Dissertations / Theses on the topic 'Inhibition'
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Booker, Samuel A. "Inhibiting inhibition : interactions amongst interneurons of the hippocampus." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2995/.
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Cortical networks comprise excitatory principal cells and interneurons (IN); the latter showing large neurochemical, morphological and physiological heterogeneity. GABA release from IN axon terminals activates fast ionotropic GABAA or slow metabotropic GABAB receptors (GABABR); ionotropic GABA mechanisms are well described in INs, whereas GABABR activity is less well understood. The primary aim of this thesis is to ascertain GABABR mediated inhibition in different IN types containing the neurochemicals parvalbumin (PV), cholecystokinin (CCK) or somatostatin (SSt). Using immunocytochemical techniques, at light and electron microscopic levels, we examined the cellular and subcellular expression of GABAB1 receptor subunits in these INs. Application of whole-cell patch clamp techniques in acute slices, allowed analysis of GABABR effects pre- and postsynaptically; in response to endogenous GABA release or pharmacological activation. Light microscopy showed GABAB1 expression in INs containing CCK or SSt, equivalent to CA1 pyramidal cells; with low expression in PV INs. Using electron microscopy, we detected GABAB1 receptor subunits in dendrites of CCK and PV INs, with densities equivalent or higher than CA1 pyramidal cell dendrites. Unexpectedly, SSt containing dendrites showed a lower density of GABAB1 receptor subunits. In axon terminals of CCK and PV containing INs, we found comparable densities of GABAB1 receptor subunits. Electrophysiological recordings confirmed the presence of functional postsynaptic GABABR in PV and CCK INs. GABABR-mediated slow inhibitory postsynaptic currents (IPSCs) had typically large amplitudes, but with high cell-to-cell variability in both IN types. Morphological separation of PV or CCK INs revealed slow IPSC amplitudes which were large in perisomatic inhibitory (PI)cells (30.8 ± 8.6 pA and 39.2 ± 5.5 pA, respectively) and small in dendritic inhibitory (DI) cells (4.0 ± 1.7 pA and 11.6 ± 2.4 pA, respectively). Consistently, SSt-immunoreactive DI INs exhibited very small IPSCs (1.5 ± 0.2 pA). Pharmacological activation of GABAB R by the selective agonist baclofen revealed variable amplitude whole-cell currents, confirming differences between IN subtypes. Examining presynaptic GABABR activity; we minimally stimulated str. pyramidale evoking monosynaptic IPSCs in CA1 pyramidal cells. IPSCs mediated by CCK or PV PI axons were pharmacologically isolated by CB1 or M2 receptor activation. Both monosynaptic responses were reduced by baclofen, albeit differentially so. To further investigate this effect we performed paired-recordings from PV or CCK INs coupled synaptically to CA1 pyramidal cells. Baclofen inhibited PV and CCK basket cell mediated IPSCs by 51% and 98%, respectively; with a smaller effect in DI INs. In summary, we have shown that functional GABABRs are expressed pre- and postsynaptically in hippocampal GABAergic INs; with distinct populations of INs under differential GABABR control. Postsynaptic inhibition was strong in PI INs, but weak or absent in DI INs, a relationship conserved presynaptically. The observed differential expression of GABABRs is likely to play a fundamental role in regulating the excitability and activity of GABAergic INs, regulating synaptic output and potentially contributing to network and oscillatory activity. Consequentially, during periods of high GABA release, GABABR activation could act as a switch, allowing DI INs to play a greater role in network inhibition, due to GABABR mediated inhibition of perisomatic-targeting INs.
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Glossop, Paul. "Thrombin inhibition." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244533.
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Bonardi, C. "Discriminative inhibition." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384313.
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Brian, Jessica Ann. "Inhibition in autism evidence of excessive inhibition-of-return /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ56219.pdf.
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Heduy, Fabrice. "Inhibition cognitive et schizophrénie : étude en situation d'auto-inhibition." Lille 3, 2001. http://www.theses.fr/2001LIL30010.
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L'inhibition cognitive est généralement représentée comme un processus qui limite et contrôle l'accès des informations à la conscience. Sa défaillance participerait à la genèse des hallucinations et des délires et pourrait sous-tendre un grand nombre de troubles observés dans la schizophrénie. Par ailleurs, deux processus différents sont proposés pour rendre compte de l'inhibition. Le premier, étudié principalement grâce au paradigme d'amorçage négatif, est appelé inhibition latérale. Son étude a montré qu'il était souvent déficient chez les patients schizophrènes. En revanche, le second processus, dispositif du type "reset" facilitant un retour au niveau de base aussi rapide que possible, n'a encore fait l'objet d'aucune recherche chez ces patients. A cette fin, nous avons éléboré une épreuve où une activité cognitive automatisée, la lecture analogique de l'heure, doit être inhibée pour laisser place à une activité sérielle et contrôlée de lecture inversée. D'autre part, notre protocole expérimental contenait plusieurs phases permettant l'étude de l'auto-inhibition lors de contextes facilitateur ou freinateur. Dans ces conditions, nous avons relevé que les schizophrènes dans leur ensemble présentaient des pertubations et qu'ils éprouvaient des difficultés particulières et distinctes selon les sous-groupes définis par le D. S. M. IV. Nous avons poursuivi par l'étude de l'influence de l'âge et du sexe des patients sur leurs performances inhibitrices et complété nos recherches en prolongeant notre étude dans la population générale selon le niveau de schizotypie. Des aptitudes diverses à l'auto-inhibition ont été relevées, certaines en accord avec les données de la littérature concernant l'inhibition latérale, d'autres originales. Nous avons terminé notre travail par une proposition d'intégration des processus inhibiteurs dans les principaux modèles rendant compte des défaillances dans la schizophrénie
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Roweth, Harvey George. "Mechanisms of platelet inhibition by the selective serotonin reuptake inhibitor citalopram." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275477.
