Relevant bibliographies by topics / Mechanism of action of electroconvulsive therapy

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Academic literature on the topic 'Mechanism of action of electroconvulsive therapy'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Mechanism of action of electroconvulsive therapy"

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Smulewicz, Klaudia, Alicja Wójcik, Wojciech Pakaszewski, Bartosz Rusin, and Bartłomiej Ziomko. "Potential mechanisms of action and effectiveness of electroconvulsive therapy in the treatment of depressive disorders." Journal of Education, Health and Sport 12, no. 11 (November 3, 2022): 216–21. http://dx.doi.org/10.12775/jehs.2022.12.11.028.

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The aim of this study is to prove the positive effect of electroconvulsive therapy on depressive disorders. Depression as a mental illness has not been fully studied in terms of its relationship in combination with electroconvulsive therapy. Nevertheless, despite many uncertainties, its positive effect on this type of treatment is indicated. Analysing a number of studies, electroconvulsive therapy is considered to be the most effective treatment for depression. As the research work shows, thanks to the use of electroconvulsive therapy in older people over 60 years of age, a positive effect on the patient's health can be observed in the entire study group. The mechanism of action of electroconvulsive therapy is multifaceted. There are several theories of how it works, affecting different areas of the individual's body. These include an anticonvulsant theory (GABAergic), effects on serotonergic and dopaminergic functions in the brain, effects on neurogenesis in the hippocampus and amygdala and neuropathicity, effects on gene transcription, an increase in the Narp protein with a presumed antidepressant effect, support for the neuroendocrine mechanism, as well as effects on inflammation (cytokines).
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Merkl, Angela, Isabella Heuser, and Malek Bajbouj. "Antidepressant electroconvulsive therapy: Mechanism of action, recent advances and limitations." Experimental Neurology 219, no. 1 (September 2009): 20–26. http://dx.doi.org/10.1016/j.expneurol.2009.04.027.

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Rojas, Milagros, Daniela Ariza, Ángel Ortega, Manuel E. Riaño-Garzón, Mervin Chávez-Castillo, José Luis Pérez, Lorena Cudris-Torres, et al. "Electroconvulsive Therapy in Psychiatric Disorders: A Narrative Review Exploring Neuroendocrine–Immune Therapeutic Mechanisms and Clinical Implications." International Journal of Molecular Sciences 23, no. 13 (June 22, 2022): 6918. http://dx.doi.org/10.3390/ijms23136918.

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Electroconvulsive therapy (ECT) is based on conducting an electrical current through the brain to stimulate it and trigger generalized convulsion activity with therapeutic ends. Due to the efficient use of ECT during the last years, interest in the molecular bases involved in its mechanism of action has increased. Therefore, different hypotheses have emerged. In this context, the goal of this review is to describe the neurobiological, endocrine, and immune mechanisms involved in ECT and to detail its clinical efficacy in different psychiatric pathologies. This is a narrative review in which an extensive literature search was performed on the Scopus, Embase, PubMed, ISI Web of Science, and Google Scholar databases from inception to February 2022. The terms “electroconvulsive therapy”, “neurobiological effects of electroconvulsive therapy”, “molecular mechanisms in electroconvulsive therapy”, and “psychiatric disorders” were among the keywords used in the search. The mechanisms of action of ECT include neurobiological function modifications and endocrine and immune changes that take place after ECT. Among these, the decrease in neural network hyperconnectivity, neuroinflammation reduction, neurogenesis promotion, modulation of different monoaminergic systems, and hypothalamus–hypophysis–adrenal and hypothalamus–hypophysis–thyroid axes normalization have been described. The majority of these elements are physiopathological components and therapeutic targets in different mental illnesses. Likewise, the use of ECT has recently expanded, with evidence of its use for other pathologies, such as Parkinson’s disease psychosis, malignant neuroleptic syndrome, post-traumatic stress disorder, and obsessive–compulsive disorder. In conclusion, there is sufficient evidence to support the efficacy of ECT in the treatment of different psychiatric disorders, potentially through immune, endocrine, and neurobiological systems.
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O'Connor, M. Kevin. "Hypotheses Regarding the Mechanism of Action of Electroconvulsive Therapy, Past and Present." Psychiatric Annals 23, no. 1 (January 1, 1993): 15–18. http://dx.doi.org/10.3928/0048-5713-19930101-06.

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Scott, Allan I. F. "Mode of action of electroconvulsive therapy: an update." Advances in Psychiatric Treatment 17, no. 1 (January 2011): 15–22. http://dx.doi.org/10.1192/apt.bp.109.007039.

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SummaryIt has become acceptable for psychiatrists to say that they simply do not know how electroconvulsive therapy (ECT) works. This frame of mind runs the risk that there will be no expectation that psychiatrists remain familiar with seminal studies on the mode of action of ECT. This article is intended as a reminder of these studies and illustrates how the original theories have evolved. This evolution has been brought about largely by modern brain imaging techniques in human studies and in patients treated with ECT. These new findings will be set in the context of contemporary ideas about the neuroanatomy of mood disorders and the cellular mechanisms of the long-term effects of antidepressant treatments.
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Malcolm, Katy. "Patients' perceptions and knowledge of electroconvulsive therapy." Psychiatric Bulletin 13, no. 4 (April 1989): 161–65. http://dx.doi.org/10.1192/pb.13.4.161.

