Tesis sobre el tema "Peripheral inflammation"
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Chapman, Katie. "Peripheral inflammation after experimental stroke". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518434.
Texto completoMcColl, Alison. "The brain response to peripheral inflammation". Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6764/.
Texto completoAdeoye, Opeolu M. D. "Peripheral Leukocytes and Intracerebral Hemorrhage". University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353100438.
Texto completoJiang, Yanyan. "The role of peripheral TNF in acute brain inflammation". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496980.
Texto completoBarr, Laura Caroline. "Peripheral blood mononuclear cell depletion for experimental human lung inflammation". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/23705.
Texto completoKarim, Salman. "Peripheral and central markers of inflammation in mild cognitive impairment". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/peripheral-and-central-markers-of-inflammation-in-mild-cognitive-impairment(bd21dafe-65c1-42c9-949b-733abfc71037).html.
Texto completoThomson, Carolyn. "Peripheral inflammation remotely triggers global gene expression changes in the brain". Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5390/.
Texto completoTzoulaki, Ioanna. "Inflammation and haemostasis in the development and progression of peripheral atherosclerotic disease". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/2148.
Texto completoParmar, Jiteshkumar H. "The role of inflammation in ischaemia reperfusion injury due to peripheral arterial revascularisation". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509840.
Texto completoHau, Vincent Sinh. "EFFECT OF PERIPHERAL INFLAMMATORY PAIN ON THE BLOOD-BRAIN BARRIER". Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1071%5F1%5Fm.pdf&type=application/pdf.
Texto completoRUSCONI, MICHELA. "Activation state and functionality of dendritic cells from peripheral blood of amyotrophic lateral sclerosis patients". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/153236.
Texto completoSeveral published data highlight the importance of inflammation for neurodegeneration in Amyotrophic lateral sclerosis (ALS) with an increased spinal cord recruitment of peripheral proinflammatory monocytes, dendritic cells (DCs) and T cells found in patients and animal models. To date no clear data are available regarding the functional state of DCs in peripheral blood of ALS patients.The aim of the present study was to examine circulating DCs in a large cohort of ALS patients taking into account their clinical phase in order to lay the basis to understand how these cells contribute to disease progression. To do this, we performed ex vivo analyses of the frequency and expression of costimulatory, MHC and migratory mole¬cules of CD1c+ DC subsets and we investigated the capacity of purified DCs to spontaneously produce inflammatory cytokines and to respond to the TLR agonist, lipopolysaccharide (LPS). We enrolled 72 ALS patients, 47 healthy donors and 25 Patients affected by neurological disorders unrelated with ALS stratified for age and sex. DC numbers and their phenotype were investigated by cytofluorimetric analyses. We found that ALS patients have much lower number of circulating DCs (identified as CD1c+ and CD19-) compared with healthy donor, and their DCs show an increased expression of the integrin CD62L. Since this integrin is required for the recruitment of leukocytes to secondary lymphoid organs or to inflammatory sites, these observations confirmed that in ALS patients DCs are actively recruited in the central nervous system with a mechanism presumably involving the CD62L molecule. We then analysed the spontaneous o LPS-induced production of inflammatory cytokines such as TNFα, IL1β, IL6, IL8, IL10 and CCL2. We noticed a subpopulation of ALS patients with a higher spontaneous and LPS-induced IL8 production. These patients, interestingly, also showed higher efficiency of CCL2 secretion. Although we could not define a correlation between the higher efficiency of these inflammatory cytokine production and disease progression, high levels of CCL2 have been shown in the spinal cord of SOD mice, a mouse model of a subclass of ALS disease, and in some ALS patients. According to our results, DCs can be a source of CCL2 in the spinal cord in a subpopulation of ALS patients. This observation suggests that a simple peripheral blood analysis can be sufficient to identify subgroups of ALS patients. We, thus, analysed the correlation between the levels of any single cytokines in ALS patients before and after LPS exposure and some disease parameters.We observed a significant inverse correlation between the time from onset to diagnosis and the ΔIL6 levels, suggesting that an increased efficiency of IL-6 production in ALS patients may accelerate the initial phases of the disease.In conclusion, DCs are one of the major cell subset recruited to the central nervous system at least in some ALS patients. Although the majority of activated DCs may migrate to the central nervous system, some differences are still observable in the peripheral blood. Based on our results, peripheral blood DC analyses can be useful to stratify patients in those that have a high inflammatory response versus those that do not show an altered inflammatory pathway.Given the high heterogeneity of ALS disease we could not observe for the moment significant correlations with disease parameters, nevertheless a more refined analysis based on specific criteria is likely to be informative on some particular disease aspects.The high levels of CD62L expression by peripheral blood DCs suggest that this molecule could be a possible target for in vivo treatment. To this regard, we are planning to perform a preclinical study in SOD mice to verify if a treatment with a blocking anti-CD62L antibody could interfere with disease progression.
Burdess, Anne. "Role of inflammation and platelet activation in the adverse cardiovascular outcomes of patients undergoing surgery for critical limb ischaemia". Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9539.
Texto completoAraújo, Lucas Guilherme de. "On cholecystokinin-opioid interaction in the spinal dorsal horn following peripheral nerve injury and inflammation /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3560-2/.
Texto completoLavinskienė, Simona. "Peripheral blood neutrophil and eosinophil activity during allergen-induced late-phase airway inflammation in asthma". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2015. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20150106_083713-90371.
Texto completoMokslininkai neabejoja, jog eozinofilai ir neutrofilai yra vienos svarbiausių ląstelių, dalyvaujančių astmos patogenezėje, kurią labiausiai atspindi vėlyva kvėpavimo takų uždegimo fazė, išsivystanti praėjus kelioms valandoms po alergeno įkvėpimo. Pasaulinėje literatūroje publikuojami darbai, nagrinėja atskirus kvė¬pavimo takų neutrofilų ir eozinofilų aktyvumo pokyčius. Ypač mažai darbų apie periferinio kraujo neutrofilų ir eozinofilų funkcijas bei jų ryšį su šių ląstelių pagausėjimu kvėpavimo takuose, sergant astma. Taip pat nėra tyrimų, vertinančių periferinio kraujo uždegimo ląstelių (neutrofilų ir eozi¬nofilų) funkcijų alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu. Todėl šio tyrimo tikslas buvo įvertinti periferinio kraujo neutrofilų ir eozinofilų funkcinį aktyvumą alergeno sukeltos vėlyvos fazės kvėpavimo takų uždegimo metu sergant astma. Tyrimo metu nustatėme, kad įkvėptas alergenas aktyvina periferinio kraujo neutrofilų ir eozinofilų funkcijas - chemotaksį, fagocitozę, reaktyvių deguonies formų susidarymą, degranuliaciją bei silpnina apoptozę vėlyvos fazės kvėpavimo takų uždegimo metu. O šių ląstelių aktyvumo pokyčiai yra susiję su kvėpavimo takų neutrofilija ir eozinofilija. Moksliniame darbe pateikiami rezultatai suteikia naujų duomenų apie sergančiųjų alergine astma periferinio kraujo neutrofilų ir eozinofilų funkcinių savybių ypatumus ir parodo jų pokyčius alergeno sukeltos vėlyvos fazes kvėpavimo takų uždegimo metu.
