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Bushell, Trevor John. "The role of group II and group III metabotropic glutamate receptors in synaptic transmission and plasticity in the mouse and rat hippocampus." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337226.
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Kiive, Evelyn. "Studies on peripheral markers of central serotonergic activity and behaviour /." Tartu : Tartu University Press, 2005. http://dspace.utlib.ee/dspace/bitstream/10062/1064/5/kiive.pdf.
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Nóbrega, Kenya Idamara Mendonça da. "Qualidade de vida, ansiedade e depressão em cuidadores de criança com neoplasia cerebral." Universidade Federal de Sergipe, 2010. https://ri.ufs.br/handle/riufs/3734.
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Background: From technological advances the patients survival with tumors of central nervous system has increased and due to this situation, it was necessary evaluate the quality of life and emotional state of both patients and their caregivers. Purposes: Distinguish in socio-demographic terms children caregivers with brain tumors treated at a public hospital in Aracaju-SE, as well as to investigate this group perception as their quality of life, anxiety and depression. Methods: 32 caregivers participated of a convenience pattern and three instruments were used: socio-demographic questionnaire, WHOQOL-bref and HADS. Data were analyzed using statistical program SPSS, 15.0. Results: The pattern showed that 100% of caregivers are female, with age greater than or equal to 18 years (32.1 ± 6.8), 96.6% were mothers (p <0.0001) and 65.6% have three or more children (p = 0.0001). Furthermore, 46.9% have primary education (p = 0.004), 43.8% were from Sergipe s counties (p = 0.01) and 75% didn t receive help to take care child (p=0.005). 46.9% caregivers didn t have a paid employment prior to the child's illness and with disease s advent, this proportion rose to 90.6% (p <0.001), although in both cases the predominant income was the minimum wage.The physical domain had the best rating among caregivers (58.7), followed by social domain (57.6). The environmental showed the worst one among caregivers (43.8), followed by psychological (55.6). There was a relevant association of environmental field with the physical domains only (p <0.0001) and social (p = 0.05). The psychological domain was positively correlated with the physical one. (p = 0.01).The prevalence of anxiety was 50% while depression was 46.9%. Conclusions: The perception of caregivers quality of life was moderate, the average caregivers QOL among the areas was 53.9. The social domain were associate with presence for anxiety and the physical and environment were associate with presence for depression.Fundamentação: A partir dos avanços tecnológicos a sobrevida dos pacientes com tumores no Sistema Nervoso Central aumentou e com isso surgiu a necessidade de avaliar a qualidade de vida e o estado emocional tanto destes pacientes quanto de seus cuidadores. Objetivos: Caracterizar em termos sócio-demográfico cuidadores de crianças com neoplasia cerebral atendidas em um hospital público de Aracaju/SE, bem como investigar a percepção desse grupo quanto a sua qualidade de vida, ansiedade e depressão. Métodos: Participaram do estudo 32 cuidadores de uma amostra por conveniência. Foram utilizados 3 instrumentos: um questionário sócio-demográfico, WHOQOL-abrev e HADS. Os dados obtidos foram analisados utilizando-se o programa estatístico SPSS, 15.0. Resultados: A amostra indicou que 100% dos cuidadores são do gênero feminino, com idade superior ou igual a 18 anos (32,1± 6,8), 96,6% são mães (p < 0,0001) e 65,6% delas possuem três filhos ou mais (p = 0,0001). Além disso, 46,9% possuem ensino fundamental (p = 0,004), 43,8% eram procedentes do interior do Estado de Sergipe (p = 0,01) e 75% não recebiam ajuda externa para cuidar da criança (p = 0,005). 46,9% dos cuidadores não possuía uma ocupação remunerada antes da doença da criança e com o advento da doença, essa proporção se elevou para 90,6% (p < 0,001), no entanto em ambos os casos a renda predominante foi a de um salário mínimo. O domínio físico obteve a melhor avaliação entre os cuidadores (58,7), seguido pelo domínio social (57,6). O domínio ambiental foi o que apresentou pior avaliação entre os cuidadores (43,8), seguido pelo psicológico (55,6). Houve uma associação significativa do domínio ambiental somente com os domínios físicos (p < 0,0001) e social (p = 0,05). O domínio psicológico se correlacionou positivamente com o domínio físico (p = 0,01). A prevalência de ansiedade na amostra foi de 50%, enquanto que a prevalência de depressão foi de 46,9%. Conclusões: A percepção da qualidade de vida dos cuidadores foi moderada, pois a média da QV dos cuidadores entre os domínios foi de 53,9. O domínio social esteve associado à presença de ansiedade e os domínios social e ambiental estiveram associados à depressão.
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GONDIM, Mariana Barros e. Silva. "Nutrição, natação e desenvolvimento cerebral em ratos: efeitos eletrofisiológicos sobre a potenciação do eletrocorticograma associada à depressão alastrante." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/18051.
