Made available in DSpace on 2016-06-02T20:30:56Z (GMT). No. of bitstreams: 1 5216.pdf: 2501037 bytes, checksum: 1c749233a3e1aa698840c7fea2c19aa2 (MD5) Previous issue date: 2013-03-27 / Universidade Federal de Minas Gerais / It is noticed that children learn about 14.000 words to the age of five years old. One of the phenomenon related to this remarkable language development is known as exclusion responding. This responding, described as the immediate selection of an undefined comparison stimulus given and also undefined stimulus, excluding familiar stimuli, is being robustly verified among different populations. It s been also noticed that learning the relation between the new stimuli does not seem to occur through a single exclusion trial. However, exclusion trials have revealed itself an efficient procedure to teach new relations to individuals with typical and atypical development. This study, carried out with 22 participants where 8 had typical development, 11 had autism and 3 had Down syndrome and ages five to 46 years old, investigated, from a particular set of procedures and learning tests, the number of exclusion trials needed for the participants to learn the relations between undefined figures and undefined dictated names. At each trial, the researcher said a word and the participant selected one figure out of three that he/she considered correct. The procedure consisted of five phases: base line (1), introduction of the mask as neutral stimulus (2), exclusion trials (3), learning tests (4) and a nomination test (5). Phases 3 and 4 were repeated until learning was observed or until the number of 10 repetitions was reached. The procedure was replicated for four times, and the relations between the undefined dictated words Mido, Fani, Duca, Pagu and its respective figures were teached. All participants completed phases 1 and 2; 21 participants responded by exclusion; 19 participants learned all the relations presented. Concerning the amount of exclusion trials needed for learning the relation between new dictated names and figures, it was observed that a variation from 2 (the minimum programmed by the procedure) to 10 trials were needed for the learning of each stimuli pair to occur. Despite the relative variation, it is clear that the data were mostly concentrated on the minimum number of repetitions (2) and this was the trend line observed for the learning of all the stimuli pairs. The observed average was 2,1 trias for two of the stimuli pairs (Pagu and Duca) with standard deviations equal to 0,1. For the learning of Mido and Fani were needed, in average, 2,6 and 3,2 exclusion trials, with standard deviations 1,8 and 0,9 respectively. It is considered that the experimental conditions favored the learning outcomes and the typically used procedure can be configured in a kind of teaching technology of arbitrary relations and widely used in different educational contexts. / Crianças aprendem cerca de 14.000 palavras antes de completarem cinco anos de idade. Um dos fenômenos atribuídos a este notável desenvolvimento de linguagem é o responder por exclusão. Este responder, descrito como a seleção imediata de um estímulo de comparação novo diante de um estímulo modelo novo, excluindo estímulos de comparação familiares, tem sido verificado de forma robusta em diferentes populações. Observa-se também que a aprendizagem da relação entre os estímulos novos não parece ocorrer após uma única tentativa de exclusão. Por outro lado, a utilização de tentativas de exclusão como procedimento de ensino de novas relações a indivíduos com desenvolvimento típico e atípico tem se revelado eficaz. Este estudo, conduzido com 22 participantes oito crianças de desenvolvimento típico, 11 indivíduos com autismo, e três com Síndrome de Down , com idades entre cinco e 46 anos, investigou, a partir de um conjunto de procedimentos e testes de aprendizagem, o número de tentativas necessárias para que cada participante aprendesse a relação entre figuras indefinidas e nomes ditados indefinidos. A cada tentativa, a experimentadora dizia uma palavra e o participante selecionava a figura que considerava correta, diante de três comparações. O procedimento foi composto por cinco fases; linha de base (1), introdução da máscara como estímulo neutro (2), tentativas de exclusão (3), testes de aprendizagem (4) e teste de nomeação (5). As fases 3 e 4 foram repetidas até a observação