Relevant bibliographies by topics / Liver disease; Immunology

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Liver disease; Immunology'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Liver disease; 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 "Liver disease; Immunology"

1

Leevy, Carroll B., and Hany A. Elbeshbeshy. "Immunology of Alcoholic Liver Disease." Clinics in Liver Disease 9, no. 1 (February 2005): 55–66. http://dx.doi.org/10.1016/j.cld.2004.11.002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Duddempudi, Anupama T. "Immunology in Alcoholic Liver Disease." Clinics in Liver Disease 16, no. 4 (November 2012): 687–98. http://dx.doi.org/10.1016/j.cld.2012.08.003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chedid, Antonio, Selma Arain, Ann Snyder, Philippe Mathurin, Frédérique Capron, and Sylvie Naveau. "The Immunology of Fibrogenesis in Alcoholic Liver Disease." Archives of Pathology & Laboratory Medicine 128, no. 11 (November 1, 2004): 1230–38. http://dx.doi.org/10.5858/2004-128-1230-tiofia.

Full text
Abstract:
Abstract Context.—Alcoholic liver disease in humans frequently leads to cirrhosis. Experimental models of hepatic fibrogenesis are available, but extrapolation of those findings to human ethanol-induced liver injury is difficult. Hepatic ethanol-induced fibrosis in humans has often been studied in relatively small patient populations. During the past decade, several animal models and human studies have attributed fibrogenesis in the liver to the role played by hepatocytes, Kupffer cells, endothelial cells, and especially stellate cells. Objective.—To determine the contribution of the main liver cell types to ethanol-induced fibrogenesis. For that purpose, we studied the expression of the following immunologic parameters: smooth muscle–specific α actin (SMSA), CD68, CD34, transforming growth factor β1, intercellular adhesion molecule 1, and collagen types 1 and 3. The Dako LSAB+ kit (peroxidase method) was used. Design.—We recently studied a large cohort of patients with alcoholic liver disease in France. In this cohort, we found 87 cases in which liver biopsies revealed only pericentral injury with nonpathologic portal areas. We compared cases in which the portal areas were nonpathologic with 324 patients in whom staging ranged from F0 to F3. Patients with cirrhosis (F4) were excluded from evaluation. To stage fibrosis, we used the METAVIR system. Furthermore, we selected 40 cases in which the biopsies measured at least 25 mm in length for further histochemical evaluation. Ten additional normal cases from our archives were used as controls. We divided this patient population into the following 5 groups of 10 patients each: group 1A, F0 with steatosis; group 1B, F0 without steatosis; group 2, F0 to F1, central injury; group 3, F3, fibrosis with multiple septa; and group 4, nonpathologic livers (controls). Results.—Smooth muscle–specific α actin was expressed by stellate cells, pericentrally, with increasing severity and intensity in the advanced stage of fibrosis of group 3, less intense expression was noted in group 2, and expression was practically absent in group 1 and in nonpathologic controls. CD68 was the best marker for Kupffer cells and was expressed diffusely within the lobules in all groups. Its expression correlated directly with the degree of disease severity, progressing from stage I through stage III, but was absent in nonpathologic livers. CD34 was consistently expressed by endothelial cells in the periportal areas in all groups. The expression of collagen type 1 was intense in the bands of fibrosis or bridging, while type 3 expression was poor. Transforming growth factor β1 and intercellular adhesion molecule 1 were not expressed in any group. Conclusions.—In this study, stellate cell activation (SMSA) was most intense pericentrally in the early stages and diffusely with progression to fibrosis and maximum intensity in stage III. Kupffer cell activation, as determined by CD68 expression, was intense and diffuse, while endothelial cells expressed CD34 periportally in a similar manner in all stages. Fibrogenesis in human ethanol injury is due to the activity of stellate cells, Kupffer cells, and to a lesser extent, to endothelial cells.
APA, Harvard, Vancouver, ISO, and other styles
4