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Background: Selective serotonin reuptake inhibitor (SSRI) antidepressants prevent serotonin (5-HT) uptake by the serotonin transporter (SERT). Since blood platelets express SERT, SSRIs may modify platelet function and the risk of cardiovascular disease. However, the beneficial or adverse effects of SSRIs on arterial thrombosis are poorly characterised and detailed in vitro experimental data is limited. The SSRI citalopram is a racemate, the (S)-isomer being the more potent SERT inhibitor. Although citalopram has been shown to inhibit platelets in vitro, it is unclear whether this is mediated via SERT blockade. Aim: To determine if citalopram inhibits platelet function via SERT blockade, or through a novel mechanism of action. Findings: 5-HT uptake into platelets was blocked by both citalopram isomers at concentrations that had no apparent effect on platelet function. Despite the (S)-citalopram isomer being the more potent SERT inhibitor, (R)-citalopram was equally potent at inhibiting other platelet functions. These findings strongly suggest that inhibition of platelet function by citalopram in vitro is not mediated by blocking SERT. Subsequent experiments identified two putative mechanisms for citalopram-mediated platelet inhibition: 1) citalopram did not inhibit calcium store release induced by the platelet agonist U46619, despite blocking subsequent Rap1 activation. A credible target for this inhibitory mechanism is the calcium and diacylglycerol guanine nucleotide exchange factor-1 (CalDAG-GEFI): 2) citalopram suppressed early protein phosphorylation within the GPVI pathway, resulting in the inhibition of subsequent platelet responses. Further experiments show that other commonly used antidepressants also inhibit platelets. As with citalopram, inhibition was only observed at concentrations above those required to block SERT, suggesting that alternative inhibitory mechanism(s) are responsible. Conclusions: Data presented in this thesis support two novel putative mechanisms of citalopram-induced platelet inhibition. These findings demonstrate that citalopram and other antidepressants inhibit platelets independently of their ability to block SERT-dependent 5-HT transport. The identification of thesemechanisms provides a pharmacological approach to develop novel antiplatelet agents based on current antidepressants.
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Bowditch, William Antony. "Response inhibition and associative learning : training stimulus specific response inhibition." Thesis, University of Exeter, 2016. http://hdl.handle.net/10871/24923.
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Response inhibition, which refers to the ability to cancel an already initiated motor response, is often considered to be a hallmark of Executive Control. The popular view conceptualises these control processes as deliberate and top-down. How- ever, what if you have cancelled the same response (say stopping at a pedestrian crossing) to a given stimulus (in this example the red do not cross pictogram) many times before? Does the resulting action cancellation remain an exclusively top down act of control, or does it become bottom-up with practise. Research suggests that repeatedly pairing a stimulus with withholding a response results in slowed reaction times and a decreased probability of responding, even when no longer appropriate (a phenomenon first reported by Verbruggen & Logan, 2008a). This thesis attempts to answer this question from an associative learning per- spective: Asking if repeatedly pairing a stimulus with action cancellation results in stimulus-stop associations. Chapter One introduces current perspectives on response inhibition, the dual- process model of associative learning, and a theoretical framework that attempts to integrate these areas. Chapters Two and Three ask what is learnt when a stimulus is repeatedly paired with stopping in response inhibition task: Specif- ically, Chapter Two investigate the contribution of stimulus detection. Chapter Three asks whether subjects are learning not to respond or withhold and pro- vides evidence for the feature-positive effect in stimulus-stop learning. Chapter Four investigates the role of explicit expectancies and incidental associations in this form of learning, whilst also exploring whether transcranial direct cur- rent stimulation can enhance the acquisition of stimulus-stop associations. Both Chapters Five and Six investigate how stimulus-stop training may transfer to other tasks and behaviours with a specific focus on why stimuli tend to be devalued after stimulus-stop training. Finally, Chapter Seven relates the findings of each respective chapter back to the theoretical model introduced in Chapter One.
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Chowdhury, Nahian Shahmat. "Intracortical Inhibition and Response Inhibition in healthy adults and gamblers." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21945.
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This thesis investigated whether the strength of primary motor cortex (M1) short-interval Intracortical inhibition (SICI) can predict an individual’s ability to stop prepotent actions. Experiments involved measuring SICI at rest (i.e. during relaxed muscle activity) or during a stop signal task. Chapter 3 showed that stronger resting-state SICI predicted more efficient stopping. Chapter 4 showed that more efficient stopping was associated with stronger SICI during action stopping. Chapter 5 showed that SICI in left and right M1 uniquely predicted stopping ability of the contralateral hand but not the ipsilateral hand, suggesting there is a hemisphere-specific influence of SICI over stopping ability. This was further supported by Chapter 6, which showed that left M1 SICI was stronger when the contralateral (right) hand vs. ipsilateral (left) hand was selected to stop. Chapter 6 also showed that subjects trained in the stop signal task either within one session and across multiple sessions, displayed increases in resting-state SICI strength and increased SICI strength during action stopping. These findings demonstrate a strong link between stopping ability and SICI measured outside of and during task context, with a stronger influence of SICI over the stopping ability in contralateral actions. This thesis also had an applied question, which was to investigate whether SICI is altered in gamblers, a population associated with impaired stopping ability. Chapter 2 consisted of a meta-analysis which showed that gambling disorder is associated with impairments in action stopping. Chapter 3 showed that those classified as problem gamblers exhibited reduced SICI and increased glutamate-mediated Intracortical facilitation relative to controls. This suggests intracortical circuits within M1 altered in problem gamblers, which may be functionally implicated in the inability to stop gambling urges. This thesis makes contributions to our understanding of the mechanisms of action stopping, and the aetiology of gambling problems.
