Дисертації з теми "Tumor-inflammation"
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Huang, Hua. "Endothelial activation and inflammation in the tumor microenvironment." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-247889.
Повний текст джерелаDe, Cock Jasmine M. (Jasmine Morgan). "Inflammation triggers Zeb1-dependent escape from tumor dormancy." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104098.
Повний текст джерелаThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 167-181).
Metastasis-related mortality for breast cancer patients often occurs many years after treatment of the primary tumor. Inflammation, through the orchestra of immune cells and released inflammatory cytokines, can predispose certain tissues to cancer development and can create a favorable environment for metastatic outgrowth. I evaluated whether lipopolysaccharide (LPS) could induce an inflammatory response, leading to the activation of the cell-biological epithelial-mesenchymal transition (EMT) program in dormant disseminated cancer cells in vivo, and subsequent metastatic outgrowth. To model metastatic cellular dormancy, I used a dormant subpopulation of cells (D2A1-d) that were enriched for in vivo from the highly metastatic carcinoma cell line D2A1, that was derived from spontaneous murine mammary tumor. The ability of the EMT program to awaken dormant disseminated D2A1-d cells was directly assessed in vivo, which resulted in the formation of macro-metastases following a transient induction of either the EMT-transcription factor Snail or Zeb1. Furthermore, the transient induction of Zeb1 led to the generation of CD29+ CD24- metastasis-initiating cells. In mice bearing dormant disseminated D2A1-d cells, my findings demonstrated that LPS-treatment resulted in the awakening of D2A1-d cells and metastatic outgrowth in the lungs and bone. The awakening of dormant disseminated D2A1-d cells was dependent, albeit through unknown mechanism, on the presence of neutrophils. The LPS-mediated awakening of dormant disseminated cancer cells was also dependent upon the activation of the EMT-inducing transcription factor Zeb1 in the D2A1-d cells. In conclusion, my thesis work demonstrated that inflammation can trigger the escape of metastatic dormancy in vivo.
by Jasmine M. De Cock.
Ph. D.
Nygren, Emma. "The role of Sema3A in inflammation mediated tumor progressions." Thesis, KTH, Skolan för bioteknologi (BIO), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-172790.
Повний текст джерелаMånga olika sorters celler är närvarande i tumörers mikromiljö och immunceller utgör en stor andel av dessa. Makrofager är centrala spelare o tumörimmunförsvaret och dessa kan indelas i olika aktiveringsgrader eller fenotyper, M1 eller M2 makrofager. M1 polariserade makrofager är tumörsuppressiva medan M2 makrofager bidrar till tumörtillväxt. De faktorer som reglerar skiftningen mellan M1 och M2 fenotyperna är under utredning. Vårt labb har identifierat att Immunsemaforinen 3A (Sema3A) spelar en roll i att reglera ackumuleringen av antitumorala M1 makrofager vilket leder till hämmad tumörtillväxt. Med denna information som bakgrund har detta examensarbete fokuserat på Sema3As roll i tumörmikromiljön. Med hjälp av lentivirusmedierad genterapi skapades en tumörcellinje som uttrycker shRNA mot Sema3AmRNA. Denna cellinjes visade 72% lägre Sema3A mRNA uttryck jämfört med kontorll och utvärderades sedan in vivo genom att följa tumörtillväxten i BALB/c mushonor. Immuncellsammansättningen i tumörerna analyserades sedan med hjälp av flödescytometri. Resultaten från in vivo experimentet visar att endogent Sema3A har en begränsad effekt på tumörutvecklingen. En något mer tumörgynnande immunprofil observerades i de tumörer där Sema3A uttryck var minskat. Utöver detta skapades också ett lentivirus för att transducera celler så att de överuttrycker Sema3A under en passande promotor för systemisk tillförsel.
Ng, Bernice Yu Jing. "Chronic Inflammation-Driven Tumor Promotion Asociated with CD8+ T Cells." Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08232007-122524/.
Повний текст джерелаDieterich, Lothar. "Molecular Regulation of Inflammation and Angiogenesis in the Tumor Microenvironment." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-152257.
Повний текст джерелаMa, Xiaojun. "Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth." Kyoto University, 2016. http://hdl.handle.net/2433/215461.
Повний текст джерелаKyoto University (京都大学)
0048
新制・課程博士
博士(医科学)
甲第19635号
医科博第73号
32671
京都大学大学院医学研究科医科学専攻
(主査)教授 妹尾 浩, 教授 渡邊 直樹, 教授 椛島 健治
学位規則第4条第1項該当
Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.
Повний текст джерелаKumari, Vandana. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17389.
Повний текст джерелаThe skin is the largest organ of an individuum and builds the barrier for a host against the environment. Skin barrier disruption by exogenous or endogenous stimuli can lead to skin inflammation. As a consequence, irritant or atopic eczema, frequent skin diseases, may evolve. Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine which plays a central role in inflammatory processes. The main aim of this thesis was to clarify whether and how endogenous TNF-α is contributing to skin inflammation driven by exogenous and endogenous triggers. The role of endogenous TNF-α was studied using TNF knockout (-/-) mice. In an irritation model, chemical and physical stimuli were applied on to mouse skin. Thymic stromal lymphopoietin (TSLP) was significantly induced by the used irritants. This TSLP induction was independent from endogenous TNF-α proven by using TNF-/- mice. Next the role of TNF-α in atopic dermatitis (AD) promoting an allergic skin inflammation was investigated. TNF-/- mice developed more severe AD compared to the wildtype mice and TSLP was significantly increased and correlated with the severity of the eczema. To prove the pathophysiological role of TSLP for AD progression, TNF-/- mice were pretreated with an TSLP antibody. Indeed, these mice developed less AD symptoms compared to the control mice. Mast cells (MCs) were also significantly increased in lesional skin in the AD model and moreover, correlated with AD severity, but also with TSLP expression.
CONSONNI, FRANCESCA MARIA. "Inflammation and cancer: relevance of myeloid cells recruitment and plasticity in tumor biology." Doctoral thesis, Università del Piemonte Orientale, 2017. http://hdl.handle.net/11579/86903.
Повний текст джерелаF, Consonni. "Inflammation and cancer: relevance of myeloid cells recruitment and plasticity in tumor biology." Doctoral thesis, Università del Piemonte Orientale, 2017. http://hdl.handle.net/11579/96173.
Повний текст джерелаShakya, Sajina. "ROLE OF TUMOR NECROSIS FACTOR-STIMULATED GENE-6 IN CUTANEOUS WOUND HEALING AND INFLAMMATION." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1572915446243341.
Повний текст джерелаScott, Alasdair James. "The regulation of tumor necrosis factor-alpha converting enzyme (TACE/ADAM17) during acute inflammation." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6041.