de aprendizagem, ou até alcançar o critério máximo de 10 repetições. O procedimento foi replicado por quatro vezes, e as relações entre as palavras indefinidas Mido, Fani, Duca e Pagu e suas respectivas figuras indefinidas foram ensinadas. Todos os participantes completaram as fases 1 e 2; 21 participantes responderam por exclusão; 19 participantes demonstraram aprendizagem. No que concerne à quantidade de tentativas de exclusão necessárias para aprendizagem da relação entre nomes e figuras novas, observou-se uma variação de 2 (mínimo programado pelo procedimento) a 10 tentativas necessárias para que a aprendizagem da cada par de estímulos ocorresse. Apesar da relativa variação, observa-se que os dados ficaram concentrados em sua maioria no número mínimo de repetições (2) sendo esta a moda verificada para aprendizagem de todos os pares de estímulos. A média observada também foi de 2,1 tentativas para 2 dos pares de estímulos (Pagu e Duca) com desvios padrão iguais a 0,1. Para a aprendizagem de Mido e Fani foram necessárias, em média, 2,6 e 3,2 tentativas de tentativas de exclusão, com desvios padrão iguais a 0,9 e 1,8 respectivamente. Avalia-se que o delineamento experimental favoreceu a aprendizagem das relações auditivo-visuais novas e que o procedimento utilizado pode ser configurado em uma espécie de tecnologia de ensino de relações arbitrárias e amplamente utilizado em diferentes contextos educacionais.

Submitted by Regina Correa (rehecorrea@gmail.com) on 2016-09-26T20:18:08Z No. of bitstreams: 1 DissTPG.pdf: 2328311 bytes, checksum: e10d0fd3320f470ffc369ea4cb30908b (MD5) / Approved for entry into archive by Marina Freitas (marinapf@ufscar.br) on 2016-09-27T19:31:39Z (GMT) No. of bitstreams: 1 DissTPG.pdf: 2328311 bytes, checksum: e10d0fd3320f470ffc369ea4cb30908b (MD5) / Approved for entry into archive by Marina Freitas (marinapf@ufscar.br) on 2016-09-27T19:31:45Z (GMT) No. of bitstreams: 1 DissTPG.pdf: 2328311 bytes, checksum: e10d0fd3320f470ffc369ea4cb30908b (MD5) / Made available in DSpace on 2016-09-27T19:31:50Z (GMT). No. of bitstreams: 1 DissTPG.pdf: 2328311 bytes, checksum: e10d0fd3320f470ffc369ea4cb30908b (MD5) Previous issue date: 2016-02-26 / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Responding by exclusion is defined, in conditional discriminations tasks, as the immediate selection of a new stimulus, among other known stimuli, when a new sample stimulus is presented. Responding by exclusion is usually investigated by using nameobject relations as a baseline. However, generalization data of this behavior pattern to other classes of words, such as verbs, are scarce. This study investigated exclusion responding and learning of word-object (nouns) and word-action (verbs) relations in children aged 24 to 29 months. The presentation order of conditions (Noun or Verb) was counterbalanced across participants. After one, four, seven and 10 exclusion trials learning probes were presented. Results showed that baseline training for the Verb condition required a higher number of trials compared to the Noun condition. On the first exclusion probe, participants consistently selected the new stimulus, although greater variability was observed for the Verb condition. Only one participant showed positive outcomes on the learning probes, for one of the relations of the Noun condition. The study replicated previous findings on exclusion responding using nouns and extended it to name-action (verb) relations and to children aged about two years. The data points to the existence of different levels of learning and the need for a clear specification of how to measure learning outcomes of exclusion responding. / O responder por exclusão é definido, em tarefas de discriminação condicional, como a seleção imediata de um novo estímulo, entre outros estímulos familiares, quando um estímulo modelo também novo é apresentado. O responder por exclusão é usualmente investigado por meio do uso de uma linha de base de relações nome-objeto. No entanto, os dados de generalização desse padrão comportamental para outras classes de palavras, como verbos, é escasso. O presente estudo investigou o responder por exclusão e a aprendizagem por exclusão de relações nome-objeto (substantivos) e nome-ação (verbos) em crianças com idade entre 24 e 29 meses. A ordem de apresentação de ambas as condições (Substantivo e Verbo) foi contrabalanceada entre os participantes. Após