Komla, Essie S. "Antinociceptive tolerance to morphine is driven by colonic inflammation and mediated by peripheral opioid receptors". VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5818.
Texto completoCristante, Enrico. "Impact of peripheral inflammation in the brain : new roles for the anti-inflammatory molecule Annexin A1". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14415.
Texto completoJäger, Amelie [Verfasser] y Christine [Akademischer Betreuer] Dierks. "JAK Pathway inhibition as a novel therapeutic strategy in peripheral t-cell lymphomas with associated inflammation". Freiburg : Universität, 2018. http://d-nb.info/1216826420/34.
Texto completoRiester, Karin Dorota [Verfasser]. "The effect of peripheral inflammation on in vivo functional properties of cortical networks / Karin Dorota Riester". Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1217249265/34.
Texto completoHernández, Aguilera Anna. "Peripheral Artery Disease: The search for a biological marker". Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/442958.
Texto completoLa enfermedad arterial periférica (EAP) es una manifestación común de aterosclerosis sistémica que afecta a las arterias periféricas. Aunque su prevalencia es elevada, está infradiagnosticada porque los primero estadíos de la enfermedad son asintomáticos. El índice tobillo-brazo es el test más usado para el diagnóstico, aunque presenta limitaciones. Existen otros marcadores circulantes pero son para aterosclerosis en general. La inflamación, oxidación, remodelación vascular y disfunción mitocondrial tienen un papel clave en el desarrollo de la aterosclerosis. Creemos que un mejor conocimiento de estos procesos puede proporcionar marcadores circulantes de enfermedad y también posibles dianas terapéuticas. En el estudio 1, investigamos la expresión inmunohistoquímica de las paraoxonasas (PON) y quimiocinas en arterias de pacientes con EAP. Los resultados mostraron que PON1, PON3, la quimiocina CCL2 y los receptores inespecíficos (ACKRs) DARC y D6 estaban incrementados en arterias ateroscleróticas, sugiriendo que paraoxonasas y quimiocinas tienen un papel clave en el desarrollo de la enfermedad. El recambio de la matriz extracelular (ECM) también está involucrado en la remodelación vascular. En el estudio 2, combinando histología y proteómica, observamos que las arterias ateroscleróticas tenían un perfil proteico donde los componentes de la ECM estaban menos expresados. De entre un conjunto de neo-epítopos, los fragmentos de degradación de versican y colágeno IV mostraron potencial como biomarcadores para segregar pacientes con diferentes grados de EAP. La alteración del metabolismo y la disfunción mitocondrial también pueden predisponer a la enfermedad. En el estudio 3, utilizamos técnicas metabolómicas en el plasma de pacientes con EAP. La mayoría de metabolitos cuantificados se relacionaron con las comorbilidades asociadas a la EAP. De entre los metabolitos restantes, el (iso)citrato y glutamato resultaron útiles para el diagnóstico de la EAP, y también para una detección precoz de la enfermedad.
Peripheral artery disease (PAD) is a common manifestation of systemic atherosclerosis affecting peripheral arteries. Despite its high prevalence, PAD is often underdiagnosed because first stages of the disease are asymptomatic. The ankle-brachial index (ABI) is the most used test for PAD diagnosis although its limitations. There are additional circulating biomarkers of diagnosis not exclusively for PAD but for atherosclerosis in general. Inflammation, oxidation, vascular remodeling and mitochondrial dysfunction play an important role in the development of atherosclerosis. We hypothesized that an increased knowledge on these processes may provide circulating biomarkers for the disease as well as possible therapeutic strategies. In Study 1, we investigated the immunohistochemical expression of paraoxonases (PON) and chemokines in arteries of PAD patients. Results showed that PON1, PON3, chemokine (C-C motif) ligand 2 (CCL2) and atypical chemokine receptors (ACKR) DARC and D6 were increased in atherosclerotic arteries, suggesting that both paraoxonases and chemokines play a key role in the development of atherosclerosis. Extracellular matrix (ECM) turnover is also involved in vascular remodeling. In Study 2, by combining histological and proteomics approaches, we observed that atherosclerotic arteries had a specific protein profile in which ECM-related components were underexpressed, suggesting a possible degradation of the ECM. Among a measured a panel of neo-epitopes, Versican and type IV collagen degradation fragments showed potential as biomarkers to segregate patients across the spectrum of PAD. Impaired metabolism and mitochondrial dysfunction may also predispose to disease. In Study 3, we used a targeted metabolomics methodology to assess the plasma metabolome of PAD patients. Many of measured metabolites were connected not with PAD, but with associated comorbidities, age or body mass index. Among remaining metabolites, (Iso)citrate and glutamate were useful for PAD diagnosis and also for an early detection of the disease.
Doak, Gregory J. "Peripheral mechanisms of adenosine and 5-hydroxytryptamine contributing to nociception and inflammation in the rat formalin model". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24735.pdf.
Texto completoPitcher, Mark Henry. "Role of the NKCC1 co-transporter in spinal nociceptive mechanisms in a rodent model of peripheral inflammation". Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96700.
