tbuckley/cabot-search huggingface dataset:
Interlaboratory Comparability Study of Cancer Gene Expression Analysis Using Oligonucleotide Microarrays
Authors: Kevin K. Dobbin, David G. Beer, Matthew Meyerson, Timothy J. Yeatman, William L. Gerald, James W. Jacobson, Barbara Conley, Kenneth H. Buetow, Mervi Heiskanen, Richard M. Simon, John D. Minna, Luc Girard, David E. Misek, Jeremy M.G. Taylor, Samir Hanash, Katsuhiko Naoki, D. Neil Hayes, Christine Ladd-Acosta, Steven A. Enkemann, Agnes Viale, Thomas J. Giordano
Journal: Clinical Cancer Research (2005)

Abstract A key step in bringing gene expression data into clinical practice is the conduct of large studies to confirm preliminary models. The performance of such confirmatory studies and the transition to clinical practice requires that microarray data from different laboratories are comparable and reproducible. We designed a study to assess the comparability of data from four laboratories that will conduct a larger microarray profiling confirmation project in lung adenocarcinomas. To test the feasibility of combining data across laboratories, frozen tumor tissues, cell line pellets, and purified RNA samples were analyzed at each of the four laboratories. Samples of each type and several subsamples from each tumor and each cell line were blinded before being distributed. The laboratories followed a common protocol for all steps of tissue processing, RNA extraction, and microarray analysis using Affymetrix Human Genome U133A arrays. High within-laboratory and between-laboratory correlations were observed on the purified RNA samples, the cell lines, and the frozen tumor tissues. Intraclass correlation within laboratories was only slightly stronger than between laboratories, and the intraclass correlation tended to be weakest for genes expressed at low levels and showing small variation. Finally, hierarchical cluster analysis revealed that the repeated samples clustered together regardless of the laboratory in which the experiments were done. The findings indicate that under properly controlled conditions it is feasible to perform complete tumor microarray analysis, from tissue processing to hybridization and scanning, at multiple independent laboratories for a single study.
Using Peripheral Blood Mononuclear Cells to Determine a Gene Expression Profile of Acute Ischemic Stroke
Authors: David F. Moore, Hong Li, Neal Jeffries, Violet Wright, Ronald A. Cooper, Abdel Elkahloun, Monique P. Gelderman, Enrique Zudaire, Gregg Blevins, Hua Yu, Ehud Goldin, Alison E. Baird
Journal: Circulation (2005)

Direct brain biopsy is rarely indicated during acute stroke. This study uses peripheral blood mononuclear cells (PBMCs) to determine whether a systemic gene expression profile could be demonstrated in patients with acute ischemic stroke.Using oligonucleotide microarrays, we compared the gene expression profile of an index cohort of 20 patients with confirmed ischemic stroke on neuroimaging studies with that of 20 referent subjects. Validation studies used quantitative real-time polymerase chain reaction to measure the levels of 9 upregulated genes in the index cohort, and an independent cohort of 9 patients and 10 referent subjects was prospectively studied to determine the accuracy of the Prediction Analysis for Microarrays list to classify stroke. After correction for multiple comparisons with the Bonferroni technique, 190 genes were significantly different between the stroke and referent groups. Broad classes of genes included white blood cell activation and differentiation (approximately 60%), genes associated with hypoxia and vascular repair, and genes potentially associated with an altered cerebral microenvironment. Real-time polymerase chain reaction confirmed increased mRNA expression in 9 of 9 upregulated stroke-associated genes in the index cohort. A panel of 22 genes derived from the Prediction Analysis for Microarrays algorithm in the index cohort classified stroke in the validation cohort with a sensitivity of 78% and a specificity of 80%. Control for the Framingham stroke risk score revealed only a partial dependence of the stroke gene expression profile in PBMCs on vascular risk.This study demonstrated an altered gene expression profile in PBMCs during acute ischemic stroke. Some genes with altered expression were consistent with an adaptive response to central nervous system ischemia.
Evaluating the Accuracy of Continuous Glucose-Monitoring Sensors
Authors: Boris P. Kovatchev, Linda A. Gonder-Frederick, Daniel J. Cox, William L. Clarke
Journal: Diabetes Care (2004)