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Frings, Christian. "Inhibition von Distraktorinformation." Kassel : Kassel Univ. Press, 2004. http://deposit.d-nb.de/cgi-bin/dokserv?idn=97180110X.
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Smith, Gary Thomas. "Inhibition of IPNS." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.276831.
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Elfant, David J. "Inhibiting inhibition : GABAergic networks in the CA1 area of the rat hippocampus." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496867.
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Shkirskiy, Viacheslav. "Corrosion inhibition of galvanized steel by LDH - inhibitor hybrids : Mechanisms of Inhibitor Release and Corrosion Reactions." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066216/document.
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Le travail présenté essaie de comprendre les mécanismes de l’action d’un inhibiteur de corrosion présent dans un revêtement hybride sous forme de pigments intercalés dans les hydroxydes double lamellaires (HDL) pour la protection de l’acier galvanisé. Trois étapes clés ont été choisies pour ce travail : (1) l’identification d’un inhibiteur de corrosion hydrosoluble pour l’acier galvanisé avec une compréhension de sa réactivité, (2) la détermination des facteurs et des mécanismes contrôlant la libération de l’inhibiteur à partir d’HDL et (3) la compréhension des mécanismes de protection dans un système modèle avec le revêtement hybride contrôlé par la libération de l’inhibiteur et la réactivité d’inhibiteur. MoO42- a montré la meilleure efficacité d'inhibition comparable à CrO42- dans des solutions alcalines et neutres. L’effet inhibiteur de MoO42- a été associé à la formation d’un film riche en Mo(V). L'effet de cet anion sur la dissolution de l'acier à bas carbone a été également vérifié pour exclure la possibilité d'un effet d'accélération des espèces choisies. Les tests de lixiviation ont montré que la libération de MoO42- à partir d’HDL a été contrôlée par la nature des ions échangés à partir du support par un mécanisme d'échange d'ions à un pH neutre et par la dissolution du cadre de la LDH à un pH alcalin. La présence de seulement Cl- conduit à moins de 40% de libération de MoO42- après 24 h d'immersion alors que les additions des carbonates ont abouti à libération de 100% après 1 h. Les tests d'immersion ont montré léger effet d'inhibition du système de revêtement dans Cl- et une augmentation dans CO32- en accords avec le niveau plus élevé de MoO42- libéréThe current work was dedicated to the investigation of the fundamental mechanisms of the action of a layered double hydroxide (LDH) inhibitor hybrid coated systems for the corrosion protection of galvanized steel. The objective of the work was achieved by the realization of three milestones: (1) the identification of the effective water soluble inhibitor on Zn and steel substrates and the understanding the mechanisms of its action, (2) the revealing the factors and mechanisms controlling the release of the selected inhibitor from Zn2Al/-LDH hosts and (3) the understanding the mechanisms of coated system controlled by inhibitor release and its action. MoO42- showed the best inhibition efficiency comparable to CrO42- in alkaline and neutral solutions. The protective properties of MoO42- were assigned to the fast formation of Mo(V) film. The effect of MoO42- on the dissolution of low carbon steel was also verified to exclude the possible accelerating effect of chosen species. The leaching tests showed that MoO42- release from LDH was controlled by the nature of the exchanged ions from the media by ion-exchange mechanism at neutral pH and by the dissolution of the LDH framework at alkaline pH. The presence of only Cl- resulted in less than 40 % of MoO42- release after 24 hours of the immersion while the additions of the carbonates resulted in 100 % release after 1 hour. The immersion tests showed slight inhibiting effect of coated system in Cl and high in CO32- medias coherent with higher level of MoO¬42- released. The ways to control the inhibitor release and hence, the inhibition performance of coated systems were discussed in the vein of environment composition
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Mizon, Guy Andrew. "Selective attention and inhibition : effects of inhibition tasks on subsequent distractor rejection." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404990.
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Bearss, Nicole R. "Inhibition of Prostate Cancer via Inhibition of Peptidylglycine α-Amidating Monooxygenase (PAM)." University of Toledo / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1302200866.
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Köhncke, Clemens [Verfasser]. "Zerebrale Oxygenierungsänderungen bei Inhibition in einem Modell der transkallosalen Inhibition / Clemens Köhncke." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024743128/34.
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McCready, Tara Lyn. "Inhibition of protein phosphatase-1 by endogenous inhibitor proteins and natural product toxins." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0032/NQ46885.pdf.
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Guerrant, William. "Targeted histone deacetylase inhibition." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/44907.
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Histone deacetylase (HDAC) inhibitors (HDACi) have demonstrated a wealth of biological effects, including anti-proliferative, anti-inflammatory, anti-parasitic, and cognition-enhancing activities. The recent FDA approvals of the inhibitors SAHA and FK-228 have validated HDACi clinical use in cutaneous T cell lymphoma, while numerous clinical trials are currently ongoing using HDACi against a variety of disease states. While the future of the HDAC field looks increasingly promising, there are lingering issues hindering broader use. Recent data point to dysregulation of specific HDAC isoforms in many disease states. However, most current HDACi are pan-inhibitors, lacking the specificity to target individual isoforms. Adding to this, there are currently 18 identified HDAC isoforms, and most lack a defined crystal structure, further complicating the task of designing isoform-specific inhibitors. Most importantly, HDACi have demonstrated a lack of efficacy against solid tumors in the clinic, a major obstacle to broader use in cancer therapy. Several of these issues could more fully be addressed through specific targeting of HDACi, and could bring HDACi into wider and more efficacious pharmaceutical use. Targeting the specific tissue or organelle where HDAC dysregulation occurs could confer greater efficacy in vivo. To this end, we have created four classes of compounds: (1) aryltriazolyl HDACi that potently inhibit HDAC activity and prostate cancer cell growth, (2) dual-targeted inhibitors of Topoisomerase II and HDAC and (3) dual-targeted inhibitors of Topoisomerase I and HDAC, both of which have potent inhibition against both target enzymes as well as cancer cell lines, and finally (4) macrocyclic HDACi that potently inhibit the growth of lung cancer cell lines and preferentially target lung tissue in vivo.
