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1
Ng, Tat-fong. "Molecular basis for regeneration of CNS : a possible regulatory role of growth associated protein-43 /". Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17538786.
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吳達方 y Tat-fong Ng. "Molecular basis for regeneration of CNS: a possible regulatory role of growth associated protein-43". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31235219.
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Roshan, Payam. "Cellular basis of inflammation in the enteric nervous system". Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26759.
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There is limited knowledge of immunocyte-myenteric neuronal interaction and the role of iNOS in myenteric neuronal injury. This research sought to examine the role of macrophages, NO, and iNOS inhibitors in myenteric neurodegeneration.
Increased NO synthesis in macrophages and its effects on myenteric neurons were investigated in cell cultures. Using rodent models of inflammation, we further examined NO-dependent neurotoxicity.
In the presence of activated macrophages neuronal injury and degeneration occurred; however the myenteric neurons showed greater resistance to oxidative challenge than cortical neurons. Pretreatment with iNOS inhibitors significantly reduced these inflammatory effects. Myenteric neuronal injury was also evident in experimental colitis, and iNOS selective inhibitor protected the myenteric neurons from inflammation and degeneration.
In conclusion, these results show that activated macrophage-derived NO is important in inflammation-dependent myenteric neurodegeneration, and iNOS inhibitors can protect myenteric neurons from degeneration. Two potential strategies for neuroprotection in gut inflammation are defined.
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Jaramillo, Martinez Diana. "Epidemiology and pathogenesis of Nervous Necrosis Virus". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13088.
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Viral Nervous Necrosis (VNN) is a globally distributed disease that affects a large number of finfish species, causing significant economic losses on affected farms. The causative agent is a small single stranded RNA virus called Nervous Necrosis Virus (NNV) from the genus Betanodavirus. NNV is neurotropic; clinical signs involve abnormal behaviour and high mortality associated with histopathological findings of vacuolating necrosis in the central nervous system and retina. In Australia, NNV has been isolated from Australian bass (Macquaria Novemaculeata) and barramundi (Lates calcarifer) populations recurrently for the past 10 and 25 years, respectively. However, the prognosis of NNV infection is highly variable. Although NNV became notorious for mass mortalities in marine fish hatcheries, it is often detected in apparently healthy individuals in the absence of clinical signs or histopathological lesions. Current knowledge on NNV epidemiology and pathogenesis is fragmentary. It is still unclear how the virus is transmitted between hosts and why some individuals are susceptible to VNN while others are not. The aim of this work was to study the epidemiology and pathogenesis of NNV in Australian native species with a focus on transmission and disease determinants to provide a basis for the development of prevention and control strategies. In Chapter 3, a partially retrospective study was conducted on the occurrence of NNV at the Darwin Aquaculture Centre (DAC), a barramundi hatchery. Observations on NNV detection frequency and distribution provided clues to the possible transmission pathways of the virus, including the potential role of broodstock as reservoirs, and the age-dependency of the disease. To assess the NNV exposure distribution among populations of adult fish, an indirect antibody detection ELISA was developed (Chapter 4). The assay was optimized and compared with a competitive ELISA format to provide the best discriminatory power between sera from immunized and non-immunized populations. After defining the best antibody detection protocol (the indirect ELISA), the diagnostic accuracy of the assay was assessed in naturally exposed subjects using a Bayesian approach in the absence of a gold standard (Chapter 5). After validation of the ELISA, a single point and repeated cross sectional analysis of NNV seroprevalence was conducted on native Australian adult fish populations (barramundi, Australian bass and groupers Epinephelus sp.) (Chapter 6). Survey results discredited the role of broodstock as NNV reservoirs based on the lack of correspondence between NNV seroprevalence and the occurrence of NNV outbreaks at the hatchery level. Results also suggested that the exposure of adult fish to NNV antigens must be progressive as seroconversion was often observed and the seroprevalence tended to be higher in older fish populations. From this and previous accumulated epidemiological evidence, horizontal transmission of NNV was considered most likely. An environmental reservoir outside the hatcheries has yet to be investigated. In Chapter 7, the factors influencing the pathogenesis of NNV in barramundi were explored. Juveniles of different ages were challenged by immersion to analyse the influence of the age of the host on VNN disease expression. Additionally, to test the influence of the virus isolate, juveniles were challenged with two inoculums obtained from NNV outbreaks in barramundi populations with different disease presentation (clinical and subclinical). Results showed that fish from all the age groups tested (range 20 to 63 days post hatch) were susceptible to NNV infection. However, the survival of the fish following NNV challenge was highly influenced by the age of the host. Juveniles of 5 weeks of age and older showed no clinical signs and their survival odds were the same as the non-challenged controls, whereas younger fish developed clinical disease. No significant effect on disease severity was noted between different NNV isolates. In Chapter 8, the factors influencing the pathogenesis of NNV in Australian bass were explored. In addition to the age of the host and the isolate factor, the influence of the dose of the virus and the water temperature on VNN expression was examined. As with barramundi, the disease expression in Australian bass was age dependent. The severity of the disease was affected by the water temperature in younger fish but it did not affect the outcome in fish above 5 weeks of age. The dose of the virus influenced the incidence of infection but not the severity of the disease expression. Again, no significant effect on disease severity was noted between the two isolates tested. From the experimental challenge of barramundi and Australian bass, further observations on NNV pathogenesis were provided: incubation period, minimum infectious dose, tissue distribution, shedding and humoral immune response. The results from this study narrow the knowledge gap on NNV transmission mechanisms and provide important insights into the virus pathogenesis in barramundi and Australian bass. The virus is most likely being transmitted horizontally and VNN disease expression as distinct from infection with NNV is highly age dependent. From this evidence, recommendations are made on the direction of efforts to control VNN at the farm level.
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Caruso, Giuseppe. "Basi Molecolari dei DCP (disoridni conformazionali proteici) a carico del sistema nervoso: condizioni microambientali e interrelazioni cellulari". Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1532.
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La funzione biologica di una proteina dipende dalla sua struttura tridimensionale, che è determinata dalla sua sequenza aminoacidica durante il processo di folding proteico. Il folding proteico nella cellula è un processo strettamente regolato che coinvolge una serie di proteine, dai chaperon molecolari alle proteasi, che assistono il processo folding e monitorano la qualità del prodotto finale. Molte malattie hanno mostrato di derivare da misfolding e sono raggruppate sotto il nome di disordini conformazionali proteici (DCP) . L'evento distintivo nei PCD è un cambiamento nella struttura secondaria e/o terziaria di una proteina normale senza alterazione della struttura primaria. Il cambiamento conformazionale può promuovere la malattia aumentando l attività tossica o causando la mancanza di funzione biologica della proteina nativa. I DCP comprendono il morbo di Alzheimer (AD) , il morbo di Huntington (HD), la fibrosi cistica, il diabete mellito di tipo II (T2DM), il morbo di Parkinson (PD), e molte altre malattie. Nella maggior parte dei DCP la proteina mal ripiegata è ricca di strutture beta-sheet. Sia T2DM che AD sono caratterizzati da aggregati proteici insolubili con conformazione fibrillare. L aggregazione dell amilina è associata alla perdita delle cellule beta pancreatiche, mentre Abeta e la formazione grovigli neurofibrillari sono associati alla perdita di cellule neuronali. Sono stati mostrati sia condivisi che separati modelli di tossicità per le due molecole amiloidogeniche Amilina e Abeta, che sono in parte mediati da recettori, con i recettori, almeno in una certa misura, condivisi tra le due molecole. Fattori microambientali quali gli ioni metallici sono noti interagire con queste molecole amiloidogeniche, rendendole tossiche per le cellule in coltura.
Nel presente studio abbiamo dimostrato come i peptidi amiloidogenici formano spontaneamente aggregati amorfi o fibrillari. In presenza di rame la fibrillogenesi di Abeta25 35 subisce delle modifiche strettamente legate al tempo di incubazione, in particolare nel passaggio da una specie all altra. Questi cambiamenti possono essere correlati al grado di tossicità misurato dopo il trattamento di colture cellulari di neuroblastoma (SH-SY5Y). L aumento della tossicità cellulare, indotta mediante incubazione con rame, può essere spiegata con un rallentamento nell evoluzione verso strutture non tossiche, e con la conseguente stabilizzazione di aggregati oligomerici, notoriamente molto più tossici rispetto alle specie fibrillari.
L'incubazione favorisce la formazione di strutture beta-sheet da parte di hA17-29. Lo stato di aggregazione cambia in funzione del tempo di incubazione. La presenza di rame in soluzione rallenta il processo di fibrillogenesi e favorisce la stabilizzazione di specie oligomeriche, mentre altri fattori, quali lo zinco e il ribosio, favoriscono la formazione di grandi aggregati. La vitalità delle cellule di neuroblastoma diminuisce in relazione al tempo di incubazione del frammento peptidico. La pre-incubazione in presenza di rame aumenta ulteriormente la tossicità del peptide. Questa diminuzione della vitalità potrebbe anche dipendere dalla formazione di radicali liberi tossici prodotti come risultato di reazioni di Fenton.
L'analisi del medium condizionato da cellule endoteliali ha mostrato il collegamento fra la produzione di alphaB-cristallina e lo stress cellulare. È stato dimostrato che la produzione di alphaB cristallina è direttamente proporzionale alla concentrazione di peptide Abeta25-35 usato per trattare le colture cellulari. Questo è in accordo con i dati di letteratura in cui l aumentata produzione di HSP, necessarie per il corretto ripiegamento delle proteine e per la protezione delle cellule, è collegata ad eventi di stress cellulare.
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CARUSO, GIUSEPPE. "Basi Molecolari dei DCP (disoridni conformazionali proteici) a carico del sistema nervoso: condizioni microambientali e interrelazioni cellulari". Doctoral thesis, Università degli studi di Catania, 2014. http://hdl.handle.net/20.500.11769/490585.
