tbuckley/cabot-search huggingface dataset:
Time Course and Mechanism of Myocardial Catecholamine Release During Transient Ischemia In Vivo
Authors: Thomas W. Lameris, Sandra de Zeeuw, Gooitzen Alberts, Frans Boomsma, Dirk J. Duncker, Pieter D. Verdouw, Arie J. Man in ’t Veld, Anton H. van den Meiracker
Journal: Circulation (2000)

Background —Elevated concentrations of norepinephrine (NE) have been observed in ischemic myocardium. We investigated the magnitude and mechanism of catecholamine release in the myocardial interstitial fluid (MIF) during ischemia and reperfusion in vivo through the use of microdialysis. Methods and Results —In 9 anesthetized pigs, interstitial catecholamine concentrations were measured in the perfusion areas of the left anterior descending coronary artery (LAD) and the left circumflex coronary artery. After stabilization, the LAD was occluded for 60 minutes and reperfused for 150 minutes. During the final 30 minutes, tyramine (154 nmol · kg −1 · min −1 ) was infused into the LAD. During LAD occlusion, MIF NE concentrations in the ischemic region increased progressively from 1.0±0.1 to 524±125 nmol/L. MIF concentrations of dopamine and epinephrine rose from 0.4±0.1 to 43.9±9.5 nmol/L and from &lt;0.2 (detection limit) to 4.7±0.7 nmol/L, respectively. Local uptake-1 blockade attenuated release of all 3 catecholamines by &gt;50%. During reperfusion, MIF catecholamine concentrations returned to baseline within 120 minutes. At that time, the tyramine-induced NE release was similar to that seen in nonischemic control animals despite massive infarction. Arterial and MIF catecholamine concentrations in the left circumflex coronary artery region remained unchanged. Conclusions —Myocardial ischemia is associated with a pronounced increase of MIF catecholamines, which is at least in part mediated by a reversed neuronal reuptake mechanism. The increase of MIF epinephrine implies a (probably neuronal) cardiac source, whereas the preserved catecholamine response to tyramine in postischemic necrotic myocardium indicates functional integrity of sympathetic nerve terminals.
C1q deviation test for the detection of immune complexes, aggregates of IgG, and bacterial products in human serum.
Authors: A T Sobel, V A Bokisch, H J Müller-Eberhard
Journal: The Journal of Experimental Medicine (1975)

This report describes a new, rapid, sensitive, and quantitative method for the detection of immune complexes, endotoxins, and other complement activating materials in patients sera utilizing the ability of these substances to react with isolated C1q. The procedure is based on the inhibition of radiolabeled C1q binding to sensitized sheep erythrocytes by C1q-reactive substances in pathological sera. The C1q deviation test may be performed on 50 mu1 of serum, using 1 mug of radiolabeled C1q per sample. The procedure may be completed in 1.5-2 h, it is capable of detecting 5 mug of aggregated human IgG per ml of serum, and its coefficient of variation is 4.2%. Application of the test to the study of 193 sera from 43 patients with Dengue hemorrhagic fever showed a positive correlation between degree of C1q deviation and severity of disease.
Osteoporosis in chronic obstructive pulmonary disease
Authors: A.A. Ionescu, E. Schoon
Journal: European Respiratory Journal (2003)

Osteoporosis is one of the systemic effects associated with chronic obstructive pulmonary disease (COPD). Potential risk factors of osteoporosis may be due to the lifestyle, genetics, treatment with corticosteroids, endocrine abnormalities or the impairment of the body composition and peripheral skeletal muscles. Evidence for the possible contribution of such factors is reviewed. The occurrence of fractures, as a consequence of osteoporosis, can contribute to the disability and mortality of patients with COPD and add to the economic burden of the disease. The treatment with corticosteroids for the lung disease is associated with increased prevalence of fractures, but other factors may contribute. There is a remarkable paucity of interventional studies targeting the osteoporosis in patients with COPD. The results of studies on the treatment of osteoporosis in chronic lung diseases, some including small numbers of patients with COPD, are reviewed in the paper. Prospective longitudinal studies on the incidence of osteoporosis in chronic obstructive pulmonary disease need to assess patients with various degrees of disease severity and investigate the possible contribution of etiological factors. Randomised placebo-controlled trials are required to assess the effect of intervention, such as bisphosphonates, hormone replacement, calcium supplementation, on the prevention and treatment of osteoporosis and fractures in chronic obstructive pulmonary disease.
Bevacizumab Plus Irinotecan in Recurrent Glioblastoma
Authors: Marc C. Chamberlain
Journal: Journal of Clinical Oncology (2008)