Texto completoLa théorie du portillon décrit un circuit spinal dans lequel l'activation des fibres mécano-sensitives de bas seuil atténue l'activité des fibres nociceptives, de tel sorte que le toucher léger réduit la douleur. Paradoxalement, pour plusieurs personnes souffrant de douleur chronique, la stimulation tactile de la région affectée (région primaire) ou la région adjacente à la lésion (région secondaire) provoque de la douleur au lieu de la réduire, phénomène respectivement nommé allodynie primaire et allodynie secondaire. Nous suggérons que dans les cas de douleur persistante, l'augmentation de l'activité du co-transporteur de chlore, NKCC1, pourait expliquer ce phénomène. NKCC1 est le principal responsable de l'accumulation intracellulaire de chlore au niveau des fibres sensitives primaires; en ajustant la concentration intracellulaire de chlore, NKCC1 détermine la magnitide de la dépolarisation afférente primaire et, par conséquant, déterminera si une stimulation mécanique de basse intensité activera ou inhibera les fibres nociceptives afférentes. Dans cette thèse, plusieurs techniques de recherche sont utilisées pour déterminer le rôle de NKCC1 dans l'allodynie induite par capsaicine. La capsaicine, la molécule active des piments forts, produit des potentiels d'action au niveau des fibres nociceptives afférentes en activant les récepteurs TRPV1 dans les terminaisons périfériques. Premièrement, nous démontrons que lorsque NKCC1 ou TRPV1 sont bloqués au niveau spinal, il y a une réduction de l'allodynie induite par la capsaicine intracolonique ainsi que de l'allodynie induite par l'administration spinal d'un agoniste de TRPV1. Ensuite, nous démontrons que le blocage des récepteurs AMPA/kainate atténuent l'augmentation de l'expression de NKCC1 par la capsaicine, alors que le blocage des récepteurs TRPV1 n'ont pas d'effet. Cela suggère un rôle des récepteurs pre-synaptiques AMPA/kainate comme régulateur de l'expression d'NKCC1. Dans la moelle épinière, le blocage de NKCC1 réduit aussi l'augmentation de l'expression de FOS induite par la capsaicine intracolonique. Il est aussi intéressant de noté que le blocage de NKCC1 prévient partiellement l'augmentation de l'expression de FOS suivant une stimulation de faible intensité de la région d'allodynie secondaire. Finalement, le blocage de NKCC1 prévient la sensibilisation par la capsaicine des neurones nociceptives de la corne dorsal de la moelle épinière. Cela illustre que l'augmentation de l'activité de NKCC1 joue un rôle modulateur sur les signaux nociceptif afférant. L'ensemble de ces études soutiennent le rôle d'NKCC1 dans la persistance de la douleur et démontre que NKCC1 est une cible thérapeutique prometteuse.
Wendeln, Ann-Christin [Verfasser]. "Long-lasting epigenetic microglial memory of peripheral inflammation modulates hallmarks of Alzheimer's disease pathology / Ann-Christin Wendeln". Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1217249214/34.
Texto completoMarimuthu, Rekha. "Study of Monocytes in Diabetic Foot Ulcer (DFU) patients with Peripheral Arterial Disease (PAD)". Thesis, The University of Sydney, 2018. https://hdl.handle.net/2123/21374.
Texto completoBernards, Nicholas. "PET molecular imaging of peripheral and central inflammatory processes targeting the TSPO 18 kDa". Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112211/document.
Texto completoPurpose : The purpose of this study was to determine the in vivo potential of the TSPO 18 kDa as a biomarker of inflammation, with the use of its radioligand [ ¹ ⁸F]DPA-714, to non-invasively quantify the inflammatory state within the scope of various pathologies. Procedure : Multiple animal models of various inflammatory diseases, to include : inflammatory bowel disease, neuroinflammation, and septic shock, were developed and put in place by adapted measures. The animals well-being and the subsequent inflammation was evaluated. The inflammatory state was measured using quantitative PET imaging with the TSPO radioligand [ ¹ ⁸F]DPA-714 and correlated to the expression of conventional inflammatory markers using microscopy. Results : Based on the observed data, we were able to distinguish control groups from treated groups when using [ ¹ ⁸F]DPA-714. This TSPO radioligand permitted us to quantify the inflammatory level and to observe evolutionary changes in the inflammatory state of the disease in multiple models. The PET results, using the [ ¹ ⁸F]DPA-714 signal was correlated with an increased TSPO expression at cellular level. Conclusion : Results indicate that [ ¹ ⁸F]DPA-714 is a suitable tracer for studying inflammation of multiple diseases.[ ¹ ⁸F]DPA-714 could be a good molecular probe to non-invasively evaluate the level and localization of inflammation. Moreover, in vivo imaging using this TSPO ligand is potentially a powerful tool to stage and certainly to follow the evolution and therapeutic efficiency at molecular level in inflammatory diseases
Rankin, Gregory. "Investigation of the role of IgE-dependent cytokine release from human peripheral lung tissue in allergic lung inflammation". Thesis, University of Southampton, 2011. https://eprints.soton.ac.uk/378565/.
Texto completoParkinson, Sarah. "Neuroinflammation, Peripheral Inflammation and Gut Microbiome Profiles in Male Mice from Two Proposed Mouse Models of Social Behavior Deficits". Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/etd/3972.
Texto completoPitcher, Mark H. "The effects of persistent peripheral inflammation on the ultrastructural localization of spinal cord dorsal horn group I metabotropic glutamate receptors /". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98770.
Texto completoGelinas, Jinelle Crystal Marie. "The effects of aerobic exercise training on peripheral vascular structure and function and inflammation in patients with Chronic Obstructive Pulmonary Disease". Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45454.
Texto completoCarroll, Mark. "A stereological study assessing the validity of using endobronchial biopsies to assess mast cell density in the central and peripheral bronchial tree". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0005.
Texto completoTarkowski, M. S. "ANALYSIS OF THE FREQUENCIES OF CD235A+CD71+ PRE-ERYTHROID CELLS IN PERIPHERAL BLOOD AND THEIR FUNCTION IN HIV INFECTED PEOPLE". Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/487852.
Texto completoPre-erythroid cells, characterized by expression of glycophorin A (CD235a) and transferrin receptor (CD71) were demonstrated before to modulate immune responses and to suppress inflammatory reactions. As the process of erythropoiesis is often disturbed during HIV infection it was assumed that pre-erythroid cells, normally not present in peripheral blood of healthy adults, may be found in this tissue of HIV infected people and exert immunomodulatory activity. The purpose of the study was to investigate the presence and function of pre-erythroid cells found in peripheral blood of HIV and HIV/HCV co-infected adults. It was found that pre-erythroid cells are present in peripheral blood of HIV and HIV/HCV co-infected adults, especially those who developed anemia. Pre-erythroid cells of these people were found to be a significant source of Arg1 expression, and plasma activity of this enzyme was significantly higher in both groups of HIV infected patients in comparison to healthy group. In vitro analyses of activity of cord blood derived pre-erythroid cells confirmed previously reported findings and showed that these cells diminish the processes of immune activation. Although these observations could be confirmed in some cases of HIV infected patients, the immunosuppressive effect exerted by their pre-erythroid cells was less evident. Despite the findings of increased number pre-erythroid cells with potentially immunosuppressive activity, anemic HIV infected and HIV/HCV co-infected demonstrated similar or for some parameters even higher values of immune activation or inflammation than not anemic, infected people. The discrepancy between these observations can indicate that despite potential immunosuppressive character of the pre-erythroid cells their short term presence in peripheral blood may not be significant enough to affect more sustained pro-inflammatory reactions. It needs also to be considered that in this study limited number of immune activation and inflammation markers were studied. Explanation of the potential effect of pre-erythroid cells during the course of anemia in HIV and HIV/HCV co-infected people requires further studies as it can help to better understand the association between anemia and increased mortality, increased disease progression, and reduced quality of life in these groups of patients.