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Camp, Gino. "Forgetting: inhibition or interference?" Rotterdam : Rotterdam : Erasmus Universiteit ; Erasmus University [Host], 2006. http://hdl.handle.net/1765/8200.
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Carter, Wendy Jayne. "Legumain structure and inhibition." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615940.
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Richardson, J. "Corrosion inhibition with amides." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381056.
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Corin, Karolina A. (Karolina Ann) 1981. "Inhibition of myofibroblast contraction." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/32381.
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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2005.Includes bibliographical references (p. 46-49).
Although current medical procedures cannot restore complete function of a transected nerve, inserting both of its ends in a tube helps it regenerate. The regenerate is inferior to the uninjured nerve: it has a smaller diameter and poorer electrical conduction. Layers of contractile cells known as myofibroblasts have been observed around regenerated nerve portions. An inverse relationship between the layer thickness and the quality of the regenerate has also been observed. These findings suggest that the cells are exerting contractile forces which prevent the regenerating nerve from fully developing. Inhibiting this contraction should thus improve the quality of nerve regeneration. Alpha smooth muscle actin ([alpha]-SMA) is a critical contractile protein. Its expression can be upregulated by the growth factor TGF-[beta]1, and blocked by the pharmacological agent PP2. To investigate whether blocking SMA expression alone can inhibit myofibroblast contraction, NR6 wild type fibroblasts were seeded into short cylindrical collagen-GAG matrices, and administered either media alone, media with TGF-[beta]1 (3ng/ml), or media with TGF-[beta]1 and PP2 (10 [mu]M). Non-seeded matrix samples were also prepared. The matrix diameters were measured every day for 12 days, after which the matrices were digested and the number of adhered cells were counted. The daily change in matrix diameter was calculated. The results showed that the cells contracted the matrices. TGF-[beta]1 increased cell contractility, while PP2 inhibited it..
(cont.) Normalizing the Day 12 diameter change measurements to cell number and the original matrix diameter showed that TGF-[beta] increased the strain generated by each cell ... relative to ... for untreated cells), and that PP2 counteracted this effect (...). Using the linear elastic constitutive relations, the average force exerted per cell was calculated for the untreated cells (...), TGF-[beta]1 stimulated cells (...), and TGF-[beta] + PP2 stimulated cells (...). The cell counts after Day 12 indicate that PP2 interferes with cell adhesion to the matrices. After 6 hours in culture, 21% of untreated cells, 25% percent of cells treated with TGF-[beta] 1, and 25% of cells treated with TGF-[beta]1 and PP2 had adhered. By Day 12, only 12% of the seeded untreated cells, 14% of cells treated with TGF-[beta] I, and 3.2% of cells treated with both TGF-[beta]1 and PP2 remained adhered. This study thus indicates that PP2 inhibits cellular contraction, possibly by preventing cell-substrate adhesion
by Karolina A. Corin.
S.M.
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Roberts, Henrietta Whitley. "Rumination and cognitive inhibition." Thesis, University of Exeter, 2013. http://hdl.handle.net/10871/10281.
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The focus of the thesis is the investigation of the causal nature of the established association between rumination and that ability to resolve interference from task-irrelevant information, and prepotent responses. Rumination is a term used to refer to both unhelpful dwelling on negative moods and depressive symptoms (e.g., Nolen-Hoeksema, 1991), and repetitive intrusive thoughts around the theme of unresolved personal goals (Martin & Tesser, 1996). It has been proposed that rumination occupies working memory resources, thereby depleting cognitive control capabilities necessary for the performance of concurrent effortful tasks (Hartlage, Alloy, Vasquez, & Dykman, 1993; Hertel, 2004; Watkins & Brown, 2002). This model constitutes one possible account of the considerable data demonstrating an association between depressive rumination and deficits on tasks invoking inhibitory processes (Joormann, Yoon, & Gotlib, 2007). An inhibition construct is invoked to account for the empirical observation of interference; however there are few instances where inhibition is unambiguously driving interference (MacLeod, 2007). Moreover, there is evidence that inhibition is not a unitary construct (Friedman & Miyake, 2004). Five experiments manipulated rumination on depressive symptoms and on personal goals in dysphoric and unselected samples in order to test Watkins and Brown’s (2002) hypothesis that state rumination impairs interference control capabilities. The causal impact of state rumination was examined on interference control tasks that implicate different inhibitory sub-types: resistance to proactive interference from positive and negative material (Studies One, Two, and Five), and prepotent response inhibition on a go/no-go paradigm (Studies Three and Four). No evidence was found to support the prediction that state rumination about depressed mood (Studies One and Two) or on-going personal goal discrepancies (Study Five) causes difficulties resolving interference from irrelevant emotional material relative to non-ruminative control conditions in both dysphoric (Studies One and Two) and unselected (Study Five) samples. No evidence was found to support the prediction that state rumination about personal goal discrepancies impairs prepotent response inhibition relative to non-ruminative control conditions (Studies Three and Four). There was some tentative evidence to suggest that ruminating on personal goal discrepancies increased efficiency in holding a single goal active in working memory without reinforcement (Study Four). The implications of these findings for existing models of the causal nature of the relationship between rumination and interference control processes is discussed (Chapter Nine). It is concluded that models proposing a causal impact of state rumination on available working memory capacity are insufficient to fully account for the established association between the trait tendency to ruminate and increased susceptibility to interference from irrelevant material.
