tbuckley/cabot-search huggingface dataset:
Definition of T cell idiotypes using anti-idiotypic antisera produced by immunization with T cell clones.
Authors: A J Infante, P D Infante, S Gillis, C G Fathman
Journal: The Journal of Experimental Medicine (1982)

Alloreactive T cell clones with distinct specificities were used to raise anti-idiotypic antisera via an F1 anti-(parent anti-F1) protocol. Antisera were raised that could stimulate the proliferation of the appropriate T cell clone, but not other clones. The active fraction of the antisera for T cell proliferation was immunoglobulin. In addition to proliferation, an anti-idiotypic antiserum could induce the appropriate T cell clone to secrete substantial amounts of interleukin 2 (IL-2). Production of IL-2 appeared independent of the involvement of accessory cells. These accessory cells may be unnecessary for IL-2 production in our assay, or their effect may be produced by anti-idiotype. Thus, anti-idiotype may provide two or more specific T cell signals.
Pathology of chronic hepatitis C in children
Authors: M Kage, T Fujisawa, K Shiraki, T Tanaka, A Kimura, K Shimamatsu, E Nakashima, M Kojiro, M Koike, Y Tazawa, D Abukawa, M Okaniwa, H Takita, A Matsui, T Hayashi, T Etou, S Terasawa, K Sugiyama, H Tajiri, A Yoden, Y Kajiwara, M Sata, Y Uchimura
Journal: Hepatology (1997)

Limited information is available regarding the histology of hepatitis C virus infection in children. The aim of this study was to determine the histological pattern of chronic hepatitis C (CHC) in children, and liver biopsy specimens from 109 pediatric patients with CHC were examined. Each biopsy specimen was evaluated based on a numerical scoring system for the stage of fibrosis (1-4), the grade of portal/periportal necroinflammation (0-4), the grade of lobular necroinflammation (0-4), and their sum (final grade). The histological lesions considered to be characteristic of chronic hepatitis were also evaluated. None of the children had liver cirrhosis, and 105 cases (97%) were stage 1 or 2. Only 4 children were stage 3. Two of these 4 cases showed hemosiderosis. A significant correlation was observed between the staging score and the final grade in the pediatric patients (r = .59; P < .0001). The histological characteristics of adult CHC, such as lymphoid aggregate, bile duct injury, and fatty changes, were also observed in the children. In conclusion, the majority of children with CHC presented with mild fibrosis, but a few showed CHC with lobular distortion and hemosiderosis. Frequent blood transfusion may aggravate hepatic lesions in pediatric CHC.
ENZYMES OF THE GLYCOLYTIC PATHWAY IN SKIN. VII: Triosephosphate Isomerase.
Authors: P. D. Mier, D. W. K. Cotton
Journal: British Journal of Dermatology (1967)

Journal Article ENZYMES OF THE GLYCOLYTIC PATHWAY IN SKIN. VII: Triosephosphate Isomerase. Get access P. D. Mier, P. D. Mier The Institute of Dermatology, St. John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 Search for other works by this author on: Oxford Academic Google Scholar D. W. K. Cotton D. W. K. Cotton The Institute of Dermatology, St. John's Hospital for Diseases of the Skin, Homerton Grove, London, E.9 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 79, Issue 11, 1 November 1967, Pages 598–602, https://doi.org/10.1111/j.1365-2133.1967.tb11423.x Published: 01 November 1967
Postnatally Induced Inactivation of gp130 in Mice Results in Neurological, Cardiac, Hematopoietic, Immunological, Hepatic, and Pulmonary Defects
Authors: Ulrich A.K. Betz, Wilhelm Bloch, Maries van den Broek, Kanji Yoshida, Tetsuya Taga, Tadamitsu Kishimoto, Klaus Addicks, Klaus Rajewsky, Werner Müller
Journal: The Journal of Experimental Medicine (1998)

The pleiotrophic but overlapping functions of the cytokine family that includes interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin 1 are mediated by the cytokine receptor subunit gp130 as the common signal transducer. Although mice lacking individual members of this family display only mild phenotypes, animals lacking gp130 are not viable. To assess the collective role of this cytokine family, we inducibly inactivated gp130 via Cre-loxP–mediated recombination in vivo. Such conditional mutant mice exhibited neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects, demonstrating the widespread importance of gp130-dependent cytokines.
Double-Edged Role of Statins in Angiogenesis Signaling
Authors: Carmen Urbich, Elisabeth Dernbach, Andreas M. Zeiher, Stefanie Dimmeler
Journal: Circulation Research (2002)

