Tesi sul tema "Latent inhibition"
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1
Jakob, Andrea F. (Andrea Frances). "The effects of serotonergic ligands on latent inhibition". Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23401.
Testo completoAbstract (sommario):
Latent inhibition (LI) is the attenuation in the acquisition of Pavlovian conditioning to a conditioned stimulus (CS) due to prior extensive exposure to that CS. It is assumed that LI is an animal model of attention in that animals learn to ignore the preexposed CS. The present series of experiments investigated the effects of selective serotonergic (5-HT) ligands known to increase 5-HT neurotransmission on LI using a conditioned emotional response (CER) procedure. In experiment 1, rats preexposed (PE) to 40 presentations of a tone CS acquired CER suppression more slowly than vehicle-treated nonpreexposed (NPE) animals, suggesting LI was obtained. Administration of 10 mg/kg fluoxetine (i.p.) did not influence CER acquisition in PE animals, suggesting that LI was not affected by fluoxetine. However, it was assumed that 40 CS presentations exerted a powerful LI effect, which might mask any effect of fluoxetine. Consequently, we assessed the effects of 5-HT ligands on LI following 10, rather than 40, CS preexposures. Under these conditions, both acute fluoxetine (experiment 2), and chronic (14 day) fluoxetine (experiment 3) administration, were found to augment LI. Experiment 4 suggested that acute administration of the 5-HT2 agonist DOI (2.5 mg/kg) also enhances LI. Experiment 5 revealed that 1 mg/kg 8-OH-DPAT did not influence LI, suggesting that postsynaptic 5-HT1a receptors are not involved in LI. These results suggest that enhancement of 5-HT neurotransmission enhance LI and that this effect is mediated, in part, through the 5-HT2 receptor subtype. The results are discussed within the context of the switching model of LI, which suggests that the effects of 5-HT are mediated through the modulation of the mesolimbic dopamine pathway.
2
Killcross, Andrew Simon. "Dopaminergic mechanisms and latent inhibition : implications for schizophrenia". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261541.
Testo completo
3
Leung, Hiu Tin Psychology Faculty of Science UNSW. "Spontaneous recovery in Pavlovian fear extinction and latent inhibition". Publisher:University of New South Wales. Psychology, 2009. http://handle.unsw.edu.au/1959.4/43701.
Testo completoAbstract (sommario):
The experiments reported in the present thesis examined the behavioural processes of Pavlovian fear extinction and latent inhibition. The first series of experiments studied the reacquisition of extinguished fear responses following different amounts of extinction training. Rapid reacquisition occurred when rats were reconditioned after moderate extinction, showing that the original learning remained intact across this extinction. In contrast, when reconditioning was given after massive extinction, reconditioned responding was first depressed but then spontaneously recovered over time. This suggests that massive extinction produces a relatively permanent loss of the originally learned responding, while additionally imposes on the extinguished CS a transient latent inhibitory process that prevented the immediate but not the delayed expression of reconditioning. The second series of experiments studied the impact of spontaneous recovery of extinguished fear responses on their additional extinction. These experiments demonstrated that a CS that had time to show spontaneous recovery underwent greater response loss across additional extinction than one lacking recovery. They also showed that an excitor extinguished in compound with a CS showing recovery suffered greater response loss than an excitor extinguished in compound with a CS lacking recovery. Further, extinction of a compound composed of two CSs, one showing recovery and a second lacking recovery, produced greater extinction to the CS that showed recovery. These results show that spontaneous recovery of extinguished responses deepens their extinction through an error-correction mechanism regulated by both common and individual error terms. The third series of experiments studied the spontaneous recovery of latently inhibited and extinguished fear responses in within-subject designs. Using a compound test procedure, a CS that had received extensive preexposure or extensive extinction was found to have undergone greater spontaneous recovery relative to a CS just moderately preexposed or moderately extinguished. A CS given a mixed history of preexposure and extinction also underwent greater recovery relative to a CS just preexposed or just extinguished. These results suggest that both latent inhibition and extinction share a transient depressive process, and that the resulting recovery of responding is proportional to the amount of this depression.
4
Tsakanikos, Elias. "Latent inhibition and psychometrically defined schizotypy : an experimental investigation". Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405897.
Testo completo
5
Martins, Serra Ana Maria. "Latent inhibition and the Kamin blocking effect in schizophrenia and schizotypy". Thesis, King's College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307402.
Testo completo
6
Gray, Nicola Susan. "The attentional deficit in schizophrenia : a neurobiological account". Thesis, King's College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319152.
Testo completo
7
Schmidt-Hansen, Mia. "Evaluation of latent inhibition and learned irrelevance as assays of attentional abnormalities in schizotypy". Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/56176/.
Testo completoAbstract (sommario):
The claim that the positive symptoms of schizophrenia are associated with attentional abnormalities was investigated by using naturally occurring individual differences in schizotypic characteristics in a normal population of undergraduate students. Attention was measured using a variety of novel procedures that assessed latent inhibition (Chapters 2 and 3), learned irrelevance (Chapters 4 and 5) and stimulus detection (Chapter 6). The results provide restricted support for the claim that attentional processes are aberrant in groups of participants with high schizotypy scores (in particular high levels of unusual experiences on the Oxford-Liverpool Inventory of Feelings and Experiences).
8
Quinn, Veronica Frances. "Sources of learning and their role in the experience of placebo nausea". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15541.
Testo completoAbstract (sommario):
The purpose of the project was to better understand sources of learning that lead to placebo nausea, with the aim of developing interventions with clinical utility. After introducing theory regarding placebo effects and nausea in Chapter 1, Chapter 2 systematically reviewed studies that had previously attempted to manipulate nausea via the placebo effect. This review revealed that there were some features of interventions associated with success, but that results were often conflicting and a better paradigm to model placebo nausea in healthy participants was required. Chapter 3 introduced such a paradigm, illustrating how Galvanic Vestibular Stimulation (GVS) could be used to administer both placebo and nauseating stimulation under the guise of an experiment looking at the effects of GVS on spatial ability. Chapter 4 presented a study that used this paradigm to explore the development of placebo-induced relief from nausea through instruction, conditioning, and their combination. Both sources of learning reduced nausea on test relative to controls. Chapter 5 refocused on the problem of nausea that is incidentally conditioned in the treatment context. A model of conditioned nausea was tested, and it appeared that conditioning had developed and had also generalized perfectly well to a new test context. This finding was taken as evidence that the GVS device had overshadowed any context-nausea learning, and was used to inform the development of a new latent inhibition paradigm tested in Chapters 6 and 7. Chapter 6 pre-exposed these GVS-related reactive cues in the form of placebo stimulation in an attempt to retard conditioning through latent inhibition. Here, pre-exposure reduced conditioned nausea to the placebo on test relative to a group who did not receive pre-exposure, and had reduced nausea to the level of a control group who received no conditioning. Given that the applicability of any such intervention to applied settings rests on its ethicality, in a novel extension, Chapter 7 tested whether this latent inhibition effect required deception. This study replicated the effect of pre-exposure observed in Chapter 6, as well as finding that latent inhibition occurred to the same extent in a group fully informed as to the nature of the pre-exposure phase. Together, these findings suggest that placebo effects can occur after both instruction and conditioning, and that taking advantage of placebo effects in the clinic could offer an important method of intervening to reduce nausea.
