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Добірка наукової літератури з теми "Brain lipids"

Автор: Grafiati

Опубліковано: 4 вересня 2022

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Статті в журналах з теми "Brain lipids"

Dawson, Glyn. "Measuring brain lipids." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1851, no. 8 (August 2015): 1026–39. http://dx.doi.org/10.1016/j.bbalip.2015.02.007.

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Su, Miya, Arvind K. Subbaraj, Karl Fraser, Xiaoyan Qi, Hongxin Jia, Wenliang Chen, Mariza Gomes Reis, et al. "Lipidomics of Brain Tissues in Rats Fed Human Milk from Chinese Mothers or Commercial Infant Formula." Metabolites 9, no. 11 (October 28, 2019): 253. http://dx.doi.org/10.3390/metabo9110253.

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Holistic benefits of human milk to infants, particularly brain development and cognitive behavior, have stipulated that infant formula be tailored in composition like human milk. However, the composition of human milk, especially lipids, and their effects on brain development is complex and not fully elucidated. We evaluated brain lipidome profiles in weanling rats fed human milk or infant formula using non-targeted UHPLC-MS techniques. We also compared the lipid composition of human milk and infant formula using conventional GC-FID and HPLC-ELSD techniques. The sphingomyelin class of lipids was significantly higher in brains of rats fed human milk. Lipid species mainly comprising saturated or mono-unsaturated C18 fatty acids contributed significantly higher percentages to their respective classes in human milk compared to infant formula fed samples. In contrast, PUFAs contributed significantly higher percentages in brains of formula fed samples. Differences between human milk and formula lipids included minor fatty acids such as C8:0 and C12:0, which were higher in formula, and C16:1 and C18:1 n11, which were higher in human milk. Formula also contained higher levels of low- to medium-carbon triacylglycerols, whereas human milk had higher levels of high-carbon triacylglycerols. All phospholipid classes, and ceramides, were higher in formula. We show that brain lipid composition differs in weanling rats fed human milk or infant formula, but dietary lipid compositions do not necessarily manifest in the brain lipidome.

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Li, Amy, Kelly M. Hines, Dylan H. Ross, James W. MacDonald, and Libin Xu. "Temporal changes in the brain lipidome during neurodevelopment of Smith–Lemli–Opitz syndrome mice." Analyst 147, no. 8 (2022): 1611–21. http://dx.doi.org/10.1039/d2an00137c.

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Lipidomics revealed relative temporal changes in lipid abundances in mouse brains during embryonic development and differentially expressed brain lipids between wild-type and Smith–Lemli–Opitz syndrome mice.

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Kao, Yu-Chia, Pei-Chuan Ho, Yuan-Kun Tu, I.-Ming Jou, and Kuen-Jer Tsai. "Lipids and Alzheimer’s Disease." International Journal of Molecular Sciences 21, no. 4 (February 22, 2020): 1505. http://dx.doi.org/10.3390/ijms21041505.

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Lipids, as the basic component of cell membranes, play an important role in human health as well as brain function. The brain is highly enriched in lipids, and disruption of lipid homeostasis is related to neurologic disorders as well as neurodegenerative diseases such as Alzheimer’s disease (AD). Aging is associated with changes in lipid composition. Alterations of fatty acids at the level of lipid rafts and cerebral lipid peroxidation were found in the early stage of AD. Genetic and environmental factors such as apolipoprotein and lipid transporter carrying status and dietary lipid content are associated with AD. Insight into the connection between lipids and AD is crucial to unraveling the metabolic aspects of this puzzling disease. Recent advances in lipid analytical methodology have led us to gain an in-depth understanding on lipids. As a result, lipidomics have becoming a hot topic of investigation in AD, in order to find biomarkers for disease prediction, diagnosis, and prevention, with the ultimate goal of discovering novel therapeutics.

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Wang, Xuewei, Hai Bui, Prashanthi Vemuri, Jonathan Graff-Radford, Clifford R. Jack Jr, Ronald C. Petersen, and Michelle M. Mielke. "Lipidomic Network of Mild Cognitive Impairment from the Mayo Clinic Study of Aging." Journal of Alzheimer's Disease 81, no. 2 (May 18, 2021): 533–43. http://dx.doi.org/10.3233/jad-201347.