OBJECTIVE—The objective of this study was to introduce continuous glucose–error grid analysis (CG-EGA) as a method of evaluating the accuracy of continuous glucose-monitoring sensors in terms of both accurate blood glucose (BG) values and accurate direction and rate of BG fluctuations and to illustrate the application of CG-EGA with data from the TheraSense Freestyle Navigator. RESEARCH DESIGN AND METHODS—We approach the design of CG-EGA from the understanding that continuous glucose sensors (CGSs) allow the observation of BG fluctuations as a process in time. We account for specifics of process characterization (location, speed, and direction) and for biological limitations of the observed processes (time lags associated with interstitial sensors). CG-EGA includes two interacting components: 1) point–error grid analysis (P-EGA) evaluates the sensor’s accuracy in terms of correct presentation of BG values and 2) rate–error grid analysis (R-EGA) assesses the sensor’s ability to capture the direction and rate of BG fluctuations. RESULTS—CG-EGA revealed that the accuracy of the Navigator, measured as a percentage of accurate readings plus benign errors, was significantly different at hypoglycemia (73.5%), euglycemia (99%), and hyperglycemia (95.4%). Failure to detect hypoglycemia was the most common error. The point accuracy of the Navigator was relatively stable over a wide range of BG rates of change, and its rate accuracy decreased significantly at high BG levels. CONCLUSIONS—Traditional self-monitoring of BG device evaluation methods fail to capture the important temporal characteristics of the continuous glucose-monitoring process. CG-EGA addresses this problem, thus providing a comprehensive assessment of sensor accuracy that appears to be a useful adjunct to other CGS performance measures.
Secretory leukocyte proteinase inhibitor is preferentially increased in patients with acute respiratory distress syndrome
Authors: J.-M. Sallenave, S.C. Donnelly, I.s Grant, C Robertson, J Gauldie, C. Haslett
Journal: European Respiratory Journal (1999)

Inappropriate release of proteases from inflammatory and stromal cells can lead to destruction of the lung parenchyma. Antiproteinases such as alpha-1-proteinase inhibitor (alpha1-Pi), secretory leukocyte proteinase inhibitor (SLPI) and elastase-specific inhibitor (elafin) control excess production of human neutrophil elastase. In the present study, the concentrations of alpha1-Pi, SLPI and elafin found in bronchoalveolar lavage (BAL) fluid from control subjects, patients at risk of developing acute respiratory distress syndrome (ARDS) and patients with established ARDS were determined. Levels of all three inhibitors were raised in patients compared with normal subjects. SLPI was increased in the group of patients who were at risk of ARDS and went on to develop the condition, compared with the "at-risk" group who did not progress to ARDS (p=0.0083). Alpha1-Pi and elafin levels were similar in these two populations. In patients with established ARDS, both alpha1-Pi and SLPI levels were significantly increased, compared to patients at risk of ARDS who did (p=0.0089) or did not (p=0.0003) progress to ARDS. The finding of increased antiproteinases shortly before the development of acute respiratory distress syndrome provide further evidence for enhanced inflammation prior to clinical disease.
Efficacy and safety of raltegravir for treatment of HIV for 5 years in the BENCHMRK studies: final results of two randomised, placebo-controlled trials
Authors: Joseph J Eron, David A Cooper, Roy T Steigbigel, Bonaventura Clotet, Jose M Gatell, Princy N Kumar, Jurgen K Rockstroh, Mauro Schechter, Martin Markowitz, Patrick Yeni, Mona R Loutfy, Adriano Lazzarin, Jeffrey L Lennox, Kim M Strohmaier, Hong Wan, Richard JO Barnard, Bach-Yen T Nguyen, Hedy Teppler
Journal: The Lancet Infectious Diseases (2013)
Identification of dendritic cell colony-forming units among normal human CD34+ bone marrow progenitors that are expanded by c-kit-ligand and yield pure dendritic cell colonies in the presence of granulocyte/macrophage colony-stimulating factor and tumor necrosis factor alpha.
Authors: J W Young, P Szabolcs, M A Moore
Journal: The Journal of Experimental Medicine (1995)