Pisi, Paula Carolina Bezzan. "Influência da perda de peso induzida por cirurgia bariátrica na resposta imune em paciente com obesidade grau III". Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-06062017-163504/.
Texto completoThe obesity-associated inflammation is characterized by a chronic and low intensity activation of the immune system. Several authors have shown changes in inflammatory parameters after weight loss. Bariatric surgery is a method for treating obesity with high efficiency and less risk of recurrence. Peripheral blood mononuclear cells (PBMC) are an interesting biological material for research, due to the ability to reflect changes in gene expression in different tissues and easy access to analysis. This study aimed to evaluate the effects of obesity and weight loss induced by bariatric surgery on immune activity through PBMC culture of morbidly obese patients (BMI >= 40 kg/m2). Peripheral vein blood samples were collected from 10 volunteers with normal weight (control group) and before and after the surgery in 20 volunteers with morbid obesity. After separation of the mononuclear cells by Ficoll-Hypaque gradient centrifugation, cells were stimulated with lipopolysaccharide (LPS) and concanavalin A (Con-A) and culture supernatants collected for IL-1?, IL-6, TNF-?, IFN-?, IL-10 and IL-17 dosage by ELISA. Blood samples were also used for biochemical examinations and adiponectin, leptin and serum cytokine dosage. The results showed higher concentrations of IL-6, TNF-?, IL-1? and IL-10 in the supernatants of the MNSP cultures of the obesity group in relation to the control group. In the comparison between cytokine dosages of the obesity group, we observed reduction of TNF-?, IL-1? and IL-10 after 6 months of surgery, which was not observed after 1 year, and IL-17 increased after 1 year of treatment. There was no significant difference in serum cytokine concentrations in the comparison between obesity and control groups or operated group. We observed correlations of cytokines obtained in PBMC culture supernatant and serum with laboratory results related to glucose homeostasis in patients with obesity before and after bariatric surgery, as well as correlation between cytokines of the supernatant and the state of adiposity postoperatively. We conclude that morbid obesity is associated with changes in cytokine production by PMNC and weight loss induced by bariatric surgery influences cytokine production in the first year of treatment.
Quinteiro, Mariana da Silva 1982. "Evaluation of peripheral effect of 15d-PGJ2 on inflammatory process induced by rheumatoid arthritis into rats' temporomandibular joint = Avaliação do efeito periférico da 15d-PGJ2 no processo inflamatório induzido pela artrite reumatoide na articulação temporomandibular de ratos". [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/289486.
Texto completoTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
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Resumo: O processo inflamatório induzido pela Artrite Reumatoide (AR) na articulação temporomandibular (ATM) resulta em uma dor persistente causando estresse em muitos pacientes. ... Observação: O resumo, na íntegra, poderá ser visualizado no texto completo da tese digital
Abstract: Inflammation of the temporomandibular joint (TMJ) induced by Rheumatoid Arthritis (RA) have often resulted in persistent pain and caused distress to many patients... Note: The complete abstract is available with the full electronic digital thesis or dissertations
Doutorado
Fisiologia Oral
Doutora em Odontologia
Wachtel, Nikolaus Constantin [Verfasser]. "Polyunsaturated fatty acids, colorectal cancer, and inflammation: Effects of three major polyunsaturated fatty acids on the lipid metabolism of colorectal adenocarcinoma HT-29 cells and on the cytokine secretion by peripheral blood mononuclear cells / Nikolaus Constantin Wachtel". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1218076240/34.
Texto completoMartinez, Caroline Silveira. "Efeitos da exposição ao alumínio sobre parâmetros neurológicos, reprodutores, cardiovasculares e bioquímicos em ratos". Universidade Federal do Pampa, 2017. http://dspace.unipampa.edu.br:8080/jspui/handle/riu/3363.
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O Alumínio (Al) é o metal de maior exposição humana, no entanto os efeitos do metal em nível de exposição humana ainda são pouco conhecidos. Assim, o objetivo desse estudo foi investigar os efeitos da exposição ao Al por 60 dias em dose equivalente a exposição humana ao metal através da dieta sobre o Sistema Nervoso Central (SNC), Sistema Nervoso Periférico (SNP), sistema reprodutor masculino e sistema cardiovascular e, comparar com os efeitos de uma exposição alta ao metal com efeitos tóxicos conhecidos. Para isso, ratos Wistar com 3 meses de idade foram divididos em: 1) Grupo 1: baixas doses de Al, onde durante 60 dias os ratos receberam por água de beber: a) Controle – água ultrapura; b) Al na dose de 1,5 mg/kg de peso corporal e, c) Al na dose de 8,3 mg/kg de peso corporal e, 2) Grupo 2: alta dose de Al, onde durante 42 dias os ratos receberam por gavagem: a) Controle – água ultrapura; b) Al na dose de 100 mg/kg de peso corporal. O tratamento com Al mesmo em baixas doses prejudicou a memória de reconhecimento de objetos e promoveu o desenvolvimento de catalepsia nos ratos. Somado a isso, a exposição ao Al aumentou os níveis de espécies reativas de oxigênio (EROs) e de peroxidação lipídica, reduziu a capacidade antioxidante e inibiu a atividade da acetilcolinesterase no hipocampo dos animais. No SNP, o Al promoveu o desenvolvimento de alodínea mecânica, aumentou o estresse oxidativo sistêmico, induziu inflamação com recrutamento de macrófagos e, o metal foi capaz de depositar-se entre as fibras do nervo ciático. Já no sistema reprodutor masculino, a exposição ao Al reduziu a contagem espermática, a motilidade e a produção diária de espermatozides, aumentou a porcentagem de espermatozoides com anormalidades morfológicas, alterou a estrutura testicular, aumentou os níveis de estresse 14 oxidativo e a inflamação testicular, demonstrando que uma baixa concentração do metal nos testículos (3.35 μg/g) é o suficiente para comprometer a espermatogênese e a qualidade dos gametas masculinos. No sistema cardiovascular, o Al aumentou a pressão arterial sistólica, reduziu a resposta vasodilatadora a acetilcolina, aumentou a resposta vasoconstritora a fenilefrina, reduziu a modulação endotelial na resposta vasoconstritora, reduziu a biodisponibilidade de óxido nítrico, o envolvimento dos canais de potássio nas respostas vasculares e aumentou a produção de EROs principalmente via NAD(P)H oxidase e de prostanóides contráteis da via da COX-2. A exposição ao Al aumentou o estresse oxidativo em artérias aorta e mesentérica, reduziu a expressão de mRNA de eNOS e SOD1 e aumentou a expressão da isoforma da NAD(P)H oxidase 1, COX-2 e a expressão de TXA-2 R. Tomados em conjunto, nossos dados demonstram que a exposição subcrônica ao Al por 60 dias em baixa dose, que reflete a exposição humana ao metal através da dieta, alcança um limiar tóxico suficiente para promover efeitos adversos no SNC, SNP, sistema reprodutor masculino e sistema cardiovascular. Além disso, os efeitos de uma exposição em baixa dose são praticamente os mesmos de uma exposição alta ao metal.