Повний текст джерелаVendramini-Costa, Débora Barbosa 1984. "Goniotalamina : atividade antitumoral e anti-inflamatória." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317629.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-09-28T18:41:42Z (GMT). No. of bitstreams: 1 Costa_DeboraBarbosaVendramini_D.pdf: 5920460 bytes, checksum: d6638ad4d3d0a96e4bbcdb55823f3254 (MD5) Previous issue date: 2012
Resumo: A carcinogênese é um processo longo, multi-etapas, onde células normais progressivamente adquirem um fenótipo neoplásico. Sua origem é favorecida por fatores genéticos, exposição à carcinógenos químicos, infecções crônicas e incorporação de mutações em genes envolvidos com a regulação da homeostase celular. O crescente entendimento da biologia tumoral tem fornecido alvos moleculares para a triagem orientada de quimioterápicos e de agentes quimiopreventivos, geralmente de origem natural ou sintetizados com base em produtos naturais. A evolução da química orgânica permitiu que compostos naturais fossem sintetizados de forma econômica e aperfeiçoados quanto às suas propriedades físico-químicas, favorecendo sua disponibilidade. Esse trabalho teve como foco a goniotalamina, uma estiril-lactona naturalmente encontrada na forma enantiomérica (R) em plantas do gênero Goniothalamus (Annonaceae). Foram sintetizadas as formas (R), (S) e racêmica, que em painel de nove linhagens tumorais humanas levaram à inibição de crescimento e morte celular com elevada potência. Apesar da potência sobre a MCF-7 (carcinoma mamário responsivo ao estrógeno), estudos com estimulação estrogênica revelaram que a atividade da goniotalamina é independente da via hormonal. De qualquer maneira, a goniotalamina racêmica inibiu em 65% a proliferação da MCF-7 implantada em fibras semipermeáveis (hollow fiber) em camundongos. A citometria de fluxo revelou que o racemato de goniotalamina induz apoptose na linhagem tumoral de cólon HT-29 em baixa concentração (10 ?g/mL), com participação das caspases 8 e 9, sugerindo ativação das vias extrínseca e intrínseca. Houve também indução de apoptose na linhagem de melanoma humano SK-MEL-2, mas esse efeito diminuiu quando essa linhagem foi transfectada com Bcl-XL, inibidor apoptótico ligado à mitocôndria, sugerindo ativação principalmente da via apoptótica extrínseca, com ativação da via intrínseca para amplificação do sinal. A goniotalamina em suas três formas comprovou in vivo a atividade apresentada in vitro, pela inibição do desenvolvimento tumoral em modelo de tumor sólido e ascítico de Ehrlich, sem sinais de toxicidade nas doses efetivas. Esses resultados, aliados aos bons rendimentos na rota sintética, favoreceram a continuidade dos estudos com a forma racêmica. Considerando que aproximadamente 25% dos tumores estão relacionados com inflamações crônicas, a goniotalamina racêmica foi avaliada em modelos de edema de pata induzido por carragenina e por diversos mediadores (fosfolipase A2, histamina/serotonina, prostaglandina E2 e bradicinina), apresentando atividade anti-edematogênica em todos os modelos. Corroborando com esses resultados, a goniotalamina apresentou efeito antinociceptivo em modelos de algesia induzidos por processos inflamatórios. A goniotalamina inibiu o desenvolvimento de colite induzida por TNBS e o tratamento oral (30 mg/kg, três vezes por semana/três meses) preveniu o desenvolvimento de inflamação e câncer em animais deficientes em interleucina 10, sem apresentar sinais de toxicidade. Tais dados foram revelados após análise de dano macroscópico e microscópico (histologia) do cólon, havendo diminuição da expressão relativa dos genes para TNF? e MMP9, importantes no processo inflamatório e de invasão e metástase. Além disso, a goniotalamina diminuiu a incidência de metástase pulmonar em modelo de melanoma metastático. Os resultados obtidos e o perfil multi-alvos apresentado pela goniotalamina sugerem sua avaliação em terapias combinatórias para tratamento de processos inflamatórios crônicos e de câncer
Abstract: Carcinogenesis is a long process involving several steps, in which normal cells progressively acquire a neoplastic phenotype. Its origin is favored by genetic factors, exposure to chemical carcinogens, chronic infections and incorporation of mutations into genes involved in regulation of cellular homeostasis. The increasing understanding of tumor biology has provided molecular targets for screening of targeted chemotherapeutic and chemopreventive agents, usually from natural sources or synthesized based on natural products. The improvement of organic chemistry allowed the synthesis of natural products in an economic and refined way, with improvement on their physicochemical properties and availability. This work focuses on goniothalamin, a styryl-lactone naturally found on its enantiomeric form (R), in plants of Goniothalamus (Annonaceae) genus. The (R), (S) and racemic forms were synthesized and led to growth inhibition and cell death in a panel of nine human tumor cell lines, with high potency. Despite the potency against MCF-7 (breast carcinoma responsive to estrogen), estrogen stimulation studies revealed that the goniothalamin activity is independent of the hormone pathway. Anyway, racemic goniothalamin inhibited on 65% the proliferation of MCF-7 implanted into semi permeable fibers (hollow fiber) in mice. Flow cytometry analysis showed that low concentration of racemic goniothalamin (10 ?g/mL) leads colon tumor cell line (HT-29) to apoptosis with involvement of caspase 8 and 9, suggesting the activation of the extrinsic and intrinsic pathways. Apoptosis was also induced in human melanoma cell line SK-MEL-2, but the activity was decreased in SK-MEL-2 transfected with Bcl-XL, a mitochondrial related apoptotic inhibitor, suggesting mainly activation of the extrinsic apoptotic pathway, with activation of the intrinsic pathway to amplify the signal. Goniothalamin on its three forms comproved in vivo the in vitro activity by inhibiting tumor development in models of Ehrlich solid and ascitic tumor in mice, without signals of toxicity at the effective doses. These results, combined with good yields in the synthetic rout favored the racemic form to continue the in vivo studies. Considering that about 25% of tumors are related to chronic inflammation, racemic goniothalamin was evaluated in models of paw edema induced by carrageenan and various mediators (phospholipase A2, histamine/serotonin, prostaglandin E2 and bradykinin) displaying anti-edematogenic activity in all models. Corroborating these results, goniothalamin showed antinociceptive effect in models of algesia induced by inflammatory processes. It also inhibited the development of TNBS-induced colitis and oral treatment (30mg/kg, three times/week, three months) prevented the development of inflammation and cancer in interleukin-10 deficient mice, without signals of toxicity. These data were revealed after macroscopic and microscopic (histology) colon damage analysis, with decreased expression of TNF? and MMP9, which are important in inflammation, invasion and metastasis process. Furthermore, goniothalamin reduced the incidence of lung metastasis in a metastatic melanoma model. These results and the multitarget profile presented by goniothalamin suggest its evaluation in combinatory therapies for treatment of chronic inflammation and cancer
Doutorado
Biologia Celular
Doutor em Biologia Celular e Estrutural
Garcia, Stéphane. "TP53INP1 [Tumor Protein 53 Induced Nuclear Protein 1] : un nouvel acteur dans le processus inflammation-cancer." Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX20661.