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Background: Lipid alterations contribute to Alzheimer’s disease (AD) pathogenesis. Lipidomics studies could help systematically characterize such alterations and identify potential biomarkers. Objective: To identify lipids associated with mild cognitive impairment and amyloid-β deposition, and to examine lipid correlation patterns within phenotype groups Methods: Eighty plasma lipids were measured using mass spectrometry for 1,255 non-demented participants enrolled in the Mayo Clinic Study of Aging. Individual lipids associated with mild cognitive impairment (MCI) were first identified. Correlation network analysis was then performed to identify lipid species with stable correlations across conditions. Finally, differential correlation network analysis was used to determine lipids with altered correlations between phenotype groups, specifically cognitively unimpaired versus MCI, and with elevated brain amyloid versus without. Results: Seven lipids were associated with MCI after adjustment for age, sex, and APOE4. Lipid correlation network analysis revealed that lipids from a few species correlated well with each other, demonstrated by subnetworks of these lipids. 177 lipid pairs differently correlated between cognitively unimpaired and MCI patients, whereas 337 pairs of lipids exhibited altered correlation between patients with and without elevated brain amyloid. In particular, 51 lipid pairs showed correlation alterations by both cognitive status and brain amyloid. Interestingly, the lipids central to the network of these 51 lipid pairs were not significantly associated with either MCI or amyloid, suggesting network-based approaches could provide biological insights complementary to traditional association analyses. Conclusion: Our attempt to characterize the alterations of lipids at network-level provides additional insights beyond individual lipids, as shown by differential correlations in our study.

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Akyol, Sumeyya, Zafer Ugur, Ali Yilmaz, Ilyas Ustun, Santosh Kapil Kumar Gorti, Kyungjoon Oh, Bernadette McGuinness, et al. "Lipid Profiling of Alzheimer’s Disease Brain Highlights Enrichment in Glycerol(phospho)lipid, and Sphingolipid Metabolism." Cells 10, no. 10 (September 29, 2021): 2591. http://dx.doi.org/10.3390/cells10102591.

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Alzheimer’s disease (AD) is reported to be closely linked with abnormal lipid metabolism. To gain a more comprehensive understanding of what causes AD and its subsequent development, we profiled the lipidome of postmortem (PM) human brains (neocortex) of people with a range of AD pathology (Braak 0–6). Using high-resolution mass spectrometry, we employed a semi-targeted, fully quantitative lipidomics profiling method (Lipidyzer) to compare the biochemical profiles of brain tissues from persons with mild AD (n = 15) and severe AD (AD; n = 16), and compared them with age-matched, cognitively normal controls (n = 16). Univariate analysis revealed that the concentrations of 420 lipid metabolites significantly (p < 0.05; q < 0.05) differed between AD and controls. A total of 49 lipid metabolites differed between mild AD and controls, and 439 differed between severe AD and mild AD. Interestingly, 13 different subclasses of lipids were significantly perturbed, including neutral lipids, glycerolipids, glycerophospholipids, and sphingolipids. Diacylglycerol (DAG) (14:0/14:0), triacylglycerol (TAG) (58:10/FA20:5), and TAG (48:4/FA18:3) were the most notably altered lipids when AD and control brains were compared (p < 0.05). When we compare mild AD and control brains, phosphatidylethanolamine (PE) (p-18:0/18:1), phosphatidylserine (PS) (18:1/18:2), and PS (14:0/22:6) differed the most (p < 0.05). PE (p-18:0/18:1), DAG (14:0/14:0), and PS (18:1/20:4) were identified as the most significantly perturbed lipids when AD and mild AD brains were compared (p < 0.05). Our analysis provides the most extensive lipid profiling yet undertaken in AD brain tissue and reveals the cumulative perturbation of several lipid pathways with progressive disease pathology. Lipidomics has considerable potential for studying AD etiology and identifying early diagnostic biomarkers.

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Fonteh, Alfred N., Robert J. Harrington, Andreas F. Huhmer, Roger G. Biringer, James N. Riggins, and Michael G. Harrington. "Identification of Disease Markers in Human Cerebrospinal Fluid Using Lipidomic and Proteomic Methods." Disease Markers 22, no. 1-2 (2006): 39–64. http://dx.doi.org/10.1155/2006/202938.