9
Gracey, David J. "An investigation of some CCK ligands as potential antipsychotic compounds using latent inhibition in rats". Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388091.
Testo completo
10
Lawrence, Natalia Sophie. "The role of ventral pallidal GABA transmission in latent inhibition : a behavioural and neurochemical study". Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251870.
Testo completo
11
Kirsch, Philine Elea [Verfasser]. "Targeting the Latent Persistence of KSHV through Inhibition of LANA – DNA Interaction / Philine Elea Kirsch". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1214640826/34.
Testo completo
12
Lee, Dong Hyung. "Testing executive function models of ADHD and its comorbid conditions: A latent variable approach". Diss., Texas A&M University, 2004. http://hdl.handle.net/1969.1/2801.
Testo completoAbstract (sommario):
Current theoretical models of ADHD (i.e., Disinhibition Model: Barkley, 1997; Working Memory Model: Rapport et al., 2001) conceptualize ADHD as the disorder of executive function (EF) with some variation in their emphases on particular components of the broadly-defined EF (e.g., working memory vs. inhibition) and in their postulated relationships with ADHD symptoms. Although these models provide systematic accounts of the manifestation of ADHD, they have not been extensively tested from an empirical standpoint. Moreover, despite the fact that ADHD is highly comorbid with other additional conditions such as learning and behavioral problems and EF deficits are found in individuals with these conditions as well as in those with ADHD, current EF models have not specified the developmental relationship between ADHD and its comorbid conditions. This study was: (1) to examine the extent to which two current models of ADHD are supported in a sample of 102 adults; (2) to present an ??integrated?? model by combining two current models of ADHD and linking them to recent research findings on two common comorbid conditions with ADHD (i.e., reading difficulty and substance abuse); and (3) to test and revise such an integrated model in the light of data using a latent variable analysis. Major findings provided a strong support for the Working Memory Model with a lesser degree of support for the Disinhibition Model. Preliminary evidence of working memory as the primary deficit in ADHD was also obtained in the present sample. Finally, the integrated EF model and its revised model (final model) demonstrated a very good fit to the data. These findings suggest that the integrated model provides a unified account of how EF deficits contribute to the manifestation of ADHD symptoms and comorbid conditions with ADHD. Given some limitations (e.g., sample size and scope) of the present study, current findings need to be replicated.
13
Cassaday, Helen John. "The effects of pharmacological and neurotoxic manipulation of serotonergic activity on latent inhibition in the rat". Thesis, King's College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294276.
Testo completo
14
Chandra, Sathees B. C. "Heritable variation for learning : molecular analysis of reversal learning and latent inhibition in the honeybee, Apis millifera /". The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu148819515435839.
Testo completo
15
Shockley, Natalie. "Schizophrenia & information processing : a comparison of the prepulse inhibition, latent inhibition, P-50 gating, and mismatch negativity paradigms, with schizophrenia, bipolar and well control samples /". [St. Lucia, Qld.], 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17131.pdf.
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16
Bay-Richter, Cecilie. "The Role of Dopamine D2 adn D1 Receptor Subtypes in Latent Inhibition : Behavioural Studies in Gene Knockout Mice". Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508158.
Testo completo
17
Yang, Xinhai, e 楊新海. "Latent membrane protein 1 of Epstein-barr virus induces cell proliferation and participates in the inhibition of replicativesenescence". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31241256.
Testo completo
18
Trimble, Karen M. "The development and evaluation of latent inhibition in the rat as an animal model of schizophrenic attentional deficit". Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286859.
Testo completo
19
Harrington, Nicholas R. "The role of the nucleus accumbens in the development of latent inhibition : implications for animal models of schizophrenia". Thesis, University of York, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242202.
Testo completo
20
Yap, Carol Sue Lynn Psychology Faculty of Science UNSW. "An analysis of late-developing learning and memory systems in rats: fear-potentiated startle and context-specific latent inhibition and extinction". Awarded by:University of New South Wales. Psychology, 2006. http://handle.unsw.edu.au/1959.4/24374.
Testo completoAbstract (sommario):
Eleven experiments examined two late-developing learning and memory systems in rats: fear-potentiated startle (FPS) and the contextual regulation of latent inhibition and extinction. The first study was based on three previous developmental findings on FPS: (1) FPS to an odour CS emerges at postnatal day (PN) 23; Rats conditioned at PN16 to an odour CS express freezing but not FPS when tested at PN23, and (3) FPS to an odour CS trained at PN16 is activated if rats are also trained to a difference odour at PN23 (Yap, Stapinski, & Richardson, 2005). Yap et al. (2005) hypothesised that the activation effect only occurs if rats are given training to the second odour at an age when FPS has emerged. Study 1 assessed this hypothesis and trained the second odour CS at either PN23 or PN20. Contrary to expectations, the results of this study showed the activation effect for both groups of rats. Surprisingly, the results also revealed a significant FPS effect to the odour CS trained at PN20. Subsequent experiments examined this unexpected result, and found that learning to odour 1 at PN16 facilitated the age of onset for FPS at PN20. The results of Study 1 are discussed in relation to past findings on enrichment, cumulative learning, and neurobiological models of conditioned fear. The second section of this thesis (Studies 2 and 3) examined the context-specificity of two memory interference paradigms, latent inhibition and extinction, in developing rats. The studies found that both phenomena were context-specific at PN23-25 but not at PN16-18. Moreover, the results suggest that the context-specificity of both latent inhibition depended on the age of the rat during the second phase of training, but not their age during the first phase of training or their age at test. The implications of these findings for theoretical and neural models of learning, as well as the occurrence of latent inhibition and extinction during development are discussed.
21
McCartan, D. "The effects of antipsychotic medication on latent inhibition and other measures of cognition : studies in healthy volunteers and people with schizophrenia". Thesis, Queen's University Belfast, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273097.
Testo completo
22
McDonald, Louise Mary. "The effects of 5 HTâ‚‚â†A antagonists and noise on latent inhibition in rats : a model of schizophrenic attentional dysfunction". Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249512.
Testo completo
23
Barnes, Gary W. "Retrograde amnesia and reconsolidation of a context-no US association". Kent State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=kent1311122134.
Testo completo
24
Heim, Whitefield Karen Elizabeth. "Mechanism of RRR-[alpha]-tocopheryl succinate activation of latent TGF-[beta] and induction of cell growth inhibition in the human breast cancer cell line MDA-MB-435 /". Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.
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25
Opgen-Rhein, Carolin Stephanie. "Stimuluskomplexgrad-abhängige konditionierte Hemmung und latente Inhibition". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97441784X.
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26
Zimmermann, Mark. "Latente Inhibition ein lernpsychologisches Paradigma in der psychopathologischen Forschung /". [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965600041.
Testo completo
27
Gosselin, Valérie. "Injections systémiques de phencyclidine et inhibition latente chez le rat". Master's thesis, Université Laval, 2002. http://hdl.handle.net/20.500.11794/42952.