Повний текст джерелаPeyvandi, Sanam. "Les cellules Myéloïdes Dans le Microenvironnement Tumoral : Rôle de FasL." Phd thesis, Université Paris Sud - Paris XI, 2013. http://tel.archives-ouvertes.fr/tel-00968103.
Повний текст джерелаZeidler, Patti C. "Particle-induced pulmonary inflammation and fibrosis role of inflammatory mediators in the initiation and progression of occupational lung disease /." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3022.
Повний текст джерелаTitle from document title page. Document formatted into pages; contains xv, 190 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Kostyk, Amanda Gail. "Tumor necrosis factor-[alpha] : a critical cytokine at the crossroads of fibrosis and inflammation in the lung /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 182-208). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Yasuda, Michiko. "Studies of Food Factors that Suppress Inflammation and Tumor Promotion via Regulation of Programmed Cell Death 4." Kyoto University, 2010. http://hdl.handle.net/2433/120915.
Повний текст джерела0048
新制・課程博士
博士(農学)
甲第15587号
農博第1837号
新制||農||984(附属図書館)
学位論文||H22||N4460(農学部図書室)
28108
京都大学大学院農学研究科食品生物科学専攻
(主査)教授 入江 一浩, 教授 井上 國世, 教授 河田 照雄
学位規則第4条第1項該当
Mola, Silvia. "Tumor Associated Macrophages (TAMs) a pivotal orchestrator in cancer-related inflammation and a new important target in cancer-therapy." Doctoral thesis, Università del Piemonte Orientale, 2021. https://hdl.handle.net/11579/127797.
Повний текст джерелаPenglis, Peter Savas. "The relationships between eicosanoid production and pro-inflammatory cytokines." Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09php3985.pdf.
Повний текст джерелаGaré, Ricardo Rodrigues. "Efeitos do reiki na evolução do granuloma induzido através da inoculação do BCG em hamsters e do tumor ascítico de Ehrlich induzido em camundongos." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-12012009-094100/.
Повний текст джерелаWe studied the effects of the influence of Reiki in the evolution of the experimental induced granuloma by the inoculation of BCG in the footpad of hamsters, and the effects of the same therapy in mice with Ehrlich ascitic tumor in vivo and in vitro. In the chronic granulomatous inflammation model, it was used, 40 male hamsters, which, after been inoculated with BCG in day 0, it was separated in two groups with 20 animals per group: control and reiki. The control group received no treatment, and reiki group, which was treated with Reiki by 15 minutes, daily, from 30 cm of the box. Immediately before the inoculation, the footpad diameter was measured, and after this measure was made in every other day, until complete 54 days. In the Ehrlich ascitic tumor model, it was used, 26 female mice inoculated with Ehrlich tumor cells, by intraperitoneal via, in the day 0. After that, the mice were separated in three groups: control (n=8), reiki A (n=9) and reiki B (n=9). The control group received no treatment, reiki A group received Reiki treatment by 10 minutes, daily, from 30 cm of the box, and reiki B group, which was manipulated and received a different way of Reiki treatment. The mice were observed daily until death in order to analyze survival rate. As regards granuloma evaluation it was observed a reduced footpad edema in hamsters inoculated with BCG and treated with Reiki. In relation to survival rate assay, it was observed an increased lifespan of those mice of the reiki A group.
Lima, Joanna Darck Carola Correia. "O papel do infiltrado inflamatório no tumor e sua contribuição para inflamação sistêmica e desenvolimento da caquexia." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-12082016-100836/.
Повний текст джерелаCancer cachexia is characterized by severe weight loss and large metabolic imbalance.It is a result of the interaction between the host\'s cells and the tumour, which induces systemic inflammation.Understand the relationship is required for the discovery of diagnostic markers.The aim of the present study was to characterize differences in inflammatory tumour infiltrate and molecular aspects in order to assess whether the presence of cachexia is determined by the inflammatory tumour profile. The study involved patients diagnosed with colorectal cancer and then distributed into two groups: cancer without cachexia(WSC) and cancer cachexia(CC).Histopathological analysis showed that the presence of cachexia in patients with colo-rectal cancer was independent from tumour staging.Characterization of infiltrating macrophages revealed a lower percentage of M2 profile in CC.Protein expression of cytokines demonstrated lower of IL-13 in CC and pro-inflammatory cytokines is higher in CC. Correlation between macrophages and cytokines was shown positive with macrophages type M1.These results provide evidence that tumor has a different secretion profile between the groups with regard to inflammatory factors and different percentages of macrophage phenotype.
Caughey, Gillian Elizabeth. "Regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phc371.pdf.
Повний текст джерелаBerkhout, Laura Katharina [Verfasser], and Gisa [Akademischer Betreuer] Tiegs. "Role of Tumor necrosis factor receptor 1 in a mouse model of chronic liver inflammation / Laura Katharina Berkhout ; Betreuer: Gisa Tiegs." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://d-nb.info/1214370373/34.
Повний текст джерелаCOCCO, MARTINA. "Polarization of tumor associated macrophages in ovarian cancer ascites: relationship with cancer-related anemia and associated inflammation and iron metabolism changes." Doctoral thesis, Università degli Studi di Cagliari, 2018. http://hdl.handle.net/11584/255967.
Повний текст джерелаBeringer, Audrey. "IL - 17 et réponse inflammatoire systémique : focus sur le foie et le muscle." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSE1318/document.