Aluminum (Al) is the most important environmental and human contaminant. While a good deal of research has been conducted on the acute toxic effects of Al, little is known about the effects of longer-term exposure at human dietary Al levels. Therefore, the purpose of this study was to investigate the effects of 60-day Al exposure at low doses on Central Nervous System (CNS), Peripheral Nervous System (PNS), male reproductive system and cardiovascular system for comparison with a model of exposure known to produce toxicity in rats. Three-month-old male Wistar rats were divided into two major groups: 1) Grou 1, low aluminum levels - rats were treated orally by drinking water for 60 days as follows: a) Control – received ultrapure drinking water; b) Aluminum at 1.5 mg/kg b.w. and c) Aluminum at 8.3 mg/kg b.w. and 2) Group 2, high aluminum level - rats were treated through oral gavages for 42 days as follows: a) Control – received ultrapure water; b) Aluminum at 100 mg/kg b.w. Al treatment even at low doses promoted recognition memory impairment seen in object recognition memory testing and catalepsy behavior in rats. Moreover, Al increased hippocampal reactive oxygen species (ROS) and lipid peroxidation levels, reduced antioxidant capacity and decreased acetylcholinesterase activity. On PNS, Al promoted the development of mechanical allodynia, increased inflammation in the sciatic nerve, systemic oxidative stress and, is able to be retained in the sciatic nerve. Regarding the male reproductive system, Al decreased sperm count, daily sperm production, sperm motility, normal morphological sperm, impaired testis histology; increased oxidative stress in reproductive organs and inflammation in testis, showing that low concentrations of Al in testes (3.35 μg/g) are sufficient to impair 16 spermatogenesis and sperm quality. On cardiovascular system, Al increased systolic blood pressure, decreased acetylcholine-induced relaxation, increased response to phenylephrine, decreased endothelial modulation of vasoconstrictor responses, the bioavailability of nitric oxide, the involvement of potassium channels on vascular responses, as well as increased ROS production from NAD(P)H oxidase and contractile prostanoids mainly from COX-2 in both aorta and mesenteric resistance arteries (MRA). Al exposure increased vascular ROS production and lipid peroxidation as well as altered the antioxidant status in aorta and MRA. Al decreased vascular eNOS and SOD1 mRNA levels and increased the NAD(P)H oxidase 1, COX-2 and TXA-2 R mRNA levels. Taken together, our data demonstrate that 60-day subchronic exposure to low doses of Al from feed and added to the water, which reflect human dietary Al intake, reaches a threshold sufficient to promote adverse effects on SNC, PNS, male reproductive system and cardiovascular system. Moreover, these effects were almost the same as Al exposure at much higher levels.
Janahi, Noor. "The role of pro-inflammatoy cytokines and autoimmune antibodies in diabetic peripheral neuropathy". Thesis, Queen Margaret University, 2014. https://eresearch.qmu.ac.uk/handle/20.500.12289/7430.
Texto completoKuster, Robin. "Modulation sexe-dépendante du traitement des informations nociceptives par l'inhibition GABAergique spinale". Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ016.
Texto completoThe short-term plasticity of GABAergic synapses in the lamina II of the spinal cord is essential for processing nociceptive information. This plasticity varies depending on the type of postsynaptic neuron, whether excitatory or inhibitory. Our findings indicate a sex-specific modulation of GABAergic synaptic transmission, particularly in response to acute peripheral inflammation. These observations highlight the importance of maintaining a balance between inhibition and excitation in processing nociceptive information. They also suggest that mechanisms regulating GABAergic synaptic transmission may explain differences in mechanical and thermal sensitivity between males and females.Our work enhances understanding of the neurobiological mechanisms of nociception, considering often overlooked sex-related differences
Marques, Fernanda Cristina Gomes de Sousa. "The choroid plexus as a sensor of peripheral inflammation". Doctoral thesis, 2008. http://hdl.handle.net/1822/8942.
Texto completoParticular interest has been raised in the last few years, regarding the contribution of the immune system in neurological and psychiatric diseases. It is recognized that an inflammatory component underlies disorders such as Alzheimer’s disease and multiple sclerosis. However, whether these are a consequence, a cause, or just a trigger of disease progression remains to be clarified. In this context, understanding how peripheral inflammatory stimulus reach the brain may contribute to better understand the mechanisms involved in such conditions. Most studies on the communication between the periphery and the central nervous system (CNS) focus on the bloodbrain barrier, which is composed by the endothelial cells of the brain capillaries. However, the blood-cerebrospinal fluid barrier (BCSFB) may as well convey signals from the periphery into the CSF and backwards. The BCSFB is formed by the choroid plexus (CP) epithelial cells. Given its role as the major producer of the CSF, and the presence of several receptors and transporters both in the apical and in the basolateral membranes, the CP is ideally positioned to transmit signals between the immune and the CNS. In the present study we address the CP response to inflammatory stimuli induced in the periphery. We show that the CP displays a specific, rapid and transient response to an acute inflammatory stimulus induced by the intraperitoneal administration of the Gram negative bacteria cell wall lipopolysaccharide (LPS). As soon as 1h after the injection, the CP responds by altering the expression of several genes. This response reaches a maximum at 3h, in which the level of 324 (out of 24 000 studied) transcripts are altered, and returns to the basal profile for most of the transcripts at 72h. Most of the up-regulated genes belong to immune-mediated cascades while those down-regulated encode for proteins involved in the maintenance of the CP barrier function. When LPS is administered repetitively every 2 weeks for 3 months, the CP response persists for longer periods but is attenuated. The biological pathway with higher up-regulation includes genes encoding for proteins that facilitate cells entry into the CSF, which may be particularly relevant in diseases such as multiple sclerosis. Of notice, in both conditions of acute and sustained inflammatory response, we observed altered expression of genes that participate in the innate immune response to infection by microorganisms, and that are related to iron homeostasis. In both conditions, the CP responds by decreasing iron availability for bacterial growth. Specifically, lipocalin 2, a sequester for bacteria iron-loaded siderophores is rapidly secreted into the CSF, persisting in the sustained inflammatory conditions. In addition, the CP is here suggested to play an identical role of that played by the liver, in regulating iron uptake and release, through the synthesis and secretion of hepcidin. Of interest, iron deregulation has been implicated in neurodegenerative diseases including Alzheimer’s disease and multiple sclerosis. Taken together, the data presented here highlights the role of the CP in mediating immune signals into the brain. How, this ultimately corresponds to neuroprotective or deleterious consequences for the brain and how this may relate to diseases of the CNS needs to be further investigated.
