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1
Freemantle, Erika. "Brain lipids and cholesterol in neuropsychiatric disorders." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116838.
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Neuropsychiatric disorders and suicidal behaviour represent major contributions to mortality in Canada. Among the many factors associated with psychiatric disorders and suicide, alterations in lipids and cholesterol have been demonstrated both peripherally and centrally, supporting their roles as mediating variables in the underlying neuropathology. Cholesterol (CHL) regulation is a complex and dynamic system, and while animal studies also support a mediating role of CHL on brain function, efforts to determine a biological association in humans have achieved only modest gains. While mechanisms governing cholesterol regulation are not entirely understood, cholesterol is well accepted to have important impacts on a variety of brain functions from neurotransmission to synaptic plasticity and neurodegeneration, with unique contributions from neurons, astrocytes, and oligodendrocytes. Given the extensive regulatory feedback mechanisms and the implications in neurological function, determining a biological basis for the association of cholesterol with neuropsychiatric disorders remains an important area of research. This research aimed to explore the neurobiological mechanism whereby alterations in CHL may relate to neuropsychiatric phenotypes. The results presented in chapter 3 suggest, while no clear differences were found in suicide completers with major depressive disorder, expression of several CHL related genes associate more strongly with white matter CHL levels compared to grey matter, suggesting a potential contribution of SORT1, LPL, and ABCA2, in the regulation of white matter CHL. The results of chapter 4 suggest altered phospholipid levels and expression of lysosomal acid lipase A gene in violent suicides in the prefrontal cortex, which would have important consequences for inhibitory neurotransmission. The results of chapter 4 suggest an increase in 24-hydroxycholesterol in the prefrontal cortex of suicide completers and this could have implications for synapse maintenance and loss in the neuropathology of suicide. In regards to CHL levels, however, little evidence in support of alterations in CNS CHL in neuropsychiatric disorders and suicidal behaviour was noted.Les troubles neuropsychiatriques et les comportements suicidaires contribuent de façon importante au taux de mortalité au Canada. Parmi les facteurs associés aux troubles neuropsychiatriques, on retrouve des altérations lipidiques autant périphériques que centrales, ce qui supporte une implication lipidique dans les mécanismes neuropathologiques. Étant donné la complexité des mécanismes régissant le cholestérol, et malgré les études animales qui soutiennent un rôle fonctionnel dans le cerveau, les déterminants biologiques sous-jacents à une telle association chez les humains demeurent incertains. Alors que les mécanismes impliqués dans la régulation du cholestérol ne sont pas entièrement compris, on attribue au cholestérol un rôle important dans la régulation de plusieurs fonctions cérébrales telles que la neurotransmission, les modifications synaptiques, et la neurodégénération avec des contributions uniques aux neurones, astrocytes et oligodendrocytes. Compte tenu de l'étendue de ces mécanismes, de leur relation entre les différents types cellulaires et de leur implication dans les troubles neuropsychiatriques, déterminer une association biologique demeure d'une importance majeure afin de comprendre l'implication du cholestérol dans les troubles psychiatriques. Ce projet de recherche vise à explorer les mécanismes neurobiologiques et génétiques supportant une relation entre le cholestérol et différents phénotypes psychiatriques. Les résultats présentées aux chapitre 3 suggère, tandis que pas de différences distinctes ont été remarqués dans les suicidés, l'expression de plusieurs gènes liés à la CHL associer plus fortement avec les niveaux de CHL dans la substance blanche par rapport à la substance grise, ce qui suggère une contribution potentielle des SORT1 , LPL, et ABCA2, dans la régulation de CHL dans la substance blanche. Les résultats du chapitre 4 indiquent une altération des niveaux de phospholipides et l'expression du gène lipase acide lysosomale A chez le cortex préfrontal des suicides violent, qui aurait des conséquences importantes pour la neurotransmission inhibitrice. Les résultats du chapitre 4 suggèrent une augmentation de 24-hydroxycholestérol dans le cortex préfrontal des suicidés, ce qui pourrait avoir des implications pour l'entretien et la perte des synapses dans la neuropathologie de suicide. En ce qui concerne les niveaux de CHL, cependant, peu de preuves ont été constatées à l'appui des altérations de cholestérol du système nerveux central aux troubles neuropsychiatriques et aux comportements suicidaire.
2
Jaddoa, Estabraq. "Analysis of rat brain lipids and metabolites after antidepressant drug treatment." Thesis, De Montfort University, 2018. http://hdl.handle.net/2086/16575.
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Depression is a major debilitating disorder and the key aim of the current project was to investigate some of the molecular/biochemical mechanisms of antidepressant drugs with an emphasis on the relatively unexplored role of sphingolipids. For this purpose, the current study used two antidepressant drugs: the tricyclic antidepressant desipramine, and the selective serotonin re-uptake inhibitor paroxetine. The effects of the drugs in rat brain regions implicated in depression: the prefrontal cortex (PFC), hippocampus (HP) and striatum (ST) were investigated both acutely (single administration) and chronically (daily treatment for 15 days). In Chapter Three, 1H NMR spectroscopy was used to explore the metabolic response of acute and chronic administration of desipramine and paroxetine. These experiments showed significant changes in a number of water-soluble metabolites (i.e. N-acetylaspartylglutamate, glutamate, glutamine, lactate and creatine) following acute but not chronic treatment of the drugs. Sphingolipids including ceramide and its main metabolite sphingosine are key modulators of numerous cellular functions and in Chapter Four, it was shown by using liquid chromatography with mass spectrometry (LC-MS) that chronic but not acute administration of the antidepressant drugs decreased sphingosine levels in the HP and PFC but not in the ST. The effect of the drugs (e.g. paroxetine) on ceramide levels was also tested (HP only) by benzoylation of ceramide using high-performance liquid chromatography with ultraviolet detection (HPLC-UV) and in Chapter Four, it was shown that hippocampal levels of ceramide were as for sphingosine decreased by chronic paroxetine treatment. This chapter also demonstrated a highly significant correlation for the two sphingolipids in both controls and drug-treated animals. In Chapter Five , the effect of chronic paroxetine and desipramine administration was investigated on gene expression for two key enzymes of the brain sphingolipid pathway namely, acid sphingomyelinase (ASM) and acid ceramidase (AC). By using real-time quantitative polymerase chain reaction (RT-qPCR) it was shown that paroxetine and desipramine significantly reduced mRNA levels of ASM in the HP while effects in the PFC and ST did not reach significance. Similar effect was seen for desipramine but not paroxetine on mRNA levels for AC in the HP. Recent studies indicate that ceramide modifies monoaminergic neurotransmission. In Chapter Six, the effect of carmofur, a potent inhibitor of acid ceramidase (AC) was investigated on monoamine neurotransmitters levels and their corresponding metabolites in rat brain regions by using HPLC with electrochemical detection (HPLC-ECD). Carmofur significantly increased 5-HT and decreased its metabolite 5-hydroxyindole-3-acetic acid (5-HIAA) in tissue samples from the PFC, HP and ST. In contrast, carmofur failed to significantly alter brain levels of dopamine, noradrenaline and the dopamine metabolite 3, 4- dihydroxyphenylacetic acid (DOPAC). In conclusion, findings of this project are supportive of a putative role for sphingolipids in the mechanism of action by antidepressant drugs. The potential clinical significance of these findings requires further studies.
3
Apaydin, Serpil. "Effect Of Lipids On Binding Characteristics Of Opioid Receptors." Phd thesis, METU, 2005. http://etd.lib.metu.edu.tr/upload/3/12605971/index.pdf.
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Effect of lipids on binding characteristics of opioid receptors in membranes prepared from rat brain were studied. Lipid concentrations causing changes in specific binding of [3H]Endomorphin-1 (ProE1), an opioid agonist highly specific to mu-type opioid, [3H]Ile5,6deltorphin II (DIDI), an agonist ligand highly specific to delta type receptor and [3H]Naloxone (Nlx), a universal opioid receptor antagonist were determined. Inhibition of [3H]ProE1, [3H]DIDI and [3H]Nlx specific binding was also examined by homologous displacement experiments in the presence and absence of lipids. In order to understand whether the changes occurring in the specific binding is due to changes in equilibrium dissociation constant (KD) or maximum number of binding sites (Bmax), the equilibrium binding experiments were performed.
Arachidonic acid (AA) inhibited binding of both agonist and antagonist ligand in a dose dependent manner with IC50 values of 0.15, 0.1, and 0.6 mM for [3H]ProE1, [3H]DIDI and [3H]Nlx, respectively. Kd values were not affected while Bmax values decreased 38 % and 76 % for mu, and delta receptor subtypes, respectively. For [3H]Nlx, Bmax values decreased 20 and 56 % in the absence and presence of 100 mM NaCl, respectively.
Cholesteryl hemisuccinate (CHS) enhances (100 % of control) ligand binding at mu-sites however no effect was encountered at delta sites. Furthermore, CHS also enhances (50 % of control) the binding of antagonist ligand in the absence of NaCl. Bmax values were increased by 70 % for mu sites and 40% for antagonist ligand binding site. Under similar conditions Kd values were not affected.
Phosphatidic acid (PA) and phosphatidylcholine (PC) exhibited negligible effect on ligand binding. PA decreased specific binding of ProE1 and DIDI by 16 and 10 %, respectively. Specific binding of antagonist ligand Nlx decreased 11 % in the presence of NaCl whereas in the absence of NaCl specific binding is very close to control. In the presence of PC specific binding of both agonist and antagonist ligands were around control values.
In this study modulatory effect of lysophospholipids, lysophosphatidic acid and lysophosphatidylcholine on opioid binding sites were evaluated for the first time. Both lysophospholipids exhibited similar effects: decreasing specific binding in receptor subtype independent manner between 0.1 to 1 mM range. Kd values were not significantly affected, while remarkable decrease (45-75 %) in Bmax values were observed.
4
Anyakoha, Ngozi G. "Fatty acid and lipid profiles in models of neuroinflammation and mood disorders. Application of high field NMR, gas chromotography and liquid chromotography-tandem mass spectrometry to investigate the effects of atorvaststin in brain and liver lipids and explore brain lipid changes in the FSL model of depression." Thesis, University of Bradford, 2009. http://hdl.handle.net/10454/4328.
Full textAbstract:
Lipids are important for the structural and physiological functions of neuronal cell
membranes. Alterations in their lipid composition may result in membrane dysfunction
and subsequent neuronal deficits that characterise various disorders. This study
focused on profiling lipids of aged and LPS-treated rat brain and liver tissue with a view
to explore the effect of atorvastatin in neuroinflammation, and examining lipid changes
in different areas of rat brain of the Flinders Sensitive Line (FSL) rats, a genetic model
of depression.
Lipids and other analytes extracted from tissue samples were analysed with proton
nuclear magnetic resonance spectroscopy (1H-NMR), gas chromatography (GC) and
liquid chromatography-tandem mass spectroscopy (LC/ESI-MS/MS).
Changes in the lipid profiles suggested that brain and liver responded differently to
ageing and LPS-induced neuroinflammation. In the aged animals, n-3 PUFA were
reduced in the brain but were increased in the liver. However, following treatment with
LPS, these effects were not observed. Nevertheless, in both models, brain
concentration of monounsaturated fatty acids was increased while the liver was able to
maintain its monounsaturated fatty acid concentration. Atorvastatin reversed the
reduction in n-3 PUFA in the aged brain without reducing brain and liver concentration
of cholesterol. These findings further highlight alterations in lipid metabolism in agerelated
neuroinflammation and show that the anti-inflammatory actions of atorvastatin
may include a modulation of fatty acid metabolism.
When studying the FSL model, there were differences in the lipid profile of different
brain areas of FSL rats compared to Sprague-Dawley controls. In all brain areas,
arachidonic acid was increased in the FSL rats. Docosahexaenoic acid and ether lipids
were reduced, while cholesterol and sphingolipids were increased in the hypothalamus
of the FSL rats. Furthermore, total diacylglycerophospholipids were reduced in the
prefrontal cortex and hypothalamus of the FSL rats. These results show differences in
the lipid metabolism of the FSL rat brain and may be suggestive of changes occurring
in the brain tissue in depression.
5
Anyakoha, Ngozi Gloria. "Fatty acid and lipid profiles in models of neuroinflammation and mood disorders : application of high field NMR, gas chromotography and liquid chromotography-tandem mass spectrometry to investigate the effects of atorvaststin in brain and liver lipids and explore brain lipid changes in the FSL model of depression." Thesis, University of Bradford, 2009. http://hdl.handle.net/10454/4328.