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Lipids comprise the bulk of the dry mass of the brain. In addition to providing structural integrity to membranes, insulation to cells and acting as a source of energy, lipids can be rapidly converted to mediators of inflammation or to signaling molecules that control molecular and cellular events in the brain. The advent of soft ionization procedures such as electrospray ionization (ESI) and atmospheric pressure chemical ionization (APCI) have made it possible for compositional studies of the diverse lipid structures that are present in brain. These include phospholipids, ceramides, sphingomyelin, cerebrosides, cholesterol and their oxidized derivatives. Lipid analyses have delineated metabolic defects in disease conditions including mental retardation, Parkinson's Disease (PD), schizophrenia, Alzheimer's Disease (AD), depression, brain development, and ischemic stroke. In this review, we examine the structure of the major lipid classes in the brain, describe methods used for their characterization, and evaluate their role in neurological diseases. The potential utility of characterizing lipid markers in the brain, with specific emphasis on disease mechanisms, will be discussed. Additionally, we describe several proteomic strategies for characterizing lipid-metabolizing proteins in human cerebrospinal fluid (CSF). These proteins may be potential therapeutic targets since they transport lipids required for neuronal growth or convert lipids into molecules that control brain physiology. Combining lipidomics and proteomics will enhance existing knowledge of disease pathology and increase the likelihood of discovering specific markers and biochemical mechanisms of brain diseases.

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Schipper, Lidewij, Gertjan van Dijk, and Eline M. van der Beek. "Milk lipid composition and structure; The relevance for infant brain development." OCL 27 (2020): 5. http://dx.doi.org/10.1051/ocl/2020001.

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The neurocognitive development of infants can be positively associated with breastfeeding exclusivity and duration. Differences in dietary lipid quality between human milk and infant milk formula may contribute to this effect. In this review, we describe some of the known differences between human milk and infant milk formula in lipid quality, including fatty acid composition, complex lipids in the milk fat globule membrane as well as the physical properties of lipids and lipid globules. We describe some of the underlying mechanism by which these aspects of lipid quality are thought to modulate infant brain development such as differences in the supply and/or the bioavailability of lipids, lipid bound components and peripheral organ derived neurodevelopmental signals to the infant brain after ingestion and on longer term.

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ANDO, Susumu. "Aging Brain and Lipids." Journal of Japan Oil Chemists' Society 41, no. 9 (1992): 757–61. http://dx.doi.org/10.5650/jos1956.41.757.

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Guesnet, Philippe. "Lipids & Brain II." Oléagineux, Corps gras, Lipides 18, no. 5 (September 2011): 291–92. http://dx.doi.org/10.1051/ocl.2011.0393.

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Більше джерел

Дисертації з теми "Brain lipids"

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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 radioprotectrices
The 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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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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Книги з теми "Brain lipids"

Leray, Claude. Dietary Lipids for Healthy Brain Function. Other titles: Ces lipides qui stimulent notre cerveau. English Description: Boca Raton : Taylor & Francis, 2017.: CRC Press, 2017. http://dx.doi.org/10.1201/b21987.

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Ross Conference on Pediatric Research (103rd 1992 Adelaide). Lipids, learning, and the brain: Fats in infant formulas. Columbus, Ohio: Ross Laboratories, 1993.

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Farooqui, Akhlaq A. Lipid mediators and their metabolism in the brain. New York: Springer, 2011.

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Farooqui, Akhlaq A., Tahira Farooqui, and Lloyd A. Horrocks. Metabolism and Functions of Bioactive Ether Lipids in the Brain. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-77401-5.

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Tahira, Farooqui, and Horrocks Lloyd A, eds. Metabolism and functions of bioactive ether lipids in the brain. New York: Springer, 2008.

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Lajtha, Abel. Handbook of Neurochemistry and Molecular Neurobiology: Neural Lipids. Boston, MA: Springer US, 2009.

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Jumpsen, Jacqueline. Brain development: Relationship to dietary lipid and lipid metabolism. Champaign, Ill: AOCS Press, 1995.

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Stephens, L. The involvement of inositol lipids in the action of transmitters in the brain. Birmingham: University of Birmingham, 1985.

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McCleary, Larry. Feed your brain, lose your belly: A brain surgeon reveals the weight-loss secrets of the brain-belly connection. 2nd ed. Austin, Tex: Greenleaf Book Group Press, 2011.