Texto completoResumen
La funzione biologica di una proteina dipende dalla sua struttura tridimensionale, che è determinata dalla sua sequenza aminoacidica durante il processo di folding proteico. Il folding proteico nella cellula è un processo strettamente regolato che coinvolge una serie di proteine, dai chaperon molecolari alle proteasi, che assistono il processo folding e monitorano la qualità del prodotto finale. Molte malattie hanno mostrato di derivare da misfolding e sono raggruppate sotto il nome di disordini conformazionali proteici (DCP) . L'evento distintivo nei PCD è un cambiamento nella struttura secondaria e/o terziaria di una proteina normale senza alterazione della struttura primaria. Il cambiamento conformazionale può promuovere la malattia aumentando l’attività tossica o causando la mancanza di funzione biologica della proteina nativa. I DCP comprendono il morbo di Alzheimer (AD) , il morbo di Huntington (HD), la fibrosi cistica, il diabete mellito di tipo II (T2DM), il morbo di Parkinson (PD), e molte altre malattie. Nella maggior parte dei DCP la proteina mal ripiegata è ricca di strutture beta-sheet. Sia T2DM che AD sono caratterizzati da aggregati proteici insolubili con conformazione fibrillare. L’aggregazione dell’amilina è associata alla perdita delle cellule beta pancreatiche, mentre Abeta e la formazione grovigli neurofibrillari sono associati alla perdita di cellule neuronali. Sono stati mostrati sia condivisi che separati modelli di tossicità per le due molecole amiloidogeniche Amilina e Abeta, che sono in parte mediati da recettori, con i recettori, almeno in una certa misura, condivisi tra le due molecole. Fattori microambientali quali gli ioni metallici sono noti interagire con queste molecole amiloidogeniche, rendendole tossiche per le cellule in coltura. Nel presente studio abbiamo dimostrato come i peptidi amiloidogenici formano spontaneamente aggregati amorfi o fibrillari. In presenza di rame la fibrillogenesi di Abeta25 35 subisce delle modifiche strettamente legate al tempo di incubazione, in particolare nel passaggio da una specie all’altra. Questi cambiamenti possono essere correlati al grado di tossicità misurato dopo il trattamento di colture cellulari di neuroblastoma (SH-SY5Y). L’aumento della tossicità cellulare, indotta mediante incubazione con rame, può essere spiegata con un rallentamento nell’evoluzione verso strutture non tossiche, e con la conseguente stabilizzazione di aggregati oligomerici, notoriamente molto più tossici rispetto alle specie fibrillari. L'incubazione favorisce la formazione di strutture beta-sheet da parte di hA17-29. Lo stato di aggregazione cambia in funzione del tempo di incubazione. La presenza di rame in soluzione rallenta il processo di fibrillogenesi e favorisce la stabilizzazione di specie oligomeriche, mentre altri fattori, quali lo zinco e il ribosio, favoriscono la formazione di grandi aggregati. La vitalità delle cellule di neuroblastoma diminuisce in relazione al tempo di incubazione del frammento peptidico. La pre-incubazione in presenza di rame aumenta ulteriormente la tossicità del peptide. Questa diminuzione della vitalità potrebbe anche dipendere dalla formazione di radicali liberi tossici prodotti come risultato di reazioni di Fenton. L'analisi del medium condizionato da cellule endoteliali ha mostrato il collegamento fra la produzione di alphaB-cristallina e lo stress cellulare. È stato dimostrato che la produzione di alphaB cristallina è direttamente proporzionale alla concentrazione di peptide Abeta25-35 usato per trattare le colture cellulari. Questo è in accordo con i dati di letteratura in cui l’aumentata produzione di HSP, necessarie per il corretto ripiegamento delle proteine e per la protezione delle cellule, è collegata ad eventi di stress cellulare.The biological function of a protein depends on its tridimensional structure, which is determined by its amino acid sequence during the process of protein folding. Protein folding in the cell is a tightly regulated process, involving a series of proteins, from molecular chaperones to proteases that assist the folding process and monitor the quality of the final product. Several diseases have been shown to arise from protein misfolding and are grouped together under the name of protein conformational disorders (PCDs). The hallmark event in PCDs is a change in the secondary and/or tertiary structure of a normal protein without alteration of the primary structure. The conformational change may promote the disease by either gain of a toxic activity or by the lack of biological function of the natively folded protein. The PCDs includes Alzheimer's disease (AD), Huntington disease (HD), cystic fibrosis, diabetes mellitus type II (T2DM), Parkinson disease (PD), and many other diseases. In most of PCDs the misfolded protein is rich in beta-sheet conformation. Both T2DM and AD are characterized by insoluble protein aggregates with a fibrillar conformation. Amylin aggregation is associated with pancreatic beta-cell loss, whereas Abeta and tangle formation is associated with neuronal cell loss. For the two amyloidogenic molecules Amylin and Abeta, shared and separate modes of toxicity have been revealed, that are in part receptor-mediated, with the receptors, at least to some degree, being shared between the two molecules. Microenvironmental factors such as metal ions are known to interact with these amyloidogenic molecules, and make them toxic for cultured cells. In the present study, we show that amyloidogenic peptides spontaneously form amorphous or fibrillary aggregates. In presence of copper Abeta25 35 fibrillogenesis undergoes changes, tightly linked to the time of incubation, especially in the shift from one species to another. These changes may be related to the toxicity degree measured after treatment of neuroblastoma cell cultures (SH-SY5Y). Cellular toxicity increase, induced by incubation with copper, may be explained with a slowdown in the evolution toward not toxic structures, and a consequent stabilization of oligomeric aggregates, notoriously much more toxic than fibrillary species. The incubation favors the formation of beta-sheet structures by hA17-29. The state of aggregation changes as a function of incubation time. The presence of copper in solution slows the fibrillogenesis process, and favors the stabilization of oligomeric species, instead other factors such as zinc and ribose favor the formation of large aggregates. The neuroblastoma cells viability decreases in relation to incubation time of the peptide fragment. The pre-incubation in the presence of copper further increases the toxicity of the peptide. This decrease of viability could also depend on the formation of toxic free radical species produced as a result of Fenton reactions. The analysis of the conditioned medium from endothelial cells shown a connection between alphaB-cristallin production and cellular stress. The production of alphaB-crystallin has been shown directly proportional to the concentration of Abeta25-35 peptide used to treat cell cultures. This is in agreement with literature data in which increased production of HSP, necessary for the proper folding of proteins and for the cell protection, is connected to events of cellular stress.
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Lloyd, Edward John y mikewood@deakin edu au. "A common structural basis for central nervous system drug design". Deakin University. School of Biological Sciences, 1986. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050902.115505.
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The main theme of this thesis is that there is a common structural basis for drugs acting on the central nervous system (CNS), and that this concept may be used to design new CNS-active drugs which have greater specificity and hence less side-effects.
To develop these ideas, the biological basis of how drugs modify CMS neurotransmission is described, and illustrated using dopaminergic pathways. An account is then given of the use of physicochemical concepts in contemporary drug design. The complete conformational analysis of several antipsychotic drugs is used to illustrate some of these techniques in the development of a model for antipsychotic drug action.
After reviewing current structure-activity studies in several classes of CNS drugs (antipsychotics, anti-depressants, stimulants, hal1ucinogens, anticonvulsants and analgesics), a hypothesis for a common structural basis of CNS drug action is proposed- This is based on a topographical comparison of the X-ray structures of eight representative CNS-active drugs, and consists of three parts: 1.there is a common structural basis for the activity of many different CNS-active drug classes; 2. an aromatic ring and a nitrogen atom are the primary binding groups whose topographical arrangement is fundamental to the activity of these drug classes;
3. the nature and placement of secondary binding
determines different classes of CNS drug activity. A four-Point model for this common structural basis is then defined using 14- CNS-active drug structures that include the original eight used in proposing the hypothesis. The coordinates of this model are: R1 (0. 3.5, 0), R2 (0, -3.5, O), N (4.8. -0.3, 1.4), and R3 (6.3, 1.3, 0), where R1 and R2 represent the point locations of a hydrophobic interaction of the common aromatic ring with a receptor, and R3 locates the receptor point for a hydrogen bond involving the common nitrogen, N. Extended structures were used to define the receptor points R1, R2 and R3, and the complete conformational space of each of the 14 molecules was considered.
It is then shoun that the model may be used to predict whether a given structure is likely to show CNS activity: a search over 1,000 entries in the current Merck Index shows a high probability (82%) of CNS activity in compounds fitting the structural model.
Analysis of CNS neurotransmitters and neuropeptides shows that these fit the common model well. Based on the available evidence supporting chemical evolution, protein evolution, and the evolution of neurotransmitter functions, it is surmised that the aromatic ring/nitrogen atom pharmacophore proposed in the common model supports the idea of the evolution of CNS receptors and their neurotransmitters, possibly from an aromatic amine or acety1cho1ine acting as a primaeval communicating molecule.
The third point in the hypothesis trilogy is then addressed. The extensive conformation-activity analyses that have resulted in well-defined models for five separate CNS drug classes are used to map out the locations of secondary binding groups relative to the common model for anti-psychotics, antidepressants, analgesics, anticholinergics, and anticonvulsants. With this information, and knowledge derived from receptor-binding data, it is postulated that drugs having specified activity could be designed.
In order to generate novel structures having a high probability of CNS-activity, a process of drug design is described in which known CNS structures are superimposed topographically using the common model as a template. Atoms regarded as superfluous may be selectively deleted and the required secondary binding groups added in predicted locations to give novel structures.
It is concluded that this process provides the basis for the rational design of new lead compounds which could further be optimized for potent and specific CNS activity.
8
Shi, Huilin. "The common basis of sympathetic nervous system and neuroblastoma development". Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1244058100.
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Thesis (Ph. D.)--University of Toledo, 2009."In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences (Cancer Biology)." Title at OhioLINK ETD site: Investigation of common bases of sympathetic nervous system and neuroblastoma development. Title from title page of PDF document. Includes bibliographical references (p. 72-75, 119-125, 152-192).
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Nazer, Manoel Brandes. "Sistematização das artérias da base do encéfalo de avestruz (struthio camelus)". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2009. http://hdl.handle.net/10183/16335.