Повний текст джерелаInterleukin-17A (IL-17) and tumor necrosis factor-a (TNFa) are two pro-inflammatory cytokines playing an important role in various systemic inflammatory and autoimmune disorders affecting different organs and tissues including the liver and the muscles. However, the roles of IL-17 and TNFa are not fully understood in the muscles and also in liver, which is crucial in the acute phase response. By using cultures of human myoblasts, primary human hepatocytes, human HepaRG cells and LX-2 hepatic stellate cells, we found that IL-17 and TNFa increase in synergy the production of the pro-inflammatory cytokine IL-6 and chemokines (IL-8, CCL20, MCP-1). In myoblasts, the IL-17 and TNFa stimulation induces endoplasmic reticulum stress and calcium dysregulation showing that immune and non-immune pathogenic mechanisms interplay. In hepatocytes, IL-17 and TNFa mediate systemic inflammation and cell damage by increasing in synergy the CRP acute-phase protein and transaminase levels through the induction of IL-6. Since active liver and muscle disorders are characterized by inflammatory infiltrates of immune cells, the cell interactions play certainly an important role in the chronicity of the inflammation. Peripheral blood mononuclear cells activated or not were therefore co-cultured with myoblasts, hepatocytes and/or hepatic stellate cells to assess the inflammatory role of the cell-cell interactions. Co-cultures enhance the production of IL-6 and IL-8 compared to monocultures. IL-17 and TNFa contribute partially to these inductions. The systemic effects of IL-17 and/or TNFa make them attractive therapeutic targets for the treatment of various systemic inflammatory disorders
Tjomsland, Vegard. "Studies of the tumor microenvironment : Local and systemic effects exerted by the cross-talk between tumor and stroma cells in pancreatic cancer." Doctoral thesis, Linköpings universitet, Molekylär virologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-67632.
Повний текст джерелаMindre än 5% av patienterna som drabbas av cancer i bukspottkörteln förväntas överleva i mer än fem år. De typiska symtomen kommer sent och sjukdomen framskrider snabbt. Några av de riskfaktorer som identifierats är tobaksrökning, fetma och typ 2 diabetes. Forskningen har hittills siktat in sig på tumörcellerna och de mekanismer de använder för att överleva och föröka sig. Men en tumör innehåller också normala kroppsceller och vid bukspottkörtelcancer kan så mycket som 70 procent bestå av i sig ofarliga bindvävsceller. Miljön i tumören skapas av samspelet mellan dessa celltyper. De cancerceller som är bäst på att utnyttja omgivningen för sin tillväxt fortlever och för sina egenskaper vidare. En sådan egenskap är att kunna manipulera bindvävsceller till att producera signalsubstanser och tillväxtfaktorer som gynnar tumören. Mekanismerna bakom denna kommunikation har studerats och ett viktigt fynd var att tumörcellerna producerar signalämnet interleukin 1-alpha (IL-1a). Detta protein upptäcktes i 90 procent av de undersökta tumörerna, och var kopplat till dålig prognos hos patienterna. Signalen via IL-1a sätter igång tillverkningen av substanser som behövs för nybildning och tillväxt av blodkärl, i sin tur en förutsättning för att tumören ska leva vidare och växa. Proteinet stimulerar också celldelning i tumören, bidrar till att lura kroppens immunförsvar och underlättar spridning av dottertumörer till andra delar av kroppen. När vi slår ut signaleringen kan tumörcellerna inte längre påverka bindvävscellerna lika effektivt, och således minskar förekomsten av flera faktorer som gynnar tumörtillväxten. IL-1a kan därför vara en lovande kandidat att utforska vidare för framtida som ett läkemedel mot bukspottkörtelcancer.
Mumprecht, Viviane Denise. "In vivo imaging of tumor- and inflammation-induced lymph node lymphangiogenesis and proteomic profiling for the identification of surface-accessible lymphatic markers /." [S.l.] : [s.n.], 2009. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=18414.
Повний текст джерелаKumari, Vandana [Verfasser], A. [Akademischer Betreuer] Radbruch, M. [Akademischer Betreuer] Worm, and P. [Akademischer Betreuer] Franken. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation / Vandana Kumari. Gutachter: A. Radbruch ; M. Worm ; P. Franken." Berlin : Lebenswissenschaftliche Fakultät, 2015. http://d-nb.info/1081211180/34.
Повний текст джерелаWilkie, Tasha Wilkie. "Tumor Commensal Microbiota Activates an S100A7-TLR4-STAT-3 Signaling to Induce Chronic Inflammation and Consequent Growth and Metastasis of Breast Cancer." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1524214470077411.
Повний текст джерелаYuan, Kai. "Metabolic inflammation and immunomodulation in dairy cows." Diss., Kansas State University, 2014. http://hdl.handle.net/2097/17294.
Повний текст джерелаDepartment of Animal Sciences and Industry
Barry J. Bradford
The transition period in dairy cows is characterized by dramatic increases in nutrient requirements for lactation and substantial metabolic stress. The disturbed metabolic balance, coupled with suppressed immune function, contributes to markedly elevated incidence of health disorders. Several lines of evidence suggest that increased inflammation is common during the transition period. Unlike the classical inflammation associated with acute infection, the postpartum inflammatory state is low-grade and often of metabolic origin. This metabolic inflammation plays a key role in numerous disorders; an improved understanding of inflammatory pathways in transition cows may improve our ability to predict and prevent disorders. To mimic metabolic inflammation, in Experiment 1, we administered low amounts of recombinant bovine tumor necrosis factor-α (rbTNFα), a pro-inflammatory cytokine, to early lactation cows, and evaluated whether rbTNFα affects milk production, metabolism, and health. We found that rbTNFα administration increased systemic inflammation, decreased feed intake and milk yield, and increased incidence of disorders. Conversely, preventing excessive inflammation has the potential to improve productivity and health of dairy cows. To identify nutritional strategies that could enhance metabolism and immunity, we evaluated the efficacy of several feed additives. In Experiment 2, we evaluated effects of chromium propionate, rumen-protected lysine and methionine, or both on metabolism and immunity in lactating dairy cows, and found that supplementation of these nutrients may enhance neutrophil function. In Experiment 3, we determined whether supplementation of yeast product to transition cows could enhance production, metabolism, and immunity, and found that yeast product modulated feeding behavior, metabolism, immunity, and uterine inflammation. Overall, a greater understanding of the role of metabolic inflammation in the transition period and the nutritional strategies that could modulate these signals may improve the production and health of dairy cows.
Esteves, Bruna. "Avaliação da atividade anti-inflamatória e antitumoral dos extratos de Solidago chilensis, Aristolochia cymbifera e Piper umbellatum." Universidade Federal de Juiz de Fora (UFJF), 2017. https://repositorio.ufjf.br/jspui/handle/ufjf/4032.
