Relevant bibliographies by topics / Toxicologic pathology

Contents

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

Academic literature on the topic 'Toxicologic pathology'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Toxicologic pathology"

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Boyle, Molly H., Bindu Bennet, Karyn Colman, et al. "Publication Categories in Toxicologic Pathology." Toxicologic Pathology 49, no. 5 (2021): 1042–47. http://dx.doi.org/10.1177/0192623321992305.

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Toxicologic Pathology is the official journal of the Society of Toxicologic Pathology (STP), the British Society of Toxicological Pathology, and the European STP (ESTP). Toxicologic Pathology publishes articles related to topics in various aspects of toxicologic pathology such as anatomic pathology, clinical pathology, experimental pathology, and biomarker research. Publications include society-endorsed Best Practice/Position and Points to Consider publications and ESTP Expert Workshop articles that are relevant to toxicologic pathology and scientific regulatory processes, Opinion articles under the banner of the STP Toxicologic Pathology Forum, Original Articles, Review Articles (unsolicited/contributed, mini, and invited), Brief Communications, Letters to the Editor, Meeting Reports, and Book Reviews. This article provides details on the various publication categories in Toxicologic Pathology and will serve as a reference for authors and readers.
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Cohen, Samuel M., Wanda M. Haschek-Hock, and Carl Alden. "Obituary: Dr Gordon Charles Hard (1931-2021)." Toxicologic Pathology 50, no. 2 (2022): 164–65. http://dx.doi.org/10.1177/01926233211068853.

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Dr Gordon Hard, of Tairua, New Zealand, a preeminent international toxicology thought leader and international consultant in toxicologic pathology of the kidney, passed on November 22, 2021. He was a key player in shaping and developing the global field of toxicologic pathology and the role of toxicologic pathology in risk assessment of environmental chemicals and pharmaceuticals.
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Schwetz, Bernard A. "Toxicologic Pathology: Looking Ahead." Toxicologic Pathology 31, no. 1_suppl (2003): 2–5. http://dx.doi.org/10.1080/01926230390174869.

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The field of toxicologic pathology is being impacted, as are other fields of science and medicine, by rapid transitions to take advantage of new science and technology. The new technology represents great opportunities to advance our understanding of toxicology and pathology to exciting new levels, but it also poses new challenges. We must be seriously engaged in that transition to assure that the outcome reflects the knowledge and discipline that are hallmarks of today's decision-making process in areas of product development and approval. New expertise will be required to deal with new issues. How well and how rapidly we adapt as the field moves from “... icities” to “ ... omics” will, at least in part, determine the role of toxicologic pathologists in the product development and approval processes of the future.
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Bolon (Chair), Brad, Erio Barale-Thomas, Alys Bradley, et al. "International Recommendations for Training Future Toxicologic Pathologists Participating in Regulatory-type, Nonclinical Toxicity Studies." Toxicologic Pathology 38, no. 6 (2010): 984–92. http://dx.doi.org/10.1177/0192623310378137.

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The International Federation of Societies of Toxicologic Pathologists (IFSTP) proposes a common global framework for training future toxicologic pathologists who will support regulatory-type, nonclinical toxicology studies. Optimally, trainees should undertake a scientific curriculum of at least five years at an accredited institution leading to a clinical degree (veterinary medicine or medicine). Trainees should then obtain four or more years of intensive pathology practice during a residency and/or on-the-job “apprenticeship,” at least two years of which must be focused on regulatory-type toxicologic pathology topics. Possession of a recognized pathology qualification (i.e., certification) is highly recommended. A nonclinical pathway (e.g., a graduate degree in medical biology or pathology) may be possible if medically trained pathologists are scarce, but this option is not optimal. Regular, lifelong continuing education (peer review of nonclinical studies, professional meetings, reading, short courses) will be necessary to maintain and enhance one’s understanding of current toxicologic pathology knowledge, skills, and tools. This framework should provide a rigorous yet flexible way to reliably train future toxicologic pathologists to generate, interpret, integrate, and communicate data in regulatory-type, nonclinical toxicology studies.
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Gauthier, Béatrice E., Frédéric Gervais, Gregory Hamm, Donal O’Shea, Alain Piton, and Vanessa L. Schumacher. "Toxicologic Pathology Forum*: Opinion on Integrating Innovative Digital Pathology Tools in the Regulatory Framework." Toxicologic Pathology 47, no. 4 (2019): 436–43. http://dx.doi.org/10.1177/0192623319827485.