Mutchnick, Milton G. "Immunology of liver disease. Seminars in liver disease, vol. 4, number 1." Gastroenterology 89, no. 4 (October 1985): 923–24. http://dx.doi.org/10.1016/0016-5085(85)90598-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bejarano, P. A. "The Immunology of Fibrogenesis in Alcoholic Liver Disease." Yearbook of Pathology and Laboratory Medicine 2006 (January 2006): 30–31. http://dx.doi.org/10.1016/s1077-9108(08)70025-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Heymann, Felix, and Frank Tacke. "Immunology in the liver — from homeostasis to disease." Nature Reviews Gastroenterology & Hepatology 13, no. 2 (January 13, 2016): 88–110. http://dx.doi.org/10.1038/nrgastro.2015.200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Neuberger, James, and Roger Williams. "12 Immunology of drug and alcohol-induced liver disease." Baillière's Clinical Gastroenterology 1, no. 3 (July 1987): 707–22. http://dx.doi.org/10.1016/0950-3528(87)90054-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

TODA, GOTARO. "Immunology on the digestive system.5.Disease state of autoimmune liver diseases." Nihon Naika Gakkai Zasshi 82, no. 9 (1993): 1403–8. http://dx.doi.org/10.2169/naika.82.1403.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Utiyama, Shirley R. R., Katiane B. Zenatti, Heloisa A. J. Nóbrega, Juliana Z. C. Soares, Thelma L. Skare, Caroline Matsubara, Dominique A. Muzzilo, and Renato M. Nisihara. "Rheumatic Disease Autoantibodies in Autoimmune Liver Diseases." Immunological Investigations 45, no. 6 (July 13, 2016): 566–73. http://dx.doi.org/10.1080/08820139.2016.1186173.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Schimpf, Kl. "Liver disease in hemophilia." Transfusion Science 11 (January 1990): S15—S22. http://dx.doi.org/10.1016/0955-3886(90)90078-w.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Liver disease; Immunology"

1

Than, Nwe Ni. "Stem cell therapy in liver disease." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8482/.

Full text
Abstract:
Liver cirrhosis is the fifth leading cause of death worldwide and the definitive treatment for liver cirrhosis is liver transplantation although there are limitations such as organ availability and surgical risks. Therefore, alternative therapies have been studied extensively and stem cell therapies have shown some promising results although most studies are small and not randomised. The aim of this thesis was to explore the effectiveness of stem cell therapy in patients with chronic liver disease as well as explore the mechanism behind fibrosis resolution achieved with cell therapy. There were three parts to the thesis: firstly, I examined the mechanistic actions behind fibrosis reduction by the infusion of bone marrow derived haematopoietic stem cells (HSC) in mice chronic fibrosis liver injury model. I worked on both immune-histochemical staining and qPCR to measure the effect oval cell response, matrix metalloproteinases and macrophage subsets within the liver with HSC therapies. Secondly, I recruited patients with chronic liver diseases for a multicentre, randomised, controlled trial to assess the clinical effectiveness of either subcutaneous granulocyte-colony stimulating factor (GCSF) or GCSF with repeated HSC infusions. The co-primary outcomes were improvement in severity of liver disease measured by model for end stage live disease (MELD) at 3 months and the trend of MELD change over time. The results showed that neither of the treatments improved the clinical outcomes. Lastly, I performed a systematic review of current published studies of stem cells therapies in liver diseases. The results showed that stem cells improved patients’ clinical parameters in the short term (< 6 months) but had no benefit on long term outcomes. In conclusion, bone marrow derived stem cell therapy did not seem to be effective in liver cirrhosis.
APA, Harvard, Vancouver, ISO, and other styles
2

Lo, Su Kong. "The immunology and treatment of primary sclerosing cholangitis." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386640.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Martins, Eduardo B. G. "Lymphocyte subsets and immune mechanisms in primary sclerosing cholangitis (PSC)." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294347.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Rajoriya, Neil. "CD161+ Gamma Delta T-cells in health and liver disease." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:fd3fb46a-bd46-4096-8f9f-0f8d092682dd.