Nos últimos anos tem aumentado o interesse no estudo da participação do sistema imunológico em doenças neurológicas e psiquiátricas. A inflamação é hoje aceite com estando presente em doenças como a de Alzheimer e a esclerose múltipla. No entanto, ainda está por esclarecer se esta é uma causa, consequência ou estímulo de progressão e agravamento da doença. Neste contexto, a compreensão do modo como estímulos inflamatórios periféricos influenciam o cérebro pode contribuir para a compreensão dos mecanismos envolvidos nestas doenças. A maioria dos estudos sobre a comunicação entre a periferia e o sistema nervoso central têm incidido na barreira hemato-encefálica, que é constituída pelas células endoteliais dos capilares sanguíneos. No entanto, a barreira sangue-líquido céfalo-raquidiano (BCSFB) pode, igualmente, participar na transmissão de sinais entre a periferia e o CSF. A BCSFB é formada pelas células epiteliais dos plexus coroideus (CP). Tendo como função principal a produção de CSF, e uma vez que possuem vários receptores e transportadores, tanto na membrana apical como na basolateral, os CP estão idealmente posicionados para facilitar a interacção entre os sistemas imunológico e nervoso central. O trabalho desenvolvido nesta tese avalia a resposta dos CP a estímulos inflamatórios periféricos induzido pela administração intraperitoneal do lipopolissacarídeo (LPS) da parede de bactérias de Gram negativo. Quando este estímulo é agudo, observa-se uma resposta específica, rápida e transitória nos níveis de expressão de vários genes. Esta resposta é evidente 1h após a injecção, atinge um máximo às 3h, com a expressão diferencial de 324 (num total de 24 000 estudados) transcritos, e volta ao estado basal para a maioria dos transcritos ao fim de 72h. De entre os genes cuja expressão se encontra alterada os que têm expressão mais aumentada codificam moléculas envolvidas em cascatas imunológicas, enquanto que aqueles com expressão mais diminuída incluem genes que codificam proteínas que participam na manutenção da função de barreira do CP. Quando o LPS é administrado a cada 2 semanas durante 3 meses, a resposta dos CP persiste mais tempo e é de pequena amplitude. A via metabólica com maior aumento na expressão inclui genes que codificam proteínas que facilitam a migração de células para o CSF, o que pode ser relevante em doenças como a esclerose múltipla. De realçar, tanto na resposta inflamatória aguda como na continuada, observa-se expressão alterada de genes que participam na resposta imunológica inata à infecção por microorganismos, e que estão relacionados com o metabolismo do ferro. Em ambos os casos, o CP responde diminuindo a disponibilidade de ferro necessário para o crescimento bacteriano. Especificamente, a lipocalina 2, uma proteína que sequestra sideroforos bacterianos que ligam ferro, é rapidamente segregada para o CSF; uma resposta que persiste na inflamação continuada. Para além disso os resultados obtidos sugerem que o CP desempenha uma função idêntica à do fígado na regulação da captação e libertação de ferro, através da regulação da síntese e segregação de hepcidina. É de notar que alterações no metabolismo do ferro têm sido implicadas em doenças neurodegenerativas como a doença de Alzheimer e a esclerose múltipla. No seu conjunto, os resultados desta tese apontam para uma função clara do CP na transmissão da resposta inflamatória periférica para o cérebro. Se a consequência final desta resposta é benéfica ou deletéria para o cérebro, ou se contribui para doenças do sistema nervoso central fica ainda por esclarecer.
Arioli, Jessica. "TIM-1 glycoprotein mediates neutrophil peripheral recruitment during inflammation". Doctoral thesis, 2020. http://hdl.handle.net/11562/1017959.
Texto completoVale, Ana Margarida Gonçalves Candeias do. "Impact of Peripheral Inflammation on the Susceptibility to Neurodegenerative Diseases". Master's thesis, 2021. http://hdl.handle.net/10400.6/11501.
Texto completoO lipopolissacarídeo (LPS) é um agente inflamatório amplamente utilizado para induzir respostas inflamatórias periféricas em modelos animais. Quando administrado a baixas concentrações e durante um curto intervalo temporal, tem a capacidade de induzir neuroproteção em modelos animais da Doença de Alzheimer e de Acidente Vascular Cerebral. Este efeito neuroprotetor deve-se à ativação do sistema imunitário periférico e, subsequentemente, ativação e indução da memória imunitária inata nas células da microglia. Assim, o principal objetivo deste trabalho foi compreender os efeitos do LPS e da histamina, uma amina biogénica também envolvida em reações inflamatórias periféricas, na capacidade de induzir memória imunitária inata e, consequentemente, promover neuroproteção dos neurónios dopaminérgicos num modelo animal da Doença de Parkinson (DP). Para tal, murganhos C57BL/6J foram sujeitos à administração intraperitoneal com LPS ou histamina e, após 3 semanas, foram expostos à lesão intraestriatal com 6-hidroxidopamina (6-OHDA) para mimetizar a DP. A resposta inflamatória foi avaliada através da expressão de citocinas pro-inflamatórias (TNF-a e IL-1ß) e anti-inflamatórias (IL-10) no plasma sanguíneo, e da expressão da molécula adaptadora de ligação ao cálcio ionizado 1 (Iba-1), marcador celular de células de microglia e macrófagos, no cérebro. Para avaliar a sobrevivência dopaminérgica e o comportamento motor, recorreu-se às técnicas de imunohistoquímica para tirosina hidroxilase (TH) e ao teste da apomorfina, respetivamente. Os resultados obtidos sugerem que o LPS e a histamina induzem ativação da resposta inflamatória periférica com consequente ativação da microglia, desencadeando memória imunitária inata. A longo prazo, verifica-se que estes estímulos inflamatórios protegem os neurónios dopaminérgicos num modelo da DP, bem como a recuperação motora, traduzindo-se num novo mecanismo de prevenção e melhoria celular e funcional da DP.
Fang-YiKo y 柯芳宜. "Brain region-specific microglial activation in response to peripheral LPS-induced inflammation". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/27222561195714367804.
