tbuckley/cabot-search huggingface dataset:
Cigarette smoke induces interleukin-8 release from human bronchial epithelial cells.
Authors: T Mio, D J Romberger, A B Thompson, R A Robbins, A Heires, S I Rennard
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Cigarette smoking causes the development of chronic bronchitis and chronic obstructive pulmonary disease. We hypothesized that exposure to cigarette smoke might initiate release of inflammatory mediators by bronchial epithelial cells. To evaluate this, the effect of cigarette smoke extract (CSE) on IL-8 release from cultured human bronchial epithelial cells was examined. CSE augmented IL-8 release from bronchial epithelial cells in a concentration- and time-dependent manner. Most of the augmenting activity of CSE on IL-8 release from bronchial epithelial cells was lost after volatilization or lyophilization treatment. Two major volatile factors in cigarette smoke, acrolein and acetaldehyde, augmented IL-8 release. Four cell strains were tested and showed increased IL-8 release in response to CSE. In addition, bronchoalveolar lavage was performed on 11 nonsmokers and 12 smokers. IL-8 concentration was greater in the proximal, bronchial samples than in distal, alveolar samples, and IL-8 in BAL from smokers was higher than in BAL from nonsmokers. There was a significant correlation between IL-8 concentration and neutrophil count in bronchial samples of BAL fluid. These data support the hypothesis that exposure to cigarette smoke may induce bronchial epithelial cells to release IL-8 and that this may contribute to airway inflammation in smokers.
Correction: "Leukocytoblastic" for "Leukocytoclastic;" "Farmington" for "Hartford"
Authors: Henry Schneiderman
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 February 1983Correction: "Leukocytoblastic" for "Leukocytoclastic;" "Farmington" for "Hartford"HENRY SCHNEIDERMAN, M.D.HENRY SCHNEIDERMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-98-2-262_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the November 1982 issue, in the letter by Cordonnier and associates (1), the adjective "leukocytoclastic" is misprinted four times as "leukocytoblastic," a neologism. Both the context of the letter and the references cited confirm this; the term describes the breakdown products of neutrophils (leukocytoclasis) seen pathologically.Also, the University of Connecticut Health Center (2) is located in Farmington, not Hartford, Connecticut....References1. CORDONNIERROUJEAUVERNANTMATHERONGANEM CJJSG. Cancer chemotherapy and acral erythema [Letter]. Ann Intern Med. 1982;97:783. LinkGoogle Scholar2. SCHNEIDERMANROBERT HN. Cancer chemotherapy and acral erythema [Letter]. Ann Intern Med. 1982;97:783. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 February 1983Volume 98, Issue 2Page: 262-262KeywordsNeutrophils ePublished: 1 December 2008 Issue Published: 1 February 1983 PDF downloadLoading ...
Factors influencing non-approval of new drugs in Europe
Authors: Michelle Putzeist, Aukje K. Mantel-Teeuwisse, Bo Aronsson, Malcolm Rowland, Christine C. Gispen-de Wied, Spiros Vamvakas, Arno W. Hoes, Hubert G. M. Leufkens, Hans-Georg Eichler
Journal: Nature Reviews Drug Discovery (2012)
Decreased Level of Vascular Endothelial Growth Factor in Bronchoalveolar Lavage Fluid of Normal Smokers and Patients with Pulmonary Fibrosis
Authors: Sekiya Koyama, Etsuro Sato, Masayuki Haniuda, Hiroki Numanami, Sonoko Nagai, Takateru Izumi
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Vascular endothelial growth factor (VEGF) plays multifunctional roles in both the development of vasculature and the maintenance of vascular function. A decrease in VEGF reduces angiogenesis and induces apoptosis of vascular endothelial cells. Inhibition of the VEGF receptor causes endothelial cell apoptosis and emphysema. We postulated that VEGF concentrations might be reduced in patients with chronic lung diseases. The level of VEGF was evaluated by enzyme-liked immunosorbant assay in bronchoalveolar lavage fluid (BALF) from normal smokers, nonsmoking volunteers, idiopathic pulmonary fibrosis, pulmonary fibrosis associated with a connective tissue disease, and sarcoidosis. The isoforms of VEGF in BALF were determined by high-performance liquid chromatography. VEGF in nonsmoking volunteers was detectable at a high concentration. In contrast, VEGF in most of the normal smokers was below the detectable limit. The VEGF found in nonsmoking volunteers BALF was VEGF165. VEGF was significantly decreased in idiopathic pulmonary fibrosis, pulmonary fibrosis associated with a connective tissue disease, and sarcoidosis compared with nonsmoking volunteers. The smoking patients showed a further decrease in VEGF. These data suggest that the decrease in VEGF in smokers and patients with chronic lung diseases may reduce angiogenesis and induce apoptosis of vascular endothelial cells.
Deadly Dust: Silicosis and the Politics of Occupational Disease in Twentieth-Century America
Authors: Robert N. Proctor
Journal: JAMA (1992)