Full textAbstract:
Lipids are important for the structural and physiological functions of neuronal cell membranes. Alterations in their lipid composition may result in membrane dysfunction and subsequent neuronal deficits that characterise various disorders. This study focused on profiling lipids of aged and LPS-treated rat brain and liver tissue with a view to explore the effect of atorvastatin in neuroinflammation, and examining lipid changes in different areas of rat brain of the Flinders Sensitive Line (FSL) rats, a genetic model of depression. Lipids and other analytes extracted from tissue samples were analysed with proton nuclear magnetic resonance spectroscopy (1H-NMR), gas chromatography (GC) and liquid chromatography-tandem mass spectroscopy (LC/ESI-MS/MS). Changes in the lipid profiles suggested that brain and liver responded differently to ageing and LPS-induced neuroinflammation. In the aged animals, n-3 PUFA were reduced in the brain but were increased in the liver. However, following treatment with LPS, these effects were not observed. Nevertheless, in both models, brain concentration of monounsaturated fatty acids was increased while the liver was able to maintain its monounsaturated fatty acid concentration. Atorvastatin reversed the reduction in n-3 PUFA in the aged brain without reducing brain and liver concentration of cholesterol. These findings further highlight alterations in lipid metabolism in agerelated neuroinflammation and show that the anti-inflammatory actions of atorvastatin may include a modulation of fatty acid metabolism. When studying the FSL model, there were differences in the lipid profile of different brain areas of FSL rats compared to Sprague-Dawley controls. In all brain areas, arachidonic acid was increased in the FSL rats. Docosahexaenoic acid and ether lipids were reduced, while cholesterol and sphingolipids were increased in the hypothalamus of the FSL rats. Furthermore, total diacylglycerophospholipids were reduced in the prefrontal cortex and hypothalamus of the FSL rats. These results show differences in the lipid metabolism of the FSL rat brain and may be suggestive of changes occurring in the brain tissue in depression.
6
Chang, Hsiu-Ming Samuel. "Interactions between membrane lipids and integral proteins: Effects of bilayer structure on the reconstituted calcium-activated potassium channel from rat brain." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186738.
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The plasma membrane isolates the interior of cells from the external environment. In addition to acting as an insulating barrier, it permits selective interactions across the cell membrane through the presence of membrane-integral proteins which playa major role in the regulation of the internal environment of the cell. One class of membrane-integral proteins forms channels through which solutes pass in and out of the cell. In this dissertation, the properties of one such channel--the high conductance calcium-activated potassium (BK) channel--are examined subsequent to reconstituting the channel into bilayer membranes whose structure is experimentally altered. The central theme of this dissertation is to ask whether an alteration in membrane lipids, which results in different structural properties, provides information on the regulation of membrane-integral proteins such as ion channels. It is known that the lipid composition of cell membranes changes during development and aging, during adaptation to different temperatures, and in some disease states. A better understanding of lipid-channel interactions is therefore likely to provide key information concerning cellular homeostasis. Natural and induced changes in membrane lipid composition, and hence membrane structure, alter the physico-chemical environment at the membrane--protein interface. I propose in this dissertation that changes in membrane structure are ultimately expressed as physical changes that affect ion channel behavior in predictable ways. To test the hypothesis that the lipid environment modifies channel function, I examined the properties of the BK channel reconstituted from rat brain into lipid bilayers of different compositions. The bilayer was modified with phospholipids of different headgroups (altering charge and size), or with phospholipids which have different fatty acid chains (altering the order parameter). Changing the bilayer surface charge is expected to change the concentration of ions near the channel thereby. Therefore the properties of BK channels is expected to be changed due to the interactions of calcium and potassium ions with the surface charge. Furthermore, the interaction between negatively charged lipid and calcium is known to order the lipid structure and may introduce structure stress in bilayers. This structural stress in bilayers may act on the BK channel and modify its properties. Altering the size of phospholipid headgroups and the order of fatty acid chains are likely to change the packing of lipids in the bilayer. Also, such structural alteration in lipid changes the lateral elastic and curvature stress within the bilayer. Addition of cholesterol to phospholipid bilayers is known to increase the orderliness of the fatty acid chains and increase the modulus of compressibility of the membrane, thus increasing the lipid structural stress. Adding general anesthetics into bilayers has been shown to disorder the lipid structure but also increase the lipid structural stress. These physical changes in bilayers may, in tum, act on the channel protein and altering its properties. The results showed that increasing the negatively charged lipid in the bilayer surface resulted in an increase in channel mean opentime, open probability and conductance of the BK channel. Increasing the lipid structural stress, in general, reduces channel mean opentime and open probability. In the case of cholesterol, the conductance is also reduced in addition to mean opentime and open probability. Taking together, these results suggest that the lipid environment plays a profound role in shaping ion channel properties.
7
Martigne, Patrick. "Neuropathologie radio-induite : des effets précoces aux séquelles tardives : études comportementales et métaboliques chez le rat après irradiation globale sublétale." Grenoble, 2010. http://www.theses.fr/2010GRENS012.
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Le dogme relatif à la radiorésistance du Système Nerveux Central (SNC) a vécu. Les progrès en neurosciences permettent aujourd'hui de reconsidérer les dysfonctionnements cognitifs radio-induits observés au décours des radiothérapies ou après un accident d'irradiation, et d'envisager des moyens diagnostiques et thérapeutiques adaptés. Nous avons développé un modèle Rat afin d'étudier les effets d'une irradiation gamma corps entier à dose sublétale (4,5 Gy). Celle-ci induit des troubles de l'apprentissage et de la mémorisation d'une tâche en cours d'acquisition durant le premier mois – lesquels sont prévenus par l'administration d'une molécule radioprotectrice de référence (amifostine) – tandis qu'elle ne semble pas perturber la mémoire rétrograde. Précocement, une vague apoptotique survient 5 à 9 heures après exposition dans la zone sous-ventriculaire avec, en parallèle, une neurogenèse anéantie. Deux jours après irradiation, l'étude métabolique ex vivo réalisée par RMN HRMAS (High Resolution Magic Angle Spinning) suggère la présence d'un œdème cérébral tandis que l'étude des lipides cérébraux en RMN liquide confirme l'atteinte membranaire (élévation du cholestérol et des phospholipides). Le profil lipidique se normalise ensuite tandis qu'une réaction gliale apparait. Enfin, 1 mois post-irradiation, l'élévation du GABA, neurotransmetteur inhibiteur du SNC, dans 2 structures cérébrales distinctes, s'accompagne d'une diminution de la taurine dans l'hippocampe qui persiste 6 mois. Notre modèle intégré permet ainsi de valider des biomarqueurs quantifiables en spectroscopie RMN in vivo – prochaine étape expérimentale – et de tester de nouvelles thérapeutiques radioprotectricesThe radioresistance dogma of Central Nervous System (CNS) is now obsolete. Recent progress in neuroscience allow us to reconsider the radiation-induced cognitive dysfunctions observed after radiation therapy or after a nuclear accident, and to devise appropriate diagnostic and therapeutic means. We have developed a Rat model to study the effects of total body irradiation at a sublethal dose (4. 5 Gy). This leads to impaired learning and memory of a task being acquired during the first month – which is prevented by administration of a radioprotector (amifostine) – while it does not appear to affect retrograde memory. Early, an apoptotic wave occurs in the sub-ventricular zone, 5 to 9 hours after exposure, while neurogenesis is suppressed. Two days after irradiation, the metabolic study conducted by NMR HRMAS (High Resolution Magic Angle Spinning) suggests the presence of cerebral oedema and the study of brain lipids in liquid NMR confirms the membrane damages (elevated cholesterol and phospholipids). The lipid profile is then normalized while a gliosis appears. Finally, 1 month post-irradiation, the elevation of GABA, an inhibitory neurotransmitter, in 2 separate brain structures, occurs simultaneously with a taurine decrease in the hippocampus that lasts 6 months. Our integrated model allows validating biomarkers measurable in vivo NMR spectroscopy – the next experimental stage – and testing new radiation-protective agents
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Queiroz, Michelly Pires. "Impacto da suplementação materna com ácido linoleico conjugado sobre a maturação reflexa e função cognitiva da prole de ratos." Universidade Federal da Paraíba, 2016. http://tede.biblioteca.ufpb.br:8080/handle/tede/9445.
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Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
The essential fatty acids are important lipids for formation of the central nervous system. During pregnancy and lactation the intake need is increased to further development of this system. The conjugated linoleic acid (CLA) is a fatty acid consisting of isomers of linoleic acid. The CLA is naturally produced by ruminant animals and is found in food products such as milk fat and meat of these animals. The CLA has been widely investigated because of its many beneficial health effects, however the effects of CLA on isolated CNS changes at this stage of life have not yet been investigated. This study aims to investigate the impact of maternal diet with different concentrations of CLA during pregnancy and lactation on the neonatal reflex maturation and cognitive function in rats. To this end, three groups were formed: the control group (GC) received a standard diet without added CLA; The GCLA1 group received the experimental diet containing 1% CLA and GCLA3 containing 3% CLA. After birth, the reflex responses were surveyed between 1 and 21 postnatal day, as well as the measurement of head size and body weight. At 42 days old, the animals participated in the habituation to the open field test, the second exposure occured after 7 days. For the evaluation of declarative memory, it was performed for object recognition test 3 days after the habituation test using the open field. After the test the animals were anesthetized and euthanized by cardiac puncture. The analyzes were compared by one way ANOVA test followed by the Holm Sidak test, considering significant difference for p <0.05. We used the Sigma start program for data analysis. The GCLA 1 and GCA3 showed acceleration in reflex maturation of puppies for most of the evaluated parameters. Body weight was higher compared to the control group (p <0.05). To assess the extent of the head, it can be seen that the GCLA1 and GCLA3 presented in laterolateral size measurements when compared to controls. In the anteroposterior extent GCLA1 and GCA3 shown to be lower when compared to the control group on day 1, with an increase in the perimeter evaluated in GCLA3 to compare it GCLA1 on the 7th and 21th day (p <0.05). On habituation in the open field test just wandered GCLA3 least the second open field indicating exposure to facilitating memory (p <0.05). In the long term object recognition test, a significant difference when comparing the time of exploration of familiar object to the time of operation of the new object occured in the GC, GCLA1 and GCLA3. Moreover, with respect to the explored ratio of the objects in GCLA1 there was a significant increase compared to GC and GCLA3 compared with GCLA1 (p <0.05). Maternal treatment with CLA anticipates reflex maturation, increases body weight, head size and improves responses in memory tests in the offspring of rats.
Os ácidos graxos essenciais são lipídios muito importantes para a formação do sistema nervoso central (SNC). Durante a gestação e lactação sua necessidade encontra-se aumentada para melhor desenvolvimento deste sistema. O Ácido Linoleico Conjugado (CLA) é um ácido graxo formado por isômeros de ácido linoleico. Este ácido graxo vem sendo investigado devido aos seus prováveis efeitos benéficos à saúde, porém os efeitos da mistura de CLA sobre alterações do SNC durante a fase de gestação e lactação ainda não foram investigados. Assim, este estudo tem como objetivo investigar o impacto de dieta materna com diferentes concentrações de CLA durante a gestação e lactação sobre a maturação reflexa neonatal e função cognitiva em ratos. Para tanto, foram formados 3 grupos: O Grupo Controle (GC) recebeu a dieta padrão sem adição de CLA; O Grupo GCLA1, a dieta experimental contendo 1% de CLA e o GCLA3, contendo 3% de CLA. Após o nascimento, as respostas reflexas foram avaliadas entre o 1º e 21º dia pós-natal, como também a aferição do tamanho da cabeça e o peso corporal. Aos 42 dias de vida, os animais participaram do teste de habituação ao campo aberto, sendo a segunda exposição após 7 dias. Para a avaliação da memória declarativa, foi realizado o teste de reconhecimento de objetos 7 dias após o teste de habituação, usando o campo aberto. Após os testes os animais foram anestesiados e eutanasiados por punção cardíaca. Os dados foram analisados pelo teste One Way ANOVA seguidas pelo teste de Tukey para os dados paramétricos e o teste Kruskal Wallis para os dados não paramétricos, considerando-se diferença significativa para p < 0,05. Utilizou-se o programa Sigma Start para a análise dos dados. Os GCLA 1 e GCA3 mostraram aceleração na maturação reflexa de filhotes para a maioria dos parâmetros avaliados. O peso corporal foi mais elevado em comparação com o grupo de controlo (p <0,05). Ao avaliar a medida da cabeça, podese observar que o GCLA1 e o GCLA3 apresentaram maior tamanho nas medidas laterolateral quando comparado ao controle. Já na medida anteroposterior o GCLA1 e GCLA3 mostraram-se menor quando comparado ao GC no 1º dia, havendo um aumento no perímetro avaliado no GCLA3 ao compara-lo GCLA1 no 7º e 21º dia (p<0,05). No teste de habituação no campo aberto apenas o GCLA3 deambulou menos na segunda exposição ao campo aberto indicando facilitação da memória (p<0,05). No teste de reconhecimento de objetos a longo prazo, houve diferença estatística significativa quando comparado o tempo de exploração do objeto familiar ao tempo de exploração do objeto novo nos GC, GCLA1 e GCLA3. Além disso, com relação à taxa de exploração dos objetos, no GCLA1 essa diferença foi observada quando comparado ao GC, e o GCLA3 ao GCLA1 (p<0,05). O tratamento materno com CLA antecipa maturação reflexa, aumenta o peso corporal, tamanho da cabeça e melhora respostas em testes de memória na prole de ratas.
