Relevant bibliographies by topics / Radiation induced liver disease

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

Academic literature on the topic 'Radiation induced liver disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Radiation induced liver disease"

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Khozouz, Radwan F., Syed Z. Huq, and Michael C. Perry. "Radiation-Induced Liver Disease." Journal of Clinical Oncology 26, no. 29 (October 10, 2008): 4844–45. http://dx.doi.org/10.1200/jco.2008.18.2931.

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Laurie, R. M., M. W. T. Chao, and C. A. Dow. "Radiation induced liver disease: is hereditary haemochromatosis a risk factor?" Journal of Radiotherapy in Practice 3, no. 2 (March 2003): 101–4. http://dx.doi.org/10.1017/s1460396903000086.

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A 71-year-old man with Stage II gastric cancer developed rapid onset radiation induced liver disease after ceasing adjuvant chemotherapy and radiotherapy. Autopsy revealed moderate hepatocellular iron overload. Posthumously, he was found to be a compound heterozygote for hereditary haemochromatosis. Since both radiation and iron overload may induce liver damage through the activation of hepatic stellate cells, it is possible that hepatocellular iron overload may potentiate the effects of irradiation and predispose the patient to radiation induced liver disease.
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Koay, Eugene J., Dawn Owen, and Prajnan Das. "Radiation-Induced Liver Disease and Modern Radiotherapy." Seminars in Radiation Oncology 28, no. 4 (October 2018): 321–31. http://dx.doi.org/10.1016/j.semradonc.2018.06.007.

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SILVEIRA, E. "Radiation-induced liver disease: a laparoscopic approach." American Journal of Gastroenterology 96, no. 9 (September 2001): S119. http://dx.doi.org/10.1016/s0002-9270(01)03113-6.

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Benson, R., R. Madan, R. Kilambi, and S. Chander. "Radiation induced liver disease: A clinical update." Journal of the Egyptian National Cancer Institute 28, no. 1 (March 2016): 7–11. http://dx.doi.org/10.1016/j.jnci.2015.08.001.

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da Silveira, Eduardo B. V., Lennox Jeffers, and Eugene R. Schiff. "Diagnostic laparoscopy in radiation-induced liver disease." Gastrointestinal Endoscopy 55, no. 3 (March 2002): 432–34. http://dx.doi.org/10.1067/mge.2002.120879.

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Bergamo, A., K. Kaweloa, A. J. Patel, P. Mavroidis, N. Papanikolaou, S. Stathakis, and A. N. Gutierrez. "Hypofractionated Liver Stereotactic Body Radiation Therapy: Biological Effective Dose Correlated Radiation-Induced Liver Disease." International Journal of Radiation Oncology*Biology*Physics 90, no. 1 (September 2014): S849. http://dx.doi.org/10.1016/j.ijrobp.2014.05.2433.

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Nakajima, Tetsuo, Yasuharu Ninomiya, and Mitsuru Nenoi. "Radiation-Induced Reactions in The Liver — Modulation of Radiation Effects by Lifestyle-Related Factors —." International Journal of Molecular Sciences 19, no. 12 (December 3, 2018): 3855. http://dx.doi.org/10.3390/ijms19123855.

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Radiation has a wide variety of effects on the liver. Fibrosis is a concern in medical fields as one of the acute effects of high-dose irradiation, such as with cancer radiotherapies. Cancer is also an important concern following exposure to radiation. The liver has an active metabolism and reacts to radiations. In addition, effects are modulated by many environmental factors, such as high-calorie foods or alcohol beverages. Adaptations to other environmental conditions could also influence the effects of radiation. Reactions to radiation may not be optimally regulated under conditions modulated by the environment, possibly leading to dysregulation, disease or cancer. Here, we introduce some reactions to ionizing radiation in the liver, as demonstrated primarily in animal experiments. In addition, modulation of radiation-induced effects in the liver due to factors such as obesity, alcohol drinking, or supplements derived from foods are reviewed. Perspectives on medical applications by modulations of radiation effects are also discussed.
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Iwasa, Satoru, Hiroshi Mayahara, Takashi Tanaka, and Yoshinori Ito. "Ring-Enhancing Lesion Associated With Radiation-Induced Liver Disease." Journal of Clinical Oncology 31, no. 14 (May 10, 2013): e243-e244. http://dx.doi.org/10.1200/jco.2012.46.7217.

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Kim, Jieun, and Youngmi Jung. "Radiation-induced liver disease: current understanding and future perspectives." Experimental & Molecular Medicine 49, no. 7 (July 2017): e359-e359. http://dx.doi.org/10.1038/emm.2017.85.

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Dissertations / Theses on the topic "Radiation induced liver disease"

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Boutin, Samuel R. 1952. "Molecular pathogenesis of Helicobacter hepaticus induced liver disease." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/35696.