ABSTRACT Dust-induced diseases have been recognized since antiquity: medieval lapidaries died of them, as did countless miners, stonecutters, and metal polishers. With the development of steamand, later, gasoline-powered machinery early in the 20th century, however, workers in such trades were exposed to dramatically increased levels of dust. The result was a minor epidemic of dustinduced diseases, notably silicosis, that aroused both popular and medical attention in the 1920s and 1930s.Rosner and Markowitz have produced a carefully crafted history of the rise and fall of this occupational disease, focusing especially on the political forces behind changing disease definitions. The central thesis is that silicosis, a disease prominent in 1930s medical literature and public consciousness, essentially disappeared from both realms in the 1950s, not just because fewer people were suffering from it, but also because industry and allied interests were able to monopolize definition of the hazard.Silicosis was recognized as a
Protein metabolism in inflammatory bowel disease.
Authors: J Powell-Tuck
Journal: Gut (1986)

Major loss of body protein mass in inflammatory bowel disease is much less common than weight loss, which is often attributable to losses of other body, particularly water and fat. It does occur, however, in a few patients, especially in those with compromised food intake. It is due principally to the combined effects of diminished intake and excessive intestinal losses of amino nitrogen. Nitrogen metabolism is influenced not only by protein nutritional state and net nitrogen intake but also by disease activity. There is some evidence for abnormally low secretion of growth hormone in adolescents with inflammatory bowel disease and growth failure. Low serum albumin concentrations are not necessarily related to protein undernutrition and are the combined result of relatively reduced albumin synthesis, increased intestinal losses, and maldistribution between intravascular and extravascular spaces. Concentrations in the plasma of IgG and acute phase reactants may be raised despite increased losses into the bowel lumen. The prevention of total body protein depletion is achieved principally by maintaining adequate and often not supranormal intakes of a balanced source of amino nitrogen in a balanced diet given orally, enterally, or parenterally, combined with a medical or surgical approach to reduce disease activity: supranormal energy intakes are not beneficial.
Role of Deformation-induced Lipid Trafficking in the Prevention of Plasma Membrane Stress Failure
Authors: Nicholas E. Vlahakis, Mark A. Schroeder, Richard E. Pagano, Rolf D. Hubmayr
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Cells experience plasma membrane stress failure when the matrix to which they adhere undergoes large deformations. In the lung, such a mechanism might explain mechanical ventilation-associated cell injury. We have previously shown that in alveolar epithelial cells, deformation induces lipid trafficking to the plasma membrane, thereby accommodating the required increase in the cell surface area. We now show that cell wounding is strain amplitude and rate dependent and that under conditions of impaired exocytosis strain-induced cell wounding is significantly increased. In addition, the susceptibility of cells to mechanical injury was not correlated with changes in cell stiffness. Using a dual-labeling technique, we differentiated between cell populations that were reversibly and irreversibly injured and showed that interventions that impair deformation-induced lipid trafficking also reduce the likelihood of plasma membrane resealing. Our findings suggest that cell plasticity and remodeling responses such as deformation-induced lipid trafficking are more important for cytoprotection from strain injury than are the innate mechanical properties of the cell. We also conclude that in deformation experiments, tests of cell membrane integrity cannot be interpreted as tests of cell viability because an intact plasma membrane after deformation does not mean that no injury had occurred.
Histamine regulation of biliary proliferation
Authors: Heather Francis, Fanyin Meng, Eugenio Gaudio, Gianfranco Alpini
Journal: Journal of Hepatology (2012)

