tbuckley/cabot-search huggingface dataset:
Secondary Disease in Irradiated Mice Grafted With Allogeneic Bone Marrow From Antilymphocyte Serum-Treated Donors&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: G D Ledney, D W van Bekkum
Journal: JNCI Journal of the National Cancer Institute (1969)

Donor mice were treated with antilymphocyte serum (ALS) and antilymphocyte serum globulin (ALG) to ascertain the influence of these substances on the symptoms of, and mortality from, delayed secondary disease. Groups of donor C57BL mice received 4 consecutive daily injections of either ALS or ALG, and 24 hours after the last treatment 20 × 106bone marrow cells were transplanted into CBA mice that had received 875 rads X radiation. As controls, other groups of donor mice were given normal rabbit serum (NRS), normal rabbit-serum globulin (NRG), or physiologic saline (NaCl) before their cells were grafted into irradiated mice. Weight loss from secondary disease occurred during the 3d week in mice grafted with marrow from NaCl- and NRG-treated donors and during the 4th week in mice grafted with marrow from NRS-, ALS-, and ALG-treated donors. Mortality from secondary disease began about 15–25 days after treatment when mice were grafted with marrow from NaCl- and NRG-treated donors and approximately 40–50 days after grafting when donor mice received NRS, ALS, or ALG. All mice grafted with marrow from NaCl-treated donors were dead within 60 days. Approximately 10% of the mice grafted with cells from NRS- or NRG-treated donors survived the 120-day observation period. Survival in mice grafted with cells from ALS-treated donors was about 10%, whereas 50% of the mice grafted with bone marrow from ALG-treated donors survived.
Correction: NIH Conference Citation
Authors: PAUL D. BERK
Journal: Annals of Internal Medicine (1975)

Comments and Correction1 July 1975Correction: NIH Conference CitationPAUL D. BERK, M.D.PAUL D. BERK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-83-1-126 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In the NIH Combined Clinical Staff Conference entitled "Unconjugated Hyperbilirubinemia" (Ann Intern Med82:552-570, 1975), we neglected to cite the classical experimental work of London and associates (1) and Gray, Neuberger, and Sneath (2) on the early-labeled peak of bile pigment production. This was the basis for our Figure 9 and the related discussion. The authors regret this omission....References1. LONDON I, WEST R, and SHEMIN D: On the origin of bile pigment in normal man. J Biol Chem 184:351-358, 1950 CrossrefMedlineGoogle Scholar2. GRAY C, NEUBERGER A, and SNEATH P: Studies in congenital porphyria. 2. Incorporation of 15N in the stercobilin in the normal and in the porphyric. Biochem J 47:87-92, 1950 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: PAUL D. BERK, M.D.Affiliations: Section on Diseases of the Liver Digestive Diseases Branch National Institute of Arthritis, Metabolism, and Digestive Diseases Bethesda, Maryland 20014 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 July 1975Volume 83, Issue 1Page: 126-126KeywordsBileEmotions ePublished: 1 December 2008 Issue Published: 1 July 1975 PDF downloadLoading ...
CLINICAL REMARKS ON SYPHILISATION
Authors: J. S. Gamgee
Journal: BMJ (1854)

WIrA,TBZZR be the judgment which experience will event- ually pronounce upon the merits of syphilisation, there can be no question as to its present claims upon the attention of every one who is interested in lessening the evils of one of the greatest scourges of the human race.Though only a few years have elapsed since the fundamental fact was an- nounced on which the doctrine and practice under consider- ation are based, it has been repeatedly debated in the medi- cal academies of the continent.Though these have for the most part condemned it, Auzias Turenne in Paris, Sperino in Turin, Boeck in Christiania, and Siegmund in Vienna, persist in its advocacy: though it has been sweepingly con- demned as chimerical and immoral, numerous well esta- blished facts connected with it await solution, and it has yet to be proved that efforts to lessen the evils of syphilis are contrary to morality.The opportunity which I have recently enjoyed of frequent interviews with Prof. Sperino, privately, and in the Turin Syphilicome, at the head of which he is placed, will, I trust, be deemed a sufficient apology for this communication.The cases I observed were of old date,the Professor having, for reasons presently to be noticed, suspended his experi-
A Case of Poisoning by Nitrate of Silver
Authors: T. Scattergood
Journal: BMJ (1871)