uma, quatro, sete e 10 tentativas de exclusão eram apresentadas tentativas de sonda de aprendizagem. Os resultados mostraram que o treino de linha de base para a Condição Verbo requereu um maior número de tentativas quando comparada com a Condição Substantivo. Na primeira sonda de exclusão, os participantes selecionaram consistentemente o estímulo novo, embora com maior variabilidade para a Condição Verbo. Apenas um participante mostrou resultados positivos na sonda de aprendizagem e isto ocorreu para uma das relações da Condição Substantivo. O presente estudo replicou os resultados de estudos prévios, sobre o responder por exclusão, que empregaram substantivos e estendeu os resultados para relações nome-ação (verbo) e para crianças com idade próxima a dois anos. Os dados apontam para a existência de diferentes níveis de aprendizagem de uma relação e a necessidade de uma especificação clara de como medir a aprendizagem que emerge do responder por exclusão. / FAPESP (Processo No. 2008/57705-8) ; CNPq (Processo No. 573972/2008-7)

Le diabète de type 2 (DT2) est une maladie métabolique complexe causée par des facteurs génétiques mais aussi environnementaux, tels la sédentarité et le surpoids. La dysfonction de la cellule β pancréatique est maintenant reconnue comme l’élément déterminant dans le développement du DT2. Notre laboratoire s’intéresse à la sécrétion d’insuline par la cellule β en réponse aux nutriments calorigéniques et aux mécanismes qui la contrôle. Alors que la connaissance des mécanismes responsables de l’induction de la sécrétion d’insuline en réponse aux glucose et acides gras est assez avancée, les procédés d’inhibition de la sécrétion dans des contextes normaux ou pathologiques sont moins bien compris. L’objectif de la présente thèse était d’identifier quelques-uns de ces mécanismes de régulation négative de la sécrétion d’insuline dans la cellule β pancréatique, et ce en situation normale ou pathologique en lien avec le DT2. La première hypothèse testée était que l’enzyme mitochondriale hydroxyacyl-CoA déshydrogénase spécifique pour les molécules à chaîne courte (short-chain hydroxyacyl-CoA dehydrogenase, SCHAD) régule la sécrétion d’insuline induite par le glucose (SIIG) par la modulation des concentrations d’acides gras ou leur dérivés tels les acyl-CoA ou acyl-carnitine dans la cellule β. Pour ce faire, nous avons utilisé la technologie des ARN interférants (ARNi) afin de diminuer l’expression de SCHAD dans la lignée cellulaire β pancréatique INS832/13. Nous avons par la suite vérifié chez la souris DIO (diet-induced obesity) si une exposition prolongée à une diète riche en gras activerait certaines voies métaboliques et signalétiques assurant une régulation négative de la sécrétion d’insuline et contribuerait au développement du DT2. Pour ce faire, nous avons mesuré la SIIG, le métabolisme intracellulaire des lipides, la fonction mitochondriale et l’activation de certaines voies signalétiques dans les îlots de Langerhans isolés des souris normales (ND, normal diet) ou nourries à la dière riche en gras (DIO) Nos résultats suggèrent que l’enzyme SCHAD est importante dans l’atténuation de la sécrétion d’insuline induite par le glucose et les acides aminés. En effet, l’oxydation des acides gras par la protéine SCHAD préviendrait l’accumulation d’acyl-CoA ou de leurs dérivés carnitine à chaîne courtes potentialisatrices de la sécrétion d’insuline. De plus, SCHAD régule le métabolisme du glutamate par l’inhibition allostérique de l’enzyme glutamate déshydrogénase (GDH), prévenant ainsi une hyperinsulinémie causée par une sur-activité de GDH. L’étude de la dysfonction de la cellule β dans le modèle de souris DIO a démontré qu’il existe une grande hétérogénéité dans l’obésité et l’hyperglycémie développées suite à la diète riche en gras. L’orginialité de notre étude réside dans la stratification des souris DIO en deux groupes : les faibles et forts répondants à la diète (low diet responders (LDR) et high diet responder (HDR)) sur la base de leur gain de poids corporel. Nous avons mis en lumières divers mécanismes liés au métabolisme des acides gras impliqués dans la diminution de la SIIG. Une diminution du flux à travers le cycle TG/FFA accompagnée d’une augmentation de l’oxydation des acides gras et d’une accumulation intracellulaire de cholestérol contribuent à la diminution de la SIIG chez les souris DIO-HDR. De