Testo completoAbstract (sommario):
L'inhibition latente (IL) correspond au retard d'acquisition d'une réponse conditionnelle (RC) suite à l'exposition répétée et non renforcée à un stimulus conditionnel (SC). Chez les patients schizophrènes et les modèles animaux de la pathologie, l'IL est abolie. La présente étude examine, chez le rat, l'effet de l'injection systémique de phencyclidine (PCP) sur l'IL dans une tâche de lapement conditionné. Des rats traités au PCP sont d'abord préexposés et conditionnés à un SC auditif après 5 jours sans traitement, ils sont préexposés et conditionnés à un SC visuel. Au premier conditionnement, huit groupes (n = 8) sont injectés avec du PCP ou une solution saline (SAL), sont préexposés (P) ou non (NP) au SC et sont traités avant et durant la préexposition (1) ou également lors du conditionnement (2). Les résultats montrent que l'IL est accentuée chez les rats PCP2-P lors du conditionnement auditif. Cet effet n'est pas persistant puisque les résultats ne sont pas reproduits lors du conditionnement visuel.
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Salgado, Joao Vinicius. "Effeito da anfetamina sobre a inibiçao latente, avaliada por paradigma de supressao condicionada, em voluntarios sadios". Université Louis Pasteur (Strasbourg) (1971-2008), 1999. http://www.theses.fr/1999STR13245.
Testo completo
29
Jeanblanc, Jérôme. "Etude des modalités d'implication des neurones dopaminergiques mésencéphaliques dans le phénomène d'inhibition latente". Université Louis Pasteur (Strasbourg) (1971-2008), 2003. http://www.theses.fr/2003STR13113.
Testo completoAbstract (sommario):
Le travail de cette thèse avait pour but d'étudier les modalités d'implication des neurones dopaminergiques (DA) mésencéphaliques dans le phénomène d'inhibition latente (IL). L'intérêt de ce travail est mis en évidence d'une part par les données montrant l'existence d'une perturbation de l'IL chez les schizophrènes non-traités et d'autre part par les données neuropsychopharmacologiques suggèrant l'existence d'un dysfonctionnement des neurones DA mésencéphaliques dans la schizophrénie. Pour étudier l'implication des neurones DA mésencéphaliques dans l'IL, nous avons développé un paradigme d'IL original dans un contexte d'aversion olfactive conditionnée. La libération de DA était mesurée par voltamétrie in vivo chez des rats en préparation chronique, libres de leurs mouvements. Dans un premier temps, les variations de la libération de DA au cours de l'IL ont été étudiées au niveau des sous-parties core, shell dorsal et shell ventral du noyau accumbens (Acc) et dans les parties antérieure et postérieure du striatum dorsal. Dans un second temps, nous avons cherché à obtenir une perturbation de l'IL. Pour ce faire nous avons étudié dans quelle mesure le blocage fonctionnel par la tétrodotoxine au niveau du cortex entorhinal (Ent) entraîne une perturbation de l'IL au niveau des réponses comportementales et des réponses DA obtenues au niveau des parties core et shell dorsal du noyau accumbens. Nous avons pu établir que les neurones DA innervant le core, le shell dorsal du Acc et la partie antérieure du striatum dorsal sont impliqués dans le phénomène d'IL. Les données obtenues ont aussi permis de montrer que l'Ent exerce une action régulatrice différentielle au niveau des parties shell dorsal et core du Acc. En conclusion, les travaux réalisés au cours de cette thèse vont grandement contribuer à la modélisation animale de la perturbation de l'IL observée chez les schizophrènes, et donc d'approcher au plus près une modélisation de la physiopathologie de la schizophrénieThe aim of this thesis was to study the ways in which mesencephalic dopaminergic (DA) neurons are involved in the latent inhibition (LI) phenomenon. This work formed part of a process of animal modelling of the physiopathology of schizophrenia. The importance of the work is demonstrated by the clinical data showing the existence of a disturbance of LI in non-treated schizophrenics. Neuropsychopharmacological data obtained over the last twenty years suggest that there is a dysfunction of the mesencephalic DA neurons in schizophrenia. To study the involvement of DA neurons in LI, we developed an original paradigm in a context of conditioned olfactory aversion. The release of DA was measured using in vivo voltammetry on freely moving rats. At first, the variations of the release of DA during the LI phenomenon were studied at the level of core, dorsal shell and ventral shell parts of the nucleus accumbens (Acc) and in the anterior and posterior subdivisions of the dorsal striatum. During the second part of the thesis, taking a physiopathological view, we tried to obtain a disturbance of LI. To this end, we studied to what extent functional blocking by tetrodotoxin of the entorhinal cortex (Ent) led to a disturbance of LI at the level of the behavioral answers and the DA answers obtained at the level of the core and dorsal shell parts of the Acc. We were able to establish that mesencephalic DA neurons innervating the core part and the dorsal shell part of the Acc and those innervating the anterior part of the dorsal striatum are involved in the LI phenomenon. The data obtained also made it possible to show that the Ent has a differential regulating effect at the level of the dorsal shell and core parts of the Acc. In conclusion, the work carried out during this thesis will contribute largely to the animal modelling of the disturbance of LI phenomenon observed in schizophrenics, and thus, ultimately, bring us closer to a model of the physiopathology of schizophrenia
30
Litten, J. Christopher. "The design, synthesis and protease inhibitor properties of latent reactive amino acid analogues". Thesis, University of Canterbury. Chemistry, 1992. http://hdl.handle.net/10092/7300.
Testo completoAbstract (sommario):
This thesis examines the synthesis and proteolytic properties of a new class of latent reactive amino acid analogue, eg: 1-(N-Phthaloyl-Lphenylalanyl)-2-hydroxymethylpyrrole 2.52, designed to inhibit serine proteases and the HN protease.
Chapter One discusses the possible mode of protease inhibition by these derivatives. The substrate specificity of chymotrypsin, and HN -1 protease suggests that the pyrrole occupies the P₁’ subsite, and the N-acyl group the P₁ subsite. Acceptance into the active site, and subsequent cleavage of the amide bond releases the highly reactive 1-azafulvene 1.3 that can alkylate an active site nucleophilic residue.
Chapter Two presents procedures for the N-acylation of pyrrole derivatives. Pyrrole-2-carboxaldehyde was successfully N-acylated with non-amino acid acylating agents using either, NaH, MeLi, or BuLi. A new mild procedure was developed for the N-acylation of pyrroles using a DMAP/organic base combination. The DMAP/organic base (TEA or Hünigs base) methodology was extended to the N-acylation of pyrrole-2-carboxaldehyde with N-Pth protected amino acid acid chlorides. The subsequent reduction of the N-acylated formyl pyrrole, 1-(N-Phthaloyl-L-phenylalanyl)-2-formylpyrrole 2.37, with Zn(BH₄)₂ produced high yields of the N-acylated hydroxymethyl pyrrole 2.52. A ¹H NMR analysis of the camphanate prepared from 2.37 demonstrated that racemisation had not occurred. A detailed ¹H and ¹³C NMR spectral analysis of the formyl and hydroxymethyl pyrroles is discussed in this chapter.