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Fouilhé, Sam-Laï Nathalie. "Caractérisation des lipides mobiles détectés par spectroscopie RMN du proton dans un modèle de gliome intracérébral chez le rat." Université Joseph Fourier (Grenoble ; 1971-2015), 1997. http://www.theses.fr/1997GRE10279.
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L'objectif de ce travail est la caracterisation des lipides mobiles detectes par spectroscopie de resonance magnetique nucleaire (srm) du proton dans un modele de gliome intracerebral chez le rat. L'analyse par microscopie electronique et srm de toutes les fractions obtenues par fractionnement subcellulaire des tumeurs montre que des gouttelettes lipidiques sont presentes dans toutes les fractions possedant sur leur spectre la resonance des lipides mobiles. L'estimation du libre parcours moyen, a partir de la mesure du coefficient de diffusion des lipides mobiles, a permis de connaitre la taille minimale du compartiment les contenant (2,7 m) et peut correspondre a celle des gouttelettes lipidiques. La cinetique d'apparition des gouttelettes lipidiques au cours de la croissance tumorale montre une presence de celles-ci en faible nombre des les premiers jours de croissance dans le residu d'agar. Le nombre et la taille peu eleves de ces gouttelettes pourrait faire qu'aucune resonance de lipides mobiles n'est visible lors des experiences en srm in vivo au debut de la croissance tumorale. Ensuite, les zones de necrose se developpant dans la tumeur, de plus en plus de gouttelettes se forment. L'analyse lipidique de la tumeur et du tissu cerebral sain montre des differences entre ces deux tissus pour plusieurs acides gras constitutifs des triglycerides ainsi qu'une elevation des triglycerides dans le tissu tumoral. Enfin, la caracterisation des lipides s'est terminee par l'evaluation de leur degre de mobilite par la mesure in vitro du temps de relaxation t#2. Ce parametre est de l'ordre de 100 ms. Cette etude nous a permis de montrer que ce sont des gouttelettes lipidiques qui sont a l'origine de la resonance des lipides mobiles dans le modele de gliome experimental et que la presence de ces gouttelettes est correlee a la presence des plages de necrose dans la tumeur.
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Grimault, Stephan. "Détermination des propriétés du signal RMN par une approche numérique : application aux expériences de diffusion et d'imagerie fonctionnelle." Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10157.
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Ce travail etaient est centre sur l'etude et la quantification du signal rmn dans certaines conditions in vivo. Une approche numerique de type monte carlo a ete utilisee. Une premiere etude porte sur la mesure in vivo du coefficient apparent de diffusion (cad) de lipides mobiles detectes dans des tumeurs cerebrales et confines dans des micro-domaines. Le modele numerique permet d'estimer la taille des micro-domaines sur la base du cad mesure. Un diametre de 10 a 12 m a ete trouve, valeur qui concorde avec les etudes par microscopie. Une seconde etudes porte sur la quantification des effets de la desoxygenation du sang sur la baisse du cad observee experimentalement lors de l'etude de l'ischemie. Une double etude numerique et experimentale nous a permis de conclure que la desoxygenation du sang n'est pas la principale cause de la baisse du cad. L'approche numerique est basee sur un modelisation du tissu cerebral prenant en compte la diffusion des molecules d'eau, le reseau vasculaire et les gradients internes generes autour ce dernier. Une troisieme etude porte sur la quantification du contraste bold (blood oxygenation level dependent) utilise en imagerie fonctionnelle. Differents parametres lies au secteur vasculaire, a la diffusion des molecules d'eau, et a la sequence d'impulsions ont ete considere. A partir de simulations basees sur une modelisation du tissu cerebral, des equations analytiques de la vitesse de relaxation de l'aimantation transversale en fonction des differents parametres d'interets ont ete. Dans ce travail, nous avons developpe un outil numerique aidant a la quantification du signal rmn et facilement adaptable aux diverses problematiques rencontrees dans differents secteurs de la rmn (diffusion, imagerie fonctionnelle).
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Kiebish, Michael Andrew. "Mitochondrial lipidome and genome alterations in mouse brain and experimental brain tumors." Thesis, Boston College, 2008. http://hdl.handle.net/2345/27.
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Thesis advisor: Thomas N. SeyfriedMitochondria are the key regulators of the bioenergetic state of the cell. Damage to mitochondrial protein, DNA, or membrane lipids can result as the cause or affect of disease pathology. Regardless, this damage can impair mitochondrial function resulting in a decreased ability to produce ATP to support cellular viability. This thesis research examined the mitochondrial lipidome by shotgun lipidomics in different populations of C57BL/6J (B6) brain mitochondria (non-synaptic and synaptic) and correlated lipid changes to differences in electron transport chain (ETC) activities. Furthermore, a comparison was made for non-synaptic mitochondria between the B6 and the VM mouse strain. The VM strain has a 1.5% incidence of spontaneous brain tumors, which is 210 fold greater than the B6 strain. I determined that differences in the brain mitochondrial lipidome existed in the VM strain compared to the B6 strain, likely corresponding to an increased rate of spontaneous brain tumor formation. Analysis of the mitochondrial genome in the CT-2A, EPEN, VM-NM1, and VM-M3 brain tumors compared to their syngeneic controls mouse strains, C57BL/6J (B6) and VM mice, was examined to determine if mutations existed in experimental brain cancer models. No pathogenic mtDNA mutations were discovered that would likely cause a decrease in the mitochondrial functionality. A novel hypothesis was devised to examine the tumor mitochondrial lipidome to determine if quantitative or molecular species differences existed that could potentially alter the functionality of the ETC. Brain tumor mitochondria were examined from tumors grown in vivo as well as in vitro. Numerous lipid differences were found in the mitochondria of brain tumors, of which the most interesting involved the unique molecular speciation of cardiolipin. ETC activities were significantly decreased in the primary ETC complexes which contribute protons to the gradient as well as the linked complexes of brain tumor mitochondria compared to controls. Taken together, it is likely that differences in the mitochondrial lipidome of brain tumors results in severe impairment of the mitochondria’s ability to produce ATP through the ETC. This research has provided a new understanding of the role of mitochondrial lipids in brain as well as brain cancer and offers an alternative explanation for metabolic dysfunction in cancer
Thesis (PhD) — Boston College, 2008
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Helynck, Gérard. "Etude chimique et physico-chimique des proteolipides de cerveau." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13019.
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Jamieson, Elizabeth Cherry. "Human brain lipid fatty acid composition in relation to infant diet." Thesis, Connect to e-thesis, 1998. http://theses.gla.ac.uk/981/.
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Thesis (Ph.D.) - University of Glasgow, 1998.Ph.D. thesis submitted to the Faculty of Medicine, University of Glasgow, 1998. Research carried out in the Departments of Pathological Biochemistry and Child Health, Royal Hospital for Sick Children, Yorkhill NHS Trust. Includes bibliographical references. Print version also available.
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Faria, Renata Alexandra Boaventura. "Lipid profile of brain and heart from mice with chronic stress." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/9196.
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Mestrado em BioquímicaO stresse crónico é uma resposta natural, adaptativa do organismo a pressões psicológicas e físicas. O stresse crónico tem vindo a ser considerado uma séria preocupação de saúde pública, já que se encontra envolvido com o desenvolvimento de vários distúrbios fisiopatológicos. Algumas das consequências do stresse crónico já descritas incluem intolerância à glucose, inflamação, defeitos cognitivos e especialmente doenças relacionadas com o cérebro, como doenças neurodegenerativas e depressão. As alterações que ocorrem no sistema nervoso, em situações de stresse crónico, relacionam-se com o desenvolvimento de alterações ao nível do cérebro e também com alterações em funções cardíacas. Apesar de várias evidências sugerirem consequências nefastas do stresse crónico, pouco se sabe ainda sobre as suas consequências a nível biomolecular, em particular sobre o seu efeito nos lípidos celulares. Assim, o objectivo deste trabalho foi estudar o perfil fosfolipídico em condições de stresse crónico, no cérebro e no coração de ratinhos. O perfil lipídico foi avaliado usando uma abordagem lipidómica. As diferentes classes de fosfolípidos foram separadas e quantificadas. A avaliação da peroxidação lipídica foi realizada pelo método de FOX II. O extrato lipídico total foi analisado por cromatografia líquida de alta resolução acoplada a espectrometria de massa (HPLC-MS e MS/MS), permitindo a identificação da estrutura dos fosfolípidos, nomeadamente o seu grupo polar e a sua composição em ácidos gordos. Os resultados revelaram alterações nos níveis cerebrais de fosfolípidos, tendose verificado o aumento significativo das fosfatidilcolinas (PC) e uma diminuição significativa dos fosfatidilinositois (PI) e das cardiolipinas (CL). Não foram detetadas, porém, alterações significativas no perfil molecular de cada classe de fosfolípidos, excepto no perfil da classe dos ácidos fosfatídicos (PA). Os nossos resultados comprovam ainda que há a formação de hidroperóxidos da CL no cérebro em situações de stressee crónico. A oxidação da CL é um indicador da apoptose celular que pode ser associado com a morte neuronal. No coração, os nossos resultados revelaram que não existem alterações significativas do perfil fosfolipídico em situações de stresse crónico, havendo apenas alguma variação no conteúdo total das classes. Assim, concluímos que em condições de stressee crónico os fosfolípidos do cérebro são os mais afectados, havendo mesmo a formação de produtos de oxidação da cardiolipina, sugerindo a ocorrência de importantes alterações a nível mitocondrial.
Chronic stress is a natural adaptive response to psychological and physical pressures. Chronic stress has been considered a serious public health concern since it is involved in many pathophysiological disturbances. Some of the consequences of chronic stress already described include glucose intolerance, inflammation, cognitive defects and especially diseases related with brain, such as neurodegenerative diseases and depression. The modifications that occur in the nervous system under chronic stress conditions are related with the development of alterations in the brain and also with changes in cardiac functions. Despite of some evidences suggesting adverse effects of chronic stress, little is known about the consequences at the molecular level, especially about its effects in lipids. Thus, the aim of this study was to evaluate the phospholipid profile changes in the brain and in the heart of chronic stressed mice. The lipid profile was evaluated using a lipidomic approach. The different phospholipid classes were separated and quantified. The lipid peroxidation was evaluated by FOX II assay. The total lipid extract was analysed by high performance liquid chromatography mass spectrometry (HPLC-MS and MS/MS), allowing the identification of the detailed structure of phospholipids, namely the polar head and fatty acyl composition. The results revealed changes in brain levels of phospholipids, with a significant increase in phosphatidylcholine (PC) content and a significant decrease in phosphatidylinositol (PI) and cardiolipin (CL) contents. No significant changes were observed in molecular profile of each phospholipid class, except in phosphatidic acid (PA) class. We were also able to identify CL hydroperoxides after chronic stress, which indicates that the increase in hydroperoxides content verified by FOX II method was due to the oxidation of CL. Interestingly CL oxidation is an early indicator of cell apoptosis that could be associated with neuronal death. In the heart, our results showed no significant changes in PL profile of the molecular species in chronic stress situations, having only some variation in the total content of the classes. Therefore, we conclude in chronic stress conditions brain phospholipids are the most affected, having the formation of CL oxidation products, suggesting the occurrence of important changes in mitochondria.
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Lassman, Daniel James. "Gut-Brain Signalling in Man: The Roles of Lipid, Cholecystokinin and Ghrelin." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492929.
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Ingested lipid releases the gut peptide cholecystokinin (CCK) which limits food intake by modulating gut function and signalling to the brain. Current understanding of this pathway and its interaction with other gut-brain signalling peptides such as ghrelin is incomplete. To clarify the roles of lipid, CCK and ghrelin in gut-brain signalling pathway in man, a series of human studies were performed in order to answer the following questions.
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Singh, Gulzar. "The measurements of indicators of oxidative stress in rat brain in vivo and in vitro." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298030.
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Lalonde, Daphnee. "Modulation of lipid homeostasis during synaptic remodelling and plasticity in response to brain injury." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107773.