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Most research on electroconvulsive therapy (ECT) has focused on technical aspects, such as indications for treatment, efficacy, side effects of treatment, and theories of mechanism of action. Little investigation has been made of the attitudes and experience of patients receiving ECT and less regarding patients' understanding and knowledge of this treatment. Earlier studies have looked at specific aspects of patients' perceptions of ECT, such as subjective side effects, (Gomez, 1975), or the effect of the media on attitudes towards ECT (Bird, 1979). Other studies have investigated these and related issues more comprehensively (Freeman & Kendell, 1980; Hughes et al, 1980). These studies were carried out some time after the ECT course had been completed; in some cases, over a year. It may be that patients' perception and knowledge of ECT are different before and after treatment. Attitudes and knowledge may also change or fade over time.
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Tullio, Valeria, Stefania Zerbo, Antonietta Lanzarone, Salvatore Procaccianti, and Antonina Argo. "Psychological and Medico-Legal Perspectives on Electroconvulsive Therapy and Patient-Centered Care: A Short Review of Cross-Cutting Issues." Open Psychology Journal 13, no. 1 (September 8, 2020): 253–63. http://dx.doi.org/10.2174/1874350102013010253.

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Electroconvulsive therapy is a treatment that, since its first administration, has been a major topic for debate within the scientific world. In recent years, the debate has become increasingly focused on the short- and/or long-term efficacy of electroconvulsive therapy, its appropriateness in clinical settings, its mechanism of action, the impact evaluation of transient and/or persistent adverse effects, and the drafting of international guidelines, etc. From the authors’ point of view, these themes are inevitably crossed by three other fundamental issues of significant psychological, relational, ethical, and medico-legal impact. Still, they are less studied than purely biomedical issues in recent times. Therefore, the aim of this article is to focus on the following cross-cutting issues: the therapist-patient relationship, the patient’s perspective, the attitude on electroconvulsive therapy, and informed consent. This short review refers to the international literature on ECT published since 2000. Analyses of the three previously listed topics are, in part, made within the context of Italian medical settings.
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Nobler, Mitchell S., and Harold A. Sackeim. "Mechanisms of Action of Electroconvulsive Therapy: Functional Brain Imaging Studies." Psychiatric Annals 28, no. 1 (January 1, 1998): 23–29. http://dx.doi.org/10.3928/0048-5713-19980101-07.

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Ryan, K. M., and D. M. McLoughlin. "From Molecules to Mind: Mechanisms of Action of Electroconvulsive Therapy." FOCUS 17, no. 1 (January 2019): 73–75. http://dx.doi.org/10.1176/appi.focus.17104.

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Ryan, K. M., and D. M. McLoughlin. "From molecules to mind: mechanisms of action of electroconvulsive therapy." Acta Psychiatrica Scandinavica 138, no. 3 (August 16, 2018): 177–79. http://dx.doi.org/10.1111/acps.12951.

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Dissertations / Theses on the topic "Mechanism of action of electroconvulsive therapy"

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GIORGI, MARIANI MICHELA. "MECHANISM OF ACTION OF ELECTROCONVULSIVE THERAPY (ECT): A NEUROIMMUNOCHEMICAL APPROACH." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071492.