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Bonetti, Kelly. "Inhibition studies of SIRT1." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12057.
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Thesis (M.A.)--Boston UniversitySilent Information Regulator 2 (Sir2) of Saccharomyces cerevisiae is the progenitor of an ancient family of proteins known as sirtuins. Sirtuins act on substrates in various regulatory pathways critical to normal cell function. Human SIRT1 is the closest known homologue of yeast Sir2. This study focuses on the function of human SIRT1 and the influence of this protein on the host inflammatory response. To better understand the role of SIRT1 and its role in disease, a working clone that expresses the SIRT1 protein is necessary. In this study, the human SIRT1 gene was amplified from commercially available template DNA using the Polymerase Chain Reaction (PCR). The SIRT1 gene was ligated into pET28b(+), a bacterial expression vector that works in Escherichia coli. The SIRT1 gene is expressed under control of the T7 promoter, which is not recognized by the transcriptional machinery in E.coli. Protein expression does not occur until a source of T7 RNA polymerase is provided. Once obtained, the SIRT1-pET28b(+) plasmid was transferred into TOP10, a bacterial maintenance strain. Once established, the SIRT1-pET28b(+) construct is transformed into an expression host containing a chromosomal copy of the T7 RNA polymerase gene. Induced by the addition of Isopropylthio-β-Galactoside (IPTG), the expression cell diverts almost all of its resources to express the target SIRT1 gene. Overexpression of the SIRT1 protein allows for characterization of enzyme activity. Characterization of the mechanism where SIRT1 is inhibited by the native inhibitor nicotinamide (NAM) and the clinical antimycobacterial agent pyrazinamide (PZA) is needed. The focus of this thesis is elucidation of the mechanism of inhibition of SIRT1. PZA, a clinical agent used to treat tuberculosis (TB), has been shown to allosterically inhibit SIRT1. It is of particular interest to determine where PZA, a NAM derivative, binds SIRT1 and if this binding can be included in natural regulatory network mechanisms within the cell. At the heart of this study, are attempts to understand the complex binding interactions of both PZA and pyrazinoic acid (POA), the chemotherapeutically active metabolite of PZA, in the presence of NAM. Competition experiments with these agents may prove useful to determine if these molecules interact at the same site, if the molecules can be displaced competitively, or if certain residues within parts of the enzyme are essential for characteristic binding.
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Rodkey, Elizabeth A. "INHIBITOR RESISTANCE MECHANISMS AND INHIBITOR DESIGN IN ¿¿-LACTAMASES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1354463033.
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Lembo, Gaia. "Substrate targeting and inhibition of editing deaminases." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1144295.
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Identification of small molecules against APOBEC3B
The APOBECs are deaminases that act on DNA and RNA to restrict exogenous nucleic acids. Yet, the signature of their mutagenic activity –especially that of APOBEC3A and APOBEC3B- has been observed in the cancer genomes and their ability to increase the genetic heterogeneity of tumours has been linked to the onset of drug resistance in cancer. As such inhibition of their enzymatic activity represents a potential target for anticancer therapies. During my PhD I worked at the identification of APOBEC3B small-molecule inhibitors. To this aim, I used a computational approach to perform a virtual screening on large library of molecules to block APOBEC3B enzymatic activity. I then tested selected molecules from the virtual screening using biochemical assays to quantify their effect on APOBEC3B activity and their capacity to interfere with APOBEC3B binding to DNA. Through this, I was able to identify two small molecules that reduce the activity of this protein, which could provide basis for the development of the first drug for anti-APOBEC activity.
Engineering ADAR2 to act on DNA
Genome editing technologies have revolutionized our ability to target and modify the genomes of living cells and organisms. The fusion of AID/APOBECs to genome editing tools such as Cas9 allowed the development the first base editor, molecules that can be targeted to mutate specific cytosines. The pool of available Base Editors is in constant expansion as new molecules are developed to target DNA with more specificity and efficiency. As the only adenine-targeting Base Editor is based on TadA- an RNA deaminase-, I focused on the development of a A•T base editor based on the catalytic domain of ADAR2. Adenosine Deaminases Acting on RNA (ADARs), are editing enzymes that catalyse the C6 deamination of adenosine (A) to produce inosine (I) in double-stranded RNA. As human ADAR2 is able to target DNA/RNA hybrids, I first tried -without success- to use chimeras of n/dCas9 and the deaminase domain of ADAR2 to induce mutations in a fluorescent reporter. I then used a bacterial screen to select for mutants of ADAR2 that act on DNA. I selected a mutant that induces a mutator phenotype in bacteria and DNA damage in mammalian cells. I am currently working to engineer this mutant into a Base Editor suitable for biotechnological applications such as gene therapy, antiviral treatment and cancer therapy.
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Vitaliti, Alessandra. "Inhibition of tumor induced angiogenesis /." [S.l.] : [s.n.], 1999. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13409.
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Bell, Theodore Anthony. "Individual differences in memory inhibition /." view abstract or download file of text, 2005. http://wwwlib.umi.com/cr/uoregon/fullcit?p3181082.
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Thesis (Ph. D.)--University of Oregon, 2005.Typescript. Includes vita and abstract. Includes bibliographical references (leaves 95-104). Also available for download via the World Wide Web; free to University of Oregon users.
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Åkerfelt, Annika. "Visual-tactile stop signal inhibition." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972887520.
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Cook, Joanna Clare. "Ageing and inhibition in memory." Thesis, University of Southampton, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288442.
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Larson, Susan Joyce. "External inhibition of ethanol tolerance." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ30100.pdf.
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Bartels-Tobin, Lori R. "Naming and inhibition in aphasia." [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0001959.