plus, l’altération de la signalisation par les voies AMPK (AMP-activated protein kinase) et PKC epsilon (protéine kinase C epsilon) pourrait expliquer certaines de ces modifications du métabolisme des îlots DIO et causer le défaut de sécrétion d’insuline. En résumé, nous avons mis en lumière des mécanismes importants pour la régulation négative de la sécrétion d’insuline dans la cellule β pancréatique saine ou en situation pathologique. Ces mécanismes pourraient permettre d’une part de limiter l’amplitude ou la durée de la sécrétion d’insuline suite à un repas chez la cellule saine, et d’autre part de préserver la fonction de la cellule β en retardant l’épuisement de celle-ci en situation pathologique. Certaines de ces voies peuvent expliquer l’altération de la sécrétion d’insuline dans le cadre du DT2 lié à l’obésité. À la lumière de nos recherches, le développement de thérapies ayant pour cible les mécanismes de régulation négative de la sécrétion d’insuline pourrait être bénéfique pour le traitement de patients diabétiques. / Type 2 diabetes (T2D) is a complex metabolic disease caused by genetic as well as environmental factors, such as sedentarity and obesity. Pancreatic β cell dysfunction is now recognized as the key factor in T2D development. Our laboratory is studying the mechanisms of regulation of insulin secretion by the pancreatic β cell in response to nutrients. While the knowledge of the mechanisms responsible for initiation of insulin secretion in response to glucose and fatty acids is quite advanced, the inhibitory processes of insulin secretion in normal or pathological situations are still poorly understood. This doctoral thesis has focused on the identification of some of the mechanisms responsible for negative regulation of insulin secretion in pancreatic β cell. We have addressed this issue under normal situation or pathological conditions related to T2D. We first tested the hypothesis by which a mitochondrial enzyme, short-chain hydroxyacyl-CoA dehydrogenase (SCHAD), negatively regulates glucose-induced insulin secretion (GIIS) by limiting the concentrations of some fatty acids and their derivatives such as acyl-CoA or acyl-carnitine molecules in the β cell. For this purpose, the downregulation of SCHAD by RNA interference (RNAi) was used in the pancreatic β cell line INS832/13. Then, we tested wether a prolonged administration of high-fat diet to mice (diet-induced obesity mouse model, DIO) would modulate intracellular metabolic and molecular pathways responsible for inhibition of insulin secretion. C57BL/6 mice were therefore fed a high-fat diet for 8 weeks followed by insulin secretion, intracellular lipid metabolism, mitochondrial function and intracellular signaling measurements on isolated pancreatic islets of Langerhans of those mice. Our results suggest that SCHAD negatively regulates GIIS and amino acid-induced insulin secretion. We propose that fatty acid oxidation by SCHAD would prevent the accumulation of short-chain acyl-CoAs or acyl-carnitines capable of potentiating insulin secretion. In addition, SCHAD regulates glutamate metabolism by the allosteric inhibition of glutamate dehydrogenase (GDH) preventing the hyperinsulinemia caused by excessive GDH activity. The study of β cell dysfunction in the DIO mouse model stratified LDR and HDR highlighted various fatty acid metabolism pathways involved in the reduction of GIIS. A decrease in the triglycerides/free fatty acid (TG/FFA) cycling associated with an increase in fatty acid oxidation and intracellular accumulation of cholesterol was shown to contribute to the decreased GIIS in DIO-HDR mice. Furthermore, alteration of AMP-activated kinase (AMPK) and protein kinase C epsilon (PKC epsilon) signaling pathways would be responsible for those alterations in metabolic pathways observed in DIO islets and cause decreased insulin secretion. In summary, we have shed light on important pathways negatively regulating insulin secretion in pancreatic β cell. These pathways could either limit the amplitude or duration of insulin secretion after a meal, or help to preserve β-cell function by delaying exhaustion. Some of those signaling pathways could explain the altered insulin secretion observed in T2D obese patients. In light of our research, the development of therapies targeting pathways that negatively regulate insulin secretion may be beneficial for treating diabetic patients.

Le diabète de type 2 (DT2) est une maladie métabolique complexe causée par des facteurs génétiques mais aussi environnementaux, tels la sédentarité et le surpoids. La dysfonction de la cellule β pancréatique est maintenant reconnue comme l’élément déterminant dans le développement du DT2. Notre laboratoire s’intéresse à la sécrétion d’insuline par la cellule β en réponse aux nutriments calorigéniques et aux mécanismes qui la contrôle. Alors que la connaissance des mécanismes responsables de l’induction de la sécrétion d’insuline en réponse aux glucose et acides gras est assez avancée, les procédés d’inhibition de la sécrétion dans des contextes normaux ou pathologiques sont moins bien compris. L’objectif de la présente thèse était d’identifier quelques-uns de ces mécanismes de régulation négative de la sécrétion d’insuline dans la cellule β pancréatique, et ce en situation normale ou pathologique en lien avec le DT2. La première hypothèse testée était que l’enzyme mitochondriale hydroxyacyl-CoA déshydrogénase spécifique pour les molécules à chaîne courte (short-chain hydroxyacyl-CoA dehydrogenase, SCHAD) régule la sécrétion d’insuline induite par le glucose (SIIG) par la modulation des concentrations d’acides gras ou leur dérivés tels les acyl-CoA ou acyl-carnitine dans la cellule β. Pour ce faire, nous avons utilisé la technologie des ARN interférants (ARNi) afin de diminuer l’expression de SCHAD dans la lignée cellulaire β pancréatique INS832/13. Nous avons par la suite vérifié chez la souris DIO (diet-induced obesity) si une exposition prolongée à une diète riche en gras activerait certaines voies métaboliques et signalétiques assurant une régulation négative de la sécrétion d’insuline et contribuerait au développement du DT2. Pour ce faire, nous avons mesuré la SIIG, le métabolisme intracellulaire des lipides, la fonction mitochondriale et l’activation de certaines voies signalétiques dans les îlots de Langerhans isolés des souris normales (ND, normal diet) ou nourries à la dière riche en gras (DIO) Nos résultats suggèrent que l’enzyme SCHAD est importante dans l’atténuation de la sécrétion d’insuline induite par le glucose et les acides aminés. En effet, l’oxydation des acides gras par la protéine SCHAD préviendrait l’accumulation d’acyl-CoA ou de leurs dérivés carnitine à chaîne courtes potentialisatrices de la sécrétion d’insuline. De plus, SCHAD régule le métabolisme du glutamate par l’inhibition allostérique de l’enzyme glutamate déshydrogénase (GDH), prévenant ainsi une hyperinsulinémie causée par une sur-activité de GDH. L’étude de la dysfonction de la cellule β dans le modèle de souris DIO a démontré qu’il existe une grande hétérogénéité dans l’obésité et l’hyperglycémie développées suite à la diète riche en gras. L’orginialité de notre étude réside dans la stratification des souris DIO en deux groupes : les faibles et forts répondants à la diète (low diet responders (LDR) et high diet responder (HDR)) sur la base de leur gain de poids corporel. Nous avons mis en lumières divers mécanismes liés au métabolisme des acides gras impliqués dans la diminution de la SIIG. Une diminution du flux à travers le cycle TG/FFA accompagnée d’une augmentation de l’oxydation des acides gras et d’une accumulation intracellulaire de cholestérol contribuent à la diminution de la SIIG chez les souris DIO-HDR. De plus, l’altération de la signalisation par les voies AMPK (AMP-activated protein kinase) et PKC epsilon (protéine kinase C epsilon) pourrait expliquer certaines de ces modifications du métabolisme des îlots DIO et causer le défaut de sécrétion d’insuline. En résumé, nous avons mis en lumière des mécanismes importants pour la régulation négative de la sécrétion d’insuline dans la cellule β pancréatique saine ou en situation pathologique. Ces mécanismes pourraient permettre d’une part de limiter l’amplitude ou la durée de la