I congratulate Vredenburgh and colleagues 1 for their article further supporting the role of bevacizumab and irinotecan in patients with recurrent glioblastoma (GBM).This article, an earlier article from the same group, a small series from the University of California, Los Angeles group, and the first report by Stark-Vance of this drug combination all seem to support the thesis that antiangiogenic therapy has substantial activity in recurrent GBM. [1]2][3][4] Several issues regarding the article are relevant and warrant discussion.
Cistrome: an integrative platform for transcriptional regulation studies
Authors: Tao Liu, Jorge A Ortiz, Len Taing, Clifford A Meyer, Bernett Lee, Yong Zhang, Hyunjin Shin, Swee S Wong, Jian Ma, Ying Lei, Utz J Pape, Michael Poidinger, Yiwen Chen, Kevin Yeung, Myles Brown, Yaron Turpaz, X Shirley Liu
Journal: Genome biology (2011)

Abstract The increasing volume of ChIP-chip and ChIP-seq data being generated creates a challenge for standard, integrative and reproducible bioinformatics data analysis platforms. We developed a web-based application called Cistrome, based on the Galaxy open source framework. In addition to the standard Galaxy functions, Cistrome has 29 ChIP-chip- and ChIP-seq-specific tools in three major categories, from preliminary peak calling and correlation analyses to downstream genome feature association, gene expression analyses, and motif discovery. Cistrome is available at http://cistrome.org/ap/ .
Bronchial hyperresponsiveness in young students of southern China: relation to respiratory symptoms, diagnosed asthma, and risk factors.
Authors: N S Zhong, R C Chen, M O-yang, J Y Wu, W X Fu, L J Shi
Journal: Thorax (1990)

A cross sectional study was carried out to determine the prevalence of bronchial hyperresponsiveness and asthma in 3067 students aged 11-17 years in an urban and a rural area of Guangzhou (Canton), China. The methods used included a self administered questionnaire, a histamine bronchial provocation test, and allergen skinprick tests. Bronchial hyperresponsiveness was defined as a 20% fall in FEV1 and peak expiratory flow at a provoking dose of histamine (PD20) less than 7.8 mumol on two occasions four weeks apart. The response rate was 98.0% and 99.2% in the two areas. The prevalence of bronchial hyperresponsiveness was 4.1% and of diagnosed asthma 2.4% in the total population. There were no significant differences in prevalence between the urban and the rural area or between boys and girls. The 11-12 year group had a higher prevalence of bronchial hyperresponsiveness (7.6%) than the older groups. Of the 125 with bronchial hyperresponsiveness, 12.0% were defined as having severe or moderate (PD20 less than 0.8 mumol), 26% mild (0.9-3.2 mumol), and 62% slight bronchial hyperresponsiveness (3.3-7.8 mumol). The severity of bronchial hyperresponsiveness was closely related to diagnosed asthma, wheezing, and cough, though half the students with bronchial hyperresponsiveness were symptom free. The most common allergens were house dust and house dust mite in the city, and hay dust, pollen, and feathers in the rural area. The odds ratios for having respectively slight, mild or moderate, and severe bronchial hyperresponsiveness were 5.9, 21.0, and 30.4 for atopy; 1.9, 1.9, and 7.3 for early respiratory infection; and 3.1, 2.5, and 5.6 for a history of parental asthma.
Training in basic and advanced life support in UK medical schools: questionnaire survey
Authors: P S Phillips
Journal: BMJ (2001)

doctors requested an autopsy themselves and most were successful in obtaining permission from the relatives.The party also recommends that "the autopsy or at least a demonstration of the major findings should be attended by a member of the clinical team."Autopsy findings differ noticeably from clinical diagnoses in 10% of cases.As awareness of clinical errors increases both within the profession and in the general public, feedback from postmortem examina-tions to clinicians responsible for patient care must be given.
Low-Fat Dietary Pattern and Cancer Incidence in the Women's Health Initiative Dietary Modification Randomized Controlled Trial
Authors: R. L. Prentice, C. A. Thomson, B. Caan, F. A. Hubbell, G. L. Anderson, S. A. A. Beresford, M. Pettinger, D. S. Lane, L. Lessin, S. Yasmeen, B. Singh, J. Khandekar, J. M. Shikany, S. Satterfield, R. T. Chlebowski
Journal: JNCI Journal of the National Cancer Institute (2007)