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Ammar, Ahmed A. "Intake inhibition by neuropeptide Y /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-308-6/.
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Strauss, Sandra Jean. "Proteasome inhibition in lymphoid malignancy." Thesis, Queen Mary, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429409.
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Day, Jonathan Robert Stewart. "Therapeutic inhibition of thrombin signalling." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434321.
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Kingsbury, Oliver William. "The inhibition of cysteine proteinases." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360390.
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Trunkfeild, Amy Elizabeth. "Inhibition of Glycosyl Transferase MurG." Thesis, University of Warwick, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487830.
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MurG is the last intracellular enzyme involved in the biosynthesis of the bacterial cell wall, it is a glycosyl transferase that catalyses the transfer of A/-acetyl glucosamine from uridine diphosphate A/-acetyl glucosamine (UDP-GlcNAc) to the 04 hydroxyl group of MurNAc(pentapeptide)-pyrophosphoryl undecaprenol.
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孫耀君 and Yiu-kwan Edmond Suen. "Backward inhibition in pathological gamblers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41712638.
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Frings, Christian [Verfasser]. "Inhibition von Distraktorinformation / Christian Frings." Kassel : Kassel Univ. Press, 2004. http://d-nb.info/97180110X/34.
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Hicks, Jake Thomas. "Surfactant aspects of corrosion inhibition." Thesis, University of Hull, 2007. http://hydra.hull.ac.uk/resources/hull:6996.
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This thesis is concerned with investigating the surfactant aspects of corrosion inhibition. Corrosion inhibitors are of great industrial importance because they are a relatively inexpensive and easily applicable method of protecting oil pipelines against internal corrosion. The performance of corrosion inhibitors is known to depend upon the prevailing conditions within the pipeline. We have used a range of experimental techniques to study corrosion of steel surfaces, adsorption of corrosion inhibitors and the behaviour of inhibitors in mixtures of oil and water in order to understand more about the factors which affect the performance of corrosion inhibitors under oil field conditions. Firstly, electrochemical and weight-loss measurements were used to measure the corrosion rate of steel immersed in aqueous environments under atmospheric conditions and in the presence of dissolved carbon dioxide and hydrogen sulphide. The measurements were repeated in the presence of dodecylbenzyldimethylammonium chloride and I-aminoethyl-2-(8- heptadecenyl)-2-imidazoline acetate, which are thought of as model corrosion inhibitors. Both surfactants were found to effectively reduce the corrosion rate of steel when the dissolved gas was hydrogen sulphide, but were found to increase the corrosion rate in some aerated and carbonated environments. The optical technique ellipsometry has been used to study the adsorption of dodecylbenzyldimethylammonium chloride at the steel-water interface. We have determined the thickness of the surfactant film adsorbed from aqueous solution in the absence of electrolyte. The results are consistent with the formation of a monolayer at inhibitor concentrations close to the critical micelle concentration and possible multilayer formation at higher concentrations. Determination of inhibitor film thickness has not been possible in the presence of electrolyte and corrosive dissolved gases which cause rapid corrosion of the steel surface. The technique has been employed subsequently to study the initial stages of corrosion in the presence and absence of dodecylbenzyldimethylammonium chloride. Scanning electron microscopy and elemental analysis have also been used to examine the changes which occur to the steel surface during corrosion. These results show that the optical properties of the steel surface undergo changes as the steel is attacked by corrosive aqueous solutions and that dodecylbenzyldimethylammonium chloride can increase the rate of these changes or completely suppress them, depending on the nature of the dissolved gas present. Finally, we have investigated the phase behaviour of alkylbenzyldimethylammonium chloride and 1-aminoethyl-2-(8-heptadecenyl)-2- imidazoline acetate using equilibrium partitioning and emulsion phase inversion methods. The results show that variations in common oil field variables, such as temperature, electrolyte concentration and oil type, can lead to the consumption of the aggregated form of water-soluble corrosion inhibitors by partitioning to the oil phase. The results are discussed in terms of the effect of these variables upon the effective geometry of the inhibitor within the monolayer of the aggregates. We have also performed electrochemical corrosion rate measurements in systems containing oil and water, under conditions which cause virtually all of the inhibitor to exist in the oil phase. The results suggest that partitioning of the aggregated form of corrosion inhibitors from water to oil does not adversely affect corrosion inhibition in the aqueous phase.
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Bullock, Anthony James. "Metabolic inhibition in the ureter." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366420.
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Reith, Alison. "Inhibition of fibrinolysis in pregnancy." Thesis, University of Aberdeen, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303338.
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Two immunologically distinct PAIs, PAI-1 and PAI-2, exist in the maternal circulation during pregnancy. SDS-PAGE with zymography showed pregnancy plasma contained 40kDa PAI-1, 75kDa α2-antiplasmin and two novel bands of PAI-2 at 130kDa and 75kDa. The size and intensity of the bands of PAI-1 and PAI-2 increased during pregnancy. Non-denaturing PAGE with zymography was developed for semiquantitative analysis of PAI-2. PAI-2 migrated as fast and slow bands on non-denaturing PAGE, which corresponded to 75kDa and 130kDa PAI-2 detected after SDS-PAGE. Fast PAI-2, the major form, was detected between nine weeks and six days postpartum. During pregnancy the bands of fast and slow PAI-2 increased in size and intensity to a maximum at 30-35 weeks. An ELISA, specific for PAI-2 antigen, was developed which used a rabbit antibody raised against human placental PAI-2. With a detection limit of 1.8 ng/ml, this ELISA was used to quantify PAI-2 in plasma and body fluids. Plasma PAI-1 and PAI-2 increased to maximum concentrations of 112.5 ± 28.9 ng/ml and 197.3 ± 56.9 ng/ml respectively during the third trimester and decreased slightly before delivery. After delivery PAI-1 decreased rapidly, while PAI-2 persisted longer in the maternal circulation. The postpartum half-lives of PAI-1 and PAI-2 were determined as 30 minutes and 24 hours respectively. Plasma from pre-eclamptic subjects showed elevated PAI-1 and decreased PAI-2. Plasma from pregnant subjects with DIC also showed increased PAI-1 and decreased PAI-2. PAI-2 was not detected in plasma during molar pregnancy. Amniotic fluid contained PAI-1 and fast PAI-2. Amniotic fluid PAI-1 doubled between 16 weeks and term, while PAI-2 decreased slightly. Term amniotic fluid PAI-1 was 8-fold higher than PAI-2. PAI-2 was also detected in ovarian cyst fluid, plasma from subjects with pancreatitis, septicaemia and leukaemia showing that PAI-2 is not a pregnancy-specific protein.
