This thesis is a critical analysis of the law of self-defence in Scotland and England. It is argued that it is far more difficult to justify the use of lethal force in self-defence than is commonly assumed and that, drawing on the work of Uniacke, the most convincing justification is on the basis of a right to life, accompanied by a theory of forfeiture. That is, the victim of an attack is entitled to protect herself from an aggressor who threatens her right to life. The reason why she is permitted to kill the aggressor, but the aggressor is not permitted to kill her, is because an aggressor forfeits her right to life by virtue of becoming an unjust immediate threat to the life of another. However, the right to life is seen as a fundamental right that should be respected in relation to all human beings, even aggressors, as far as is reasonably possible. This is because, unlike almost all other types of loss, a deprivation of life is something from which the victim can never recover and for which the victim can never be compensated. As such, it is argued that an aggressor's right to life is only forfeited at the point where it is no longer reasonably possible to save both the life of the victim and the life of the aggressor. On this basis, the thesis proceeds to argue that the law of self-defence should contain strict rules on when it is permissible to take the life of another human being. As such, relatively restrictive rules are proposed in relation to five specific aspects of self-defence law: retreat, mistake, self-generated self-defence, imminence and proportionality. It is suggested that Scots law conforms to these strict rules to a greater extent than does English law.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1956. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 61-66).

The autonomous behaviour of sex-linked recessive temperature-sensitive lethal mutants in Drosophila melanogaster could be demonstrated by the presence of mosaic patches of tissue hemizygous for the mutant created by loss of a ring X chromosome in cells at the permissive temperature (21.5°C) and the absence of such patches at the restrictive temperature (29°C), The presence of patches at both temperatures indicated that the mutant was non-autonomous. Such non-autonomous behaviour might be attributed to the existence of a substance capable of diffusing from the wild type tissue to supplement the mutant tissue. The experiments carried out showed that the presence or absence of mosaic patches could not be directly interpreted as demonstration of autonomous or non-autonomous properties of the mutant. Other factors such as the time of activity of the ts mutant and the type of tissue undergoing ring X loss affected mosaic tissue production. Therefore, the mere presence of mosaic tissue at 29°C could not be used as a criterion for the non-autonomous behaviour of the ts mutants. However, these mutants can be graded according to the degree of autonomy of ts lethality after alterations due to XO survival frequencies, lethal periods, and temperature-sensitive periods have been placed onmosaic frequencies at 29°C. Of the thirteen ts mutants studied, six can he classed as autonomous lethals. The others are equally autonomous as lethals but only in specific tissues, while others do not appear to be as autonomous. In fact, one of these may be considered non-autonomous. / Science, Faculty of / Zoology, Department of / Graduate

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Master of Science / Department of Chemical Engineering / Larry A. Glasgow / The military is interested in stopping suspicious vehicles at checkpoints or security positions while minimizing noncombatant fatalities. Preliminary work has shown that decreasing the oxygen concentration in proximity to the automobile air intake system and blocking the air flow through an automotive induction system provides the greatest probability of success for the broadest possible array of internal combustion engines. A non-lethal foam deployment system was developed that satisfies the military’s needs to stop suspicious vehicles. The foam is discharged from a pressurized tank and engulfs the air intake system of the target vehicle. The foam is drawn into the air intake and the protein additive contained in the foam would occlude pores in the air filter medium. Once the air filter was blocked, the vehicle would become immobilized so that security personnel can secure the vehicle. The work carried out in this project consisted of development and refinement of surfactant solution composition, improvement in the rate of absorption of carbon dioxide for increased foam volume, and characterization of discharge for optimum foam volume. In addition, a half-scale model apparatus was developed to test the foam’s ability to be ingested in an automotive intake system. These experiments demonstrated that the foam deployment system would stop an automobile within six seconds.

<p>Both prokaryotic and eukaryotic cells are equipped with DNA repair mechanisms to protect the integrity of their genome in case of DNA damage. In the eukaryotic organism <i>Saccharomyces cerevisiae</i>, MMS2 encodes a ubiquitin-conjugating enzyme variant protein belonging to the RAD6 repair pathway; MMS2 functions in error-free postreplication repair (PRR), a subpathway parallel to REV3 mutagenesis. A mutation in MMS2 does not result in extreme sensitivity to DNA damaging agents; however, deletion of both subpathways of PRR results in a synergistic phenotype. By taking advantage of the synergism between error-free PRR and mutagenesis pathway mutations, a conditional synthetic lethal screen was used to identify novel genes genetically involved in PRR. A synthetic lethal screen was modified to use extremely low doses of MMS that would not affect the growth of single mutants, but would effectively kill the double mutants. Fifteen potential mutants were characterized, of which twelve were identified as known error-prone PRR genes. Characterization of mutations in strains SLM-9 and SLM-11, that are conditionally synthetically lethal with mms2Ä, revealed functions for both checkpoints and mating-type heterozygosity in regulating PRR. Cell cycle checkpoints monitor the integrity of the genome and ensure that cell cycle progression is deferred until chromosome damage is repaired. The checkpoint genes genetically interact with both the error-free and error-prone branches of PRR, potentially for delaying cell cycle progression to allow time for DNA repair, and for signaling the stage of the cell cycle and thus DNA content. Other potential monitors for DNA content are the a1 and á2 proteins encoded by the mating type genes MATa and MATá, respectively. Diploid cells heterozygous for mating type (a/á) show an increased resistance to UV damage and are more recombination-proficient than haploid cells. Haploid PRR mutants expressing both mating type genes show an increased resistance to DNA-damaging agents. This phenomenon is specific to PRR: it was not seen in excision repair-deficient and recombination-deficient mutants tested. The rescuing effect seen in PRR mutants heterozygous for mating type is likely the result of channeling lesions into a recombination repair pathway and away from the non-operational PRR pathway. Both checkpoint and mating type genes play a role in regulating PRR. Almost certainly these genes are required to monitor the cell cycle stage and DNA content to determine the best mechanism to repair the damaged DNA thus preventing genomic instability.</p>