Chapter Three extends the synthesis to incorporate potential hydrogen bonding sites in the Px’ sub site direction. The imine N-(2-Pyrrolylmethylene)-L-alanine Ethyl Ester 3.12 was prepared from pyrrole-2-carboxaldehyde, by reaction with H₂N-Ala-OEt and pyrrole-2-carboxaldehyde with removal of water. The analogous imine formation using the N-acylated formyl pyrrole 1-(3-Phenylpropionyl)-2-formylpyrrole 2.31 produced high yields of the non-acylated imine 3.12. The N-acylation of 3.12 under the DMAP/Hünigs base conditions using hydroclnnamoyl chloride did not proceed.
Esterification of the hydroxymethyl pyrrole 2.52 under Mitsunobu conditions with the dipeptide N-Cbz-Val-Val-OH produced the tetrapeptide, N-benzyloxycarbonyl-L-valinyl-L-valine-l-(Nphthaloyl-L-phenylalanyl)pyrrol-2-ylmethyl Ester 3.39.
Chapter Four presents a hydrolysis and mechanistic study on the deacylation of 1-(3-Phenylpropionyl)-2-hydroxymethylpyrrole 2.32 with HO-. The deacylation of 2.32 in CD₃CN, containing one equivalent of KOH, produced 2-(3-Phenylpropionyl)-2-methylpyrrole Ester 4.5. This species was shown to form via an intramolecular mechanism. Chiral, deuterium labelling of the methylene position showed that racemisation at this position had not occurred in the formation of 4.5. An azafulvene intermediate is therefore precluded. A kinetic analysis of the subsequent conversion of 4.5 to 2-Butylaminomethylpyrrole 4.6, in the presence of n-butylamine, showed the reaction to be first order with respect to HO-.
The hydrolysis of deuterium labelled [6-d₁]-(6S)-1-(N-Phthaloyl-L-leucyl)-2-hydroxymethylpyrrole 4.14 with HO- in CD₃CN, gave the corresponding O-acetylated pyrrole 4.9 without racemisation. The addition of (S)-(+)-sec-butylamine to the reaction, trapped the azafulvene as [6-d₁]-(8S)-(+)-2-(1-methylpropionylamino)methylpyrrole 4.36.N-acylation was also shown to suppress azafulvene chemistry and therefore increase the stability of the hydroxymethyl pyrrole system. The camphanate from [6-d₁]-(6S)-1-(3-Phenylpropionyl)-2-hydroxy methylpyrrole 4.10 formed under the Mitsunobu conditions proceeded with 62% inversion of configuration of the methylene position.
Chapter Five deals with the α-chymotrypsin and HN-1 protease inhibitor properties of the pyrrole derivatives 2.32, 2.52, 1-(NPhthaloyl-D-phenylalanyl)-2-hydroxymethylpyrrole 2.55, 3.39, 1-(Undecyl)-2-hydroxymethylpyrrole 3.53 and 1-((5-Methoxycarbonyl)hexanyl)-2-hydroxymethylpyrrole 3.55. These compounds were found to be modest inhibitors of α-chymotrypsin, but poor inhibitors of HIV-1 protease. The stability of the hydroxymethyl pyrrole 2.52 was shown to be low under the HN protease assay conditions. A discussion on molecular modelling and docking the proposed inhibitors into the active site of HIV-1 protease is presented.
31
Peterschmitt, Yvan. "Etude de l'influence de différentes régions télencéphaliques sur la mise en jeu des neurones dopaminergiques mésencéphaliques dans les processus d'inhibition latente". Université Louis Pasteur (Strasbourg) (1971-2008), 2006. https://publication-theses.unistra.fr/public/theses_doctorat/2006/PETERSCHMITT_Yvan_2006.pdf.
Testo completoAbstract (sommario):
La schizophrénie est une pathologie neuropsychiatrique caractérisée par une désintégration psychique, qui reflèterait une dysconnexion fonctionnelle entre régions cérébrales intégratives. Une régulation dopaminergique (DA) inadéquate et des altérations anatomofonctionnelles du lobe temporal associées, qui auraient une origine neurodéveloppementale, pourraient contribuer à la dégradation des processus cognitifs comme l’inhibition latente (IL) ou la reconnaissance mnésique, observée chez les patients. Afin de modéliser chez l’animal certains aspects physiopathologiques de la schizophrénie, le but de cette thèse était de préciser le substrat neurobiologique dont la dysconnexion provoque une perte de l’IL, avec l’hypothèse que les structures impliquées participent à la mémoire de reconnaissance. Ainsi, une inactivation transitoire induite in situ par la tétrodotoxine a d’abord été réalisée au niveau du cortex entorhinal (ENT) ou du subiculum ventral de l’hippocampe (SUB) de rats adultes, puis dans une perspective neurodéveloppementale, de l’ENT de rats âgés de 8 jours. Les réponses comportementales d’IL chez l’adulte ont été mesurées dans un paradigme d’aversion olfactive conditionnée et la libération de DA enregistrée simultanément, dans le striatum dorsal (uniquement après blocage adulte) ou le noyau accumbens (partie core et shell dorsomédian), par voltamétrie chez les rats vigiles. Nos résultats montrent que la dysconnexion fonctionnelle de l’ENT ou du SUB adultes ou de l’ENT néonatal, apparaît suffisante pour perturber l’IL et les variations DA. Ces données originales attestent de la pertinence de notre approche de modélisation de la physiopathologie de la schizophrénie.
32
Peterschmitt, Yvan Louilot Alain. "Etude de l'influence de différentes régions télencéphaliques sur la mise en jeu des neurones dopaminergiques mésencéphaliques dans les processus d'inhibition latente". Strasbourg : Université Louis Pasteur, 2007. http://eprints-scd-ulp.u-strasbg.fr:8080/671/01/peterschmitt2006.pdf.
Testo completo
33
Croas, Joël. "Approche psychodynamique de troubles dépressifs chez l'enfant de la latence à travers deux versants contrastés, l'inhibition et l'agitation". Paris 5, 2008. http://www.theses.fr/2008PA05H005.
Testo completoAbstract (sommario):
Les troubles dépressifs chez l'enfant de la latence, étudiés depuis assez peu de temps, peuvent se manifester de diverses façons, en particulier sur un mode inhibé mais aussi sur un mode agité. Un certain nombre de questions se posent les concernant. Les fonctionnements psychiques sous-jacents, au sein de ces deux populations, sont-ils variés et/ou de même nature ? A quoi renvoient ces comportements contrastés au niveau intrapsychique, témoignent-ils d'aménagements défensifs de sens contraire ou rendent-ils compte de défenses plus spécifiques contre ces mouvements dépressifs ? Quelle pourrait être leur impact et leur influence sur les processus de pensée, notamment au niveau du registre symbolique ? Y aurait-il une spécificité de la dépression chez l'enfant et laquelle ? Quelle peut être la valence de l'étayage de l'environnement des sujets et de la reconnaissance de ces troubles par des tiers ? En corollaire quelle pourrait être l'évolution de ceux-ci en fonction ou non d'une aide thérapeutique. Cette recherche exploratoire tente, par l'intermédiaire d'une approche psychodynamique utilisant la méthodologie projective, au sein de deux populations contrastées, d'essayer de répondre partiellement à ces questions. Le corpus théorique présenté est celui de la métapsychologie freudienne, la perte d'objet, sa confrontation et la possibilité de la traiter au plan intrapsychique étant considérés comme centraux vis à vis des processus évoquésDepressive disorders in children latency, studied quite recently, may be manifested in different ways, especially in an inhibited, but also on an agitated way. A number of questions arise concerning them. Are the psychological operations underlying within these two populations varied and / or similar? What refer these contrasting behaviours at intrapsychic testify they developments defensive direction or make it account for more specific defenses against these movements depressive? What could be their impact and influence on the thought process, especially in terms of symbolization? Is there a specificity of depression among children and which? What is the valence of the backing of environmental issues and the recognition of these disorders by others? As a corollary what might be changing them in office or not a therapeutic aid. This exploratory research attempts, through a psychodynamic approach using projective methodology, with two contrasting populations, to try to answer these questions partially. The theory presented is the Freudian metapsychology, loss of object, his confrontation and the possibility of the deal in the intrapsychic area being regarded as central vis-avis the process outlined
34
Seillier, Alexandre. "Etude des mécanismes impliqués dans le déficit d'inhibition latente induit par la lésion du cortex entorhinal". Université Louis Pasteur (Strasbourg) (1971-2008), 2004. https://publication-theses.unistra.fr/public/theses_doctorat/2004/SEILLIER_Alexandre_2004.pdf.