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Thesis (Ph. D. in Molecular and Systems Bacterial Pathogenesis)--Massachusetts Institute of Technology, Biological Engineering Division, 2005.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Includes bibliographical references.
Helicobacter hepaticus infection of A/JCr mice is a model of liver cancer resulting from chronic active inflammation. We monitored hepatic global gene expression profiles and correlated them to histological liver lesions in H. hepaticus infected and control male A/JCr mice at 3 months, 6 months, and 1 year of age. We used an Affymetrix-based oligonucleotide microarray platform on the premise that a specific genetic expression signature at isolated time points would be indicative of disease status. Model based expression index comparisons generated by dChip yielded consistent profiles of differential gene expression for H. hepaticus infected male mice with progressive liver disease versus uninfected control mice within each age group. Linear discriminant analysis and principal component analysis allowed segregation of mice based on combined age and lesion status, or age alone. Up-regulated genes present throughout the 12 month study involved inflammation, tissue repair, and host immune function. Upregulation of putative tumor and proliferation markers correlated with advancing hepatocellular dysplasia. Transcriptionally down-regulated genes in mice with liver lesions included those related to peroxisome proliferator, cholesterol, and steroid metabolism pathways. Transcriptional profiling of hepatic genes documented gene expression signatures in the livers of H. hepaticus infected male A/JCr mice with chronic progressive hepatitis and preneoplastic liver lesions, complemented the histopathological diagnosis, and suggested molecular targets for the monitoring and intervention of disease progression prior to the onset of hepatocellular neoplasia. Our laboratory, in collaboration with Professors Suerbaum and Schauer, recently identified a
(cont.) 70kb genomic island in Helicobacter hepaticus strain ATCC 51488 as a putative pathogenicity island (HhPAI) (Suerbaum et al, PNAS, 2003). This region within H. hepaticus contains genes HH0233-HH0302, a differential GC content, several long tandem repeats but no flanking repeats, and three components of a type IV secretion system (T4SS). A/JCr mice were experimentally infected with three naturally occurring strains of H. hepaticus including the type strain H. hepaticus ATCC 51488 strain (Hh 3B1) isolated from A/JCr mice, MIT 96-1809 (Hh NET) isolated from mice shipped from the Netherlands, and MIT-96-284 (HhG) isolated from mice acquired from Germany.4 HhNET (missing most of the HhPAI) infected male A/JCR mice exhibited a significantly lower prevalence (p<.05) of hepatic lesions at 6 months post infection than Hh 3B1 with an intact HhPAI. Hh G also has a large segment of the genomic island deleted, but not as many genes are deleted as compared to Hh NET. Hh G also demonstrated a lower prevalence of hepatic lesions. This variable pathological effect was evident in male mice only. The severity of chronic active inflammation in the liver of the H. hepaticus infected A/JCr mice depended on H. hepaticus liver colonization levels. The in vivo results support the presence of the HhPAI as a legitimate virulence determinant and predictor of severity of liver lesions in H. hepaticus infected A/JCr male mice. To further determine the differences in virulence of the H. hepaticus strains Hh 3B1, Hh NET, Hh G and an isogenic mutant H. ...
by Samuel R. Boutin.
Ph.D.in Molecular and Systems Bacterial Pathogenesis
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Paun, Mihaela. "Detecting genetic variants in radiation-induced lung disease." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119560.