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Background: Electroconvulsive therapy (ECT) is one of the most effective and fast acting therapeutic options for treatment-resistant psychiatric diseases, in particular mood disorders. Mood disorders are highly heterogeneous, disabling and severe mental illness, at still unknown etiology, which have been associated with a multifaceted pathogenesis, encompassing genetic, epigenetic and metabolic vulnerabilities together psychosocial/lifestyle factors. Among the various biological patterns thought to be involved in the physiopathology of dysthymia, major depression, cyclothymia, bipolar I, II, mixed states and related disorders, alterations in the neuroendocrine and immune systems have been also evidenced. Additionally, an increasing number of studies have highlighted the relevance of impaired mechanisms of defense against reactive oxygen species (ROS) in the progression and severity of BD. Oxidative stress and redox states are indeed part of the metabolic and chemical networks of the immune/inflammation response. Despite such evidences, few studies have examined, by now, the impact of ECT on specific neuroendocrine, immune and oxidative stress paths in patients undergoing this therapy. It has been reported that ECT-induced epileptic seizures stimulate the intra-cerebral release of cytokines, including the cytokine network associated with the pathophysiology of affective disorders. It is therefore challenging to consider that the therapeutic efficacy of ECT may reside on the degree of activation of the immune/inflammatory system and that patients, under depressive, hypomanic, manic or mixed states, may change their specific profile of biochemical/immunological markers by ECT. ECT would thus act on complex biochemical cascades, formed by several neurotransmitters, neuro-hormones, neurotrophic factors and metabolic substrates, playing a significant therapeutic role. Hypothesis: Beside possible neurotransmitter and neurotrophin variations, mood disorder patients would also present significant changes of peripheral cytokine and oxidative stress profiles, before and after ECT; it might be thus possible to identify specific redox chemical and immune features related to the response/Non-response to this treatment. Such a result could also considerably help to detect peripheral molecular correlates of immunochemical dysregulation, refractory symptoms and ECT therapeutic benefits or adverse effects in mood disorders. Aims: The foremost aims of this study were: 1) to explore the degree of expression/activity of peripheral immune and oxidative stress markers during the course of ECT in bipolar patients; 2) to possibly evidence differences of these biochemical parameters among Remitter and Non-Remitter patients, assessed by means of suitable examinations and psychometric questionnaires, administered to recruited patients before, during and after ECT. Methods: From 2016 to 2018, we recruited and investigated 17 consecutive patients with a BD diagnosis accordingly to DSM-V diagnostic criteria, all treated by ECT at the Psychiatry section of the Department of Clinical and Experimental Medicine of the University of Pisa. All patients were examined during three main phases of ECT course, following this schedule: 1) at T0, by both psychometric and biochemical evaluations, before the first application; 2) at T1, by biochemical evaluations carried out 3 hours after the first application; 3) at T2, at the end of the treatment, by both psychometric and biochemical examinations. A forth biochemical assessment was carried out also at T3, 3 hours after the last application, in order to possible appraise a different reactivity of immune/oxidative stress patterns at the end of ECT applications. To constantly monitor patients, psychiatric and physical examinations were always performed for the duration of the study. Psychometric questionnaires carried out prior to (T0) and after (T3) the ECT course, consisted into: the Hamilton Depression Rating Scale-17 (HAM-D), Young Mania Rating Scale (YMRS), Brief Psychiatric Rating Scale (BPRS) and Clinical Global Improvement Impression (CGI) scale. The CGI subscale “global improvement”, final HAM-D and YMRS total scores were used to identify Remitter and Non-Remitter groups . Biochemical investigations, performed after blood samplings carried out at the 4 scheduled times, T0, T1, T2 and T3, were: 1)-the plasma levels of the immune/inflammatory cytokines IL-6, IL-8 and TNFα; 2)-the plasma levels/ activity of the antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD), total thiols (R-SH), the ferric reducing ability of plasma (FRAP), uric acid as well as an index of oxidative damage, the advanced oxidation plasma protein products (AOPP). Results: At the end of therapy, about the 53% of ECT-treated BD patients was found to remit. Concerning biochemical investigation, we observed that, globally, in 17 subjects, 3 hours after ECT (T1), the activity of SOD in plasma increased nearly attaining the statistical significance, while FRAP was found significantly decreased; when analyzing Remitters and Non-Remitters separately, the nearly significant increased SOD reported in all patients at T1, after the first ECT application, was due to a greater enzyme activity in Remitters, while the global T1 FRAP reduction was due to the significant decrease of plasma ferric reducing power in Non-Remitters only. We also reported that Non-Remitters had a significantly reduced CAT activity both at T1 and in the long term, at the end of ECT course (T2), and a higher percent of responce in uric acid and IL 8 after the last ECT (T3 vs. T2). Also, Non-Remitters tended to concomitantly have, at T2, higher plasma FRAP, SOD,IL6 and lower CAT, Thiols in respect to baseline (T0) values as well as in respect to Remitters. No significant effect on the plasma level of AOPP was observed at any scheduled time in all patients, indicating that no relevant protein damage, due to ROS was reported during ECT sessions. Limitations: The study, at the present stage, had a small sample size; moreover the patient group was heterogeneous, consisting of treatment resistant bipolar patients in different phases of illness and with different pharmacological regimes. Conclusions: According to literature, we showed that ECT is an effective and safe treatment able to heal drug-resistant bipolar patients with very severe clinical presentation and risk of suicide, in all phases of the illness. Preliminary results suggest that ECT can induce changes of the antioxidant system: an increased ROS scavenging activity at T1 seems to be an index of favorable response. The diminuition of antioxidant defense system would be conversely linked to reduced benefits deriving from this therapy. The recruitment of a larger cohort of patients is needed to confirm and pursue this useful investigation of peripheral biomarkers of ECT response. This will permit to perform more robust statistical tests as multivariate regression or principal component analyses and to possibly define peculiar immunochemical changes related to the clinical response.
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Griffiths, Stephen Douglas. "The mechanism of action of interferon-#alpha# in hairy-cell leukaemia." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.257124.

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Shanmugarajah, Dakshine. "Mechanism of action of BNP7787, a novel chemoprotective agent : a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1475179031&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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Dissertation (Ph.D.).--University of Texas Graduate School of Biomedical Sciences at San Antonio, 2007.
Vita. Briscoe Library received only one copy of this dissertation. It is shelved in the Archives for safekeeping. Includes bibliographical references.
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Hannan, J. M. Abdul. "Studies on the efficacy and mechanism of action of tropical plants for diabetes therapy." Thesis, University of Ulster, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414329.