Cholangiocytes, which line the biliary epithelium, are hormone-responsive and responsible for the modification of canalicular bile before reaching the duodenum. Cholangiocytes are the target cells in cholangiopathies such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) that are characterized by cholangiocyte proliferation/loss [1]. The biliary epithelium is morphologically and functionally heterogeneous and is lined by small (<15μm in diameter) and large (>15μm in diameter) cholangiocytes lining small and large bile ducts, respectively [2].
Lancet retracts Wakefield's MMR paper
Authors: C. Dyer
Journal: BMJ (2010)

The Lancet has retracted the 12 year old paper that sparked an international crisis of confidence in the safety of the measles, mumps, and rubella (MMR) vaccine when its lead author suggested a link between the vaccine and autism.

Andrew Wakefield was found guilty by the General Medical Council last week of dishonesty and flouting ethics protocols. 

The UK regulator held that Dr Wakefield abused his position, subjected children to intrusive procedures such as lumbar puncture and colonoscopy that were not clinically indicated, carried out research that breached the conditions of ethics committee approval, and brought the medical profession into disrepute.

In a statement published online (www.thelancet.com) the editors of the Lancet said: “Following the judgment of the UK General Medical Council’s Fitness to Practise Panel on Jan 28, 2010, it has become clear that several elements of the 1998 paper by Wakefield et al are incorrect, contrary to the findings of an earlier investigation.

“In particular, the claims in the original paper that children were ‘consecutively referred’ and that investigations were ‘approved’ by the local ethics committee have been …
Lead Levels and Ischemic Heart Disease in a Prospective Study of Middle-Aged and Elderly Men: the VA Normative Aging Study
Authors: Nitin B. Jain, Vijayalakshmi Potula, Joel Schwartz, Pantel S. Vokonas, David Sparrow, Robert O. Wright, Huiling Nie, Howard Hu
Journal: Environmental Health Perspectives (2007)

Lead exposure has been associated with higher blood pressure, hypertension, electrocardiogram abnormalities, and increased mortality from circulatory causes.We assessed the association between bone lead-a more accurate biomarker of chronic lead exposure than blood lead-and risk for future ischemic heart disease (IHD).In a prospective cohort study (VA Normative Aging Study), 837 men who underwent blood or bone lead measurements at baseline were followed-up for an ischemic heart disease event between 1 September 1991 and 31 December 2001. IHD was defined as either a diagnosis of myocardial infarction or angina pectoris that was confirmed by a cardiologist. Events of fatal myocardial infarction were assessed from death certificates.An IHD event occurred in 83 cases (70 nonfatal and 13 fatal). The mean blood, tibia, and patella lead levels were higher in IHD cases than in noncases. In multivariate Cox-proportional hazards models, one standard deviation increase in blood lead level was associated with a 1.27 (95% confidence interval, 1.01-1.59) fold greater risk for ischemic heart disease. Similarly, a one standard deviation increase in patella and tibia lead levels was associated with greater risk for IHD (hazard ratio for patella lead = 1.29; 95% confidence interval, 1.02-1.62).Men with increased blood and bone lead levels were at increased risk for future IHD. Although the pathogenesis of IHD is multifactorial, lead exposure may be one of the risk factors.
Termination of Implantable Pacemaker Therapy: Experience in Five Patients
Authors: Demosthenes Iskos
Journal: Annals of Internal Medicine (1997)

Background: Established guidelines direct the initial implantation of permanent pacemakers. Elective replacement of these devices is common. However, no guidelines exist for the removal of permanent pacemakers and the termination of long-term cardiac pacing. Objective: To describe the feasibility and safety of terminating cardiac pacing in carefully selected patients. Design: Case series. Setting: University hospital. Patients: Five adults with permanent pacemakers who were referred for pacemaker replacement or a complication related to cardiac pacing. All patients showed alleviation or reversal of the electric disturbance that originally led to the implantation of the device. The patients had received a pacemaker for a class I or II indication (that is, symptomatic bradycardia or asymptomatic, persistent third-degree atrioventricular block at the level of the atrioventricular node). Intervention: After an appropriate natural rhythm was documented, pacemakers were removed from all patients. Measurements: Time without recurrence of symptomatic bradycardia. Results: No patient had recurrent symptomatic bradycardia after 18 to 48 months of clinical follow-up. Conclusions: The presence of a permanent pacemaker does not necessarily imply a permanent need for cardiac pacing. Discontinuation of cardiac pacing may be considered in certain patients. Establishing consensus criteria about the potential indications, methods, and timing of the termination of cardiac pacing seems appropriate.
The effect of left ventricular systolic function on maximal aerobic exercise capacity in asymptomatic patients with coronary artery disease.
Authors: A A Ehsani, D Biello, D R Seals, M B Austin, J Schultz
Journal: Circulation (1984)