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Thoracic radiotherapy, a common treatment modality for thoracic cancers, has pulmonary side-effects of either excessive inflammation (alveolitis), or pulmonary fibrosis consisting of uncontrolled deposition of collagen in the lungs, for which no cure exists. Prior knowledge, before radiotherapy, of patients genetically predisposed to fibrosis would improve cancer treatments. Based on the known similarities between human and mouse responses to lung irradiation, we used a murine model to detect molecular pathways, immune mechanisms and genetic variants associated with the development of fibrosis. Through a gene expression study in the lungs of fibrosis-prone C57Bl/6J and alveolitis-prone A/J and C3H/HeJ mice we found that several inflammatory pathways are significantly altered and differentiate between alveolitis- and fibrosis-prone mice and that Cell Adhesion Molecule signaling is the most significantly perturbed pathway in all strains. The differences in fibrosis between inbred mice led us to perform a genome-wide association analysis in a panel of 27 strains. We found several variants in immune genes associated with fibrosis, among which several SNPs upstream of Cell adhesion molecule 1 (Cadm1), a promising potential candidate gene for susceptibility to fibrosis. The role of immunity in lung disease prompted the investigation of mice lacking Tlr2 and/or Tlr4 receptors in response to thoracic irradiation. While Tlr2-/- and Tlr4-/- mice did not differ from C57Bl/6J wildtype, Tlr2,4-/- mice have decreased survival and more severe fibrosis compared to irradiated wildtype animals. Subsequent analyses of lymphocytes infiltrating the lungs after thoracic irradiation revealed the more severe fibrosis in the Tlr2,4-/- strain to be due to increased production of Il6, Tgfβ and Il17 and lack of protective Ifnγ. These studies also showed the pro-fibrotic role of Il17, as Il17-/- mice do not develop the disease. To summarize, in this thesis we identified immune pathways and several candidate genes associated with the presence of fibrosis following thoracic radiation. We also showed that disease development is dictated, in part, by Tlr signaling and disequilibrium between pro- and anti-fibrotic cytokines.
La radiothérapie thoracique, un traitement commun pour les cancers de la cavité thoracique, a des effets secondaires au niveau des poumons: l'inflammation excessive (alvéolite) ou la fibrose pulmonaire qui consiste d'un dépôt incontrôlable de collagène dans les poumons, et pour laquelle aucun traitement n'existe. La connaissance a priori, avant l'administration de la radiothérapie, des patients susceptibles au développement de la fibrose, améliorerait considérablement les traitements du cancer. Étant données les similarités des réponses à la radiation entre l'homme et la souris, nous avons utilisé un modèle murin pour la détection des voies moléculaires, mécanismes immunitaires et des variantes génétiques associés avec le développement de la fibrose pulmonaire. A travers une étude d'expression des gènes sur les poumons des souris susceptibles à la fibrose, C57Bl/6J et à l'alvéolite, A/J and C3H/HeJ, nous avons identifié certaines voies inflammatoires significativement impactées par le traitement et différentient entre les souches susceptibles à la fibrose, et celles succombant à l'alvéolite. Parmi celles-ci, la voie de Signalisation des Molécules d'Adhésion Cellulaire est la plus perturbée dans toutes les souches. Pour déterminer la composante génétique qui détermine les différences en degré de fibrose parmi les souches des souris consanguines, nous avons fait une analyse d'association pan-génomique sur un groupe de 27 souches de souris. Nous avons identifiés plusieurs variants associés à la fibrose, situés dans des gènes immunitaires, parmi lesquels, plusieurs SNPs dans le gène Cadm1 (Cell Adhesion Molecule 1). Étant donné le rôle de l'immunité dans la maladie pulmonaire, nous avons testé la réponse des souris manquant les récepteurs Tlr2 et/ou Tlr4 à la radiation thoracique. Tandis que les souris Tlr2-/- et Tlr4-/- ne diffèrent pas dans leur phénotype de la souche sauvage C57Bl/6J, les souris Tlr2,4-/- succombent plus tôt, a une fibrose plus sévère que les souris sauvages. Des analyses ultérieures sur les lymphocytes qui s'infiltrent dans les poumons à la suite de la radiation, ont démontré que la fibrose plus sévère chez les souris Tlr2,4-/- est due à une production augmentée des cytokines Il6, Il17 et Tgfβ et à l'absence du Ifnγ qui a un rôle protecteur. Ces études ont aussi montré le rôle pro-fibrotique du Il17, étant donné que les souris Il17-/- ne développent pas la maladie. Pour conclure, dans cette thèse nous avons identifié des voies de signalisation immunitaires et plusieurs gènes candidats associés avec la présence de la fibrose suivant la radiation thoracique. Nous avons aussi montré que le développement de la maladie est dicté, en partie, par la voie de signalisation des récepteurs Tlr et aussi par un déséquilibre entre les cytokines pro- et anti-fibrotiques.
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Tomko, Tomasz. "Genetics of radiation-induced lung disease in the mouse." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114227.

