tbuckley/cabot-search huggingface dataset:
Interferon and Delta Hepatitis
Authors: Bruno Taillan
Journal: Annals of Internal Medicine (1988)

Letters and Corrections1 November 1988Interferon and Delta HepatitisBruno Taillan, MD, Jean-Gabriel Fuzibet, MD, Henri Vinti, MD, Alain Pesce, MD, Jill-Patrice Cassuto, MD, Pierre Dujardin, MDBruno Taillan, MDSearch for more papers by this author, Jean-Gabriel Fuzibet, MDSearch for more papers by this author, Henri Vinti, MDSearch for more papers by this author, Alain Pesce, MDSearch for more papers by this author, Jill-Patrice Cassuto, MDSearch for more papers by this author, Pierre Dujardin, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-9-760_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: Aach (1) states that interferon is the most promising antiviral agent for treating patients with chronic type B viral hepatitis. For patients at risk for infection with human immunodeficiency virus (HIV), however, antiviral agents do not appear to be the optimal treatment of chronic type B viral hepatitis in those patients who may be simultaneously infected with hepatitis delta virus (2). We report eight cases of severe liver disease due to hepatitis B virus and concurrent hepatitis delta virus infections in patients treated with recombinant alpha-2-interferon, 5 MU three times a week for 6 months.All patients...References1. Aach R. The treatment of chronic type B viral hepatitis. Ann Intern Med. 1988;109:89-91. LinkGoogle Scholar2. Garcia G, Smith C, and Weissberg J. Adenine arabinoside monophosphate (vidarabine phosphate) in combination with human leukocyte interferon in the treatment of chronic hepatitis B: a randomized double-blinded, placebo-controlled trial. Ann Intern Med. 1987;107:278-85. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Bruno Taillan, MD; Jean-Gabriel Fuzibet, MD; Henri Vinti, MD; Alain Pesce, MD; Jill-Patrice Cassuto, MD; Pierre Dujardin, MDAffiliations: Cimiez Hospital 06003 Nice France PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byInterferon alpha for chronic hepatitis DTreatment of hepatitis DSection Review: Anti-infectives: Recent developments in the treatment of hepatitis D infectionThe French experience of treatment of chronic type D hepatitis with a 12-month course of interferon alpha-2B. Results of a randomized controlled trialInterferon in HDV infectionTreatment of chronic type D hepatitis and concomitant human immunodeficiency infection with α-interferonUse of α-interferon in the treatment of chronic delta hepatitis 1 November 1988Volume 109, Issue 9Page: 760-760KeywordsAntiviralsHepatitis AHepatitis B virusHepatitis DHepatitis D virusHIVInfectious diseasesInterferonsLiver diseases ePublished: 1 December 2008 Issue Published: 1 November 1988 PDF downloadLoading ...
The role of transglutaminase in the rat subtotal nephrectomy model of renal fibrosis.
Authors: T S Johnson, M Griffin, G L Thomas, J Skill, A Cox, B Yang, B Nicholas, P J Birckbichler, C Muchaneta-Kubara, A Meguid El Nahas
Journal: Journal of Clinical Investigation (1997)