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) exert potent vasculoprotective effects. However, the potential contribution to angiogenesis is controversial. In the present study, we demonstrate that atorvastatin dose-dependently affects endothelial cell migration and angiogenesis. In vivo relevant concentrations of 0.01 to 0.1 μmol/L atorvastatin or mevastatin promote the migration of mature endothelial cells and tube formation. Moreover, atorvastatin also increases migration and the potency to form vessel structures of circulating endothelial progenitor cells, which may contribute to vasculogenesis. In contrast, higher concentrations (&gt;0.1 μmol/L atorvastatin) block angiogenesis and migration by inducing endothelial cell apoptosis. The dose-dependent promigratory and proangiogenic effects of atorvastatin on mature endothelial cells are correlated with the activation of the phosphatidylinositol 3-kinase–Akt pathway, as determined by the phosphorylation of Akt and endothelial NO synthase (eNOS) at Ser1177. In addition, the stimulation of migration and tube formation was blocked by phosphatidylinositol 3-kinase inhibitors. In contrast, the well-established stabilization of eNOS mRNA was achieved only at higher concentrations, suggesting that posttranscriptional activation rather than an increase in eNOS expression mediates the proangiogenic effect of atorvastatin. Taken together, these data suggest that statins exert a double-edged role in angiogenesis signaling by promoting the migration of mature endothelial cells and endothelial progenitor cells at low concentrations, whereas the antiangiogenic effects were achieved only at high concentrations.
Pharmacologic Inhibition of the Menin-MLL Interaction Blocks Progression of MLL Leukemia In Vivo
Authors: Dmitry Borkin, Shihan He, Hongzhi Miao, Katarzyna Kempinska, Jonathan Pollock, Jennifer Chase, Trupta Purohit, Bhavna Malik, Ting Zhao, Jingya Wang, Bo Wen, Hongliang Zong, Morgan Jones, Gwenn Danet-Desnoyers, Monica L. Guzman, Moshe Talpaz, Dale L. Bixby, Duxin Sun, Jay L. Hess, Andrew G. Muntean, Ivan Maillard, Tomasz Cierpicki, Jolanta Grembecka
Journal: Cancer Cell (2015)
NEURONAL CIRCUITS OF THE NEOCORTEX
Authors: Rodney J. Douglas, Kevan A.C. Martin
Journal: Annual Review of Neuroscience (2004)

We explore the extent to which neocortical circuits generalize, i.e., to what extent can neocortical neurons and the circuits they form be considered as canonical? We find that, as has long been suspected by cortical neuroanatomists, the same basic laminar and tangential organization of the excitatory neurons of the neocortex is evident wherever it has been sought. Similarly, the inhibitory neurons show characteristic morphology and patterns of connections throughout the neocortex. We offer a simple model of cortical processing that is consistent with the major features of cortical circuits: The superficial layer neurons within local patches of cortex, and within areas, cooperate to explore all possible interpretations of different cortical input and cooperatively select an interpretation consistent with their various cortical and subcortical inputs.
RADIOAUTOGRAPHIC STUDIES OF PLAQUE-FORMING CELLS
Authors: Aurelia M. C. Koros, John M. Mazur, Margaret J. Mowery
Journal: The Journal of Experimental Medicine (1968)

A method has been described for obtaining radioautographs of plaque-forming cells. The method permits radioautographic analyses of small numbers of plaque-forming cells amidst large populations of non-plaque-forming cells. Spleen cells that were pulse-labeled with tritiated thymidine could be categorized readily as labeled or not labeled. Using this method it was found that (a) at least 55% of plaque-forming cells which appear 3 days after a maximal stimulus of 4 x 10(8) sheep red cells are still capable of DNA synthesis, and must have arisen by cell proliferation; (b) the rate of proliferation of plaque-forming cells is proportional to the log of the dose of antigen; (c) the S period of plaque-forming cells is at least 2 hr, appears to be constant, and is not influenced by antigen dose. The results suggest that antigen stimulates proliferation of plaque-forming cells by hastening their transit through the G(1) phase of the generative cycle.
Immune complexes in ankylosing spondylitis.
Authors: I L MacLean, J R Archer, M I Cawley, B L Kidd, B P O'Hara, F S Pegley, P W Thompson
Journal: Annals of the Rheumatic Diseases (1992)