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Jiang, Feng. "Molecular Mechanism of Vitamin D Action and its Implications in Ovarian Cancer Prevention and Therapy." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000327.

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Menegatti, Silvia. "Anti-TNF therapy in axial spondyloarthritis : mechanism of action and prediction of therapeutic responses using immunological signatures." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC128.

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Les stratégies de traitement biologiques ciblant le TNF-α se sont avérées efficaces pour réduire l'inflammation et les symptômes cliniques dans plusieurs maladies inflammatoires chroniques et sont maintenant couramment utilisées pour les patients qui ne répondent pas aux AINS au cours de la spondyloarthrite (SpA). Cependant, 30 à 40% des patients ne répondent pas aux anti-TNF, et il est actuellement impossible de prédire la réponse des patients à ces biomédicaments. Pour améliorer les résultats cliniques, nous avons besoin d’une part d’une meilleure compréhension des mécanismes d’action des anti-TNF sur le système immunitaire, et d’autre part de biomarqueurs permettant de prédire la réponse à ces biomédicaments afin de guider la décision thérapeutique. Mon projet de doctorat a porté sur deux objectifs complémentaires: (i) l'objectif principal était de progresser dans notre compréhension des mécanismes pathogéniques impliqués dans la SpA axiale et de définir de quelle façon les anti-TNF-α affectent les réponses immunitaires des patients, (ii) de développer des biomarqueurs pour prédire la réponse thérapeutique aux inhibiteurs du TNF. En collaboration avec l'équipe du Pr. Dougados à l'Hôpital Cochin, nous avons recruté deux cohortes indépendantes de patients SpA ayant une maladie active et pour lesquels nous avons collecté des échantillons de sang avant l'initiation du traitement par anti-TNF puis 1 semaine et 3 mois après le début du traitement. Les réponses immunitaires de ces patients ont été analysées à l'aide de tests hautement standardisés réalisés ex-vivo sur sang circulant. Ces tests "TruCulture" se présentent sous forme de seringues, dans lesquelles 1 ml de sang total est mis à incuber avec un stimulus spécifique ; 20 stimuli différents ont été testé et validé avant et après traitement dans les deux cohortes de patients. Nous avons observé une réduction très significative de la sécrétion de IL-1ra, IL-1β, IL-8, and MIP-1β en réponse à des stimuli microbiens et à des agonistes des TLR dans les échantillons de sang prélevés 7 jours et/ou 3 mois après le début du traitement. Pour identifier les bases moléculaires de l’action des inhibiteurs du TNF nous avons analysé l'expression des gènes dans ces différentes conditions de stimulation. L'analyse bioinformatique quantitative de l'expression des gènes (QuSAGE) a révélé que les gènes les plus modulés par le traitement anti-TNF étaient NF-KB et les gènes cibles de NF-kB, y compris le TNF lui-même et l’IL1B. Nos données suggèrent que les inhibiteurs du TNF agissent principalement en perturbant une boucle autorégulatrice pilotée par NF-kB. Afin d'identifier les signatures immunologiques de réponse aux anti-TNF avant le début du traitement, nous avons corrélé les réponses immunitaires chez les patients analysés au temps 0 à la réponse thérapeutique aux anti-TNF mesurée à 3 mois. Nos résultats suggèrent que les patients atteints de SpA et exprimant des niveaux inférieurs de PAX5 et des niveaux supérieurs de SPP1 en réponse à la stimulation avec SEB avant l'initiation de la thérapie anti-TNF ont les meilleures réponses thérapeutiques. Notre recherche montre que les tests TruCulture sont un outil efficace pour étudier les fonctions immunitaires chez les patients atteints de SpA et que les effets du traitement anti-TNF peuvent être mesurés lorsque les cellules immunitaires sont stimulées. En terme de recherche translationnelle, nous avons identifié des molécules qui pourront être utilisés comme biomarqueurs pour aider les cliniciens à prédire les réponses thérapeutiques aux traitements anti TNF
The introduction of anti-TNF therapy has proven effective to reduce inflammation and clinical symptoms in several chronic inflammatory diseases. However, 30-40% of patients do not respond to TNF blockers and it is currently not possible to predict responsiveness of patients to anti-TNF therapy. Furthermore, their impact on the immune system is incompletely understood. The goals of my PhD project were (i) to define the impact of anti-TNF therapy on immune responses to microbial challenges and stimuli targeting specific immune pathways in spondyloarthritis (SpA) patients, and (ii) to identify immunological correlates associated with therapeutic responses to TNF-blockers.Using a set of whole-blood, syringe-based assays to perform ex vivo stimulation while preserving physiological cellular interactions (TruCulture assays), we have performed a pilot study in SpA patients and investigated immune responses to 20 different stimuli before and 3 months after initiation of anti-TNF therapy. These findings were validated in a replication cohort, also assessing the effects of anti-TNF agents after only one week of treatment. We observed a highly significant reduction of the secretion of IL-1ra, IL-1β, IL-8 and MIP-1β in response to selected stimuli after 3 months of treatment compared to the baseline. Interestingly, these changes were already detectable after a single injection of an anti-TNF agent. To gain insight into the molecular mechanism of TNF blockers, we profiled gene expression in the stimulation cultures from all patients. Quantitative set analysis for gene expression (QuSAGE) revealed that the gene modules most affected by anti-TNF therapy are NF-kB transcription factors and inhibitors and NF-kB target genes, including TNF itself and IL1B. Our data suggest that TNF-blockers primarily act by disrupting an autoregulatory loop driven by NF-kB. We also tested whether there is a correlation between the responses of immune cells to specific stimuli and the clinical response to TNF-blockers. The decision tree model that we trained and validated suggests that SpA patients who expressed lower levels of PAX5 and higher levels of SPP1 in response to SEB stimulation before initiation of anti-TNF therapy had the best therapeutic responses. Our study shows that TruCulture assays are an efficient and robust tool to monitor immune functions in SpA patients and that the effects of anti-TNF therapy can be measured when immune cells are challenged, but not at steady state. Our data also indicate that analyzing immune responses in patients before therapy is a promising strategy to develop biomarkers for prediction of therapeutic responses to TNF-blockers
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Africander, Donita Jean. "Comparative study of the molecular mechanism of action of the synthetic progestins, Medroxyprogesterone acetate and Norethisterone acetate." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/4585.