sécrétion d’insuline suite à un repas chez la cellule saine, et d’autre part de préserver la fonction de la cellule β en retardant l’épuisement de celle-ci en situation pathologique. Certaines de ces voies peuvent expliquer l’altération de la sécrétion d’insuline dans le cadre du DT2 lié à l’obésité. À la lumière de nos recherches, le développement de thérapies ayant pour cible les mécanismes de régulation négative de la sécrétion d’insuline pourrait être bénéfique pour le traitement de patients diabétiques. / Type 2 diabetes (T2D) is a complex metabolic disease caused by genetic as well as environmental factors, such as sedentarity and obesity. Pancreatic β cell dysfunction is now recognized as the key factor in T2D development. Our laboratory is studying the mechanisms of regulation of insulin secretion by the pancreatic β cell in response to nutrients. While the knowledge of the mechanisms responsible for initiation of insulin secretion in response to glucose and fatty acids is quite advanced, the inhibitory processes of insulin secretion in normal or pathological situations are still poorly understood. This doctoral thesis has focused on the identification of some of the mechanisms responsible for negative regulation of insulin secretion in pancreatic β cell. We have addressed this issue under normal situation or pathological conditions related to T2D. We first tested the hypothesis by which a mitochondrial enzyme, short-chain hydroxyacyl-CoA dehydrogenase (SCHAD), negatively regulates glucose-induced insulin secretion (GIIS) by limiting the concentrations of some fatty acids and their derivatives such as acyl-CoA or acyl-carnitine molecules in the β cell. For this purpose, the downregulation of SCHAD by RNA interference (RNAi) was used in the pancreatic β cell line INS832/13. Then, we tested wether a prolonged administration of high-fat diet to mice (diet-induced obesity mouse model, DIO) would modulate intracellular metabolic and molecular pathways responsible for inhibition of insulin secretion. C57BL/6 mice were therefore fed a high-fat diet for 8 weeks followed by insulin secretion, intracellular lipid metabolism, mitochondrial function and intracellular signaling measurements on isolated pancreatic islets of Langerhans of those mice. Our results suggest that SCHAD negatively regulates GIIS and amino acid-induced insulin secretion. We propose that fatty acid oxidation by SCHAD would prevent the accumulation of short-chain acyl-CoAs or acyl-carnitines capable of potentiating insulin secretion. In addition, SCHAD regulates glutamate metabolism by the allosteric inhibition of glutamate dehydrogenase (GDH) preventing the hyperinsulinemia caused by excessive GDH activity. The study of β cell dysfunction in the DIO mouse model stratified LDR and HDR highlighted various fatty acid metabolism pathways involved in the reduction of GIIS. A decrease in the triglycerides/free fatty acid (TG/FFA) cycling associated with an increase in fatty acid oxidation and intracellular accumulation of cholesterol was shown to contribute to the decreased GIIS in DIO-HDR mice. Furthermore, alteration of AMP-activated kinase (AMPK) and protein kinase C epsilon (PKC epsilon) signaling pathways would be responsible for those alterations in metabolic pathways observed in DIO islets and cause decreased insulin secretion. In summary, we have shed light on important pathways negatively regulating insulin secretion in pancreatic β cell. These pathways could either limit the amplitude or duration of insulin secretion after a meal, or help to preserve β-cell function by delaying exhaustion. Some of those signaling pathways could explain the altered insulin secretion observed in T2D obese patients. In light of our research, the development of therapies targeting pathways that negatively regulate insulin secretion may be beneficial for treating diabetic patients.