Tissue transglutaminase is a calcium-dependent enzyme that catalyzes the cross-linking of polypeptide chains, including those of extracellular matrix (ECM) proteins, through the formation of epsilon-(gamma-glutamyl) lysine bonds. This crosslinking leads to the formation of protein polymers that are highly resistant to degradation. As a consequence, the enzyme has been implicated in the deposition of ECM protein in fibrotic diseases such as pulmonary fibrosis and atherosclerosis. In this study, we have investigated the involvement of tissue transglutaminase in the development of kidney fibrosis in adult male Wistar rats submitted to subtotal nephrectomy (SNx). Groups of six rats were killed on days 7, 30, 90, and 120 after SNx. As previously described, these rats developed progressive glomerulosclerosis and tubulo-interstitial fibrosis. The tissue level of epsilon-(gamma-glutamyl) lysine cross-link (as determined by exhaustive proteolytic digestion followed by cation exchange chromatography) increased from 3.47+/- 0.94 (mean+/-SEM) in controls to 13.24+/-1.43 nmol/g protein 90 d after SNx, P </= 0.01. Levels of epsilon-(gamma-glutamyl) lysine cross-link correlated well with the renal fibrosis score throughout the 120 observation days (r = 0.78, P </= 0.01). Tissue homogenates showed no significant change in overall transglutaminase activity (14C putrescine incorporation assay) unless adjusted for the loss of viable tubule cells, when an increase from 5.77+/-0.35 to 13.93+/-4.21 U/mg DNA in cytosolic tissue transglutaminase activity was seen. This increase was supported by Western blot analysis, showing a parallel increase in renal tissue transglutaminase content. Immunohistochemistry demonstrated that this large increase in epsilon-(gamma-glutamyl) lysine cross-link and tissue transglutaminase took place predominantly in the cytoplasm of tubular cells, while immunofluorescence also showed low levels of the epsilon-(gamma-glutamyl) lysine cross-link in the extracellular renal interstitial space. The number of cells showing increases in tissue transglutaminase and its cross-link product, epsilon-(gamma-glutamyl) lysine appeared greater than those showing signs of typical apoptosis as determined by in situ end-labeling. This observed association between tissue transglutaminase, epsilon-(gamma-glutamyl) lysine cross-link, and renal tubulointerstitial scarring in rats submitted to SNx suggests that tissue transglutaminase may play an important role in the development of experimental renal fibrosis and the associated loss of tubule integrity.
Efficacy of human C1 esterase inhibitor concentrate compared with placebo in acute hereditary angioedema attacks
Authors: Timothy J. Craig, Robyn J. Levy, Richard L. Wasserman, Againdra K. Bewtra, David Hurewitz, Krystyna Obtułowicz, Avner Reshef, Bruce Ritchie, Dumitru Moldovan, Todor Shirov, Vesna Grivcheva-Panovska, Peter C. Kiessling, Heinz-Otto Keinecke, Jonathan A. Bernstein
Journal: Journal of Allergy and Clinical Immunology (2009)
Lassa fever: retrospective diagnosis of two patients seen in Great Britain in 1971.
Authors: H M Gilles, J C Kent
Journal: BMJ (1976)

Lassa fever: retrospective diagnosis of two patients seen in Great Britain in 1971Lassa fever was first described by Frame et all in 1970, but it was not until three outbreaks had occurred in Jos, Liberia, and Sierra Leone that the disease attracted general attention,2-4 especially as the mor- tality of these outbreaks averaged 45%.We describe two patients admitted under our care in 1971 who recovered.The diagnosis was confirmed retrospectively by serological tests. Case 1This patient, a nursing sister, had worked in Sierra Leone for nearly four years.On the morning of 10 June 1971 she became ill at Serabu Hospital with general aches and pains, fever, and rigors and treated herself for malaria without improvement.Her temperature persisted and varied between 38' and 40'C, and she had severe anorexia, nausea, and vomiting.Despite courses of chloramphenicol and ampicillin the symptoms persisted and she was transferred to Freetown, where pseudomonal septicaemia was diagnosed and she was given a course of prednisone and cloxacillin.Her condition improved and she was transferred to the Tropical Diseases Unit in Liverpool for further investigation.She arrived by air from Sierra Leone via Las
The Efficacy of Low-Dose Versus Conventional Therapy of Insulin for Treatment of Diabetic Ketoacidosis
Authors: ABBAS E. KITABCHI
Journal: Annals of Internal Medicine (1976)

The effect of low-dose intramuscular insulin therapy was compared with that of high-dose insulin therapy by intravenous and subcutaneous routes in 48 patients with diabetic ketoacidosis. A simplified protocol was devised to compare efficacy of the two methods of therapy in a randomized manner. Plasma glucose dropped to less than 250 mg/dl in the low-dose group in 6.7 ± 0.8 h and in the high-dose group in 4.5 ± 0.8 h (P = not significant). The amount of insulin necessary to lower plasma glucose to 250 mg/dl was 263 ± 45 U in the high-dose group and 46 ± 5 U in the low-dose group. Twenty five percent in the high-dose group and none in the low-dose group developed hypoglycemia. Other biochemical and clinical variables in the two groups were comparable. No treatment complications were noted in the low-dose group. Our studies suggest that low-dose intramuscular insulin therapy is simple and as effective as high-dose therapy in the treatment of diabetic ketoacidosis without the risk of hypoglycemia and with a diminished incidence of hypokalemia. Furthermore, the favorable response of these patients to low-dose insulin therapy suggests the absence of insulin resistance in diabetic ketoacidosis.
Cardiopulmonary Resuscitation in Elderly Persons
Authors: Peter Cummings
Journal: Annals of Internal Medicine (1990)