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As plantas medicinais são uma grande fonte para o desenvolvimento de novos medicamentos. Neste contexto, o objetivo do presente estudo foi avaliar a atividade anti-inflamatória e antitumoral de extratos de Solidago chilensis (G10, G11, G12), Aristolochia cymbifera (G13) e Piper umbellatum (G14). Estas espécies vegetais foram selecionadas com base em seu extenso uso na medicina popular para o tratamento de queimaduras, doenças reumáticas e inflamatórias, como sedativas, antipiréticas, entre outros. Como metodologia, primeiramente os extratos foram testados para sua citotoxicidade em células RAW264.7 (método de MTT). Em seguida, a atividade antiinflamatória dos extratos foi determinada através da produçao de óxido nítrico (método de GRIESS) e das citocinas TNF-α e MCP-1 (método de ELISA). Uma vez determinado o extrato mais promissor, sua ação foi avaliada sobre a produção de outras citocinas pro-inflamatórias (IL-1β, IL-6 e IL-12), bem como sobre a expressão de moleculas co-estimuladoras, proliferação celular e produção de IFN-. A influência do extrato no processo inflamatório também foi determinada in vivo, utilizando o modelo de edema de orelha. A atividade antitumoral foi determinada em linhagens murinas de câncer de mama (4T1) e de melanoma (B16) pelo método de MTT. Como resultados, nas concentrações não toxicas, o extrato G14 foi o único capaz de reduzir a produção de NO, TNF-α e MCP-1, sendo assim selecionado para os testes posteriores. Este extrato também inibiu a produçao de IL-1β, IL-6 e IL-12, a expressão dos coestimuladores CD40 e CD80, além de reduzir a proliferação de esplenócitos e a produção de IFN- . No ensaio in vivo, o extrato G14 foi efetivo em reduzir o edema, o infiltrado inflamatório, a produção de IL-1β, IL-6 e MCP-1 assim como da enzima mieloperoxidase. Resultados semelhantes foram encontrados nos testes in vitro realizados como o 4-nerolidilcatecol, composto majoritário presente no extrato G14. Em relação a atividade antitumoral, o extrato G12 foi o que mais se destacou, reduzindo a sobrevivência das duas linhagens estudadas em até 50%. Os resultados apresentados nos permitem concluir que tanto o extrato G14 quanto o composto 4NC foram efetivos na redução do processo inflamatório enquanto o extrato G12 se destacou por reduzir a sobrevivência de células tumorais.
Medicinal plants are a great source for the development of new medicines. In this context, the objective of the present study was to evaluate the anti-inflammatory and antitumor activity of Solidago chilensis (G10, G11, G12), Aristolochia cymbifera (G13) and Piper umbellatum (G14) extracts. These plant species were selected based on their extensive use in folk medicine for the treatment of burns, rheumatic and inflammatory diseases, such as sedatives, antipyretics, among others. As a methodology, the extracts were first tested for their cytotoxicity in RAW264.7 cells (MTT method). The anti-inflammatory activity of the extracts was determined by the production of nitric oxide (GRIESS method) and the cytokines TNF-α and MCP-1 (ELISA method). Once the most promising extract was determined, its action was evaluated on the production of other proinflammatory cytokines (IL-1β, IL-6 and IL-12), as well as on the expression of costimulatory molecules, cell proliferation and production of IFN-. The influence of the extract on the inflammatory process was also determined in vivo using the ear edema model. Antitumor activity was determined in murine (4T1) and melanoma (B16) murine cell lines by the MTT method. As a result, in the non-toxic concentrations, the G14 extract was the only one able to reduce the production of NO, TNF-α and MCP-1, being thus selected for the subsequent tests. This extract also inhibited the production of IL-1β, IL-6 and IL-12, the expression of CD40 and CD80 costimulators, as well as reducing splenocyte proliferation and IFN-γ production. In the in vivo assay, G14 extract was effective in reducing edema, inflammatory infiltrate, IL-1β, IL-6 and MCP-1 production as well as the myeloperoxidase enzyme. Similar results were found in the in vitro tests performed as 4-nerolidylcaltechol, the major compound present in the G14 extract. In relation to the antitumor activity, G12 extract was the most outstanding, reducing the survival of the two strains studied by up to 50%. The results show that both the G14 extract and the 4-NC compound were effective in reducing the inflammatory process while the G12 extract was highlighted by reducing the survival of tumor cells.
Bertling, Frederik [Verfasser], and Ursula [Akademischer Betreuer] Felderhoff-Müser. "Tumor necrosis factor-inducible gene 6 protein : A novel neuroprotective factor against inflammation-induced developmental brain injury / Frederik Bertling ; Betreuer: Ursula Felderhoff-Müser." Duisburg, 2017. http://d-nb.info/1143518705/34.
Повний текст джерелаKantola, T. (Tiina). "Systemic inflammation in colorectal cancer:the role of cytokines and endostatin." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526210544.
Повний текст джерелаTiivistelmä Paksu- ja peräsuolisyöpä (kolorektaalisyöpä) on yleisimpiä syöpämuotoja Suomessa. Sen ennustetta kuvaavat mittarit ovat tärkeitä taudin etenemisen ennustamisessa ja hoidon suunnittelussa. Käytössä olevat kolorektaalisyövän ennusteen arvioinnin menetelmät eivät ole riittäviä. Uusia merkkiaineita onkin kehitetty ja testattu, mutta rutiinikäyttöön soveltuvia menetelmiä ei ole vielä löydetty. Tässä tutkimuksessa selvitettiin immuunijärjestelmän ja muiden kasvaimen kasvua säätelevien tekijöiden keskinäisiä yhteyksiä ja niiden merkitystä kolorektaalisyövän ennusteen arvioinnissa. Tutkimusmateriaali koostui Oulun yliopistollisessa sairaalassa leikattujen kolorektaalisyöpäpotilaiden (n = 148) leikkaus- ja verinäytteistä ja terveiden verrokkihenkilöiden (n = 86) verinäytteistä. Endostatiinin ja 27 sytokiinin pitoisuudet mitattiin seeruminäytteistä. Kollageeni XVIII:n ja tulehdussolujen analysoimiseen käytettiin immunohistokemiallisia menetelmiä. Useiden sytokiinien pitoisuudet olivat korkeammat potilailla kuin verrokeilla, mutta osassa sytokiineista pitoisuudet olivat alentuneet. Seerumin sytokiiniprofiili erotteli luotettavasti potilaat verrokeista. Pidemmälle edenneeseen tautiin liittyi sytokiinien korkeampia pitoisuuksia ja etäpesäkkeitä muodostanut tauti oli yhteydessä Th1-tyypin sytokiinien esiintymiseen. Systeeminen tulehdusreaktio oli yhteydessä syövän etenemiseen. Endostatiinipitoisuudet olivat kohonneet potilailla ja olivat yhteydessä kasvaimen invaasioon suolen seinämän lihaskerroksen läpi. Endostatiinipitoisuudet korreloivat myös systeemisen tulehdusreaktion kanssa, mutta eivät liittyneet paikallisten tulehdussolujen määrään. Kollageeni XVIII ilmentyi kasvaimen stroomassa ja suolen seinämän lihaskerroksessa. Sytokiineilla ja kasvaimen paikallisilla tulehdussoluilla todettiin olevan vain vähän keskinäisiä yhteyksiä. Kolorektaalisyöpään liittyy useita erisuuntaisia muutoksia seerumin sytokiinipitoisuuksissa, joten on olennaista tutkia eri sytokiinien suhteellisia muutoksia. Seerumin sytokiiniprofiili on lupaava potilaita ja verrokeita erotteleva mittari, jolla voi olla diagnostista arvoa. Kohonneet endostatiinipitoisuudet potilailla voivat johtua kasvaimen invaasioon liittyvästä kollageeni XVIII:n hajoamisesta suolen seinämässä, mutta lisätutkimuksia tarvitaan endostatiinin ennustetta kuvaavan arvon määrittämiseksi
Behr, Delphine. "Etude de la production de marqueurs de l'inflammation lors de la circulation extra-corporelle : intérêt des cytokines." Paris 5, 1994. http://www.theses.fr/1994PA05P140.