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A nutrição no início da vida e o exercício físico podem alterar a excitabilidade cerebral, interferindo em processos de desenvolvimento e em parâmetros eletrofisiológicos. A depressão alastrante cortical (DAC) é um fenômeno relacionado com a excitabilidade cerebral. Em estudos anteriores, demonstramos potenciação da atividade elétrica cortical espontânea (ECoG) após a DAC. Nesta tese investigou-se a influência das condições de lactação e do exercício de natação, no início da vida e na idade adulta, sobre essa potenciação. Ratos Wistar machos foram amamentados em ninhadas com 6 ou 12 filhotes (grupos L6 e L12). A natação, precoce e tardia, foi realizada entre 8-23 e 60-75 dias de vida, respectivamente. O ECoG foi registrado aos 90-120 dias. Com um algoritmo específico (software Matlab™), determinou-se a amplitude do ECoG. Diferenças intergrupos de peso corporal e encefálico (L12
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Mello, Sueli Moreira de. "Cromatografia em fase gasosa como técnica de triagem para diagnóstico laboratorial das intoxicações agudas por medicamentos depressores do sistema nervoso central (OU) Cromatografia em fase gasosa como técnica de triagem para diagnóstico laboratorial das intoxicações agudas por medicamentos que causam síndrome de depressores do sistema nervoso central." Universidade de São Paulo, 1997. http://www.teses.usp.br/teses/disponiveis/9/9137/tde-23032009-095640/.
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A estatística das principais causas das intoxicações mostra que os depressores do sistema nervoso central (SNC) têm uma participação significativa. No Centro de Controle de Intoxicações da Unicamp, em 1995, 30% das intoxicações foram por medicamentos, sendo a metade por depressores do SNC. A avaliação do paciente intoxicado, freqüentemente inclui, além de exames clínicos, análises laboratoriais para identificação de agentes tóxicos presentes em amostras biológicas. Os procedimentos analíticos com esta finalidade utilizam diversas técnicas, entre elas as cromatográficas. O objetivo do presente trabalho foi desenvolver e otimizar um método de triagem para diagnóstico laboratorial das intoxicações por medicamentos que causam depressão do SNC, através da cromatografia em fase gasosa, para ser utilizado em análises de urgência em Centros de Controle de Intoxicações. Foram selecionados 21 fármacos depressores do SNC a partir de critérios de freqüência e importância clínico-toxicológica. As técnicas de extração apresentaram recuperação relativa entre 66,4 e 92,6% para a urina e entre 36,7 e 82,6% para o plasma. O estudo de precisão apresentou coeficiente de variação entre 4,3 e 13,7% para as amostras de urina e entre 7,8 e 19,4% para o plasma. A sensibilidade foi testada para concentrações próximas aos níveis terapêuticos (1 a 5 µg/mL) tendo sido considerada satisfatória e a análise de extratos de \"brancos\" de referência apresentou cromatograma sem interferentes. O tempo de análise foi compatível com a necessidade clínica (menor que duas horas) para análise concomitante dos 21 fármacos. Pode-se concluir que o método de triagem por cromatografia gasosa proposto foi adequado para o diagnóstico laboratorial das intoxicações agudas por medicamentos que causam síndrome de depressão do SNC.Drugs that cause Central Nervous System Depression Syndrome (CNSDS) have an important role in poisons. At the Poison Control Center of University of Campinas, in 1995, 30% of poisons were due to medicines and a half of that was due to CNS depressants. The evaluation of the poisoned patient includes, in addition to clinical examinations, laboratorial screenings to identify toxic agents in biological samples. The analytical procedures with this endpoint use several methods, including chromatographic analyses. The objective of this study was to develop and to optimize a procedure for screening drugs that cause CNSDS, through gas chromatography, to be used in emergency assays at the Poison Control Center. Twenty one drugs were selected using frequency and clinical-toxicology importance criteria. The extraction technique presented relative recuperation between 66.4 and 92.6% for urine and 36.7 and 82.6% for plasma. The intra-assay coefficient of variation was between 4.3 and 13.7% for urine and 7.8 and 19.4% for plasma. The sensibility was tested for concentrations near therapeutical levels (1 to 5 µg/ml) and was considered satisfactory. The chromatogram of blank sample extract presented no interferences. The time required to screen 21 drugs in plasma and urine samples was less than 2 hours, making this method appropriate for use in poison control center in hospitals.
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Almeida, Stella Pereira de. "Primeiro perfil do usuário de "êxtase" (MDMA) em São Paulo." Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/47/47132/tde-17012006-152155/.
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O presente estudo teve como objetivo identificar os padrões de uso de "êxtase" na cidade de São Paulo. Os usuários foram recrutados através da técnica de amostragem snowball, também utilizada para o recrutamento do grupo controle, composto de indivíduos com estilo de vida semelhante aos primeiros mas que nunca haviam experimentado "êxtase" (não usuários). Usuários (52) e não usuários (52) foram entrevistados quanto às características sócio-demográficas e quanto ao uso de drogas psicotrópicas; usuários também responderam questões sobre circunstâncias de uso e efeitos do "êxtase". Através da Escala de Impulsividade de Barratt e dos Inventários de Depressão de Beck e de Ansiedade Traço-Estado (IDATE-traço) foram medidas impulsividade, depressão e ansiedade de ambos os grupos. Os dois grupos apresentaram características sócio-demográficas semelhantes: a maioria pertencia à classe média, era jovem, heterossexual, solteira e com nível superior. Entre os usuários o consumo de outras drogas psicotrópicas foi expressivamente superior. Outras características mais freqüentes no grupo de usuários foram a presença de tatuagens e piercings, a frequência a "raves" e a preferência pela música eletrônica. No Inventário de Depressão de Beck os usuários apresentaram pontuação significativamente menor quanto à depressão. Os resultados das escalas de impulsividade e ansiedade não apresentaram diferenças significativas entre os dois grupos. Os padrões de uso de "êxtase" dos usuários entrevistados são semelhantes aos padrões descritos por pesquisas realizadas na Europa e em Sidney: a maioria