Immune complexes have been reported in ankylosing spondylitis (AS) and may implicate infectious agents. Serum samples from 49 patients with AS were assayed for immune complexes by polyethylene glycol precipitation, followed by radial immunodiffusion and pepsinogen binding immunoassay. Both methods showed increases in IgA containing immune complexes, which correlated with serum IgA and with IgA rheumatoid factor concentrations, but did not show increases in other immune complex components. Increased immune complexes were associated with peripheral joint synovitis, but showed no correlation with other clinical or laboratory indices of disease activity. Immune complexes from nine AS serum samples and one AS synovial fluid were electrophoretically separated then probed with anti-Klebsiella pneumoniae, but AS specific antigens were not identified. This study did not suggest a major role for immune complexes in AS without peripheral disease, nor provide serological evidence for the involvement of klebsiella antigens.
Comment re: Cancer Incidence Falls for Oldest
Authors: Tengiz Mdzinarishvili, Michael X. Gleason, Simon Sherman
Journal: Cancer Research (2008)

To the Editor: Recently, Harding and colleagues (1) have shown that the cancer incidence rates decrease in old age and may drop to zero near the end of the human life span. The authors added a linearly decreasing factor to the Armitage-Doll multistage model of cancer (2, 3) and obtained a β distribution–like model function. By this model, they obtained a good fit for incidence rates of many cancers; however, this work has several drawbacks:By introducing a lower age limit (A) in addition to the upper limit (B), in the β function (4), one can obtain the following: I(T) = aTk−1(1 − bT), where I(T) is the incidence rate, T = (t − A), b = (B − A)−1, t is the age in years, k is the number of cancer stages, and a is a combined rate constant; a and k can be used as variables, whereas A and B can be treated as a priori data extracted from observations. The use of a priori information can reduce the number of derived variables and stabilize the solution against variations of input data (5). As an example, consider pancreatic cancer incidence rates in males as reported by the Surveillance Epidemiology and End Results database for the years 1999 to 2003. One can evaluate A and B, for which the incidence rates are statistically distinguishable from zero, to be approximately equal to 30 and 100, respectively, and obtain a good fit with k ≈ 4. By contrast, the authors report a fit of comparable quality with k ≈ 7, when A is 0 and B ≈ 100.We appreciate the importance of the work, but determination of confidence intervals is crucial for the model to be applicable for rigorous statistical analysis.No potential conflicts of interest were disclosed.
Effects of fluticasone propionate on methacholine dose-response curves in nonsmoking atopic asthmatics
Authors: SE Overbeek, PR Rijnbeek, C Vons, PG Mulder, HC Hoogsteden, JM Bogaard
Journal: European Respiratory Journal (1996)

Methacholine is frequently used to determine bronchial hyperresponsiveness (BHR) and to generate dose-response curves. These curves are characterized by a threshold (provocative concentration of methacholine producing a 20% fall in forced expiratory volume in one second (PC20) = sensitivity), slope (reactivity) and maximal response (plateau). We investigated the efficacy of 12 weeks of treatment with 1,000 microg fluticasone propionate in a double-blind, placebo-controlled study in 33 atopic asthmatics. The outcome measures used were the influence on BHR and the different indices of the methacholine dose-response (MDR) curve. After 2 weeks run-in, baseline lung function data were obtained and a MDR curve was measured with doubling concentrations of the methacholine from 0.03 to 256 mg x mL(-1). MDR curves were repeated after 6 and 12 weeks. A recently developed, sigmoid cumulative Gaussian distribution function was fitted to the data. Although sensitivity was obtained by linear interpolation of two successive log2 concentrations, reactivity, plateau and the effective concentration at 50% of the plateau value (EC50) were obtained as best fit parameters. In the fluticasone group, significant changes occurred after 6 weeks with respect to means of PC20 (an increase of 3.4 doubling doses), plateau value fall in forced expiratory volume in one second (FEV1) (from 58% at randomization to 41% at 6 weeks) and baseline FEV1 (from 3.46 to 3.75 L) in contrast to the placebo group. Stabilization occurred after 12 weeks. Changes for reactivity were less marked, whereas changes in log, EC50 were not significantly different between the groups. We conclude that fluticasone is very effective in decreasing the maximal airway narrowing response and in increasing PC20. However, it is likely that part of this increase is related to the decrease of the plateau of maximal response.
Difference in Geometry of Young and Old Human Erythrocytes Explained by a Filtering Mechanism
Authors: PETER B. CONHAM
Journal: Circulation Research (1969)