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O'Connell, James P. "Matrix metalloproteinase activation and inhibition." Thesis, Open University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338338.
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Axamawaty, Mohammed Taleb Hassan. "Inhibition and inactivation of hydrolases." Thesis, University of Bristol, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481028.
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Pollux, Petra. "Cognitive inhibition in Parkinson's disease." Thesis, University of Lincoln, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263964.
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Torres, Molina Maria. "Corrosion inhibition : a spectroscopic study." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/corrosion-inhibition-a-spectroscopic-study(7279a328-ec12-4bd4-b7c0-7c3f118095f4).html.
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Although many organic compounds are known to inhibit corrosion, in most cases it remains unknown how they specifically interact with a surface and how they decrease the corrosion rate. This lack of mechanistic knowledge currently makes the design and choice of new active compounds a case of trial and error. Understanding these organic molecule-metal surface interactions could lead to the design of new corrosion inhibitors for the oil and gas industry. In this project it is intended to move the understanding of corrosion inhibition and other surface phenomena from empirical observation towards a mechanistic understanding. Using a combination of surface sensitive techniques such as vibrational sum frequency generation and X-ray photoelectron spectroscopy, and theoretical modelling through the preparation of model complexes of relevant corrosion inhibitors. Two families of corrosion inhibitors have been studied and are presented here. For nitrogen based corrosion inhibitors a combination of theoretical calculations and experimental analysis of vibrational modes of model compounds have proved to be a good method to assist in understanding of surface phenomena. For phosphorus based corrosion inhibitors an extensive study of model compounds has been done. In addition to this, different phosphonic acids and phosphate esters have been studied on a Fe (110) and steel surfaces in ultra high vacuum and in more realistic conditions using near ambient pressures in order to investigate if changes in the environmental conditions lead to a different behaviour. These have been compared to the study of PAE 136, a commercial corrosion inhibitor composed by a mixture of phosphate esters used in the extraction of oil, proving that one of the selected model compounds has a better inhibitive activity in both an ideal and a more realistic system. The results presented in this thesis demonstrate that every corrosion inhibitor needs to be tested in the conditions in which it is going to be used as it is not possible to predict if a given active compound is going to have the same behaviour for different environments.
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Hanczakowski, Maciej. "Inhibition in long-term memory." Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:6355.
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The present thesis examined the issue of inhibitory processes in long-term memory. Several theoretical frameworks, which posit various loci of an inhibitory mechanism, have been examined. The locus of an inhibitory mechanism was investigated within the retrieval practice paradigm, in which inhibition is recruited against information that competes for memory access during retrieval, and within the list-method directed forgetting paradigm, in which inhibition is voluntarily recruited. Experiments 1-8, with a total of 315 participants tested, focused on the cue-independence of forgetting in the retrieval practice paradigm. Experiments 1, 2, 4, 7, and 8 provided no evidence for the cue-independence. Although forgetting was documented when memory was tested with original cues (Experiments 1, 2, 3, 6), it failed to emerge with independent cues that were semantically related to several items in the memory set (Experiments 1 and 2), that were semantically related to individual items in the memory set (Experiments 2, 4, and 8), and that were only episodically related to individual items (Experiment 7). These findings do not support the theory of inhibition operating at the level of semantic features. Further, no support was obtained for the prediction that a broad spectrum of episodic associations established for interfering information is affected by inhibition (Experiments 4 and 7). Finally, the prediction of a constrained episodic account, according to which only the associative link directly responsible for interference is affected by an inhibitory mechanism, was assessed in Experiment 8. This hypothesis also did not gain empirical support. Experiments 9-11, with a total of 141 participants tested, focused on the list-method directed forgetting paradigm. Within this paradigm two hypotheses about the locus of inhibitory processes were tested. Predictions of the retrieval inhibition account, which postulates the general effect of inhibition on all episodic associations created during study, where contrasted with predictions of a constrained inhibitory model, according to which only episodic links directly responsible for interference are affected by inhibition. Experiments 10 and 11 did not provide support for the retrieval inhibition account, thus favouring a more constrained framework. Together, the results of the present experiments can be interpreted in two ways. They can be used to specify an inhibitory mechanism as one of associative unlearning, operating only on the associations that are the cause of interference which needs to be resolved by inhibition (but see Experiment 8). Alternatively, the present results can be used to argue that the concept of inhibition is not needed to account for forgetting in the examined paradigms.
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Cranwell, Joanne. "Inhibition training using smartphone technology." Thesis, University of Nottingham, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659213.