dos usuários consome um ou dois comprimidos a cada episódio de uso, apenas nos finais de semana ou férias, mais freqüentemente na companhia de várias pessoas, em ambientes ligados ao lazer noturno, como lugares para dançar, "raves" e festas. Os comprimidos são geralmente adquiridos de amigos ou conhecidos nesses locais. A maioria dos usuários associa "êxtase" a outras drogas psicotrópicas, particularmente maconha. As características sócio-demográficas dos usuários entrevistados e seus padrões de aquisição e consumo de "êxtase" indicam um caráter pouco marginal do uso. São sugeridas estratégias de Redução de Dano caso o uso de "êxtase" se difunda em São Paulo.The present study was aimed at identifying patterns of ecstasy (MDMA) use in the city of São Paulo. Ecstasy users were recruited through the snowball technique. Using the same technique, a control group of subjects that had never tried the drug (non users) was recruited among individuals sharing with users a similar life style. Users (N=52) and non users (N=52) were interviewed in order to obtain socio-demographic data and data on use of psychoactive drugs; users were also questionned as to the circumstances surrounding their use of the drug. Besides, levels of anxiety, depression and impulsiveness were assessed through Spielberger's IDATE Trace Inventory, Beck's Depression Inventory and Barratt Impulsiveness Scale. Both users and non users revealed similar socio-demographic characteristics: most subjects were middle class young heterosexual single men and women who had a college degree. Multiple drug use was more frequent among users than among non users. Other features that were significantly more accentuated among users than among non users were the presence of tattoos and piercings, the frequency to raves and the preference for electronic music. Beck Inventory results pointed to significantly lower depression scores among users. No differences were observed between groups in anxiety and impulsiveness scores. Ecstasy consumption patterns among users are similar to those reported in Europe and Australia: most subjects take one or two pills per episode, during weekends or vacations, usually with company and in social gatherings such as dancings, raves and parties. The drug is predominantly acquired from friends or acquaintances in these same spots. Most users reported consuming ecstasy in combination with other psychoactive drugs, particularly marihuana. The socio-demographic features of users as well as the way they buy and consume the drug suggest that the present pattern of use is not connected to illegal or marginal activities. Harm reduction strategies are suggested in case of ecstasy's use increases and spreads among the young population of the city.
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Marais, Lelanie. "The potential of exercise to reverse stress induced abnormalities in the rat brain." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/3188.
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Thesis (PhD (Biomedical Sciences. Medical Physiology.))--University of Stellenbosch, 2010.ENGLISH ABSTRACT: Adverse experiences during early life causes alterations in the development of the central nervous system structures that may result in abnormal functioning of the brain. It is well known that, in humans, adverse early-life experiences such as social separation, deprivation, maternal neglect and abuse increase the risk of developing psychiatric disorders, such as depression, later in life. We used maternal separation in the rat as a model for early life stress to firstly determine how different brain systems are dysregulated by this stressful experience and additional chronic or acute stress during adulthood. Rat pups were separated from their mothers on postnatal day 2-14 for 3 hours per day while control rats were normally reared. The behavior, stress response, neurotrophin, apoptotic marker and serotonin levels in the ventral hippocampus, striatum and frontal cortex were measured during adulthood. A different group of maternally separated rats were allowed chronic voluntary exercise and similar measurements were done to determine whether exercise was able to normalize the deficits caused by early life stress. Differentially expressed cytosolic proteins of the ventral hippocampus of maternally separated rats versus normally reared rats were also identified. Protein expression levels of maternally separated rats that received chronic voluntary exercise or escitalopram treatment were subsequently determined to unravel the mechanism of therapeutic action for these two interventions. We found that maternal separation increased the baseline corticosterone response of rats and induced a blunted adrenocorticotropin hormone after acute restraint stress. Baseline neurotrophin levels were significantly decreased in the ventral hippocampus. Maternal separation followed by chronic restraint stress during adulthood resulted in increased depressive-like behavior compared to control rats. Maternal separation alone or followed by acute restraint stress during adulthood induced changes in apoptotic marker expression in the striatum and frontal cortex. In rats subjected to maternal separation and chronic restraint stress during adulthood, we found that chronic voluntary exercise decreased their depressive-like behavior and increased brain derived neurotrophin levels in the striatum. Serotonin levels were not affected by maternal separation, but chronic voluntary exercise increased serotonin in the ventral hippocampus of normally reared rats. Maternal separation induced a number of changes in the expression of cytosolic proteins and these stress-induced changes were identified in proteins relating to cytoskeletal structure, neuroplasticity, oxidative stress, energy metabolism, protein metabolism, and cell signaling. Chronic voluntary exercise was able to restore the expression levels of a number of proteins affected by maternal separation that increased the risk for neuronal death. When comparing the efficacy of exercise to that of escitalopram treatment it was evident that, in contrast to exercise, escitalopram targets a different subset of proteins affected by maternal separation, except for a few involved in energy metabolism pathways and neuroprotection. In this study we have shown that chronic voluntary exercise has therapeutic effects in maternally separated rats, decreasing depressive-like behavior, increasing neurotrophin expression and restoring cytosolic protein expression that were dysregulated by early life stress.
