Готові списки джерел за темами / Colon fibroblasts

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Добірка наукової літератури з теми "Colon fibroblasts"

Автор: Grafiati
Опубліковано: 10 березня 2023
Оновлено: 11 березня 2023

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Статті в журналах з теми "Colon fibroblasts"

1

Laudadio, Ilaria, Alex Bastianelli, Valerio Fulci, Claudia Carissimi, Eleonora Colantoni, Francesca Palone, Roberta Vitali та ін. "ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis". International Journal of Molecular Sciences 23, № 18 (6 вересня 2022): 10261. http://dx.doi.org/10.3390/ijms231810261.

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Анотація:
Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract. Chronic inflammation is the main factor leading to intestinal fibrosis, resulting in recurrent stenosis, especially in CD patients. Currently, the underlying molecular mechanisms of fibrosis are still unclear. ZNF281 is a zinc-finger transcriptional regulator that has been characterized as an epithelial-to-mesenchymal transition (EMT)-inducing transcription factor, suggesting its involvement in the regulation of pluripotency, stemness, and cancer. The aim of this study is to investigate in vivo and in vitro the role of ZNF281 in intestinal fibrogenesis. Intestinal fibrosis was studied in vivo in C57BL/6J mice with chronic colitis induced by two or three cycles of administration of dextran sulfate sodium (DSS). The contribution of ZNF281 to gut fibrosis was studied in vitro in the human colon fibroblast cell line CCD-18Co, activated by the pro-fibrotic cytokine TGFβ1. ZNF281 was downregulated by siRNA transfection, and RNA-sequencing was performed to identify genes regulated by TGFβ1 in activated colon fibroblasts via ZNF281. Results showed a marked increase of ZNF281 in in vivo murine fibrotic colon as well as in in vitro human colon fibroblasts activated by TGFβ1. Moreover, abrogation of ZNF281 in TGFβ1-treated fibroblasts affected the expression of genes belonging to specific pathways linked to fibroblast activation and differentiation into myofibroblasts. We demonstrated that ZNF281 is a key regulator of colon fibroblast activation and myofibroblast differentiation upon fibrotic stimuli by transcriptionally controlling extracellular matrix (ECM) composition, remodeling, and cell contraction, highlighting a new role in the onset and progression of gut fibrosis.
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2

Bruckner, R. S., M. C. Barnhoorn, H. Mei, S. M. Kiełbasa, T. J. Harrijvan, S. K. Hakuno, J. J. van der Reijden, A. E. van der Meulen-de Jong, and L. J. A. C. Hawinkels. "DOP85 The role of fibroblasts in the pathogenesis of Crohn’s disease-associated fistulas and in mesenchymal stem cell therapy." Journal of Crohn's and Colitis 14, Supplement_1 (January 2020): S125. http://dx.doi.org/10.1093/ecco-jcc/jjz203.124.