Повний текст джерелаDescamps, Laurence. "Etude des mecanismes des alterations physiopathologiques de la barriere hemato-encephalique experimentalement soumise a un etat inflammatoire." Lille 2, 1996. http://www.theses.fr/1996LIL2P254.
Повний текст джерелаPerrier, Julie. "Criblage virtuel et expérimental de chimiothèques pour le développement d’inhibiteurs des cytokines TNF-alpha et IL-6." Thesis, Paris, CNAM, 2014. http://www.theses.fr/2015CNAM0978.
Повний текст джерелаAnti-cytokine biologics (monoclonal antibodies, soluble receptors) targeting TNF-alpha and IL-6in chronic inflammatory diseases have been a major success for pharmaceutical industry.However, they exhibit several drawbacks : resistance, difficult administration, high costs.Our team works on the discovery of small molecule inhibitors of cytokines suck as TNF-alphaand IL-6, in order to widen the range of therapeutic drugs. Orally active drugs would represent ahighly beneficial alternative for patients.During my PhD, I have performed an experimental screening (using cellular and biochemicalbinding testings) of the best compounds identified through virtual screening of a large chemicallibrary, and on pyridazine compounds of a medicinal chemical library. I have been able toidentify several small molecules inhibiting the interaction of TNF-! and IL-6 with their receptor.Moreover, my work will have an impact on the laboratory screening strategies.Overall, this work opens new avenues for anti-cytokine drug discovery
Simonneau, Marie. "Implication de l'Oncostatine M dans la genèse et le développement des carcinomes épidermoïdes cutanés." Thesis, Poitiers, 2018. http://www.theses.fr/2018POIT1403/document.
Повний текст джерелаCutaneous squamous cell carcinoma (cSCC) is one of the most frequent keratinocyte malignancies worldwide and is chemotherapy resistant. Surgery is the curative treatment but there isn’t any alternative in advanced cSCC. Reprogramming tumor microenvironment and tumor immunosuppressive mechanisms is a new therapeutic approach. Indeed, depending on cytokine expressed in tumor microenvironment, immune cells can inhibit (Th1/M1 cells) or enhance (Th2/M2 cells) tumor development. It was previously showed that Onconstatin M (OSM) had pleiotropic effects on cancer cells. OSM can promote cancer by inducing tumor cells motility, invasiveness or by reprogramming immune cells toward a more permissive phenotype (M2 polarization). Our previous data showed that OSM has proinflammatory effects on skin and modulate normal keratinocyte phenotype both in vitro and in vivo. In this study, we hypothesized that OSM could be involved in cSCC development. We showed that OSM was overexpressed in human cSCC as well as other cytokines such as IL-6, IL-1β, IFNγ whereas IL-4 was decreased, suggesting a Th1/M1 polarization of cSCC microenvironment. In vitro, OSM induced STAT-3 and ERK signalization, modified gene expression, promoted proliferation and migration of malignant keratinocyte PDVC57 cells. PDVC57 cells grafted in skin mice led to cSCC development associated to OSM overexpression by immune infiltrated cells. Finally, we showed that the absence of OSM led to a 30% reduction of tumor size and reduced M2 polarization in tumor microenvironment. Collectively, these results support a pro-tumoral role of OSM in cSCC development and suggest a new therapeutic approach targeting this cytokine
Sá, Carla Sandrina Rendall Moreira. "Estudo da participação dos receptores do tipo Toll-2 e Toll-4 e da molécula adaptadora MyD88 no desenvolvimento do diabetes auto-imune experimental." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-18032014-151145/.
Повний текст джерелаType 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction by activated macrophages and Th1 lymphocytes. The role of TLRs has been demonstrated in this disease, however the mechanisms involved in this process have not yet been fully explained. We evaluated the role of TLR-2, TLR-4 and MyD88 adaptor molecule in the development of experimental autoimmune diabetes induced by multiple low-doses of streptozotocin in C57Bl/6 mice. TDM1 was more severe in TLR-2 KO mice, with higher blood glucose levels and weight loss. Increased cellular infiltrate, bax and caspase-3 expression was detected in the pancreatic islets of the diabetic TLR-2 KO group suggesting a greater destruction of pancreatic cells. Interestingly, a decreased number regulatory T cells was observed in the spleen of diabetic TLR-2 KO animals. Hence, TLR-2 receptor deficiency resulted in exacerbated development of experimental autoimmune diabetes, thereby suggesting an important role for this receptor in the modulation of the immune response developed in this disease.
Hamasato, Eduardo Kenji. "A influência da convivência com um parceiro doente sobre a resposta inflamatória alérgica pulmonar em camundongos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-29092016-103925/.
Повний текст джерелаThe bidirectional relationship between the nervous system and the imune system is relevant for homeostatic organism maintenance. Studies from our laboratory showed that 14 days of cohabitation with a sick conspecific (injected with Ehrlich tumor cells-TAE) produced behavioral, endocrinological and immunological changes. This study analyzes the effects of cohabitation with an Ehrlich tumor-bearing animal on ovalbumin (OVA)-induced lung inflammatory response in mice. Pairs of male mice were separate into three groups: naïve, control and experimental. Animals of the naïve group were kept undisturbed being used for assessment of basal parameters. One animal of each experimental and control pair of mice was immunized with OVA. On D(0), these OVA-immunized animals received an OVA booster. At this day (D(0)) the experimental mice that were kept undisturbed were inoculated with 5x106 Ehrlich tumor cells; their immunized cage-mates were then referred as to CSP(companion of sick partner). The undisturbed mice of each control pair were i.p. treated on D(0) with 0.9% NaCl; their sensitized cage-mate were subsequently referred as CHP (companion of health partner). The intranasal OVA challenge was performed on CSP and CHP mice on D(12) and D(13); blood and tissue collection were performed on D (14). Fourteen days after cohabitation, in comparison to the CHP mice, the CSP mice displayed the following: (1) an increased number of eosinophils and neutrophils in the BAL, (2) a decreased bone marrow cell count, (3) increased levels of IL-4 and IL-5 and decreased levels of IL-10 and INF-ϒ in the BAL supernatant, (4) increased levels of IgG1-OVA, decreased levels of IgG2a-OVA and no changes in OVA-specific IgE in the peripheral blood, (5) increased expression of ICAM-1, VCAM-1 and L-selectin in the BAL granulocytes, (6) decreased tracheal reactivity to metacholine measured in vitro , (7) increased mast cell degranulation, (8) no changes in plasma corticosterone levels (9) increased levels of plasmatic adrenaline and noradrenaline, (10) decreased time and % of entries on open arms of elevated plus maze, (11) decreased expression of IL-6 on PVN and (12) decreased expression of C-fos on PFC. These results suggest that cohabitation with an Ehrlich tumor bearing mice exacerbates allergic lung inflammatory response in mice. Most probably, the changes observed in CSP mice are a consequence of the psychological stress induced by forced cohabitation with the sick partner. Strong involvement of the sympathetic nervous system through adrenaline and noradrenaline release and a shift of the Th1/Th2 cytokine profile toward a Th2 response were considered to be the mechanisms underlying the cell recruitment to the animal´s airways.