Several cytokines, especially granulocyte/macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha), have been identified that foster the development of dendritic cells from blood and bone marrow precursors in suspension cultures. These precursors are reported to be infrequent or to yield small numbers of dendritic cells in colony-forming assays. Here we readily identify dendritic cell colony-forming units (CFU-DC) that give rise to pure dendritic cell colonies. Human CD34+ bone marrow progenitors were expanded in semi-solid cultures with serum-replete medium containing c-kit-ligand, GM-CSF, and TNF-alpha. The addition of TNF-alpha to GM-CSF did not alter the number of typical GM colonies but did generate pure dendritic cell colonies that accounted for approximately 40% of the total colony growth. When the two distinct types of colonies were plucked from methylcellulose and tested for T cell-stimulatory activity in the mixed leukocyte reaction, the potency of colony-derived dendritic cells exceeded that of CFU-GM progeny from the same cultures by at least 1.5-2 logs. Immunophenotyping and cytochemical staining of the CFU-DC-derived progeny was also characteristic of dendritic cells. Other myeloid cells were not identified in these colonies. The addition of c-kit-ligand to GM-CSF- and TNF-alpha-supplemented suspensions of CD34+ bone marrow cells expanded CFU-DCs almost 100-fold by 14 d. We conclude that normal human CD34+ bone marrow cells include substantial numbers of clonogenic progenitors, distinct from CFU-GMs, that can give rise to pure dendritic cell colonies. These CFU-DCs can be expanded for several weeks by in vitro culture with c-kit-ligand, and their differentiation requires exogenous TNF-alpha in addition to GM-CSF. We speculate that this dendritic cell-committed pathway may in the steady state contribute cells to the epidermis and afferent lymph, where dendritic cells are the principal myeloid cell type, and may increase the numbers of these specialized antigen-presenting cells during T cell-mediated immune responses.
PREVENTING LEAD POISONING IN CHILDREN
Authors: Ellen K. Silbergeld
Journal: Annual Review of Public Health (1997)

▪ Abstract Lead poisoning is the most significant and prevalent disease of environmental origin among US children. Despite over 100 years' knowledge of the special hazards of lead exposure for young children, it has taken over a century for effective primary prevention to be adopted. Obstacles to primary prevention have included deliberate campaigns by industry to prevent restrictions upon such uses on lead as plumbing, paints, and gasoline additives; influence of industrial support of biomedical research at major US medical schools; lack of appropriate policy mechanisms to identify and control lead exposures; and opposition to investing resources in lead poisoning prevention. The removal of lead from gasoline, which began in the United States in 1972 and was completed in 1995, has resulted in almost fourfold reductions in median blood lead levels in US children from 1976 to 1991. Increased screening and interventions to identify and abate lead sources, such as lead in housing, also contributed to this major public health success. Nevertheless, lead exposures remain prevalent, although increasingly less generally distributed. Perhaps because of the renewed “ghettoization” of lead, support for lead poisoning prevention has waned. Objections to investing public and private resources in screening and source abatement have challenged the continuing commitment of public health officials to prevention. The demonstrable success and social benefits of preventing lead toxicity are cited in support of continued preventive health policies.
Clinical features of secondary pulmonary alveolar proteinosis: pre-mortem cases in Japan
Authors: H. Ishii, R. Tazawa, C. Kaneko, T. Saraya, Y. Inoue, E. Hamano, Y. Kogure, K. Tomii, M. Terada, T. Takada, M. Hojo, A. Nishida, T. Ichiwata, B.C. Trapnell, H. Goto, K. Nakata
Journal: European Respiratory Journal (2011)