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O avestruz (Struthio camelus) é uma ave da família Struthionidae, originária da África. Embora a irrigação da base do encéfalo de outras aves já tenha sido fonte de estudo por alguns pesquisadores, desconhece-se o padrão, as variações, as distribuições e o comportamento das artérias que promovem a irrigação sangüínea na base do encéfalo em avestruz. Neste trabalho, foram utilizados 30 espécimes, nos quais o sistema arterial foi preenchido com látex corado em vermelho através das artérias (Aa.) carótida comum direita e esquerda. Sistematizou-se as artérias da face ventral do encéfalo, à direita e à esquerda, com suas respectivas percentagens de ocorrência. A a. carótida do cérebro, um vaso de grosso calibre, foi predominante na direita (43,3%), esquerda (36,7%) e equivalentes (20%). A anastomose intercarótica apresentou calibre médio (46,7%), grosso (43,3%) e fino (10%), tendo inclinação de fluxo para esquerda (53,3%) e direita (46,7%). A a. oftálmica interna direita apresentou, à direita, calibre médio (43,3%), fino (33,3%) e grosso (23,3%); à esquerda, calibre médio (60%), fino (26,7%) e grosso (13,3%). O ramo caudal da a. carótida do cérebro foi, á direita, desenvolvido (53,3%) e vestigial (46,7%); à esquerda, desenvolvido (66,7%) e vestigial (33,3%). A a. tectal mesencefálica ventral foi ramo colateral do ramo caudal da a. carótida do cérebro à direita (53,3%) e à esquerda (66,7%), ramo direto da a. carótida do cérebro à direita (43,3%) e à esquerda (30%) e, ramo direto da a. basilar (3,3%) em ambos os antímeros. A a. basilar foi um vaso ímpar (80%), duplo em quase toda sua extensão calibrosa (13,3%) e, apresentou uma formação "em ilha" em seu segmento de grosso calibre (6,7%). A a. cerebelar ventral caudal foi única (96,7%) e dupla (3,3%) à direita e, única (93,3%) e dupla (6,7%) à esquerda. A a. espinhal dorsal foi ramo colateral da a. cerebelar ventral caudal à direita (96,7%) e à esquerda (93,3%), sendo também ramo da porção fina da a. basilar à direita (3,3%) e à esquerda (6,7%). A a. espinhal ventral, sempre ramo da a. basilar, foi dupla (90%) e única (10%). O ramo rostral da a. carótida do cérebro, um vaso de grosso calibre, apresentou, à direita, um trajeto padrão (86,7%) e um deslocamento rostral (13,3%) e, à esquerda, trajeto padrão (83,3%) e um deslocamento rostral (16,7%). A a. cerebral caudal, à direita, foi dupla (90%) e única (10%); à esquerda, foi dupla (53,3%) e única (46,7%). A a. cerebral média, em ambos os antímeros, foi um vaso único (100%) e de grosso calibre, sendo o segundo ramo colateral do ramo rostral da a. carótida do cérebro. A a. cerebroetmoidal foi única (100%), de médio a grosso calibre, em ambos os antímeros. A a. cerebral rostral foi única (90%) e dupla (10%) à direita e única (96,7%) e dupla (3,3%) à esquerda. A a. etmoidal foi única (100%), de médio a grosso calibre, sendo a continuação natural da a. cerebroetmoidal, após a emissão da a. cerebral rostral. O círculo arterial cerebral apresentou-se rostralmente aberto (100%) e, caudalmente, aberto (80%) e fechado (20%).The ostrich (Struthio camelus) is a bird from the Struthionidae family, originated from Africa. Although the irrigation of the base of the brain of other birds has already been the source of study by some researchers, the pattern, variations, distribution and the behavior of the arteries that promote the blood irrigation in the base of ostrich's brain are not known. In this work, 30 specimens, in which the arterial system was filled with red colored latex in the common carotid arteries left and right. We systematized the arteries of the ventral face of the brain, to the right and to the left, with their respective occurrence percentage. The carotid artery (a.) of the brain, a thick caliber vase, was predominant in the right (43.3%), left (36.7%) and equivalents (20%). The intercarotid anastomosis presented a medium caliber (46.7%), thick (43.3%) and thin (10%), with flux inclination to the left (53.3%) and right (46.7%). The inner right ophthalmic a. presented, to the right, medium caliber (43.3%), thin (33.3%) and thick (23.3%); to the left, medium caliber (60%), thin (26.7%) and thick (13.3%). The caudal branch of the carotid a. of the brain was, to the right, developed (53.3%) and vestigial (33.3%). The midbrain ventral tectal a. was the collateral branch of the caudal branch of the carotid a. of the brain to the right (53.3%) and to the left (66.7%), right branch of the carotid a. of the brain to the right (43.3%) and to the left (30%) and, right branch of the basilar a. (3.3%) in both antimeres. The basilar a. was an unpaired vase (80%), double in almost the entire caliber extension (13.3%) and, presented the "island" formation in its segment of thick caliber (6.7%). The caudal ventral cerebellar a. was single (96.7%) and double (3.3% to the right and, single (93.3%) and double (6.7%) to the left. The dorsal spinal a. was a collateral branch of the caudal ventral cerebellar a. to the right (96.7%) and to the left (93.3%), which was also a branch of the thin portion of the basilar a. to the right (3.3%) and to the left (6.7%). The ventral spinal a., always a branch of the basilar a., was double (90%) and single (10%). The rostral branch of the carotid a. of the brain, a vase of thick caliber, presented, to the right, a standard path (86.7%) and a rostral displacement (13.3%) and, to the left, a standard path (83.3%) and a rostral displacement (16.7%). The caudal brain a., to the right, was double (90%) and single (10%); to the left, it was double (53.3%) and single (46.7%). The medium cerebral a., in both antimeres, was a single vase (100%) and of thick caliber, being that the second collateral branch of the rostal branch of the brain carotid a. The brain ethmoidal a. foi single (100%), of medium to thick caliber, in both antimeres. The rostral brain a. was single (90%) and double (10%) to the right and single (96.7%) and double (3.3%) to the left. The ethmoidal a. was single (100%), of medium to thick caliber, being the natural continuity of the brain ethmoidal, after the emission of the rostral brain a.. The brain artery circle was rostrally open (100%) and, caudally, open (80%) and closed (20%).
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Hayden, James Timothy. "The molecular basis for central nervous system primitive neuroectodermal tumour development". Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1598.
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Central nervous system primitive neuroectodermal tumours (CNS-PNETs) are highly aggressive tumours with similar histopathological features to other intracranial PNETs (medulloblastomas). These two tumours have accordingly been treated using unified approaches, but CNS-PNETs have a dismal prognosis. Few studies have investigated the genetic features of CNS-PNETs. The molecular basis of CNS-PNET was therefore investigated in a cohort containing CNS-PNETs from children (n=33) and adults (n=5), to aid improvements in disease classification and treatment. The common medulloblastoma molecular defects were investigated in CNS-PNETs, and showed RASSF1A promoter hypermethylation is a frequent event (18/22, 82%), and MYC family gene amplification occurs in a subgroup (MYCN: 3/25 (12%), MYCC: 0/25 (0%)). In contrast and in distinction to medulloblastoma, chromosome 17p loss is not a common feature (2/23, 9%), whilst p53 pathway signalling appears to play a major role (20/22, 91%), and associated with TP53 mutations (4/22, 18%). Aberrant Wnt signalling was identified in 2 cases (2/22, 9%) and coupled with CTNNB1 mutation in a single case. IDH1 mutations (2/25, 8%) however, appear to occur in adult but not childhood CNS-PNETs or medulloblastoma. Subsequent genome-wide investigations of the CNS-PNET DNA methylome aimed at a wider characterisation of the molecular features of CNS-PNETs and its relationships to other childhood tumours identified CNS-PNETs as a heterogenous disease group without defined sub-clusters, which were predominantly distinct from medulloblastomas, but exhibited overlap with high-grade gliomas. A panel of 76 tumour-specific methylation events were identified as disease markers. The combination of either RASSF1A hypermethylation or HLA-DPB1 hypomethylation discerned normal brain from CNS-PNET in 94% of cases (64/68). In addition, hypermethylation of TAL1, MAP3K1 and IGFBP1 is associated with non-infant disease. In conclusion, this study has shown CNS-PNETs are a heterogenous group of tumours that are molecularly distinct from medulloblastomas, and has implicated developmental pathways and genetic events in their tumorigenesis. The associations between molecular events identified and clinical features warrant further investigation to aid classification and treatment advancements.
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Eichhorn, Klaus-Gregor. "Entwicklung eines Fragebogens zur Diagnostik von Essstörungen auf Basis von Daten etablierter diagnostischer Verfahren". Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-192711.
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Die vorliegende Arbeit entwickelt einen Vorschlag für einen neuen, kompakteren Fragebogen mit dem Akronym „BaFEK-45“ zur Diagnostik von Essstörungen, der auf einer statistischen Analyse von Daten aus fünf bereits etablierten Fragebogen (ANIS, EAT – 26, FBeK, EDI – 2, EDES) mit einer Gesamtzahl von 231 Items basiert. Dabei wurden die Antworten von Patientinnen aus den 1990er- und 2000er-Jahren der Klinik und Poliklinik für Psychiatrie, Psychotherapie und
Psychosomatik des Kindes- und Jugendalters der Universität Leipzig ausgewertet. Auf Grundlage zweier „Signalfragen“ zu Ess-Anfällen wurden die Fragebogen-Serien in drei Gruppen (anorektisch, bulimisch und grenzwertig) eingeteilt, daraufhin konnte eine Analyse zu den Unterschieden im Antwortverhalten zwischen eben diesen Gruppe vorgenommen werden. Nach einem auf dieser Analyse basierenden Auswahlverfahren wurden die verbliebenen Items einer
mehrstufigen Faktorenanalyse und kritischen inhaltlichen Differenzierung unterzogen. An deren Ende steht der o.g. Vorschlag eines neuen Diagnostikinstruments, das sich aus 45 Fragen in fünf
Skalen zusammensetzt.
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Silva, Carlos Eduardo da. "Uso de fluoresceína sódica em meningeomas da base do crânio". Pontifícia Universidade Católica do Rio Grande do Sul, 2013. http://hdl.handle.net/10923/5568.
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Previous issue date: 2013Objective: The authors present a study with the use of sodium fluorescein (SF) to enhance skull base meningiomas and perform a quantitative digital analysis of the tumors enhancement. The study intends to observe the grade of cranial base meningiomas enhancement by SF. Methods: A prospective within-subjects study was performed including twelve patients with skull base meningiomas. Digital pictures were obtained before and after the SF systemic injection, using the same light-source of the microsurgical field. The pictures were analyzed by Image Pro Plus 4. 5. 1 software, which calculated the wavelength of the sodium fluorescein pre and post injection. Results: The group of meningiomas was composed as it follows: one cavernous sinus, one olfactory groove, three petroclival, one tuberculum sellae, three sphnoid wing, one anterior clinoid and two temporal floor. The SF enhancement in all tumors was strongly positive. The digital analysis of the pictures, considering the SF wavelength pre and post injection, presented p=0. 002 (Wilcoxon T test).Conclusions: The enhancement of the skull base meningiomas by SF was consistent. The introductory results suggest the possibility of using SF as an adjuvant tool for the skull base meningioma surgery. Further studies should test the clinical application of the SF in skull base tumors.