A mechanism for the geometric difference between young and old human red blood cells is proposed. It is assumed that the bone marrow produces a population of cells with a range of sizes and shapes, but only those cells which can pass through a theoretical 3.65µ, cylindrical channel survive in the circulation. The important geometric parameters of an erythrocyte are the area and the volume. We suggest that as cells age they have a constant area but swell in proportion to their original volume. This hypothesis of aging was tested on 1,016 normal cells using the IBM 7040 computer. When the cells were theoretically swelled by approximately 15%, the population of cells which could still pass through the filter had a smaller mean area and volume and were more osmotically fragile than the same cells before swelling. Young and old cells were separated by centrifugation. The heaviest 10% of the cells (old cells) had a lower diameter, area, and volume and higher sphericity index than the lightest 20% (young cells). The calculated minimum filter diameter was not significantly different. The good agreement between the predicted and observed changes in cellular geometry between young and old cells provides supporting evidence that a cylindrical filter exists in the circulation and may play a role in determining the life span of the erythrocyte.
A phase I/II study of galiximab (an anti-CD80 monoclonal antibody) in combination with rituximab for relapsed or refractory, follicular lymphoma
Authors: J.P. Leonard, J.W. Friedberg, A. Younes, D. Fisher, L.I. Gordon, J. Moore, M. Czuczman, T. Miller, P. Stiff, B.D. Cheson, A. Forero-Torres, N. Chieffo, B. McKinney, D. Finucane, A. Molina
Journal: Annals of Oncology (2007)
STUDIES ON INFECTION AND IMMUNITY IN EXPERIMENTAL TYPHOID FEVER
Authors: Sidney Gaines, Maurice Landy, Geoffrey Edsall, Adrian D. Mandel, R.-J. Trapani, A. S. Benenson
Journal: The Journal of Experimental Medicine (1961)

A study was made of the efficacy of various antityphoid immunizing agents in immunizing chimpanzees against typhoid fever produced by feeding viable S. typhosa. It was found that both acetone-killed and heat-killed, phenol-preserved typhoid vaccines were effective in protecting against infection induced with either homologous or heterologous strains of typhoid bacilli. Purified O antigen induced no discernible protection, but some immunity was afforded by the administration of purified Vi antigen.
Identification of novel mutations in ADAMTS13 in an adult patient with congenital thrombotic thrombocytopenic purpura
Authors: Toshihiro Uchida, Hideo Wada, Minoru Mizutani, Miho Iwashita, Hiroaki Ishihara, Toshiro Shibano, Misako Suzuki, Yumiko Matsubara, Kenji Soejima, Masanori Matsumoto, Yoshihiro Fujimura, Yasuo Ikeda, Mitsuru Murata
Journal: Blood (2004)
RUNNING INTERFERENCE: Prospects and Obstacles to Using Small Interfering RNAs as Small Molecule Drugs
Authors: Derek M. Dykxhoorn, Judy Lieberman
Journal: Annual Review of Biomedical Engineering (2006)

RNA interference (RNAi) is a well-conserved, ubiquitous, endogenous mechanism that uses small noncoding RNAs to silence gene expression. The endogenous small RNAs, called microRNAs, are processed from hairpin precursors and regulate important genes involved in cell death, differentiation, and development. RNAi also protects the genome from invading genetic elements, encoded by transposons and viruses. When small double-stranded RNAs, called small interfering (si)RNAs, are introduced into cells, they bind to the endogenous RNAi machinery to disrupt the expression of mRNAs containing complementary sequences with high specificity. Any disease-causing gene and any cell type or tissue can potentially be targeted. This technique has been rapidly utilized for gene-function analysis and drug-target discovery and validation. Harnessing RNAi also holds great promise for therapy, although introducing siRNAs into cells in vivo remains an important obstacle. Pilot siRNA clinical studies began just three years after the discovery that RNAi works in mammalian cells. This review discusses recent progress and obstacles to using siRNAs as small molecule drugs.
Occupational asthma in a hairdressing salon.
Authors: A D Blainey, S Ollier, D Cundell, R E Smith, R J Davies
Journal: Thorax (1986)