Rodriguez, Alejandro. "Studies of Stroma Formation and Regulation in Human Pathological Conditions and in Experimental in vivo Models." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-120688.
Повний текст джерелаAkiel, Maaged A. "CHARACTERIZATION OF THE ROLE OF INSULIN-LIKE GROWTH FACTOR BINDING PROTEIN 7 (IGFBP7) USING A GENETIC KNOCKOUT MOUSE MODEL." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4695.
Повний текст джерелаFarrow, Michael John. "The effect of androstenediol on gene expression and NF-kappaB activation in vitro." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187109346.
Повний текст джерелаHastir, Jean-Francois. "Study of the fate of resident macrophages and monocytes upon partial liver resection and their impact on hepatocarcinoma outgrowth." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/308316.
Повний текст джерелаDoctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
Doyle, Todd A. "Inflammatory Pathways Linking Type 2 Diabetes Mellitus and Depression." Ohio University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1332460860.
Повний текст джерелаTouhami, Sara. "L’hypoxie et l’inflammation sous-rétinienne dans le contexte de la dégénérescence maculaire liée à l’âge." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS553.
Повний текст джерелаHypoxia is suspected to be one of the essential triggers in the pathogenesis of age related macular degeneration, characterized by abnormal mononuclear phagocyte (MP) infiltration. We recently showed that the inhibition of the TSP-1 (thrombospondin 1) dependent physiological elimination of MPs by complement factor H (CFH) plays an important role in subretinal MP accumulation. Here, we showed that ambient 10%O2 hypoxia increased subretinal MP infiltration and inhibited inflammation resolution after laser-induced subretinal injury, compared to normoxia (20,9%O2) in mice. In vitro, hypoxia (2%) delayed the elimination of human primary Monocytes (Mo) in coculture with immune-suppressive retinal pigment epithelium (RPE). In vivo, 10% hypoxia decreased Tsp-1 and increased Cfh and Tnfα mRNA expression in Mo that participate in the subretinal inflammation. Interestingly, contrary to wildtype animals, hypoxic ambient air had no effect on the exaggerated subretinal MP infiltration observed in normoxic Thbs1-/-mice, but diminished MP accumulation in normoxic Cfh-/-mice. Intravitreal injections of a CFH blocking antibody or recombinant TSP-1 completely reversed the pathogenic effect of hypoxia. In vitro, exogenous TNFα caused RPE cell dedifferenciation, decreasing their immunosuppressivity, which likely perpetuates Mo accumulation in the subretinal space. Together, our results demonstrate that systemic hypoxia disturbs TSP-1-dependent subretinal immune suppression, increases TNFα expression by Mo and promotes pathogenic subretinal inflammation. We show that the pathogenic effect of hypoxia can be therapeutically countered by local recombinant TSP1 or CFH inhibition
Pretorius, Rachelle Ann. "Body composition and systematic low-grade inflammation in children : the PLAY study / Rachelle A. Pretorius." Thesis, North-West University, 2006. http://hdl.handle.net/10394/1096.
Повний текст джерелаThesis (M.Sc. (Nutrition))--North-West University, Potchefstroom Campus, 2007.
Väyrynen, J. (Juha). "Immune cell infiltration and inflammatory biomarkers in colorectal cancer." Doctoral thesis, Oulun yliopisto, 2014. http://urn.fi/urn:isbn:9789526206417.
Повний текст джерелаTiivistelmä Kolorektaalisyöpä on yksi yleisimmistä pahanlaatuisista kasvaintaudeista ja syöpäkuolemien aiheuttajista Suomessa. Tulehdussolujen korkean määrän kasvainnäytteissä on havaittu olevan yhteydessä potilaiden parempaan ennusteeseen. Tarkat ja luotettavat analyysimenetelmät sekä tieto eri tulehdusmerkkiaineiden keskinäisistä yhteyksistä olisivat tärkeitä, jotta tulehdussolukon määritystä voitaisiin luotettavasti käyttää potilaiden ennusteen arviointiin. Tutkimuksessa otettiin käyttöön ja validoitiin uusi tietokonepohjainen menetelmä kasvaimen tulehdussolukon arviointiin sekä uusi menetelmä kolorektaalisyövän imukeräsreaktion arviointiin. Kasvainnäytteiden tulehdussolukon määrää ja laatua analysoitiin itsenäisissä 418 (Kohortti 1) ja 149 (Kohortti 2) kolorektaalisyöpäpotilaan aineistoissa uusia menetelmiä hyödyntäen. Lisäksi kohortilta 2 sekä 83 terveeltä ikä- ja sukupuolivalikoidulta verrokilta määritettiin seerumin matriksin metalloproteinaasi-8 (MMP-8) -taso. Tietokonepohjaisen kuva-analyysin tarkkuus ja toistettavuus todettiin erinomaiseksi. Kasvainnäytteistä analysoitujen tulehdussolutyyppien määrät olivat riippuvaisia toisistaan mast-soluja ja CD1a+ epäkypsiä dendriittisoluja lukuun ottamatta. T-solujen runsas määrä oli yhteydessä taudin vähäisempään uusiutumisriskiin. Korkea imukerästiheys kasvainnäytteissä oli yhteydessä matalaan levinneisyysasteeseen sekä potilaiden parempaan ennusteeseen levinneisyysasteesta riippumatta. Seerumin MMP-8-tason mediaani oli potilailla yli kolme kertaa korkeampi kuin terveillä verrokeilla. Tutkimus tuo lisätietoa eri tulehdussolutyyppien ja tulehdusmerkkiaineiden merkityksestä kolorektaalisyövässä, ja sen tuloksena validoitiin uusia tulehdussolukon analysointimenetelmiä. Tulosten perusteella erityisesti kasvaimen alueen T-solujen ja imukerästen tiheys tuovat hyödyllistä tietoa potilaiden ennusteesta. Lisätutkimuksia tarvitaan seerumin MMP-8:n mahdollisesta soveltuvuudesta kolorektaalisyövän diagnostiikan, seurannan tai ennusteen määrittämisen apuvälineeksi