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Radiation therapy of the thorax may result in side effects such as alve- olitis and pulmonary fibrosis, both of which limit the efficacy of cancer therapy. Previously, it was determined that mice congenic on chromosomes 2, 4 and 11 succumb to radiation-induced lung disease significantly faster than C57BL/6J mice. Herein we use chromosome 4 and 11 congenic strains and chromosome 4 sub-congenic strains to identify radiation-induced lung response susceptibility loci in C3H/HeJ congenic mice on a C57BL/6J background. Mice were treated with 18-Gy whole-thorax irradiation and their survival, lung histopathology, and BAL cell types were determined. All protein coding genes within the congenic regions were analyzed in silico and a QTL-wide association study was completed for each congenic region using the survival time phenotypes of 27 inbred strains. The C3H/HeJ strain succumbed to radiation-induced lung disease significantly faster than the C57BL/6J strain and exhibited an increase in the percentage of neutrophils combined with a decrease in the percentage of macrophages in the BAL. The survival time phenotype of the chromosome 4 congenic and sub-congenic strains, as well as the chromosome 11 congenic strain, did not differ from the C57BL/6J response. The chromosome 11 congenic strain exhibited a significant increase in alveolitis, fibrosis, and percentage of lymphocytes in the BAL in addition to a decrease in the percentage of macrophages compared to the C57BL/6J strain. Only one of five chromosome 4 sub-congenic strains differed in response from the C57BL/6J strain, these differences included a decrease in the percentage of macrophages and an increase in the percentage of lymphocytes in the BAL. In silico analysis of congenic regions decreased the number of probable candidate genes by 69% and a QWAS on the chromosome 2 congenic region determined a significant association with a SNP located in the first intron of the Wfdc8 gene. In this animal model, a locus on chromosome 2 appears to be associated with the survival time phenotype of whole-thorax irradiated mice.
La radiothérapie du thorax peut entraîner des effets secondaires tels que l'alvéolite et la fibrose pulmonaire, les deux qui limitent l'efficacité de la thérapie du cancer. Auparavant, il a été déterminé que les souris congéniques sur les chromosomes 2, 4 et 11 succombent à la maladie induite par le rayonnement du poumon significativement plus rapide que les souris C57BL/6J. Ici, nous utilisons le chromosome 4 et 11 souches congéniques et le chromosome 4 sous-souches congéniques pour identifier les radio-induites loci de susceptibilité dans pulmonaires réponse des souris C3H/HeJ congéniques sur un fond C57BL/6J. Les souris ont été traitées avec 18 Gy d'irradiation du thorax entier et leur survie, du poumon histopathologie et types de cellules BAL ont été déterminées. Toutes les gènes codant des protéines à l'intérieur des régions congéniques ont été analysés in silico et une étude de QTL à l'échelle association a été effectuée pour chaque région congéniques utilisant les phénotypes de temps de survie de 27 souches consanguines. La souche C3H/HeJ succombé à la maladie pulmonaire induite par un rayonnement beaucoup plus rapidement que la souche C57BL/6J et présentaient une augmentation du pourcentage de neutrophiles et de la baisse du pourcentage de macrophages dans la BAL. Le phénotype temps de survie des 4 chromosomes souches congéniques et sous-congéniques, ainsi que le chromosome 11 souches congéniques, ne diffère pas de la réponse C57BL/6J. Le chromosome 11 souche congénique a montré une augmentation significative de l'alvéolite, fibrose, et le pourcentage de lymphocytes dans le LBA en plus d'une diminution du pourcentage de macrophages par rapport à la souche C57BL/6J. Seulement l'un des cinq sous-chromosome 4 souches congéniques différente en réponse à partir de la souche C57BL/6J, ces différences inclus une diminution du pourcentage de macrophages et une augmentation du pourcentage de lymphocytes dans la BAL. Une analyse in silico des régions congéniques diminué le nombre de gènes candidats probables de 69% et un QWAS sur le chromosome 2 congéniques région déterminée une association significative avec un SNP situé dans le premier intron du gène Wfdc8. Dans ce modèle animal, d'un locus du chromosome 2 semble être associé avec le phénotype de toute la durée de survie des souris irradiées-thorax.
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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.

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Alghamdi, Shareefa. "Consequences of non-alcoholic fatty liver disease on drug-induced hepatocytoxicity." Thesis, University of Surrey, 2015. http://epubs.surrey.ac.uk/808210/.

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Non-alcoholic fatty liver disease (NAFLD) is characterised by the accumulation of lipid in liver. Liver is the principal organ involved in drug biotransformation. The central hypothesis of this project is that alterations in the liver environment due to lipid accumulation aggravate sensitivity of hepatocytes to toxicity of some commonly prescribed drugs (paracetamol, alcohol, phenobarbital, cisplatin or doxorubicin). The aim of this study was to investigate the effect of lipid overloading (steatosis) on drug cytotoxicity in the liver model Huh7 cell line. Hepatic steatosis was induced in Huh7 cells by exposing cells to 300 μM FFA mixture or 1 mM oleic acid. Impact of steatosis on drug toxicity was examined by co-treating the cells with FFA and paracetamol, alcohol, phenobarbital, cisplatin or doxorubicin. Cell viability MTT assay showed that neither 300 μM FFA mixture nor 1 mM OA caused significant reduction in cell viability after 24 h incubation. However, a significant reduction seen after incubation for 48 h, therefore for the subsequent experiments the time frame chosen was 24 h. The results showed that 300 μM FFA mixture did not induce a significant amount of intracellular lipid, whereas 1 mM OA induced significant amount of intracellular lipid. The subsequent experiments were carried out to test the hypothesis that lipid-loaded Huh7 cells are more sensitive to drug toxicity. Co-treatment with FFA and either paracetamol, ethanol or doxorubicin resulted in further reduction in cell viability. Phenobarbital resulted in enhanced cell viability, and no significant changes in cell viability observed after co-treatment with cisplatin. To investigate mode of cell death, caspase3/7 activity was measured as mediator of apoptosis. Generally, an advance apoptosis was observed in steatotic cells treated with the different drugs. Reactive oxygen species were measured as a possible trigger of apoptosis. A significant amount of ROS were generated by FFAs, and generally, drug treatment induced a higher significant amount of ROS in the steatotic Huh7 cells. To elucidate the specific changes observed upon treatment of steatotic cells with hepatotoxic drugs, a single FFA dose (300 μM FFA mixture) and a single drug (doxorubicin) were selected to identify major alterations in gene expression. The microarray data confirmed alterations in oxidative stress-related genes. Such changes were functionally relevant as confirmed by cellular assay and In-Cell Western blot. In conclusion, the hypothesised effect of steatosis on drug toxicity has been confirmed and steatosis may enhance drug toxicity through changing cellular oxidative state and activating the apoptotic pathway.
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Bégin, Michelle Anne. "Identifying quantitative trait loci involved in radiation-induced lung disease in mice." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=99321.