Occupational asthma among hairdressers has been recognised for some years and cases of work related asthma due to hair bleaches containing persulphates and hair dyes have been reported. The extent of the disease among hairdressers remains unknown. An investigation was carried out on an entire hairdressing salon, which specialised in hair bleaching and colouring and which employed 23 staff. On the basis of history and specific and non-specific bronchial provocation testing, four out of 23 staff were found to have occupational asthma due to the persulphate salts contained in hair bleaches. Only one of these had a positive skinprick test response to persulphate salts. Tests for non-specific bronchial reactivity to histamine in this work force were more sensitive for the diagnosis of asthma than simple lung function tests or recordings of peak flow rates performed four times daily for three weeks. The response to these agents was studied in greater detail by specific bronchial provocation tests in 14 members of the salon as well as one hairdresser from elsewhere with occupational asthma, three individuals with non-occupational asthma, and four normal subjects. Only those with a history of work related asthma and bronchial hyperreactivity responded positively, confirming that the response to bleach powders was specific. Studies of pulmonary mechanics after challenge showed that the response arose from changes in airway calibre not lung volumes. Measurement of neutrophil chemotactic activity after challenge showed significant rises in those affected, suggesting that mast cells may play a part in the pathogenesis of occupational asthma due to persulphates.
Focal Segmental Glomerulosclerosis
Authors: R C Goldszer, J Sweet, R S Cotran
Journal: Annual Review of Medicine (1984)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Induction of Renal Tubular Cell Apoptosis in Focal Segmental Glomerulosclerosis
Authors: Elif Erkan, Clotilde D. Garcia, Larry T. Patterson, Jaya Mishra, Mark M. Mitsnefes, Frederick J. Kaskel, Prasad Devarajan
Journal: Journal of the American Society of Nephrology (2004)

The hypothesis that apoptosis represents a proximate mechanism by which tubule cells are damaged in FSGS was tested. Thirty kidney biopsy specimens from children with idiopathic early FSGS were studied retrospectively. Unexpected, apoptosis was evident in both proximal and distal tubule cells. There was a significant correlation between the degree of proteinuria and the number of apoptotic cells. Fas protein was detected predominantly in the tubule cells that underwent apoptosis. When compared with patients with other chronic proteinuric states, those with FSGS displayed a proliferation/apoptosis ratio in favor of proliferation in the glomerulus but dramatically in favor of apoptosis in the tubules. When both proteinuria and apoptosis were included in a stepwise logistic regression procedure, only apoptosis was found to predict independently the development of ESRD. Prolonged incubation of cultured Madin-Darby canine kidney (distal/collecting) cells with albumin also resulted in a dose- and duration-dependent induction of apoptosis and activation of the Fas pathway, lending support to the novel finding of distal tubule cell apoptosis in patients with FSGS. The results indicate that an elevated tubule cell apoptosis rate at the time of initial biopsy represents an independent predictor of progression to ESRD in patients with early FSGS.
Multivariate Assessment of Lipid Parameters as Predictors of Coronary Heart Disease Among Postmenopausal Women
Authors: Iris Shai, Eric B. Rimm, Susan E. Hankinson, Gary Curhan, JoAnn E. Manson, Nader Rifai, Meir J. Stampfer, Jing Ma
Journal: Circulation (2004)

Background— Over the past decade, lipid measurements have been significantly improved and standardized. We evaluated the usefulness of multiple plasma lipid parameters in predicting coronary heart diseases (CHD) among women. Methods and Results— Among 32 826 women from the Nurses’ Health Study who provided blood samples at baseline, 234 CHD events were documented during 8 years of follow-up. In a nested study, these cases were matched to controls (1:2) for age, smoking, fasting status, and month of blood draw. We estimated the relative risk (RR) for each lipid parameter, adjusted for C-reactive protein, homocysteine, body mass index, family history, hypertension, diabetes, postmenopausal hormone use, physical activity, alcohol intake, and blood draw parameters. The RRs associated with an increase of ≈1 SD (mg/dL) were as follows: HDL cholesterol (HDL-C) (RR=0.6 [0.5 to 0.8], SD=17), apolipoprotein B 100 (apoB 100 ) (RR=1.7 [1.4 to 2.1], SD=32), LDL cholesterol (LDL-C) (RR=1.4 [1.1 to 1.7], SD=36), total cholesterol (TC) (RR=1.4 [1.1 to 1.6], SD=40), and triglycerides (RR=1.3 [1.0 to 1.5], SD=80). Among the lipid indexes, the RRs were: apoB 100 /HDL-C (RR=1.7 [1.4 to 2.1], SD=1.0), TC/HDL-C (RR=1.6 [1.3 to 1.9], SD=1.3), LDL-C/HDL-C (RR=1.5 [1.3 to 1.9], SD=1.0), and non–HDL-C (RR=1.6 [1.3 to 1.9], SD=42 mg/dL). After simultaneous control for several lipid biomarkers, HDL-C was the primary contributor of the variation in multivariate models ( P =0.01), followed by LDL-C ( P =0.01), whereas triglycerides and apoB 100 did not contribute further information. HDL-C–related ratios were the strongest contributors to predicting CHD ( P &lt;0.0001). Conclusions— Lower levels of HDL-C may be a key discriminator of higher CHD events among postmenopausal women. HDL-C–related ratios (such as TC/HDL-C) provide a powerful predictive tool independently of other known CHD risk factors.