AFRIKAANSE OPSOMMING: Negatiewe stresvolle ervarings gedurende die vroeë stadium van ‘n mens se lewe veroorsaak veranderinge in die ontwikkeling van breinstrukture en het ‘n nadelige uitwerking op die funksionering van die brein. Dit is bekend dat stresvolle ervarings in kinders, byvoorbeeld sosiale afsondering, verwaarlosing en mishandeling, die risiko vir die ontwikkeling van psigiatriese steurings soos depressie gedurende volwassenheid kan verhoog. In hierdie studie gebruik ons moederlike skeiding van neonatale rotte as ‘n model vir vroeë lewensstres om te bepaal hoe dit verskillende sisteme in die brein negatief beinvloed, en dan ook die effek van addisionele kroniese of akute stres gedurende volwassenheid. Die neonatale rotte is weggeneem van hulle moeders af vanaf dag 2 tot 14 vir 3 ure elke dag terwyl kontrole rotte by hulle moeders gebly het. Die gedrag, stres respons, neurotrofiene, apoptotiese merkers en serotonien vlakke is gemeet in die ventrale hippokampus, frontale korteks en striatum gedurende volwassenheid. Rotte wat van hulle moeders geskei is, is dan toegelaat om vir ses weke in wiele te hardloop om te bepaal of kroniese vrywillige oefening die negatiewe effekte wat veroorsaak is deur stres kan ophef. ‘n Bepaling van sitosoliese proteien uitdrukking in die ventrale hippokampus is ook gedoen om die uitwerking van moederlike skeiding op proteienvlak vas te stel. Hierdie protein data is dan vergelyk met die van gestresde rotte wat kroniese oefening of escitalopram behandeling ontvang het om die meganisme van werking van beide behandelings te bepaal. Ons het gevind dat moederlike skeiding die rustende kortikosteroon vlakke van rotte verhoog terwyl dit adrenokortikotropien vlakke na akute stres inhibeer. Moederlike skeiding het ook die neurotrofien vlakke in die ventrale hippokampus verlaag en addisionele kroniese stres gedurende volwassenheid het ‘n verhoging in depressie-agtige gedrag veroorsaak. Moederlike skeiding alleen, sowel as gevolg deur akute stress gedurende volwassenheid het ook veranderinge in die uitdrukking van apoptotiese merkers in die striatum en frontale korteks veroorsaak. Kroniese vrywillige oefening na moederlike skeiding en addisionele stres gedurende volwassenheid kon depressie-agtige gedrag verlaag en neurotrofienvlakke in die striatum verhoog. Serotonien vlakke was nie beinvloed deur moederlike skeiding nie, maar oefening in kontrole rotte het serotonien verhoog in die ventrale hippokampus. Moederlike skeiding het heelwat veranderinge in die uitdrukking van sitosoliese proteiene van die ventrale hippokampus veroorsaak wat ingedeel kan word in die volgende funksionele kategorieë: sitoskelet, neuroplastisiteit, oksidatiewe stres, energiemetabolisme, proteinmetabolisme en seintransduksie. Oefening kon die uitdrukking van verskeie stres-geïnduseerde veranderinge in proteiene weer herstel terwyl dit wou bleik asof escitalopram se meganisme van werking op ‘n ander vlak geskied. Ons bevindinge bewys dat kroniese vrywillige oefening ‘n goeie behandeling is na vroeë lewenstres en dat dit depressiewe gedrag verminder, neurotrofien vlakke verhoog en sitosoliese proteien skeiding alleen, sowel as gevolg deur akute stress gedurende volwassenheid het ook veranderinge in die uitdrukking van apoptotiese merkers in die striatum en frontale korteks veroorsaak. Kroniese vrywillige oefening na moederlike skeiding en addisionele stres gedurende volwassenheid kon depressie-agtige gedrag verlaag en neurotrofienvlakke in die striatum verhoog. Serotonien vlakke was nie beinvloed deur moederlike skeiding nie, maar oefening in kontrole rotte het serotonien verhoog in die ventrale hippokampus. Moederlike skeiding het heelwat veranderinge in die uitdrukking van sitosoliese proteiene van die ventrale hippokampus veroorsaak wat ingedeel kan word in die volgende funksionele kategorieë: sitoskelet, neuroplastisiteit, oksidatiewe stres, energiemetabolisme, proteinmetabolisme en seintransduksie. Oefening kon die uitdrukking van verskeie stres-geïnduseerde veranderinge in proteiene weer herstel terwyl dit wou bleik asof escitalopram se meganisme van werking op ‘n ander vlak geskied. Ons bevindinge bewys dat kroniese vrywillige oefening ‘n goeie behandeling is na vroeë lewenstres en dat dit depressiewe gedrag verminder, neurotrofien vlakke verhoog en sitosoliese proteien vlakke kan herstel.
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Schroeder, Frederick Albert. "A Role for Histone Modification in the Mechanism of Action of Antidepressant and Stimulant Drugs: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/370.
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Depression and stimulant drug addiction each result in massive losses of health, productivity and human lives every year. Despite decades of research, current treatment regimes for depression are ineffective in approximately half of all patients. Therapy available to stimulant drug addicts is largely ineffective and moreover, dedicated treatments for drug dependence (including abuse of cocaine) are non-existent. Thus, there is a pressing need to further understanding of the molecular mechanisms underlying these disorders in order to develop novel, targeted therapeutic strategies.
Chromatin remodeling, including changes in histone acetylation, has been proposed to play a role in both the etiology and treatment of depression and stimulant abuse. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) regulate numerous cellular processes, including transcription, cell cycle progression and differentiation. Moreover, histone acetylation has been shown to regulate hippocampal neurogenesis, a cellular response associated with the pathogenesis and treatment of depression and stimulant abuse (Hsieh et al., 2004, Yamaguchi et al., 2004, Fischer et al., 2007). Ultimately, such basic cellular processes impact higher order function, namely cognition and emotion.