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This study investigated the effect of an entorhinal cortex lesion (ECL) on the expression of key cholesterol homeostasis genes in relation to degeneration and reinnervation of synapses in the adult rodent brain. We report that apolipoprotein E (APOE), ATP binding cassette A1 (ABCA1) and G1 (ABCG1) play a role in the reinnervation phase following brain injury which is consistent with their known function in lipid mobilisation and recycling. Furthermore, we report an involvement of ABCA7, the most recently identified AD genetic risk factor, in the degeneration phase. In a second study using the ECL model, we examined the molecular outcome and synaptic remodelling effects of pharmacologically inducing the liver X receptor (LXR): a signalling intermediate which regulates cholesterol transporters genes. Modified cholesterol transport gene expression was observed, however the treatment did not attenuate the extent of the brain injury nor the reactive sprouting response. Finally, we investigated whether the low-density lipoprotein receptor (LDLR), APOE's main receptor in the brain, plays a key function in the internalization of the cholesterol used in the assembly of new terminals and synapses in surviving neurons following brain deafferentation. The results show that LDLR-deficient mice have modified cholesterol transport gene expression following an ECL and that the deficiency confers a neuroprotective-like effect on central nervous system injury extent, leading to an increased reactive sprouting response.Taken together, these results highlight the importance of lipoprotein metabolism and the regulated control of cholesterol delivery during synaptic remodelling and terminal proliferation in adult animals. In addition, the results presented here suggest that LDLR deficiency confers a certain level of neuroprotection in the damaged brain as opposed to LXR agonists which provide little or no benefits to the deafferented hippocampus.Le but de cette recherche consiste à étudier les effets d'une lésion du cortex entorhinal (LEC) sur l'expression des gènes directement impliqués dans le transport et la mobilisation du cholestérol durant la phase de dégénérescence et la réinnervation synaptique qui s'en suit. Les résultats obtenus montrent que l'apolipoprotéine E (APOE), le transporteur ATP-binding cassette type A1 (ABCA1) et type G1 (ABCG1) jouent un rôle prépondérant dans la phase de réinnervation. De plus, nos résultats concernant l'ABCA7, le plus récent facteur génétique identifié pour la forme commune de la maladie d'Alzheimer, suggère une participation active durant la phase de dégénérescence suite à une LCE. Dans une seconde étude avec le modèle de la LCE, nous avons étudié les effets moléculaires et synaptiques résultant de l'induction pharmacologique du transport du cholestérol par l'administration d'un agoniste du « liver X receptor » (LXR). Nous avons observé une modification significative de l'expression de certains gènes impliqués dans le transport du cholestérol alors que le traitement agoniste n'a eu aucun effet notable sur la sévérité des dommages causés par la lésion expérimentale.Finalement, nous avons déterminée si le récepteur de lipoprotéine de basse densité (LDLR) est impliqué de façon ou d'une autre dans la recapture du cholestérol utilisé par les neurones en phase de synaptogénèse réactive. Les souris exprimant un LDLR cérébral non-fonctionnel exhibent une altération significative de l'expression génétique de nombreux gènes impliqués dans le transport intra– et extra-cellulaire du cholestérol. De plus, la suppression génétique du LDLR confère une sorte de neuroprotection aux cerveaux lésionés en favorisant la plasticité neuronale locale. Globalement, l'ensemble de ces résultats confirment l'importance du métabolisme des lipoprotéines et du transport actif du cholestérol dans le processus de remodelage synaptique qui caractérise la déafférentation neuronale.
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Carreño, Fernando. "Avaliação farmacocinética da quetiapina nanoencapsulada : modelo para estudo de delivery cerebral através de um nanocarreador polimérico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/149449.
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Introdução: A barreira hematoencefálica limita a penetração de compostos farmacologicamente ativos para o cérebro devido à presença de zônulas de oclusão no endotélio cerebral e a expressão de transportadores de influxo e efluxo que modulam o acesso de fármacos para o parênquima cerebral. Nanocápsulas de núcleo lipídico (LNC) tem sido estudadas como carreadores de fármacos para o tecido cerebral devido à capacidade de modulação da farmacocinética desses compostos. Entretanto, ainda pouco se sabe sobre os processos envolvidos nas alterações farmacocinéticas e na distribuição tecidual promovidas por esses transportadores. Objetivo: Pretendeu-se investigar as alterações na farmacocinética plasmática e penetração cerebral da quetiapina (QTP) nanoencapsulada em ratos Wistar. Materiais e Métodos: QLNC (1mg/mL) foram obtidas através da metodologia de nanoprecipitação e apresentaram reduzido tamanho de partícula (143 ± 6 nm), baixo indicie de polidispersão (PI < 0.1), alta eficiência de encapsulação (96%), potencial zeta negativo (-7.65 ± 0.815 mV) e pH ácido. QLNC quando visualizadas por MET apresentaram tamanho esférico, homogêneo com ausência de agregados. Os estudos in vivo desse trabalho foram aprovados pelo CEUA/UFRGS. Análise do plasma total e a utilização da microdiálise para determinação das concentrações plasmáticas e cerebrais livres foram realizadas após administração intravenosa da formulação de nanocápsulas de QTP (5 mg /kg ) (QLCN) ou do fármaco em solução (FQ) (5 mg /kg e 10 mg /kg) na presença e na ausência de 30 mg /kg de probenecida (PB), um inibidor de transportadores de membrana. Métodos validados foram utilizados para a quantificação do fármaco em diferentes matrizes. As concentrações cerebral e hepática totais foram investigadas através da técnica de homogeneizado de tecido. Além disso, a fração livre no plasma (fu) e a penetração nos eritrócitos também foi realizada. Resultados: QTP apresentou farmacocinética linear na faixa de doses investigadas, é um substrato para transportadores de efluxo na BHE. Diferenças foram observadas na fu da QTP até 2 h após administração de QLNC indicando que LNC do tipo III promove uma liberação sustentada do fármaco do carreador. QLNC não foi capaz de alterar o coeficiente de partição nos eritrócitos determinado in vitro. As concentrações cerebrais e hepáticas totais foram aumentadas após administração da formulação de nanocápsulas, porém, as concentrações cerebrais livres não foram alteradas em comparação com o QTP em solução. Após administração de PB o fator de penetração da QTP livre no cérebro foi reduzido de 1,55 ± 0.17 para 0,94 ± 0,15. Porém, essa inibição pela probenecida não teve efeito na penetração cerebral de QLNC (0,88 ± 0,21 – 0,92 ± 0.13) provavelmente devido ao fato da QTP ser carreada pela LNC e não estar disponível para interagir com transportadores. Conclusão: Considerando todos os resultados sugere-se que as LNC do tipo III carreiam a QTP através da circulação sistêmica até o parênquima cerebral.Introduction: Blood-brain barrier (BBB) hinders the delivery of therapeutics to central nervous system due to the endothelial cells tight junctions, which restrict paracellular transport of substances, and the expression of influx and efflux transporters, which modulate drugs access to the brain. Lipid-core nanocapsules (LNC) have been proposed as drug carriers to improve brain delivery by modulating drug pharmacokinetics (PK). However, little in know about this modulation process and it is not clear whether the LCN carry the drug through the BBB or increase free drug penetration due to changes in the barrier permeability. Objective: The work aimed to investigate the alterations in the model drug quetiapine (QTP) plasma PK and brain penetration following nanoencapsulation into LNC (QLNC) using microdialysis. Methods: QLNC (1 mg.mL-1) were obtained by nanoprecipitation and presented small particle size (143 ± 6 nm), low polidispersion index (PI < 0.1), high incorporation efficiency (96%), negative zeta potential (–7.65 ± 0.815 mV) and acidic pH. TEM photomicrography showed spherically shaped particles and absence of aggregation. Animal studies approved by CEUA/UFRGS. Total plasma and free plasma and brain concentrations, last two determined by microdialysis, were analyzed after QLNC (5 mg/kg) and free drug (FQ – 5 and 10 mg/gk) i.v. dosing to Wistar rats alone or following probenecid (PB), an influx transporter inhibitor, i.v. administration (30 mg/kg). Drug was quantified in all matrices by validate LC/UV methods. Total brain and liver concentration after FQ and QLNC dosing were investigated in tissues homogenate. Furthermore, QTP free fraction (fu) in plasma and erythrocyte penetration were determined. Results: QTP presented linear PK in the dose range investigated and is substrate to influx transporters at the BBB. Differences observed on QTP fu up to 2 h after QLNC dosing indicate a drug slow release in the blood stream loaded into the LNC type III nanocarrier for this period of time. The LNC did not altered QTP erythrocytes partition coefficient. Total brain and liver concentrations were increased after QLNC dosing but free brain concentrations were not altered in comparison with FQ dosing. After PB dosing, QTP brain penetration was reduced from 1.55 ± 0.17 to 0.94 ± 0.15 when FQ was administered but the inhibition of influx transporters had no effect on QLNC brain penetration (0.88 ± 0.21 to 0.92 ± 0.13) probably because QTP is loaded into the LNC and not available to interact with transporters. Conclusions: Taking together these results suggested that LNC type III carries QTP in the blood stream and delivers the drug to the brain.
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Searcy, James Lucas. "LIPID SIGNALING IN BRAIN AGING AND ALZHEIMER'S DISEASE: PHARMACOLOGICALLY TARGETING CHOLESTEROL SYNTHESIS, TRANSPORT AND METABOLISM." Lexington, Ky. : [University of Kentucky Libraries], 2009. http://hdl.handle.net/10225/1147.
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Thesis (Ph. D.)--University of Kentucky, 2009.Title from document title page (viewed on May 12, 2010). Document formatted into pages; contains: xiv, 183 p. : ill. (some col.). Includes abstract and vita. Includes bibliographical references (p. 158-177).
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Jenschke, Blaine Edward. "Chemical, color, and sensory attributes of sorghum bran-enhanced beef patties in a high oxygen environment." Texas A&M University, 2004. http://hdl.handle.net/1969.1/3348.
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Bottom rounds were shipped to the Rosenthal Meat Science and Technology Center, ground and enhanced with one of the following predetermined treatments: control; 0.4% sodium phosphates and 0.3% salt; 0.25% sorghum bran; 2.0% sorghum bran; 0.25% sorghum bran, 0.4% sodium phosphates and 0.3% salt; and 2.0% sorghum bran, 0.4% sodium phosphates, and 0.3% salt. The ground beef was formed into 226 g ground beef patties, packaged in an 80% O2 and 20% CO2 gaseous environment, and stored under retail display at 4 degrees for 0, 3, 6, or 9d. Measurements to determine rate and extent of oxidation, rate of discoloration, and sensory characteristics were taken to evaluate the effectiveness of sorghum bran.
Patties containing the highest amount of sorghum bran had the lowest TBARS values over 9 days of storage, lower a* values, greater amounts of discoloration, darker lean color, and less cook loss (P<0.05) than control patties. Patties enhanced with the highest level of sorghum bran had lower beefy/brothy and bloody flavor aromatics, higher sorghum flavor, more bitter and burnt aftertaste, and more sandy/gritty textures (P<0.05) when compared to control patties. Patties containing the low amount of sorghum had lower TBARS values (P<0.05), but similar amounts of cook loss as the control patties. Patties containing a low sorghum level, 0.4% sodium phosphates (SP) and 0.3% salt (S) had lower (P<0.05) amounts of cook loss when compared to control patties. Patties containing low amounts of sorghum were similar to control patties in terms of redness while the addition of low sorghum, SP, and S decreased (P<0.05) the degree of redness. Patties containing low amounts of sorghum bran had similar amounts of discoloration compared to control (CONT) patties. Also, these had less bloody flavor aromatics (P<0.05), but were similar in sorghum flavor aromatics and bitter taste when compared to control patties.
The addition of sorghum bran at low levels can retard oxidative rancidity in ground beef patties without causing detrimental color changes and negatively affecting sensory attributes, while patties enhanced with 2% sorghum bran have extensive discoloration and undesirable sensory attributes.
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Klusavičiūtė, Kristina. "Sunkiųjų metalų poveikio metalotioneinų sintezei ir lipidų peroksidacijai laboratorinių pelių organuose įvertinimas." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2012. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2012~D_20120612_162632-64837.
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Atlikto darbo tikslas buvo įvertinti kadmio, nikelio bei cinko jonų poveikį metalotioneinų sintezės intensyvumui ir lipidų peroksidacijai laboratorinių pelių organuose – kepenyse ir smegenyse. Šiam tikslui įgyvendinti buvo iškelti uždaviniai: nustatyti metalotioneinų koncentraciją pelių smegenyse ir kepenyse po vienkartinio (24 val.) ir kartotinio (14 dienų) kadmio ir nikelio jonų poveikio; įvertinti ūmų vienkartinį (24 val.) ir kartotinį (14 dienų) kadmio ir nikelio jonų poveikį lipidų peroksidacijai pelių smegenyse ir kepenyse; įvertinti cinko jonų gebą apsaugoti smegenų ir kepenų antioksidacinę sistemą esant toksiniam kadmio ir nikelio jonų poveikiui.