The Women's Health Initiative Dietary Modification (DM) Randomized Controlled Trial evaluated the effects of a low-fat dietary pattern on chronic disease incidence, with breast cancer and colorectal cancer as primary outcomes. The trial protocol also listed ovarian cancer and endometrial cancer as outcomes that may be favorably affected by the intervention. A total of 48835 postmenopausal women were randomly assigned during 1993–1998 to a DM intervention (n = 19541) or comparison (usual diet; n = 29294) group and followed up for an average of 8.1 years. The intervention goal was to reduce total fat intake to 20% of energy and to increase consumption of vegetables, fruits, and grains. Cancer outcomes were verified by pathology report review. We used weighted log-rank tests to compare incidence of invasive cancers of the ovary and endometrium, total invasive cancer, and invasive cancers at other sites between the groups. All statistical tests were two-sided. Ovarian cancer risk was lower in the intervention than in the comparison group ( P = .03). Although the overall ovarian cancer hazard ratio (HR) was not statistically significantly less than 1.0, the hazard ratio decreased with increasing intervention duration ( Ptrend = .01). For the first 4 years, the risk for ovarian cancer was similar in the intervention and control groups (0.52 cases per 1000 person-years in the intervention group versus 0.45 per 1000 person-years in the comparison group; HR = 1.16, 95% confidence interval [CI] = 0.73 to 1.84); over the next 4.1 years, the risk was lower in the intervention group (0.38 cases per 1000 person-years in the intervention group versus 0.64 per 1000 person-years in the comparison group; HR = 0.60, 95% CI = 0.38 to 0.96). Risk of cancer of the endometrium did not differ between the groups ( P = .18). The estimated risk of total invasive cancer was slightly lower in the intervention group than in the control group (HR = 0.95, 95% CI = 0.89 to 1.01; P = .10). A low-fat dietary pattern may reduce the incidence of ovarian cancer among postmenopausal women.
Comparison of inhaled mannitol, daily rhDNase and a combination of both in children with cystic fibrosis: a randomised trial
Authors: C Minasian, C Wallis, C Metcalfe, A Bush
Journal: Thorax (2009)

<h3>Background:</h3> Osmotic agents, such as inhaled dry powder mannitol, may increase mucociliary clearance by rehydrating the airway surface liquid and thus act as disease-modifying treatments in cystic fibrosis (CF). This is the first therapeutic trial of inhaled mannitol in children with CF; it was compared with recombinant human deoxyribonuclease (rhDNase), the current best established mucolytic treatment. <h3>Methods:</h3> 38 children were recruited to an open crossover study. Subjects underwent an initial bronchial provocation challenge with dry powder mannitol. Those children with a negative challenge were randomly allocated to one of three consecutive 12-week treatment blocks (inhaled mannitol alone, nebulised rhDNase alone and mannitol + rhDNase). The primary outcome was forced expiratory volume in 1 s (FEV<sub>1</sub>). A number of secondary outcome measures were also studied. <h3>Results:</h3> Twenty children completed the study. Bronchoconstriction and cough associated with mannitol administration contributed to the high attrition rate. The mean increase in FEV<sub>1</sub> following 12 weeks of treatment was 0.11 litres (6.7%) (p = 0.055) for mannitol alone, 0.12 litres (7.2%) (p = 0.03) for rhDNase alone and 0.03 litres (1.88%) (p = 0.67) for rhDNase and mannitol. None of the secondary clinical outcomes was statistically significantly different between treatments. <h3>Conclusions:</h3> Inhaled mannitol was at least as effective as rhDNase after 3 months treatment. There was a marked individual variation in tolerance to mannitol and in response to treatment however. Children who do not respond to rhDNase many benefit from a trial of inhaled mannitol. The combination of mannitol and rhDNase was not useful. <h3>Trial registration number:</h3> NCT00117208
<i>In vitro</i> and <i>In vivo</i> Selective Antitumor Activity of Edelfosine against Mantle Cell Lymphoma and Chronic Lymphocytic Leukemia Involving Lipid Rafts
Authors: Faustino Mollinedo, Janis de la Iglesia-Vicente, Consuelo Gajate, Ander Estella-Hermoso de Mendoza, Janny A. Villa-Pulgarin, Mercè de Frias, Gaël Roué, Joan Gil, Dolors Colomer, Miguel A. Campanero, Maria J. Blanco-Prieto
Journal: Clinical Cancer Research (2010)

Mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) remain B-cell malignancies with limited therapeutic options. The present study investigates the in vitro and in vivo effect of the phospholipid ether edelfosine (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine) in MCL and CLL.Several cell lines, patient-derived tumor cells, and xenografts in severe combined immunodeficient mice were used to examine the anti-MCL and anti-CLL activity of edelfosine. Furthermore, we analyzed the mechanism of action and drug biodistribution of edelfosine in MCL and CLL tumor-bearing severe combined immunodeficient mice.Here, we have found that the phospholipid ether edelfosine was the most potent alkyl-lysophospholipid analogue in killing MCL and CLL cells, including patient-derived primary cells, while sparing normal resting lymphocytes. Alkyl-lysophospholipid analogues ranked edelfosine > perifosine >> erucylphosphocholine > or = miltefosine in their capacity to elicit apoptosis in MCL and CLL cells. Edelfosine induced coclustering of Fas/CD95 death receptor and rafts in MCL and CLL cells. Edelfosine was taken up by malignant cells, whereas normal resting lymphocytes hardly incorporated the drug. Raft disruption by cholesterol depletion inhibited drug uptake, Fas/CD95 clustering, and edelfosine-induced apoptosis. Edelfosine oral administration showed a potent in vivo anticancer activity in MCL and CLL xenograft mouse models, and the drug accumulated dramatically and preferentially in the tumor.Our data indicate that edelfosine accumulates and kills MCL and CLL cells in a rather selective way, and set coclustering of Fas/CD95 and lipid rafts as a new framework in MCL and CLL therapy. Our data support a selective antitumor action of edelfosine.
SPONTANEOUS EVACUATION OF A SHRAPNEL BULLET IN THE LUNG BY EXPECTORATION
Authors: R. M. Leslie
Journal: BMJ (1917)

A SHRAPNEL lUL-LET.Po. r7, I917 advanced exercises witli comparative ease.Tlli.s confirmus the previous conclusionl tlhat the remlloval of a coexistitIn, inifectioni may lead to tlle alleviation of synmptomrls of ilritable heart.'Treatment wit7 MetlIyl-Psycliolrine.In addition to these treatmeits-witlh emetine bislmuth io(idle we tested -a neiw alkaloid, nmetllyl-psyclhotrine, pre- pared from ipecacuanba by Dr. F. L. Pyman, and sent to us for trial.-bvDr.
Lipopolysaccharide-induced selective priming effects on tumor necrosis factor alpha and nitric oxide production in mouse peritoneal macrophages.
Authors: X Zhang, D C Morrison
Journal: The Journal of Experimental Medicine (1993)

Preculture of thioglycollate-elicited C3HeB/FeJ mouse peritoneal macrophages in vitro with subthreshold stimulatory concentrations of lipopolysaccharide (LPS) can induce hyporesponsiveness (desensitization) to both tumor necrosis factor alpha (TNF-alpha) and nitric oxide (NO) production when these cells are subsequently stimulated with 100 ng/ml of LPS. We have established, however, that the primary dose of LPS required for inducing downregulation of NO production is significantly lower than that required for inducing downregulation of TNF-alpha production. Further, when LPS-pretreated macrophages become refractory to subsequent LPS stimulation for NO production, the secondary LPS-stimulated TNF-alpha production is markedly enhanced, and vice versa. These results indicate that LPS-induced TNF-alpha and NO production by macrophages are differentially regulated, and that the observed desensitization process may not reflect a state in which macrophages are totally refractory to subsequent LPS stimulation. Rather, our data suggest that LPS-pretreated macrophages become selectively primed for differential responses to LPS. The LPS-induced selective priming effects are not restricted to LPS stimulation, but extend as well to stimuli such as zymosan, Staphylococcus aureus, and heat-killed Listeria monocytogenes.
THE PREVENTION OF DIPHTHERIA AND SCARLET FEVER IN NURSES
Authors: Ludvig Hektoen
Journal: JAMA (1934)