The purpose of this study was to examine the relationship between maximal O2 uptake (VO2max) and left ventricular systolic function in patients with coronary artery disease. We studied 27 patients, age 50 +/- 10 years (mean +/- SD), who were asymptomatic and able to attain true VO2max. VO2max was defined by the leveling-off criterion and/or a respiratory exchange ratio of 1.15 or greater. Left ventricular ejection fraction was determined by gated cardiac blood pool imaging. In patients whose ejection fraction decreased with exercise, VO2max was 21 +/- 4 vs 27 +/- 4 ml/kg/min in those whose ejection fraction increased (p less than .001). Systolic blood pressure/end-systolic volume relation was shifted upward and to the right in the former group in response to peak exercise. In contrast, the pressure-volume relation was shifted upward and to the left in patients whose ejection fraction increased with exercise. Ejection fraction at rest did not correlate with VO2max. There was a significant but weak correlation between peak exercise ejection fraction and VO2max (r = .43, p less than .025). Left ventricular exercise reserve, i.e., the change in ejection fraction from rest to exercise, correlated with VO2max (r = .77, p less than .0002), maximal O2 pulse (r = .50, p less than .005), and maximal heart rate during treadmill exercise (r = .61, p less than .001). Maximal heart rate during treadmill exercise correlated with VO2max (r = .70, p less than .0002).(ABSTRACT TRUNCATED AT 250 WORDS)
Life events and breast cancer prognosis.
Authors: A. J. Ramirez, J. P. Watson, M. A. Richards, I. S. Fentiman, W. M. Gregory, R. D. Rubens, T. J. Craig
Journal: BMJ (1992)

referred to in the personal communication to Swedberg, but in our trial withdrawals for this reason were according to prespecified criteria and in line with usual clinical practice.The size of our trial was indeed based on a comparison of active with placebo treatment, but, as we pointed out, an assessment of the two active agents was an important secondary objective from the outset.The advantage of the diuretic over the 3 blocker was clear, particularly for coronary events, and is also suggested by other recent results.' Swedberg is surely not suggesting that findings of such immediate clinical relevance should remain unreported.
EVALUATION OF INSTENT NEOINTIMAL TISSUE COMPONENT USING INTEGRATED BACKSCATTER INTRAVASCULAR ULTRASOUND - COMPARISON OF DRUG-ELUTING STENTS AND BARE-METAL STENTS -
Authors: Shinjo Sonoda, Yoshitaka Muraoka, Yuki Tsuda, Seiya Tanaka, Masahiro Okazaki, Yutaka Otsuji
Journal: Journal of the American College of Cardiology (2010)
A 2-step approach to myeloablative haploidentical stem cell transplantation: a phase 1/2 trial performed with optimized T-cell dosing
Authors: Dolores Grosso, Matthew Carabasi, Joanne Filicko-O'Hara, Margaret Kasner, John L. Wagner, Beth Colombe, Patricia Cornett Farley, William O'Hara, Phyllis Flomenberg, Maria Werner-Wasik, Janet Brunner, Bijoyesh Mookerjee, Terry Hyslop, Mark Weiss, Neal Flomenberg
Journal: Blood (2011)
Abstract 4914: Methylation profiling of CpG islands in multiple drug resistant cell line
Authors: Tsai-Hsien Hung, Chih-Jie Shen, Chuan-Mu Chen, Kowit Yu Chong
Journal: Cancer Research (2010)