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Thesis (PhD (Biochemistry))--University of Stellenbosch, 2010.
ENGLISH ABSTRACT: Medroxyprogesterone acetate (MPA) and norethisterone (NET) and its derivatives (norethisterone enanthate (NET-EN); norethisterone acetate (NETA)), are used by millions of women as contraceptives and in hormone replacement therapy (HRT). Although both progestins are widely used, very little is known about their mechanism of action at the molecular level. In this thesis, the differential regulation of gene expression and molecular mechanism of action via different steroid receptors by these synthetic progestons, as compared to progesterone (Prog) was investigated in human cell lines. In the first part of the study, the effect of Prog, MPA and NET-A on the expression of endogenous cytokine genes was investigated in two epithelial cell lines of the human female genital tract, Ect1/E6E7 (an ectocervical cell line) and Vk2/E6E7 (a vaginal cell line). Quantitative realtime RT-PCR (QPCR) showed ligand-specific and cell-specific regulation of the interleukin (IL)-6, IL-8 and RANTES (Regulated-upon-Activation, Normal T cell Expressed and Secreted) genes with Prog, MPA and NET-A. Moreover, the repression of the TNF -induced RANTES gene by MPA in the Ect1/E6E7 cell line was found to be mediated by the androgen receptor (AR). The second part of the study focused on elucidating the androgenic activities of these two progestins, in comparison to Prog. Competitive binding in whole cells revealed that Prog, MPA and NET-A have a similar binding affinity for the hAR as the natural androgen dihydrotestosterone (DHT). Both transactivation and transrepression transcriptional assays demonstrate that, unlike Prog, MPA and NET-A are efficacious AR agonists, with activities comparable to DHT. Using a mammalian two-hydrid assay, it was shown that MPA and NET-A exert their androgenic actions by different mechanisms. NET-A, like DHT and other well-characterised androgens, induces the ligand-dependent interaction between the NH2- and COOH-terminal domains (N/C-interaction) of the AR independent of promoter-context, while MPA does this in a promoterdependent manner. In the third part of this study, competitive binding revealed that MPA and NET-A have a similar binding affinity to each other, but about a 100-fold lower affinity than Prog for the human mineralocorticoid receptor (hMR), while RU486 has an even lower affinity for the hMR. Promoter-reporter assays showed that MPA, NET-A and RU486 are all antagonists of the hMR, but unlike Prog, they have weak antagonistic activity. However, on the endogenous MR-regulated Orm-1 (a-glycolytic protein or orosomucoid-1) gene expressed in a rat cardiomyocyte cell line, NET-A and RU486, but not MPA, has similar antagonistic activity as Prog. This study is the first to show that, NET-A and RU486, but not MPA, can dissociate between transrepression and transactivation via the hMR. Taken together, these results show that natural Prog and the synthetic progestins, MPA and NET-A display differential promoter-, cell- and receptor-specific effects on gene expression. Furthermore they may have important implications for cervicovaginal immune function, cardiovascular and other physiological functions.