THE BRIT-ISH MEDICAL _70URNAL.527 3.In anchylosis after traumatic inflammation in healthy adults, such as that which occurs after wounds of the joints, and gun-shot wounds in the neighbourhood of the joints, when the joint itself has escaped injury; and in some cases of anchylosis, chiefly from long-retained position, occurs, as a general rule, no destruction of bone even after acute suppurative inflammation, the soft tissues only being involved.
Abstract 4928: Deregulation of asymmetry genes in oligodendrogliomas and glioblastomas
Authors: Noemi Andor, Claudia Petritsch
Journal: Cancer Research (2012)

Abstract BACKGROUND. Normal neural stem cells and NG2+ oligodendrocyte progenitors (OPC) undergo asymmetric cell division to generate a balanced number of self-renewing and differentiating progeny. Our recent studies showed that NG2+ OPC are the tumor-forming cells in oligodendrogliomas (ODG), a therapy-sensitive glioma. We provide cellular and molecular evidence that defects in asymmetric division of NG2+ OPC might contribute to tumor-initiation in oligodendrogliomas. In contrast, tumor-initiating cells in the highly resistant glioblastomas (GBM) express stem cell markers and show a high number of asymmetric divisions. We propose that distinct key asymmetry genes might be deregulated in the two types of tumor-initiating cells causing them to generate progeny with distinct therapy-sensitivity. Identifying these asymmetry key regulator networks will elucidate the mechanism by which tumor-initiating cells in gliomas maintain tumors and re-grow them after therapy. METHOD. A knowledge based network, consisting of asymmetry-genes and their transcriptional regulators, was constructed and refined by correlated gene expression. Subsequently, copy number and methylation were mapped onto the network and their impact on expression was assessed. In addition, the expression profiles of asymmetry genes within glioma samples were compared against their counterparts in normal brain samples and putative associations between expression and clinical outcome were tested. RESULTS. Our study has identified cancer- and differentiation associated transcription factors as putative regulators of asymmetry genes. In GBM tumors it was found that asymmetry genes are mostly affected by single copy gains and heterozygous deletions with an apparent influence on gene expression. When considered upon ODG tumors, the pattern of deregulation was distinct from that observed in GBM: for a subset of asymmetry genes a mutually exclusive deregulation was observable in either GBM or ODG, while another gene subset was progressively deregulated in ODG- and GBM. Taken together, our results indicate that asymmetry genes are distinctly regulated in ODG and GBM. We will discuss a model how this could contribute to distinct levels of therapy resistance. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4928. doi:1538-7445.AM2012-4928
Adhesion molecules of cultured hematopoietic malignancies. A calcium-dependent lectin is the principle mediator of binding to the high endothelial venule of lymph nodes.
Authors: L M Stoolman, H Ebling
Journal: Journal of Clinical Investigation (1989)

This study documents that a calcium-dependent phosphomanosyl-binding site on human lymphoid malignancies mediates attachment to the peripheral node high endothelial venule (PNHEV). The phorbol ester PMA coordinately upregulates lectin activity and binding to the PNHEV in the human T-lymphoblastic cell line Jurkat but not in the less phenotypically mature lines HSB2, Molt4, CEM, and HPB-ALL. In contrast, expression of CD18, CD2, and several common epitopes of the putative adhesion receptor gp90Hermes (CD44) did not correlate with attachment to PNHEV in this series of cell lines. Insensitivity to inhibition by the CD18 MAb TS 1.18, temperature and divalent cation requirements further distinguish the Jurkat-PNHEV adhesive interaction from CD11a/18- and CD2-mediated adhesion. The PMA-induced phenotypic changes in the Jurkat line parallel late thymocyte differentiation as well as lymphocyte activation, suggesting that expression of the endothelial-binding lectin may be linked to one or both of these processes. The lectin-like activity on Jurkat cells is functionally indistinguishable from those previously linked to PNHEV recognition in normal human lymphocytes, normal rat lymphocytes and both normal and malignant murine lymphoid cells. In the mouse, this activity is either contained in or functionally linked to a member of the LEC-CAM family gp90Mel14, suggesting that Jurkat cells express the human homologue of the murine nodal homing receptor. Thus cultured T lymphoblastic malignancies express a variety of potential endothelial adhesion molecules but use primarily a highly conserved surface lectin to interact with PNHEV.
The relative merits of pulsus paradoxus and right ventricular diastolic collapse in the early detection of cardiac tamponade: an experimental echocardiographic study.
Authors: H S Klopfenstein, G H Schuchard, L S Wann, T E Palmer, A J Hartz, C M Gross, S Singh, H L Brooks
Journal: Circulation (1985)