Eksperimentams atlikti naudotos baltosios beveislės laboratorinės pelės. Metalotioneinų koncentracija nustatatyta pagal Peixoto ir bendraautorių, o malondialdehido – pagal Uchiyama ir bendraautorių pasiūlytas metodikas.
Tyrimo rezultatai parodė, kad tiek kadmio, tiek ir nikelio jonai pelių kepenyse metalotioneinų koncentracijos padidėjimą sukėlė ir po vienkartinio 24 val., ir po kartotinio 14 dienų šių jonų poveikio, o smegenyse – tik praėjus 24 valandoms po kadmio ar nikelio jonų poveikio. Cinko jonai veikdami kartu su kadmio jonais statistiškai reikšmingą metalotioneinų koncentracijos padidėjimą sukėlė smegenyse po 14 dienų šių jonų kompleksinio poveikio. Cinko jonams veikiant kartu su nikelio jonais, statistiškai reikšmingas metalotioneinų koncentracijos padidėjimas taip pat nustatytas smegenyse po 14 dienų šių jonų... [toliau žr. visą tekstą]The aim of the work was to evaluate the influance of cadmium, nickel and zinc ions on metallothionein synthesis and lipid peroxidation intensity in mice organs – the liver and brain. The tasks of the work were: to determine the concentration of MT in mice brain and liver after both acute (24 hours) and repeated (14 days) influence of cadmium and nickel ions, to evaluate the acute (24 hours) and repeated (14 days) effects of cadmium and nickel ions on lipid peroxidation in mouse brain and liver and to evaluate the ability of zinc ion to protect the brain and liver antioxidant system from the toxicity of cadmium and nickel ions. We used white laboratory mice in our experiments. MT concentration was established according to Peixot and contributors proposed method and MDA concentration – according to Uchiyama and contributors proposed method. The results have shown that both cadmium and nickel ions increased metallothionein concentration in the liver of mice after a single (24 hours) and after repeated (14 days) exposure of these ions. The increased metallothionein concentration in the brain was established only 24 hours after cadmium or nickel ions exposure. Zinc ions in cooperation with the cadmium ions a statistically significant increase of metallothionein levels caused in the brain 14 days after the complex effects of these ions. Zinc ions, acting with the nickel ions, a statistically significant increase of metallothionein concentration caused as well in the brain after 14... [to full text]
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Aguas-Hernandez, Raymundo Antonio. "Brain lipid binding protein expression in remyelinating Schwann cells of the spinal cord in multiple sclerosis." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54693.
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Myelin is important for axon maintenance and survival, as well as for saltatory conduction of nerve impulses. Consequently, loss of myelin after spinal cord injury or in demyelinating diseases such as Multiple Sclerosis (MS) results in dysfunction of nerve impulse propagation and progressive axonal damage and cell death.
Endogenous remyelination can occur in response to MS and is mainly mediated by oligodendrocyte precursor cell-derived oligodendrocytes, but Schwann cells (SCs) can also participate. SC remyelination has been documented in spinal cord lesions following traumatic spinal cord injury in humans, and in animal models of demyelination such as lysolecithin-induced demyelination, but endogenous remyelination by SCs in the context of MS has not been as well studied.
In the present study we used immuno-fluorescent detection to analyze the expression of brain lipid binding protein (BLBP) and peripheral myelin protein zero (P0) in MS and non-MS human spinal cord as well as in the lysolecithin-demyelinated mouse spinal cord. BLBP (also known as Fatty Acid Binding Protein 7) is a nervous system-specific fatty acid binding protein. In the context of the present study, BLBP is important because it has been previously used to identify spinal cord radial glia (RG) in the developing and adult mouse spinal cord. BLBP is also expressed by SC precursors, and by immature SCs before they differentiate into myelinating SCs. We investigated whether, like the mouse spinal cord, the aged human spinal cord preserves a population of BLBP+ spinal cord RG. We found that (1) in contrast to the mouse spinal cord RG, human spinal cord RG do not express BLBP; (2) unlike the mouse, some subpopulations human myelinating SCs express BLBP in the PNS of MS (and some non-MS) cases; (3) in the MS spinal cord, BLBP-positive SCs extensively myelinate axons in large GFAP-rich areas; (4) and that BLBP is more readily detected in uncompacted myelin sheaths.
Collectively these data provide evidence of robust SC remyelination in the human spinal cord beyond what has been previously reported, and highlight BLBP as a developmentally regulated protein whose expression is significantly different between mouse and human spinal cord RG and SCsMedicine, Faculty of
Graduate
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Augustin, Livia S. A. "The effect of wheat bran particle size and wheat protein on serum lipids and colonic health." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0014/MQ40821.pdf.
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Lalovic, Aleksandra. "The relationship between lipid metabolism and suicidal behaviour : clinical and molecular studies." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103207.
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Suicide continues to claim hundreds of thousands of lives worldwide each year, in spite of the significant progress of research efforts aimed at understanding the complexity of this tragic behaviour. Data accumulated over the last decades suggest a certain biological predisposition to suicidal behaviour. Among the possible biological risk factors, cholesterol has frequently been cited. Several lines of evidence support the relationship between altered lipid metabolism, particularly low levels of serum cholesterol, and suicidal behaviour, yet the possible mechanisms governing the relationship remain to be elucidated. Three separate strategies were employed in order to explore the link between lipid metabolism and suicidal behaviour, each one from a novel perspective on this issue. The first approach aimed to substantiate the existing evidence of an association between low serum cholesterol and suicidality by examining psychiatric data, suicidality and related behavioural characteristics in a sample of Smith-Lemli-Opitz syndrome heterozygotes---a clinically normal population with altered cholesterol metabolism due to an inherited partial deficiency in the 7-dehydrocholesterol reductase enzyme---compared with controls. The second approach consisted in measuring the lipid profile in brain tissue from suicide completers, in order to address whether there are alterations in cholesterol and/or fatty acids in the brain. The final approach involved the use of exploratory gene expression studies to identify novel candidate genes and proteins that may be involved in mediating the link between lipid metabolism and suicidality. The results of these studies will be presented and discussed.
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Asaro, Antonino [Verfasser]. "The effect of apolipoprotein E isoforms and sortilin in brain lipid homeostasis and Alzheimer’s disease / Antonino Asaro." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1200409736/34.
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Hurley, Johannah. "Lipid composition and modulation of transport function in an in vitro model of the blood-brain barrier." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268437.
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Miller, Katherine. "Genetic susceptibility in Alzheimer's Disease and the role of lipid metabolism." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1164830757.
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Thesis (Ph. D.)--Case Western Reserve University, 2006.[School of Medicine] Department of Epidemiology and Biostatistics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
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Cebak, John. "MITOCHONDRIAL AND NEUROPROTECTIVE EFFECTS OF PHENELZINE RELATED TO SCAVENGING OF NEUROTOXIC LIPID PEROXIDATION PRODUCTS." UKnowledge, 2015. http://uknowledge.uky.edu/neurobio_etds/12.
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Lipid peroxidation is a key contributor to the pathophysiology of traumatic brain injury (TBI). Traditional antioxidant therapies are intended to scavenge the free radicals responsible for either the initiation or propagation of lipid peroxidation (LP). However, targeting free radicals after TBI is difficult as they rapidly react with other cellular macromolecules, and thus has a limited post-injury time window in which they may be intercepted by a radical scavenging agent. In contrast, our laboratory has begun testing an antioxidant approach that scavenges the final stages of LP i.e. formation of carbonyl-containing breakdown products. By scavenging breakdown products such as the highly reactive and neurotoxic aldehydes (often referred to as “carbonyls”) 4-hydroxynonenal (4-HNE) and acrolein (ACR), we are able to prevent the covalent modification of cellular proteins that are largely responsible for posttraumatic neurodegeneration. Without intervention, carbonyl additions render cellular proteins non-functional which initiates the loss of ionic homeostasis, mitochondrial failure, and subsequent neuronal death. Phenelzine (PZ) is an FDA-approved monoamine oxidase (MAO) inhibitor traditionally used for the treatment of depression. Phenelzine also possesses a hydrazine functional group capable of covalently binding neurotoxic carbonyls. The hypothesis of this dissertation is that carbonyl scavenging with PZ will exert an antioxidant neuroprotective effect in the traumatically injured rat brain mechanistically related to PZ’s hydrazine moiety reacting with the lipid peroxidation (LP)-derived reactive aldehydes 4-hydroxynonenal (4-HNE) and acrolein (ACR). Data from our ex vivo experiments demonstrate that the exogenous application of 4-HNE or ACR significantly reduced respiratory function and increased markers of oxidative damage in isolated non-injured rat cortical mitochondria, whereas PZ pre-treatment significantly prevented mitochondrial dysfunction and oxidative modification of mitochondrial proteins in a concentration-related manner. Additionally, PZ’s neuroprotective scavenging mechanism was confirmed to require the presence of a hydrazine moiety based on experiments with a structurally similar MAO inhibitor, pargyline, which lacks the hydrazine group and did not protect the isolated mitochondria from 4-HNE and ACR. Our in vivo work demonstrates that subcutaneous injections of PZ following TBI in the rat are able to significantly protect brain mitochondrial respiratory function, decrease markers of oxidative damage, protect mitochondrial calcium buffering capacity, and increase cortical tissue sparing without decreasing neuronal cytoskeletal spectrin degradation. These results confirm that PZ is capable of protecting mitochondrial function and providing neuroprotection after experimental TBI related to scavenging of neurotoxic LP degradation products.
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Haraszti, Reka A. "Engineered Exosomes for Delivery of Therapeutic siRNAs to Neurons." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/971.
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Extracellular vesicles (EVs), exosomes and microvesicles, transfer endogenous RNAs between neurons over short and long distances. We have explored EVs for siRNA delivery to brain. (1) We optimized siRNA chemical modifications and siRNA conjugation to lipids for EV-mediated delivery. (2) We developed a GMP-compatible, scalable method to manufacture active EVs in bulk. (3) We characterized lipid and protein content of EVs in detail. (4) We established how protein and lipid composition relates to siRNA delivering activity of EVs, and we reverse engineered natural exosomes (small EVs) into artificial exosomes based on these data.
We established that cholesterol-conjugated siRNAs passively associate to EV membrane and can be productively delivered to target neurons. We extensively characterized this loading process and optimized exosome-to-siRNA ratios for loading. We found that chemical stabilization of 5'-phosphate with 5'-E-vinylphosphonate and chemical stabilization of all nucleotides with 2'-O-methyl and 2'-fluoro increases the accumulation of siRNA and the level of mRNA silencing in target cells. Therefore, we recommend using fully modified siRNAs for lipid-mediated loading to EVs. Later, we identified that α-tocopherol-succinate (vitamin E) conjugation to siRNA increases productive loading to exosomes compared to originally described cholesterol.
Low EV yield has been a rate-limiting factor in preclinical development of the EV technology. We developed a scalable EV manufacturing process based on three-dimensional, xenofree culture of mesenchymal stem cells and concentration of EVs from conditioned media using tangential flow filtration. This process yields exosomes more efficient at siRNA delivery than exosomes isolated via differential ultracentrifugation from two-dimensional cultures of the same cells.
In-depth characterization of EV content is required for quality control of EV preparations as well as understanding composition–activity relationship of EVs. We have generated mass-spectrometry data on more than 3000 proteins and more than 2000 lipid species detected in exosomes (small EVs) and microvesicles (large EVs) isolated from five different producer cells: two cell lines (U87 and Huh7) and three mesenchymal stem cell types (derived from bone marrow, adipose tissue and umbilical cord Wharton’s jelly). These data represent an indispensable resource for the community. Furthermore, relating composition change to activity change of EVs isolated from cells upon serum deprivation allowed us to identify essential components of siRNA-delivering exosomes. Based on these data we reverse engineered natural exosomes into artificial exosomes consisting of dioleoyl-phosphatidylcholine, cholesterol, dilysocardiolipin, Rab7, AHSG and Desmoplakin. These artificial exosomes reproduced efficient siRNA delivery of natural exosomes both in vitro and in vivo. Artificial exosomes may facilitate manufacturing, quality control and cargo loading challenge that currently impede the therapeutic EV field.
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Kulbe, Jacqueline Renee. "NEUROPROTECTIVE STRATEGIES FOLLOWING EXPERIMENTAL TRAUMATIC BRAIN INJURY: LIPID PEROXIDATION-DERIVED ALDEHYDE SCAVENGING AND INHIBITION OF MITOCHONDRIAL PERMEABILITY TRANSITION." UKnowledge, 2019. https://uknowledge.uky.edu/neurobio_etds/22.