Letters and Corrections1 January 1990Cardiopulmonary Resuscitation in Elderly PersonsPeter Cummings, MDPeter Cummings, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-112-1-74_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor: The excellent paper by Murphy and colleagues (1) reported that only 2 of 244 elderly patients with out-of-hospital cardiopulmonary arrest survived to hospital discharge.I reviewed all resuscitation attempts and deaths in our emergency department from 1 January 1982 to 31 December 1988. I included patients who were over age 69; had abrupt cessation of respiration, pulse, or blood pressure; had a resuscitation effort; and had their arrest outside the hospital. Trauma cases were excluded.These criteria were met by 199 patients. Twenty-eight were declared dead on arrival in the emergency department. After further resuscitation efforts in...References1. Murphy D, Murray A, Robinson B, and Campion E. Outcomes of cardiopulmonary resuscitation in the elderly. Ann Intern Med. 1989;111:199-205. LinkGoogle Scholar2. Smith J and Bodai B. Guidelines for discontinuing cardiopulmonary resuscitation in the emergency department after prehospital, nonparamedic-directed cardiac arrest. West J Med. 1985;143:402-5. MedlineGoogle Scholar3. Bonnin M and Swor R. Outcomes of unsuccessful field resuscitation attempts. Ann Emerg Med. 1989;18:507-12. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Peter Cummings, MDAffiliations: Kaweah Delta District Hospital Visalia, CA 93291 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRecommended Guidelines for Reviewing, Reporting, and Conducting Research on In-hospital Resuscitation: The In-hospital “Utstein Style”*Recommended Guidelines for Reviewing, Reporting, and Conducting Research on In-Hospital Resuscitation: The In-Hospital “Utstein Style”Recommended guidelines for reviewing, reporting, and conducting research on in-hospital resuscitation: the in-hospital ‘Utstein style’ 1 January 1990Volume 112, Issue 1Page: 74-75KeywordsBlood pressureCardiopulmonary resuscitationElderlyEmergency departmentHeartHeart rateRespirationResuscitation ePublished: 1 December 2008 Issue Published: 1 January 1990 PDF downloadLoading ...
Latent myeloproliferative disorder revealed by the JAK2-V617F mutation and endogenous megakaryocytic colonies in patients with splanchnic vein thrombosis
Authors: Marjorie Boissinot, Eric Lippert, Francois Girodon, Irene Dobo, Marc Fouassier, Claude Masliah, Vincent Praloran, Sylvie Hermouet
Journal: Blood (2006)
Identification of bacteria from blood and joint fluids of human subjects as Bacillus licheniformis.
Authors: P Pease
Journal: Annals of the Rheumatic Diseases (1974)

In previous papers, the occurrence of an L-form of a Gram-positive bacterium resembling Listeria, in the blood and joint fluids of arthritic, and the blood of normal persons, was reported (Pease, 1967, 1969, 1970a, b).Although similar organisms have been described from this source in the past, a satis- factory bacteriological description has been lacking, in most cases, and the purpose of this paper is to provide such a description.The organism is, in fact, identifiable as the L-form of Bacillus licheniformis, which has previously been found in association with arthritic conditions of poultry (Roberts, 1964) and probably of man (Benedek, 1955).
Serum free immunoglobulin light chain evaluation as a marker of impact from intraclonal heterogeneity on myeloma outcome
Authors: Annamaria Brioli, Hannah Giles, Charlotte Pawlyn, John P. Campbell, Martin F. Kaiser, Lorenzo Melchor, Graham H. Jackson, Walter M. Gregory, Roger G. Owen, J. Anthony Child, Faith E. Davies, Michele Cavo, Mark T. Drayson, Gareth J. Morgan
Journal: Blood (2014)
Phase 2 Trial of Neoadjuvant Axitinib in Patients with Locally Advanced Nonmetastatic Clear Cell Renal Cell Carcinoma
Authors: Jose A. Karam, Catherine E. Devine, Diana L. Urbauer, Marisa Lozano, Tapati Maity, Kamran Ahrar, Pheroze Tamboli, Nizar M. Tannir, Christopher G. Wood
Journal: European Urology (2014)
Factors associated with serum antibodies to reticulin, endomysium, and gliadin in an adult population.
Authors: S A McMillan, R P Watson, E E McCrum, A E Evans
Journal: Gut (1996)

BACKGROUND: Gluten sensitivity is thought to be significantly under-diagnosed in the population. AIMS: The aims of this study were to investigate the prevalence of antibodies associated with coeliac disease in a large representative sample of the adult population and to determine factors that are associated with their presence. PATIENTS: Serum samples from 5420 subjects with approximately equal numbers in each five year group from ages 15 to 65 years were obtained from the Belfast MONICA project and Change of Heart surveys, set up to monitor and assess risk factors associated with coronary heart disease in the population. METHODS: Using immunofluorescence and enzyme linked immunosorbent assay (ELISA) techniques autoantibodies, including those to reticulin, endomysium, and gliadin were determined. RESULTS: The results establish that IgA antigliadin antibody prevalence is high at 5.7%. Antiendomysial antibody was present in 1.2% of samples and gliadin and endomysial antibodies in 0.4%. No significant differences were found between men and women, area of residence in Northern Ireland or the year of sampling over the eight year period. However, there was a significant increase in the prevalence of IgA gliadin antibody, and to a lesser extent IgA endomysial antibody, with increasing age. CONCLUSION: The high prevalence of these positive antibodies suggests that coeliac disease may be relatively common in Northern Ireland.
Regulation of Local Angiotensin II Formation in the Human Heart in the Presence of Interstitial Fluid
Authors: Jorma O. Kokkonen, Juhani Saarinen, Petri T. Kovanen
Journal: Circulation (1997)

Background Data from in vitro studies suggest that both chymase and ACE contribute to the local generation of angiotensin (Ang) II in the heart. The enzyme kinetics under in vivo conditions are unclear. We thus studied the generation of Ang II by cardiac tissue in the presence of interstitial fluid (IF) that contains a variety of naturally occurring protease inhibitors. Methods and Results Ang I was incubated with heart homogenate in the presence of IF. IF obtained from human skin contained substantial amounts of protease inhibitors and ACE activity, the concentration of α 1 -antitrypsin being 35% and the activity of ACE 24% of the corresponding serum values. When heart homogenate was incubated with Ang I, three enzymes were responsible for its metabolism: heart chymase and heart ACE converted Ang I to Ang II, and heart carboxypeptidase A (CPA)–like activity degraded Ang I to Ang-(1-9). Incubation of heart homogenate in the presence of IF led to practically full inhibition of heart chymase–mediated Ang II formation by the natural protease inhibitors present in IF. In contrast, heart CPA–like activity was not blocked, as reflected by the continued generation of Ang-(1-9). In addition, both heart ACE– and IF ACE–mediated Ang II formation were strongly inhibited. This inhibition was shown to be due to the Ang-(1-9) formed. Conclusions The present experimental study defines two novel inhibitory mechanisms of Ang II formation in the human heart interstitium. Heart chymase–mediated Ang II formation is strongly inhibited by the natural protease inhibitors present in the IF. Similarly, both heart ACE– and IF ACE–mediated Ang II formation appear to be inhibited by the endogenous inhibitor Ang-(1-9) formed by heart CPA–like activity. These inhibitory mechanisms provide additional information about how the Ang II concentration in the heart interstitium may be controlled.
Diseases of the liver and biliary tract. Standardization of nomenclature, diagnostic criteria and prognosis. Edited by Carroll M. Leevy, Sheila Sherlock, Neils Tygstrup, and Rowen Zetterman, 205 pp. New York: Raven Press, 1994. $40
Authors: Raymond S. Koff
Journal: Hepatology (1995)

third chapter provides an excellent review by Arthur Cooper of ammonia metabolism in both liver and extrahepatic mammalian tissues.The fourth chapter is a succinct review of the clinical manifestations and management of hepatic encephalopathy.In the fifth chapter, the authors report their experience on the nutritional support of the encephalopathy-prone patient; several combinations of enteral and parenteral diets with branched chain amino acids (BCAA) are discussed.The sixth chapter provides an in-depth review of the role of the GABAhenzodiazepine receptor complex and the response of hepatic encephalopathy to flumazenil in humans and in animal models as well.In the seventh chapter, Dr W. Raabe describes the major effects of hyperammonemia on the function of neurons and their consequences.In a very charismatic manner, he demystifies difficult and complex terminology for the clinician, such as "inhibitory postsynaptic potential (IPSP)," "chloride-extrusion," and so on.References in this chapter are just superb!The eighth chapter, written by the Valencia group headed by Dr Grisolia, deals with the effects of hyperammonemia on brain microtubules.The authors present data to support their hypothesis that ammonia toxicity is mediated by the activation of the N-Methyl-D-Aspartate (NMDA) receptor.The last four chapters are devoted to the study of mechanisms that control the release of glutamate and cerebral protein breakdown and the properties of NMDA receptors that mediate glutamate toxicity, as well as the mechanism(s) of the protective effects of gangliosides against glutamate toxicity.Cirrhosis, Hyperammonemia and Hepatic Encephalopathy provides an accessible account of the state of knowledge of the role of hyperammonemia in hepatic encephalopathy in 1992.Because of the brevity of the volume, some of the subjects are not dealt with in extensive detail, but, in general, the topics are adequately covered.Overall, this is an attractive book, well-referenced, easy to read, and reasonably priced.
Abstract 5384: Frequency of gene allelic variants of the PAP prostate tumor antigen and association with immune response following antigen-specific genetic vaccination
Authors: Jordan T. Becker, Douglas G. McNeel
Journal: Cancer Research (2012)