Full text
Abstract:
CD161 γδ T-cells have been implicated in the pathogenesis of Multiple Sclerosis however their role in health and chronic liver disease requires further exploration. In health, the majority of γδ T-cells expressed CD161 – a C-type lectin, and predominantly expressed the Vδ2 chain. The CD161+ γδ T-cells demonstrated a Th1-like pattern, expressing IFN-γ, TNF-α and Granzymes/Perforin when compared to the CD161- subset. The CD161+ γδ T-cells also expressed CCR6 and IL-18R thus also displaying a Th17-like pattern. These cells were also found in the lamina propria in the gut and rapidly expanded in the 1st few weeks of life in the periphery. On gene array analysis, there were 409 genes expressed on the CD161+ γδ T-cells when compared to their CD161-ve counterparts including those coding for β2 receptors, CCL20, Acetycholinesterase, CCR1 and IL-18R. A potential clinical correlation to cardiac diseases was found when the upregulated genes were analysed. When the CD161+ γδ and CD161+ αβ T-cell populations were compared via gene-array, an association with a risk variant for coeliac disease was found. Thus in health, CD161+ γδ T-cells are not only a distinct subset of T-cells (confirmed by a FACS approach and gene array methods), but also the expression of CD161 may be linked to common genetic signals downstream in cell processes and disease pathogenesis, irrespective of T-cell subset population. In chronic liver disease there was a significant reduction in the periphery of CD161+ γδ T-cells in patients with chronic Hepatitis C (HCV) and an increase in patients with Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis when compared with healthy individuals. The CD161+ γδ T-cells appeared to be of a different phenotype in HCV infection. There was no overall significant localisation into of CD161+ γδ T-cells patients with chronic liver disease or specifically in HCV infection. There was however a CD161+ γδ T-cell enrichment in the liver in patients with Non-Alcoholic Fatty Liver disease. The CD161+ γδ T-cells were also found in Hepatocellular Carcinoma tissue. Overall it appears the CD161+ γδ T-cells are indeed a unique subset, playing a distinct role in health, as part of an early innate response, but also potentially involved in disease pathogenesis.
APA, Harvard, Vancouver, ISO, and other styles
5

Ren, Hui. "REGULATION OF HEPATIC GENE EXPRESSION DURING LIVER DEVELOPMENT AND DISEASE." UKnowledge, 2012. http://uknowledge.uky.edu/microbio_etds/6.

Full text
Abstract:
My first project was to investigate the role of Hepatocyte Nuclear Factor 1 (HNF1) and Nuclear Factor I (NFI) on alpha-fetoprotein (AFP) promoter activity during liver development. AFP is highly expressed in the fetal liver, silenced at birth, and remains at very low levels in the adult liver. A GA substitution located at -119 of the human AFP promoter is associated with hereditary persistence of AFP (HPAFP) expression in the adult liver (Hum Molec Genet, 1993, 2:379). The -120 region harbors overlapping binding sites for HNF1 and NFI. While it has been shown that the GA substitution increases HNF1 binding, the role of NFI in AFP regulation has not been investigated. This overlapping HNF1/NFI site is conserved in other mammals, including mice. In this study, I used a combination of biochemical, tissue culture, and animal studies to explore further the role of this HNF1/NFI site in AFP regulation. Transient co-transfections in Hep3B hepatoma cells indicate that HNF1 activates while NFI represses the mouse AFP promoter. EMSAs indicate that HNF1 and NF1 compete for binding to this site. Transgenes regulated by the wild-type AFP promoter are expressed at low levels in the adult liver. Transgenes with a GGAA mutation (similar to the G-A human mutation) are more active in the adult liver. My data indicate that HNF1 and NFI compete for binding to the -120 region of the AFP promoter and this competition is involved in postnatal AFP repression. My second project was to study the control of Elongation of very long chain fatty acids like 3 (Elovl3) in the liver by Zinc fingers and homeoboxes 2 (Zhx2). The Zhx2 gene was originally characterized in our lab based on its ability to control the developmental repression of several hepatic genes, including AFP (PNAS, 102:401). Zhx2 is a member of a small family of proteins found only in vertebrates that also includes Zhx1 and Zhx3. These proteins all contain two zinc fingers and four homeodomains, suggesting that they function as regulators of gene expression. My study shows that Zhx2 regulates Elovl3 expression in female liver. Mouse strain-specific differences in adult liver Elovl3 mRNA levels and transgenic mouse data indicate that Zhx2 activates Elovl3 expression in the female adult liver. I also demonstrate that Elovl3 is repressed in the regenerating liver and that the level of Elovl3 repression is controlled by alpha-fetoprotein regulator 2 (Afr2). In addition, I show that Elovl3 expression is reduced in liver tumors, fibrotic livers and fatty livers, raising the possibility that Elovl3 can serve as a marker for HCC and liver damage.
APA, Harvard, Vancouver, ISO, and other styles
6

John, Ani K. "Incidence and Factors Associated With Nonalcoholic Fatty Liver Disease Among Patients With Rheumatoid Arthritis." ScholarWorks, 2016. https://scholarworks.waldenu.edu/dissertations/1972.