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Digital pathology is defined as the ability to examine digitized microscopic slides and to generate qualitative and quantitative data. The field of digital pathology is rapidly evolving and has the potential to revolutionize toxicologic pathology. Techniques such as automated 2-D image analysis, whole slide imaging, and telepathology are already considered “mature” technologies and have been used for decades in exploratory studies; however, many organizations are reluctant to use digital pathology in regulatory toxicology studies. Innovative technologies using digitized slides including high-content imaging modalities and artificial intelligence are still under development but are increasingly used in toxicologic pathology. While software validation requirements are already described, clear guidance for application of these rules to the digital pathology field are few and the acceptance of these technologies by regulatory authorities remains necessary for successful adoption of digital pathology into the mainstream of toxicologic pathology. This topic was discussed during a roundtable at the 2018 Annual Congress of the French Society of Toxicologic Pathology. This opinion article summarizes the discussion regarding the current questions and challenges on the integration of innovative digital pathology tools within a good laboratory practice framework and is meant to stimulate further discussion among the toxicologic pathology community. [Box: see text]
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Dagli, Maria L. Z., Arun Pandiri, Jeff Wolf, Sibylle Groeters, and Wanda M. Haschek-Hock. "Global Perspective on Careers in Environmental Toxicologic Pathology: The 2019 Society of Toxicologic Pathology Annual Symposium Lunchtime Career Development Session." Toxicologic Pathology 47, no. 8 (2019): 1088–95. http://dx.doi.org/10.1177/0192623319877859.

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A wide range of career options is available globally in the environmental toxicologic pathology (ETP) arena including academia, government, contract research organizations, and the agrichemical/chemical industry. This small and specialized subset of toxicologic pathologists addresses the effects of contaminants and pollutants on human, animal, and ecological health (One Health). Veterinary students and pathology trainees are primarily exposed to diagnostic pathology and often have limited exposure to toxicologic pathology and even less so to the issues and opportunities in environmental toxicology. The speakers provided a brief overview of global opportunities in their work sector and personal perspectives of their careers in ETP. The following panel discussion provided an opportunity to discuss issues related to careers in this specialty.
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Prasse, Keith, Paul Hildebrandt, and David Dodd. "In Toxicologic Pathology." Toxicologic Pathology 14, no. 2 (1986): 274–75. http://dx.doi.org/10.1177/019262338601400218.

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Haschek-Hock, Wanda M. "Diagnostic Toxicologic Pathology." Toxicologic Pathology 20, no. 3-1 (1992): 454–55. http://dx.doi.org/10.1177/019262339202000316.

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Hubbs, Ann F., Linda M. Sargent, Dale W. Porter, et al. "Nanotechnology: Toxicologic Pathology." Toxicologic Pathology 41, no. 2 (2013): 395–409. http://dx.doi.org/10.1177/0192623312467403.

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Maronpot, Robert R., and Maria L. Z. Dagli. "Contemporary Activities of Toxicologic Pathology Societies." Toxicologic Pathology 48, no. 2 (2019): 295–301. http://dx.doi.org/10.1177/0192623319880885.

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Educational activities and training opportunities in toxicologic pathology are major goals of 9 formally established Toxicologic Pathology Societies and the International Academy of Toxicologic Pathology. Some Toxicologic Pathology Societies have examination-based certification programs while others accept certification or registration by veterinary pathology organizations including the American College of Veterinary Pathologists, the European College of Veterinary Pathologists. We summarize here the membership numbers and current activities of formally established Toxicologic Pathology Socities.
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Dissertations / Theses on the topic "Toxicologic pathology"

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Hard, Gordon Charles. "Renal Carcinogenesis: Animal Models, Toxicologic Pathology And Risk Assessment." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13990.