Vieira, Cristiano Pedrozo 1986. "Efeito da nutrição terapêutica a base de Camellia sinensis (chá verde) e ração rica em glicina sobre a tendinite do tendão calcanear de rato = Effect of therapeutic nutrition on the basis of Camellia sinensis (green tea) and glycine-diet on the tendinitis of Achilles tendon of rats." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317356.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Nutrição terapêutica é a administração de alguns nutrientes, em doses maiores que as necessidades alimentares diárias que podem prevenir deficiências orgânicas e atuar como agentes farmacológicos. A glicina apresenta amplos efeitos benéficos em processos inflamatórios e tumorais. O Chá verde feito de folhas e brotos da planta Camellia sinensis, é a segunda bebida mais consumida em todo mundo. O interesse econômico e social tem ganhado espaço no mercado e atualmente seu consumo faz parte da rotina diária de muitas pessoas que utilizam essa bebida como uma finalidade terapêutica. O Chá verde possui propriedades antimutagênicas, antidiabéticos, antiinflamatórias, antioxidante, antimicrobial e hipocolesterolêmica. A tendinite é reconhecidamente um problema clínico que motiva a comunidade científica a buscar tratamentos que auxiliem no restabelecimento das propriedades funcionais dos tendões. O presente estudo investigou o efeito do chá verde e ou da ração rica em glicina após 7 e 21 dias da indução da tendinite com colagenase. Ensaios bioquímicos, moleculares, morfológicos e biomecânicos foram desenvolvidos. Além disso, tenócitos em cultura foram tratados com glicina após inflamação induzida por TNF-?. Nossos ensaios in vivo mostraram altas concentrações de hidroxiprolina e glicosaminoglicanos no grupo glicina e chá em 21 dias de tratamento. Nos ensaios biomecânicos os grupos chá verde e dieta de glicina em 21 dias suportaram maiores cargas biomecânicas antes da ruptura. Além disso, uma melhor organização das fibras de colágeno foi observada no grupo chá verde em 7 dias. Análises bioquímicas e moleculares da junção miotendínosa mostraram que a inflamação instalada na região osteotendinea pode provocar alterações significativas nesse local. Marcantes alterações foram notadas nas metaloproteínases (MMP) tais como MMP-2, MMP-8 e MMP-9 em animais com tendinite tratados ou não com chá verde e glicina. No estudo in vitro, tenócitos extraídos a partir de tendão de Aquiles foram tratados com TNF-?, seguindo ou não de tratamento com glicina em meio de cultura. Antes e após 24 horas da inflamação foi adicionado glicina. Tenócitos inflamados e tratados com glicina mostraram expressão de colágeno tipo I próxima aos grupos tratados com glicina previamente e depois da inflamação quando comparado ao grupo controle. Todos os grupos tratados com glicina mostraram menor expressão de MMP-2. A atividade da MMP-9 foi alta apenas no grupo tratado com glicina em 48 horas. A concentração de ácido urônico foi menor no grupo tratado com glicina 24 horas após a inflamação. No ensaio de migração celular, resultados em 24 horas de tratamento foram similares ao grupo controle. Em geral, tanto a glicina quanto o chá verde influenciam na síntese dos componentes do tendão, melhoram a organizaçao das fibras colagênicas, aumentam a resistência a cargas do tendão inflamado e consequentemente aceleram o processo de remodelamento após indução da tendinite. Além disso, o tratamento com glicina em cultura de tenócitos mostrou uma reorganização eficiente da matriz extracelular, corroborando com os resultados encontrados in vivo
Abstract: Therapeutic nutrition is the administration of some nutrients, in higher doses than those recommended for the daily food needs that can prevent dysfunctions and act as pharmacological agents. Glycine has large beneficial effects in inflammatory and tumor processes. Green tea made from leaves and buds of the Camellia sinensis plant, is the second most consumed beverage in the world. The economic and social interest has gained space in the market and currently its consumption is part of the daily routine of many people who use this drink as a therapeutic purpose. Green tea has antimutagenic, antidiabetic, anti-inflammatory, antioxidant, antimicrobial and hypocholesterolemic properties. Tendinitis is recognized as a clinical problem that motivates the scientific community to investigate treatments that help in restoring the functional properties of tendons. The present study investigated the effect of green tea and/or diet rich in glycine after 7 and 21 days of tendinitis collagenase-induced. Biochemical, molecular, morphological and biomechanical tests were developed. Furthermore, tenocytes in culture were treated with glycine after inflammation induced by TNF-?. Our tests in vivo showed high concentrations of hydroxyproline and glycosaminoglycans in glycine and green tea group in 21 days of treatment. In biomechanical assay, green tea and glycine diet groups in 21 days showed a high biomechanical loads bore before rupture. In addition, better organization of collagen fibers was observed in green tea group in 7 days. Biochemical and molecular analyzes of myotendinous junction showed that the inflammation installed in osteotendinious region can cause significant change in that region. Remarkable changes were noted in metalloproteinases (MMP) such as MMP-2, MMP-8 and MMP-9 in animals with tendinitis treated with or without glycine and green tea. In the in vitro study, tenocytes from Achilles tendon were treated with TNF-?, or not following treatment with glycine in the culture medium. Before and 24 hours after inflammation was added glycine. Tenocytes inflamed and treated with glycine showed expression of collagen type I close to the treated groups with glycine previously and after the inflammation when compared to the control group. All treated groups showed less glycine MMP-2 expression. The activity of MMP-9 was high only in the group treated with glycine for 48 hours. In the cell migration assay results in 24 hours of treatment were similar to the control group. In general, both glycine and green tea influenced the synthesis of the tendon components, improve the organization of the collagenous fibers, increase the load resistance of the inflamed tendon and consequently accelerate the remodeling process after inducing tendinitis. In addition, the treatment with glycine in tenocytes culture showed efficient reorganization of the extracellular matrix, confirming the results found in vivo
Doutorado
Biologia Celular
Doutor em Biologia Celular e Estrutural
Bleve, Augusto. "Decoding of epigenetic and metabolic events driving immune diversion of myeloid cells in cancer." Doctoral thesis, Università del Piemonte Orientale, 2020. http://hdl.handle.net/11579/114772.
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