An inspiratory decline in systolic arterial blood pressure exceeding 10 mm Hg has been used clinically to identify hemodynamically significant pericardial effusions. Recently, the echocardiographic sign of right ventricular diastolic collapse (RVDC) has been shown to occur early in the course of cardiac tamponade in association with a hemodynamically important decline in cardiac output. This study was undertaken to compare the relative merits of pulsus paradoxus and the onset of RVDC in the early detection of cardiac tamponade in an unanesthetized canine preparation. We studied six chronically instrumented, conscious dogs with two-dimensional echocardiography during cardiac tamponade induced by continuous infusion of saline into the pericardial space. We recorded intrapericardial pressure, cardiac output (electromagnetic flowmeter), aortic (catheter-tip transducer) and right atrial blood pressures, heart rate, and respiration. None of the dogs had RVDC when the pericardial space was empty, but all dogs showed RVDC during cardiac tamponade. We found that RVDC was strongly related to all of the cardiac parameters evaluated (intrapericardial pressure, cardiac output, aortic blood pressure, heart rate, and stroke volume) and provided information on each that was independent of that provided by pulsus paradoxus. Furthermore, RVDC appeared to be more strongly related to most cardiac parameters than was pulsus paradoxus and to be more sensitive and specific than pulsus paradoxus in detecting changes in intrapericardial pressure early in cardiac tamponade.
Transcriptional targeting of dendritic cells in gene gun-mediated DNA immunization favors the induction of type 1 immune responses
Authors: Stephan Sudowe, Isis Ludwig-Portugall, Evelyn Montermann, Ralf Ross, Angelika B Reske-Kunz
Journal: Molecular Therapy (2003)

Cutaneous dendritic cells (DC) are pivotal for the elicitation of antigen-specific immune responses following gene gun-mediated biolistic transfection of the skin. We transcriptionally targeted transgene expression to DC using vectors containing the murine fascin promoter (pFascin) to control antigen production and compared the immune response elicited with conventional DNA immunization using plasmid constructs with the ubiquitously active CMV promoter (pCMV). Biolistic transfection with pFascin initiated a marked type 1 immune response characterized by the occurrence of a large population of IFN-γ-producing T helper (Th) cells in spleen and draining lymph nodes. Consistently, immunoglobulin production was dominated by IgG2a antibodies. In contrast, the humoral response after repeated administration of pCMV was strongly enhanced and characterized by a type 2-like isotype pattern (IgG1 > IgG2a). Cytokine production analysis in vitro indicated compartmentalization of the immune response, revealing large numbers of IL-4-producing Th cells in the lymph nodes and dominant presence of IFN-γ-producing Th cells in the spleen. Biolistic transfection with pFascin, like immunization with pCMV, led to potent induction of cytotoxic T cells as was assessed by JAM test. Thus gene gun immunization with plasmids that focus transgene expression and antigen production specifically to DC propagates type 1-biased cellular immune responses.
Epigenetic Regulation of <i>miR-17∼92</i> Contributes to the Pathogenesis of Pulmonary Fibrosis
Authors: Duaa Dakhlallah, Kara Batte, Yijie Wang, Carmen Z. Cantemir-Stone, Pearlly Yan, Gerard Nuovo, Adel Mikhail, Charles L. Hitchcock, Valerie P. Wright, S. Patrick Nana-Sinkam, Melissa G. Piper, Clay B. Marsh
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