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This thesis presented for Doctor of Veterinary Science is a collection of 50 papers dealing with aspects of experimental renal carcinogenesis published in peer-reviewed cancer research, pathology and toxicology journals, or in one case, in a WHO International Agency for Research on Cancer (IARC) volume. The work, conducted from 1979 since award of Doctor of Science to the present (2014), concerns the further development of animal models of kidney cancer, the modes-of-action of certain chemical compounds in the induction of renal toxicity and carcinogenesis, and toxicologic pathology of the rodent renal response to chemically-mediated injury. For the last decade or more, the intent of the papers has been to help inform the risk assessment process by defining the relevance of certain aspects of laboratory animal renal carcinogenesis for assessing chemical hazard in humans. Hence, the title selected for this thesis is “Renal Carcinogenesis: Animal Models, Toxicologic Pathology, and Risk Assessment”. The papers are presented in 10 sections, the first of which continues the theme of developing animal models of renal cancer. The papers in Section 2 represent an extension of previous studies with an in vivo model of chemical induction of renal tumors in rats by administration of a single dose of dimethylnitrosamine (DMN). DMN is capable of inducing two types of tumors with high incidence in rats, renal mesenchymal tumor (RMT) and renal tubule tumor (RTT). One of the papers in this section traces the sequence of target cell events involved in the acute toxicologic response of rat kidney to the carcinogen. The DMN model also enabled development of in vitro correlates of these two tumor types, and the present (as well as some previous) studies confirmed that malignant mesenchymal or epithelial cell lines could be established from DMN-treated rats within a few hours or days following administration of the single dose of carcinogen. The papers in Section 3 comprise an extension of this in vitro work, focusing on renal tubule tumor as it has greater significance for humans. Section 4 contains papers representing research on hyaline droplet nephropathy and its involvement in renal tubule tumor induction in the male rat. One paper, a review of the syndrome and its pathology, was used for the US Environmental Protection Agency statement on the science policy for chemicals inducing renal tubule tumors through this mechanism. Section 5 describes the Author’s work supporting the conclusion that spontaneous progressive nephropathy (CPN), a frequent confounding factor for kidney in rat safety evaluation studies, is, in itself, a risk factor for a low incidence of renal tubule tumor development in rats. Dose-related exacerbation by chemicals of CPN to advanced stages of severity is often associated with a low incidence of renal tubule tumors, an outcome which can be attributed as a direct effect of the chemical, and in consequence, misclassification of the chemical as a renal carcinogen. Section 6 contains papers that have contributed to the recognition of a morphologically distinctive form of renal tubule tumor encountered in rat toxicology studies that is of spontaneous origin and independent of chemical treatment. Section 7 contains papers studying the pathology of certain fungal toxins exhibiting toxicity for the kidney, including ochratoxin A and fumonisin B1. For some time ochratoxin A has been considered to be involved in the etiology of Balkan Endemic Nephropathy (BEN), a chronic renal condition linked with renal pelvic carcinoma, occurring in subsistence-farming communities along the tributaries of the Danube River in certain parts of Eastern Europe. Section 8 contains papers either reviewing the information on mechanisms of renal carcinogenesis in rodents, or papers contributing to recognition of key events in chemically-induced rodent kidney carcinogenesis for use in hazard evaluation in human risk assessment. In Section 9 the papers describe the toxicologic pathology induced by several unrelated chemicals in rat kidney, namely ethoxyquin, ethylene glycol, and melamine. In the case of ethoxyquin, lesions in the rat kidney had been previously (and incorrectly) considered to be preneoplastic, while ethylene glycol was studied to determine the potential contribution of toxicokinetic differences as a basis for variability in rat strain sensitivity. Melamine was involved in an epidemic of kidney injury in infants in China due to consumption of adulterated infant milk formula. The last section of papers, Section 10, contains publications solicited mainly by the Society of Toxicologic Pathology, or IARC, providing diagnostic guidelines for toxicologic pathology of non-proliferative and proliferative lesions of the rat and mouse kidney. Section 11 is a list of titles of invited book chapters reviewing aspects of renal carcinogenesis and toxicologic pathology, while Section 12 provides a list of other paper titles published in the peer-reviewed literature during the period covered by this thesis, that is, from 1979 to 2014.
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Frank, Evan A. "Toxicology and Mechanisms of Lung Responses to Carbon Nanotube Exposures." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1448037426.