Full text
Abstract:
Nonalcoholic fatty liver disease (NAFLD) has become one of the most common hepatic diseases worldwide, making the diagnosis and management of NAFLD an emerging public health issue. Theories associated with NAFLD surmise that inflammation may be the root cause, along with the complex interplay of other chronic conditions such as obesity, metabolic syndrome, diabetes, dyslipidemia, and cardiovascular disease (CVD). It is unknown if other inflammatory conditions such as rheumatoid arthritis (RA), along with the use of methotrexate (MTX), might confer increased risk for NAFLD. Longitudinal data collected from a retrospective cohort of 17,481 adult RA patients in the United States were used to determine the incidence and factors associated with the development of NAFLD using a noninvasive tool (Fibrosis-4 score). Results of the Kaplan Meier analysis showed that 31% of this cohort developed NAFLD, in about 7 years from baseline, with most having mild to moderate disease and only 1.4% with advanced disease. RA patients also had a prevalence of chronic conditions associated with NAFLD, as seen in the general population. In the Cox proportional hazard multivariate analysis, age (middle and elderly), hypertension, CVD, dyslipidemia, metabolic syndrome, exercise, use of MTX, and non-MTX antirheumatic drugs were independent predictors for the development of NAFLD. This research could improve early diagnosis of NAFLD using a novel noninvasive tool. Increase awareness of the prevalence and causes of NALFD inform clinical practice and management of the disease and influence policy about this chronic condition in patients with RA.
APA, Harvard, Vancouver, ISO, and other styles
7

Tickle, Joseph. "The role of vascular adhesion protein (VAP)-1 during inflammatory liver disease." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8217/.

Full text
Abstract:
Liver disease is the fifth largest killer in the United Kingdom and with the numbers of diagnoses increasing each year there is an urgent need for novel therapeutic interventions. This thesis examines one potential target, Vascular Adhesion Protein (VAP)-1: an amine oxidase enzyme with reported adhesin functionality. The results herein confirm a primarily sinusoidal localisation of VAP-1, expression of which was upregulated in the liver during chronic inflammation correlated with diminished enzyme activity. Functional analysis of sinusoidal VAP-1 in vitro did not demonstrate any effect of inhibition on leukocyte recruitment, unlike that observed in other tissues. Furthermore, only neutrophils were capable of binding to recombinant VAP-1 under flow conditions. Further investigation highlighted the importance of this intimate relationship during neutrophil-endothelial interactions; revealing the first evidence that neutrophils also express catalytically active VAP-1. Neutrophil effector functions, such as the formation of extracellular traps, were also hindered by recombinant VAP-1. This was also observed in wild-type mice but not those expressing a catalytically inactive form of VAP-1 (SSAOKO). Following acute injury, these mice also exhibited expanded intrahepatic macrophage and NKT cell populations compared to control. In combination, these data highlight the complex role that VAP-1 plays during inflammatory liver disease.
APA, Harvard, Vancouver, ISO, and other styles
8

Barnes, Mark Aaron Jr. "MACROPHAGE MIGRATION INHIBITORY FACTOR AND LIVER DISEASE: THE ROLE OF MIF IN ALCOHOL-INDUCED LIVER INJURY AND CARBON TETRACHLORIDE (CCI4)-INDUCED LIVER FIBROSIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396429556.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Roscioli, Tony Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "The genetic basis of veno-occlusive disease with immunodeficiency syndrome." Awarded by:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/40599.

Full text
Abstract:
This thesis addresses the genetic basis of a rare autosomal recessive primary immunodeficiency disorder with the characteristic additional feature of venoocclusive disease of the liver (VODI). The interest in this condition was stimulated both by the potential to identify the genetic basis of a rare immunodeficiency and the opportunity to gain an insight into the biological basis of hepatic veno-occlusive disease, a poorly understood condition that is encountered most frequently in Australia as a consequence of bone marrow transplantation. The gene responsible for VODI was identified by homozygosity mapping and DNA sequence analysis of positional candidates and was shown to be the PML Nuclear Body expressed protein Sp110. This is the first time a PML Nuclear Body protein has been shown to be involved in immunodeficiency disorder. Subsequent immunofluorescence studies of affected patient cell lines showed absence of Sp110 in patient B cells. The role of SP110 alleles in the susceptibility of bone marrow transplant patients to hepatic veno-occlusive disease was investigated using a cohort of patients from the Fred Hutchinson Cancer Center, Seattle. A SNP association study identified initial evidence for an association, but the study lacked sufficient power after correction for multiple testing. Contemporaneously, Dr Igor Kramnik published a report that the murine homologue of Sp110, Ifi75 (also termed Ipr1) was deleted in mice that were supersusceptible to infection with Mycobacterium tuberculosis. A further SNP association study was therefore performed utilising a NSW cohort of Mantouxpositive South East Asian migrants, which detected evidence that alleles of SP110 may be associated with progression of M. tuberculosis infection. Again, the limited size of this cohort precluded definitive findings.
APA, Harvard, Vancouver, ISO, and other styles
10