Indeed, recent studies suggest that HDAC activity in selected forebrain regions, including ventral striatum and hippocampus, modulate stimulant- and antidepressantinduced behavior (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). These reports highlight an association between chromatin remodeling and diverse behavioral changes, including changes induced by the pleiotropic HDAC inhibitor, sodium butyrate (SB), (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). However, behavioral, brain-metabolic and molecular effects of SB treatment in the context of rodent models of depression, dopaminergic sensitization and repeated cocaine administration remained unclear.
The work described in this thesis illustrates the potential for chromatin modifying drugs in mechanisms underlying the experimental pharmacology of depression and stimulant addiction. Specifically, the data presented here support the view that treatment with the short chain fatty acid, sodium butyrate enhances: (1) antidepressant-like behavioral effects of the selective serotonin reuptake inhibitor (SSRI), fluoxetine (2) locomotor sensitization induced by repeated administration of the dopamine D1/D5 receptor agonist SKF82958; and(3) brain metabolic activation upon repeated cocaine administration as evidenced by fMRI in awake rats.
Furthermore, this report provides evidence that these treatment paradigms will result in chromatin modification changes associated with active transcription, in addition to increased mRNA levels of plasticity-associated genes, including brain-derived neurotrophic factor (BDNF) at key brain regions implicated in the pathogenesis of depression and stimulant addiction.
To date, little is known regarding the underlying mechanisms of action mediating the enhancing effects of sodium butyrate on the various antidepressant- and stimulantrelated paradigms. Our findings underscore the potential of chromatin-modifying drugs to profoundly affect the behavioral response of an animal to antidepressant and stimulant drugs and warrants consideration in the context of developing novel therapeutic strategies.
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GALET, PATRICK. "Peut-on se faire du mauvais sang ou contribution a une revue de la litterature sur la neuro-immunomodulation et la psycho-immunologie." Toulouse 3, 1988. http://www.theses.fr/1988TOU31049.
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Solomon, Thomas. "Central nervous system infections in Vietnam." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340736.
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Zhang, Hui. "Remyelination in the central nervous system." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8095.
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Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhance remyelination. The aim of this thesis was to first characterize a fast and reliable model to study CNS remyelination in vitro, and second to investigate the role of semaphorin 3a (Sema3A) and semaphorin 3f (Sema3F) signaling in CNS remyelination. Various in vivo models have been developed to investigate the pathology of multiple sclerosis, and can be used to test remyelination therapies. However, in vivo models are expensive, animal- and time- consuming. Until now, there has been no well-characterized and robust in vitro model for remyelination study. In this thesis, an ex vivo slice culture system with mouse brain and spinal cord was developed, and characterized by immunofluorescent microscopy and transmission electron microscopy, for CNS remyelination study. Automated (re)myelinating quantification by image pro plus software was developed and validated to provide a fast and reliable way for testing factors that change remyelination efficiency. Two such factors are Sema3A and 3F, which were initially identified as axon guidance cues during development. Sema3A (repulsive) and 3F (attractive) were proved to play a role in oligodendrocyte precursor cell (OPC) migration during development, and hypothesized to be important in remyelination. In this thesis, I investigated the effects and mechanisms for this by adding recombinant SEMA3A or SEMA3F or by knockdown their obligatory receptors Neuropilin (Nrp) 1 and 2, using lentivirus induced miRNAi. Slice culture and primary OPC culture were used to determine the effect on OPC survival, migration, proliferation, differentiation and myelination.
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Poland, Stephen D. "Central nervous system infection with human cytomegalovirus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21311.pdf.
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Hüppi, Petra Susan. "Serum antibodies to central nervous system antigens /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Bernick, Kristin Briana. "Cell biomechanics of the central nervous system." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67202.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2011.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 133-153).
Traumatic brain injury (TBI) is a significant cause of death and morbidity in both the civilian and military populations. The major causes of TBI, such as motor vehicle accidents, falls, sports concussions, and ballistic and explosive blast threats for military personnel, are well established and extensively characterized; however, there remains much to be learned about the specific mechanisms of damage leading to brain injury, especially at the cellular level. In order to understand how cells of the central nervous system (CNS) respond to mechanical insults and stimuli, a combined modeling/experimental approach was adopted. A computational framework was developed to accurately model how cells deform under various macroscopically imposed loading conditions. In addition, in vitro (cell culture) models were established to investigate damage responses to biologically relevant mechanical insults. In order to develop computational models of cell response to mechanical loading, it is essential to have accurate material properties for all cells of interest. In this work, the mechanical responses of neurons and astrocytes were quantified using atomic force microscopy (AFM) at three different loading rates and under relaxation to enable characterization of both the elastic and viscous components of the cell response. AFM data were used to calibrate an eight-parameter rheological model implemented in the framework of a commercial finite element package (Abaqus). Model parameters fit to the measured responses of neurons and astrocytes provide a quantitative measure of homogenized nonlinear viscoelastic properties for each cell type. In order to ensure that the measured responses could be considered representative of cell populations in their physiological environment, cells were also grown and tested on substrates of various stiffness, with the softest substrate mimicking the stiffness of brain tissue. Results of this study showed both the morphology and measured force response of astrocytes to be significantly affected by the stiffness of their substrate, with cells becoming increasingly rounded on soft substrates. Results of simulations suggested that changes in cell morphology were able to account for the observed changes in AFM force response, without significant changes to the cell material properties. In contrast, no significant changes in cell morphology were observed for neurons. These results highlight the importance of growing cells in a biologically relevant environment when studying mechanically mediated responses, such as TBI. To address this requirement, we developed two model systems with CNS cells grown in soft, 3D gels to investigate damage arising from dynamic compressive loading and from a shock pressure wave. These damage protocols, coupled with the single cell computational models, provide a new tool set for characterizing damage mechanisms in CNS cells and for studying TBI in highly controllable in vitro conditions.
by Kristin Briana Bernick.