AFRIKAANSE OPSOMMING: Medroksieprogesteroon asetaat (MPA), noretisteroon (NET) en derivate daarvan (noretisteroon enantaat (NET-EN); noretisteroon asetaat (NET-A), word deur miljoene vroue gebruik as voorbehoedmiddels en vir hormoon vervangingsterapie (HVT). Tenspyte daarvan dat beide hierdie progestiene algemeen gebruik word, is min bekend oor hulle meganisme van werking op molekulêre vlak. In hierdie proefskrif word die differensiële regulering van geenuitdrukking asook die molekulêre meganisme van werking deur middel van steroïedreseptore van beide hierdie sintetiese progestiene, ondersoek, en vergelyk met progesteroon (Prog), in menslike sellyne. In die eerste deel van die studie is die effek van Prog, MPA en NET-A op die uitdrukking van endogene sitokinien gene ondersoek in twee epiteel sellyne van die menslike vroulike geslagskanaal, Ect1/E6E7 (‘n ektoservikale sellyn) en Vk2/E6E7 (‘n vaginale sellyn). Kwantitatiewe intydse RT-PKR het ligand-spesifieke en selspesifieke regulering van interleukien (IL)-6, IL-8 en RANTES (Regulering-na- Aktivering, Normale T-sel Uitgedrukte en Afgeskei) gene getoon met Prog, MPA en NET-A. Verder is gevind dat die onderdrukking van die TNF- - geïnduseerde RANTES geen deur MPA in die Ect1/E6E7 sellyn bemiddel word deur die androgeen reseptor (AR). Die tweede deel van die studie het gefokus op die toeligting van die androgeniese aktiwiteit van die twee progestiene in vergelyking met Prog. Kompeterende binding in volselle het getoon dat Prog, MPA en NET-A ‘n soortelyke bindings affiniteit vir die menslike AR as die natuurlike androgeen dehidrotestosteroon (DHT) vir die menslike AR het. Beide transaktiverings en transonderdrukkings transkripsionele analieses toon dat, anders as Prog, MPA en NET-A effektiewe AR agoniste is met aktiwiteite wat vergelykbaar is met die van DHT. Deur die gebruik van ‘n soogdier twee-hibried toets, kon gewys word dat MPA en NET-A hul androgeniese effekte uitoefen deur verskillende meganismes. NET-A, soos DHT en ander goed gekarakteriseerde androgene, induseer die ligand-afhanklike interaksie tussen die NH2- en COOH-terminale domeine (N/C-interaksie) van die AR, onafhanklik van die promoter-konteks. MPA, aan die ander kant, doen dit op ‘n promoter-afhanklike manier. In die derde deel van die studie het kompeterende binding getoon dat MPA en NETA soortelyke relatiewe bindings affiniteite vir die menslike mineralokortikoïed reseptor (hMR) het, maar dat hierdie affiniteit ongeveer 100-voud laer is as die van Prog en dat die affiniteit van RU486 vir hMR selfs nog laer is. Promoter-rapporteerder toetse het getoon dat MPA, NET-A en RU486 almal antagoniste van die hMR is, maar anders as Prog, is hierdie ‘n swak antagonistiese aktiwiteit. Nietemin, op die endogene MR-gereguleerde Orm-1 ( -glikolitiese proteïen of orosomukoïed-1) geen, uitgedruk in ‘n rot kardiomiosiet sellyn, het NET-A en RU486, maar nie MPA nie, ‘n soortgelyke antagonistiese aktiwiteit as Prog. Hierdie studie is die eerste om te wys dat NET-A en RU486, maar nie MPA nie, kan onderskei tussen transrepressie en transaktivering deur middel van die hMR. Samevattend toon die resultate dat natuurlike Prog en die sintetiese progestiene, MPA en NET-A, ‘n differentiële promoter-, sel- en reseptor-spesifieke effek op geenuitdrukking het. Verder mag die resultate belangrike implikasies vir servikovaginale immuunfunksie, asook kardiovaskulêre en ander fisiologiese funksies, inhou.
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Nishimura, Takeshi. "Studies on Usefulness of 3-Oxa-methano-prostaglandin I1 for Therapy of Peripheral Circulatory Insufficiency and Involved Mechanism of Action." Kyoto University, 2000. http://hdl.handle.net/2433/151617.