Full textAbstract:
Traumatic brain injury (TBI) represents a significant health crisis. To date there are no FDA-approved pharmacotherapies available to prevent the neurologic deficits caused by TBI. Following TBI, dysfunctional mitochondria generate reactive oxygen and nitrogen species, initiating lipid peroxidation (LP) and the formation of LP-derived neurotoxic aldehydes, which bind mitochondrial proteins, exacerbating dysfunction and opening of the mitochondrial permeability pore (mPTP), resulting in extrusion of mitochondrial sequestered calcium into the cytosol, and initiating a downstream cascade of calpain activation, spectrin degradation, neurodegeneration and neurologic impairment.
As central mediators of the TBI secondary injury cascade, mitochondria and LP-derived neurotoxic aldehydes make promising therapeutic targets. In fact, Cyclosporine A (CsA), an FDA-approved immunosuppressant capable of inhibiting mPTP has been shown to be neuroprotective in experimental TBI. Additionally, phenelzine (PZ), an FDA-approved non-selective irreversible monoamine oxidase inhibitor (MAOI) class antidepressant has also been shown to be neuroprotective in experimental TBI due to the presence of a hydrazine (-NH-NH2) moiety allowing for the scavenging of LP-derived neurotoxic aldehydes.
The overall goal of this dissertation is to further examine the neuroprotective effects of the mPTP inhibitor, CsA, and the LP-derived neurotoxic aldehyde scavenger, PZ, using a severe controlled cortical impact injury (CCI) model in 3-month old male Sprague-Dawley rats.
First, the effects of CsA on cortical synaptic and non-synaptic mitochondria, two heterogeneous populations, are examined. Our results indicate that compared to non-synaptic mitochondria, synaptic mitochondria sustain greater damage 24h following CCI and are protected to a greater degree by CsA.
Second, the neuroprotective effects of a novel 72h continuous subcutaneous infusion of CsA combined with PZ are compared to monotherapy. Following CCI, our results indicate that individually both CsA and PZ attenuate modification of mitochondrial proteins by LP-derived neurotoxic aldehydes, PZ is able to maintain mitochondrial respiratory control ratio and cytoskeletal integrity, but together, PZ and CsA, are unable to improve and in some cases negate monotherapy neuroprotective effects.
Finally, the effects of PZ (MAOI, aldehyde scavenger), pargyline (PG, MAOI, non-aldehyde scavenger) and hydralazine (HZ, non-MAOI, aldehyde scavenger) are compared. Our results indicate that PZ, PG, and HZ are unable to improve CCI-induced deficits to learning and memory as measured by Morris water maze (post-CCI D3-7). Of concern, PZ animals lost a significant amount of weight compared to all other group, possibly due to MAOI effects. In fact, in uninjured cortical tissue, PZ administration leads to a significant increase in norepinephrine and serotonin. Additionally, although PZ, PG, and HZ did not lead to a statistically significant improvement in cortical tissue sparing 8 days following CCI, the HZ group saw a 10% improvement over vehicle.
Overall, these results indicate that pharmacotherapies which improve mitochondrial function and decrease lipid peroxidation should continue to be pursued as neuroprotective approaches to TBI. However, further pursuit of LP-derived aldehyde scavengers for clinical use in TBI may require the development of hydrazine (-NH-NH2)-compounds which lack additional confounding mechanisms of action.
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Alaei, Zohreh. "Molecular Dynamics Simulations of Axonal Membrane in Traumatic Brain Injury." Thesis, KTH, Skolan för teknik och hälsa (STH), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-211109.
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The following project presents in silico investigation of axonal damage in Diffuse Axonal Injury (DAI). When axons face a shear force, orientation of the lipids in the axonal membrane gets disrupted. Depending on the value of the force, a tensile strain causes the axons to get partially or fully deformed and in some cases a pore forms in the membrane. Using Molecular Dynamic (MD) simulation and a coarse grain model, a series of bilayers with various bilayer structure (single bilayer, parallel bilayer and cylindrical bilayer) and similar composition to biological axonal membrane were simulated. This was initially done to investigate the strain rate dependency of the bilayers, and their viscoelastic ability on returning to their original shape from their deformed forms. To achieve this, various deformation velocities were applied to the bilayers reaching 20% strain and relaxing the bilayer after. Additionally, the bilayers were deformed further until they reached a pore. It was found that the bilayers can almost recover from their deformed forms to their original length when they were deformed at 20% strain level. In conjunction, no correlation between the deformation velocity and lipid deformation was observed. Further, it was found that bilayers with different lipid percentage to axonal bilayer has different strain values for water penetration and for pore formation. The strain value for cylindrical bilayer was found very high compared to the strain values found in vitro. The strain for pore formation of parallel and single bilayer was found to be around 80% to 90% and for water penetration was found to be 70% for single bilayer and 50% for parallel bilayer. A slight difference in strain for pore formation between single and parallel bilayer was found which showed the bilayer structure can play a role in simulation results. The effect of the length in the simulations results was also observed where shorter bilayers showed lower strain for pore formation compared to longer bilayers.
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Williams, Anest. "Lipid profilling of polyunsaturated fatty acid - treated mouse brain and plasma. Investigation into polyunsaturated fatty acid (PUFA)-induced neuroprotection." Thesis, University of Bradford, 2010. http://hdl.handle.net/10454/4414.
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Pre-treatment with polyunsaturated fatty acids or bioactive lipid mediators has been shown to reduce neuronal injury in rodent models of focal ischaemia, but the molecular mechanisms underlying this neuroprotection are unclear. In this study, we aimed to investigate whether systemic administration of alpha linolenic acid (ALA) leads to changes in the profile of mouse brain phospholipid and bioactive lipid mediators in both mouse brain and plasma within the previously determined neuroprotection time window. Mass spectrometry (MS) and tandem mass spectrometry (MS/MS) allowed us to detect and identify 47 phospholipids in mouse cerebral cortex, including several phospholipid species not previously reported in brain lipidomic studies. These included a phosphatidylethanolamine species with m/z 720 that has been associated with retinal stem cells. No widespread changes in cerebral cortex phospholipid composition were observed following intravenous ALA. Several significant changes in lipid mediators (P<0.05 with two-way ANOVA and post hoc Dunnett's t test) were detected in ALA-treated animals compared to untreated and vehicle-injected animals. Many of the affected lipid mediators are ligands for prostanoid receptors which have been demonstrated to play a role in the development of brain injury following cerebral ischaemia, implying that changes in bioactive lipid mediators or modulation of prostanoid receptors may occur following ALA pre-treatment in mice. This study illustrates the potential of advanced lipidomic analysis as a novel tool for neurochemists.
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Yamashita, Yui. "Brain-specific natriuretic peptide receptor-B deletion attenuates high-fat diet-induced visceral and hepatic lipid deposition in mice." Kyoto University, 2016. http://hdl.handle.net/2433/217139.
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Arango, Nicolas(Nicolas S. ). "Sequence-phase optimal (SPO) [d̳e̳l̳t̳a̳]B₀ field control for lipid suppression and homogeneity for brain magnetic resonance spectroscopic imaging." Thesis, Massachusetts Institute of Technology, 2020. https://hdl.handle.net/1721.1/128411.
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Thesis: S.M., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, February, 2020Cataloged from PDF version of thesis. [d̳e̳l̳t̳a̳] in title on title page appears as upper case Greek letter.
Includes bibliographical references (pages 33-35).
This work develops sequence-phase optimal (SPO) [delta]B₀ shimming methods to reduce lipid contamination and improve brain metabolite spectra in proton spectroscopic imaging. A rapidly reconfigurable 32-channel, local-multi-coil-shim-array is used to enhance lipid suppression and narrow metabolite linewidth in magnetic resonance spectroscopic imaging (MRSI) of the brain. The array is optimally reconfigured dynamically during each MRSI repetition period, first during the lipid-suppression phase, by widening the spectral gap between spatially separate lipid and metabolite regions, and then to narrow metabolite linewidth during readout, by brain-only [delta]B₀ homogenization. This sequence-phase-optimal (SPO) shimming approach is demonstrated on four volunteer subjects using a commercial 3T MRI outfitted with a 32-channel integrated RF receive and local multi-coil shim array. This proposed sequence-phase-optimal shimming significantly improves brain-metabolite MRSI in vivo, as measured by lipid suppression, brain metabolite chemical shift, and line widths. The time required to compute patient specific SPO shims negligibly impacted scan time. Sequence-phase-optimal shimming reduced lipid energy in the brain volume across four subjects by 88%, improved NAA FWHM by 23%, and dramatically reduced lipid ringing artifacts in quantified NAA and Glutamate metabolites, without increasing scan time or SAR.
by Nicolas Arango.
S.M.
S.M. Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science
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Hemphill, Susan Patricia. "Effect of sorghum bran addition on lipid oxidation and sensory properties of ground beef patties differing in fat levels." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4399.
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Oxidation of lipids influences the color and sensory qualities of meat products.
Meat with a high fat content, such as ground meat, is susceptible to lipid oxidation that
leads to the development of negative flavor and color changes. Antioxidants, such as
butylated hydroxanisole (BHA), butylated hydroxytolune (BHT) and extracts of
rosemary, are used in meat products to control the effects of lipid oxidation. Awika
(2000, 2003) found that sorghum bran phytochemicals have high antioxidant properties.
Our objective is to evaluate the pH, color, sensory and antioxidant effect of 10, 20 and
30% ground beef patties containing rosemary, BHA/BHT, and three levels of sorghum
bran during 5 d of aerobic storage at 4ðC.
Beef trimmings containing either 50% or 90% lean were formulated into three
meat blocks containing either 10, 20 or 30% lipid. Within a fat content, ground beef was
equally divided into one of six treatments: 1) control-no added ingredients; 2) BHA and
BHT at .01% of the meat weight; 3) rosemary at 0.2% of the meat weight; 4) high level
of sorghum at 1.0% of the meat weight; 5) medium level of sorghum at 0.5% of the meat
weight; and, 6) a low level of sorghum at 0.25% of the meat weight. The ground beef was aerobically packaged and stored for 0, 1, 3, or 5 days at 4ðC. pH, thiobarbituric acid
reactive substances (TBARS), fatty acid methyl esters (FAME), sensory color, Minolta
color space values and descriptive sensory evaluations were determined.
Antioxidant addition reduced TBARS values and increased hardness (P<0.020)
and springiness (P=0.002) over time compared to controls. The addition of the high
sorghum bran level resulted in lower raw color scores (2.0 vs. 2.9) (P<0.0001) and
slightly increased bitter basic taste (2.47 vs. 2.65) (P=0.0069) when compared to control
patties. The high sorghum level slightly increased pH (6.33 vs. 6.41) (P<0.0001) and
resulted in darker (P<0.0001) and less yellow colored (P<0.0001) patties. With storage,
patties had higher pH (P<0.0001) and color space values decreased (P<0.0001). Sensory
properties of the patties differed across fat levels (P<0.05); however, interactions
between fat level and antioxidant treatment were not significant (P>0.05).
Moreover, the addition of sorghum bran at low levels can retard oxidative
rancidity in ground beef patties without causing detrimental color changes and
negatively affecting sensory attributes.
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Pourbaghi, Masouleh Milad. "Development of lipid nanocapsules for antiangiogenic treatment of glioblastoma and evaluation of their potential for nose-to-brain drug delivery." Thesis, Angers, 2018. http://www.theses.fr/2018ANGE0037.