Testo completoAbstract (sommario):
Ce travail a cherché à préciser les mécanismes par lesquels la lésion du cortex entorhinal (CE) pouvait supprimer l'inhibition latente (IL) chez le Rat. Dans un premier temps, nous avons montré, dans une situation de réponse émotionnelle conditionnée (REC), que l'IL dépendait à la fois de l'impact de la préexposition et de l'impact du conditionnement. Dans un deuxième temps nous nous sommes attachés à reproduire le déficit d'IL induit par la lésion du CE. Nos travaux ont permis de montrer que la lésion bilatérale (excitotoxique) du CE produit un déficit d'IL dans la situation de REC quand le conditionnement est fort, mais pas lorsqu'il est faible, et que cette même lésion n'affecte pas l'IL dans une situation d'aversion gustative conditionnée. Nous avons ensuite montré que la lésion du CE induit une facilitation de conditionnement, cette facilitation ne résultant pas d'une réactivité supérieure au stimulus inconditionnel (chocs électriques), ni d'une augmentation du niveau d'anxiété et/ou de stress. Nous avons également pu établir que la lésion du CE affectait le fonctionnement du système dopaminergique méso-accumbens, évalué par i) les mesures d'activité locomotrice induite par la nouveauté ou par la d-amphétamine, ii) la réponse génomique (expression du gène c-fos) induite par des composés antipsychotiques (halopéridol, olanzapine et clozapine) et par un antagoniste des récepteurs D3 à la dopamine, iii) mais pas par la mesure de préférence de place induite par la d-amphétamine, iv) ni par l'activité locomotrice induite par des ligands des récepteurs D3 à la dopamine. Enfin, une approche d'inactivation réversible (par l'utilisation de tétrodotoxine) a permis de montrer que l'intégrité fonctionnelle du CE était nécessaire lors de la phase de préexposition de l'IL. Dans leur ensemble, ces résultats suggèrent que la lésion du CE pourrait supprimer l'IL via une facilitation de conditionnement résultant vraisemblablement d'une activité dopaminergique méso-accumbens exacerbée. Ces résultats ne remettent cependant pas en question l'implication du CE dans l'IL, l'intégrité fonctionnelle de ce dernier étant requise lors de la phase de préexpositionThe experiments presented herein aimed at clarifying the mechanisms involved in entorhinal cortex (EC)-induced deficit of latent inhibition (LI) in rats. First, we showed that, in a conditioned emotional response (CER) paradigm, LI is expressed under a balance between the impact of pre-exposure and conditioning. Second, we assessed the effects of bilateral excitotoxic EC lesions on LI and showed that EC lesions disrupted LI in a CER paradigm under condition of high, but not low, conditioning, and that these same lesions do not affect LI in a conditioned taste aversion paradigm. We then showed that EC lesions enhanced conditioning, this enhancement being not attributable to an increase of sensitivity to unconditioned stimulus (footshock), nor an increase in anxiety and/or stress. We also showed that EC lesions modify dopaminergic meso-accumbens functioning, as assessed by i) novelty- or amphetamine-induced locomotor activity, ii) c-fos expression induced by antipsychotic compounds (haloperidol, olanzapine and clozapine) and a D3-receptor antagonist, iii) but not by amphetamine-induced place preference, iv) nor by locomotor activity induced by D3 receptors ligands. Finally, using reversible inactivation of EC (by tetrodotoxin), we showed that EC is involved during the preexposure phase of LI. Taken together, these results suggest that the disruptive effect of EC lesions on LI may be consecutive to a lesion-induced increase of the impact of stimulus-reinforcer association, probably induced itself by an increased dopaminergic meso-accumbens activity. These results do not however question the involvement of EC in LI, the integrity of this brain area being necessary during the preexposure phase
35
McDonough, Suzanne. "The development of short latency inhibition from triceps brachii to biceps brachii in man". Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283056.
Testo completo
36
Guinard, Frédérik. "Psychopathologie des processus d'appropriation à l'âge de latence : intérêt thérapeutique des groupes à médiation dans la clinique des apprentissages". Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE2104.
Testo completoAbstract (sommario):
Cette recherche trouve son origine dans une pratique clinique quotidienne auprès d'enfants en âge de latence accompagnés pour leurs difficultés d'apprentissage. L'âge de latence est pour l'enfant une étape importante de réaménagement cognitif et de désintrication pulsionnelle. Si les troubles des apprentissages et l'échec scolaire peuvent trouver leur origine dans des temps plus anciens du développement psycho-cognitif du sujet, la période de latence est cruciale pour le déploiement de la curiosité intellectuelle et la réalisation de "conquêtes" importantes de la symbolisation. Ne pas savoir lire, écrire, compter, ne constitue bien souvent que la partie émergée de difficultés plus profondes qui touchent chez certains sujets tous les modes de figurabilités et différents niveaux de symbolisation. Cette thèse explore les différentes significations des conduites anti-apprentissages que développent ces enfants dans leurs expériences d'appropriation, d'exploration et de manipulation de l'environnement. Enfin, ce travail présente un outil de repérage clinique et d'évaluation qualitative des groupes à médiation thérapeutique qui sont proposés pour accompagner cette clinique des apprentissages. L'intérêt thérapeutique de ces dispositifs sera questionné et illustré au travers de trois expériences de groupe : un atelier à médiation sensorielle, un atelier peinture et un groupe à médiation théâtraleThis research finds its origin in a daily clinical practice with children in latence period in treatment for their learning disabilities. The latence period is an important stage of cognitive reorganization and drive defusion. If the learning disabilities and the academic failure can find their origin in older times of the psychic and cognitive development of the subject, the time of latence period is crucial for the growth of the intellectual curiosity and achieve important symbolic “conquests”. Deep, unresolved psychic issues can perturb all modes of abstraction and symbolic understanding as well as causing difficulties in the acquisition of reading and writing. This dissertation explore the various meanings of the anti-learnings conducts which develop these children in their experiences of appropriation, exploration and manipulation of the environment. Finally, this work presents a tool of clinical analysis and qualitative evaluation of the groups of therapeutic mediation which are proposed to treat these context of learning disorder. The therapeutic interest of these settings will be questioned and illustrated through three experiences of group : a workshop with sensory mediation, a painting group experience and a therapeutic group with the medium of theater
37
Rascle, Claire. "Etude de l'inhibition latente dans la schizophrénie : Analyse des performances dans un paradigme de détection de contingence et de conditionnement classique". Strasbourg 1, 2001. http://www.theses.fr/2001STR13196.