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Human self-regulation has, throughout time, been held as one of the most centrally important human virtues. Those who are prone to lapses in self control may be at risk of exposure to a myriad of individual problems such as alcoholism, drug addiction and gambling. The impact of poor self-control also extends far beyond the individual and is responsible for a wide range of economic problems globally and in the United Kingdom (UK). The ubiquity and ever evolving computing power of the mobile phone now affords greater opportunities for behaviour change professionals to design and deliver self-control interventions as people go about their everyday life. Better understanding of how people interact with these technologies and accept such interventions will help professionals to design mobile applications to support good self-control. First, based on an energy or strength model of self-control, the work in thesis presents evidence that self-control resources can be strengthened through regular discrete bouts of exercise (response inhibition training) using smartphone technology, as reported in two longitudinal self-control training studies. Second, insight into how patticipants interacted with the teclmology used to deliver the intervention was gained through a series of post-training interviews. Third, through recorded focus groups, lay perceptions of self-control are explored to see if participant conceptualisations of self-control can help inform the content and design of future mobile training interventions. Finally, this thesis concludes with a general discussion of the thesis findings. Broadly, the work presented centres on the effect of the training, the efficacy and acceptance of the mode of delivery of the intervention, and providing insight for future interventions by delivering a core set of guidelines essential for future designers. The research addresses gaps in the ego-depletion literature and contributes to the advancement of theory and practice.
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Cook, Erik C. "Calcineurin: From Activation to Inhibition." UKnowledge, 2016. http://uknowledge.uky.edu/biochem_etds/29.
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Calcineurin is a Ser/Thr phosphatase whose function is implicated in critical physiological processes such as immune system activation, fetal heart development, and long-term depression in neurons. Calcineurin has been implicated in the progression of Alzheimer’s disease and cardiac hypertrophy. It is not well understood how calcineurin is activated on a molecular level by Ca2+ and its activating protein calmodulin. Previous data from our lab show that calmodulin interaction induces the folding of the intrinsically disordered regulatory domain of calcineurin in two discrete and distant regions into α-helical conformations and that this folding is critical for complete activation of calcineurin. It was also discovered that one of the helical elements which we call the “distal helix” was unstable at a human body temperature of 37°C in dilute buffer. This raises the question; how can a structure critical for the complete activation of calcineurin be unstable at average human body temperature? Proteins do not exist in solutions of the dilute buffer, but rather in a crowded cosmos that ranges between 200 and 400 g/L of macromolecules such as proteins, DNA, and other cellular components. We show here that phenomenon known as macromolecular crowding can stabilize the distal helix and that stabilization increases the activity of calcineurin at human body temperature.
Much about intrinsically disordered proteins (IDPs) remains a mystery, especially what influences the rate at which they interact with their target molecules. IDPs lack any sort of stable three-dimensional structure because of their lack of sufficient hydrophobic or aromatic amino acids while having a large proportion of polar and charged amino acids. Because of the high degree of charged amino acids, electrostatic forces play a significant role in their interaction other proteins. This is known to be the case for calmodulin which is net negatively charged protein that has over 300 binding targets of which are usually basic amphipathic alpha-helices. The calmodulin-binding site located in the intrinsically disordered regulatory domain of calcineurin is net positively charged, and, interestingly, is flanked by acidic patches on either side. These acidic patches might perturb attractive electrostatic forces between the calmodulin-binding site and calmodulin. Using fluorescence spectroscopy in conjunction with a stopped-flow apparatus to measure the kinetics between calmodulin and calcineurin we seek to characterize the influence of the steric and electrostatic forces between the two proteins.
Also, we present data on RCAN1-4 (Regulator of Calcineurin Isoform 1-4) which has been shown to be an inhibitor in some contexts and an activator of calcineurin in other. RCAN1-4 is expressed in the heart and its upregulation has been shown to prevent calcineurin-mediated pathological cardiac hypertrophy suggesting that it plays an inhibitory role in this context. The work shown demonstrates that RCAN1-4 is a competitive inhibitor of calcineurin and whose binding affinity is modulated by Ca2+/calmodulin. These data unveil a binding site utilized by RCAN1-4 which is commonly used among other calcineurin substrates.
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Billard, 1959 Jean-Marie. "Olive inférieure et inhibition cérébelleuse." Paris 6, 1986. http://www.theses.fr/1986PA066044.
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Etude du rôle de l'olive inferieure dans l'inhibition cérébelleuse chez le rat, après destruction sélective de l'O. I. Cette destruction élimine l'action de suppression tonique qu'exercent les fibres grimpantes sur les décharges simples des Purkinje. On observe : a) un accroissement de l'inhibition cérébelleuse dans les premiers jours, ainsi qu'une disfacilitation rubrale et une dépression des activités motrices; b) ces effets régressent jusqu'à 1 mois; c) passe 1 mois le déficit moteur persiste.
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Edge, Colin Michael. "Theoretical studies of enzyme inhibition." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/14388.
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The glyoxalase enzyme system catalyses the conversion of methylglyoxal to D-lactic acid. The first of the two component enzymes, glyoxalase I, is responsible for the transfer of two protons in an iscmerisation reaction. This enzyme has been ascribed a role in tumorigenesis in the past and some of its inhibitors are known to be carcinostatic. This thesis describes quantum chemical calculations on the enzyme mechanism and on some enzyme inhibitors. The calculations on the mechanism of the enzyme take the form of studies of model reaction schemes, with minimal and split-valence basis sets. The calculation of the energies of various intermediates has led to the evaluation of different pathways as models of the enzyme mechanism. The comparison of different substituted compounds has led to further conclusions on the part played by the sulphur atom in the enzyme-catalysed reaction. Two main groups of inhibitor molecules are discussed; these are flavone and coumarin derivatives. The molecular electrostatic potential of these molecules has been calculated on various surfaces, using a minimal basis set, to attempt to correlate this property with the compounds' inhibitory power. A FORTRAN program is presented which depicts calculated properties on the surfaces. This program allowed the identification of various regions which seemed to be indicative of the inhibitory strength of the compounds.