Objetivo: Apresenta-se o primeiro estudo com o uso de Fluoresceína Sódica (FS) para contrastar meningeomas localizados na base do crânio e realiza-se uma análise quantitativa digital do contraste tumoral. O estudo tem por objetivo observar o grau de captação de FS pelos meningeomas da base do crânio.Métodos: Estudo descritivo com observação intragrupo (antes e depois), incluindo 12 pacientes com lesões da base do crânio. Fotografias digitais foram realizadas antes e após a administração sistêmica de FS, utilizando-se a mesma fonte de iluminação do campo microcirúrgico. As fotografias pré e pós-injeção de FS foram analisadas usando-se o software Image Pro Plus 4. 5. 1, que calculou o comprimento de onda da FS nas respectivas imagens. Resultados: O grupo de meningeomas foi distribuído topograficamente da seguinte forma: um do seio cavernoso, um da goteira olfatória, três petroclivais, um do tubérculo selar, três da asa do esfenóide, um da clinóide anterior e dois do assoalho temporal. O contraste dos tumores pela FS foi fortemente positivo. A análise digital das fotografias, considerando a presença do comprimento de onda da FS nas imagens obtidas pré e pós-injeção de FS, apresentou uma diferença significativa, com p=0,002 (Teste T de Wilcoxon).Conclusões: A captação da FS pelos meningeomas foi consistente. Os resultados introdutórios sugerem a possibilidade de uso da FS como uma ferramenta adjuvante para a cirurgia dos meningeomas de base de crânio. Estudos complementares são necessários para definir aplicação clínica da FS em tumores da base do crânio.
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Mapes, Richard John. "The biophysical basis of accommodation in human peripheral nerve fibres". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397992.
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Vermeren, Matthieu M. "Molecular basis of peripheral nerve segmentation in the chick embryo". Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621857.
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Ue, Hidetoshi. "Non-Invasive Assessment of Human Cardiac Autonomic Nervous System : Basic and Clinical Applications". Kyoto University, 2001. http://hdl.handle.net/2433/150745.
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Kyoto University (京都大学)0048
新制・課程博士
博士(人間・環境学)
甲第9030号
人博第123号
12||125(吉田南総合図書館)
新制||人||30(附属図書館)
UT51-2001-F360
京都大学大学院人間・環境学研究科文化・地域環境学専攻
(主査)教授 森谷 敏夫, 教授 家森 幸男, 教授 津田 謹輔
学位規則第4条第1項該当
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Thompson, Samantha Lee. "A genetic basis for the development of prognostic indication in childhood primitive neuroectodermal tumours". Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324697.
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Medrado, Andreone Teles. "An Atlas of catfish brain - Steindachneridion parahybae (Teleostei: Siluriformes): a detailed cytoarchitectonic study of the different brain areas and nuclei as a basis for further morphological and functional studies". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04112015-150105/.
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In the present Master\'s Dissertation, a detailed cytoarchtectonic study of the brain of the juvenile catfish - Steindachneridion parahybae, has been performed. The animals used for this Atlas were juvenile specimens of one hundred days post-fertilization. The coronal (transverse) sections (5µm-thick) were obtained by using a rotary microtome, stained with cresyl-violet and examined under a photomicroscopy with the help of a digital system of analysis. Some criteria have been used to classify the different cell masses of the catfish brain: (i) characteristic size, shape and intensity of the staining from the perykarya; (ii) packing density and distribution pattern of the cell bodies; (iii) neuropil surrounding the cell groups and (iv) consistency of cell groups in both hemispheres and different brains of catfish. Thus, around one hundred and thirty nuclei have been described in the catfish brain, which are distributed in four main region that are from rostral to caudal: telencephalon, diencephalon, mesencephalon and rhombencephalon. Although we have observed important similarities between the brain of catfish and other teleosts, we have also noticed some differences in the characteristics and placement of several nuclei in relation to other teleosts, or even when compared to the brain of species of the same Order, the Siluriformes. Some of these differences could be related with the age of the animals studied here, but probably represent species-specific differences because the brain of adult catfish specimens has a great similarity in cytoarchitecture and overall organization compared to younger animals. The main outcome of this study has been the availability of a complete Atlas of the brain of catfish, which has been used to localize precisely the distribution of cells and fibers of the Gonadotropin-releasing hormone in the brain. This Atlas will also represent a valuable tool for future endocrine analyses, allowing the precise mapping of the different neurohormones in the brain of catfish, as well as for the study of neural connections among different brain areasEsta Dissertação de Mestrado, apresenta-se estruturalmente como um Atlas, em que é apresentado um detalhado estudo citoarquitetônico do encéfalo de catfish- Steindachneridion parahybae. Para a realização deste, foram utilizados 7 juvenis de 100 dias após a eclosão, analisados por técnicas rotineiras de histologia, cujas secções coronais(transversais) - 5&um;m de espessura-, foram obtidas utilizando-se de um micrótomo rotativo, coradas com violeta de cresil e examinadas a partir de sistema digital de análise. Alguns critérios foram utilizados para classificar as diferentes massas de células do cérebro catfish, tais como: (i) o tamanho característico, forma e intensidade da coloração do pericário; (ii) padrão de densidade de agrupamento e distribuição dos corpos celulares; (iii) a presença de neurópilos ao redor dos desses agrupamentos celulares e (iv) a consistência/coerência destes agrupamentos em ambos os hemisférios dos diferentes encéfalos, então analisados. Dessa forma, são descritos aproximadamente130 massas celulares para o encéfalo de S. parahybae, as quais estão distribuídas em quatro principais regiões que, da parte rostral para caudal, são: telencéfalo, diencéfalo, mesencéfalo e rombencéfalo. Embora são observadas semelhanças entre o cérebro de S. parahybae e de outros teleósteos, nota-se, também, certas diferenças quanto às características e/ou localização das massas celulares em relação ao encéfalo de outros teleósteos, ou mesmo quando comparado com o cérebro de espécies da mesma ordem, Siluriformes. Algumas destas diferenças pode estar relacionada com a idade dos animais estudados, no entanto,também podem representar diferenças espécie-específicas, uma vez que o encéfalo adultos de S. parahybae apresentam grande similaridade citoarquitetônica, além da organização geral do encéfalo, previamente observadas em animais acima dos 100 dias após a eclosão. Portanto, como resultado deste estudo tem-se a disponibilidade de um Atlas completo do encéfalo de S. parahybae, o qual representa uma ferramenta valiosa para o estudo das conexões neurais entre diferentes áreas do encéfalo, bem como para futuras análises endócrinas, permitindo o mapeamento preciso de neuro-hormônios nesta espécie, como demonstrado ao longo deste estudo, para o hormônio liberador de gonadotropinas
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Beaudoin, Danelle Rae. "T-cell signaling in response to altered myelin basic protein peptides /". Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/8535.
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Dombrowski, Mary A. "Sciatic nerve remyelination and nodal formation following olfactory ensheathing cell transplantation". Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08092007-114648/.
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Transplantation of olfactory ensheathing cells (OECs) into injured spinal cord results in improved functional outcome through axonal regeneration, remyelination, and neuroprotection. However, because little is known of the fate of OECs transplanted into injured peripheral nerve, their myelin forming potential requires investigation. To study these issues OECs were isolated from the olfactory bulbs of adult green fluorescent protein (GFP)-expressing transgenic rats and transplanted into a sciatic nerve crush lesions. Five weeks to six months after transplantation the nerves were studied histologically and it was determined that GFP-expressing OECs survived in the lesion and distributed longitudinally across the lesion zone. Immunostaining revealed a high density of isoform Nav1.6 at the newly formed nodes of Ranvier which were flanked by paranodal Caspr staining. Immuno-electron microscopy for GFP revealed transplanted OECs form peripheral type myelin. These results indicate that transplanted OECs extensively integrate into transected peripheral nerve, form myelin on regenerated peripheral nerve fibers, and reconstruct nodes of Ranvier with proper sodium channel structure.
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Carvalho, Michelle Figueiredo. "Dieta Experimental com Base nos Alimentos da Pesquisa de Orçamento Familiar (POF)- 2002/2003 Durante Gestação e Lactação: Repercussões Sobre Desempenho Reprodutivo, Dimensões Corporais e Perfil Bioquímico de Filhotes". Universidade Federal de Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/12071.
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license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5)Made available in DSpace on 2015-03-11T19:15:50Z (GMT). No. of bitstreams: 2 Tese Michelle Carvalho Nutrição 2012.pdf: 2269037 bytes, checksum: fcecb05acf122ab934ca168e509e7260 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2012-04-11
O presente estudo avaliou os efeitos de uma dieta experimental baseada nos alimentos adquiridos para consumo pelos brasileiros segundo a Pesquisa de Orçamento Familiar (POF) 2002/2003 durante a gestação e lactação e/ou pós-desmame sobre os desempenhos maternos crescimento, desenvolvimento, adiposidade, dimensões corporais e perfil bioquímico na prole. Ratas Wistar (n= 12), alimentadas ad libitum com dieta comercial Labina®, Brasil ou dieta experimental na gestação e lactação formaram os grupos GC e GPOF. Do desmame aos 120 dias novos subgrupos foram formados: Controle-controle (GCC); controle-POF (GCP); POF-controle (GPC) e POF-POF (GPP). A significância adotada em todas as análises foi de 5%. A dieta POF aumentou a duração da gestação [GC:21,00(21,00-21,00); GPOF: 22,00(21,25-22,00)] e provocou nas mães perda de peso ao final da lactação (GC: 27,92±18,47g; GPOF: -15,66±16,90g), menor consumo alimentar, energético e de nutrientes, exceto de lipídeos. A prole GPOF apresentou menor peso ao desmame e menor comprimento naso-anal. No entanto, não diferiu nos eixos cranianos, na maioria dos reflexos e caracteres físicos e até adiantou alguns desses parâmetros: colocação pelas vibrissas [GC: 12,00 (9,00-15,00); GPOF: 9,50 (9,00-14,00)] e queda livre [GC: 18,00 (17,00-20,00); GPOF: 16,00 (13,00-18,00)] e da característica física de abertura do pavilhão auditivo [GC: 3,00 (3,00-3,00); GPOF: 2,00 (2,00-3,00)]. A dieta POF oferecida na fase perinatal e/ ou pós-desmame incrementou o ganho de peso (%) ao final do estudo (GPP=878,2±93,5%;GPC=871,7±102,9%; GCP=682,6±98,4%; GCC=678,28±91,69%), mas reduziu o peso do fígado (GPP=2,59±0,13g; GPC=2,94±0,31g; GCP=2,67±0,28g; GCC= 2,80±0,08g) e rins (GPP=0,31±0,02g; GPC=0,33±0,04g; GCP=0,30±0,01g; GCC=0,38±0,03g). Alteração na gordura visceral foi evidenciada em todos os grupos com dieta POF (GPP=16,06±1,57g; GPC=16,82±3,44g; GCP= 20,65±3,68g; GCC= 12,46±3,24g) e o GPP mostrou maior glicemia de jejum. A dieta POF causou maior agressão ao crescimento somático que ao desenvolvimento do sistema nervoso da prole e demonstrou aumento no depósito de gordura visceral, e, da glicemia se ingerida continuamente.
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Lim, S. P. "Electrical basis for inhibition and excitation in non-propulsive autonomically innervated smooth muscle". Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377171.
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Aggarwal, Anuradha 1964. "Basis for a sympatholytic approach in the treatment of human heart failure". Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8091.