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TREGUER, MONA. "Nouvelles approches pour accroitre le rendement effectif de formation de l'image latente dans agx par inhibition de la recombinaison e /h +". Paris 11, 1999. http://www.theses.fr/1999PA112284.
Testo completoAbstract (sommario):
En photographie, les proprietes specifiques des agregats metalliques jouent un role primordial dans l'etape de la formation photochimique de l'image latente et dans l'etape du developpement. Concernant la catalyse du developpement, notamment dans les procedes par inversion-transfert qui requierent des germes exogenes, une etude a ete menee afin de maitriser la structure de nanoagregats multimetalliques et de s'assurer que tous les metaux se trouvent en surface de la particule comme dans un alliage (agau, agpd, agaucu, agpdcu). Les resultats ont montre l'influence preponderante des cinetiques en competition des processus de reduction et coalescence avec ceux de transfert d'electron intermetallique. La segregation ou l'association intime des metaux est controlee par la vitesse de reduction (debit de dose d'irradiation). Seule une reduction rapide et totale de tous les ions metalliques peut faire echec au transfert d'electron intermetallique se produisant lors de la coalescence des agregats et favorisant donc la segregation des metaux. Les clusters trimetalliques allies sont de loin les germes les plus efficaces pour catalyser le developpement. Concernant la formation de l'image latente, le rendement quantique effectif de reduction des ions ag + est toujours tres faible et tres inferieur a la limite theorique d'un evenement par photo absorbe en raison des phenomenes rapides de recombinaison des paires electrons-trous. Pour faciliter l'echappement des electrons et accroitre ainsi le rendement quantique effectif dans les microcristaux d'halogenure d'argent, differents types d'intercepteurs de trous ont ete examines : dimeres ag 2, clusters moleculaires ((pt 3(co) 6) 2 n, et petits anions organiques acetate et formiate. Les dimeres argentiques formes par pre-reduction avant l'exposition captent les trous photoproduits, mais le risque de ce mode de sensibilisation est de faire apparaitre du voile des qu'un exces local de reducteur correspond a plus de deux atomes d'argent par cristal (en raison de la distribution de poisson). A l'inverse, les clusters moleculaires de platine (pt 3(co) 6) 2 n ne reduisent pas spontanement les cations ag + dans le noir et le voile est donc negligeable. Les clusters (pt 3(co) 6) 2 n permettent en outre d'accroitre le rendement quantique effectif en capturant les trous et en empechant en partie les recombinaisons entre les paires de charges photoproduites. Une etude par radiolyse impulsionnelle de ces clusters en solution a permis de determiner leurs proprietes redox et de preciser leur mecanisme d'action lorsqu'ils sont inclus au cur des microcristaux agx. Quant a l'acetate ou au formiate, ils captent egalement les trous et leur efficacite est telle que les rendements de reduction se rapprochent de la limite theorique d'un evenement par photon absorbe. En presence de formiate, le radical co _ 2 forme lors de la reaction avec le trou constitue une source secondaire de reduction de ag + comme en radiolyse des solutions d'ions metalliques. Pour chaque trou capte, 2 atomes d'argent sont formes dans le milieu ; et en association avec des pieges a electrons, le rendement quantique approche la limite theorique de transformation integrale de l'energie lumineuse en effet chimique irreversible. Comme le procede concerne l'etape de base de la formation d'une image, il peut donc etre applique a tous les types d'emulsions. Ces progres apportent donc a l'image argentique de nouveaux atouts pour accroitre ses performances.
39
Fischer, Maximilian [Verfasser], e Michael [Akademischer Betreuer] Orth. "Short-latency sensory afferent inhibition : conditioning stimulus intensity, recording site, and effects of 1 Hz repetitive TMS / Maximilian Fischer. Betreuer: Michael Orth". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/1047440407/34.
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Freitas, Ana Paula Fragoso de. "Protein fraction of latex Calotropis procera protects against induced oral mucositis 5-Fluorouracil in hamsters through inhibition proinflammatory mediators". Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=9245.
Testo completoAbstract (sommario):
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorCoordenaÃÃo de AperfeiÃoamento de NÃvel Superior
Oral mucositis (OM) induced by antineoplasic drugs is an important, dose-limiting, and costly side effect of cancer therapy. Calotropis procera is a plant plant constitutively produces abundant latex that is reported to possess anti-inflammatory, bacteriolytic, insecticidal, analgesic properties. The present work aimed to describe the effect of laticifer proteins of Calotropis procera (LP) in the expression of pro-inflammatory cytokines and inducible enzymes, such as, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in the model of OM in Hamsters. OM was induced by two intraperitoneal (i.p.) administrations of 5-Fluorouracil (5-FU) on the 1st and 2nd days (60 and 40 mg/kg, respectively) in hamsters (n=5). LP (0,25; 1; 5 E 25 mg / kg) was injected i.p. 24h before and 24h after mechanical trauma of the cheek pouches. Control group received only saline. On the 10th day, the animals were sacrificed and tissues from the cheek pouches were harvested. Macroscopical and histopathological (inflammatory cell infiltration, edema, hemorrhage and the formation of ulcerations and abscess) analysis as well as immunohistochemistry for TNF-, IL-1β, iNOS and COX-2 was performed in the cheek pouch tissue. Kruskal Wallis/Dunn was used as statistical tests. P<0.05 was accepted. Ethics Committee 036/10. The LP significantly inhibited macroscopical and histopathological parameters when compared to control group with maximum effect in macroscopic scores reaching 75% and 66% of maximum effect at the histopathological evaluation. The MPO activity was also significantly inhibited by LP in 91% at the same dose (p<0,001) and also inhibited the lost weight of 5- FU induced-oral mucositis. The cheek pouches of hamsters submitted to OM showed marked immunostaining for TNF-, IL-1β, iNOS and COX-2 on inflamed conjunctive (Cj) and epithelial (Ep) tissue compared with the cheek pouches of the normal control group. LP caused considerable reduction in the immunostaining for TNF- (62%,Cj; 70%,Ep), IL-1β (87%,Cj; 80%,Ep), iNOS (82%Cj; 52%Ep) and COX-2 (70%,Cj; 100%,Ep) in the check pouches tissue when compared with the group of animals subjected to experimental mucositis that received saline instead of LP. These findings show anti-inflammatory effects of LP in 5-FU-induced OM. The protective effect could be supported by the reduction of the expression of pro-inflammatory cytokines, such as TNF- and IL-1β and the enzymes iNOS and COX-2. The protective mechanism appears to involve inhibition of the expression of iNOS, COX-2, TNF-, and IL- 1β.