CHDS State/Local / Approved for public release, distribution is unlimited / The planning methodologies used today by most U.S. fire departments are excellent for traditional missions, but wholly inadequate for the threats posed by terrorism. Planning in the fire service and the rest of the first responder community historically has relied on a one-dimensional approach that uses a scenario-based planning (SBP) methodology. This thesis argues that the fire service and others in the first responder community will be able to contribute to homeland security missions much more effectively, and efficiently, by switching to specially adapted versions of capabilities-based planning. This thesis proposes a new integrated planning methodology that combines the planning strengths of scenariobased planning, threat-based planning, and capabilities-based planning. The new method identifies capabilities that could be used to manage and mitigate the consequences of the different types of contingencies within the various response spectrums. It allows an organization to perform analysis and efficiency studies to evaluate the different spectrums of contingencies against existing capabilities and create a menu of capabilities necessary for the first responder to respond to all its missions, including immediate threats and terrorism, in the most efficient and cost-effective manner. / Battalion Chief, Fire Department City of New York

The aim of this research was to evaluate the role of the first responder at the crime scene, focusing on visible policing members at Ivory Park Police Station situated in Gauteng Province. A qualitative approach was employed in which the multiple data sources of literature, documents (SAPS directives) and structured interviews were compared in an attempt to substantiate the research findings. The interviews were conducted with visible policing members who attended to crime scenes as first responders and with detective branch commanders. This research discussed a number of key concepts: crime scene, criminal investigation, first responder, Locard’s Principle and physical evidence. It explained that criminal investigation is a logical and systematic process of gathering, locating and collecting evidence and the subsequent apprehension of perpetrators of crime in an attempt to secure a conviction. The objectives of criminal investigation are to detect crime; locate and identify possible offenders; gather, collect and process evidence; arrest offenders; recover stolen property; and bring the perpetrators before court to secure a conviction. The basic purpose of investigation is to prevent crime. Locard’s Principle, also known as the “the contact theory”, is that every contact leaves a trace. This research also suggests the processes that must be followed when crime is reported, the meaning of preliminary investigation, and the basic considerations during preliminary investigation, the main mistakes made by the first responder and the solutions to the identified mistakes. It is imperative that visible policing members familiarise themselves with the purpose of investigation and develop an understanding of the term “Locard’s Principle”, the process that must be followed when crime is reported, the basic considerations in the preliminary investigation of a crime and the main mistakes made by the first responders at the scene of crime, as these carry significant weight in the execution of their daily duties. These must be understood by the first responder as they contribute to the successful investigation and prosecution of offenders. This research hopes to assist in securing convictions and decreasing the number of repeat offenders who commit crimes. / Criminology and Security Science / M.A. (Criminal Justice)

<p>This dissertation examines the impact of active shooters upon patrons attending large outdoor events. There has been a spike in shooters targeting densely populated spaces in recent years, to include open-air venues. The 2019 Gilroy Garlic Festival was selected for modeling replication using AnyLogic software to test various experiments designed to reduce casualties in the event of an active shooter situation. Through achievement of validation to produce identical outcomes of the real-world Gilroy Garlic Festival shooting, the researcher established a reliable foundational model for experimental purposes. This active shooter research project identifies the need for rapid response efforts to neutralize the shooter(s) as quickly as possible to minimize casualties. Key findings include the importance of armed officers patrolling event grounds to reduce response time, the need for adequate exits during emergency evacuations, incorporation of modern technology to identify the shooter’s location, and applicability of a 1:548 police to patron ratio.</p>