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The goal of this thesis was to identify genetic loci involved in radiation-induced lung disease in mice. Phenotypic analysis was completed for alveolitis, pulmonary fibrosis, survival time, mast cells/mm2 and cell counts in bronchoalveolar lavage (BAL) to assess lung damage. Genome scans and linkage analysis were completed for two backcross cohorts (75%C3H/HeJ-25%C57Bl/6J or 25%C3H/HeJ-75%C57BU6J) using each of the phenotypes measured. Putative susceptibility loci were identified for alveolitis on chromosomes 12 (LOD=3.35), 14 (LOD=2.22) and 19 (LOD=1.7) in the mostly C3H/HeJ backcross cohort and on chromosome 14 (LOD=2.7) in the mostly C57BI/6J backcross cohort. Linkage using the pulmonary fibrosis scores provided supportive evidence for a quantitative trait loci (QTL) on chromosome 17 (LOD=2) in the mostly C57BI/6J background, and two unique putative linkage regions were localized on chromosome 2 (LOD=2.2) in the mostly C3H/HeJ cohort and 14 (LOD=2) in the mostly C57BI/6J cohort. Supporting evidence for linkage on chromosomes 12 and 14 in the mostly C3H/HeJ background and chromosome 14 in the mostly C57BI/6J background was obtained using cellular markers. Additionally, survival time mapped to the linkage regions isolated for alveolitis and pulmonary fibrosis, suggesting that the development of radiation-induced lung disease influences the survival time of the mice. Within each cohort there were sex dependent linkage intervals, indicating that male and female mice may possess different factors involved in the development of alveolitis and/or pulmonary fibrosis. These results suggest that there are multiple genetic loci involved in the development of radiation-induced lung disease in mice.
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Martin, Daniel Richard. "The Role of Phosphohistidine Phosphatase 1 in Ethanol-induced Liver Injury." Scholar Commons, 2018. http://scholarcommons.usf.edu/etd/7194.

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Chronic liver diseases, which includes alcoholic liver disease (ALD), are consistently among the top 15 leading causes of death in the United States. ALD is characterized by progression from a normal liver to fatty liver disease (hepatic steatosis), which can lead to cirrhosis, alcoholic hepatitis, and liver failure. We have identified a novel role of phosphohistidine signaling, mediated through phosphohistidine phosphatase 1 (PHPT1), in the onset of hepatic steatosis. We have identified PHPT1 as a target of selective oxidation following acute ethanol exposure as well as being downregulated following chronic ethanol exposure. We mapped the oxidative modification site and developed a mass-spectrometry based phosphohistidine phosphatase assay to determine the impact of PHPT1 oxidative modification during acute ethanol exposure. To further understand the role of PHPT1 and phosphohistidine signaling during chronic ethanol exposure, we have developed PHPT1 overexpression and knockout mouse models. These mouse models were characterized using mass spectrometry-based proteomics. They were then utilized in a 10-day chronic ethanol plus binge model to determine the impact of PHPT1 expression on the onset of ethanol-induced hepatic steatosis. In addition, advanced mass spectrometry-based phenotypic characterization was performed on the treated liver tissues to determine the key regulators and canonical pathways influencing phosphohistidine signaling during chronic ethanol exposure. We have evidence to suggest that PHPT1 overexpression plays a protective role in the onset of hepatic steatosis, the PHPT1 heterozygous model is more susceptible to liver damage, and the complete knockout model is embryonically lethal. Additionally, we have identified novel pathways and regulators involved in phosphohistidine signaling during the development of ethanol-induced hepatic steatosis.
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Schultes, Klaus. "Ultrastructural characterization of ultraviolet induced corneal disease : an animal model." Master's thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/27046.