Mucosite oral (MO) induzida por drogas antineoplÃsicas à um importante fator limitante da dose e efeitos colaterais da terapia do cÃncer. Calotropis procera à uma planta que produz lÃtex constitutivamente abundante que à relatado possuir propriedades antiinflamatÃrias, bactericidas, inseticidas, analgÃsicas. O presente trabalho teve como objetivo descrever o efeito das proteÃnas do lÃtex da Calotropis procera (LP) na expressÃo de citocinas prÃ-inflamatÃrias (TNF-α e IL-1) e enzimas induzÃveis, como, ciclooxigenase-2 (COX-2) e Ãxido nÃtrico sintase induzÃvel (NOSi) no modelo de MO em hamsters. A mucosite oral foi induzida por duas administraÃÃes intraperitoneal (i.p) de 5-fluorouracil (5-FU) no 1  e 2 dias nas doses de 60 e 40 mg/kg, respectivamente nos animais (n = 5). As LP (0,25; 1; 5 E 25 mg/kg) foi injetado via i.p. 24h antes e 24h apÃs o trauma mecÃnico da mucosa jugal. O grupo controle recebeu apenas soluÃÃo salina. No 10 dia, os animais foram sacrificados e os tecidos da mucosa jugal foram colhidos. Foram realizadas no tecido mucosa jugal as anÃlises macroscÃpicas e histopatolÃgicas (infiltraÃÃo de cÃlulas inflamatÃrias, edema, hemorragia e à formaÃÃo de ulceraÃÃes e abscessos), bem como a imunohistoquÃmica para TNF-α, IL-1β, NOSi e COX-2. Foram utilizados Kruskal Wallis / Dunn como testes estatÃsticos, onde P <0,05 foi aceito. O estudo foi submetido ao Comità de Ãtica sob o protocolo 036/10. Observou-se que a LP inibiu significativamente parÃmetros macroscÃpicos e histopatolÃgicos, quando comparado ao grupo controle, com efeito mÃximo nos escores macroscÃpicos atingindo 75% e 66% do efeito mÃximo na avaliaÃÃo histopatolÃgica. A atividade de Mieloperoxidase (MPO) tambÃm foi significativamente inibida por LP em 91% com a mesma dose (p <0,001) quando comparado ao grupo controle e tambÃm inibiu a perda de peso em animais submetidos a mucosite oral e tratados com LP. A mucosa jugal dos animais submetidos a MO mostrou imunomarcaÃÃo para TNF-α, IL-1β, NOSi e COX-2 na conjuntiva inflamada (Cj) e tecido epitelial (Ep) em comparaÃÃo com o tecido jugal do grupo normal. LP causou reduÃÃo considerÃvel na imunomarcaÃÃo para TNF-α (62%, Cj, 70%, Ep), IL-1β (87%, Cj, 80%, Ep), NOSi (82% Cj; Ep 52%) e COX -2 (70%, Cj, 100%, Ep) no tecido jugal quando comparado com o grupo de animais submetidos à mucosite experimental que receberam salina, em vez de LP. Esses achados demonstram efeitos anti-inflamatÃrios de LP em MO induzida por 5-FU. O efeito protetor poderia ser suportado pela reduÃÃo da expressÃo das citocinas prÃ-inflamatÃrias, como TNF-α e IL-1β e na expressÃo de enzimas COX-2 e NOSi. O mecanismo de proteÃÃo parece envolver a expressÃo inibitÃria da NOSi, COX-2, TNF-α e IL-1β.
41
Ansari, Yekta. "The Effect of Thermal Stimulation on Corticospinal Excitability". Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39328.
Testo completoAbstract (sommario):
This thesis describes a series of experiments to investigate the effect of thermal stimulation on corticospinal excitability using transcranial magnetic stimulation (TMS). Experiment I showed that innocuous cooling or warming of a single digit, produced short-lasting and mixed patterns of modulation only during actual thermal stimulation, with the inhibition being the most common pattern observed. In line with this finding, cooling stimulation applied to a larger area (i.e. multi-digits) produced variable but more sustained modulation in motor evoked potential (MEP) amplitude in the post-cooling phase (Exp II). Notably, the responses to cooling in terms of either suppressed or enhanced corticospinal excitability tended to be fairly consistent in a given individual with repeated applications. When examining possible sources of the observed variable MEP modulation, we found that individual characteristics such as age, sex and changes in skin temperature had no major influences. We hypothesized that the variability of responses might be related to individual differences in the excitability of intra-cortical circuits involved in sensorimotor integration. To test this hypothesis, we performed Experiment III using conditioning TMS paradigms. This experiment revealed that TMS markers of sensorimotor integration (SAI and SAF levels) were good predictors of individual variations in cooling-induced modulation in corticospinal excitability. This provided evidence supporting the role of SAI and SAF as markers to predict individual’s response to focal thermal stimulation. The identification of such predictors could enhance the therapeutic applicability of this form of stimulation in neurorehabilitation. Collectively, these findings advance our understanding of the neurophysiological basis of thermal stimulation and shed light on the development of a more rational application of neurofacilitation techniques based on afferent stimulation in clinical populations, such as stroke survivors.
42
Yates, David Ira. "Latex of Sciadopitys verticillata (Thunb.) Siebold and Zuccarini: Antibiotic Properties, Phytochemistry, and Inhibition of Adventitious Rooting of Stem Cuttings". Digital Commons @ East Tennessee State University, 2006. https://dc.etsu.edu/etd/2228.
Testo completoAbstract (sommario):
Sciadopitys verticillata was subjected to three propagation treatments designed to inhibit coagulation of its latex-like sap at the cut ends of the stem cuttings. Twenty-four hour soaking in water prior to rooting hormone application significantly enhanced production of adventitious roots. Old wood stem cuttings from shade-grown trees rooted at higher proportions than stem cuttings collected from sun-grown trees. Height, age, and place of origin of the source trees were not important factors in successful rooting. Antibacterial activity against some human pathogens and soil bacterial species was detected in latex application trials but the antibiotic activity was not related to the bacterial Gram reaction. The latex-like sap inhibited none of four plant pathogens tested. A suspension of the water insoluble latex-like sap of S. verticillata had a pH of 5.8. Antibacterial activity of S. verticillata sap was heat stable, which indicates the activity was not protein-based.
43
Shinde, Neelam V. "Establishment of a Quiescent Infection of HSV-1 in L929 Fibroblasts using a Mitotic Inhibitor and IFN-γ". Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1334631020.
Testo completo
44
Williams, Lisa Marie. "Cell cycle inhibitors in control of chronic gammaherpesvirus infection /". Connect to abstract via ProQuest. Full text not available online, 2007.
Cerca il testo completoAbstract (sommario):
Thesis (Ph.D. in Microbiology) -- University of Colorado Denver, 2007.Typescript. Abstract available online via ProQuest Digital Dissertations. Includes bibliographical references (leaves 207-223).
45
Chang, Shu-Hui, e 張淑慧. "Molecular mechanism of EBV latent membrane protein-1 induced inhibition of tissue inhibitor of metalloproteinase-3". Thesis, 2006. http://ndltd.ncl.edu.tw/handle/86392507708066462674.