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Kharrazian, Datis. "Association between Immunological Reactivity with Tetrabromobisphenol-A and Autoimmune Target Sites of the Nervous System". Diss., NSUWorks, 2018. https://nsuworks.nova.edu/hpd_hs_stuetd/12.
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Tetrabromobisphenol-A (TBBPA) is the most widely used flame retardant. Flame retardants are sprayed on furniture, mattress beds, children’s pajamas, car seats, upholstery, carpets, and rugs in the United States. Chemical immune reactivity may play a role in the epidemic of autoimmune disease. The goal of this research is to investigate whether any correlation exists between immunological reactivity to TBBPA, a key chemical used in most flame retardants, and neurological autoimmune target sites that are associated with neurological autoimmune diseases with a diverse and specific list of antibodies that include myelin basic protein, myelin-associated glycoprotein, alpha-synuclein, aquaporin receptors, and S100B antibodies with human serum samples. The outcomes of this research can be used to support the development of safety regulations and for identifying potential health concerns for current mandatory flame-retardant legislation. Additionally, this research may support the decisions made in respect of those suffering from neurological autoimmune diseases, as to whether removing flame retardant chemicals is a factor for consideration.
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Silva, Carlos Eduardo da. "Uso de fluoresce?na s?dica em meningeomas da base do cr?nio". Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2013. http://tede2.pucrs.br/tede2/handle/tede/1746.
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Previous issue date: 2013-06-26Objective: The authors present a study with the use of sodium fluorescein (SF) to enhance skull base meningiomas and perform a quantitative digital analysis of the tumors enhancement. The study intends to observe the grade of cranial base meningiomas enhancement by SF. Methods: A prospective within-subjects study was performed including twelve patients with skull base meningiomas. Digital pictures were obtained before and after the SF systemic injection, using the same light-source of the microsurgical field. The pictures were analyzed by Image Pro Plus 4.5.1 software, which calculated the wavelength of the sodium fluorescein pre and post injection. Results: The group of meningiomas was composed as it follows: one cavernous sinus, one olfactory groove, three petroclival, one tuberculum sellae, three sphnoid wing, one anterior clinoid and two temporal floor. The SF enhancement in all tumors was strongly positive. The digital analysis of the pictures, considering the SF wavelength pre and post injection, presented p=0.002 (Wilcoxon T test). Conclusions: The enhancement of the skull base meningiomas by SF was consistent. The introductory results suggest the possibility of using SF as an adjuvant tool for the skull base meningioma surgery. Further studies should test the clinical application of the SF in skull base tumors.
Objetivo: Apresenta-se o primeiro estudo com o uso de Fluoresce?na S?dica (FS) para contrastar meningeomas localizados na base do cr?nio e realiza-se uma an?lise quantitativa digital do contraste tumoral. O estudo tem por objetivo observar o grau de capta??o de FS pelos meningeomas da base do cr?nio. M?todos: Estudo descritivo com observa??o intragrupo (antes e depois), incluindo 12 pacientes com les?es da base do cr?nio. Fotografias digitais foram realizadas antes e ap?s a administra??o sist?mica de FS, utilizando-se a mesma fonte de ilumina??o do campo microcir?rgico. As fotografias pr? e p?s-inje??o de FS foram analisadas usando-se o software Image Pro Plus 4.5.1, que calculou o comprimento de onda da FS nas respectivas imagens. Resultados: O grupo de meningeomas foi distribu?do topograficamente da seguinte forma: um do seio cavernoso, um da goteira olfat?ria, tr?s petroclivais, um do tub?rculo selar, tr?s da asa do esfen?ide,um da clin?ide anterior e dois do assoalho temporal. O contraste dos tumores pela FS foi fortemente positivo. A an?lise digital das fotografias, considerando a presen?a do comprimento de onda da FS nas imagens obtidas pr? e p?s-inje??o de FS, apresentou uma diferen?a significativa, com p=0,002 (Teste T de Wilcoxon). Conclus?es: A capta??o da FS pelos meningeomas foi consistente. Os resultados introdut?rios sugerem a possibilidade de uso da FS como uma ferramenta adjuvante para a cirurgia dos meningeomas de base de cr?nio. Estudos complementares s?o necess?rios para definir aplica??o cl?nica da FS em tumores da base do cr?nio.
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Kvarnström, Maria. "Mechanisms in inflammatory demyelinating diseases of the nervous system : immunological and methodological aspects /". Linköping : Linköpings universitet, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med892s.pdf.
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NEAL, MARY ELIZABETH. "DIAGNOSTIC PREDICTION OF EATING DISORDER PATIENTS ON THE BASIS OF MEASURES OF PERSONAL EFFECTIVENESS, FAMILY DYNAMICS AND TRADITIONAL SEX-ROLE BELIEFS (ANOREXIA NERVOSA, BULIMIA)". Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183900.
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This study explored three areas believed to play a central role in the pathogenesis and presenting clinical picture of the eating disorders, anorexia nervosa and bulimia. Measures of personal effectiveness, family dynamics, and traditional sex-role beliefs were assessed in groups of restricted anorexics, bulimic anorexics, normal weight bulimics and controls. Control subjects manifested the highest degree of psychological adjustment, resourcefulness, and self-direction, while restricting anorexics obtained the lowest score on this measure. Bulimics experienced the highest degree of personal effectiveness of the patient groups, with bulimic anorexics falling in-between restricting anorexics and bulimics. Control subjects also reported that they felt more independent, accepted and tolerated in their family than any of the eating disorder groups. Bulimic subjects scored closest to controls on this measure, with bulimic anorexics experiencing the least degree of acceptance, tolerance and independence of all groups. Finally, control subjects defined themselves in a more traditionally masculine role than did any of the eating disorder groups. Restricting anorexics were most likely to describe themselves as passive, submissive, constricted and sensitive; bulimic subjects were more likely to endorse such self-descriptive adjectives as assertive, uninhibited, self-confident and competitive. Bulimic anorexics perceived themselves to be less traditionally feminine than did restricting anorexics, but more than bulimics or controls. The results of this study support the theory that ego deficits contribute to the development of eating disorders.
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Lekholm, Emilia. "Solute Carriers in Metabolism : Regulation of known and putative solute carriers in the central nervous system". Doctoral thesis, Uppsala universitet, Funktionell farmakologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-331328.
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Solute carriers (SLCs) are membrane-bound transporter proteins, important for nutrient, ion, drug and metabolite transport across membranes. A quarter of the human genome codes for membrane-bound proteins, and SLCs make up the largest group of transporter proteins. Due to their ability to transport a large repertoire of substances across, not just the plasma membrane, but also the membrane of internal organelles, they hold a key position in maintaining homeostasis affecting metabolic pathways. Unfortunately, some of the more than 400 identified SLCs are still not fully characterized, even though a quarter of these are associated with human disease. In addition, there are about 30 membrane-bound proteins with strong resemblance to SLCs, of which very little is known. The aim of this thesis is to characterize some of these putative SLCs, focusing on their localization and function in the central nervous system. Since many of the known SLCs play a vital part in metabolism and related pathways, the response to different nutritional conditions has been used as a key method. MFSD14A and MFSD14B, characterized in Paper I, are putative SLCs belonging to the Major Facilitator Superfamily (MFS) and found to be neuronal, differentially expressed in the mouse central nervous system and transiently upregulated in mouse embryonic cortex cultures due to amino acid deprivation. They were also altered in areas of the mouse brain after starvation as well as after high fat diet. In Paper II, the effect on gene regulation due to complete amino acid starvation was monitored in a mouse hypothalamic cell line and 47 different genes belonging to SLCs, or putative SLCs, were found to be affected. Of these, 15 genes belonged to already known amino acid transporters, whereas 32 were putative SLCs with no known function or SLCs not known to react to amino acids. The three SV2 proteins, SV2A, SV2B and SV2C, were studied in Paper III using human neuroblastoma cell lines. The high metabolic state of cancers often result in an upregulation and alteration of transporter proteins, and alterations of the SV2 proteins were found following different treatments performed in this study. Paper IV focused on putative SLCs of MFS type and their role in glucose metabolism. Mouse embryonic cortex cultures were subjected to glucose starvation and the gene expression of 19 putative transporters were analyzed. All but four of the putative transporters were affected either at 3h or 12h of glucose deprivation. In conclusion, several SLCs and putative SLCs studied in this thesis are strongly affected by alteration in metabolism, either due to amino acids or glucose or both. This makes the putative SLCs dynamic membrane-bound proteins, possibly transporters, highly affected by nutritional status and most likely regulated to maintain homeostasis.
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Zibetti, C. "ALTERNATIVE SPLICING AND PHOSPHORYLATION PROVIDE A MECHANISTIC BASIS FOR FUNCTIONAL SPECIALIZATION OF LSD1/KDM1 HISTONE DEMETHYLASE IN THE CENTRAL NERVOUS SYSTEM". Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150261.
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Chromatin represents the physiological substrate of epigenetic regulation, underlying several biological processes, from replication and transcriptional activity to cell lineage commitment and adaptation in response to specific cues. In the central nervous system, chromatin integrates a plethora of converging signaling pathways, leading to short- and long-term changes in gene expression that are crucial for neuronal commitment, terminal differentiation and neuroplasticity throughout life. Although a variety of ubiquitously expressed chromatin-remodeling complexes assist tissue-specific transcription factors in mediating histotype-restricted transcriptional regulation, neuro restricted chromatin-remodeling factors have just been recently described.
Here, I report the identification of four mammal-specific variants of the histone demethylase LSD1 / KDM1 arising from combinatorial retention of two alternatively spliced exons, resulting in either ubiquitous isoforms or neuro-restricted ones, which are dynamically regulated during cortical development. The neuro-specific variants, whose functional diversification partly relies on the phosphorylation status, contribute to the acquisition of neurite morphology in an exclusive way.
The expression of LSD1 splice variants is particularly regulated during perinatal stages, with a progressive increase of LSD1 neuro-specific isoforms over the ubiquitous ones and the same LSD1 splice dynamics can be fairly recapitulated in cultured cortical neurons reflecting the early synaptic establishment. While LSD1 isoforms exhibit a comparable demethylase activity in vitro, the sole neuro-specific isoforms display an altered repressor activity on a reporter gene in cortical neurons, where their overexpression enhances neurite morphogenesis. Conversely, the imbalance of LSD1 isoforms that are devoid of the neurospecific exon elicits no morphogenic effect, indicating that the arousal of neuronal LSD1 isoforms pace-makes early neurite morphogenesis. The genome wide-location of LSD1 in cortical neurons by chromatin immunoprecipitation sequencing reveals its extensive role in the regulation of promoters related to developmental processes, pattern specification and forebrain organogenesis, as well as the control of cell fate decisions and calcium induced neuronal signaling, confirming its neurogenic implication.