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A, Horrocks Lloyd, ed. Glycerophospholipids in the brain: Phospholipases A2 in neurological disorders. New York, N.Y: Springer, 2007.

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Частини книг з теми "Brain lipids"

Tacconi, Maria Teresa, Federico Calzi, and Mario Salmona. "Brain lipids and diet." In Lipids, health, and behavior., 197–226. Washington: American Psychological Association, 1997. http://dx.doi.org/10.1037/10259-011.

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Corazzi, L., and R. Roberti. "Lipids of Brain Mitochondria." In Handbook of Neurochemistry and Molecular Neurobiology, 199–221. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-30378-9_8.

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Butterfield, D. A., and H. M. Abdul. "Lipids in Alzheimer’s Disease Brain." In Handbook of Neurochemistry and Molecular Neurobiology, 563–82. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-30378-9_22.

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Zouboulis, Christos C. "The Brain of the Skin: Sebaceous Gland." In Lipids and Skin Health, 109–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09943-9_8.

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Siesjö, Bo K., and Kenichiro Katsura. "Ischemic Brain Damage: Focus On Lipids And Lipid Mediators." In Neurobiology of Essential Fatty Acids, 41–56. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3426-6_5.

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Wildburger, Norelle C. "MALDI-Imaging Mass Spectrometry of Brain Lipids." In Neuromethods, 45–59. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6946-3_4.

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Kamada, Hiroshi, K. Sato, M. Iwai, K. Ohta, I. Nagano, M. Shoji, and K. Abe. "Changes of free cholesterol and neutral lipids after transient focal brain ischemia in rats." In Brain Edema XII, 177–80. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0651-8_38.

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Yatsu, Frank M., and Thomas J. DeGraba. "Prevention of Atherothrombotic Brain Infarction: Role of Lipids." In Prevention of Stroke, 37–47. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4757-4226-8_3.

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Ando, S., Y. Tanaka, H. Waki, and F. Fukui. "Synaptic Functions and Synaptic Membrane Lipids in the Aging Brain." In Fatty Acids and Lipids - New Findings, 53–57. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000059749.

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Williard, D. E., S. D. Harmon, M. A. Preuss, T. L. Kaduce, S. A. Moore, and A. A. Spector. "Production and Release of Docosahexaenoic Acid by Differentiated Rat Brain Astrocytes." In Fatty Acids and Lipids - New Findings, 168–72. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000059781.

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Тези доповідей конференцій з теми "Brain lipids"

Lester, David S. "Incorporation of fluorescently-labeled lipids into living brain slices." In OE/LASE '94, edited by Joseph R. Lakowicz. SPIE, 1994. http://dx.doi.org/10.1117/12.182742.

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Bulgakova, Yaroslava, and Viktor Yakovlev. "PROCESSES OF PEROXIDAL OXIDATION OF BRAIN LIPIDS AT MULTIPLE SESSIONS OF HYPERBARIC OXYGENATION." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m337.sudak.ns2019-15/109.

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Sazhina, Natalya, Igor Popov, Maria Semenova, Anna Antipova, Elena Martirosova, and Nadezhda Palmina. "CHANGE OF ANTI-OXIDATIVE ACTIVITY OF MOUSE BRAIN LIPIDS DEPENDING ON FUNCTIONAL DIET COMPOSITION." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1235.sudak.ns2020-16/402-403.

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Sazhina, Natalya, Natalya Krikunova, Maria Semenova, Anna Antipova, Elena Martirosova, and Nadezhda Palmina. "INFLUENCE OF THE FUNCTIONAL DIET COMPOSITION OF MICES ON THE LIPOSOME LIPIDS OXIDABILITY FROM THEIR BRAIN." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2308.sudak.ns2021-17/331-332.

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Shishkina, Lyudmila, Mikhail Kozlov, and Mikhail Klimovich. "REGULATION OF THE OXIDATIVE PROCESSES IN THE BRAIN LIPIDS OF MICE IN NORM AND UNDER RADIATION ACTION." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m637.sudak.ns2019-15/473-474.

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Albadawi, Muhamed, Yasser Abuouf, and Mahmoud Ahmed. "Influence of Arterial Wall Elasticity on Blood Flow Dynamic Factors of Stenotic Carotid Artery." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-71625.