Texto completo國立成功大學
細胞生物及解剖學研究所
98
Microglia, one of three glial cell types in the central nervous system (CNS), play an important role as resident immunocompetent and phagocytic cells in the CNS in the event of injury and disease. Numerous studies indicated that peripheral inflammation may induce CNS inflammation and microglia activation. Activation of microglia is associated with cell transformation to phagocytes, capable of releasing potentially cytotoxic substances such as oxygen radicals, proteases, and proinflammatory cytokines. Recent studies indicated that CNS in?ammation and microglial activation is a common component of the pathogenesis for multiple neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, etc. It has been shown that the densities of microglia are unevenly distributed across different brain regions. However, whether the uneven distribution of microglia has any effect on peripheral inflammation-induced microglia activation remains unknown. The objective of this study is to investigate the temporal and spatial profiles of microglia activation after the peripheral inflammation in male C57BL/6 mice. Microglia morphological changes and densities of microglial cells in various brain regions were visualized using an immunohistochemical method with a polyclonal antibody recognizing the mouse ionized calcium binding adaptor protein-1 (Iba-1). Our results showed that substantia nigra (SN) had the highest microglia densities among the brain regions, followed by (in a high to low order) cortex, limbic system, basal nucleus, midbrain, thalamus, hypothalamus, brain stem, and the lowest in cerebellum. Microglia activation (soma enlargement, Iba-1-positive cell area and cell density) were observed after intraperitoneal LPS injection, with the highest degree of change in SN. I hypothesize that the integrity of blood-brain barrier (BBB) is involved in the transmission of inflammatory responses from the periphery to the CNS. The results showed that the BBB leakage was most pronounced in the SN among other brain regions. . Previously, it has been shown that TNFα/TNFα receptor 1 (TNFR1) play critical role in transmitting the inflammation signal from periphery into CNS. Therefore, we also investigated the expression of TNFR1 one day after LPS injection. The results showed that the highest LPS-induced TNFR1 levels was in the SN. Furthermore, activated microglia is capable of release cytokines and chemokines; among them monocyte chemoattractant protein (MCP-1) is vital in attracting peripheral monocytes into CNS. Hence, the levels of MCP-1 were measured. The results showed that the expressions of MCP-1 were elevated in all brain regions, with the highest in the SN. Furthermore, we used the Ly6C, a surface marker for monocytes but not microglia, to distinguish peripheral monocytes from residual microglia and found that the number of Ly6C-positve cells was highest in the SN. In conclusion, this study indicates that SN has the highest microglia density in the CNS. Upon peripheral inflammation stimulation, the degree of microglia activation was most prominent in the SN. This phenomenon may be due to the higher TNFR1 expression in the SN after the stimulation of inflammation, leading to larger leakage of BBB, higher expression of MCP-1 and more monocyte infiltration into the SN. Therefore, the SN is the most susceptible brain region in response to systemic immunological insults.
Rosenkranz, Melissa A. "Reciprocal modulation of peripheral inflammation and affective neural circuitry in health and disease". 2008. http://www.library.wisc.edu/databases/connect/dissertations.html.
Texto completoTian, Tin-Yi y 田婷怡. "Peripheral inflammation induces cytokine expression in brain and increases the permeability of blood-brain barrier". Thesis, 1999. http://ndltd.ncl.edu.tw/handle/07223055509356639351.
Texto completo國立成功大學
微生物暨免疫學研究所
87
英文摘要 The CNS (central nervous system) of mammal is considered to be an immunologically privileged site because it lacks lymphatic drainage, the brain is separated from the blood compartment by the blood-brain barrier (BBB). The brain also expresses FasL and TGFβ that can down-modulate the immune response. However, peripheral administration of lipopolysaccharide has been found to stimulate the hypothalamic- pituitary- adrenocortical axis to induce fever and influence behavior. This result showed that communication between peripheral immune system and CNS exists. It is general believed that cytokines produced in peripheral tissue can not cross the BBB because of the unique features of brain microvascular endothelial cells that wrapped by astrocyte. In this study, we reported that the peripheral stimulation with complete Freund’s adjuvant (CFA) induced the cytokine expression in brain. With immunohistochemical staining, TNFα and cyclooxygenase type 2 (COX-2) were detected on brain microvascular vessels post CFA or poly (Glu60 Ala30 Tyr10 , GAT ) in CFA injection. IL-1βwas detected in microvascular vessels only in mice injected with GAT/CFA. On the contrary, the constitutive expression of IL-6 on brain microvascular vessels and IL-1α on brain neuron bundle were found to decrease. The cytokine induction was also confirmed by semiquantitative reverse-transcription polymerase chain reaction, indicating its de novo synthesis. Using the M4 E. coli that constitutive expresses β-galactosidaseas as a tracer to quantitate the increased permeability of BBB, we found that the vasopermeability of BBB increased maximum at 96 h post CFA injection and 48 h post GAT/CFA injection. The increase of BBB permeability was inhibited by either NS398 (COX-2 inhibitor) or anti-TNFα antiserum. Using immunohistochemistry staining, the TNFαexpression was inhibited by NS398 treatment while COX-2 induction was blocked by anti-TNFαadministration. Furthermore, peripheral administration of GAT/CFA were found to induce fever at 48 h. The fever was not inhibited by anti-TNFαantiserum, but could be inhibited by NS398 or indomethacin (COX-1 and COX-2 inhibitor). Based on the above data, we conclude that peripheral inflammation stimulates TNFα or IL-1βexpression on brain microvascular vessels. The TNFαwould further cause COX-2 induction that involved in the increase of BBB permeability. The IL-1βinduction might be responsible for the fever that can be inhibited by COX inhibitor.
Cuhlmann, S., W. Gsell, der Heiden K. Van, J. Habib, J. L. Tremoleda, M. Khalil, F. Turkheimer et al. "In vivo mapping of vascular inflammation using the translocator protein tracer 18F-FEDAA1106". 2014. http://hdl.handle.net/10454/10331.
Texto completoNon-invasive imaging methods are required to monitor the inflammatory content of atherosclerotic plaques. FEDAA1106 (N-(5-fluoro-2-phenoxyphenyl)-N-(2-(2-fluoroethoxy)-5- methoxybenzyl) acetamide) is a selective ligand for TSPO-18kDa (also known as peripheral benzodiazepine receptor), which is expressed by activated macrophages. We compared 18F- FEDAA1106 and 18F-FDG (a marker of glucose metabolism) for PET imaging of vascular inflammation. This was tested using a murine model where focal inflammation was induced in the carotid artery via placement of a constrictive cuff. Immunostaining revealed CD68-positive cells (macrophages) at a disturbed flow site located downstream from the cuff. Dynamic PET imaging using 18F-FEDAA1106 or 18F-FDG was registered to anatomical data generated by CT/CT angiography. Standardized uptake values (SUV) were significantly increased at cuffed compared to contralateral arteries using either 18F-FEDAA1106 (p<0.01) or FDG (p<0.05). However, the 18F-FEDAA1106 signal was significantly higher at the inflamed disturbed flow region compared to the non-inflamed uniform flow regions, whereas differences in FDG uptake were less distinct. We conclude that 18F-FEDAA1106 can be used in vivo for detection of vascular inflammation. Moreover, the signal pattern of 18F-FEDAA1106 correlated with vascular inflammation more specifically than FDG uptake.