Furthermore, for those genes where multiple binding locations can be found at short and long distance from the same transcriptional start site, a wide-range LSD1 regulatory role can be hypothesized, possibly related to enhancers function.
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Chénard, Carol Anne. "Ribonucleoprotein complexes and protein arginine methylation : a role in diseases of the central nervous sytem". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115894.
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For the past 45 years, QKI has been studied for its role in the processes of development and central nervous system myelination using the qkv mouse. The presence of a single KH domain and the recent identification of a high-affinity binding site in mRNAs, suggests that it can bind to and regulate mRNAs through processes such as stability, splicing and transport. As a member of the STAR RNA binding family of proteins the QKI isoforms may also be involved in cell signaling pathways.QKI's involvement in all of these processes, lead us to examine both the protein partners and the mRNA targets of the QKI complex in order to identify potentially new pathways regulated by QKI. In doing so, we identified a novel direct protein-protein interaction with PABP and for the first time described the relocalization of QKI to cytoplasmic granules following oxidative stress. In addition, in vivo mRNA interaction studies were performed and allowed the identification of approximately 100 new mRNA targets in human glioblastoma cells. One of the targets identified was VEGF mRNA.
Another QKI target mRNA is MBP, a major protein component of the myelin sheath and the candidate auto-antigen in multiple sclerosis (MS). In vivo MBP is symmetrically dimethylated on a single arginine residue. To further establish the role of the methylation of MBP in myelination, a methyl-specific antibody and an adenovirus expressing a recombinant protein arginine methyltransferase 5 (PRMT5) was generated. We show that methylated MBP is found in areas of mature myelin and that overexpression of the PRTM5 blocked the differentiation of oligodendrocytes.
Taken together these datas implicate QKI for the first time in the process of human cancer angiogenesis and could explain the vascularization defects observed in some of the qkI mutant mice. In addition, arginine methylation of MBP may prove to have an important role in the process of myelination and in the pathogenesis of demyelination and the autoimmune reaction in diseases such as MS.
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Silvas, Tania V. "Investigating the Structural Basis for Human Disease: APOBEC3A and Profilin". eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/955.
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Analyzing protein tertiary structure is an effective method to understanding protein function. In my thesis study, I aimed to understand how surface features of protein can affect the stability and specificity of enzymes. I focus on 2 proteins that are involved in human disease, Profilin (PFN1) and APOBEC3A (A3A). When these proteins are functioning correctly, PFN1 modulates actin dynamics and A3A inhibits retroviral replication. However, mutations in PFN1 are associated with amyotrophic lateral sclerosis (ALS) while the over expression of A3A are associated with the development of cancer. Currently, the pathological mechanism of PFN1 in this fatal disease is unknown and although it is known that the sequence context for mutating DNA vary among A3s, the mechanism for substrate sequence specificity is not well understood.
To understand how the mutations in Profilin could lead to ALS, I solved the structure of WT and 2 ALS-related mutants of PFN1. Our collaborators demonstrated that ALS-linked mutations severely destabilize the native conformation of PFN1 in vitro and cause accelerated turnover of the PFN1 protein in cells. This mutation-induced destabilization can account for the high propensity of ALS-linked variants to aggregate and also provides rationale for their reported loss-of-function phenotypes in cell-based assays. The source of this destabilization was illuminated by my X-ray crystal structures of several PFN1 proteins. I found an expanded cavity near the protein core of the destabilized M114T variant. In contrast, the E117G mutation only modestly perturbs the structure and stability of PFN1, an observation that reconciles the occurrence of this mutation in the control population. These findings suggest that a destabilized form of PFN1 underlies PFN1-mediated ALS pathogenesis.
To characterize A3A’s substrate specificity, we solved the structure of apo and bound A3A. I then used a systematic approach to quantify affinity for substrate as a function of sequence context, pH and substrate secondary structure. I found that A3A preferred ssDNA binding motif is T/CTCA/G, and that A3A can bind RNA in a sequence specific manner. The affinity for substrate increased with a decrease in pH. Furthermore, A3A binds tighter to its substrate binding motif when in the loop region of folded nucleic acid compared to a linear sequence. This result suggests that the structure of DNA, and not just its chemical identity, modulates A3 affinity and specificity for substrate.
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Head, David John. "Molecular basis of nerve insensitivity resistance to pyrethroid insecticides in Heliothis virescens (Fabricius) and Helicoverpa armigera (Hübner) (Lepidoptera:Noctuidae)". Thesis, University of Reading, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393841.
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Morgan, H. M. C. "Developmental expression of the KCa2.3 channel subunit in the central nervous system and unravelling the molecular basis of the sAHP current regulation". Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19392/.
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Neuronal calcium-activated potassium currents are intimately involved in the regulation of cellular membrane potential. Different currents have been identified with diverse pharmacological and physiological properties and in many cases the molecular correlates of the currents have been identified. This thesis will seek to provide information about the molecular biology of two distinct Ca2+-activated K+ currents. In this study the distribution of the small conductance Ca2+-activated K+ channel SK3\alpha-subunit in rat brain during development will be described. Firstly, a polyclonal anti-CSK3 antibody was developed and affinity purified. Secondly, this antibody along with a commercial polyclonal antibody against the N-terminus of SK3 have been used to assess the developmental expression pattern of SK3 at five distinct post-natal time points (P1, P3, P6, P12 and P25). The distribution and level of SK3 expression remains constant throughout development and is in accordance with the pattern previously described for adult rat brain. SK3 is highly expressed in many different neuronal populations but of most interest are the high levels of expression seen in monoaminergic regions such as the substantia nigra pars compacta, locus coeruleus and the dorsal raphe nucleus, regions that have been examined in detail here. The slow afterhyperpolarisation is a Ca2+-activated potassium current present in a restricted number of cell types, chiefly the pyramidal cells of the hippocampus and neocortex. A study recently published identified the neuronal calcium sensor hippocalcin, whose expression is also limited to these cell types, as a key molecule responsible for gating the calcium activation of this current (Tzingounis et al. 2007). I have undertaken a yeast two-hybrid screen to identify potential interacting partners of hippocalcin in an attempt to elucidate the molecular pathway underlying the sAHP. This thesis will present the novel interaction between hippocalcin and the Mitogen- Activated Protein Kinase Kinase Kinase (MAP3K), Mixed Lineage Kinase 2 (MLK2 or MAP3K10).
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Baer, Matthew L. "Elucidating the Role of Endogenous Electric Fields in Regulating the Astrocytic Response to Injury in the Mammalian Central Nervous System". VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/4007.
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Endogenous bioelectric fields guide morphogenesis during embryonic development and regeneration by directly regulating the cellular functions responsible for these phenomena. Although this role has been extensively explored in many peripheral tissues, the ability of electric fields to regulate wound repair and stimulate regeneration in the mammalian central nervous system (CNS) has not been convincingly established. This dissertation explores the role of electric fields in regulating the injury response and controlling the regenerative potential of the mammalian CNS. We place particular emphasis on their influence on astrocytes, as specific differences in their injury-induced behaviors have been associated with differences in the regenerative potential demonstrated between mammalian and non-mammalian vertebrates. For example, astrocytes in both mammalian and non- mammalian vertebrates begin migrating towards the lesion within hours and begin to proliferate after an initial delay of two days; subsequently, astrocytes in non-mammalian vertebrates support neurogenesis and assume a bipolar radial glia-like morphology that guides regenerating axons, whereas astrocytes in mammals do not demonstrate robust neurogenesis and undergo a hypertrophic response that inhibits axon sprouting. To test whether injury-induced electric fields drive the astrocytic response to injury, we exposed separate populations of purified astrocytes from the rat cortex and cerebellum to electric field intensities associated with intact and injured mammalian tissues, as well as to those electric field intensities measured in regenerating non-mammalian vertebrate tissues. Upon exposure to electric field intensities associated with uninjured tissue, astrocytes showed little change in their cellular behavior. However, cortical astrocytes responded to electric field intensities associated with injured mammalian tissues by demonstrating dramatic increases in migration and proliferation, behaviors that are associated with their formation of a glial scar in vivo; in contrast, cerebellar astrocytes, which do not organize into a demarcated glial scar, did not respond to these electric fields. At electric field intensities associated with regenerating tissues, both cerebellar and cortical astrocytes demonstrated robust and sustained responses that included morphological changes consistent with a regenerative phenotype. These results support the hypothesis that physiologic electric fields drive the astrocytic response to injury, and that elevated electric fields may induce a more regenerative response among mammalian astrocytes.
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FERRARI, BEATRICE. "Un nuovo profarmaco a base di platino: il suo effetto antitumorale e nuovi approcci in vitro per comprendere nuovi target per il trattamento di tumori del sistema nervoso". Doctoral thesis, Università degli studi di Pavia, 2020. http://hdl.handle.net/11571/1301306.
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Jacquesson, Timothée. "Tractographie des nerfs crâniens : état de l'art, développement et application en chirurgie des tumeurs de la base du crâne". Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1309/document.
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Apparue à la fin des années 1990, la tractographie utilise le signal diffusion de l’imagerie par résonance magnétique (IRM) pour détecter l’orientation préférentielle des molécules d’eau et reconstruire l’architecture des tissus biologiques, notamment celle des fibres blanches intra cérébrales. Cette technique a suscité l’engouement de la communauté scientifique en permettant, pour la première fois, l’étude in vivo non invasive des structures anatomiques, et en particulier celle du cerveau. Néanmoins, la description de la trajectoire des fibres blanches reste imprécise dans les zones de croisement de fibres et pour les faisceaux de petite taille comme les nerfs crâniens. De multiples méthodes sont développées aux différents étapes d’acquisition et de post-traitement afin d’améliorer la résolution spatiale et angulaire et augmenter la précision de la reconstruction des fibres. En pratique clinique, la détection de la trajectoire des nerfs crâniens déplacés au contact des tumeurs de la base du crâne pourrait apporter une aide significative dans la stratégie chirurgicale et améliorer le résultat fonctionnel pour les patients.Après avoir rappelé les notions fondamentales nécessaires à la compréhension de chaque étape de la tractographie, nous en présentons l’ « état de l’art » dans le cas particulier des nerfs crâniens. A partir de 21 études de la littérature scientifique, nous détaillons tous les paramètres d’acquisition et de tracking, les algorithmes de reconstruction, le design des régions d’intérêt et le filtrage. Puis, nous développons notre propre pipeline de tractographie et montrons son impact sur la prise en charge chirurgicale à travers une série de 62 cas de tumeurs variées de la base du crâne et 2 vignettes cliniques illustratives. Enfin, nous proposons une nouvelle approche, la full-tractography, avec une utilisation potentielle en routine clinique, notamment lors du planning pré-chirurgicalTractography is a recent imaging tool that used the diffusion signal from the magnetic resonance imaging (MRI) to detect the preferential orientation of water molecules within the tissues and particularly along white fibers of the brain. This technique has caught the attention of the scientific community describing non-invasively the in vivo white matter architecture. Nonetheless, its application to fiber crossing areas or to small-scale structures, such as cranial nerves, remains inaccurate. New methods are being developed for both the acquisition and post-processing steps to provide a higher angular and spatial resolution imaging, and improve the reconstruction of fibers. In the clinical setting, the detection of the trajectory of the cranial nerves displaced by skull base tumors could be a relevant asset for the surgical strategy and the functional outcome. After reminding the basics to understand each step involved in tractography, we present the current state-of-the-art for application to cranial nerves. From 21 selected studies, we report all parameters of acquisition and tracking, algorithms of reconstruction, the design of the regions of interest, and filtering. We then develop our tractography pipeline and show its value for the surgical management through a 62 case series of various skull base tumors and two clinical images. Finally, we propose a new full-tractography approach that could be implemented in routine, notably for presurgical planning
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Gruenhagen, Jason Alan. "Bioanalytical Applications of Real-Time ATP Imaging Via Bioluminescence". Washington, D.C. : Oak Ridge, Tenn. : United States. Dept. of Energy. Office of Science ; distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy, 2003. http://www.osti.gov/servlets/purl/822057-FTilZ3/native/.