Sharma, Vishakha. "Aging and Gender Effects in Diet-Induced Obesity and its Metabolic Sequelae." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1522320845867142.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Liver disease; Immunology"

1

Thomas, H. C., and J. Waters, eds. Immunology of Liver Disease. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1428-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Peter, Dienes Hans, ed. Autoimmune liver disease: Proceedings of the Falk Symposium 142 held in Freiburg, Germany, October 12-13, 2004. Dordrecht: Springer, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shimizu, Ichiro. Female hepatology: Favorable role of female factors in chronic liver disease. Hauppauge, NY: Nova Science Publishers, 2009.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

International Symposium on Viral Hepatitis and Liver Disease (9th 1996 Rome, Italy). Viral hepatitis and liver disease: Proceedings of IX Triennial International Symposium on Viral Heptatis and Liver Disease, Rome, Italy, 21-25 April 1996. Edited by Rizzetto Mario. Turin: Edizioni Minerva Medica, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Falk Symposium (114th 1999 Basel, Switzerland). Immunology and liver. Dordrecht: Kluwer Academic Publishers, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

missing], [name. Liver immunology. Philadelphia, PA: Hanley & Belfus, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Takahashi, Memorial Forum (1998 Tokyo Japan). Liver and immunology: Proceedings of the "Takahashi Memorial Forum", held in Tokyo, Japan, on 14 November 1998. Amsterdam: Elsevier, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Falk, Symposium (114th 1999 Basel Switzerland). Immunology and liver: Proceedings of the Falk Symposium 114 held in Basel, Switzerland, October 120-21 October, 1999 (part 1 of the Basel Liver Week 1999). Dordrecht: Kluwer Academic Publishers, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Karl-Hermann, Meyer zum Büschenfelde, Hoofnagle Jay H, and Manns Marianne, eds. Immunology and liver: Proceedings of the 70th Falk Symposium held in Basel, Switzerland, October 18-20, 1992. Dordrecht: Kluwer Academic Publishers, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Dying to live: How our bodies fight disease. Cambridge: Cambridge University Press, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Liver disease; Immunology"

1

Szabo, Gyongyi. "Alcoholic Liver Disease." In Liver Immunology, 331–43. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Mieli-Vergani, Giorgina, Rodrigo Liberal, and Diego Vergani. "Paediatric Liver Disease." In Liver Immunology, 361–71. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Gupta, Rishi, and Nanda Kerkar. "Pediatric Liver Disease." In Liver Immunology, 453–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_28.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Patel, Vaishali, and Arun J. Sanyal. "Nonalcoholic Fatty Liver Disease." In Liver Immunology, 345–59. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Raza, Ali, and John M. Vierling. "Graft-Versus-Host Disease." In Liver Immunology, 425–41. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_29.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Liu, Mengfei, Tejasav S. Sehrawat, Gyongyi Szabo, and Vijay H. Shah. "Alcohol-Associated Liver Disease." In Liver Immunology, 309–24. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Alazawi, William, and Gideon Hirschfield. "Nonalcoholic Fatty Liver Disease." In Liver Immunology, 325–34. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ahmed, Zunirah, and John M. Vierling. "Graft-Versus-Host Disease." In Liver Immunology, 551–82. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Selmi, Carlo, Cecilia B. Chighizola, Angela Ceribelli, Maria De Santis, Pier Luigi Meroni, and Renqian Zhong. "The Geoepidemiology of Autoimmune Liver Disease." In Liver Immunology, 27–43. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Trivedi, Palak Jitendrakumar, Ka-Kit Li, and James Neuberger. "Immune-Mediated Liver Disease in the Transplanted Liver." In Liver Immunology, 443–62. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02096-9_30.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Liver disease; Immunology"

1

Argirion, Ilona, Ruth M. Pfeiffer, Zhiwei Liu, Allan Hildesheim, Ligia Pinto, Katherine A. McGlynn, Jessica L. Petrick, et al. "Abstract 836: Immunologic markers and the progression of liver disease in HCV-positive individuals." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-836.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Rettke, S. R., C. A. Owen, E. J. W. Bowie, T. L. Cole, R. H. Wiesner, R. A. F. Krom, and C. Jensen. "HEMOSTATIC EVALUATION OF PATIENTS UNDERGOING LIVER TRANSPLANTATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643070.

