to small solute mole- cules is retained.Since the water is considered to move in bulk through aqueous channels in such circumstances (1, 2), an explanation has been needed to account for the concomitant low perme- ability of these channels to small hydrophilic sol- utes.Andersen and Ussing (3) postulated the existence of a double series permeability barrier to account for this discrepancy in toad skin, and this concept has been extended to the toad bladder (4).A homogeneous outer diffusion barrier, highly permeable to water but of low permeability to most hydrophilic solutes, is considered to overlie a deeper porous barrier in which the porosity is in- creased by neurohypophyseal hormones.Since water crosses the diffusion barrier readily, changes in the porous layer will determine the character- istics of net water transport.The penetration of the bladder by small solute molecules, effectively blocked at the outer diffusion barrier, is unaffected by hormonally induced changes in the porous layer.It became apparent that these considerations could not be restricted to water alone, on the one hand, and to all solutes, on the other, because the permeability of the toad bladder to urea and a small group of related, uncharged amides was found to be markedly enhanced by neurohypo- physeal hormones (4, 5).These hormones also specifically stimulate the active transport of sodium *
Pituitary imaging is essential for women with moderate hyperprolactinaemia.
Authors: P M Stewart, S Maheshwaran, J Griffith, J Li, M C Sheppard, J Olliff, J A Franklyn
Journal: BMJ (1993)

Case 2A 32 year old Asian man presented with a three week history of poor appetite, weight loss, diarrhoea, sweating, tremor of the hands, and paraesthesia in the extremities and face.Symptoms developed four weeks after treatment for eczema had been started by the same hakim who had treated the first patient.On examination the patient was anxious, flushed, tachycardic, and hypertensive, with a fine tremor of the outstretched hands.Neurological examination showed reduced pinprick sensation in both feet.Standard laboratory investigations, including thyroid function tests, all gave normal findings.Mercury poisoning was confirmed by a urinary mercury concen- tration of 105 ,ug/l (normal < 10 ,ug/l, toxic concen- tration > 100 ,ug/l) 12 weeks after the last exposure to the ethnic remedies.Analysis of the handmade red- brown pills which the hakim had prescribed at a dose of six daily showed each to contain 30-42 mg of inorganic mercuric sulphide (table).
Abstract 3110: Targeting the Wnt/PCP signaling through ROCK: A new neuroblastoma drug target
Authors: Cecilia Dyberg, David Forsberg, Panos Papachristou, Jessika Lannerholm-Palm, Bjorn Helge Haug, Baldur Sveinbjörnsson, Hugo Lagercrantz, Per Kogner, John inge Johnsen, Malin Wickstrom
Journal: Cancer Research (2014)

Abstract Background: The non-canonical Wnt/planar cell polarity (PCP) pathway regulates cytoskeletal organization, migration and neuritogenesis. Signaling is characterized by activation of the GTPases Rho and Rac, and the downstream Rho-associated protein kinases (ROCKs). Neuroblastoma is a malignant embryonal tumor of the sympathetic nervous systems, often with poor prognosis. The need for novel therapeutic approaches is great. Genetic analyses have revealed mutations and aberrations in the regulators Rho/Rac in neuroblastoma. The aim of this study was to characterize the Wnt/PCP signaling and the effects of ROCK inhibition in neuroblastoma. Methods: Cytotoxic activity of ROCK inhibitors was studied in cell viability assays. Morphology and invasion were studied with microscopy. The molecular mechanisms were characterized using cell- and molecular biology techniques. In vivo studies in mice were carried out to validate the therapeutic effects and toxicity. Results: Several mediators in the pathway were differentially expressed in cell lines and patient samples. Using compounds blocking ROCK1 and ROCK2 activity revealed that the ROCK2 inhibitor HA-1077 effectively repressed proliferation and reduced cell viability in neuroblastoma. Additionally, HA-1077 inhibited migration and induced differentiation through initiating neural outgrowth. Furthermore, HA-1077 reduced the growth of established neuroblastoma xenografts in nude mice. Conclusions: These results suggest that non-canonical Wnt signaling in general and ROCK in particular is a promising new therapeutic target for high-risk neuroblastoma. Citation Format: Cecilia Dyberg, David Forsberg, Panos Papachristou, Jessika Lannerholm-Palm, Bjorn Helge Haug, Baldur Sveinbjörnsson, Hugo Lagercrantz, Per Kogner, John inge Johnsen, Malin Wickstrom. Targeting the Wnt/PCP signaling through ROCK: A new neuroblastoma drug target. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3110. doi:10.1158/1538-7445.AM2014-3110
Idiopathic Pulmonary Fibrosis — A Sticky Business
Authors: Richard C. Boucher
Journal: New England Journal of Medicine (2011)

Pulmonary fibrosis comprises a spectrum of disease phenotypes, including familial and idiopathic forms. Current research suggests that pulmonary fibrosis is a “two-hit” disease: a genetic predisposition to abnormal alveolar epithelial-cell regulation of the cell cycle and apoptosis combined with environmental stressors, including exposure to known fibrogenic materials (e.g., asbestos, silica, and cigarette smoke).1 Indeed, the identification of mutations in genes expressed in alveolar epithelia in association with pulmonary fibrosis — such as the surfactant proteins A and C (SPA and SPC, respectively)2,3 — and genes associated with cell stability — such as telomerase4 (hTERT and hTER) . . .
Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase-Derived Superoxide and Vascular Endothelial Dysfunction in Human Heart Failure
Authors: Rafał Dworakowski, Simon Walker, Aziz Momin, Jatin Desai, Ahmed El-Gamel, Olaf Wendler, Mark T. Kearney, Ajay M. Shah
Journal: Journal of the American College of Cardiology (2008)
Sphingosine Kinase 2 Promotes Acute Lymphoblastic Leukemia by Enhancing <i>MYC</i> Expression
Authors: Craig T. Wallington-Beddoe, Jason A. Powell, Daochen Tong, Stuart M. Pitson, Kenneth F. Bradstock, Linda J. Bendall
Journal: Cancer Research (2014)

Sphingosine kinase 2 (SK2) may have utility as a prognostic marker in inflammatory diseases such as cancer in which it has been rationalized as a candidate therapeutic target. Here, we show that SK2 has an oncogenic role in acute lymphoblastic leukemia (ALL) by influencing expression of MYC. Genetic ablation of SK2 impaired leukemia development in a mouse model of ALL and pharmacologic inhibition extended survival in mouse xenograft models of human disease. SK2 attenuation in both the settings reduced MYC expression in leukemic cells, with reduced levels of acetylated histone H3 within the MYC gene associated with reduced levels of MYC protein and expression of MYC-regulated genes. Our results demonstrated that SK2 regulates MYC, which has a pivotal role in hematologic malignancies, providing a preclinical proof of concept for this pathway as a broad-based therapeutic target in this setting.