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The majority of ancient people worshipped the sun and viewed it as a health - bringing deity. During the eighteenth and nineteenth century therapeutic benefits of sunlight exposure were beginning to be understood and by the end of the nineteenth century the importance of ultraviolet radiation was being realized. Danish physician Niels Finsen, whom many regard as the father of ultraviolet phototherapy, also stressed that it was ultraviolet radiation in the solar spectrum which cause sunburn. We now recognize that the small portion of ultraviolet radiation which reaches the earth's surface is not necessarily therapeutic, but in fact could be harmful to humans. There are numerous accounts of the harmful effects of UV radiation to the skin and the eye as a whole. These effects may be caused by either acute or chronic exposure to UV radiation. For example, some acute effects of UV-B radiation include conjunctivitis and photokeratitis. "Snow blindness" and "arc welders eye" are further examples of acute ultraviolet damage specifically to the surface of the cornea. On the other hand, chronic exposure to ultraviolet radiation is thought to be responsible for pterygia, climatic droplet keratopathy Hill and Maske (1989), cancers of the external eye, cataracts and various types of retinal diseases. The present study is an extension of ongoing studies on ultraviolet radiation damage to the cornea in the Department of Ophthalmology, University of Cape Town and Groote Schuur Hospital. Their specific interest lies in the causes and treatment of climatic droplet keratopathy. The aims of the present study are: 1) Establish a possible role of ultraviolet B radiation in human corneal diseases such as climatic droplet keratopathy and pterygium using the rabbit as an animal model. 2) Determine by means of SEM the initial effects and subsequent recovery of the epithelium after a 3-hour dose of ultraviolet B radiation. We refer to this study as "acute" response to ultraviolet B radiation. 3) To try and confirm the effects observed by SEM with ultrastructural studies using TEM. 4) In addition, we are also looking at the possible effects after exposing rabbit cornea to a daily dose of low level ultraviolet B radiation, over a long period of time. We refer to this as chronic exposure to ultraviolet B radiation. It is hoped that by exposing rabbits to ultraviolet light, principally ultraviolet B radiation, diseases similar to those found in humans could be simulated and disease progression studied. People are generally exposed to substantial amounts of UV radiation for a very long time. Since people generally live longer they will be exposed to an ever-increasing amount of solar UV radiation and subsequently, there is an increasing risk of developing corneal diseases. The possible threat to the ozone is also a real possibility and could lead to increased levels of ultraviolet radiation reaching the earth's surface. This will require a greater understanding of the very nature of corneal damage due to acute and chronic exposure. This study focusses mainly on the acute response to UV-B radiation since most studies have investigated effects of prolonged exposure to UV light. Accordingly, much less is known about acute exposure. Many people suffering from acute UV B radiation effects probably never visit the ophthalmologist or wait for a couple of days. This could also contribute to the fact that effects of short-term damage is not well documented.
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Taylor, Carolyn W. "Breast cancer radiotherapy and heart disease." Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:c9dda3ca-8cb3-4a38-938d-0b75b4f6471d.

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Introduction: Some past breast cancer radiotherapy regimens led to an increased risk of death from heart disease. Although heart dose from breast cancer radiotherapy has generally reduced over the past few decades, there may still be some cardiac risk. Estimation of future risk for women irradiated today requires both measurement of their cardiac dose and dose-response relationships, which depend on cardiac dosimetry of past regimens, in conjunction with long-term follow-up data. Methods: Virtual simulation and computed tomography 3-dimensional treatment planning on a representative patient were used to estimate mean heart and coronary artery doses for women irradiated since 1950 in 71 randomised trials in the Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) overview. Patient-to-patient variability in cardiac dose was assessed. Heart and coronary artery doses were also calculated for breast cancer radiotherapy regimens used since the 1950s in Sweden. Cardiac doses from contemporary (year 2006) radiotherapy were assessed for 55 patients who received tangential breast cancer irradiation at a large UK radiotherapy centre. The maximum heart distance (i.e. the maximum distance between the anterior cardiac contour and the posterior tangential field edges) was measured for the left-sided patients, and its value as a predictor of cardiac doses assessed. Results: Mean heart dose for women irradiated in the EBCTCG trials varied from <1 to 18 Gray, and mean coronary artery dose from <1 to 57 Gray. Patient-to-patient variability was moderate. Mean heart dose for women irradiated in Sweden since the 1950s varied from <1 to 24 Gray, and mean coronary artery dose from <1 to 46 Gray. Heart dose from tangential irradiation has reduced over the past four decades. However, mean heart dose for left-sided patients irradiated in 2006 was 2 Gray and around half of them still received >20 Gray to parts of the heart and left anterior descending coronary artery. For these patients, maximum heart distance was a reliable predictor of cardiac doses. For the other patients, mean heart dose varied little and was usually less than 2 Gray. Conclusions: Cardiac doses from breast cancer radiotherapy can be estimated reliably and are now available for use in deriving dose-response relationships in the EBCTCG data and in a Scandinavian case-control study. Cardiac dose has reduced over the past four decades. Therefore the cardiac risk is also likely to have reduced. Nevertheless, for some patients, parts of the heart still receive >20 Gray in the year 2006.
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Sethi, Mieran Kaur. "Xeroderma pigmentosum : a disease model for clinical, cellular and molecular consequences of ultraviolet radiation-induced damage." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/xeroderma-pigmentosum(e3241e71-b997-4830-826c-06c898c76a59).html.