Abstract Multiple drug resistance (MDR) is a major issue to attenuate the effectiveness of chemotherapy to many human malignancies. Despite extensively investigation, MDR inhibitors have been discovered serve side effect. Recently, scientists have reported that proteasome inhibitor, Bertezomib (PS-341), induced apoptosis in a variety of cancer cells and recognized as a novel anticancer therapy approach. Previous study revealed that bertezomib inhibits DNA methyltransferase and led to DNA hypomethylation in myeloid leukemia. Despite its success, some patients are resistant to ongoing proteasome inhibitor treatment. These reports suggested that chemoresistant cell line may develop a novel mechanism to against proteasome inhibitor. To verify the hypothesis, we used human CpG island microarray to indentify epigenetic change and genes expression profile in parental human uterus sarcoma cell line (MES-SA) and MES-SA variant drug resistant cell line (Dx5-C5) Our data has shown that the global genes were hypomethylated in both PS-341 treated MES-SA and Dx5-C5 cell line. Furthermore, the Wnt signalling pathway and cell cycle related gene have significant altered in DNA methylation pattern of Dx5-C5. In summary, our study demonstrated that the cell cycle related gene(s) and upstream gene(s) of Wnt pathway altered its DNA methylation pattern and mRNA expression level in MDR cell line. These data may help us to develop a new strategy for treatment of multiple drug resistance cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4914.
Circulating and tissue endothelin immunoreactivity in hypercholesterolemic pigs.
Authors: A Lerman, M W Webster, J H Chesebro, W D Edwards, C M Wei, V Fuster, J C Burnett
Journal: Circulation (1993)

BACKGROUND Hypercholesterolemia is characterized by a coronary vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. This abnormality may be due to reduced synthesis of endothelium-derived relaxing factor and/or enhanced synthesis and release of an endothelium-derived contracting factor. Endothelin is an endothelium-derived vasoconstrictor and mitogenic peptide that is present in normal plasma, and its circulating concentrations are elevated in disease states that are characterized by abnormal endothelium-dependent relaxation to acetylcholine. The current studies were designed to test the hypotheses that experimental hypercholesterolemia results in elevation of plasma and tissue endothelin immunoreactivity and that the abnormal acetylcholine-evoked coronary vasoconstriction in the hypercholesterolemic animals is associated with further elevation of plasma endothelin. METHODS AND RESULTS Plasma concentrations and molecular forms of endothelin immunoreactivity were determined following 2% cholesterol diet for 4 months in pigs and during intracoronary acetylcholine administration. Second, we assessed the presence of endothelin in the coronary vascular wall by using immunohistochemistry. Hypercholesterolemia elevated plasma endothelin concentration and enhanced coronary artery tissue endothelin immunoreactivity. The endothelium-dependent vasodilator acetylcholine further increases plasma endothelin in hypercholesterolemia in association with coronary vasoconstriction. The predominant molecular form of endothelin in hypercholesterolemia is the biological active endothelin-1. CONCLUSIONS This study suggests a role for endothelin as an early participant and a marker for the endothelial dysfunction in hypercholesterolemia as well as a participant in the atherogenic process.
Amoxicillin-induced exanthema in young adults with infectious mononucleosis: demonstration of drug-specific lymphocyte reactivity
Authors: C.N. Renn, W. Straff, A. Dorfmuller, T. Al-Masaoudi, H.F. Merk, B. Sachs
Journal: British Journal of Dermatology (2002)

Summary Background Teenagers and young adults frequently develop maculopapular exanthema following amoxicillin intake within infectious mononucleosis. The underlying pathomechanisms are still largely unknown. Objectives To investigate whether amoxicillin-induced exanthema in florid infectious mononucleosis is a disease-associated phenomenon or results from specific sensitization to the drug. Methods Four patients with amoxicillin-induced exanthema within infectious mononucleosis were analysed in vivo by prick, intradermal and patch tests and in vitro by means of the lymphocyte transformation test (LTT) employing amoxicillin, ampicillin, benzylpenicillin and phenoxymethylpenicillin. Results Drug-specific sensitization to amoxicillin in the LTT was observed in three patients, two of whom showed a side-chain-specific sensitization to amoxicillin and ampicillin. The in vitro results were confirmed in vivo by skin tests. Conclusions These data suggest that real sensitization to amoxicillin and ampicillin may occur within infectious mononucleosis and may be detected in vivo and in vitro by means of skin tests and the LTT.