Full text
Abstract:
Significant hemostatic abnormalities can occur during orthotopic liver transplantation (OLT). This study addressed three goals: 1)evaluation of the hemostatic mechanism at each stage of the OLT; 2) the relationship of the coagulation process with the thrombelastograph (TEG); and 3) comparison of results in patients requiring retransplantation or who died, with the overall pattern. To evaluate hemostasis during 50 consecutive OLTs, a detailed coagulation and TEG study was done. The surgical procedure was divided into the following stages: Stage I--induction of anesthesia to occlusion of blood flow to the patient’ s diseased liver; Stage II—occlusion of blood flow to the patient’ s diseased liver to reperfusion of the patient’ s new liver; and Stage III—reperfusion of the new liver until skin closure. 28 ml of arterial blood were sampled at the beginning and end of each stage and up to five days posttransplantation for the following: platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin, factors V, VII, IX, and X, plasminogen, antiplasmin, antithrombin III (functional and immunologic), fibrinolytic split products, and TEG. The patient’ s core temperature and amount of blood products transfused were obtained intraoperatively during each of the six data times. The ischemia time of the donor liver was recorded. Significant hemostatic abnormalities developed during each of the 50 OLTs, especially during reperfusion of the donor liver. In some instances, this was corrected within one hour, but platelet counts continued to fall, and a number of coagulation factors rebounded only partially. The TEG values correlated with laboratory data and blood loss, but the correlations were not strong. The patient’ s requirement for red cells varied with the operative drop in temperature; however, the donor liver ischemia time and length of Stage II made no significant difference. It is concluded that 1) significant deterioration of coagulation factors occurs during OLT, 2) the TEG is an effective screening test that affords prompt information, 3) aggressive measures should be taken to maintain the patient’ s body temperature at 37°C, 4) patient outcome was not predicted by intraoperative hemostatic evaluation.
APA, Harvard, Vancouver, ISO, and other styles
3

Abshire, T., L. Fink, J. Christian, J. O'Connell, and W. Hathaway. "THE DYSFIBRINOGEN OF CHILDHOOD NEPHROSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643334.

Full text
Abstract:
An abnormal fibrinogen (Fib) related to increased sialic acid (SA) has been described in adults with liver disease. This dysfibrinogen (Dysfib) seems most like fetal Fib. A review of 11 patients with nephrosis revealed an unexplained prolonged thrombin time (TT) and otherwise normal coagulation studies. Based on these observations, we sought to answer whether the prolonged TT defined a Dysfib and if this abnormal Fib was similar to fetal Fib. Pooled adult, fetal plasma, and the plasma of 3 patients with nephrosis were studied with TT and reptilase times (RT). Fib was measured by functional (Fib-act) and immunologic (Fib-ag) assays. An enzyme linked immunosorbent assay (ELISA) was established using antifibrinogen as the first antibody and either peroxidase conjugated Fib or a lectin (Limulus Polyphemus) specific for SA as the second antibody. The optical density was recorded per μgm Fib for both conjugated antifibrinogen or lectin and the ratio compared in order to estimate SA reactivity. Patient 3 was also studied by: 1) crossed immunoelectrophoresis (CIE) employing lectin in the first dimension and 2) polyacrylamide gel electrophoresis (PAGE) with transfer to nitrocellulose paper using Western Blot technique.Results of the CIE showed patient 3 and fetal plasma were similar in electrophoretic pattern and different from adult plasma. The PAGE with Western Blot revealed a similar pattern of Fib for patient 3, fetal and adult plasma. We conclude that the prolonged TT and RT, the greater amount of Fib-ag when compared to Fib-act in patients 1-3 and fetal plasma and the absence of evidence for Fib degradation products, support the diagnosis of Dysfib. The similarity of the CIE for patient 3 and fetal plasma and the difference between ELISA lectin/Fib ratio of patients 1-3 and fetal compared with adult plasma suggest that the Dysfib of nephrosis may be similar to fetal Fib.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Liver disease; Immunology' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography