Master of Science / Department of Statistics / Weixing Song / The potency of a pesticide or some materials is widely studied in agricultural and biological fields. The level of a stimulus that results in a response by 50% of individuals in a population under study is an important characterizing parameter and it is denoted by the median lethal concentration (LC50) or the median lethal dose (LD50) or median. Estimation of LC50 is a type of quantal response assays that belong to qualitative indirect bioassays. In this report, seven methods of estimating LC50 are reviewed with reference to two normal distributions of tolerance in four different cases. Some modified methods are also discussed. Simulation shows that the maximum likelihood method generally outperforms all other traditional methods, if the true tolerance distribution is available. The comparison results indicate that the modified Dragstedt-Behrens method and modified Reed-Muench method are good substitutes for the original ones in most scenarios.

No description available.

The objective of this thesis was to evaluate hsp70 expression as an indicator of arsenic exposure in zebrafish larvae and to assess the accuracy of the hsp70-eGFP reporter gene construct as a reliable indicator of endogenous hsp70 expression. The relative toxicity of arsenite and arsenate was also examined and gross developmental effects were recorded following an acute 96 hour range finding exposure. Gross effects observed included edema, trunk abnormalities, immobility, and mortality for both arsenite and arsenate, with arsenite more toxic than arsenate. The median lethal concentrations (LC50) for arsenite and arsenate were calculated from the data obtained in the 96 hour exposure. They were determined to be 771.98 μM and 1347 μM respectively. The effective concentrations (EC50) were determined to be 570 μM for arsenite and 1172 μM for arsenate. Results from the 96 hour exposures were also used to determine concentrations used in subsequent exposures. Induction of hsp70 was examined in wild-type larvae following a three hour exposure to arsenic and subsequent in situ hybridization. It was determined that both trivalent and pentavelant arsenic induced expression in the olfactory rosette, gills and skin, GIT, liver, and pericardial muscle. Expression was found to be dose-dependent and tissue-specific for both. Induction of hsp70 was evident in the skin, liver, and gastrointestinal tract of zebrafish larvae exposed to 700 μM arsenite and in the skin, gills, liver, pericardial muscle, and gastrointestinal tract in those exposed to 1000 μM or 2000 μM arsenite. Exposure to 1500 μM arsenate resulted in expression in skin, liver, and gastrointestinal tract, while induction was observed in skin, gills, liver, pericardial muscle and gastrointestinal tract of larvae exposed to 2500 μM or 7500 μM arsenate. Overall expression patterns of hsp70-eGFP in transgenic zebrafish larvae exposed to arsenic were found to closely mimic that of endogenous hsp70 expression patterns in wild-type larvae suggesting that it is an accurate indicator of endogenous hsp70 expression.

The objective of this thesis was to evaluate hsp70 expression as an indicator of arsenic exposure in zebrafish larvae and to assess the accuracy of the hsp70-eGFP reporter gene construct as a reliable indicator of endogenous hsp70 expression. The relative toxicity of arsenite and arsenate was also examined and gross developmental effects were recorded following an acute 96 hour range finding exposure. Gross effects observed included edema, trunk abnormalities, immobility, and mortality for both arsenite and arsenate, with arsenite more toxic than arsenate. The median lethal concentrations (LC50) for arsenite and arsenate were calculated from the data obtained in the 96 hour exposure. They were determined to be 771.98 μM and 1347 μM respectively. The effective concentrations (EC50) were determined to be 570 μM for arsenite and 1172 μM for arsenate. Results from the 96 hour exposures were also used to determine concentrations used in subsequent exposures. Induction of hsp70 was examined in wild-type larvae following a three hour exposure to arsenic and subsequent in situ hybridization. It was determined that both trivalent and pentavelant arsenic induced expression in the olfactory rosette, gills and skin, GIT, liver, and pericardial muscle. Expression was found to be dose-dependent and tissue-specific for both. Induction of hsp70 was evident in the skin, liver, and gastrointestinal tract of zebrafish larvae exposed to 700 μM arsenite and in the skin, gills, liver, pericardial muscle, and gastrointestinal tract in those exposed to 1000 μM or 2000 μM arsenite. Exposure to 1500 μM arsenate resulted in expression in skin, liver, and gastrointestinal tract, while induction was observed in skin, gills, liver, pericardial muscle and gastrointestinal tract of larvae exposed to 2500 μM or 7500 μM arsenate. Overall expression patterns of hsp70-eGFP in transgenic zebrafish larvae exposed to arsenic were found to closely mimic that of endogenous hsp70 expression patterns in wild-type larvae suggesting that it is an accurate indicator of endogenous hsp70 expression.

No description available.

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 54-59).

Thesis (M.S.)--Eastern Illinois University, 2010. / Includes bibliographical references (leaves 31-38).

University, Diss., 2002--Regensburg.

Assays based on a biological response (bioassays) offer the possibility of screening foodstuffs for both known and uncharacterised mycotoxins. The sensitivity of several bioassays, namely brine shrimp, rat liver cells, baby hamster kidney cells, Bacillus megaterium, B. stearothermophilus Tetrahymena pyriformis and pea seedlings, to mycotoxin standards was established. Based on these results, the bacterial assays were found to be relatively insensitive to the majority of mycotoxins tested. A biological screen consisting of the above bioassays (excluding the bacterial assays) was capable of detecting twelve mycotoxins. This screen was applied to the testing of moulds isolated from mould-spoiled foods, identified, and tested in a ratio corresponding to their percentage occurrence. They included species of Aspergillus, Penicillium, Cladosporium, Rhizopus, Mucor, Alternaria and Wallemia. Approximately 60% of the moulds, when grown in culture media, caused a toxic effect in three or more of the bioassays. Some of the moulds caused enhanced toxicity when grown on a foodstuff; other extracts from mould-inoculated foods were found to be non-toxic to the bioassays. It was of interest to note the toxicity to bioassays caused by moulds such as Mucor and Wallemia. These are not well-recognised mycotoxin producers. A further study was made on toxin production by Wallemia. A scheme of chemical purification, involving TLC and HPLC, linked with bioassay testing, was used to isolate the toxic compound. The toxin, to be named walleminol A, has a molecular weight of 236 and probable composition of C15-H24O2. The minimum inhibitory dose of the toxin to bioassays was approximately 50 mug/ml. Toxicity of ochratoxin A to cell lines was not enhanced by the inclusion of microsomal enzymes. The acute toxicity of aflatoxin B1 and sterigmatocystin, was, however, greatly enhanced by the microsomal enzymes. Aflatoxin B1 and sterigmatocystin were metabolised to form the more polar metabolites. The effects of these toxins on cells was also examined by flow cytometry. This demonstrated that aflatoxin B1 and sterigmatocystin had no effect on the cell cycle unless activated by microsomal enzymes. The activated toxins inhibited DNA synthesis and showed that apparently surviving cells died on subculture.

No description available.