Our purpose in this note is to complete the records of the prevention of diphtheria and scarlet fever among the nurses in the Durand Hospital, which was closed, at least temporarily, at the beginning of this year. Since the opening of the hospital in March, 1913, special efforts have been made to protect the nurses against the infectious diseases with which they were dealing and especially diphtheria and scarlet fever. As tests for susceptibility and immunization of susceptibles developed, these methods were applied to the nurses. Accurate records of the health of the nurses while in the hospital have been kept. The capacity of the hospital was sixty beds. Only patients with acute infectious diseases (mostly diphtheria and scarlet fever) were received. At first the nursing was done principally by graduate nurses, but after the end of the second year the bedside nursing was in the hands of student nurses
The beta subunit of human granulocyte-macrophage colony-stimulating factor receptor forms a homodimer and is activated via association with the alpha subunit.
Authors: A Muto, S Watanabe, A Miyajima, T Yokota, K Arai
Journal: The Journal of Experimental Medicine (1996)

Human granulocyte-macrophage colony-stimulating factor (hGM-CSF) receptor (hGMR) consists of alpha and beta subunits, and the precise stoichiometry of these subunits has remained to be determined. In this work, oligomerization of the beta subunit was studied using a chemical cross-linker. In Ba/F3, a mouse interleukin-3-dependent cell line expressing both subunits of hGMR (Ba/F3-alpha,beta), a protein with a molecular mass corresponding to that of a homodimer of the beta subunit (beta homodimer) was detected only when cells were treated with the cross-linker. Dimerization of the beta subunit was confirmed by coimmunoprecipitation of a tagged beta subunit with the wild type beta subunit COS7 cells. The beta homodimer had already formed in the absence of hGM-CSF, whereas stimulation with the ligand brought both alpha and beta subunits into a complex, the result being tyrosine phosphorylation of the beta homodimer. Tyrosine phosphorylation of the subunit was impaired by deletion of the cytoplasmic domain of the alpha subunit without interfering with the association of both subunits. These results indicate that the beta homodimer, which alone is insufficient for signaling, forms the functional hGMR with the alpha subunit in response to hGM-CSF.
A Four-Kallikrein Panel Predicts Prostate Cancer in Men with Recent Screening: Data from the European Randomized Study of Screening for Prostate Cancer, Rotterdam
Authors: Andrew J. Vickers, Angel M. Cronin, Monique J. Roobol, Caroline J. Savage, Mari Peltola, Kim Pettersson, Peter T. Scardino, Fritz H. Schröder, Hans Lilja
Journal: Clinical Cancer Research (2010)

Abstract Purpose: We have developed a statistical prediction model for prostate cancer based on four kallikrein markers in blood: total, free, and intact prostate-specific antigen (PSA), and kallikrein-related peptidase 2 (hK2). Although this model accurately predicts the result of biopsy in unscreened men, its properties for men with a history of PSA screening have not been fully characterized. Experimental Design: A total of 1,501 previously screened men with elevated PSA underwent initial biopsy during rounds 2 and 3 of the European Randomized Study of Screening for Prostate Cancer, Rotterdam, with 388 cancers diagnosed. Biomarker levels were measured in serum samples taken before biopsy. The prediction model developed on the unscreened cohort was then applied and predictions compared with biopsy outcome. Results: The previously developed four-kallikrein prediction model had much higher predictive accuracy than PSA and age alone (area under the curve of 0.711 versus 0.585, and 0.713 versus 0.557 with and without digital rectal exam, respectively; both P &amp;lt; 0.001). Similar statistically significant enhancements were seen for high-grade cancer. Applying the model with a cutoff of 20% cancer risk as the criterion for biopsy would reduce the biopsy rate by 362 for every 1,000 men with elevated PSA. Although diagnosis would be delayed for 47 cancers, these would be predominately low-stage and low-grade (83% Gleason 6 T1c). Conclusions: A panel of four kallikreins can help predict the result of initial biopsy in previously screened men with elevated PSA. Use of a statistical model based on the panel would substantially decrease rates of unnecessary biopsy. Clin Cancer Res; 16(12); 3232–9. ©2010 AACR.
High Risk for Bradyarrhythmic Complications in Patients With Brugada Syndrome Caused by SCN5AGene Mutations
Authors: Takeru Makiyama, Masaharu Akao, Keiko Tsuji, Takahiro Doi, Seiko Ohno, Kotoe Takenaka, Atsushi Kobori, Tomonori Ninomiya, Hidetada Yoshida, Makoto Takano, Naomasa Makita, Fumiko Yanagisawa, Yukei Higashi, Youichi Takeyama, Toru Kita, Minoru Horie
Journal: Journal of the American College of Cardiology (2005)