: This study was funded by the British Heart Foundation and through a grant from the Swiss National Science Foundation (310030_143343/1 to B.R.K.)
Ho, Ying-Hao y 何英豪. "Peripheral inflammation increases seizure susceptibility via the induction of neuroinflammation and oxidative stress in the hippocampus". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/52580917089874888255.
Texto completo國立中山大學
生物科學系研究所
103
Epilepsy is a common neurological disorder. Neuroinflammation is involved in the pathophysiology of epilepsy. Tissue oxidative stress is another confounding factor in epilepsy. While both neuroinflammation and brain oxidative stress are involved, relationship between these two factors in epileptogenesis, however, is not fully understood. In this study, I investigated the relationship and the underlying molecular mechanism. In aim 1, I established a rodent model of chronic neuroinflammation via peripheral inflammation induced by continuous infusion of E. coli lipopolysaccharide (LPS; 2.5 mg/kg/day) in the peritoneum for 7 or 14 days. Results showed an increased proinflammatory cytokines level, including IL-1β, IL-6 and TNF-α in plasma and various areas of brain (frontal lobe, temporal lobe, hippocampus, striatum, rostral ventrolateral medulla (RVLM), nucleus tractus solitarii (NTS)), increased number of the activated microglia in brain and sensitivity to induction of seizure by KA (KA, 10 mg/kg) injection. Based on these findings, I focused my study on the hippocampus, which is associated with temporal lobe epilepsy, a common form of epilepsy in human. Pharmacological agents were delivered via intracerebroventricular infusion with an osmotic minipump in chronic neuroinflammation model for 7 days. In aim 2, a cycloxygenase-2 inhibitor, NS398 (5 μg/μl/h), was used to study the relationship between neuroinflammation and tissue oxidative stress in seizure susceptibility after the LPS-induced peripheral inflammation. The results showed that NS398 significantly blunted the increase in microglia activation, production of proinflammatory cytokines, and tissue oxidative stress (upregulations of the NADPH oxidase subunits) in the hippocampus. The same treatment also ameliorated the increase in seizure susceptibility in the KA-induced seizure model. In aim 3, a reactive oxygen species scavenger, tempol (2.5 μg/μl/h), was used to study the relationship between neuroinflammation and oxidative stress in the increase in seizure susceptibility under peripheral inflammation. The results showed that tempol did not blunt the increase in activated microglia, production of proinflammatory cytokines, but significantly blunted tissue oxidative stress (upregulations of the NADPH oxidase subunits) in the hippocampus and ameliorated the increase in seizure susceptibility in the KA-induced seizure model. These results indicated that peripheral inflammation evoked neuroinflammation and the subsequent oxidative stress in the hippocampus, resulting in the increase seizure susceptibility. Moreover, protection from neuroinflammation and oxidative stress in the hippocampus exerted beneficial effect on seizure susceptibility following peripheral inflammation.
KASSA, Roman Mehari. "The role of peripheral challenges and inflammation in motoneuron degeneration caused by nerve trauma and disease". Doctoral thesis, 2007. http://hdl.handle.net/11562/338054.
Texto completoThe experiments presented in sections 2, 3 and 4 focused on the motor circuit implying crosstalk between neurons, as well as between motoneurons and target muscles, between a neural circuit and the environment. The experiments also focused on the motor circuit as a model of neurodegenerative motoneuron disease.
Oruebor, Jennifer Nkem. "Peripheral blood biomarkers in youth with bipolar disorder: a systematic review". Thesis, 2019. https://hdl.handle.net/2144/36613.
Texto completoChen, Ying-Ju y 陳映儒. "Increased expression of a proton-sensing G-protein coupled receptor, TDAG8, in DRG neurons after peripheral inflammation". Thesis, 2006. http://ndltd.ncl.edu.tw/handle/32750630763754454077.
Texto completo國立中央大學
生命科學研究所
94
High concentrations of hydrogen ions are usually found in local area surrounding the insulted tissues during several inflammatory responses. The tissue acidosis phenomenon is thought to be associated with inflammatory pain because the proton molecule can activate nociceptors (pain-related neurons) directly through proton-sensing ion channels. Several proton-sensing receptors expressed in dorsal root ganglia neurons. Some of them, such as vallinoid receptor1 and acid-sensing ion channel 3 are thought to be involved in inflammatory hyperalgesia. However, it is still unclear that whether there are any other proton-sensing receptors involved in inflammation. Here we have demonstrated that a proton-sensing G-protein-coupled receptor, mouse T-cell Death Associated gene 8 (mTDAG8), was predominantly expressed in small-diameter neurons, which give rise to the majority of nociceptors. The transcripts of mTDAG8 were increased 24 hours after complete Freund’s Ajuvant (CFA)-induced inflammation, suggesting that the TDAG8 receptors might associate with inflammatory pain. Consistently, data of in situ showed that the total TDAG8-expressing neurons increased approximately 15% in DRG neurons after CFA-inflammation. Most of the increased TDAG8-expressing neurons are large-diameter neurons (9-10%), and the increased small-diameter neurons expressing TDAG8 are restricted in IB4-positive neurons (5-7%). Since the large-diameter neurons can be activated by non-noxious stimulations during inflammation, and the responses of IB4-positive neurons are enhanced after treating with inflammatory mediators, the increased number of neurons expressing TDAD8 receptors may associate with allodynia and hyperalgesia in inflammation. In addition, the mTDAG8-transfected HEK 293 cells accumulated the cAMP in responding to pH 6.0 buffers. Thus the TDAG8 may mediate certain responses through cAMP-pathway in neurons after inflammation.
Maseroli, Elisa. "Central and peripheral effects of Dihydrotestosterone (DHT) in females: a preclinical perspective". Doctoral thesis, 2020. http://hdl.handle.net/2158/1192669.
Texto completoKallur, Sailaja. "Investigation of Circadian Clock in Peripheral Tissues and Immune-Circadian Interaction in the Domestic Fowl, Gallus Domesticus". Thesis, 2012. http://hdl.handle.net/1969.1/148255.
Texto completoHe, Rong-Heng y 何榕恒. "FK506-Binding Protein 51 Regulates GABAergic Neurotransmission-related Protein Expression in Peripheral Inflammation- versus Glucocorticoid- induced Anxiety Mouse Models". Thesis, 2017. http://ndltd.ncl.edu.tw/handle/16676195364561600806.
Texto completo