Academic literature on the topic 'Theses – Immunology'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Theses – Immunology.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Theses – Immunology"
1
Salem, M. Dr Rafid Abdel Kadhim. "Book of Mena Mannan in the defense of the Koran to Mr. Mohammed Sadr Reading in light of the reference method." ALUSTATH JOURNAL FOR HUMAN AND SOCIAL SCIENCES 227, no. 3 (December 5, 2018): 417–41. http://dx.doi.org/10.36473/ujhss.v227i3.790.
Full textAbstract:
His Eminence was not excluded from the academic study. He combined the study of Al-Hawzawi and Al-Jamaa'i. He even contributed to the introduction of the academic lessons of the estate and he obtained the rank of ijtihad. He was 34 years old and in the same year he studied arfan and used various sources and references. He was not keen on them, because most of theses contained in his book of the daughters of his ideas. In his book, he adopted an innovative approach in most of his writings, to develop the mind and the works of thought, especially the book in question. He contradicted his predecessor in his interpretive approach, beginning with the last line of the Holy Book. He emphasized the theory of inspiration, The number of signs recorded in the minyan (37) is a reference divided into several sections, including those related to the divinity, judgments, ethics, etc., as shown in the research table
2
Rasheed, Dr Wesam Ahmed. "Map valuation of Map elements in the Geographic studies Comparative study of theses and distraction of department of Geography college of Education for girls and college of Education ( Ibn- Rushid ) University of Baghdad for the period ( 2000- 2015 )." ALUSTATH JOURNAL FOR HUMAN AND SOCIAL SCIENCES 219, no. 2 (November 9, 2018): 57–72. http://dx.doi.org/10.36473/ujhss.v219i2.515.
Full textAbstract:
This research aims to study elements of map through evaluation of using elements of map ofone hundred theses and dissertations of geography department in the college of Education for girls –university of Baghdad. The researcher makes a comparison between this department and the department of geography in the college of Education – IbnRushid – university of Baghdad that he would know which department is better in producing maps having accuracy in using elements of map especially if we know that the first department is in need of specialized professors, the other department has specialist in cartography. The research reaches to that some researchers fails in following some basic rules of maps. From other side, the research realizes that there is a clear development in producing a high quality map through using new technologies and programs by researchers. As to comparison which is made between two departments, the second department has a wide maintaining in elements of maps as there are specialized professors of cartography having the ability in producing accurate and scientific maps through supervision or giving advice .
3
Guillemin, Marie-Claude, Emmanuel Raffoux, Dominique Vitoux, Scott Kogan, Hassane Soilihi, Valérie Lallemand-Breitenbach, Jun Zhu, et al. "In Vivo Activation of cAMP Signaling Induces Growth Arrest and Differentiation in Acute Promyelocytic Leukemia." Journal of Experimental Medicine 196, no. 10 (November 18, 2002): 1373–80. http://dx.doi.org/10.1084/jem.20021129.
Full textAbstract:
Differentiation therapy for acute myeloid leukemia uses transcriptional modulators to reprogram cancer cells. The most relevant clinical example is acute promyelocytic leukemia (APL), which responds dramatically to either retinoic acid (RA) or arsenic trioxide (As2O3). In many myeloid leukemia cell lines, cyclic adenosine monophosphate (cAMP) triggers growth arrest, cell death, or differentiation, often in synergy with RA. Nevertheless, the toxicity of cAMP derivatives and lack of suitable models has hampered trials designed to assess the in vivo relevance of theses observations. We show that, in an APL cell line, cAMP analogs blocked cell growth and unraveled As2O3-triggered differentiation. Similarly, in RA-sensitive or RA-resistant mouse models of APL, continuous infusions of 8-chloro-cyclic adenosine monophosphate (8-Cl-cAMP) triggered major growth arrest, greatly enhanced both spontaneous and RA- or As2O3-induced differentiation and accelerated the restoration of normal hematopoiesis. Theophylline, a well-tolerated phosphodiesterase inhibitor which stabilizes endogenous cAMP, also impaired APL growth and enhanced spontaneous or As2O3-triggered cell differentiation in vivo. Accordingly, in an APL patient resistant to combined RA–As2O3 therapy, theophylline induced blast clearance and restored normal hematopoiesis. Taken together, these results demonstrate that in vivo activation of cAMP signaling contributes to APL clearance, independently of its RA-sensitivity, thus raising hopes that other myeloid leukemias may benefit from this therapeutic approach.
4
Smith, Daniel J., William F. King, Christine D. Wu, Bella I. Shen, and Martin A. Taubman. "Structural and Antigenic Characteristics of Streptococcus sobrinus Glucan Binding Proteins." Infection and Immunity 66, no. 11 (November 1, 1998): 5565–69. http://dx.doi.org/10.1128/iai.66.11.5565-5569.1998.
Full textAbstract:
ABSTRACT Three purified glucan binding proteins (GBP-2, GBP-3, and GBP-5) from Streptococcus sobrinus 6715 were compared structurally by mass spectroscopy of tryptic fragments and antigenically by Western blot analysis with rat antisera to each GBP or to peptides containing putative glucan binding epitopes of mutans streptococcal glucosyltransferases. Structural and antigenic analyses indicated that GBP-3 and GBP-5 are very similar but that both are essentially unrelated to GBP-2. None of theseS. sobrinus GBPs appeared to have a strong antigenic relationship with GBPs from Streptococcus mutans. Thus,S. sobrinus GBP-2 and GBP-3 appear to be distinct proteins with potentially different functions. S. sobrinusGBP-5 may be a proteolytic fragment of GBP-3, or, alternatively, the genes coding for these proteins may be closely related.
5
Villanueva-Romero, Raúl, Irene Gutiérrez-Cañas, Mar Carrión, Selene Pérez-García, Iria V. Seoane, Carmen Martínez, Rosa P. Gomariz, and Yasmina Juarranz. "The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis." Journal of Immunology Research 2018 (August 1, 2018): 1–11. http://dx.doi.org/10.1155/2018/6043710.
Full textAbstract:
Genetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic joint inflammation and an imbalance between different T helper (Th) subsets. Vasoactive intestinal peptide (VIP) is a mediator that modulates all the stages comprised between the arrival of pathogens and Th cell differentiation in RA through its known anti-inflammatory and immunomodulatory actions. This “neuroimmunopeptide” modulates the pathogenic activity of diverse cell subpopulations involved in RA as lymphocytes, fibroblast-like synoviocytes (FLS), or macrophages. In addition, VIP decreases the expression of pattern recognition receptor (PRR) such as toll-like receptors (TLRs) in FLS from RA patients. These receptors act as sensors of pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP) connecting the innate and adaptive immune system. Moreover, VIP modulates the imbalance between Th subsets in RA, decreasing pathogenic Th1 and Th17 subsets and favoring Th2 or Treg profile during the differentiation/polarization of naïve or memory Th cells. Finally, VIP regulates the plasticity between theses subsets. In this review, we provide an overview of VIP effects on the aforementioned features of RA pathology.
6
Herrington, CS, and PA Hall. "Molecular and cellular themes in inflammation and immunology." Journal of Pathology 214, no. 2 (January 2008): 123–25. http://dx.doi.org/10.1002/path.2303.
Full text
7
Y. Nasir, Dr Adel. "Identity and ideological reading paths in the conflict and developments." ALUSTATH JOURNAL FOR HUMAN AND SOCIAL SCIENCES 212, no. 2 (November 12, 2018): 243–68. http://dx.doi.org/10.36473/ujhss.v212i2.673.
Full textAbstract:
Ideology and identification is one of the main and big subjects nowadays, especially after the ideology specified the ideology and main nationality identification existence by process which leads to Replacement and paddlefish of ideology existence rather than identification , while ideology makes so much efforts ( intellectual and beliefs efforts ) to solve century problems and presents mental and intellectual developments which characterized by realism in such disturbed and Dispersion world in political, social, economic factions and dominated by cases of conflict and chaos . Identification seeks to connect the individual similarities participating in the land, history and real affiliation, which tend to personal fulfillment of humanity in its social and cultural frame and confirms his affiliation root. But while that facing the impact of ideological conflict which aims to achieve an intellectual image and adopts cultures and ideas from another civilization might disagree with identification characteristics existence. Ideology trying to dismantling in all Civilization and national directions, as well as seeks to Skepticism of identification with its ideological features while the weakness of the Factors affiliation , the local organizations , National parties and Religious institutions and their branches in its special directions . Which lead to the disability of resists the ideological Invasion weather is was local, regional or global. But despites of the some ideologies presents humanitarian and reformative theses .In different political shapes and frames still mainly defending to the Elements of existence which resulting the ideological conflict – identificational despite of that both of them have weakness in its Staff fundamental parts thus the ideology Remain to protect the benefits of the interests of the political elite and leaders while facing Cases of rejection and acceptance in social circles . Whereas the main nationality identification went through a conflict with sub-identification ,Sectarianism and loyalty instead of main identification or the national identification and from that description we can conclude that the conflicts and its pathways are continuous in such a world full of existence and hegemony and superiority .