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Thesis (Ph.D.); Submitted to Iowa State Univ., Ames, IA (US); 12 Dec 2003.Published through the Information Bridge: DOE Scientific and Technical Information. "IS-T 2604" Jason Alan Gruenhagen. 12/12/2003. Report is also available in paper and microfiche from NTIS.
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Brabb, Thea. "The fate of MBP-specific T cells in MBP TCR transgenic mice /". Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/10853.
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Saarikettu, Juha. "Calcium regulation and functions of basic Helix-Loop-Helix transcription factors". Doctoral thesis, Umeå : Department of Molecular Biology, Umeå University, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-537.
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Allan, Douglas Watt. "Prenatal development of the rat phrenic nerve and diaphragm, basic embryology, role of PSA-NCAM and the pathogenesis of congenital diaphragmatic hernia". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0009/NQ59925.pdf.
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Flanagan, Shawn D. "Neurological Basis of Persistent Functional Deficits after Traumatic Musculoskeletal Injury". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1469031876.
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Pertici, Vincent. "Récupération induite par l'implantation d'hydrogels, à base de polymères et de copolymères à blocs, suite à un traumatisme médullaire : analyse comportementale, électrophysiologique et histologique". Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM4026/document.
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Il n'existe actuellement aucun traitement efficace pour les patients présentant une blessure au niveau de la moelle épinière. Ce triste constat est, en partie, dû à la présente d'une cicatrice empêchant la repousse des tissus. Dans ce contexte, des biomatériaux (composés non-toxiques) pourraient être implantés afin de réduire la cicatrice en formation et de fournir un support de repousse aux fibres nerveuses. Parmi ces biomatériaux, certains semblent induire de nombreuses améliorations chez le rat. Nous avons renforcé ces résultats, à l'aide de techniques électrophysiologiques. De plus, nous avons développé un nouveau matériau dégradable afin de limiter toutes réactions délétères à long terme. Après avoir synthétisé notre matériau, combinant les qualités de dégradabilité de l'acide poly(lactique) et les propriétés mécaniques du poly(méthacrylate d'hydroxyéthyle), nous avons évalué ses différentes caractéristiques et ses effets thérapeutiques. Les résultats obtenus sont encourageants. Il serait maintenant intéressant de coupler notre biomatériau à des molécules bioactives ou à des cellulesCurrently, there is no treatment for patients with spinal cord injury. This pessimistic statement is, in part, due to the presence of a scar that prevents tissue regrowth. In this context, biomaterials (non-toxic compounds) could be implanted in order both to reduce the scar formation and to provide a growth support for nervous fibers. Among those biomaterials, many seem to induce numerous benefic effects in the rat model. We confirmed these data by the use of electrophysiological techniques. In addition, we developed a new degradable material so as to limit any long term deleterious reactions. After having synthesized our material, combining the degradable quality of the poly(lactic acid) and the mechanical properties of the poly(hydroxyethyl methacrylate), we analyzed its different characteristics and its therapeutic effects. The obtained results are encouraging. Now, it would be interesting to couple bioactive molecules or cells with our biomaterial scaffold
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Carmo, Samuel Sullivan. "Sistema de gerenciamento da informação: alterações neurológicas em chagásicos crônicos não-cardíacos". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/17/17140/tde-26052010-105637/.
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O presente trabalho ocupa-se no desenvolvimento de um sistema computacional de gerenciamento da informação para auxiliar os estudos científicos sobre o sistema nervoso de chagásicos crônicos não-cardíacos. O objetivo é desenvolver o sistema requerido, pelo pressuposto de praticidade nas análises decorrentes da investigação. O método utilizado para desenvolver este sistema computacional, dedicado ao gerenciamento das informações da pesquisa sobre as alterações neurológicas de seus sujeitos, foi; compor o arquétipo de metas e a matriz de levantamento de requisitos das variantes do sistema; listar os atributos, domínios e qualificações das suas variáveis; elaborar o quadro de escolha de equipamentos e aplicativos necessários para sua implantação física e lógica e; implantá-lo mediante uma modelagem de base de dados, e uma programação lógica de algoritmos. Como resultado o sistema foi desenvolvido. A discussão de análise é; a saber, que a informatização pode tornar mais eficaz as operações de cadastro, consulta e validação de campo, além da formatação e exportação de tabelas pré-tratadas para análises estatísticas, atuando assim como uma ferramenta do método científico. Ora, a argumentação lógica é que a confiabilidade das informações computacionalmente registradas é aumentada porque o erro humano é diminuído na maioria dos processamentos. Como discussão de cerramento, estudos dotados de razoável volume de variáveis e sujeitos de pesquisa são mais bem geridos caso possuam um sistema dedicado ao gerenciamento de suas informações.This is the development of a computer information management system to support scientific studies about the nervous system of non-cardiac chronic chagasic patients. The goal is to develop the required system, by assumption of the convenience in the analysis of research results. The method used to develop this computer system, dedicated to information management of research about the neurological disorders of their human subject research, were; compose the archetypal matrix of targets and requirements elicitation of the system variants; list the attributes, qualifications and domains of its variables; draw up the choice framework of equipment and required applications for its physical and logic implementation, and; deploying it through a data modeling, an adapted entity-relationship diagram and programmable logic algorithms. As a result the required system was developed. The analytical discussion is that the computerization makes the data processing faster and safer. The more practical information management processes are: the operations of registration, queries and fields\' validations, as well as the advanced and basic queries of records, in addition to table formatting and exporting of pre-treated for statistical analysis. The logical argument is that the reliability of the recorded computationally information is increased because is insured that bias of human error is absent from most of the steps, including several the data processing operations. As end discussion, scientific studies with reasonable amount of variables and research subjects are better managed if they have a dedicated system to managing their information.
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Kele, Olovsson Julianna M. V. "Regulation of midbrain dopaminergic neuron development by Wnts, sFRPs and bHLH proteins/". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-242-2/.
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Fischer, Linda [Verfasser], Felix Christian [Akademischer Betreuer] Felmy, Anaclet [Akademischer Betreuer] Ngezahayo y Evgeni [Akademischer Betreuer] Ponimaskin. "Input-Output Functions of Sensory Neurons in the Central Nervous System with Focus on the Physiological Basis underlying Information Transfer in the VNLL / Linda Fischer ; Felix Felmy, Anaclet Ngezahayo, Evgeni Ponimaskin". Hannover : Stiftung Tierärztliche Hochschule Hannover, 2020. http://d-nb.info/1224232968/34.
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Castelnovo, L. F. "MOLECULAR BASIS FOR THE DEVELOPMENT OF INNOVATIVE THERAPIES FOR PERIPHERAL NEUROPATHIES TREATMENT: ROLE AND CROSS-REGULATION OF THE GABAERGIC SYSTEM AND NEUROACTIVE STEROIDS". Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/465187.
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Peripheral neuropathies are a heterogeneous group of pathologies with a high prevalence worldwide, which are characterized by alterations of peripheral nerves structure and function. Their treatment is currently a challenge for clinicians. Indeed, even if continuous progresses are made in the study of the basic mechanisms underlying these pathologies, etiology is still unknown in a significant number of cases. Different compounds, such as growth factors, adhesion proteins, neurotransmitters, enzymes, peptides and neuroactive steroids, have been proposed to play important roles in the patho-physiology of the peripheral nervous system. Therefore, most of the research is addressed to identify the molecules that might represent the more promising therapy for this set of pathologies.
This thesis focuses on some aspects of the patho-physiological role of the GABAergic system and neuroactive steroids in the peripheral nervous system.
Several papers in literature strongly support the hypothesis that they are both present and active in the peripheral nervous system, in particular in Schwann cells, the myelinating cells of the peripheral nervous system. These cells are indeed able to synthesize GABA and neuroactive steroids and express both the ionotropic GABA-A and the metabotropic GABA-B receptor. In order to deepen the knowledge on this topic, four research lines were pursued in my PhD program and are described in this thesis. The first line regarded the analysis of the effects of specific GABA-B ligands on nerve regeneration in a model of neuropathic pain caused by nerve ligation. These studies showed that the specific GABA-B antagonist CGP56433 was able to recover some morphological, functional and biochemical parameters in peripheral nerves. Surprisingly, some of these effects were potentiated by the co-treatment with GABA-B specific agonist baclofen, suggesting the co-activation of possible central and peripheral mechanisms. The second research line regarded the analysis of different GABA-A subunits in dorsal root ganglia (DRG) neurons of a model of conditional knockout mice, in which the GABA-B1 receptor is specifically deleted in Schwann cells. The results showed a modulation of different GABA-A subunits, pointing to a down-regulation of GABA-A receptors, mainly regarding the synaptic ones. This evidence may contribute to understand some of the alterations that were previously observed in this conditional knockout mouse model. The third research line dealt with the study of the modulation of protein kinase C-type ε (PKCε), an important neuropathic pain mediator, and its possible cross-talk with the GABA-A receptor and the neuroactive steroid allopregnanolone. The results showed that allopregnanolone down-modulates PKCε expression in Schwann cells, but the direct treatment on DRG neurons did not lead to any significant effect. However, Schwann cells conditioned medium was able to induce a significant up-regulation of PKCε gene expression in DRG neurons. Also the membrane expression of PKCε phosphorylated form resulted to be modulated in similar way. These findings suggest a possible involvement of PKCε in the GABA-A mediated control of pain transmission exerted by allopregnanolone, also pointing out to a Schwann cell-mediated process. Finally, the fourth research line regarded the identification of a novel family of progestogen receptors localized on the cell membrane (mPRs) and PGRMC1 in Schwann cells; moreover, their putative role in the modulation of Schwann cell physiology was also investigated. The data demonstrated the expression of these receptors in Schwann cell plasma membrane. The treatment with a specific mPR agonist proved able to induce cell migration at short time points (2-4 hours) and increased the expression of myelin associated glycoprotein (MAG) at longer time points (24-36 hours), giving a first demonstration of a role for these receptors in Schwann cells. The identification of this new signaling pathway will allow a better understanding of progestogen actions in Schwann cells.