Abstract Prostatic acid phosphatase (PAP) and prostate-specific antigen (PSA) are target antigens in genetic vaccines (viral and DNA plasmid vaccines) being evaluated as treatments for prostate cancer. Amino acid allelic variants and different splicing variants of each protein have been identified as part of the human genome sequencing project. We hypothesized that allelic variants in the coding sequence of one of these target proteins in a vaccine recipient, different from the amino acid sequence of the gene encoded by the vaccine, could account for some immune responses observed following genetic vaccination. Such a finding would be essentially analogous to xenoantigen vaccination approaches using highly homologous antigens. In this report, we used direct Sanger sequencing to identify allelic variations in the genes encoding PAP and PSA from 33 patients with prostate cancer who had been previously immunized with a DNA vaccine encoding PAP. The goal of this study was to identify the frequency of variants encoding amino acid changes for two common tumor antigens, and to specifically determine if PAP-specific amino acid variants were more frequent in patients with evidence of immunological response following genetic vaccination and whether these responses localized to regions of allelic variance. Three synonymous coding mutations within the coding sequence of PAP were observed, one of which was observed in 10/33 patients (30.3%), another in 15/33 patients (45.5%), and another in 17/33 patients (51.5%). These variants appear to be linked, as 9 patients possessed all three. No non-synonymous coding mutations were identified. Thus, while a small and somewhat homogeneous patient population, these findings suggest that PAP amino acid variants may be uncommon and immune responses observed are indeed reactive to the host PAP amino acid sequence, not to antigen amino acid variants. Studies are currently underway to alternatively determine whether immune responses were elicited to peptides spanning four known splice variants of PAP. In contrast, we observed four synonymous coding mutations as well as three non-synonymous coding mutations among the five exons of the non-target antigen PSA. Synonymous or non-synonymous mutations were detected in 11/33 individuals (33.3 %). However, while more variations were observed, each occurred in a smaller frequency of patients and did not appear to be linked. The more heterogeneous sequence of PSA may warrant further investigation to determine whether immune responses elicited by genetic vaccines encoding PSA are reactive to host or vaccine-encoded epitopes. 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 5384. doi:1538-7445.AM2012-5384
Dysgranulopoietic neutropenia and abnormal monocytes in childhood vitamin B<sub>12</sub> deficiency
Authors: William M. Crist, Richard T. Parmley, C. Tate Holbrook, Robert P. Castleberry, Francis R. Denys, Ahmad Malluh
Journal: American Journal of Hematology (1980)

Abstract Neutropenia and/or leukopenia (associated with elevated serum lysozyme levels) in three children with vitamin B 12 deficiency were evaluated using soft agar culture and ultrastructural and cytochemical techniques. In two patients a marked increase in peripheral blood myeloid colony forming cells (CFC) was observed; whereas a marginal increase in CFC was present in the third, less symptomatic, patient. Marrow CFC was normal or slightly increased. Serum colony stimulating activity (CSA) was normal but elaboration of CSA by white blood cells was low. Normal maturation of the progenitors was present in vitro and serum inhibitors of myelopoiesis were absent. Megaloblastic neutrophils and monocytes with nuclear‐cytoplasmic asynchrony were observed ultrastructurally in directly sampled marrow specimens. These cells contained autophagic and/or heterophagic vacuoles and an increase in cytoplasmic granules. Both monocytes and neutrophils also contained enlarged‐disrupted centrioles. Many marrow macrophages contained phagocytic vacuoles, which enclosed disrupted neutrophils and cellular debris. We conclude that although a large number of dysmorphic myeloid cells degenerate in the marrow, sufficient marrow CFC are present and peripheral blood CFC are elevated, suggesting abnormal release and/or maturation failure. All of these abnormalities are corrected by administration of vitamin B 12 .