Idiopathic pulmonary fibrosis (IPF) is a disease of progressive lung fibrosis with a high mortality rate. In organ repair and remodeling, epigenetic events are important. MicroRNAs (miRNAs) regulate gene expression post-transcriptionally and can target epigenetic molecules important in DNA methylation. The miR-17~92 miRNA cluster is critical for lung development and lung epithelial cell homeostasis and is predicted to target fibrotic genes and DNA methyltransferase (DNMT)-1 expression.We investigated the miR-17~92 cluster expression and its role in regulating DNA methylation events in IPF lung tissue.Expression and DNA methylation patterns of miR-17~92 were determined in human IPF lung tissue and fibroblasts and fibrotic mouse lung tissue. The relationship between the miR-17~92 cluster and DNMT-1 expression was examined in vitro. Using a murine model of pulmonary fibrosis, we examined the therapeutic potential of the demethylating agent, 5'-aza-2'-deoxycytidine.Compared with control samples, miR-17~92 expression was reduced in lung biopsies and lung fibroblasts from patients with IPF, whereas DNMT-1 expression and methylation of the miR-17~92 promoter was increased. Several miRNAs from the miR-17~92 cluster targeted DNMT-1 expression resulting in a negative feedback loop. Similarly, miR-17~92 expression was reduced in the lungs of bleomycin-treated mice. Treatment with 5'-aza-2'-deoxycytidine in a murine bleomycin-induced pulmonary fibrosis model reduced fibrotic gene and DNMT-1 expression, enhanced miR-17~92 cluster expression, and attenuated pulmonary fibrosis.This study provides insight into the pathobiology of IPF and identifies a novel epigenetic feedback loop between miR-17~92 and DNMT-1 in lung fibrosis.
Why Prion Diseases Are a Mystery, and Why They Matter
Authors: Jennifer Fisher Wilson
Journal: Annals of Internal Medicine (2005)

Current Clinical Issues15 November 2005Why Prion Diseases Are a Mystery, and Why They MatterJennifer Fisher WilsonJennifer Fisher WilsonAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-143-10-200511150-00037 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Prion diseases are rare in humans. Only about 300 Americans per year develop these fatal brain-wasting diseases, such as sporadic Creutzfeldt-Jakob Disease (CJD), Gerstmann-Sträussler-Scheinker syndrome, or fatal insomnia. New variant CJD, from consumption of beef infected with bovine spongiform encephalopathy, is even more rare—only about 150 people worldwide have been infected so far, and the number of new cases is waning. Prion diseases that infect animals other than cows—scrapie in goats and sheep and chronic wasting disease in elk and deer—do not appear to infect humans.However, just because these diseases are rare in humans does not make them irrelevant. ... Author, Article, and Disclosure InformationAffiliations: Disclosures: None disclosed.E-mail:[email protected]org PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byScientific Visuals, Language, and the Commercialization of a Scientific Idea: The Strange Case of the Prion 15 November 2005Volume 143, Issue 10Page: 773-776KeywordsBrainBrain diseasesCellsInfectious diseasesNeurodegenerative diseasesPrion diseasesPrionsProteinsResearch laboratoriesScientists ePublished: 15 November 2005 Issue Published: 15 November 2005 Copyright & PermissionsCopyright © 2005 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Effect of diltiazem and propranolol on left ventricular segmental relaxation during temporary coronary arterial occlusion and one month reperfusion in conscious dogs.
Authors: G D Tilton, L R Bush, P G Apprill, L M Buja, J T Willerson
Journal: Circulation (1985)

Using sonar microcrystals implanted in conscious dogs, we have characterized left ventricular segmental relaxation (LVSR) by measuring the mean rate to half end-diastolic thinning (RHEDT) and the late diastolic thinning fraction (TF). In protocol 1 (five nonischemic dogs), RHEDT correlated with changes in left ventricular dP/dt (r = .87) and systemic arterial pressure (r = -.80) but not with alterations in heart rate. Only systemic arterial pressure importantly influenced TF (r = -.65). In protocol 2 (21 dogs), LVSR paralleled net systolic segmental wall thickness (NET) during both 2 and 4 hr of coronary occlusion followed by 1 month reperfusion. Both LVSR and NET remained depressed during 2 and 4 hr of coronary occlusion and through 24 hr of reperfusion, but both also gradually improved afterwards. In protocol 3, 31 dogs underwent 4 hr of coronary occlusion with 1 month of reperfusion. Among these animals, 11 dogs (group S4) received saline after 1 hr of occlusion, nine dogs (group P4) received propranolol, and 11 dogs (group D4) received diltiazem. Drug therapy was stopped at 2 hr of reperfusion. In segments with mildly and moderately depressed NET, LVSR was significantly increased in group D4 vs group S4 animals during the diltiazem infusion. Expressed as mean percentage of control value +/- SEM, RHEDT of moderately dysfunctional segments in group D4 compared with group S4 measured 53 +/- 10% vs 25 +/- 5%, respectively, at 2 hr of occlusion of the left anterior descending coronary artery (p = .03), 76 +/- 17% vs 28 +/- 8%, respectively, at 4 hr of occlusion (p = .01), and 74 +/- 11% vs 33 +/- 10%, respectively, at 1 hr of reperfusion (p less than .05). The differences in TF at these same time points were 106 +/- 10% vs 70 +/- 9% (p less than .03), 105 +/- 7% vs 65 +/- 16% (p less than .02), and 106 +/- 11% vs 74 +/- 13% (p less than .05), respectively. The improvement in LVSR occurred independently of changes in NET. The values of LVSR in the diltiazem-treated dogs fell to the levels of groups S4 and P4 within 24 hr of stopping the intervention. Propranolol did not significantly alter LVSR over the short or long term. The increase in LVSR during administration of diltiazem did not appear to be mediated by changes in contractility or regional myocardial blood flow, but were probably mediated in part by afterload reduction and possibly by a reduction in calcium entry into ischemic myocardium.
Cancer Surveillance Series: Non-Hodgkin's Lymphoma Incidence by Histologic Subtype in the United States From 1978 Through 1995
Authors: F. D. Groves, M. S. Linet, L. B. Travis, S. S. Devesa
Journal: JNCI Journal of the National Cancer Institute (2000)