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Ooko, Edna [Verfasser]. "Molecular mechanism of action and pharmacogenomics of curcumin, curcumin synthetic derivatives and combinations with curcumin in cancer therapy / Edna Ooko." Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/1128922738/34.

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Stefanovska, Bojana. "New Mechanism of Action of Rapalogs : Transcriptional Regulation of TRIB3 and Alteration of Pre-mRNA Splicing." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS195.

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La voie de signalisation mTOR intègre une variété de signaux environnementaux pour réguler la croissance et le métabolisme cellulaire. Cette voie est altérée dans 70% des cancers. Les inhibiteurs allostériques de mTOR, comme la rapamycine et ses dérivés (évérolimus et temsirolimus), sont administrés aux patients atteints de tumeurs métastatiques du sein, du rein et neuroendocrines. Cependant, leur efficacité reste modeste et une majorité de patients rechutent. L'utilisation de rapalogues fait donc face à deux problèmes cliniques majeurs : 1/l’absence de biomarqueur qui permette de stratifier les patients qui bénéficieraient le plus d'un traitement par rapalogues ; 2/ l’existence de plusieurs mécanismes de résistance décrits ou non. L’objectif de mon travail de thèse est d’identifier des nouveaux gènes cible des rapalogues utilisables comme biomarqueurs prédicteurs de l’efficacité du traitement ou comme cibles thérapeutiques pour vaincre la résistance.Nous avons identifié le gène TRIB3 comme cible des rapalogues. Sous traitement, son expression est diminuée dans un panel de lignées tumorales et des échantillons tumoraux. Nous avons démontré que cette régulation est indépendante de l’inhibition de la voie mTOR, mais médiée par le répresseur transcriptionnel GCF2. Des analyses protéomiques à haut débit ont identifié TRIB3 en tant que composant du spliceosome. De plus, nous avons démontré que la régulation négative de TRIB3 est nécessaire aux rapalogues pour modifier l'épissage des pré-ARNm. A l’inverse, la surexpression de TRIB3 supprime ces effets des rapalogues. En conclusion, ce travail de thèse ouvre plusieurs perspectives: 1 / l'utilisation potentielle de TRIB3 comme biomarqueur pour prédire ou évaluer l'efficacité du traitement par les rapalogues; 2 / de nouvelles opportunités thérapeutiques ciblant ces mécanismes indépendants de mTor ; 3/ la combinaison possible des rapalogues avec des composés ciblant l’épissage afin de surmonter la résistance
The mTOR signaling pathway senses variety of environmental cues and integrates them to regulate cellular growth and metabolism. This pathway is altered in 70% of cancers. Allosteric inhibitors of mTOR like rapamycin and its derivatives (everolimus and temsirolimus) have become standard of care in patients with metastatic breast, kidney and neuroendocrine tumors. Unfortunately, their role is modest and most of patients will relapse. Thus, in clinic there are two major concerns related to the use of rapalogs: 1/ the absence of accurate biomarker to stratify patients who would benefit from rapalogs treatment; 2/ the existence of known and unknown mechanisms of resistance. Accordingly, the aim of my PhD project is to identify new target genes of rapalogs that could be used as biomarkers to predict treatment efficacy, or as therapeutic targets, to overcome resistance.We identified TRIB3 gene as a novel target of rapalogs. Upon treatment, its expression is down-regulated both in a panel of cancer cell lines and in cancer patient samples. We showed that this regulation is independent of the mTOR signaling inhibition, but relies on a transcriptional regulation via the co-repressor GCF2. High-throughput proteomic analyses identified TRIB3 as a component of the spliceosome. Additionally, we demonstrated that the down-regulation of TRIB3 is necessary for rapalogs to alter pre-mRNA splicing. In contrast, the, overexpression of TRIB3 abolishes these effects of rapalogs. In conclusion, this PhD work leads to the following important perspectives: 1/ the potential use of TRIB3 as a biomarker to predict or asses the efficacy of rapalogs treatment; 2/ new window of therapeutic possibilities by targeting this mTOR - independent mechanism of action; 3/ the potential combination of rapalogs with splicing targeting agents to overcome resistance
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Books on the topic "Mechanism of action of electroconvulsive therapy"

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International Conference on Tumor Necrosis Factor and Related Cytokines (2nd 1989 Napa, Calif.). Tumor necrosis factor: Structure, mechanism of action, role in disease and therapy. Edited by Bonavida Benjamin and Granger Gale. Basel: Karger, 1990.

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Hannan, J. M. Abdul. Studies on the efficacy and mechanism of action of tropical plants for diabetes therapy. [S.l: The Author], 2004.

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Godfrey, Tunnicliff, Eison Arlene S, and Taylor Duncan P, eds. Buspirone: Mechanisms and clinical aspects. San Diego: Academic Press, 1991.

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Godfraind, T. Calcium channel blockers. Boston, MA: Birkhauser Verlag, 2003.

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A, Hickman John, and Tritton Thomas R, eds. Cancer chemotherapy. Oxford: Blackwell Scientific Publications, 1993.

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Calcium channel blockers. Basel: Birkhäuser Verlag, 2004.

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Lithium: Actions and mechanisms. Washington, DC: American Psychiatric Press, 1996.

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N, Herrington Reginald, ed. Biological treatments in psychiatry. Oxford: Oxford University Press, 1990.

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Biological treatments in psychiatry. 2nd ed. Oxford: Oxford University Press, 1996.

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1944-, Yaksh T. L., ed. Anesthesia: Biologic foundations. Philadelphia: Lippincott-Raven, 1998.

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Book chapters on the topic "Mechanism of action of electroconvulsive therapy"

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Green, A. Richard, and David J. Nutt. "Psychopharmacology of Repeated Seizures: Possible Relevance to the Mechanism of Action of Electroconvulsive Therapy." In Handbook of Psychopharmacology, 375–419. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1819-4_6.

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Rossetto, O., M. Pirazzini, F. Fabris, and C. Montecucco. "Botulinum Neurotoxins: Mechanism of Action." In Botulinum Toxin Therapy, 35–47. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/164_2020_355.