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Sargeant, Aaron Matthew. "Preclinical Efficacy and Safety Evaluation of Novel Small-Molecule Targeted Agents for the Prevention and Treatment of Prostate Cancer." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243948876.

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Lourens, Denise. "The epidemiology, pathology and toxicology of suicide." Master's thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26780.

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Complete suicides and parasuicides are a major cause of death and disability in South Africa and the rest of the world. The epidemiology, pathology and toxicology of complete suicides were investigated in this study. All the complete suicide cases, which were presented to Salt River Medicolegal Laboratory over a period of one year (1 January 1997 - 31 December 1997), were analysed. The candidate personally conducted 148 of the alleged 180 suicide cases that presented in this time period (82%). The candidate did all the follow up investigations herself. The main findings were: 1. The male to female ratio was 5: 1. (131: 26) 2. Shooting and hanging were the most commonly used methods. 3. The racial distribution of violent deaths showed a high rate of suicides amongst the White population. 4. Suicides accounted for the Joss of young lives, the average age being 37,8 years. The mean age was 34 years. 5. Most victims committed suicide in and around their own homes. 6. The majority did not leave suicide notes. 7. Psychiatric disorders, poor health, arguments with close family members and friends, financial problems and long-standing relationship problems were the most common reasons for the suicides. 8. Suicides by prisoners accounted for 3,8% of the study (6 cases). 9. Two cases of double suicide (group suicide) were identified. 10. Five cases of homicide-suicide were identified in the study material. 11. One case of an attempted suicide by means of a high-speed motor vehicle accident, followed by the successful suicide by other means, was identified.
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Xavier, Fabiana Galtarossa. "Intoxicação por aldicarb (\"chumbinho\"): I. Estudo das alterações post mortem microscópicas em cães e gatos - II. Avaliação dos efeitos tóxicos agudos em camundongos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-22122008-145055/.

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O presente trabalho propôs estudar as alterações microscópicas observadas em 100 casos de intoxicação por aldicarb em cães e gatos e os efeitos agudos (14 dias) induzidos por esse praguicida em camundongos após a administração de dose única oral, avaliando-se as alterações clínicas, laboratoriais, microscópicas e ultraestruturais. As principais lesões microscópicas em cães e gatos foram observadas nos pulmões (congestão, edema, hemorragia, enfisema e atelectasia), fígado (congestão, degeneração vacuolar e hemorragia) e rins (congestão, hemorragia e nefrose). Nos demais órgãos, apenas alterações circulatórias (congestão e hemorragia) foram encontradas. Em ambas espécies, considerando as alterações significantes de acordo com a faixa etária, observou-se que os animais idosos apresentaram o maior grau de intensidade de degeneração vacuolar hepática e que a congestão renal foi mais intensa nos adultos. Em camundongos, observou-se que: 1) doses superiores a 0,08 mg/kg de aldicarb promoveram a morte de todos os animais em 2,6 - 4,7 minutos após a exposição, sendo o óbito precedido por convulsões; 2) a dose de 0,08 mg/kg promoveu o rápido aparecimento dos sinais clínicos clássicos da intoxicação por anticolinesterásicos, com duração de 45 - 120 minutos, sendo esta a dose escolhida para os demais experimentos in vivo; 3) os camundongos expostos mostraram consumo de água superior ao do grupo controle até o 5° dia após a exposição e inferior a partir do 10° dia até o término do experimento (14º dia); 4) quanto ao consumo de ração, de forma geral, camundongos expostos ao praguicida consumiram menos que os não expostos, sendo o ganho de peso inferior ao do grupo controle nas primeiras 48 horas após a intoxicação; 5) as alterações histopatológicas, como observado em cães e gatos, ocorreram principalmente nos pulmões (edema, congestão e hemorragia), fígado (congestão e degeneração vacuolar, principalmente em zona 3) e rins (congestão, hemorragia e nefrose), sendo que as alterações degenerativas em fígado e rins foram significantemente mais intensas até 48 horas após a exposição; 6) na avaliação ultraestrutural (microscopia eletrônica de transmissão) após 24 e 48 horas da exposição, foi observada a presença de tumefação celular e mitocondrial e, após 48 horas, a presença de vacúolos citoplasmáticos hepáticos, os quais continham gordura pela avaliação histoquímica; nos rins foram observadas também desorganização, tumefação e despregamento celulares, além da presença de conteúdo intratubular; 7) os principais achados do hemograma foram a diminuição no número de hemácias após 24 horas da exposição e leucopenia, que persistiu ate o 7° dia da intoxicação; 8) entre as alterações bioquímicas relevantes estão o aumento da glicemia e da amilase após 24 horas da exposição, bem como dos triglicerídeos e da creatinina até 48 horas após o quadro agudo; 9) os principais achados nos ensaios de imunotoxicidade foram o aumento do peso relativo do timo e da celularidade do baço, bem como a diminuição da celularidade da medula óssea nas primeiras 48 horas após a exposição; 10) avaliando-se a indução de morte celular por apoptose e/ou necrose pelo aldicarb em hepatócitos e leucócitos in vitro, constatou-se que o aldicarb promove tanto apoptose quanto necrose de leucócitos de camundongos e que é capaz de aumentar a porcentagem de hepatócitos com apoptose, tanto in vivo quanto in vitro. Tomando-se estes resultados em conjunto, foi possível constatar que a exposição oral aguda grave ao aldicarb produz efeitos nocivos graves, principalmente nos pulmões, fígado, rins, pâncreas e sistema imune, notadamente nas primeiras 48 horas após a exposição.<br>The present study evaluated microscopic post mortem findings in 100 cases of aldicarb intoxication in dogs and cats and the acute toxicity in mice induced by a single dose of aldicarb, assessing the clinical, laboratorial, microscopic and ultrastructural alterations caused by aldicarb up to 14 days after exposition. The most commonly affected organs in dogs and cats were lung (congestion, edema, hemorrhage, emphysema and/or atelectasy), liver (congestion, vacuolar degeneration and/or hemorrhage) and kidney (congestion, hemorrhage and/or nephrosis); the other organs showed circulatory alterations, as congestion and hemorrhage. Considering both species and age we observed that old animals had the most intensity of hepatic vacuolar degeneration and the adult animals the most intensity of renal congestion. Experimental oral aldicarb poisoning resulted in death if mice were exposed to more than 0.08mg/kg, preceded by seizures. Rapid and classical symptoms of anticholinesterase poisoning occurred within 45 minutes to 2 hours after exposure to 0.08mg/kg of oral aldicarb. Animals exposed to 0.08mg/kg of aldicarb presented increased water intake until day 5, followed by decreased water intake from day 10 to day 14 after exposure to the drug in comparison to control animals. Food intake was also decreased in the experimental group. Blood analyses revealed decreased erythrocyte count and leukopenia started 24 hours after exposure and persistent for 7 days. Hyperglycemia, hypertriglyceremia, elevation of amylase and creatinine happened after 24 to 48 hours after exposure. Microscopic evaluation revealed: (i) lung edema, pulmonary congestion and/or pulmonary hemorrhage; (ii) liver congestion and zonal vacuolar degeneration of the liver; (iii) renal congestion, nephrosis and/or kidney hemorrhage. Those alterations were more prominent after 24 to 48 hours of exposure to aldicarb. Ultrastructural analysis (transmission electron microscopy) demonstrated: (i) cellular edema and mitochondrial swelling after 24 and 48 hours after exposure to aldicarb; (ii) lipid vacuoles in hepatocytes after 48 hours of exposure; (iii) renal tubular epithelium disorganization with swelling and intratubular cell exfoliation. Increased thymus/body weight ratio and spleen cellularity and decreased bone marrow cellularity were also found after 48 hours of aldicarb exposure. Aldicarb was able to induce leukocyte dead by necrosis and/or apoptosis in vitro and hepatocyte apoptosis in vivo and in vitro. Altogether, our findings demonstrated that acute oral exposure to aldicarb induces toxic effects mainly to the lungs, liver, kidneys, pancreas, and immune system. Those effects are more evident up to 48 hours after intoxication.
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Doit, Catherine. "Toxicologie de la D-pénicillamine." Paris 5, 1988. http://www.theses.fr/1988PA05P095.