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Le glioblastome (GB), tumeur primitive du cerveau, la plus agressive, et la plus fréquente chez l’adulte, présente une prolifération vasculaire importante. Des agents thérapeutiques innovants ciblant à la fois l'angiogenèse et les cellules tumorales sont recherchés, ainsi que des systèmes pour augmenter leur délivrance dans la tumeur cérébrale. Un de ces agents est le sorafénib (SFN), un inhibiteur de tyrosine kinase. Sa mauvaise solubilité aqueuse et ses effets secondaires indésirables limitent son utilisation. Le premier objectif de cette thèse était d'encapsuler cet agent dans des nanocapsules lipidiques (NCL) pour contrer ces inconvénients. Nous avons développé des NCL avec une haute efficacité d'encapsulation du SFN qui inhibaient in vitro l'angiogenèse et la viabilité de la lignée de GB humain U87MG. La délivrance intratumorale de SFN-NCL chez des souris porteuses d’une tumeur intracérébrale U87MG induit une normalisation vasculaire tumorale précoce qui pourrait améliorer l'efficacité de la chimiothérapie et de la radiothérapie. Le second objectif était de définir si la délivrance intranasale de NCL pouvait constituer une voie non-invasive alternative. Nous avons étudié via le transfert d'énergie par résonance de type Förster, le devenir des NCL chargées d’un fluorochrome à travers des monocouches de cellules Calu-3, un modèle de l'épithélium nasal. L'utilisation de NCL augmente le passage du fluorochrome à travers les cellules Calu-3, mais les particules sont rapidement dégradées après leur capture. Ces données mettent en évidence que les NCL sont appropriées pour la délivrance locale du SFN mais doivent être modifiées pour une délivrance intranasaleGlioblastoma (GB), the most aggressive, and the most frequent primary tumor of the brain in adults, present a prominent vascular proliferation. Innovative therapeutic agents targeting both angiogenesis and tumor cells are urgently required, along with competent systems for their delivery to the brain tumor. One such agent is sorafenib (SFN), a tyrosine kinase inhibitor. However, poor aqueoussolubility and undesirable side effects limit its clinical application. The first objective of this thesis was to encapsulate this drug inside lipid nanocapsules(LNCs) to overcome these drawbacks. We developed LNCs with a high SFN encapsulation efficiency (>90%) that inhibited in vitro angiogenesis and the viability of the human U87MG GB cell line. Intratumoral delivery of SFN-LNCs in mice bearing intracerebral U87MG tumors induced early tumor vascular normalization which could be used to improve the efficacy of chemotherapy and radiotherapy in the treatment of GB. The second objective was to define whether intranasal delivery of LNCs could be an alternative non-invasive route. In this regard, we investigated through Förster resonance energy transfer, the fate of dye-loaded LNCs across Calu-3 cell monolayers, a model of the nasal mucosa. We showed that employment of LNCs dramatically increased the delivery of the dye acrossCalu-3 cell monolayer but they were rapidly degraded after their uptake. These data highlight that LNCs are suitable nanocarriers for the local delivery of SFN but must be redesigned for enhancing their nose-to-brain delivery
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Ta, Nathan. "Role of glucose and glutamine in lipogenesis in the VM-M3 glioblastoma cell line and the inheritance of brain cardiolipin fatty acid abnormality in the VM/Dk mice." Thesis, Boston College, 2014. http://hdl.handle.net/2345/bc-ir:103739.
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Thesis advisor: Thomas SeyfriedLipids, in all their forms from structural components of the membranes (phosphoglycerides, glycolglycerolipids) to signaling molecules (IP3, DAG, prostaglandins, etc.,) post-translational modification of proteins (palmitoylated, farnesylated, prenylated, and GPI anchoring) play an essential role in cancer cell survival, proliferation, and metastasis. Alteration in structural lipids can impair transport, and signaling cascades. Abnormalities in lipids, such as cardiolipin (Ptd2Gro), impair mitochondrial function, bioenergetics, and could play a role in precipitatting the high incidence of spontaneous tumors in VM/Dk mice. This thesis explores the role of glucose and glutamine in their incorporation into lipids in the VM-M3 murine glioblastoma cell line as well as the inheritance of brain cardiolipin fatty acids abnormalities in VM/Dk mice. I used labeled [14C]-U-D-glucose and [14C]-U-L-glutamine to examine the profile of de novo lipid biosynthesis in the VM-M3 cell line. The major lipids synthesized included phosphatidylcholine (PtdCho), phosphatidylethanolamine (EtnGpl), phosphatidylinositol (PtdIns), phosphatidylserine (PtdSer), sphingomyelin (CerPCho), bis(monoacylglycero)phosphate (BMP) / phosphatidic acid (PtdOH), cholesterol (C), Ptd2Gro, and the gangliosides. The data show that the incorporation of labeled glucose and glutamine into synthesized lipids was dependent on the type of growth environment, and that the VM-M3 glioblastoma cells could acquire lipids, especially cholesterol, from the external environment for growth and proliferation. In addition, this thesis also explores and evaluates the abnormality of Ptd2Gro fatty acid composition in VM mice in comparison to B6 mice. Although previously reported, I confirmed the finding in the abnormal cardiolipin fatty acid composition in the VM mice. The abnormal brain cardiolipin fatty acid composition was found to be inherited as an autosomal dominant trait in reciprocal B6 x VM F1 hybrids for both male and female. Impaired cognitive awareness under hypoxia observed for the VM mice and reciprocal F1 hybrids is associated with abnormalities in neural lipid composition
Thesis (PhD) — Boston College, 2014
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Robberts, Theunis Christoffel. "The influence of lipid changes in bran and offall on the baking properties of wheaten flour." Thesis, Cape Technikon, 1991. http://hdl.handle.net/20.500.11838/821.
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Thesis (Masters Diploma (Food Technology)) -- Cape Technikon, Cape Town,1991Bread is an important commodity in South Africa for its nutritional value and contribution to the economy. As such anything that enhances consumption of bread is of economic importance. Variation in bread volumen influences its utility value aand consumer acceptance of the product- The variation of brown bread volume is much greater than that of white bread. Bakers will benefit if they could control the variation in brown bread volume since consumer studies indicate that brown bread sales could surpass that of white bread in the near future. The baking industry uses an automated, continuous baking process that is difficult to alter. Variance of flour thus causes variance in bread volume. Flour variance is caused by the availability of suitable wheat cultivars to blend the grist, the sxtraction rate of the flour, the amount of bran and germ materials inclusionan and the amount of cake flour divided off. Although millers strive to control variation in flour quality, they must operate their mills within constraints of profitability and wheat availability. Deregulation is only applied to bread and excludes the raw material. Since the total deregulation of bread, the fixed price structure has been abolished. Bakers can now use more expensive additives to negate any shortfalls in floUT quality. This could ensure standard bread quality at a slightly higher price. The problem at this stage is that very little is known about the factors that cause variable bread volume. In most cases decreased volumes are attributed to shortfalls in protein quality and quantity and bran content. Baking quality of brown bread flour deteriorates during storage. The deterioration is mor pronounced in flour blended with bran before storage. This study centres around the effects of changing lipid composition during storage on the baking quality of the flour. A review of the literature, with respect to the formation of gluten and the lipidprotein interactions during this process) shows that the various authors have contradictory opinions. The effects of bran and its contribution to the baking process led to even more contradictions. The research approach of this study differed from the approach published in the literature where the researchers use a specific sample of wheat and then generalise for wheat in total. fn this study the samples were selected such that variation between samples are as high as possible. The lipids were extracted as total lipid, and were not separated into various fractions. This allowed the determination of the effect of the changed total lipid content on bread volume. The separation of the different flour samples, that was necessary in the analysis of the results, indicates that one or more important parameters were absent in the design. With this approach it was shown that the changes in total lipids are caused by enzymatic action and that total lipid profIles correlate with bread volumes. It was however impossible to generalise for all the different samples of flour.
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Westendorf, Kathryn A. "Brain lipid binding protein expression in lamina-propria olfactory ensheathing cells is regulated by delta/notch-like epidermal growth factor-related receptor." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/3196.
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The olfactory system exhibits remarkable regenerative ability in it’s neuronal population. The success of continuous neurogenesis is thought to be due, at least in part, to its unique glia – olfactory ensheathing cells (OECs). OECs bear characteristics of both peripheral and central glia, and serve to ensheath, guide and promote growth of olfactory receptor neurons (ORNs) throughout both development and adult life. Brain lipid binding protein (BLBP) is most highly expressed by radial glia during embryonic development. It is largely down-regulated in the adult CNS, but BLBP expression is retained in the adult by special subpopulations of glia, including OECs. BLBP expression is induced in radial glia via Notch signaling, but it is not known if these same mechanisms regulate BLBP expression in the adult CNS. Axonal-glial signaling is a dynamic process whereby closely apposed neuronal and glial cells regulate the growth, maintenance and plasticity of one another through direct cell-cell signaling. Delta/Notch-like EGF-related receptor (DNER) is a transmembrane protein expressed by Purkinje cells which has been implicated in the regulation of BLBP in Bergmann glia during cerebellum development through Notch1 deltex-dependent non-canonical signaling. We have found that DNER is expressed in more mature ORNs, and other exclusive subpopulations of cells within the CNS. OECs in close apposition with DNER-expressing ORNs in vivo appear to maintain the highest BLBP expression found in the nervous system through development and adulthood. Immunofluorescence shows that this close relationship between BLBP expressing cells and DNER expressing cells also appears to be retained in specialized areas such as the hippocampus, retina and spinal cord, throughout mouse CNS development as well as in the mature system. Removing DNER or axonal input in vivo decreases the robustness of OEC BLBP expression, and the number of cells in OEC culture expressing BLBP decreases rapidly with time. OEC co-culture with a DNER expressing monolayer increases the number of OECs in vitro which express BLBP, providing evidence for the regulation of BLBP expression in OECs by DNER expression in apposing ORNs.
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Lémeret, Sabrina. "Etude de la relation entre le métabolisme lipidique et les marqueurs de vieillissement cérébral en imagerie par résonance magnétique." Thesis, Bordeaux, 2016. http://www.theses.fr/2016BORD0063.
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L’augmentation de la longévité et une meilleure prise en charge des maladies cardiovasculaires entraînent un accroissement de la fréquence des maladies liées au vieillissement cérébral, les accidents vasculaires cérébraux (AVC) et la démence étant les plus fréquents. Les marqueurs IRM de vieillissement cérébrovasculaire (hypersignaux de la substance blanche [HSB], infarctus silencieux, microhémorragies) sont de forts prédicteurs d’AVC et de démence, très fréquents en population générale âgée et facilement mesurables. Nous avons étudié l’association entre des composantes du métabolisme lipidique (taux de lipides plasmatiques, génotype ε de l’Apolipoprotéine E [APOE]) et les marqueurs IRM de vieillissement cérébrovasculaire. Nous rapportons dans une revue systématique et méta-analyse que l’allèle APOEε4 est associé à un volume accru de HSB et à un risque accru de microhémorragies et que l’allèle APOEε2 est associé avec un volume accru de HSB et une fréquence plus élevée d’infarctus silencieux. Nous rapportons dans les études 3C-Dijon et EVA, que les taux croissants de triglycérides (TG) sont associés à un volume accru de HSB et à une fréquence plus élevée de lacunes (petits infarctus silencieux). Enfin nous avons exploré la signification clinique de ces associations dans l’étude 3C. Nous rapportons que des taux plus élevés de TG, LDL-cholestérol, et cholestérol total sont associés à un risque accru de démence et de ses sous-types, en population générale âgée de 74 ans à l’inclusion et suivie pendant 12 ans. Nous concluons que le métabolisme lipidique est associé aux marqueurs IRM de vieillissement cérébrovasculaire et à la démenceIncreasing longevity and improved management of cardiovascular diseases has led to an increase in the frequency of age-related neurological diseases, especially stroke and dementia. MRI markers of vascular brain injury (white matter hyperintensities [WMH], silent infarcts and microbleeds) are powerful predictors of stroke and dementia, very frequent in the elderly, and can be measured easily. We studied the association between some components of lipid metabolism (plasma lipid levels, Apolipoprotein E [APOE] ε genotype) and MRI markers of vascular brain injury. We found in a systematic review with meta-analysis that the ε4 allele of the APOE gene is associated with larger WMH volume and a higher frequency of cerebral microbleeds, and that the APOEε2 allele is associated with larger WMH volume and a higher frequency of silent brain infarcts. We also report in the 3C-Dijon Study and in the EVA study that higher triglyceride levels are associated with an increased WMH volume and with a higher frequency of silent lacunar (small subcortical) brain infarcts. Finally, we investigated the clinical significance of these associations the 3C Study. We observed that higher triglycerides, LDL-cholesterol and total cholesterol levels, were associated with an increased risk of all dementia and its subtypes, in community persons aged 74 years at baseline and followed for up to 12 years. We conclude that lipid metabolism is associated with MRI-markers of cerebrovascular aging and dementia
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Bôas, Eloísa Aparecida Vilas. "Tratamento crônico com ácido palmítico aumenta o conteúdo de superóxido e a apoptose de células BRIN-BD11com participação da NADPH oxidase, sem envolvimento do GPR40." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-18062014-132020/.