Ph.D.
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Coutinho, Maria Ester Freitas Barbosa Pereira. "Central nervous system autoimmunity in neuropsychiatric disorders." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3.
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The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment has hardly been considered. To study the relationship between maternal antibodies towards neuronal surface proteins and neurodevelopmental disorders in the foetus a dual approach was undertaken. First, pregnancy serum samples from mothers of children later diagnosed with a neurodevelopmental disorder and from mothers of children with typical development were screened for the presence of neuronal surface antibodies. Next, the effects of pathogenic neuronal surface antibodies in the offspring were assessed in a maternal-to-foetal transfer mouse model. Antibodies to neuronal surface proteins in the gestational serum, particularly CASPR2 antibodies, were found to associate with an increased risk of mental retardation and disorders of psychological development in the progeny. The animal model showed that mice exposed in utero to CASPR2 antibodies have long term behavioural sequelae and histological findings suggestive of abnormalities in brain development. These findings support a model in which maternal antibodies towards foetal neuronal proteins cause long-term behavioural deficits and permanent abnormalities at the cellular and synaptic level in a subset of children with neurodevelopmental disorders.
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Suzumura, Akio. "Microglia : Immunoregulatory cells in the central nervous system." Nagoya University School of Medicine, 2002. http://hdl.handle.net/2237/5375.
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Piani, Daniela. "Immune-mediated cytotoxicity in the central nervous system /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10423.
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Lamvik, Kate K. "Central Nervous System Associations in Neurofibromatosis Type 1." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1179426618.
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Thesis (M.S.)--University of Cincinnati, 2007.Advisor: Dr. Elizabeth K. Schorry. Title from electronic thesis title page (viewed June 30, 2010). Includes abstract. Keywords: Neurofibromatosis type 1 (NF1); optic pathway glioma (OPG); central nervous system (CNS). Includes bibliographical references.
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Lee, Yong Beom. "Cytokine network in the human central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ38925.pdf.
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Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.
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Jackson, Johanna Sara. "Stem cell tracking in the central nervous system." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446551.
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Bell, Michael David. "Factors regulating inflammation in the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308694.
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Smith, Imogen. "Cannabinoid receptor signalling in the central nervous system." Thesis, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553656.
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The GPCRs CB1R and CB2R are targets for endocannabinoids, exogenous synthetic agents and phytocannabinoids derived from Cannabis plants. However, the pharmacological properties of many phytocannabinoids remain to be elucidated. The present work focused on activity of cannabinoids at CB1R, and potentially other targets, in brain membrane preparations and a cell culture model of epileptiform activity. The synthetic cannabinoids WIN55,212-2 (CB1/2R agonist) and AM251 (CB1R antagonist), and the phytocannabinoids fl9_THCV, CBO and CBG were investigated using radioligand binding and [35SjGTPyS assays to assess pharmacological actions, and patch-clamp electrophysiology to study functional effects. Radioligand competition binding assays using the CB1R antagonist [3HjSR141716A demonstrated high affinity binding of AM251 and WIN55,212-2, moderate affinity of fl9_ THCV, and weak affinity of CBO and CBG. [35SjGTPyS binding assays were used to construct concentration response curves for all compounds, and showed potent efficacious agonism by WIN55,212-2, whilst fl9_THCV, CBO, and CBG showed no agonist activity. AM251 and fl9_ THCV were used in Schild analyses, and demonstrated potent antagonism of CB1R at submicromolar concentrations. At higher concentrations, AM251 and fl9_THCV caused depression of [35SjGTPyS binding. For AM251, but not fl9_THCV, further investigations demonstrated an adenosine Al receptor component of this depression. To enable functional studies, a novel cell culture model of Mg2+-free pre-treatment induced epileptiform activity in mouse cortical neurones was successfully developed. In electrophysiological investigations WIN55,212-2 and fl9 -THCV reduced action potential firing in epileptiform neurones. The effects of WIN55,212 were blocked by AM251, suggesting a CB1R-mediated mechanism. fl9_THCV, CBG and AM251 reduced peak action potential amplitude, potentially via a non-CBR mechanism. Further investigations showed fl9_THCV and CBG reduced peak Na+ conductance suggesting functional, potentially therapeutic, effects via voltage-gated Na+ channels. These data demonstrate novel forms of cannabinoid signalling in the CNS, show that phytocannabinoids have a range of CBR affinities, and may have additional targets in the CNS.
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Sussman, Jonathan David. "Glial lineages in the adult central nervous system." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625026.
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McQuaid, Stephen. "Measles virus infection of the central nervous system." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287361.
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Davies, M. "5-hydroxytryptamine receptors in the central nervous system." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382505.
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Panni, Moeen. "Neuron-target interactions in the central nervous system." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337889.
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Staley, Kristina. "Targeting gene expression to the central nervous system." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319537.
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Galtrey, Clare Margaret. "Central nervous system plasticity and peripheral nerve repair." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614254.
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Roberts, Malcolm Ian. "Death receptor 3 in the central nervous system." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615645.
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Rist, Julia Maria. "Rejuvenating remyelination in the ageing central nervous system." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608517.
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Almeida, Rafael. "Axon-glia interactions during central nervous system myelination." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21038.