which may suggest shared predisposition to these autoimmune diseases and lung cancer.Advice on smoking control would be appropriate for patients with these diseases.In conclusion, the increased risk of COPD but not lung cancer in patients with many autoimmune diseases suggests that the defined autoimmunity may predispose to COPD.Another possibility is that smoking is a risk factor for some of these autoimmune diseases and the effects on lung cancer cannot be recognised because of the small number of cases.This possibility could not be ruled out because data on smoking were lacking.The four-fold risks of lung cancer in patients with systemic sclerosis, discoid lupus erythematosus and polymyositis/dermatomyositis may indicate susceptibility to lung cancer, which should be considered in the counselling of these patients.
<scp>l</scp>-Arginine-Induced Vasodilation of the Renal Vasculature Is Preserved in Uremic Type 1 Diabetic Patients After Kidney and Pancreas but not After Kidney-Alone Transplantation
Authors: Francesco De Cobelli, Paolo Fiorina, Gianluca Perseghin, Marta Magnone, Massimo Venturini, Gianpaolo Zerbini, Alessandro Zanello, Gabriella Mazzolari, Lucilla Monti, Valerio Di Carlo, Antonio Secchi, Alessandro Del Maschio
Journal: Diabetes Care (2004)

OBJECTIVE—In uremic type 1 diabetic patients, kidney and pancreas transplantation (KP) and kidney-alone transplantation (KD) provide full restoration of normal renal function; however, only KP, i.e., curing diabetes, is expected to prevent endothelial damages. Our aim was to study l-arginine-induced vasodilation of the renal vasculature in uremic type 1 diabetic patients after KP or KD using magnetic resonance (MR). RESEARCH DESIGN AND METHODS—MR quantitative flow measurements were performed in 15 KP patients (mean age 39.0 ± 1.7 years, 10 men and 5 women), in 11 KD patients (mean age 47.3 ± 1.9 years, 7 men and 4 women), and in 8 nondiabetic kidney transplant patients (mean age 44.0 ± 4.8 years, 7 men and 1 woman), who were used as control subjects, to measure renal blood flow and velocity and renal vascular resistance before and immediately after infusion of l-arginine. RESULTS—Renal blood flow and velocity were not different at baseline in KP, KD, and control subjects. In contrast, during l-arginine administration renal blood flow increased significantly in KP subjects (basal 8.4 ± 0.6 vs. post 9.6 ± 0.8 ml/s, Δ 14.3 ± 4.4%, P &amp;lt; 0.05) and in control subjects (basal 9.3 ± 0.8 vs. post 9.1 ± 0.8 ml/s, Δ 17.3 ± 6.2%, P &amp;lt; 0.01), while it remained unchanged in KD subjects (basal 10.0 ± 0.8 vs. post 11.6 ± 0.9 ml/s, Δ −1.36 ± 6.9%, NS). Parallel results have been achieved for renal blood velocity (KP subjects: 20.1 ± 4.9%, P &amp;lt; 0.01; control subjects: 23.0 ± 7.99%, P &amp;lt; 0.01; and KD subjects: −0.3 ± 6.5%; NS). A reduction in renal vascular resistance in response to l-arginine was evident in KP and control subjects but not in KD patients. CONCLUSIONS—l-Arginine vasodilatory response was successfully assessed with MR quantitative flow measurements. KP patients and control subjects, but not those with KD, showed a preserved l-arginine-induced vasodilation of the renal vasculature.
New Predictive Equations Improve Monitoring of Kidney Function in Patients With Diabetes
Authors: Marie-Christine Beauvieux, Françoise Le Moigne, Catherine Lasseur, Christelle Raffaitin, Caroline Perlemoine, Nicole Barthe, Philippe Chauveau, Christian Combe, Henri Gin, Vincent Rigalleau
Journal: Diabetes Care (2007)