Background: Clinical investigations have shown prognostic heterogeneity within the non-Hodgkin's lymphomas (NHLs) according to histology, but few descriptive studies have considered NHLs by subgroup. Our purpose is to assess the demographic patterns and any notable increases in population-based rates of different histologic subgroups of NHL. Methods: Using data collected by the Surveillance, Epidemiology, and End Results Program of the National Cancer Institute, we calculated incidence rates for the major clinicopathologic categories of NHL by age, race, sex, geographic area, and time period. Results: Among the 60 057 NHL cases diagnosed during the period from 1978 through 1995, total incidence (per 100 000 person-years) was 17.1 and 11.5 among white males and females, respectively, and 12.6 and 7.4 among black males and females, respectively. However, rates for follicular NHLs were two to three times greater among whites than among blacks, with little sex variation. Blacks demonstrated much higher incidence than whites for peripheral T-cell NHL, with the incidence rates higher in males than in females. For other NHL subgroups, the incidence rates for persons less than 60 years of age were generally higher among males than among females, with little racial difference; at older ages, the rates were higher among whites than among blacks, with little sex difference. High-grade NHL was the most rapidly rising subtype, particularly among males. Follicular NHL increased more rapidly in black males than in the other three race/sex groups. Overall, the broad categories of small lymphocytic, follicular, diffuse, high-grade, and peripheral T-cell NHL emerged as distinct entities with specific age, sex, racial, temporal, and geographic variations in rates. Conclusions: Findings from our large, population-based study reveal differing demographic patterns and incidence trends according to histologic group. Future descriptive and analytic investigations should evaluate NHL risks according to subtype, as defined by histology and new classification criteria.
MATURATION OF HEMOLYSIN-PRODUCING CELL CLONES
Authors: George C. Saunders
Journal: The Journal of Experimental Medicine (1969)

INVESTIGATIONS OF THE INDUCTION PERIOD OF AN IN VITRO HEMOLYSIN RESPONSE TO SHEEP ERYTHROCYTE ANTIGEN REVEALED THE FOLLOWING: 1. After antigen stimulation precursors of plaque-forming cells rapidly maturate to the point of hemolysin production. 2. Initial maturation probably occurs in the absence of cell division. 3. After initial maturation, a latent period of about 12 hr occurs before the first doubling of PFC. 4. At least the first three cell doublings are synchronous, with a generation time of 7-8 hr. 5. Synchronous cell division implies that all precursor cells are at the same point in the cell cyde when they are initially stimulated.
Postinfarction Risk Stratification
Authors: George A. Diamond
Journal: JAMA (1993)

On August 29, 1949, the Soviet Union exploded its first nuclear bomb. Advocates of "preventive war"—including such luminaries as Bertrand Russell and John von Neumann— argued that an eventual armed confrontation with the Soviets was inevitable, and that the United States should therefore seize the opportunity to launch a pre-emptive first strike. To those who countenanced a more cautious wait-and-see attitude, von Neumann responded, "If you say why not bomb them tomorrow, I say why not today? If you say today at five o'clock, I say why not one o'clock?"<sup>1</sup> See also p 2379. The medical counterpart of preventive war is currently being waged under the pseudonym "risk stratification." Risk stratification strategies are based on the tacit assumption that physicians can accurately predict the unfavorable outcome of individual patients and that they possess effective ways to mitigate that unfavorable outcome. If so, the sooner one intervenes, the better. Indeed,