<p>Both prokaryotic and eukaryotic cells are equipped with DNA repair mechanisms to protect the integrity of their genome in case of DNA damage. In the eukaryotic organism <i>Saccharomyces cerevisiae</i>, MMS2 encodes a ubiquitin-conjugating enzyme variant protein belonging to the RAD6 repair pathway; MMS2 functions in error-free postreplication repair (PRR), a subpathway parallel to REV3 mutagenesis. A mutation in MMS2 does not result in extreme sensitivity to DNA damaging agents; however, deletion of both subpathways of PRR results in a synergistic phenotype. By taking advantage of the synergism between error-free PRR and mutagenesis pathway mutations, a conditional synthetic lethal screen was used to identify novel genes genetically involved in PRR. A synthetic lethal screen was modified to use extremely low doses of MMS that would not affect the growth of single mutants, but would effectively kill the double mutants. Fifteen potential mutants were characterized, of which twelve were identified as known error-prone PRR genes. Characterization of mutations in strains SLM-9 and SLM-11, that are conditionally synthetically lethal with mms2Ä, revealed functions for both checkpoints and mating-type heterozygosity in regulating PRR. Cell cycle checkpoints monitor the integrity of the genome and ensure that cell cycle progression is deferred until chromosome damage is repaired. The checkpoint genes genetically interact with both the error-free and error-prone branches of PRR, potentially for delaying cell cycle progression to allow time for DNA repair, and for signaling the stage of the cell cycle and thus DNA content. Other potential monitors for DNA content are the a1 and á2 proteins encoded by the mating type genes MATa and MATá, respectively. Diploid cells heterozygous for mating type (a/á) show an increased resistance to UV damage and are more recombination-proficient than haploid cells. Haploid PRR mutants expressing both mating type genes show an increased resistance to DNA-damaging agents. This phenomenon is specific to PRR: it was not seen in excision repair-deficient and recombination-deficient mutants tested. The rescuing effect seen in PRR mutants heterozygous for mating type is likely the result of channeling lesions into a recombination repair pathway and away from the non-operational PRR pathway. Both checkpoint and mating type genes play a role in regulating PRR. Almost certainly these genes are required to monitor the cell cycle stage and DNA content to determine the best mechanism to repair the damaged DNA thus preventing genomic instability.</p>

YDL100Cp is the ArsA homologue protein found in S. cerevisiae. In bacteria, ArsA protein is involved in As3+detoxification but the function of YDL100Cp is still unknown. Previous studies show that deletion of YDL100C in S. cerevisiae was not lethal and had no effect on As3+ sensitivity or growth at 30¢J. However, when grown at 40¢J, growth of YDL100C disrupted strain (JSY1) was inhibited. To study the role of YDL100C in response to lethal heat shock, wild type (W303-1B) and JSY1 cells were exposed to 50¢J for 15 min. The survival rate of JSY1 cells was half of W303-1B cells and the difference in survival rate was complemented by introduction of plasmid carrying YDL100C. It suggests that YDL100Cp plays a role in acquisition of thermotolerance to lethal heat shock. It is believed that there are two factors involved in heat-induced cell death: the heat damage and the oxidative damage. Determinations of heat-damage related defense system in S. cerevisiae, including trehalose (a thermoprotectant) content, Hsp70 expression and Hsp104 expression, demonstrate that heat damage should not be the major cause of JSY1 cell death during heat shock. For the oxidative damage, the measurement of in vivo reactive oxygen species reveal the lower protein damage caused by reactive oxygen species (ROS) in JSY-1 after 50¢J 15 min heat shock, this might reflect the difference in viability of three strains under lethal heat shock. And with the intra cellular content of glutathione, it revels that the YDL100C deficient caused cell got more serious oxidative damage under 50¢J heat shock. But the observation of thermotolerance related ROS scavenger system (including the catalase, and superoxide dismutase) expression with reverse transcription polymerase chain reaction suggested that YDL100C deficient had no effect on triggering these system. As the result, it is suggested that the function of YDL100Cp in S. cerevisiae might be an oxidative damage repair system, such as the glutathione peroxidase. It might react with the oxidative damage substance and function as a deoxidizer.