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XP is considered a disease of failed repair of direct UVR-induced DNA photoproducts, leading to severe sunburn, extremely high rates of skin cancer, and death in young adulthood from complications relating to malignancy and neurodegeneration. Most experiments in the literature on XP cells, both for diagnosis and interpretation of photobiological processes, have used non-solar UVC radiation. Discernable differences in clinical phenotype have emerged from long-term follow-up of XP patients in the UK National XP clinic. The development of a sunburn severity score revealed that XP-C, XP-E and XP-V patients have normal sunburn reactions; a cohort of milder XP-A patients has been identified, arising from a likely founder mutation yielding less than 5% read-through of normal XPA protein. Deep phenotyping, including the development of ocular and neurological severity scores, has resulted in precise correlation of XP phenotype with the causal mutation, enabling the development of personalized prognostic advice for XP patients worldwide. Based on XP phenotype patterns, molecular experiments were conducted on skin fibroblasts from a range of XP complementation groups using environmentally relevant 385nm UVA-1 compared with 254nm UVC. UVA-1 was a more effective inducer of MMP mRNA and protein than UVC, by a mechanism independent of CPD. MMP upregulation was proportional with ROS generation, and this effect was attenuated when vitamin E was added to cell culture, providing indirect evidence that UVA-1-induced ROS was the main cause of MMP upregulation. The effects of UVA in XP literature have been largely ignored; studies here highlight that XP is a disease of impaired defenses against direct and indirect UVR-induced damage, which may explain sunburn, photoageing, skin cancer and neurological phenotype. These studies demonstrate the importance of translational research in this rare genetic disease. Photoprotection from solar-UVA, together with antioxidants, may provide a future gold standard for photoageing in the general population.
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Books on the topic "Radiation induced liver disease"

1

Farrell, Geoffrey C. Drug-induced liver disease. Edinburgh: Churchill Livingstone, 1994.

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Second primary cancers and cardiovascular disease after radiation therapy. Bethesda, Md: National Council on Radiation Protection and Measurements, 2011.

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Gofman, John W. Preventing breast cancer: The story of a major, proven, preventable cause of this disease. San Francisco, Calif., U.S.A: C.N.R. Book Division, Committee for Nuclear Responsibility, 1995.

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Gofman, John W. Preventing breast cancer: The story of a major, proven, preventable cause of this disease. 2nd ed. San Francisco, Calif., U.S.A: C.N.R. Book Division, Committee for Nuclear Responsibility, Inc., 1996.

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Drug-Induced Liver Disease. Elsevier Science & Technology Books, 2013.

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Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. 2nd ed. New York: Informa Healthcare USA, 2007.

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(Editor), Neil Kaplowitz, and Laurie D. DeLeve (Editor), eds. Drug-Induced Liver Disease. Informa Healthcare, 2002.

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Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. New York: Marcel Dekker, 2003.

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Kaplowitz, Neil. Drug-Induced Liver Disease. Edited by Neil Kaplowitz and Laurie D. DeLeve. CRC Press, 2007. http://dx.doi.org/10.3109/9781420021141.

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Keshav, Satish, and Palak Trivedi. Drug-induced liver disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0215.

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Drugs are an important and common cause of hepatic injury. This is unsurprising, as the liver is a major site for drug clearance, biotransformation, and excretion. A careful history of drugs taken (prescribed, over the counter, herbal, or illicit) is vital when assessing anyone with abnormal liver function tests. Although toxic or idiosyncratic adverse reactions may occur with many therapeutic agents, drug-induced jaundice is not so common.
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Book chapters on the topic "Radiation induced liver disease"

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Sourati, Ainaz, Ahmad Ameri, and Mona Malekzadeh. "Radiation-Induced Liver Disease." In Acute Side Effects of Radiation Therapy, 137–44. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55950-6_14.

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Yue, Ning J., Kent Lambert, Jay E. Reiff, Anthony E. Dragun, Ning J. Yue, Jay E. Reiff, Jean St. Germain, et al. "Radiation-Induced Liver Disease (also RILD)." In Encyclopedia of Radiation Oncology, 726. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_226.

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Shung, Dennis L., and Joseph K. Lim. "Drug-Induced Liver Injury." In Liver Disease, 1–10. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98506-0_1.

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Dancygier, Henryk, and Peter Schirmacher. "Radiation-Induced Liver Damage." In Clinical Hepatology, 203–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-93842-2_22.

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Bobrow, Martin. "Radiation-Induced Disease." In Ciba Foundation Symposium 175 - Environmental Change and Human Health, 182–96. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514436.ch11.