8
Roccaro, Aldo M., Xavier Leleu, Antonio Sacco, Xiaoying Jia, Molly Melhem, Anne-Sophie Moreau, Hai T. Ngo, et al. "Dual targeting of the proteasome regulates survival and homing in Waldenström macroglobulinemia." Blood 111, no. 9 (May 1, 2008): 4752–63. http://dx.doi.org/10.1182/blood-2007-11-120972.
Full textAbstract:
AbstractWaldenström macroglobulinemia (WM) is an incurable low-grade B-cell lymphoma characterized by high protein turnover. We dissected the biologic role of the proteasome in WM using 2 proteasome inhibitors, NPI-0052 and bortezomib. We found that NPI-0052 inhibited proliferation and induced apoptosis in WM cells, and that the combination of NPI-0052 and bortezomib induced synergistic cytotoxicity in WM cells, leading to inhibition of nuclear translocation of p65NF-κB and synergistic induction of caspases-3, -8, and -9 and PARP cleavage. These 2 agents inhibited the canonical and noncanonical NF-κB pathways and acted synergistically through their differential effect on Akt activity and on chymotrypsin-like, caspaselike, and trypsinlike activities of the proteasome. We demonstrated that NPI-0052–induced cytotoxicity was completely abrogated in an Akt knockdown cell line, indicating that its major activity is mediated through the Akt pathway. Moreover, we demonstrated that NPI-0052 and bortezomib inhibited migration and adhesion in vitro and homing of WM cells in vivo, and overcame resistance induced by mesenchymal cells or by the addition of interleukin-6 in a coculture in vitro system. Theses studies enhance our understanding of the biologic role of the proteasome pathway in WM, and provide the preclinical basis for clinical trials of combinations of proteasome inhibitors in WM.
9
Posada, Ana C., Stacey L. Kolar, Renata G. Dusi, Patrice Francois, Alexandra A. Roberts, Chris J. Hamilton, George Y. Liu, and Ambrose Cheung. "Importance of Bacillithiol in the Oxidative Stress Response of Staphylococcus aureus." Infection and Immunity 82, no. 1 (October 28, 2013): 316–32. http://dx.doi.org/10.1128/iai.01074-13.
Full textAbstract:
ABSTRACTInStaphylococcus aureus, the low-molecular-weight thiol called bacillithiol (BSH), together with cognateS-transferases, is believed to be the counterpart to the glutathione system of other organisms. To explore the physiological role of BSH inS. aureus, we constructed mutants with the deletion ofbshA(sa1291), which encodes the glycosyltransferase that catalyzes the first step of BSH biosynthesis, andfosB(sa2124), which encodes a BSH-S-transferase that confers fosfomycin resistance, in severalS. aureusstrains, including clinical isolates. Mutation offosBorbshAcaused a 16- to 60-fold reduction in fosfomycin resistance in theseS. aureusstrains. High-pressure liquid chromatography analysis, which quantified thiol extracts, revealed some variability in the amounts of BSH present acrossS. aureusstrains. Deletion offosBled to a decrease in BSH levels. ThefosBandbshAmutants of strain COL and a USA300 isolate, upon further characterization, were found to be sensitive to H2O2and exhibited decreased NADPH levels compared with those in the isogenic parents. Microarray analyses of COL and the isogenicbshAmutant revealed increased expression of genes involved in staphyloxanthin synthesis in thebshAmutant relative to that in COL under thiol stress conditions. However, thebshAmutant of COL demonstrated decreased survival compared to that of the parent in human whole-blood survival assays; likewise, the naturally BSH-deficient strain SH1000 survived less well than its BSH-producing isogenic counterpart. Thus, the survival ofS. aureusunder oxidative stress is facilitated by BSH, possibly via a FosB-mediated mechanism, independently of its capability to produce staphyloxanthin.
10
Kim, Hee Nam, Huong Thi Thanh Tran, Il-Kwon Lee, Yeo-Kyeoung Kim, Deok-Hwan Yang, Je-Jung Lee, Myung-Geun Shin, et al. "Polymorphisms of Thymidylate Synthase in the 5′- and 3′-Untranslated Regions Associated with Risk of Non-Hodgkin’s Lymphoma." Blood 108, no. 11 (November 1, 2006): 2394. http://dx.doi.org/10.1182/blood.v108.11.2394.2394.
Full textAbstract:
Abstract Thymidylate synthase (TS) catalyzes the conversion of dUMP by 5,10-methylenetetrahydrofolate to dTMP in DNA synthesis. Polymorphisms in the untranslated regions(UTRs) of TS, which may modulate TS transcription and expression, have been associated with susceptibility to several malignancies. In this study, to evaluate the association with TS the 28-bp tandem repeat(2R→3R) and the 6-bp deletion(6 bp-) and susceptibility to non-Hodgkin’s lymphoma(NHL), large-scale population-based case-control study was conducted in Chonnam National University Hospital between Mar 1997 and Feb 2006. 553 patients with histologically comfirmed lymphoma and 1,324 controls were evaluated. The cases consisted of 275 diffuse large B-cell lymphomas (DLBCL), 109 T-cell lymphomas and 169 unclassifiable lymphomas. TS 2R2R genotype was significantly associated with increased risk for NHL and T-cell lymphoma, but not for DLBCL. Using subjects with the TS 3R3R as a reference group, the OR of TS 2R2R was 2.00 (95% CI 1.21–3.31, p=0.007) for NHL and 3.30 (95% CI 1.52–7.17, p=0.003) for T-cell lymphoma. The association was 1.65 fold higher and more evident for T-cell lymphoma than NHL. However, there was no significant association of TS 6bp- with NHL. In conclusion, theses results suggest that TS (2R→3R) may play an important role in the pathogenesis of NHL, and that DNA synthesis may play a crucial roles in the pathogenesis of specific NHL subtypes.
Dissertations / Theses on the topic "Theses – Immunology"
1
Zhao, Yuan. "Immunology of granulomatosis with polyangiitis." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/immunology-of-granulomatosis-with-polyangiitis(91230752-735f-41ea-8695-f26f8b2e5c97).html.
Full textAbstract:
Granulomatosis with polyangiitis (GPA, formerly known as Wegener’s granulomatosis) is a rare and sometimes fatal systemic autoimmune disease. Anti-neutrophil cytoplasmic antibodies (ANCAs) specific for proteinase 3 (PR3) are associated with GPA. However, the pathogenesis of GPA is not yet clear. Our aim was to investigate the local autoimmune response, circulating immune modulatory cells and cells expressing the immune suppressor molecules programmed death 1 (PD-1) and its ligands in GPA. In mucosa from GPA patients, activated B cells were observed located alongside PR3 expressing cells and B cell survival factors BAFF and APRIL, which was produced by the granulomas and giant cells. B cells were proliferating and persistent in biopsies. However no evidence of B cell clones from the mucosal biopsies circulating in peripheral blood was observed in GPA. An increased frequency of circulating TFH cells and a reduced frequency of Treg cells was observed in peripheral blood from GPA patients on conventional therapies compared to healthy controls. No such difference was found in GPA patients treated with rituximab. The frequency of circulating TFH and Treg cells was found to be inversely correlated in human peripheral blood. No difference in the relative quantity of mRNA encoding PD-1 in lymphocytes and monocytes was found in GPA patients compared with healthy controls. Lower percentage of CD14+ monocytes expressing PD-1 was observed in GPA patients. Lower relative quantity of mRNA encoding PD-1 ligands PD-L1 and PD-L2 in T cells and monocytes was observed in GPA patients. In conclusion, data in this thesis identifies activated B cells alongside auto-antigens and B cell survival factors in the mucosa in GPA. A negative correlation between TFH and Treg cells is observed that implies the balance between T cell subsets and its B cell dependence are associated with disease activity in GPA. The deficiency of PD-L1 and PD-L2 mRNA in lymphocytes and monocytes may contribute to the pathogenesis of GPA.
2
Fashola, Bola. "The Effect of Sodium Chloride on Beta-Hemolytic Streptococci." TopSCHOLAR®, 1987. https://digitalcommons.wku.edu/theses/2321.
Full textAbstract:
The drug of choice for the treatment of Stieptococcal pharyngitis is penicillin G. However, a common home remedy prescribes the use of salt-water solutions for gargling.
Members of Beta -hemolytic streptococcal groups A, B, and C were isolated from the upper -respiratory tracts of patients diagnosed as having streptococcal pharyngitis. These cultures we:e obtained from HCA Greenview Hospital (Bowling Green, Kentucky) and used to study the effects of sodium chloride on the isolates.
The minimum inhibitory concentration of sodium chloride was determined for each of eight hospital isolates. Croup A streptococci were inhibited at a concentration of 7.2% sodium chloride while Group C streptococci were inhibited at a 7.0% concentration. Group P streptococci were more resistant, and inhibition of growth occurred at 12.0% sodium chloride concentrations.
Scanning electron microscopic studies showed no significant differences in the external structure of cells treated with sodium chloride when compared to non-treated cells. Despite the lack of changes in the external structure of treated cells, fine structural alterations were observed with transmission electron microscopic studies.
Treatment of the cells with sodium chloride resulted in a condensation of nucleoid deoxyribonucleic acid (DNA) and some loss of ribosomes. These changes were followed by a dissolution of the cytoplasmic cell contents resulting in an intact cell wall with capsule.
Other parameters such as the rate of growth, minimum bactericidal concentrations, DNA content and protein content of cells treated with sodium chloride were examined and compared to control cells.
3
Ventevogel, Melissa Samo. "Cytokine Modulation of Thymopoiesis." NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-03182008-100350/.
Full textAbstract:
The thymus is an organ derived from embryonic endoderm and mesoderm differentiation. It is located above the heart and is made up of two compartments, the thymic epithelial space and the perivascular space. The thymic epithelial space consists of the cortex and the medulla, which is where T cell development, maturation and induction of self tolerance occur in a process known as thymopoiesis. The thymus is susceptible to chronic and acute stressors that result in thymic involution. A consequence of thymic involution is reduced thymopoiesis, which affects the generation of a diverse T cell repertoire and establishment of central T cell tolerance. Many thymosuppressive and thymostimulatory cytokines are involved in thymopoiesis and thymic involution. Keratinocyte growth factor and IL-7 are two cytokines that function in driving early thymic progenitor proliferation and T cell development, respectively. We hypothesized that IL-7 and Keratinocyte growth factor, delivered via recombinant adenovirus, can improve thymopoiesis and T cell reconstitution in mice in an endotoxin model of acute thymic atrophy. Analysis of thymus weight, cellularity, phenotype and TCR gene rearrangement showed moderate increases in thymic function with delivery of IL-7 or Keratinocyte growth factor versus control. Taken together, these data suggested that IL-7 and Keratinocyte growth factor, delivered via recombinant adenoviruses, have thymostimulatory effects on the thymus in normal thymus or settings of acute thymic atrophy and maybe beneficial for future development as therapeutics.
4
Chilcoat, Clayton Douglas. "Protein Kinase A Regulates β2 Integrin Avidity Activation and Subsequent Neutrophil Activation via Modulation of Myosin Light Chain Kinase." NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-03312005-093042/.
Full textAbstract:
β2 integrins are adhesion molecules on the surface of neutrophils. Avidity activation of β2 integrins includes transportation of pre-formed integrins to the cell surface and a conformational change in the integrin to a high-binding state. Upon binding ligand, β2 integrins initiate a signaling cascade that results in activation of the neutrophil to a pro-inflammatory state, and the inhibition of this signal can prevent further activation of the neutrophil. cAMP and it effector protein kinase A (PKA) exert a generally inhibitory effect upon neutrophil activation. PKA has been shown to inactivate myosin light chain kinase (MLCK). Myosin light chain (MLC) phosphorylation is crucial for actin-myosin complex formation, which is required for stability and contraction of the actin cytoskeleton in neutrophils as well as β2 integrin-dependent adhesion. We hypothesize that the inhibitory effect of PKA upon neutrophils is due to inhibition of β2 integrin avidity activation resulting in the subsequent inhibition of neutrophil activation. Furthermore we hypothesize that the effect of PKA upon β2 integrin avidity activation is mediated through PKA?s effect upon MLCK. We demonstrate that inhibition of PKA induces β2 integrin-dependent adhesion and that augmentation of cAMP prevented β2 integrin-dependent adhesion and subsequent respiratory burst activity. Further, we demonstrate via flow cytometric detection of antibodies directed against β2 integrins that pharmacologic inhibition of PKA activity results in overall increased β2 integrin expression on the neutrophil surface, as well as increased expression of the activated form of the integrin. This upregulation and activation of β2 integrins due to inhibition of PKA is abolished by pharmacologic MLCK inhibition. Inhibition of MLCK also blocked β2 integrin-dependent neutrophil adhesion achieved by inhibition of PKA, as well as neutrophil migration along towards a PKA inhibitor. These findings demonstrate that PKA regulation of β2 integrin affinity activation and subsequent neutrophil activation is via an MLCK-dependent pathway.
5
Pressler, Barrak. "The Role of Complementary Proteins in Autoimmune Glomerulonephritis." NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-05062008-155750/.
Full textAbstract:
Although numerous theories exist proposing mechanisms whereby autoimmune diseases may be initiated, as of yet none of these have been definitively shown to be responsible for the induction of any naturally-occurring disease. One of these theories, known as autoantigen complementarity, states that the initiator of an autoimmune response may not be the target autoantigen itself or an exogenous mimic, but instead is a peptide or protein that is âantisenseâ or âcomplementaryâ in shape and/or charge to the autoantigen. The first immune response is therefore production of an antibody specific for this complementary protein, followed by an anti-antibody (i.e. anti-idiotypic antibody) that reacts with the paratope of the first antibody and also recognizes the âsenseâ or self-protein due to surface contour, charge, and/or hydropathy complementarity. Our laboratory group has published evidence for autoantigen complementarity in one autoimmune glomerular disease, proteinase-3 specific antineutrophil cytoplasmic autoantibody glomerulonephritis. The overall objective of the work described here was to provide further evidence for complementary proteins as inciting antigens in autoimmune glomerulonephritis using anti-GBM disease as the classic antibody-mediated autoimmune glomerulopathy; our central hypothesis was that anti-GBM disease is caused by a protein or peptide complementary to the anti-GBM autoantigen. The design of synthetic peptides complementary in sequence to portions of the human and rat α3(IV)NC1 collagen domains, and the design and production of a recombinant complementary α3(IV)NC1 protein more likely to possess appropriate tertiary structure to be complementary in sequence and in structure to the full-length anti-GBM epitope are described. These antigens were used to demonstrate that a subset of patients with anti-GBM disease have anti-idiotypic antibodies specific for α3(IV)NC1-complementary peptides and proteins, that these antibodies are distinct from their pathogenic idiotypic partners, and that the anti-GBM antibodies bind to these anti-complementary protein antibodies as expected by idiotypic:anti-idiotypic partners. Finally, we describe the immunologic and clinicopathologic consequences of immunization of two rodent models with anti-GBM-complementary peptides, thus providing provisional evidence for autoantigen complementarity-induced anti-GBM disease.
6
Rogers, Melinda Cadd. "Differential thrombospondin expression on T lymphocytes in a Feline Immunodeficiency Virus model." NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-06152007-103921/.
Full textAbstract:
CD4+CD25+ T regulatory cells represent an important subset of lymphocytes whose function is to suppress autoimmune disease and control normal immune responses. There is much research indicating a direct role for TGF-beta expressed on the surface of Tregs in the suppressor function of these cells. TGF-beta, whether bound to the cell surface or secreted, is produced as part of a complex that renders the cytokine inactive. Thrombospondin is the primary activator of biologically latent TGF-beta. This research demonstrates that thrombospondin is expressed on the surface of T lymphocytes isolated from the blood and lymph nodes of normal and FIV positive felines. Thrombospondin is expressed at significantly higher levels on CD4+CD25+ T lymphocytes, but can be induced in culture by activating T helper cells in the presence of LPS and IL2. We also observed that the CD4+CD25- T helper cells isolated from FIV negative control lymph nodes were able to markedly upregulate surface thrombospondin expression compared with similarly stimulated CD4+CD25- T helper cells from FIV positive sources. These findings are initial steps in working to understand the mechanism behind latent TGF-beta activation on CD4+CD25+ T regulatory cells and the role this cell type plays in FIV/HIV pathogenesis.
7
lee, kang mi. "Antibody and Cellular Immune Responses of Swine Exposed to Porcine Reproductive and Respiratory Syndrome Virus or a GP5 Subunit Vaccine." NCSU, 2007. http://www.lib.ncsu.edu/theses/available/etd-07052007-104723/.
Full textAbstract:
Developing effective vaccines against the porcine reproductive and respiratory syndrome virus (PRRSV) has proved difficult, highlighting the need for basic information on the nature of the immune response against this virus and the mechanisms of resistance that the virus employs. In this investigation our goal was to characterize the immune response against the major outer membrane protein of the virus, GP5, in pigs experimentally infected with a North Carolina isolate of PRRSV known as the NC Powell strain. In addition, we compared this response with the immune response seen after vaccination with purified recombinant GP5 (rGP5) protein. Humoral immune responses were monitored by western blot and immunofluorescence while T cell responses were monitored using proliferation assays and flow cytometry. Our results show strong humoral recognition of rGP5 protein during both natural and vaccine induced Ab responses. In addition, epitope mapping via western blot revealed that Ab responses were directed largely against the C-terminal endodomain of rGP5 protein in both experimentally infected and vaccinated pigs. We also investigated T cell responses to rGP5 protein. Our experiments revealed that T cells from vaccinated animals also responded to both rGP5 protein and inactivated NC Powell strain of PRRSV suggesting that T cells may play an important role in vaccine-induced resistance. Interestingly, we found that the inactivated NC Powell strain of PRRSV caused a strong proliferative response in naïve T cells from control animals, perhaps indicating the presence of a superantigen as a component of this highly virulent strain of PRRSV.
8
Madison, Sharon L. "THE EFFECTS OF PM2.5 ON ALLERGIC INFLAMMATION IN MAST CELL DEFICIENT MICE." NCSU, 2002. http://www.lib.ncsu.edu/theses/available/etd-05082002-132938/.