Testo completoAbstract (sommario):
碩士高雄醫學大學
公共衛生學研究所碩士班
94
Epstein-Barr virus is a prototype gamma herpes virus which is widely spreaded infection in the adults. EBV has been implicated in the pathogenesis of several human malignancies such as Burkitt’s lymphoma, Hodgkin’s disease and nasopharyngeal carcinoma (NPC). Latent membrane protein 1 (LMP-1) is the oncoprotein of EBV associated NPC. Some evidences showed that LMP-1 enhanced the MMP-9 expression in the EBV-infected human epithelial cell lines C33A. In addition, numerous studies indicated that many NPC patients have lymph-node metastasis. In the physical condition, MMPs are regulated by natural inhibitor called tissue inhibitor of metalloproteinases (TIMPs). Until now, there are four kinds of TIMPs: TIMP-1, TIMP-2, TIMP-3 and TIMP-4. The biological function of TIMP-3 is different from the others. First, it could inhibit ADAM-17 (a disintergrin and metaloproteinases) , ADAMT-4 and ADAMT-5 (ADAM with thrombospondin domain). TIMP-3 could inhibit TNF-α release from the cells and regulate cellular inflammation. Second, TIMP-3 could promote cancer cells to undergo apoptosis. Third, TIMP-3 could inhibit the metastasis and angiogenesis of cancer cells. Fourth, TIMP-3 played a key role in the inhibition of tumor growth. Some evidences showed that the TIMP-3 promoter was hypermethylated in the tumor, and its expression was significantly down-regulated in tumors.The goal of our study is to elucidate the molecular mechanism by which LMP-1 regulates TIMP-3 in the NPC cell line TW04. Our results showed that TIMP-3 was decreased in LMP-1-expressing TW04 cells. Promoter activity assays indicated that the -44 / +28 region of TIMP-3 promoter was regulated by LMP-1. By using different kinds of protein kinase inhibitors, it was showed that the TIMP-3 mRNA level was restored after treatment with p38 kinase inhibitor SB203580. We found that the LMP-1 induced TIMP-3 inhibition could increase the migration and invasion of TW04 cells. While co-expression with TIMP-3 attenuated LMP-1-evoked the migration and invasion. According to our results, we suggest that LMP-1 might increase the cell migration and invasion through p38 mediated down-regulation of TIMP-3.
46
Brown, Rick D. "Latent inhibition goes social : reducing the expression of the attractiveness stereotype". 2004. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=80231&T=F.
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47
"The Role of the Biogenic Amine Tyramine in Latent Inhibition Learning in the Honey Bee, Apis mellifera". Master's thesis, 2017. http://hdl.handle.net/2286/R.I.44293.
Testo completoAbstract (sommario):
abstract: Animals must learn to ignore stimuli that are irrelevant to survival, which is a process referred to as ‘latent inhibition’. This process has been shown to be genetically heritable (Latshaw JS, Mazade R, Sinakevitch I, Mustard JA, Gadau J, Smith BH (submitted)). The locus containing the AmTYR1 gene has been shown through quantitative trait loci mapping to be linked to strong latent inhibition in honey bees. The Smith lab has been able to show a correlation between learning and the AmTYR1 receptor gene through pharmacological inhibition of the receptor. In order to further confirm this finding, experiments were designed to test how honey bees learn with this receptor knocked out. Here this G-protein coupled receptor for the biogenic amine tyramine is implemented as an important factor underlying latent inhibition in honey bees. It is shown that double-stranded RNA (dsRNA) and Dicer-substrate small interfering RNA (dsiRNA) that are targeted to disrupt the tyramine receptors specifically affects latent inhibition but not excitatory associative conditioning. The results therefore identify a distinct reinforcement pathway for latent inhibition in insects.Dissertation/Thesis
Masters Thesis Biology 2017
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Puga, Frank. "Functional neural networks underlying latent inhibition and the effects of the metabolic enhancer methylene blue". Thesis, 2009. http://hdl.handle.net/2152/ETD-UT-2009-12-584.
Testo completoAbstract (sommario):
The present research reports the first comprehensive map of brain networks underlying latent inhibition learning, the first application of structural equation modeling to cytochrome oxidase data, and the first effects of methylene blue, a known metabolic enhancer, on latent inhibition. In latent inhibition, repeated exposure to a stimulus results in a latent form of learning that inhibits subsequent associations with that stimulus. As neuronal energy demand to form learned associations changes, so does the induction of the respiratory enzyme cytochrome oxidase. Therefore, cytochrome oxidase can be used as an endpoint metabolic marker of the effects of experience on regional brain metabolic capacity. Quantitative cytochrome oxidase histochemistry was used to map brain regions in mice trained on a tone-footshock fear conditioning paradigm with either tone preexposure (latent inhibition), conditioning only (acquisition), conditioning followed by tone alone (extinction), or no handling or conditioning (naïve). In normal latent inhibition, the ventral cochlear nucleus, medial geniculate, CA1 hippocampus, and perirhinal cortex showed modified metabolic capacity due to latent inhibition. Structural equation modeling was used to determine the causal influences in an anatomical network of these regions and others thought to mediate latent inhibition, including the accumbens and entorhinal cortex. An uncoupling of ascending influences between auditory regions was observed in latent inhibition. There was also a reduced influence on the accumbens from the perirhinal cortex in both latent inhibition and extinction. These results suggest a specific network with a neural mechanism of latent inhibition that involves sensory gating, as evidenced by modifications in metabolic capacity, effective connectivity between auditory regions, and reduced hippocampal influence on the accumbens. The effects of methylene blue on disrupted latent inhibition were also investigated. Reduced tone-alone presentations disrupted the latent inhibition effect and led to an increase in freezing behavior. Repeated low-dose administration of methylene blue decreased freezing levels and facilitated the disrupted latent inhibition effect. Methylene blue administration also resulted in changes in metabolic capacity in limbic and cortical regions. A unique functional neural network was found in methylene blue-restored latent inhibition that emphasized sensory gating of auditory information, attention processing, and cortical inhibition of behavior.text
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Příplatová, Lenka. "Úleková reakce u osob s latentní toxoplasmosou". Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-312746.
Testo completoAbstract (sommario):
Possible connection between latent toxoplasmosis and schizophrenia is a very interesting and medically important topic. In this thesis I tried to map current state of knowledge in the interdisciplinary research of schizophrenia and Toxoplasma gondii and their possible connections as well as to show differences in responses between Toxoplasma-positive and Toxoplasma-negative subjects using simple computer-administered tests of prepulse inhibition of startle reaction (PPI). Such differences would suggest another similarity between schizophrenia patients and subjects with latent toxoplasmosis as the sensorimotor gating responsible for PPI was found to be disrupted in schizophrenia patients. Side goal of the study was to test newly developed PC software for testing PPI and to determine its applicability in further research. Subjects for the tests were recruited among adepts of professional military service; 409 subjects completed the test of acoustic PPI and 276 subjects completed the test of visual PPI. All the subjects were tested on presence of specific anti-Toxoplasma IgG in their blood serum. Both tests revealed significant (p<0.001) differences between responses on prepulse-preceded stimuli and plain stimuli without prepulse, no significant results were, however, gained for the effects of latent...
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Zimmermann, Mark [Verfasser]. "Latente Inhibition : ein lernpsychologisches Paradigma in der psychopathologischen Forschung / vorgelegt von Mark Zimmermann". 2002. http://d-nb.info/965600041/34.
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