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Abecassis, Isaac Josh, Christopher C. Young, Rajeev D. Sen, Cory M. Kelly, and Michael R. Levitt. "Radiation-Induced Stenosis." In Carotid Artery Disease, 113–23. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41138-1_8.

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Hamilton, James P., and Jacqueline M. Laurin. "Drug-Induced Cholestasis." In Cholestatic Liver Disease, 21–43. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-118-5_2.

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Ahmad, Shahzaib, and Beverley J. Hunt. "Coagulopathy of Liver Disease." In Trauma Induced Coagulopathy, 471–82. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28308-1_29.

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Ebel, Noelle H., and Karen F. Murray. "Drug-Induced Liver Disease." In Diseases of the Liver and Biliary System in Children, 169–90. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119046936.ch12.

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Murray, Karen F. "Drug-Induced Liver Disease." In Diseases of the Liver and Biliary System in Children, 207–30. Oxford, UK: Wiley-Blackwell, 2009. http://dx.doi.org/10.1002/9781444300536.ch9.

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Conference papers on the topic "Radiation induced liver disease"

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Linh, Ha Phuong, and Tran Huu Ngoc. "IDDF2020-ABS-0218 The values of acoustic radiation force impulse elastography of liver in evaluating the degree of liver fibrosis in alcoholic liver disease." In Abstracts of the International Digestive Disease Forum (IDDF), 22–23 November 2020, Hong Kong. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2020. http://dx.doi.org/10.1136/gutjnl-2020-iddf.170.

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Ansari, Sana, Imran Shafi, Aiza Ansari, Jamil Ahmad, and Syed Ismail Shah. "Diagnosis of liver disease induced by hepatitis virus using Artificial Neural Networks." In 2011 IEEE 14th International Multitopic Conference (INMIC). IEEE, 2011. http://dx.doi.org/10.1109/inmic.2011.6151515.

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Dujunco, Ma Marylaine, and Juliet Gopez-Cervantes. "IDDF2018-ABS-0011 Use of acoustic radiation force impulse (ARFI) imaging for the diagnosis of malignant liver tumour among patients with liver tumours: a cross-sectional study." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.188.

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Meena, Ramesh Kumar, and Tejpal Singh. "IDDF2019-ABS-0320 Terminalia arjuna bark extract protects against early alcohol-induced liver injury in the rat." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.109.

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Najmie Muhammad Yusuf, Allia, Raja Affendi Raja Ali, Khairul Najmi Muhammad Nawawi, and Norfilza Mohd Mokhtar. "IDDF2019-ABS-0167 Identification of cancer-related exosomal mirnas in NASH-induced liver cirrhosis with hepatocellular carcinoma." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.276.

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Nasehi, L., A. Ghandour, X. Li, S. Shrikanthan, R. Gurajala, and G. McLennan. "Radiation Activity Delivered to the Tumor by Sir-Sphere versus TheraSphere in Liver Masses Treated with Yttrium 90." In Abstracts of 3rd Annual Meeting of the American Society of Digestive Disease Interventions. Thieme Medical Publishers, 2017. http://dx.doi.org/10.1055/s-0037-1603713.

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Ashfaq-Khan, M., M. Aslam, MA Qureshi, SY Weng, V. Zevallos, and YO Kim. "Ingestion of wheat amylase trypsin inhibitors promotes a proinflammatory liver and adipose tissue phenotype in diet induced non-alcoholic fatty liver disease in mice." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605070.

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Gadour, Eyad, and Zeinab Hassan. "P009 Biologic induced Hepatotoxicity in Inflammatory Bowel Disease (IBD); a Systematic Review and Meta-Analysis." In Abstracts of the British Association for the Study of the Liver Annual Meeting, 22–24 November 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-basl.18.

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Yee, D., R. Cangemi, B. Osler, K. E. Cox, Y. Vayntrub, and C. J. Mullin. "Profound Shock from Metformin-Induced Lactic Acidosis in a Patient with End Stage Liver Disease and Hepatic Encephalopathy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5157.

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Bui Thi Quynh, Nhung, and Son Nguyen Van. "IDDF2019-ABS-0218 Evaluation on the protection effect of the vismisco in the liver damage induced by paracetamol in mice experiment." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.99.

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Reports on the topic "Radiation induced liver disease"

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Osman, Mohamed, Portia Allen, Nimer Mehyar, Gerd Bobe, Johann Coetzee, and Donald C. Beitz. Acute Effects of Postpartal Subcutaneous Injection of Glucagon and/or Oral Administration of Glycerol on Blood Metabolites and Hormones and Liver Lipids and Glycogen of Holstein Dairy Cows Induced with Fatty Liver Disease. Ames (Iowa): Iowa State University, January 2007. http://dx.doi.org/10.31274/ans_air-180814-754.

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