Full textAbstract:
MADISON, SHARON LYNN. The effects of PM2.5 on allergic inflammation in mast cell deficient mice. (Under the direction of Bruce Hammerberg.) Animal models of asthma have confirmed epidemiological findings that exposure to fine particulate matter (PM2.5) can enhance asthmatic symptoms, including eosinophilic inflammation and airway hyperresponsiveness. Critics have dismissed the possibility that these studies utilizing artificial exposure scenarios, like intratracheal instillation (i.t.), can be legitimately extrapolated to human risk largely due to the fact that the doses required for this type of model exceed the normal ambient concentrations of PM2.5. In order to improve the credibility of the findings from previous animal studies utilizing the i.t. method for delivery of aqueous particle suspensions to the lung, and to determine the biological mechanisms responsible for the observed enhancement of allergic inflammation following PM2.5 exposure, large-scale air samplers have been developed making it possible to directly expose wild type (WT) and genetically altered mice to fine, concentrated ambient particles (CAPs). In this study allergic asthma was modeled in both WT and mast cell deficient (MCD) mice by local (L) or systemic (S) sensitization to ovalbumin (OVA). Two weeks later mice were challenged with OVA (day 0) and then exposed to CAPs (day 0 & 1) with numerous endpoints collected (day 0-2). Overall, there was a temporal difference in the bronchoalveolar lavage cell profile between L and S sensitized mice, and the contribution of mast cells (MC) to this differential response was best observed for neutrophils at day 0 and day 1. Compared to air exposed mice, CAPs depressed total inflammatory cell infiltrates in the bronchoalveolar lavage fluid at day 0 and day 1 after OVA challenge for all groups. This overwhelming difference of limited cellular infiltration of monocytes and neutrophils in the bronchoalveolar lavage fluid following CAPs exposure, and the significant difference between the L and S sensitization protocols, confound interpretation for all of the factors examined. However, the specific finding that CAPs can enhance eosinophil recruitment by day 2 after OVA challenge indicates that the results from previous animal studies utilizing i.t. PM2.5 exposures do in fact support the epidemiological associations linking PM2.5 exposures with the enhancement of allergic inflammation indicative of the asthmatic phenotype. Given the strict regulation of immunological tolerance at mucosal surfaces like the lung, the genetic variability of different mouse strains, and the daily changes in ambient PM2.5 composition, the findings of this study prompt many unique questions. However, the bottom line is that this study demonstrates that ambient PM2.5 does alter Th2-like responses in mice by enhancing pulmonary BAL eosinophils in the late phase response (day 2), and that mast cells are critical to their recruitment.
9
Chen, Hsin-Ying. "T CELL RESPONSE TO INFECTION BY THE PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS." NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-01062005-170050/.
Full textAbstract:
The purpose of the research has been to characterize the response of naïve or virus-specific swine T lymphocytes from different lymphoid compartments to Porcine Reproductive and Respiratory Syndrome Virus (PRRSV). Peripheral blood mononuclear cells (PBMCs), tracheobronchial lymph node (TLN) and lateral retropharyngeal lymph node (LLN) cells were labeled with PKH67 green fluorescence dye to measure cell proliferation and surface phenotypes were examined using anti-CD4, anti-CD8 or anti-CD25 monoclonal antibodies. Stimulation with Concanavalin A was also included as a positive control. Our results show that potential virus-specific T lymphocytes were found in the peripheral blood, although no cell proliferation was found in cultures of lymph node cells. We did find that the percentages of CD8+ T cells in cultures of lymph node cells from the virus-infected pig increased after in vitro stimulation with the Powell virus compared to the lymph node cells cultured in media only, suggesting that CD8+ T lymphocytes may play a role in the virus clearance and immune memory to PRRSV.
10
Emani, Sirisha. "MOLECULAR CHARACTERIZATION OF T REGULATORY CELLS IN FIV-INFECTION." NCSU, 2006. http://www.lib.ncsu.edu/theses/available/etd-01192006-105756/.
Full textAbstract:
Naturally occurring CD4+CD25+ T regulatory cells (Treg) play important roles in maintaining immunologic self-tolerance in addition to controlling the magnitude of anti-microbial immune responses. However, the capacity of these CD4+CD25+ Treg cells to control immune responses both in vivo and in vitro is not well established. CD4+CD25+ Treg cell-mediated suppression can control autoimmune diseases; transplantation tolerance and graft verses host disease and, in contrast hinder tumor immunity and immunity to infectious agents. As Treg cells have been reported to be involved in several diseases, this study focused on molecular characteristics that enables them to maintain anergy and also resistance to programmed cell death along with the effect of FIV-infection on regulation of the above phenotypic characteristics. Our results show that feline CD4+CD25+ Treg cells are phenotypically and functionally anergic as indicated by elevated levels of the cyclin dependent kinase inhibitors, CdkI¡¦s, (p21cip1,p16ink4, and p27kip1) , and resistance to mitogen-induced proliferation compared to their counter parts CD4+CD25- T cells. Importantly, CdkI¡¦s are constitutively over-expressed only in FIV-infected cats. As expected Treg cells from FIV-infected cats that over-expressed CdkI¡¦s expressed low levels of the cyclins (mainly cyclins D) and phosphorylated retinoblastoma protein (pRb) that are responsible for cell cycle progression. We investigated the role of TGF?Ò signaling and found that TGF?Ò1 plus ConA stimulation was able to convert CD4+CD25- T cells to CD4+CD25+ T cells with functional and phenotypic characteristics including upregulation of CdkI¡¦s and bcl-2. The differential expression of CdkI¡¦s and bcl-2 between the two CD4+ T cell subsets may be linked to TGF?Ò-Smad pathway. Consistent with upregulation of CdkI¡¦s and bcl-2, we found that although natural and TGF?Ò1 converted CD4+CD25+ Treg cells are anergic, they are more resistant to activation induced cell death compared to CD4+CD25- T cells functionally which correlated with increased bcl-2 to bax ratio in Treg cells. Thus, the molecular characterization of this unique population of Treg cells may be essential for understanding their role and function for developing effective therapeutics and vaccination especially against chronic infections such as Acquired Immune Deficiency Syndrome (AIDS).
Books on the topic "Theses – Immunology"
1
(Editor), Gavin Spickett, and Ian G. Lewin (Editor), eds. Current Themes in Allergy and Immunology. Royal College of Physicians of London, 1994.
Find full text
2
Kirkham, Bruce. Immunology and cytokine pathways. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0007.
Full textAbstract:
Psoriatic arthritis immunopathology has become the subject of intense study. These findings show differences to other forms of inflammatory arthritis in key pathways. Increased knowledge of innate immunity and the important role of IL-17/23 biology in both psoriasis and psoriatic arthritis, have led to new theories of immunopathogenesis in both conditions. Direct environmental stimuli could trigger innate immune cells resident in skin, which may then initiate a chronic adaptive immune response. The joint has fewer resident innate immune cells, but new studies show cells producing IL-17 may play key roles in immunopathology. The new information summarized here will provide important hypotheses for investigation of pathogenic pathways. Differences in non-immune cell function may also be critical mediators of response, for example, production of IL-12 or IL-23 by dendritic cells. Keratinocytes in skin and fibroblasts in joints may be critical in mediating cytokine production and effector function.
3
Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.
Full textAbstract:
Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.
4
Keshav, Satish, and Alexandra Kent. Immunology and genetics in gastrointestinal and hepatic medicine. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0196.
Full textAbstract:
The gut has a pivotal role in immune homeostasis. It is constantly exposed to a wide array of antigens in food, and resident and consumed microorganisms. It is estimated that the number of bacterial cells in the gastrointestinal tract is tenfold greater than the number of cells in the human body. The gut needs to recognize harmful bacteria, and consequently contains the largest number of immune cells in the body. However, it must remain tolerant to commensal bacteria. Bacteria express antigens that stimulate an immunological response via the gut-associated lymphoid tissue (GALT). The GALT includes the appendix, tonsils, Peyer’s patches, and mesenteric lymph nodes. Therefore, the intestinal immune system is finely balanced between tolerance and reactivity. An example of an abnormal response that generally the individual should be tolerant to is gliadin peptides in coeliac disease. An example of excessive tolerance to an otherwise controllable infection is cryptosporidiosis, which causes diarrhoea in patients with HIV infection. The understanding of genetics in disease has progressed rapidly with the introduction of genome-wide association studies. The Welcome Trust Case Control Consortium has performed extensive research on the genetics of many illnesses, including Crohn’s disease, ulcerative colitis, Barrett’s oesophagus, oesophageal adenocarcinoma, and primary biliary cholangitis. Although these studies have increased our understanding of the molecular basis of disease, they have had little impact on clinical management. This may change as studies associate genotype and phenotype. Several gastrointestinal diseases have an etiology based on immunological or genetic aberrations, and these immunological mechanisms and genetic mutations can be utilized for diagnostic purposes. However, there is no genetic or immunological marker that is 100% specific to a disease and, consequently, the markers are used to support clinical, histological, and/or radiological findings.
5
Foster, Brogan, and Paul A. Brogan. Juvenile idiopathic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738756.003.0003.
Full textAbstract:
This chapter describes the JIA subtypes, uveitis, prognostic indicators, the spectrum of JIA in adults and updated chapters on the genetics and immunology of JIA. There are updated sections on treatment approaches, pathways (including reference to NICE and guidance from North America and Europe) and disease activity scores.
6
Gavin, Spickett, Lewin Ian G, and Royal College of Physicians of London., eds. Current themes in allergy and immunology: Papers based on an Interfaces in Medicine Conference organised by the Royal College of Physicians, London. London: Royal College of Physicians of London, 1994.
Find full text
7
Giesser, Barbara S., ed. Primer on Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.001.0001.
Full textAbstract:
Primer on Multiple Sclerosis, second edition is designed to be a practical guide to the basic science and clinical manifestations of multiple sclerosis. It is intended primarily for neurologists and other health care professionals who treat persons with this disease. The book starts with a review of the history of multiple sclerosis and the basic genetics, immunology, electrophysiology, and pathophysiology that are central to the disease. It then reviews the common and uncommon clinical signs and symptoms of multiple sclerosis and the management of these conditions. The latest diagnostic strategies are presented. There is extensive coverage of approved and experimental disease-modifying therapies, including algorithms to assist clincians in choosing these therapies. Complementary and alternative therapies that are popular among persons with multiple sclerosis are examined. New additions to this edition include a chapter for nursing health care professionals, and updates on therapeutics. Unique to this book are the chapters on the legal, psychosocial, and vocational issues that often present challenges for person with multiple sclerosis, topics that typically are not covered in standard texts.
8
Bielekova, Bibiana, Gary Birnbaum, and Robert P. Lisak, eds. Neuroimmunology. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190050801.001.0001.
Full textAbstract:
This book provides clinical and supporting scientific background on a diverse group of neurological disorders in an expanding field of neurology, that of neuroimmunology. It includes chapters on multiple sclerosis and related disorders in adults and children, neuromyelitis optica spectrum disorder, Guillain-Barré syndrome, chronic inflammatory deymyelinating polyradiculoneuropathy and variants, immune-mediated disorders of the neuromuscular junction, inflammatory myopathies, paraneoplastic disorders and autoimmune encephalitities, and neurologic manifestations of systemic immune-mediated diseases. In addition there is an introductory chapter dealing with basic of immunology and another on mechanisms of action of therapies used in neuroimmunologic disorders. The clinical chapters cover epidemiology, pathology, pathogenesis, and pathophysiology of the different diseases along with clinical presentation, diagnostic testing, differential diagnosis, and treatment.
9
Swash, Michael. Myology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0012.
Full textAbstract:
Diseases of muscle have become better understood by careful clinical observations, resulting in a clinically useful classification of the different groups of disorders e.g. inherited muscular dystrophies such as Duchenne muscular dystrophy, limb-girdle and metabolic myopathies, and myotonic disorders. A number of scientific approaches have determined the directions taken by this evolving classification. Understanding of the anatomy of the motor unit’s distribution in muscle transformed muscle pathology and muscle electrophysiology, and key to these pathological advances was the use of the histochemical technique for identifying myofibrillar ATPase in muscle fibres. This allowed studies of the distribution of fibre types in muscle in many different disorders. The inflammatory muscle diseases have been better understood since recent advances in immunology have characterized the underlying processes. The limb-girdle and childhood myopathies have proven to be heterogeneous, with many different, apparently causative, underlying genetic mutations.
10
Kirk, Robert G. W., and Michael Worboys. Medicine and Species: One Medicine, One History? Edited by Mark Jackson. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780199546497.013.0031.
Full textAbstract:
This article surveys the present position of the animal within the history of human medicine, linking this to work in the history of veterinary medicine, and also speculates on the value of making ‘species’ a central and unifying theme of a new history of medicine. It mentions that re-conceiving medicine as a set of knowledge-practices grounded in interspecies interactions promises to reinvigorate the subject. It draws on a diverse theoretical literature ranging from ‘animal studies’ to ‘post-human’ literature in order to suggest how such an approach could allow us to re-imagine what medicine has been and still may be. This is a timely project as the medical and veterinary professions, after long debating the notion of ‘one medicine’ as ‘a common pool of knowledge in microbiology, immunology, physiology, pathology and epidemiology’, are now calling to develop the field.
Book chapters on the topic "Theses – Immunology"
1
Kroese, F. G. M., and N. A. Bos. "Peritoneal B-1 Cells Switch in vivo to IgA and these IgA Antibodies can bind to Bacteria of the Normal Intestinal Microflora." In Current Topics in Microbiology and Immunology, 343–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60162-0_42.
Full text
2
Golz, Julia Carolin, and Kerstin Stingl. "Natural Competence and Horizontal Gene Transfer in Campylobacter." In Current Topics in Microbiology and Immunology, 265–92. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65481-8_10.
Full textAbstract:
AbstractThermophilic Campylobacter, in particular Campylobacter jejuni, C. coli and C. lari are the main relevant Campylobacter species for human infections. Due to their high capacity of genetic exchange by horizontal gene transfer (HGT), rapid adaptation to changing environmental and host conditions contribute to successful spreading and persistence of these foodborne pathogens. However, extensive HGT can exert dangerous side effects for the bacterium, such as the incorporation of gene fragments leading to disturbed gene functions. Here we discuss mechanisms of HGT, notably natural transformation, conjugation and bacteriophage transduction and limiting regulatory strategies of gene transfer. In particular, we summarize the current knowledge on how the DNA macromolecule is exchanged between single cells. Mechanisms to stimulate and to limit HGT obviously coevolved and maintained an optimal balance. Chromosomal rearrangements and incorporation of harmful mutations are risk factors for survival and can result in drastic loss of fitness. In Campylobacter, the restricted recognition and preferential uptake of free DNA from relatives are mediated by a short methylated DNA pattern and not by a classical DNA uptake sequence as found in other bacteria. A class two CRISPR-Cas system is present but also other DNases and restriction–modification systems appear to be important for Campylobacter genome integrity. Several lytic and integrated bacteriophages have been identified, which contribute to genome diversity. Furthermore, we focus on the impact of gene transfer on the spread of antibiotic resistance genes (resistome) and persistence factors. We discuss remaining open questions in the HGT field, supposed to be answered in the future by current technologies like whole-genome sequencing and single-cell approaches.
3
Lambourne, Jonathan, and Ruaridh Buchanan. "Basic Immunology." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0012.
Full textAbstract:
There are four major components of the immune system. These include: 1. mechanical barriers to pathogen entry. 2. the innate immune system. 3. the adaptive immune system. 4. the lymphoid organs. Mechanical barriers include skin and mucous membranes and tight junctions between epithelial cells prevent pathogen entry. Breaches can be iatrogenic, for example, IV lines, surgical wounds, and mucositis, and are a large source of healthcare- associated infections. The innate immune system provides the first internal line of defence, as well as initiating and shaping the adaptive immune response. The innate system comprises a range of responses: phagocytosis by neutrophils and macrophages (guided in part by the adaptive immune system), the complement cascade, and the release of antimicrobial peptides by epithelial cells (e.g. defensins, cathelicidin). The adaptive immune system includes both humoral (antibody- mediated) and cell-mediated responses. It is capable of greater diversity and specificity than the innate immune system, and can develop memory to pathogens and provide increased protection on re-exposure. Immune cells are divided into myeloid cells (neutrophils, eosinophils, basophils, mast cells, and monocytes/macrophages) and lymphoid cells (B, T, and NK cells). These all originate in the bone marrow from pluripotent haematopoietic stem cells. The lymphoid organs include the spleen, the lymph nodes, and mucosal-associated lymphoid tissues—which respond to antigens in the blood, tissues, and epithelial surfaces respectively. The three main ‘professional’ phagocytes are macrophages, dendritic cells, and neutrophils. They are similar with respect to how they recognize pathogens, but differ in their principal location and effector functions. Phagocytes express an array of Pattern Recognition Receptors (PRRs) e.g. Toll-like receptors and lectins (proteins that bind carbohydrates). PRRs recognize Pathogen- Associated Molecular Patterns (PAMPs)— elements which are conserved across species, such as cell-surface glycoproteins and nucleic acid sequences. Though limited in number, PRRs have evolved to recognize a huge array of pathogens. Binding of PRRs to PAMPs enhances phagocytosis. Macrophages are tissue-resident phagocytes, initiating and co-ordinating the local immune response. The cytokines and chemokines they produce cause vasodilation and alter the expression of endothelial cell adhesion factors, recruiting circulating immune cells.
4
Lazarus, John H., L. D. Kuvera, and E. Premawardhana. "Thyroid disease during pregnancy." In Oxford Textbook of Endocrinology and Diabetes, 547–52. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.3255.
Full textAbstract:
Thyroid disorders are common. The prevalence of hyperthyroidism is around 5/1000 in women and overt hypothyroidism about 3/1000 in women. Subclinical hypothyroidism has a prevalence in women of childbearing age in iodine-sufficient areas of between 4% and 8%. As these conditions are generally much more common in females, it is to be expected that they will appear during pregnancy. Developments in our understanding of thyroid physiology (1) and immunology (2) in pregnancy, as well as improvements in thyroid function testing (3), have highlighted the importance of recognizing and providing appropriate therapy to women with gestational thyroid disorders. Before considering the clinical entities occurring during and after pregnancy it is useful to briefly review thyroid physiology and immunology in relation to pregnancy.
5
Wallin, Elizabeth, and Kathryn J. Wood. "Principles of transplantation immunology." In Oxford Textbook of Medicine, edited by John D. Firth, Christopher P. Conlon, and Timothy M. Cox, 392–408. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0044.
Full textAbstract:
Since the first successful transplant of a kidney between identical twins in 1954, transplantation has progressed from being an experimental procedure to a routine clinical therapy offering immense benefits for patients with organ failure. However, the survival of transplanted organs remains limited by the body’s immune responses, and many of the complications of transplantation result from the crude nature of our attempts to suppress these. This chapter explains how the survival of transplanted organs remains limited by the body’s immune responses, which are designed to discriminate between ‘self’ and ‘non-self’ or ‘altered-self’, and how many of the complications of transplantation result from the crude nature of our attempts to suppress these.
6
Ferreira, Adaliene Versiani Matos, Laís Bhering Martins, Nayara Mussi Monteze, Geneviève Marcelin, and Karine Clément. "Immunology of Eating Disorders." In Immunopsychiatry, 241–50. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0014.
Full textAbstract:
Eating disorders (EDs) are characterized by dysregulation in eating behavior leading to extreme increase or decrease in food intake that, in turn, changes body weight, adiposity, and physical health. Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) are the three major eating disorders. Peculiar immune abnormalities occur in these conditions. Previous studies have reported a higher number of CD4+ T lymphocytes in patients with AN, which are related to a relative resistance to viral infections, even in the presence of leukopenia. It has also been proposed that a cluster of cytokines is altered in these patients. A chronic low-grade inflammation has been observed in obese people with BED and in patients with AN, but with a different profile in each condition. In this context, antagonist drugs of specific cytokines, such as anti-TNF, showed improvement of AN-related symptoms, but increased weight gain in obese subjects. The identification of specific molecules and/or immune cells that impair neuronal circuits implicated in eating behaviors may contribute to the development of pharmacological strategies for eating disorders.
7
Mallard, Bonnie, Mehdi Emam, Shannon Cartwright, Tess Altvater-Hughes, Alexandra Livernois, Lauri Wagter-Lesperance, Douglas C. Hodgins, et al. "Advances in understanding immune response in dairy cattle." In Improving dairy herd health Improving, 121–62. Burleigh Dodds Science Publishing, 2021. http://dx.doi.org/10.19103/as.2020.0086.06.
Full textAbstract:
From the beginning, cattle have made important contributions to the field of immunology, including the development of the first Mycobacterium bovis BCG vaccine for human tuberculosis in 1921. In 1981 the first report of a biosynthesized polypeptide vaccine against Foot and Mouth Disease Virus (FMDV) using the VP3 protein expressed in Escherichia coli (E. coli) was made for cattle. Cattle also possess a substantial proportion of T cells expressing the γδ T-cell receptor which helped to elucidate the role of these unique cells in host defence. More recently, it was discovered that cattle produce antibodies with ultra-long Complementarity Determining Region (CDR) - 3. This seminal finding has allowed the production of bovine therapeutic broadly neutralizing antibodies with ultra-long CDRs to passively treat various virial infections in humans and play a key role in protecting cattle. This chapter will review advances in bovine immunology, particularly as it relates to dairy cattle.
8
Spickett, Gavin. "Autoantibodies." In Oxford Handbook of Clinical Immunology and Allergy, edited by Gavin Spickett, 511–76. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198789529.003.0018.
Full textAbstract:
There are many hundreds of reported autoantibodies, not all of clinical value. The repertoire of the typical regional immunology laboratory will cover most of the ones described within this chapter. Some will only be available through specialist referral laboratories, or through research laboratories. This chapter covers techniques, then the units, principles, indications, and interpretation for tests for individual autoantibodies.
9
Peakman, Mark. "Immunology of type 1 diabetes mellitus." In Oxford Textbook of Endocrinology and Diabetes, 1723–33. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1319.
Full textAbstract:
The concept that the pathological hallmark of type 1 diabetes—namely, irreparable damage to β cells—is the result of an autoimmune process has gained sustained credence since it was first intimated in the 1970s. Forty years on, a robust set of criteria can be applied to settle this important question. As a result of numerous, reproducible research findings (Table 13.2.3.1), there is now an overwhelming case to support the assertion that type 1 diabetes is an autoimmune disease. Perhaps the most persuasive evidence is provided by the case reports of diabetes arising in recipients of bone marrow from patients with type 1 diabetes (1, 2). In these cases, the recipients underwent bone marrow ablation as part of the treatment for their underlying condition (e.g. relapsed haematological cancers) that effectively removed all autologous innate and adaptive immune cells. To reconstitute their immune system, they then received bone marrow from a sibling with type 1 diabetes. They developed the disease themselves some years later. It is hard to argue against the proposal that immune cells transferred in the bone marrow inoculum were responsible for β cell destruction. Indeed, current practice in these circumstances is to ensure immune depletion of any mature T lymphocytes that may be present in the transplanted bone marrow using specific monoclonal antibodies. This successfully circumvents the problem—and also provides clear evidence for the pivotal role for T lymphocytes in causing β cell damage. It should be noted that the overwhelming majority of patients with type 1 diabetes—especially those inhabiting the Western, developed world—have evidence of the underlying autoimmune processes, as discussed in this chapter. However, there is a recognition that type 1 diabetes may be heterogeneous, as, in some patients, evidence of autoimmunity is lacking (WHO diabetes classification type 1B). In Japan, a fulminant form of diabetes has been described as representing 15–20% of type 1 disease (15). Presentation is characterized by a high prevalence of preceding common cold-like and gastrointestinal symptoms, a near-normal level of HbA1c (despite very high plasma glucose levels and ketoacidosis), raised serum pancreatic enzyme levels, and absent C-peptide—but only rarely any evidence of autoantibodies against islet cell autoantigens (16). Some cases of type 1 diabetes arising in sub-Saharan Africa have also been described as lacking evidence of autoimmunity against islet cells (see Chapter 13.4.3.4); however, these data require clarification, since it is known that the autoantibodies decline and may disappear from the circulation soon after diagnosis, making retrospective classification of cohorts with established disease highly problematic (17). Future studies in these locations will need to establish evidence of autoimmunity at diagnosis in currently equivocal situations, using the most comprehensive, up-to-date range of serological markers (see Table 13.2.3.2, below), as well as to establish the clinical and immunogenetic features of the disease.
10
Salem, Haitham, Scott D. Lane, and Antonio L. Teixeira. "Immunology of Substance Use Disorders." In Immunopsychiatry, 165–78. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.003.0009.
Full textAbstract:
As in other psychiatric disorders, the role of the immune system is gathering increasing attention as an important mechanism in substance use disorders. Addiction is a complex condition in which a person engages in drug-seeking and drug-taking behaviors to accentuate the reward processes in the brain and avoid negative withdrawal states. Due in part to the activation of stress responses during drug withdrawal, high levels of peripheral pro-inflammatory cytokines are observed in this phase, and these immune changes might contribute to the behavioral negative reinforcing effects of the drug. This and other observations suggest that the immune system might play a role in the development of substance use disorders, also representing a potential target for biomarker and therapeutic strategy development (e.g., vaccines).
Conference papers on the topic "Theses – Immunology"
1
Fulcher, C. A., R. A. Houghten, S. de Graaf Mahoney, J. R. Roberts, and T. S. Zimmerman. "SYNTHETIC PEPTIDE PROBES OF FACTOR VIII IMMUNOLOGY AND FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644768.
Full textAbstract:
In order to develop specific immunologic reagents for mapping functionally important sites on FVIII, we have prepared rabbit polyclonal antibodies against synthetic peptides of FVIII derived from regions along the entire FVIII amino acid sequence. To date, a total of 70 peptides have been synthesized and characterized by amino acid and HPLC analysis. The peptides were coupled to keyhole limpet hemocyanin with glutaraldehyde as a linkage reagent and used to immunize rabbits. Antisera were tested by ELISA assay on polystyrene microtiter plates coated with either the peptide immunogen, or purified FVIII. The antisera were also tested for their ability to inhibit FVIII clotting activity and to react with separated FVIII polypeptides on immunoblots.Of the 70 peptides, all reacted with the peptide immunogen, 45 reacted with purified FVIII and 33 reacted with FVIII on immunoblots. Because we had obtained evidence that cleavage of the amino terminal region of the 80 kDa polypeptide may play a role in FVIII activation by thrombin, a series of partially overlapping peptides, 15 residues in length, were synthesized in this area. After affinity purifying these antibodies on columns of FVIII immobilized on agarose, adjusting the antibodies to equal antigen binding titers by dot immunoblotting and testing for inhibition of FVIII activity, only one antibody could strongly inhibit FVIII clotting activity. This inhibition could be blocked by the peptide itself at nanomolar concentrations and no significant inhibition could be shown by antibodies to partially overlapping peptides individually, or in combination. These data suggest that a site important to FVIII function can be localized to a 15 amino acid residue region of the 80 kDa polypeptide of FVIII. In addition, a second inhibitoryantibody was identified which was produced against a peptide in the carboxy terminal region of the 54 kDa thrombin fragment of FVIII and this area is currently being studied in a similar manner. In addition, two monoclonal anti-FVIII synthetic peptide antibodies have been produced which react with purified FVIII on immunoblots. One of these antibodies also functions as an immunoadsorbent when linked to agarose and FVII can be purified in this manner, using the synthetic peptide as eluant. It is evident that antibodies to synthetic peptides of FVIII can be useful probes of FVIII structure, function and interactions as well as being of use in FVIII purification.
2
Rossi, L., A. M. Gianregorio, S. Bartolai, L. Lecchini, M. Bendinelli, and F. Panicucci. "IMMUNOLOGIC EVALUATIONOF ITALIAN HAEMOPHILIACS TREATED WITH COMMERCIAL CONCENTRATES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644146.
Full textAbstract:
The presence of the antibody to human immunodeficiency virus (HIV) was investigated in 487 serum samples withdrawn from 216 haemophiliacs (186 haemophiliacs A and 30 B) who came to the Pisa Centre between 1977 and 1986. Results show that a considerable proportion of haemophiliacs (15%) were already positive in 1982. In haemophiliacs A, who were treated up to 1983 with concentrates made from US plasma, but from 1984 on began to use concentrates made from Italian plasma, this proportion in 1986 was 16%. In haemophiliacs B who have continued using concentrates from US plasma, the prevalcence rate of Anti-HIV was found to be much higher (63%). As regards the contact with the virusof hepatitis B (HBV), antibodies werefound in 64% of haemophiliacs and theviral antigens in 6%. 137 of these haemophiliacs (112 A and 25 B) were examined between 1985 and 1986 for indexof hepatic cytoli-sis, immunological and clinical status. In 65% of haemophiliacs the level of serum glutamic pyruvate transaminase (SGPT) was mildly increased, perhaps for the presenceof chronic hepatitis. In Anti-HIV negative subjects we found a decrease of T helper/T suppressor (Th/Ts) ratio, with a mean of 1.3 (in controls, 1.7),due especially to an increase of Ts (mean 0.8 × 103Vcu.mm.; incontrols, mean 0.6). Also in Anti-HIVpositive haemophiliacs there was a decrease ofTh/Ts ratio (mean 1.1), but this was mainly due to a decrease of Th (mean 0.7 × 103/cu.mm.;in controls, mean 1.1). Clinical evaluation of the Anti-HIVpositive subjectsshowed 2 patients with AIDS related illness with opportunistic infections and 13 haemophiliacs (33% of seropositive subjects) withone or more of these abnormalities: thrombocytopenia, lymphoadenopathy, slight persistentfever, diarrhea.
3
Karpatkin, S. "MECHANISMS OF IMMUNOLOGIC THROMBOCYTOPENIA IN INDIVIDUALS AT RISK FOR AIDS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644759.
Full textAbstract:
HIV-seropositive homosexuals, narcotic addicts and hemophiliacs develop a new syndrome of immunologic thrombocytopenic purpura (ITP) which is clinically indistinguishable from classic autoimmune thrombocytopenic purpura (ATP) with respect to increased megakaryocytes in the bone marrow, peripheral destruction of antibody-coated platelets, negative serology for SLE, response to treatment with prednisone and/or splenectomy. However, their platelet immunologic profiles are different.Homosexuals appear to have an immune complex-mediated mechanism: markedly elevated platelet-bound IgG and C3C4 (3.8 and 4.2-fold greater than classic ATP, respectively), elevated circulating immune complexes (3-fold greater than classic ATP), anti-F(ab')2 antibodies and absence of 7S anti-platelet IgG. There is no inverse correlation between platelet count and platelet-bound IgG or platelet-elutable anti-platelet antibody as in classic ATP.Hemophiliacs appear to have an autoimmune 7S IgG-mediated mechanism similar to classic ATP: inverse relationship betweem platelet count and platelet-bound IgG, r = 0.84, p less than 0.001, 26 df, anti-platelet reactive 7S IgG which reacts by its F(ab')2 domain, (reactive at 60-130 ug/ml compared to control IgG), platelet-elutable anti-platelet antibody. However, these patients also have elevated circulating immune complexes (2.4-fold classic ATP level) and markedly elevated platelet-bound IgG and C3C4 (3.4 and 1.2-fold classic ATP level, respectively). Anti-HIV antibody correlated with circulating immune complexes, r = 0.833, p less than 0.001.Narcotic addicts appear to have a mixture of both mechanisms (immune complex as well as autoimmune 7S IgG): markedly elevated platelet-bound IgG and C3C4 (2.6 and 2.4-fold classic ATP level, respectively), elevated circulating immune complexes (7.3-fold classic ATP level), anti-F(ab')2 antibodies, absence of an inverse correlation between platelet count and platelet-bound IgG. However, these patients do have specific 7S IgG anti-platelet antibody, which reacts by its F(ab')2 domain.F(ab')2antibodies were of the IgG class and correlated with circulating immune complex level. They react with autologous, homologous patient and healthy control F(ab')2 fragments. Some anti-F(ab')2 antibodies have broad reactivity, others are more limited. Some immune complexes were shown to contain HIV antibody. It is postulated that the immune complex platelet deposition noted with homosexual and narcotic addict thrombocytopenia may in part be due to HIV antibody complexes, some of which may exist as anti-antibody complexes.
4
Fabbrini, N., J. M. Walenga, D. Hoppensteadt, and J. Fareed. "LABORATORY EVALUATION OF A MULTICHANNEL VERTICAL PHOTOMETRIC ANALYZER FOR TEE TESTING OF CLOT, CHROMOGENIC AND ELISA BASED METHODS FOR HEMOSTATIC SYSTEM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644605.
Full textAbstract:
Due to major developments in the molecular understanding of the hemostatic system, many newer tests to evaluate bleeding and clotting disorders have been developed. These newer tests are based on clotting, enzymatic and immunologic techniques. Since routine coagulation laboratories are not equipped with instruments capable of enzymatic or immunologic measurements, adaptation of these newer tests to the clinical laboratory has been rather limited. As these tests have a significant impact on the basic diagnostics of hemostatic disorders and the monitoring of antithrombotic therapy, the need for instruments capable of performing each of these tests is evident. We have evaluated a new multiprobe instrument, the FP-910 Coagulation Analyzer (Lab-Systems, Helsinki, Finland), for numerous clot-based, immunologic and amidolytic assays. This instrument has a programmable microprocessor controlled analyzer, mixer and incubator in a semi-automated system capable of hight throughput due to multiple processing. A unique vertical light path system allows quantification of even particulate reactions. It is compatible with most commercially available reagents for clot-based synthetic substrate and ELISA methodologies. Individual methods are preprogrammed in the instrument and additional methods can be programmed for all detection modes. For the clot-based assays (P.T, APTT, Heptest®) , excellent correlations were obtained with the BBL Fibrometer and General Diagnostics Coagamate X2 (n=50, r>0.95). The chromogenic assay kits from various suppliers (AT III, heparin, plasminogen, a-antiplasmin) also correlar-ted well (n=50, r>0.95). Similarly the ELISA based protein C assay also correlated well with the Dynatech® system (n=50, r>0.98). The instrument is easy to operate, has a high throughput in all modes (50-100/hr.), high reproducibility and is economically feasible for routine laboratories involved in multi-parametric testing of hemostasis.
5
Roncaglioni, M. C., A. Falanga, A. P. Bolognese Dalessandro, B. Casali, and M. B. Donti. "ENZYMATIC AND IMMUNOLOGIC CHARACTERIZATION OF A CYSTEINE PROTEINASE PROCOAGULANT IN SEVERAL MURINE METASTASIZING TUMO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643663.
Full textAbstract:
Involvement of the hemostatic systemin tumor metastasis growth has been repeatedly suggested and several tumor-associated procoagulants have been described. We have studied here the procoagulant activity (PCA) of tissue extracts from 4 murine metastasizing tumors: Lewis Lung Carcinoma (3LL), B16 melanoma (B16), JW sarcoma (JWS) and the M4 variant of the mFS6 fibrosarcoma (M4). The experiments were designed to identify cancer procoagulant (CP) a FVII independent FX activating cysteine proteinase or tissue factor (TF) in these tumors. Tissue extracts from 3LL, B16 and JWS initiated coagulation both in the presence and absence of FVII (FVII independent activity ranging from 70% to 86% of the total activity). The PCA of the same tumors was significantly decreased (p < 0.01) by cysteine proteinase inhibitors (1 mM iodoacetamide (IA) and 0.1 mM HgCl2 ) and the inhibitionby HgCl2 was reversed by -SH group activators (di-thiatreital, KCN, IiDTA). In addition these samples were able of directly activating pure bovineFX in a two stage clotting assay. The PCA of M4 extract was dependent on FVII,was not significantly affected by IA and HgCl2 and was inhibited by concanavalin A, a known TF inhibitor. An Ouchterlony double immunodiffusion study showed immunological cross-reactivity of 3LL, B16 and JWS to a polyclonal antibody to purified CP (from rabbit V2 carcinoma; obtained from S.G. Gordon, Denver, USA). No cross-reactivity was present between this antibody and M4. This study shows that the PCA of M4 is TF, whereas the procoagulant(s) of 3LL, B16 and JWS are enzymatically and immunologically indistinguishable from CP.
6
Pengo, V., M. J. Heine, P. Thiagarajan, and s. s. Shapiro. "A GENERAL MECHANISM FOR LUPUS ANTICOAGULANTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643660.
Full textAbstract:
Although- a number of observations have implied that lupus anticoagulants have immunologic specificity towards anionic. phospholipids, thereby prolonging phospholipid-dependent coagulation tests, this assumption has been directly demonstrated in only one patient with a monoclonal IgM paraprotein. We have tested the generality of this hypothesis directly by isolating five IgG lupus anticoagulants from patients with lupus-like syndromes and/or thrombosis. IgG lupus anticoagulant fractions were isolated free of other plasma proteins and free of contaminating phospholipid by adsorption to and elution from cardiolipin-cholesterol-dicetylphosphate liposomes , followed by chromatography on protein A-Sepharose. Cardiolipin liposomes, but not phosphatidylcholine liposomes, were capable of removing all, or nearly all, lupus anticoagulant activity from patient plasma. Anticardiolipin and lupus anticoagulant activity were both present in acidic fractions on isoelectric focusing. F(ab’)2 fragments retained lupus anti coagulant activity and bound to cardiolipin in an ELISA assay. The affinity-purified IgG preparations reacted with cardiolipin, phosphatidyl serine , phosphatidylinositol and phosphatidic acid, but not with phosphatidylcholine or phosphatidyl ethanol amine, and inhibited calcium-dependent binding of prothrombin and of factor X to phosphatidy1serine-coated surfaces. These data demonstrate a general mechanism for the action of lupus anticoagulants: antibodies that have immunologic specificity towards anionic phospholipids, thereby blocking the calcium-mediated binding of vitamin K-dependent coagulation factors to coagulation-active phospholipid surfaces.
7
Slattery, Robyn Maree. "Objective versus subjective methods to assess discipline-specific knowledge: a case for Extended Matching Questions (EMQs)." In Third International Conference on Higher Education Advances. Valencia: Universitat Politècnica València, 2017. http://dx.doi.org/10.4995/head17.2017.5473.
Full textAbstract:
Background: Extended matching questions (EMQs) were introduced as an objective assessment tool into third year immunology undergraduate units at Monash University, Australia. Aim: The performance of students examined objectively by multiple choice questions (MCQs) was compared to their performance assessed by EMQs; there was a high correlation coefficient between the two methods. EMQs were then introduced and the correlation of student performance between related units was measured as a function of percentage objective assessment. The correlation of student performance between units increased proportionally with objective assessment. Student performance in tasks assessed objectively and subjectively was then compared. The findings indicate marker bias contributes to the poor correlation between marks awarded objectively and subjectively. Conclusion: EMQs are a valid method to objectively assess students and their increased inclusion in the assessment process increases the consistency of student marks. The subjective assessment of science communication skills introduces marker bias, indicating a need to identify, validate and implement, more objective methods for their assessment. Keywords: Extended matching question (EMQ); Objective assessment (OA); SA (SA); Marker bias; Discipline-specific assessment; Science communication assessment
8
Cunningham-Rundles, C., J. Bussel, and A. Lipscombs. "CHANGES IN ANTI-CARD10LIPIN ANTIBODY TITER IN SERA OF I TP PATIENTS AFTER TREATMENT WITH INTRAVENOUS IMMUNOGLOBULIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643924.
Full textAbstract:
Antibodies to cardiolipin have previously been demonstrated in the sera of patients with idiopathic thrombocytopenia purpura (ITP). We questioned whether the levels of anti-cardiolipin in the sera of patients with ITP would be altered after treatment with intravenous immunoglobulin (IVGG). Using flexible polyvinyl chloride microtiter plates coated with bovine cardiolipin, we measured IgG and IgM anti-cardio1ipin levels by ELISA before and at multiple intervals during and after IVGG treatment for 17 patients who had ITP. We found that within 7-10 days of treatment, 16 of 17 patients had further increases of IgG anti-cardiolipin antibody. This is probably due to the infusion of IVGG concentrates, which we found contained substantial amounts of IgG anti-cardio1ipin. Increases in platelet counts had significant correlation with increased IgG anti-cardio1ipin (p>0.01), presumably also due to the infusion of IVGG. Surprisingly, 16 of 17 patients had a marked increase in serum levels of IgM anti-cardiolipin 7-10 days post IVGG treatment. Since IVGG does not contain IgM anti-cardiolipin and our assay is specific for this isotype, this antibody represents de novo synthesis. We previously reported and have also confirmed here, that 16 of these 17 patients had increased serum IgM levels after IVGG treatment. The increase in serum IgM anti-cardio1ipin antibody may explain part of the increased total serum IgM observed. IVGG has been believed to be potentially suppressive of various immunologic activities; our data shows that immunologic stimulation also occurs. The biologic effect of increased serum IgG and IgM anti-cardiol ipin after IVGG treatment in ITP, particularly since cardiolipin may be a constituent of platelet membranes, is still uncertain.
9
Gordon, Stuart, Bonnie Sloane, Phil Cavanugh, Barbara Cross, Kenneth Honn, and Mohanathasan Chelladurai. "PURIFICATION AND CHARACTERIZATION OF TWO PROCOAGULANTS FROM WALKER 256 CARCINOSARCOMA TUMORS,." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643666.
Full textAbstract:
Activation of the coagulation system bytumor cells may play an important role in tumor growth and metastases. Becauseprocoagulant activities have been identified in different tumor cells by different investigators, effective comparison of these activities has been difficult. Therefore, we purified and characterized two different procoagulant proteins from the same Walker 256 tumors. The first procoagulant activity/platelet aggregating activity (PCA/PAA) was purified from a 1% CHAPS detergent extract oftumor homogenate followed by (NH4)2SO4 fractionation, anion exchange and hydrophobic chromatography. The protein had a molecular weight of 58,000, required phospholipid and an intact coagulation pathway from factor X through fibrinogen for activity, but did not require factors VII or IX forits procoagulant activity. The procoagulant activity was not inhibited by 5mMphenyl-methyl sulfonyl fluoride, iodoacetamide or phenanthroline; there was noevidence of proteinase activity. The PAA was due to thrombin generation during coagulation. The second procoagulant,cancer procoagulant (CP), was extracted from tumors in barbital buffer (pH 7.4) without detergent, purified by immunoaffinity (using a polyclonal goat antibody to CP from V2 carcinoma) and mercurial-benzoate affinity chromatography. CP had a molecular weight of 68,000, an isoelectric point of 4.8 and initiated coagulation by directly activating factor X in the coagulation system. CP was inhibited by Hg++ and iodoacetamide, cysteine proteinase inhibitors. The purified CP formed an immunodiffusion precipitin band against the polyclonal anti-CP goat antibody. Thus, thepurified CP had the same physicochemical, enzymatic and immunologic propertiesas CP from rabbit V2 carcinoma. Neither procoagulant had the properties of tissue factor. These results suggest that there aretwo distinct procoagulant activities inWalker 256 and that both may contributeto the coagulation abnormalities that are associated with tumor growthand metastases.
10
Godal, H. C., F. Brosstad, and B. Holm. "CONGENITAL HYPOFIBRINOGENEMIA, DEEP VEIN THROMBOSIS AND RECURRENT PLACENTAL ABRUPTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644279.
Full textAbstract:
A patient with hypofibrinogenemia, deep vein thrombosis and recurrent placental abruption is reported. The persistently low plasma fibrinogen concentration strongly suggested that the condition was inherited, and this was supported by low fibrinogen levels and thrombosis tendency in the patient's brother. The exact nature of the condition is not known, but the close agreement between the clottable and immunologic fibrinogen -indicates the presence of a hyperfibrinogenemia sensu stricte rather than dysfibrinogenemia, and this was supported by uniformly negative tests to detect fibrinogen abnormalitied.Up to now, less than 50 cases of congenital hypofibrinogenemia have been reported. It is not entirely clear whether hypofibrinogenemia represents the heterozygous form of afibrinogenemia or whether itrepresents some sort- of dysfibrinogenemia with abnormal rate of biosynthesis but normal clotting and crosslinking functions. Four of the reported patients with hypofibrinogenemia had placental abruption, a complication which occursin less than of pregnancies. In addition, a relatively high proportion of patients withcongenital hypofibrinogenemiahad increased tendency to thrombosis. On this background it is tempting to speculate that the elevated fibrinogen during pregnancy serves other functions than to facilitate the formation of haemostatic plugs. Thus, during pregnancy and other socalled "acute phase" situations, minute amounts of fibrin may be generatedwithin the circulating blood. Since, moreover, the solvent for these fibrin molecules isfibrinogen, the possibility exists that hyperfibrinogenemia contributes to the prevention of thromboembolism by keeping trace amounts of fibrin in solution.