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Myelination drastically speeds up action potential propagation along axons, which is fundamental for the correct function of neuronal circuits. However, axon-oligodendrocyte interactions regulating the onset of myelin formation remain unclear. I sought to determine how reticulospinal axons control myelination, as they are the first myelinated in the zebrafish spinal cord. I genetically manipulated zebrafish in order to either remove such axons from a region of the spinal cord, or to increase their number, and characterized oligodendrocyte-lineage cells following this axonal loss- or gain-of-function. In kinesin-binding protein (kbp) mutants, reticulospinal hindbrain neurons start axonogenesis but axons fail to grow along the entire spinal cord as in wildtype, providing an axon-deficient posterior spinal cord and an intact anterior region. I found that early stages of oligodendrocyte development, such as the specification of oligodendrocyte precursors, their distribution and migration were not affected in the posterior spinal cord of these mutants. However, both the proliferation and the survival of late precursors were impaired, resulting in a significant reduction of mature oligodendrocytes in the posterior region of mutants at the onset of myelination. Since the anterior spinal cord of mutants is indistinguishable from wildtype, these results demonstrate that reticulospinal axons provide a mitogenic and a survival signal to a subset of developing OPCs, enabling their differentiation and lineage progression. I then found that the absence of reticulospinal axons did not affect the timing of oligodendrocyte differentiation, which matured on time, suggesting that this follows an intrinsic timer, as previous studies suggested. Oligodendrocytes also did not myelinate incorrect axonal targets, but instead adapted to the reduced axonal surface by elaborating fewer myelin sheaths. Additionally, oligodendrocytes made shorter sheaths, and also incorrectly ensheathed neuron somas in the mutant spinal cord, suggesting that either kbp function or a precise amount of axonal surface are required to prevent ectopic myelination of somas and to promote the longitudinal growth of myelin sheaths. In wildtype animals, the two reticulospinal Mauthner axons are the very first myelinated in the spinal cord. In animals where Notch1a function is temporarily abrogated or hoxb1 genes are temporarily upregulated, supernumerary Mauthner neurons are generated. I found that these extra axons are robustly myelinated, with no impairment of myelination of adjacent axons. Surprisingly, the number of oligodendrocytes was not altered, but I found that each individual oligodendrocyte elaborated more myelin sheaths, whose total length was also longer than in wildtypes. Additionally, dorsal oligodendrocytes, which normally myelinate only small-calibre dorsal axons, readily extended processes ventrally to myelinate the supernumerary large-calibre Mauthner axons, in addition to small-calibre axons. These results suggest that oligodendrocytes are plastic and are not destined to myelinate a particular type of axon, and conversely, that axonal signals that induce myelination are similar for different axons. The long-standing observation that oligodendrocytes tend to myelinate either few large axons or many small axons thus reflects local interactions of oligodendrocyte processes with the nearby axons, rather than different subtypes of oligodendrocytes specified by an intrinsic programme of differentiation. Collectively, this work shows that axons extensively influence both oligodendrocyte lineage progression and oligodendrocyte myelinating potential in vivo.
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Gifford, Andrew Neal. "Catecholaminergic neurotransmission in the insect central nervous system." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/15042.
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Wheeler, Natalie A. "Autotaxin in Central Nervous System Development and Disease." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4104.
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During development, oligodendrocytes (OLGs), the myelinating cells of the central nervous system (CNS), undergo a stepwise progression during which OLG progenitors, specified from neural stem/progenitor cells, differentiate into fully mature myelinating OLGs. This progression along the OLG lineage is characterized by well-synchronized changes in morphology and gene expression patterns. The studies presented in this dissertation identified the extracellular factor Autotaxin (ATX) as a novel upstream signal modulating HDAC1/2 activity and gene expression in cells of the OLG lineage. Using the zebrafish as an in vivo model system, as well as rodent primary OLG cultures, this functional property of ATX was found to be mediated by its lysoPLD activity, which has been well-characterized to generate the lipid signaling molecule lysophosphatidic acid (LPA). LPA binds to Gprotein-coupled LPA receptors (LPARs) on the surface of OLGs to initiate downstream signaling events. ATX’s lysoPLD activity was found to modulate HDAC1/2 regulated gene expression during a time window coinciding with the transition from OLG progenitor to early differentiating OLG. When looking further downstream of the ATX-LPA axis, down-regulation of LPA receptor 6 (LPA6) was found to reduce the expression of OLG differentiation genes as well as the overall process network area of OLGs. Thus, LPA6 plays a role in both the gene expression and morphology changes seen in OLG differentiation. These findings prove useful for future therapeutic targets needed for demyelinating diseases of the CNS such as Multiple Sclerosis (MS), in which OLGs fail to differentiate into mature OLGs, needed for remyelination.
Additionally, white matter injury has been frequently reported in HIV+ patients. Previous studies showed that HIV-1 Tat (transactivator of transcription), a viral protein that is produced and secreted by HIV-infected cells, is a toxic factor to OLGs. We show here that Tat treatment reduces the expression of OLG differentiation genes and the overall process network area of OLGs. Additionally, Tat-treated OLGs have reduced ATX lysoPLD activity and there is a physical interaction between Tat and ATX. Together, these data strongly suggest functional implications of Tat blocking ATX’s lysoPLD activities and thus the ATX-LPA signaling axis proves to play a significant role in the development of OLGs.
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Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.
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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.
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Foster, Michelle Tranace. "Central nervous system regulation of fat cell lipid mobilization the role of the sympathetic nervous system /." restricted, 2005. http://etd.gsu.edu/theses/available/etd-11162005-154631/.