OBJECTIVE—The Cockcroft-Gault and Modification of Diet in Renal Disease (MDRD) equations poorly predict glomerular filtration rate (GFR) decline in diabetic patients. We sought to discover whether new equations based on serum creatinine (the Mayo Clinic Quadratic [MCQ] or reexpressed MDRD equations) or four cystatin C–based equations (glomerular filtration rate estimated via cystatin formula [Cys-eGFR]) were less biased and better predicted GFR changes. RESEARCH DESIGN AND METHODS—In 124 diabetic patients with a large range of isotopic GFR (iGFR) (56.1 ± 35.3 ml/min per 1.73 m2 [range 5–164]), we compared the performances of the equations before and after categorization in GFR tertiles. A total of 20 patients had a second determination 2 years later. RESULTS—The Cockcroft-Gault equation was the least precise. The MDRD equation was the most precise but the most biased according to the Bland-Altman procedure. By contrast with the MDRD and, to a lesser extent, the MCQ, three of the four Cys-eGFRs were not biased. All equations overestimated the low GFRs, whereas only the MDRD and Rule's Cys-eGFR equations underestimated the high GFRs. For the subjects studied twice, iGFR changed by −8.5 ± 17.9 ml/min per 1.73 m2. GFR changes estimated by the Cockcroft-Gault (−4.5 ± 6.8) and MDRD (−5.7 ± 6.2) equations did not correlate with the isotopic changes, whereas new equation-predicted changes did: MCQ: −8.7 ± 9.4 (r = 0.44, P &amp;lt; 0.05) and all four Cys-eGFRs: −6.2 ± 7.4 to −7.3 ± 8.4 (r = 0.60 to 0.62, all P &amp;lt; 0.005), such as 100/cystatin-C (r = 0.61, P &amp;lt; 0.005). CONCLUSIONS—The new predictive equations better estimate GFR than the Cockcroft-Gault equation. Although the MDRD equation remains the most accurate, it poorly predicts GFR decline, as it overestimates low and underestimates high GFRs. This bias is lesser with the MCQ and Cys-eGFR equations, so they better predict GFR changes.
Autoantibodies against the specific epitope of human tropomyosin(s) detected by a peptide based enzyme immunoassay in sera of patients with ulcerative colitis show antibody dependent cell mediated cytotoxicity against HLA-DPw9 transfected L cells
Authors: S Sakamaki
Journal: Gut (2000)

Recent studies suggest that tropomyosin (TM) may act as a putative autoantigen in ulcerative colitis (UC). Recently, we identified, by computer homology analysis, a specific peptide (HIAEDADRK) in human TM that can bind to HLA-DPw9. The aim of this study was to investigate the presence of autoantibodies against this peptide in UC.Antibodies were measured by ELISA with a synthetic peptide in 20 healthy volunteers, 48 patients with UC, 26 with Crohn's disease (CD), eight with primary sclerosing cholangitis (PSC), and six with primary biliary cirrhosis (PBC). The functional significance of antibodies was investigated by antibody dependent cell mediated cytotoxicity (ADCC) against DPw9 transfected L cells using a standard (51)Cr release assay.Optical density values (mean (SD)) of sera from patients with UC (1.40 (0. 52)) and PSC (1.65 (0.12)) were significantly higher than those from healthy volunteers (0.32 (0.28)) (p<0.05), CD (0.50 (0.34)) (p<0.05) and PBC (0.14 (0.09)) (p<0.05). Values in UC decreased with clinical improvement. The ADCC activity of UC sera correlated well with antibody titre against this synthetic peptide.Anti-TM antibody was detected in UC sera by a specific peptide based ELISA with high reproducibility. This peptide may be an antigenic epitope of TM involved in the immunopathogenesis of UC and, perhaps, PSC.
Virologic response and resistance to adefovir in patients with chronic hepatitis B
Authors: Scott K. Fung, Hee Bok Chae, Robert J. Fontana, Hari Conjeevaram, Jorge Marrero, Kelly Oberhelman, Munira Hussain, Anna S.F. Lok
Journal: Journal of Hepatology (2005)