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Jepson, Paul David. "Pathology and toxicology of stranded harbour porpoises (Phocoena phocoena in UK waters." Thesis, Royal Veterinary College (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406450.

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Allen, Jeremy George. "Studies of the pathogenesis, toxicology and pathology of lupinosis and associated conditions." Thesis, Allen, Jeremy George (1989) Studies of the pathogenesis, toxicology and pathology of lupinosis and associated conditions. PhD thesis, Murdoch University, 1989. https://researchrepository.murdoch.edu.au/id/eprint/53693/.

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Lupinosis is caused by phomopsins, which are toxic metabolites of the fungus Phomopsis leptostromiformis. This thesis records a series of studies of aspects of the pathogenesis, toxicology and pathology of lupinosis and associated conditions. A sheep bioassay developed for the estimation of phomopsins-associated toxicity in feed samples infected with Phomopsis leptostromiformis is described. Toxicity ratings provided by this bioassay were compared with results provided by a nursling rat bioassay and a chemical assay for phomopsin A. There was a poor correlation between the results from the two bioassays, but results from the sheep bioassay correlated well with those from the chemical assay. The procedure for scoring microscopic liver damage in the sheep bioassay was modified to enable assessment of the severity of lupinosis in sheep grazing toxic lupin stubbles for various periods. Individual sheep were awarded liver injury scores as a measure of the severity of their lupinosis. The microscopic changes assessed had a dynamic interrelationship with each other, and with other parameters including the daily intake of phomopsins and the period over which they were consumed. For this reason liver injury scores could only be used to compare the severity of lupinosis in sheep in individual experiments, and at the same times during experiments. Nevertheless, liver injury scores proved to be a valuable experimental tool and were used in several of the investigations reported in this thesis. The roles of copper and the hepatic microsomal enzymes in the pathogenesis of lupinosis were examined. It was established that copper accumulates in the liver of sheep with subacute and chronic lupinosis. The concentration of copper in the liver was positively correlated with the degree of liver injury. It was also found that the degree of liver injury was correlated positively with the concentration of selenium and negatively with the concentration of zinc. Induction of the hepatic microsomal enzymes with DDT and phenobarbitone, and inhibition with SKF 525A and carbon disulphide, did not alter the toxicity of phomopsin A in rats. However, the toxicity in both males and females was significantly increased when hepatic microsomal enzymes were inhibited by adrenalectomy, and was significantly increased in males only when they were inhibited by cobalt chloride. Toxicological studies established 50% lethal doses for phomopsin A in sheep and pigs following a single subcutaneous administration, and in sheep following a single oral administration and daily oral administrations. Sheep were approximately 40 times more susceptible than pigs to phomopsin A, and in sheep phomopsin A was approximately 65 times more toxic following a single subcutaneous injection rather than a single oral administration. It was demonstrated that only the Biotype A strains of P. leptostromiformis were toxicogenic when grown on autoclaved wheat. The different strains of this biotype had varying potentials to produce phomopsin A. Evidence for a toxic phomopsin additional to phomopsins A and B is presented, and it was referred to as phomopsin C. Aspects of the pathology, clinical chemistry and haematology of experimental phomopsins toxicosis in sheep and rats, which complemented or differed from previous descriptions, are reported. Special attention was given to lupinosis-associated spongy degeneration of the brain and lupinosis-associated myopathy in sheep. Specific experiments conducted to study the pathogenesis and pathology of these conditions are documented.
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Dezfulian, A. Rahman. "Microscopical application of design based stereological methods in histopathology and toxico-pathology." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284162.