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Thesis (Ph. D.)--Georgia State University, 2005.Timothy Bartness, committee chair; Elliott Albers, Ruth Harris , Sarah Pallas, committee members. Electronic text (181 p. : ill.)) : digital, PDF file. Description based on contents viewed July 17, 2007. Includes bibliographical references (p. 148-181).
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Tep-Cullison, Chhavy R. "Distinct roles of p75 regulation on myelination in the peripheral nervous system and central nervous system." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1299179635.
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Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.
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Zhang, Xiaochun. "Involvement of neuroinflammation in models of neurodegeneration." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1663059561&sid=3&Fmt=2&clientId=18949&RQT=309&VName=PQD.
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Fundytus, Marian Elaine. "Central nervous system and peripheral signs of opioid abstinence." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56639.
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It was hypothesized that a metabolite of morphine, morphine-3-glucuronide (M3G), contributes to the expression of symptoms seen during withdrawal from morphine. To test this hypothesis, the behaviors observed during precipitated withdrawal from morphine and sufentanil were compared. Sufentanil was chosen because, like morphine, it acts primarily at the mu opioid receptor, but has different metabolites. Differences in the abstinence syndromes produced by the two drugs may therefore be attributable to the actions of metabolites, rather than the primary opioid actions of morphine and sufentanil. Although there were some differences in the occurrence of symptoms, morphine and sufentanil withdrawal were very similar. Therefore, the evidence was inconclusive as to the contribution of metabolites during withdrawal.Systemic administration of M3G alone and in combination with morphine produced no withdrawal-like behaviors. However, when these drugs were given centrally, withdrawal-like behaviors were observed in conjunction with seizures. The seizures were not attenuated by naloxone (but were alleviated by an anti-convulsant), indicating that they were not mediated by opioid receptors. The behaviors resembled those seen by previous investigators following high doses of morphine. The results suggest that M3G may play a role in the toxic effects of high doses of morphine.
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Goudreau, Guy. "Transgenic models of retrovirus-mediated central nervous system diseases." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39908.
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Neurological diseases are a common consequence of retroviral infections. The pathogenesis of these diseases however remains undetermined. In an attempt to elucidate the mechanisms involved in certain of these disorders, we have used an experimental approach involving transgenic mice. Transgenic animals provide an important tool in the study of retroviral diseases, since they allow us to circumvent the complex process of retroviral infection. In addition, when retroviral sequences are expressed under the regulation of a CNS-specific promoter, transgenic experiments allow us to evaluate the effects of expressing viral gene products in a given CNS cell population. Specific aspects of the neurological disorders caused by HIV-1, HTLV-1, and Cas-Br-E MuLV were evaluated. Transgenic mice experiments were generated in order to study the pathogenesis of the CNS white matter diseases caused by human retroviruses HIV-1 and by HTLV-1, and to evaluate the function of astroglial cells in mediating the CNS disease associated with Cas-Br-E MuLV infection. On the basis of our experimental results, we propose novel pathogenic mechanisms which may contribute to our understanding of the CNS diseases caused by these retroviruses.
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Akers, Stephen Matthew. "Modeling central nervous system involvement in acute lymphoblastic leukemia." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11227.
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Thesis (Ph. D.)--West Virginia University, 2010.Title from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Mabon, Joy. "Strategies to reduce inflammation in the central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ39851.pdf.
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Lyng, Eric E. Bottiglieri Teodoro. "Gamma Hydroxybutyrate (GHB) : mechanisms of central nervous system toxicity /." Waco, Tex. : Baylor University, 2006. http://hdl.handle.net/2104/4211.
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Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.
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Vidyadaran, Sharmili. "Neuroprotective properties of HSP27 in the central nervous system." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424392.
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Matyszak, M. K. "Immune mediated inflammatory responses in the central nervous system." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334846.
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Tran, Thi Hong Chau. "Clinical and pathological aspects of central nervous system infection." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578010.
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Central nervous system (CNS) infection remains a major cause of mortality and morbidity worlwide. This thesis focuses on the causes, prognostic markers, and pathogenesis of meningitis in adults in Viet Nam and explores the pharmacokinetic properties of fluoroquinolones in the treatment of tuberculous meningitis (TBM). Chapter One provides an introduction to infections of the CNS in Viet Nam. Chapter Two describes the clinical studies of CNS infections at the Hospital for Tropical Diseases in Viet Nam which underpin this thesis. Mycobacterium tuberculosis is the most common cause of CNS infections with the three commonest causes of acute pyogenic meningitis Streptococcus suis, Streptococcus pneumoniae and Neisseria meningitidis. In Chapter Three, I report on a study of the pathogenesis of meningitis and encephalitis in particular the role for Metalloproteinase/Tissue Inhibitor of Metalloproteinase. One of the most challenging situations is to distinguish partially treated pyogenic meningitis from TBM and viral meningitis and encephalitis. I identified two major clinical factors that can help distinguish TBM from pyogenic meningitis- gingivo-herpes and deafness are very much more common in pyogenic meningitis than in TBM (Odds Ratio 32). In Chapter Four, I develop a clinical aligorithm and in Chapter Five, a prognostic system to determine which variables can be used to predict the clinical outcome.TBM remains very difficult to treat. In Chapter Six, I report the results of a pharmacokinetic study aimed to identify the optimal fluoroquinolone to be used for the treatment of TBM. My results demonstrate levofloxacin has a better pharmacokinetic profile than ciprofloxacin or gatifloxacin for the treatment of TBM.
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Ives, N. K. "Bilirubin transport and toxicity in the central nervous system." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604974.
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Ruddick, Jon Paul. "Characterisation of ABCG transporters in the central nervous system." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289547.
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