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Raut, Mohan, and Mugdha Raut. "Mechanism of Action of LIT." In Lymphocyte Immunization Therapy (LIT) in Reproductive Failures, 67–71. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2960-1_8.

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Liu, Leroy F., and Shyamal D. Desai. "Mechanism of Action of Topoisomerase 1 Poisons." In Camptothecins in Cancer Therapy, 3–21. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-866-8:003.

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Porzsolt, F., W. Digel, C. Buck, A. Raghavachar, M. Stefanic, and W. Schöniger. "Possible Mechanism of Interferon Action in Hairy Cell Leukemia." In Cancer Therapy, 124–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73721-3_15.

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Bjordal, Jan Magnus, Rodrigo Alvaro Brandão Lopes-Martins, and Lucio Frigo. "Low level laser therapy - mechanism of action." In Lasers in Dentistry, 27–33. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118987742.ch5.

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Chow, Roberta. "Low level laser therapy - mechanism of action." In Lasers in Dentistry, 34–39. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118987742.ch6.

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Schneeweiss, Adam, and Marija Weiss. "The Mechanism of Action of Nitrates in Angina Pectoris." In Advances in Nitrate Therapy, 14–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-97066-5_4.

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Schneeweiss, Adam, and Marija Weiss. "The Mechanism of Action of Nitrates in Angina Pectoris." In Advances in Nitrate Therapy, 14–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75834-8_4.

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Bromberg, Kenneth D., and Neil Osheroff. "Mechanism of action of topoisomerase II-targeted anticancer drugs." In DNA Topoisomerases in Cancer Therapy, 53–78. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0141-1_3.

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Conference papers on the topic "Mechanism of action of electroconvulsive therapy"

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Ovsiannikov, Victor, T. Sologub, N. Pustashova, N. Kuznetsov, O. Masterova, A. Rakhmanova, N. Sizova, and I. A. Karpushina. "Laser therapy of infectious diseases: results and mechanism of therapeutic action." In Laser Florence 2000: A Window on the Laser Medicine World, edited by Leonardo Longo, Alfons G. Hofstetter, Mihail-Lucian Pascu, and Wilhelm R. Waidelich. SPIE, 2001. http://dx.doi.org/10.1117/12.446707.

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Buettner, Ralf R., Renzo Corzano, Jianping Lin, Nagarajan Vaidehi, Richard Yip, Yuan Chen, Richard Jove, David Horne, and John Williams. "Abstract 2576: Mechanism of action of a novel Stat3 inhibitor for cancer therapy." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2576.

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Hwang, Larn, David Nam, Fatih Uckun, and Vuong Trieu. "Abstract 5029: OT-101/Chemotherapy- A novel mechanism of action (MOA) in glioblastoma immunization therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-5029.

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Hwang, Larn, David Nam, Fatih Uckun, and Vuong Trieu. "Abstract 5029: OT-101/Chemotherapy- A novel mechanism of action (MOA) in glioblastoma immunization therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-5029.

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Thomas, Matthew J., Olivier Bonneau, Loredana Ciuclan, Nicholas Duggan, David Rowlands, Jenny Grieve, Andrew Baker, Mandy MacLean, Gabor Jarai, and John Westwick. "Imatinib As A Therapy For Pulmonary Arterial Hypertension - Insights Into Mechanism Of Action From Rodent Models." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3420.

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Dong, Shujun, Yuqing Zhang, Xiao Cen, Xiaojing Li, Lixia Yu, Zhongjie Li, and Xiaoqin Zhu. "Mechanism of action of cognitive behavioral therapy on pain in adult women with major TMJ disorders." In ICMHI 2022: 2022 6th International Conference on Medical and Health Informatics. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3545729.3545769.

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Nam, David, Larn Hwang, and Vuong Trieu. "Abstract 3968: OT-101/Chemotherapy - A novel mechanism of action (MOA) in pancreatic cancer immunization therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3968.

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Nam, David, Larn Hwang, and Vuong Trieu. "Abstract 3968: OT-101/Chemotherapy - A novel mechanism of action (MOA) in pancreatic cancer immunization therapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3968.

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Schwab, Richard J., Christopher Kim, Larry C. Siegel, J. Black, M. Farid-Moayer, Jonathan L. Podmore, and Matt Vaska. "Mechanism Of Action Of A Novel Device Using Oral Pressure Therapy (OPT) For The Treatment Of OSA." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6811.

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Bacha, Jeffrey A., Guangan He, Xiaolei Xie, Anne Steino, Dennis M. Brown, and Zahid H. Siddik. "Abstract A01: Distinct mechanism of action of DNA-damaging agent dianhydrogalactitol (VAL-083) suggests combination therapy with PARP inhibitors." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a01.

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Reports on the topic "Mechanism of action of electroconvulsive therapy"

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Reiter, Robert. Mechanism of Action of Prostate Stem Cell Antigen Targeted Antibody Therapy and Its Relevance to Clinical Application in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada512783.

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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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