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Dorlhiac, Bénédicte. "Rôle des acariens domestiques en pathologie allergique." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M193.

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Books on the topic "Toxicologic pathology"

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Sahota, Pritam S., James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, and Page R. Bouchard, eds. Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624.

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Steinbach, Thomas J., Daniel J. Patrick, and Mary Ellen Cosenza, eds. Toxicologic Pathology for Non-Pathologists. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9777-0.

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Pathologists, Society of Toxicologic. Standardized system of nomenclature and diagnostic criteria: Guides for toxicologic pathology. The Society, 1990.

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Principles of toxicological pathology. Taylor & Francis, 1986.

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Gopinath, Chirukandath, and Vasanthi Mowat. Atlas of Toxicological Pathology. Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-998-7.

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E, Prentice D., and Lewis D. J, eds. Atlas of experimental toxicological pathology. MTP Press, 1987.

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Gopinath, C., D. E. Prentice, and D. J. Lewis. Atlas of Experimental Toxicological Pathology. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3189-3.

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Bruslé, Jacques. The impact of harmful algal blooms on finfish: Mortality, pathology, and toxicology = impact des toxines algales sur les poissons : mortalité, pathologie, toxicologie. Ifremer, 1995.

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Walum, Erik. Understanding cell toxicology: Principles and practice. E. Horwood, 1990.

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Kjell, Stenberg, and Jenssen Dag, eds. Understanding cell toxicology: Principles and practice. Ellis Horwood, 1990.

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Book chapters on the topic "Toxicologic pathology"

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Pandiri, Arun R., David E. Malarkey, and Mark J. Hoenerhoff. "Toxicogenomics in Toxicologic Pathology." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-9.

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Tripathi, Niraj K., and Jacqueline M. Tarrant. "Principles of Clinical Pathology." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-7.

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Popp, James A., and Jeffery A. Engelhardt. "Overview of Drug Development." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-1.

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Johnson, Robert C., Robert H. Spaet, Gitte Jeppesen, Ursula Junker, and Robert Stull. "Spontaneous Lesions in Control Animals Used in Toxicity Studies." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-10.

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Markovits, Judit E., Graham R. Betton, Donald N. McMartin, and Theresa Boulineau. "Gastrointestinal Tract." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-11.

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Cattley, Russell C., James A. Popp, and Steven L. Vonderfecht. "Liver, Gallbladder, and Exocrine Pancreas." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-12.

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McKevitt, Tom P., and David J. Lewis. "Respiratory System." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-13.

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Frazier, Kendall S., and John Curtis Seely. "Urinary System." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-14.

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Henson, Kristin, Tanasa Osborne, and Gregory S. Travlos. "Hematopoietic System." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-15.

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Haley, Patrick J. "The Lymphoid System." In Toxicologic Pathology. CRC Press, 2018. http://dx.doi.org/10.1201/9780429504624-16.

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Conference papers on the topic "Toxicologic pathology"

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Dreher, Rachel, Ryan Power, and Binil Starly. "Biofabrication of Multi-Material 3D Neural Constructs Embedded With Patterned PC12 Neural Cell Lines." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14249.

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Abstract:
In Vitro models are being used as a bridge between animal and human studies. Being able to reproduce specific tissue-like structures, functions and responses in a way that is more physiologically relevant allows for huge advantages for tissue engineering, pharmaco-toxicology and food research. These systems are not designed to be directly implanted into patients, but can be used to study human tissue physiology and pathophysiology in vitro. In vitro models are based on human cells, which can capture the responses of the human body, particularly those that are species specific. Models of tissues and organs can give enhanced predictive power, particularly for large-scale screening assays and to understand complex disease pathology.
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