The incidence and risk factors for adefovir-resistant HBV have not been clearly defined.To characterize the virologic response to adefovir, to determine the rate of adefovir resistance and to explore factors associated with initial virologic response (IVR) and adefovir resistance.All hepatitis B patients who received adefovir for > or =6 months at our center were prospectively monitored for virologic response and adefovir resistance.Forty three patients were included; mean treatment duration was 18 months (range 6-45). Thirty four (79%) patients had prior lamivudine. IVR was observed in 44% patients and associated with higher pretreatment ALT (P = 0.05) and the absence of HBeAg (P = 0.02). Six (14%) patients were found to have adefovir-resistant mutations. The cumulative probability of genotypic resistance to adefovir at month 24 was 22%. Patients with adefovir resistance were more likely to have been switched from lamivudine to adefovir monotherapy (P = 0.01), to be older (P = 0.04), and to be infected with HBV genotype D (P = 0.02).Roughly 50% of patients failed to achieve IVR on adefovir. The cumulative probability of adefovir resistance at 2 years was 22%. Our data suggest that combination of lamivudine and adefovir may prevent emergence of adefovir resistance in patients with lamivudine-resistant HBV.
Anaphylaxis After Bitten By Domestic Hamster: A Case Report
Authors: Leila Borges, Danielle Bichueti Silva, Tessa Rachel Tranquilini Gonçalves, Rafael Rota, Camila Gonzaga da Silva, Danieli Hirari, Marcia Mallozi, Dirceu Sole
Journal: Journal of Allergy and Clinical Immunology (2014)
Apparent predisposition to systemic lupus erythematosus in Chinese patients in West Malaysia.
Authors: A O Frank
Journal: Annals of the Rheumatic Diseases (1980)

In the first 9 years following the opening of the University Hospital in kuala Lumpur nearly 130,000 patients have been admitted (excluding obstetric patients), and, of these, 175 fulfilled the American Rheumatism Association criteria for the diagnosis of systemic lupus erythematosus. This diagnosis was made significantly more frequently in Chinese patients than in other races. SLE is more often reported from Chinese communities in Asia than from India and tropical Africa. There may be a lower susceptibility to autoimmune disease in black Africans than the suspected increased susceptibility to autoimmune disease in black Africans than the suspected increased susceptibility in their American Negro and West Indian descendants. A careful study of racial and geograhical factors in autoimmune disease should throw further light on the interaction between the host and his environment which results in autoimmune disease.
Ditiocarb Sodium and HIV Infection
Authors: M. P. O'Meara
Journal: JAMA (1991)

<h3>To the Editor.</h3> —Hersh et al<sup>1</sup>demonstrated in a controlled study that oral sodium diethyldithiocarbamate (ditiocarb), given once weekly, reduced the incidence of opportunistic infections by approximately 50% in patients with symptomatic human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS). Patients were advised to avoid alcohol for 12 hours before and 48 hours after the weekly dose because of "disulfiram (Antabuse)—like effects." Ditiocarb is the principal metabolite of disulfiram. After absorption in the gut, disulfiram is rapidly reduced to two molecules of ditiocarb. Disulfiram and ditiocarb are similar in many biologic effects, including effectiveness in chelation therapy of nickel poisoning<sup>2</sup>and potentiation of hyperbaric oxygen poisoning in rats.hyper<sup>3</sup> Disulfiram is inexpensive, widely available, and has a well-defined and acceptable side-effect profile based on more than 40 years of extensive use in alcoholism. Should there not be clinical trials of this agent in HIV infection and AIDS?