In conclusion, the results presented in this thesis shed some light on some basic mechanism controlling the patho-physiology of the peripheral nervous system, whose comprehension may lead to the identification of new more specific drugs for peripheral neuropathies treatment.
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Chan, Kara Y. "MECHANISMS OF TRINUCLEOTIDE REPEAT INSTABILITY DURING DNA SYNTHESIS". UKnowledge, 2019. https://uknowledge.uky.edu/toxicology_etds/29.
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Genomic instability, in the form of gene mutations, insertions/deletions, and gene amplifications, is one of the hallmarks in many types of cancers and other inheritable genetic disorders. Trinucleotide repeat (TNR) disorders, such as Huntington’s disease (HD) and Myotonic dystrophy (DM) can be inherited and repeats may be extended through subsequent generations. However, it is not clear how the CAG repeats expand through generations in HD. Two possible repeat expansion mechanisms include: 1) polymerase mediated repeat extension; 2) persistent TNR hairpin structure formation persisting in the genome resulting in expansion after subsequent cell division. Recent in vitro studies suggested that a family A translesion polymerase, polymerase θ (Polθ), was able to synthesize DNA larger than the template DNA. Clinical and in vivo studies showed either overexpression or knock down of Polθ caused poor survival in breast cancer patients and genomic instability. However, the role of Polθ in TNR expansion remains unelucidated. Therefore, we hypothesize that Polθ can directly cause TNR expansion during DNA synthesis. The investigation of the functional properties of Polθ during DNA replication and TNR synthesis will provide insight for the mechanism of TNR expansion through generations.
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Mao, Weiming. "The role of bHLH gene ash1 in the developing chick eye". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/mao.pdf.
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Grenier, Etienne. "Evaluation des effets physiologiques, neurophysiologiques et comportementaux liés au port de bas médicaux de compression". Thesis, Lyon, INSA, 2013. http://www.theses.fr/2013ISAL0130.
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La thérapie par compression médicale est reconnue comme une composante essentielle dans le traitement des pathologies veineuses et demeure incontournable dans la prise en charge des affections veineuses aux différents stades de la pathologie (jambes lourdes, œdèmes, ulcères). Si le bénéfice est reconnu par les patients eux-mêmes ainsi que par les médecins, il n’existe à l’heure actuelle que peu d’éléments permettant de quantifier ce bénéfice. Dans ce contexte, l’objectif de ces travaux de thèse est d’apporter des éléments de compréhension et d’objectiver les effets bénéfiques des bas médicaux de compression (BMC) aux niveaux physiologique, neurophysiologique et comportemental. Trois axes de recherche ont été dégagés. Le premier axe de recherche est l’étude de l’effet de la compression sur l’activité microcirculatoire cutanée dans les membres inférieurs en utilisant le dispositif Hématron, dispositif ambulatoire exclusif d’évaluation de l’activité microcirculatoire cutanée. Les résultats ont montré une amélioration de l’activité microcirculatoire pour différentes classes de BMC et pour différentes positions. Ces résultats tendraient à mettre en cause l’hypothèse, largement admise, que les BMC améliorent le retour veineux principalement en diminuant la section des veines (superficielles voire profondes). La deuxième piste de recherche concerne l’objectivation de l’amélioration de la qualité de vie liée au port des BMC, généralement exprimée subjectivement par les personnes atteintes de pathologie veineuse. Les résultats préliminaires montrent que l’analyse de la variabilité cardiaque permet de mettre en évidence une relation entre le paramètre indicateur de l’activité de la balance sympatho-vagale et le port de la compression médicale au cours d’une journée. Compte tenu de la grande dispersion des résultats, cette étude serait à poursuivre sur une population plus large pour aboutir à des conclusions fiables. Le dernier axe de recherche est lié à l’impact du port des BMC sur le comportement du sujet et plus précisément sur sa déambulation. Les patients déclarent une fatigue physique dans les membres inférieurs moins intense en fin de journée grâce à la compression médicale. Notre hypothèse est que le port des BMC impacterait directement la dynamique de la déambulation. Pour évaluer la cinétique de la marche, nous avons conçu, développé et validé une instrumentation intégrant des capteurs accéléromètres. Des tests préliminaires ont permis de dégager des paramètres pertinents caractéristiques de la déambulation. La prochaine étape sera de conduire une campagne d’expérimentation destinée à objectiver la fatigue comportementale en fin d’après-midi mesurée avec ou sans compression médicale portée au cours de la journéeMedical compression therapy is recognized as an essential component in the treatment of venous diseases and is indispensable in the treatment of venous diseases at different stages of the disease (heavy legs, edema and ulcers). Although the benefit is recognized by the patients themselves and by physicians, there is at present little evidence to quantify this benefit. Against this background, the aim of this thesis is to provide more understanding and objectify the benefits of compression stockings (MCS) on in terms of physiology, neurophysiology and gait dynamics. Three areas of research were identified and studied. The first line of research is the study of the effect of compression on skin microcirculatory activity in the lower limbs using the Hematron ambulatory device. The results showed an improvement in skin blood flow activity for different classes of MCS and at different positions. These results would tend to challenge the widely accepted assumption that MCS improve venous return primarily by decreasing the cross-sectional area of (superficial or deep) veins. The second line of research involves the objectification of the improvement in the quality of life resulting from the wearing of MCS, usually this is expressed subjectively by people with venous disease. Preliminary results show that the analysis of heart rate variability highlights a relationship between the indicators of sympathovagal balance activity and the use of medical compression during the day. Given the wide dispersion in the results, this study should be carried out on a larger population to draw more reliable conclusions. The last line of research relates to the impact of MCS on the behavior and, in particular, the gait of the subject. Patients report that physical fatigue in the lower limbs is less prevalent at the end of the day with compression therapy. Our hypothesis is that the wearing of MCS has a direct impact on gait. To evaluate the kinetics of walking, we have designed, developed and validated an instrumentation involving accelerometers sensors. Preliminary tests have yielded relevant parameters characteristic of gait dynamics. The next step is to conduct an experimental campaign to objectify behavioral fatigue, with or without the wearing of medical compression, at the end of the afternoon
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Hou, Tianfei. "MECHANISMS AND POTENTIAL THERAPY ON DISRUPTED BLOOD PRESSURE CIRCADIAN RHYTHM IN DIABETES". UKnowledge, 2018. https://uknowledge.uky.edu/pharmacol_etds/26.
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Arterial blood pressure (BP) undergoes a 24-hour oscillation that peaks in the active day and reaches a nadir at night during sleep in humans. Reduced nocturnal BP fall (also known as non-dipper) is the most common disruption of BP circadian rhythm and is associated with increased risk of untoward cardiovascular events and target organ injury. Up to 75% of diabetic patients are non-dippers. However, the mechanisms underlying diabetes associated non-dipping BP are largely unknown. To address this important question, we generated a novel diabetic db/db-mPer2Luc mouse model (db/db-mPer2Luc) that allows quantitatively measuring of mPER2 protein oscillation by real-time mPer2Luc bioluminescence monitoring in vitro and in vivo. Using this model, we demonstrated that the db/db-mPer2Luc mice have a diminished BP daily rhythm. The phase of the mPER2 daily oscillation is advanced to different extents in explanted peripheral tissues from the db/db-mPer2Luc mice relative to that in the control mice. However, no phase shift is found in the central oscillator, the suprachiasmatic nucleus (SCN). The results indicate that the desynchrony of mPER2 daily oscillation in the peripheral tissues contributes to the loss of BP daily oscillation in diabetes.
Extensive research over the past decades has been focused on how the components of food (what we eat) and the amount of food (how much we eat) affect metabolic diseases. Only recently has it become appreciated that the timing of food intake (when we eat), independent of total caloric and macronutrient quality, is also critical for metabolic health. To investigate the potential effect of the timing of food intake on the BP circadian rhythm, we simultaneously monitored the BP and food intake profiles in the diabetic db/db and control mice using radiotelemetry and BioDAQ systems. We found the loss of BP daily rhythm is associated with disrupted food intake rhythm in the db/db mice. In addition, the normal BP daily rhythm is altered in the healthy mice with abnormal feeding pattern, in which the food is available only during the inactive-phase. To explore whether imposing a normal food intake pattern is able to prevent and restore the disruption of BP circadian rhythm, we conducted active-time restricted feeding (ATRF) in the db/db mice. Strikingly, ATRF completely prevents and restorers the disrupted BP daily rhythm in the db/db mice. While multiple mechanisms likely contribute to the protection of ATRF on the BP daily rhythm, we found that ATRF improves the rhythms of energy metabolism, sleep-wake cycle, BP-regulatory hormones and autonomic nervous system (ANS) in the db/db mice. To further investigate the molecular mechanism by which ATRF regulates BP circadian rhythm, we determined the effect of ATRF on the mRNA expressions of core clock genes and clock target genes in the db/db mice. Of particular interest is that we found among all the genes we examined, the mRNA oscillation of Bmal1, a key core clock gene, is disrupted by diabetes and selectively restored by the ATRF in multiple peripheral tissues in the db/db mice. More importantly, we demonstrated that Bmal1 is partially required for ATRF to protect the BP circadian rhythm.
In summary, our findings indicate that the desynchrony of peripheral clocks contributes to the abnormal BP circadian pattern in diabetes. Moreover, our studies suggest ATRF as a novel and effective chronotherapy against the disruption of BP circadian rhythm in diabetes.
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Daval, Jean-Luc. "Les dérivés puriques au niveau du système nerveux central : Caractérisation de la libération des dérivés adenyliques par des préparations synaptosomales : implication possible des purines dans le mécanisme d'action des benzodiazepines". Nancy 1, 1986. http://www.theses.fr/1986NAN10045.
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Étude des mécanismes impliqués, le métabolisme et la libération des dérivés adényliques ont été étudiés à partir de terminaisons nerveuses isolées du néocortex de cobaye. Hypothèse d'une participation des mécanismes "purinergiques" dans le mode d'action des benzodiazépines au niveau du système nerveux central