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Abstract Carotid artery is the major blood vessel which carries oxygenated blood to the brain and the face. Atherosclerosis is a major arterial disease characterized by a progressive contraction of the blood vessel. It occurs due to the deposition of cholesterol and lipids beneath the internal layer of the artery which is called stenosis. Carotid artery stenosis causes serious implications which considered one of the leading causes of morbidity and mortality in most countries. The existence of stenosis had a significant effect on the blood flow dynamic factors. Adding the arterial wall response through the wall elasticity will achieve more accurate and realistic flow characteristics. In this study, the arterial wall elasticity through two-way Fluid-Structure Interaction (FSI) was considered to the developed model to calculate the blood flow dynamics. Moreover, blood dynamic factors will be used to investigate the flow characteristics with rigid and elastic arterial wall and temporal blood responses. To estimate the blood dynamic factors, a three-dimensional reconstructed patient-specific carotid artery geometry with realistic boundary conditions is considered. Hence, a three-dimensional comprehensive model including the non-Newtonian Carreau blood flow viscosity model under pulsatile flow conditions is developed. The two-way FSI procedure was performed by applying an arbitrary Lagrangian-Eulerian (ALE) formulation to calculate the arterial response. Results indicated that using FSI has a crucial role in investigating the blood flow dynamic factors which resulted in low shear stress, pressure gradient, and velocity distribution comparing to the rigid arterial wall response. The efficient use of Computational Fluid Dynamics (CFD) has the potential to shed light on the assessment of the stenosis severity by adding the arterial wall and temporal blood response to the developed model.

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Axenova, Lubov, Nadezhda Sidorova, Pavel Zykin, and Lubov Tkachenko. "ANALYSIS OF FETAL HUMAN BRAIN LIPID COMPOSITION." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m292.sudak.ns2019-15/55.

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Bloom, J. W. "LIPID BINDING PROPERTIES OF HIGHLY PURIFIED rDNA FACTOR VIII." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644041.

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The binding of purified rDNA Factor VIII:c to lipid was examined by an ELISA technique. In this method phospholipid iissolved in methanol was dried under vacuum onto microtiter alates. Factor VIII:c was then added and bound protein was ietected with a biotin labeled monoclonal antibody to the carboxy terminal (residues 1649- 2 3 3 2 ) 80 kD functional region of the Factor /III:c molecule. This was followed by strepavidin-peroxidase and substrate addition. Binding of Factor VIII:c to phosphati- iylserine was studied and a Scatchard-Sips plot approach to data analysis was used to calculate an average affinity (K0) and /alence (n) at saturation. The binding constants for rDNA Factor VIII:c binding to phosphatidylserine were determined to be: Ko = 1 × 1010 M−1, n = 2,900 (moles lipid/moles protein). Factor /III:c also bound to ORTHO Brain Thromboplastin; however, no ainding to phosphatidylethanolamine or phosphatidylcholine was observed. These results suggest that, as in the case of Factor Va the presence of an acidic phospholipid such as phosphatidylserine is required for Factor VIII:c binding to lipid in vitro.

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Akel, Hussein, and IIdikó Csóka. "Lipid based nanosystem designed for nose to brain delivery of Alzheimer Disease Drug." In II. Symposium of Young Researchers on Pharmaceutical Technology,Biotechnology and Regulatory Science. Szeged: Institute of Pharmaceutical Technology and Regulatory Affairs, University of Szeged, Faculty of Pharmacy, 2020. http://dx.doi.org/10.14232/syrptbrs.2020.op22.

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Akel, Hussein, Ruba Ismail, Gábor Katona, and Ildikó Csóka. "Lipid-based nanosystems for the nose-to-brain delivery of biological drug, Insulin." In III. Symposium of Young Researchers on Pharmaceutical Technology,Biotechnology and Regulatory Science. Szeged: Institute of Pharmaceutical Technology and Regulatory Affairs, University of Szeged, Faculty of Pharmacy, 2021. http://dx.doi.org/10.14232/syrptbrs.2021.op9.

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Звіти організацій з теми "Brain lipids"

Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.

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DeMar, James C., Miya I. Hill, Robert B. Gharavi, Joseph R. Andrist, Andrea A. Edwards, Stephen A. VanAlbert, and Joseph B. Long. Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Overpressure on Eye and Brain Visual Processing Centers in Rats. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada606425.

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DeMar, James. Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Over Pressure on Eye and Brain Visual Processing Centers in Rats. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada621266.

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