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A exposição crônica a ácidos graxos (AG) saturados leva à disfunção da célula beta pancreática com redução da secreção de insulina e apoptose, fenômeno conhecido como lipotoxicidade, que está relacionado a: estresse de retículo endoplasmático (RE), estimulação crônica do receptor de AG GPR40 e aumento de espécies reativas de oxigênio (ERO) provenientes, entre outras fontes, da enzima NADPH oxidase. Pretendeu-se explorar como mecanismos de lipotoxicidade: o estresse de RE, a estimulação crônica do GPR40 e a geração de ERO pela NADPH oxidase, bem como relações entre NADPH oxidase e estresse de RE. Verificamos que cronicamente o ácido palmítico (AP) provocou aumento do conteúdo de superóxido, proveniente em parte da NADPH oxidase. A inibição da NADPH oxidase com VAS2870 reverteu a apoptose provocada pela exposição crônica ao AP e apresentou relação com menor expressão proteica de um marcador do estresse de RE (PERK). O GW9508 (agonista do GPR40) não provocou os mesmos efeitos crônicos do AP, sugerindo que a ativação da via do GPR40 não está envolvida nos processos.Chronic exposure to saturated fatty acids can lead to pancreatic beta cell dysfunction, reduction of insulin secretion and apoptosis, condition known as lipotoxicity, that has been related to: endoplasmic reticulum stress, chronic stimulation of GPR40 and increased production of reactive oxygen species (ROS) from, among other sources, the enzime NADPH oxidase. We intended to explore as mechanisms of lipotoxicity: reticulum stress, chronic stimulation of GPR40 and NADPH oxidase generation of ROS, as well as relations between NADPH oxidase and reticulum stress. Our results show that chronically palmitic acid induced an increase in the superoxide, in part from NADPH oxidase. NADPH oxidase inhibition by VAS2870 reverted the apoptosis induced by chronic exposure to palmitic acid, and was related to a lower expression of a reticulum stress marker (PERK). GW9508, GPR40 agonist, did not produced the same effects observed after chronic treatment with palmitic acid, suggesting that activation of GPR40 pathway is not involved in these processes.
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Smine, Selima. "Obésité induite par un régime riche en lipides (HFD) et effet protecteur d'un extrait polyphénolique de raisin (GSSE) : approche protéomique." Thesis, Normandie, 2017. http://www.theses.fr/2017NORMR111/document.
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Les effets du GSSE (Grape seed and skin extract), extrait de raisin particulièrement riche en antioxydants, ont été étudiés pour prévenir les troubles métaboliques et cardiovasculaires liés à l’obésité. L’obésité est caractérisée par une accumulation ectopique de graisse dans les tissus non adipeux tels que le cerveau. Cette lipotoxicité cérébrale induit une inflammation chronique au niveau du cerveau. Dans ce présent travail, nous avons décrit l’effet anti-obésité du GSSE dans un modèle expérimental d’obésité induite par un régime alimentaire à haute teneur en graisses (HFD) tout en mettant l’accent sur le stress oxydant ainsi que le dysfonctionnement métabolique du cerveau qui n’est pas organe cible de l’obésité. Grâce à ce travail, nous avons développé une approche protéomique quantitative Nano LCMS/MS Label free afin d’identifier les biomarqueurs liés au traitement riche en lipides (HFD) et à la protection apportée au cerveau par le GSSE. Pour ce faire, on a eu recours à un modèle animal afin de mieux comprendre les voies métaboliques potentielles altérées par l’obésité et la protection apportée par le GSSE. Plusieurs protéines ont été identifiées et quantifiées en comparant le protéome cérébral total chez les rats dans les différentes conditions de traitements. On a eu recours à des outils de bioinformatique qui nous ont permis de conclure que ces protéines significativement différenciées sont principalement liées à la voie de la phosphorylation oxydative, de la glycolyse / néoglucogenèse et celle de la signalisation du calcium. Ces résultats ont été confirmés par la mesure de quelques activités enzymatiques métaboliques. Fait intéressant, qu’elles soient sous ou surexprimées par le traitement du HFD, le GSSE corrige l’effet délétère apporté aux différentes protéines et enzymes suite au traitement du HFD. D’autres voies métaboliques cérébrales ont été induites par le GSSE telle que le « HIF signaling pathway ». Ces résultats nous permettent de fournir un élan pour l’investigation thérapeutique du GSSE contre différents désordres métaboliquesThe effects of GSSE (Grape seed and skin extract) extracted from grapes particularly rich in antioxidants have been studied to prevent metabolic and cardiovascular disorders related to obesity. Obesity is characterized by an ectopic accumulation of fat in non-adipose tissues such as the brain. This cerebral lipotoxicity induces chronic inflammation of the brain. In this work, using quantitative proteomic analysis, biochemical and bio-informatic tools allows us to identify actors of metabolic and biological pathways that were disregulated in brain of experimentally-induced obese rats and corrected by GSSE treatment. While our data are consistent with previous findings of obesity-induced brain lipotoxicity, such as enhancement of proteins belonging to the OXPHOS and calcium pathways, they also unveiled novel pathways including the up-regulation of HIF-signaling pathway in HFD brains. In the same context, GSSE abrogated HFD-induced signaling pathway elevation either by modulating several proteins or by inducing some others that were not affected by HFD
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Günther, Ann-Kathrin Verfasser], Gregor [Akademischer Betreuer] Eichele, Gregor [Gutachter] Eichele, and Eberhard [Gutachter] [Bodenschatz. "Transport of lipid vesicles via the cilia logistic network in the brain of mice / Ann-Kathrin Günther ; Gutachter: Gregor Eichele, Eberhard Bodenschatz ; Betreuer: Gregor Eichele." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2019. http://d-nb.info/1195215886/34.
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Günther, Ann-Kathrin [Verfasser], Gregor Akademischer Betreuer] Eichele, Gregor [Gutachter] Eichele, and Eberhard [Gutachter] [Bodenschatz. "Transport of lipid vesicles via the cilia logistic network in the brain of mice / Ann-Kathrin Günther ; Gutachter: Gregor Eichele, Eberhard Bodenschatz ; Betreuer: Gregor Eichele." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2019. http://d-nb.info/1195215886/34.
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Braun, Christian Julian [Verfasser], Gerhard [Akademischer Betreuer] Thiel, and Adam [Akademischer Betreuer] Bertl. "Structure/function correlates and protein/lipid interaction of the viral potassium channel KcvNTS / Christian Julian Braun. Betreuer: Gerhard Thiel ; Adam Bertl." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2014. http://d-nb.info/1110902069/34.
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Braun, Christian J. [Verfasser], Gerhard [Akademischer Betreuer] Thiel, and Adam [Akademischer Betreuer] Bertl. "Structure/function correlates and protein/lipid interaction of the viral potassium channel KcvNTS / Christian Julian Braun. Betreuer: Gerhard Thiel ; Adam Bertl." Darmstadt : Universitäts- und Landesbibliothek Darmstadt, 2014. http://nbn-resolving.de/urn:nbn:de:tuda-tuprints-40761.
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Hallinan, Robert Michael. "Increasing the Oral Bioaccessibility of Curcumin Using Oleogels Structured by Rice Bran Wax." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1578004597209035.
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Lyras, Leonidas. "Oxidative stress and neurodegenerative diseases : measurement of lipid, protein and DNA damage in brain tissue from Alzheimer's disease, amyotrophic lateral sclerosis and dementia with Lewy bodies." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298464.
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Aidoud, Nacima. "Modulation de l'apport qualitatif post-natal en lipides sur le fonctionnement cérébral du nouveau-né." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0105.
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La qualité des lipides des préparations pour nourrissons est primordiale, notamment en termes d’acides gras polyinsaturés (AGPI) comme l’acide arachidonique (ARA) et docosahexaénoïque (DHA). Ces derniers pourraient favoriser le développement neurosensoriel de l’enfant. Nous avons ainsi évalué 4 standards commerciaux contenant des lipides végétaux ou laitiers et supplémentés ou non en ARA/DHA, sur le développement neurosensoriel au travers d’un modèle d’allaitement artificiel « pups in the cups ». En TEP-cs, nous observons que la supplémentation en ARA/DHA permet de normaliser le fonctionnement cérébral.L’exploration des lipides tissulaires indique des différences en DHA particulièrement bas avec l’allaitement en lipides végétaux purs. Nous proposons un algorithme de prédiction du DHA cérébrale et oculaire via les profils en acides gras érythrocytaires. Dans ces tissus un tiers des espèces à DHA sont affectées et corrélées à l’activité cérébrale. Les neuromédiateurs issus de l’AL, ARA, DHA par la voie LOX sont impactés ainsi que la distribution spatiale en DHA en IMS. Les autres données omiques soulignaient l’impact des interactions fond lipidique x ajout DHA/ARA (transcriptomique) ou fond lipidique (métabolomique) sur la régulation du métabolisme cérébral impactant le métabolisme neuronal et le métabolisme cérébral du microbiote probablement via l’axe de signalisation intestin-cerveau. Nous identifions alors un métagénome sensible à l’ajout DHA/ARA corrélé à la fonction cérébrale. Enfin, des modifications épigénétiques (méthylation du génome et miARN) touchant le groupe FC suggèrent potentiellement un impact à long termeThe quality of lipids in infant formula is essential, especially in terms of polyunsaturated fatty acids (PUFAs) such as arachidonic acid (ARA) and docosahexaenoic acid (DHA). These could promote the neurosensory development of the child. We thus evaluated 4 commercial standards containing plant or dairy lipids and supplemented or not with ARA / DHA, on the neurosensory development through an artificially feeding model "pups in the cups". In PET-cs, we observe that the supplementation in ARA / DHA makes it possible to normalize the cerebral functioning. The exploration of tissue lipids indicates differences in DHA which are particularly low with pure plant lipids intake. We propose an algorithm for predicting cerebral and ocular DHA via erythrocyte fatty acids profiles. In these tissues one-third of the DHA species are affected and correlated with brain activity. The neuromediators resulting from AL, ARA, DHA by the LOX pathway are impacted as well as the spatial distribution of DHA in IMS imaging. Other omics data underlined the impact of lipid background x combination DHA / ARA (transcriptomics) or lipid background (metabolomics) on the regulation of cerebral metabolism impacting neuronal metabolism and brain metabolism of the microbiota probably through the signalling of gut-brain axis. We then identify a metagenome sensitive to the addition of DHA / ARA correlated to brain function. Finally, epigenetic modifications (methylation of the genome and miRNA) affecting the FC group potentially suggest a long-term impact
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Drbal, Abed Alnaser Anter Amer. "Studies on bioactive lipid mediators involved in brain function and neurodegenerative disorders : the effect of ω-3PUFA supplementation and lithium treatment on rat brain sphingomyelin species and endocannabinoids formation : changes in oxysterol profiles in blood of ALS patients and animal models of ALS." Thesis, University of Bradford, 2013. http://hdl.handle.net/10454/6285.
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Lipids are important for structural and physiological functions of neuronal cell membranes. They exhibit a range of biological effects many are bioactive lipid mediators derived from polyunsaturated fatty acids such as sphingolipids, fatty acid ethanolamides (FA-EA) and endocannabinoids (EC). These lipid mediators and oxysterols elicit potent bioactive functions in many physiological and pathological processes of the brain and neuronal tissues. They have been investigated for biomarker discovery of ageing, neuroinflammation and neurodegenerative disorders. The n-3 fatty acids EPA and DPA are thought to exhibit a range of neuroprotective effects many of which are mediated through production of such lipid mediators. The aims of this study were to evaluate the effects of n-3 EPA and n-3 DPA supplementation on RBC membranes and in this way assess dietary compliance and to investigate brain sphingomyelin species of adult and aged rats supplemented with n-3 EPA and n-3 DPA to evaluate the effects and benefits on age-related changes in the brain. Furthermore, to study the effects of lithium on the brain FA-EAs and ECs to further understand the neuroprotective effects of lithium neuroprotective action on neuroinflammation as induced by LPS. Finally to examine if circulating oxysterols are linked to the prevalence of ALS and whether RBC fatty acids are markers of this action in relation to age and disease stages. These analytes were extracted from tissue samples and analysed with GC, LC/ESI-MS/MS and GC-MS. It was found that aged rats exhibited a significant increase in brain AA and decrease in Σn-3 and Σn-6 PUFAs when compared to adult animals. The observed increase of brain AA was reversed following n-3 EPA and n-3 DPA supplementation. Sphingomyelin was significantly increased when aged animals were supplemented with n-3 DPA. LPS treatment following lithium supplementation increased LA-EA and ALA-EA, while it decreased DHA-EA. Both oxysterols 24-OH and 27-OH increased in ALS patients and SOD1-mice. Eicosadienoic acid was different in ASL-patients compared to aged SOD1-mice. These studies demonstrated that dietary intake of n-3 EPA and n-3DPA significantly altered RBC fatty acids and sphingolipids in rat brain. They suggest that n-3 DPA can be a potential storage form for EPA, as shown by retro-conversion of n-3 DPA into EPA in erythrocyte membranes, ensuring supply of n-3 EPA. Also, n-3 EPA and n-3 DPA supplementation can contribute to an increase in brain sphingomyelin species with implications for age effects and regulation of brain development. Effects of lithium highlight novel anti-neuroinflammatory treatment pathways. Both 24-hydroxycholesterol and eicosadienoic acid may be used as biomarkers in ALS thereby possibly helping to manage the progressive stages of disease.