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Abstract Background Perianal fistulas are a severe and frequent complication in Crohn’s disease (CD) patients, significantly affecting their quality of life. High recurrence rates, incomplete fistula healing and non-responding patients make the treatment challenging. Despite some novel insights, current knowledge about the pathogenesis of fistula formation is still limited. Fibroblasts are abundantly present in CD fistulas and were recently reported to regulate Th1 cell activity in inflammatory bowel disease (IBD) (Beswick EJ et al. 2018). We hypothesised that fibroblasts act as the key drivers of fistula pathogenesis by regulating inflammatory cell recruitment. Methods Fibroblasts were isolated from curettage material of perianal CD fistulas, non-CD-associated fistulas, and the normal colon (obtained at surgery for colorectal cancer at least 10 cm away from the primary tumour). For all experiments, fibroblast populations were identified by qPCR and flow cytometry analysis first. Then gene expression profiling via mRNA sequencing of cultured fistula- and colon-derived fibroblasts was performed. The characterisation was complemented by flow cytometry analysis. Furthermore, the interaction of fistula-derived fibroblasts with regulatory T cells (Tregs) was studied in co-culture experiments. Results mRNA sequencing analysis revealed no significant differences in gene expression between perianal CD fistulas and non-CD-associated fistulas. However, comparing fistula-derived samples to fibroblasts derived from the normal colon, we found over 6000 significantly differentially expressed genes. Among the 20 most significant differentially expressed genes between CD fistulas and colon fibroblasts were genes related to epithelial-mesenchymal transition, cell migration or the NF-κB signalling pathway. Furthermore, co-culture experiments with CD fistula-derived fibroblasts, revealed increased proliferation rates of CD25+FoxP3+ Treg cells. In addition, more CD4+ T cells differentiated into Treg cells after exposure to CD fistula fibroblasts. Conclusion Our data indicate a pathogenic role of fibroblasts located in the fistula tract. Their gene expression profile markedly differed from fibroblasts derived from the normal part of the colon. Based on our data, there is no difference between CD-associated and non-CD-associated fistula fibroblasts. CD fistula-derived fibroblasts seem to increase both the proliferation of Treg cells, and the differentiation of CD4+ T cells into Treg cells, indicating an important immunoregulatory role of fibroblasts. Ongoing experiments should reveal which cytokines and chemokines are involved in this process.
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3

Jasso, Guadalupe J., Alok Jaiswal, Mukund Varma, Tyler Laszewski, Angelo Grauel, Abdifatah Omar, Nilsa Silva, et al. "Colon stroma mediates an inflammation-driven fibroblastic response controlling matrix remodeling and healing." PLOS Biology 20, no. 1 (January 27, 2022): e3001532. http://dx.doi.org/10.1371/journal.pbio.3001532.

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Chronic inflammation is often associated with the development of tissue fibrosis, but how mesenchymal cell responses dictate pathological fibrosis versus resolution and healing remains unclear. Defining stromal heterogeneity and identifying molecular circuits driving extracellular matrix deposition and remodeling stands to illuminate the relationship between inflammation, fibrosis, and healing. We performed single-cell RNA-sequencing of colon-derived stromal cells and identified distinct classes of fibroblasts with gene signatures that are differentially regulated by chronic inflammation, including IL-11–producing inflammatory fibroblasts. We further identify a transcriptional program associated with trans-differentiation of mucosa-associated fibroblasts and define a functional gene signature associated with matrix deposition and remodeling in the inflamed colon. Our analysis supports a critical role for the metalloprotease Adamdec1 at the interface between tissue remodeling and healing during colitis, demonstrating its requirement for colon epithelial integrity. These findings provide mechanistic insight into how inflammation perturbs stromal cell behaviors to drive fibroblastic responses controlling mucosal matrix remodeling and healing.
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Fuhr, Abreu, Carbone, El-Athman, Bianchi, Laukkanen, Mazzoccoli, and Relógio. "The Interplay between Colon Cancer Cells and Tumour-Associated Stromal Cells Impacts the Biological Clock and Enhances Malignant Phenotypes." Cancers 11, no. 7 (July 15, 2019): 988. http://dx.doi.org/10.3390/cancers11070988.

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Cancer cells interrelate with the bordering host microenvironment that encompasses the extracellular matrix and a nontumour cellular component comprising fibroblasts and immune-competent cells. The tumour microenvironment modulates cancer onset and progression, but the molecular factors managing this interaction are not fully understood. Malignant transformation of a benign tumour is among the first crucial events in colorectal carcinogenesis. The role of tumour stroma fibroblasts is well-described in cancer, but less well-characterized in benign tumours. In the current work we utilized fibroblasts isolated from tubulovillous adenoma, which has high risk for malignant transformation, to study the interaction between benign tumour stroma and the circadian clock machinery. We explored the role of the biological clock in this interplay taking advantage of an experimental model, represented by the co-culture of colon cancer cells with normal fibroblasts or tumour-associated fibroblasts, isolated from human colorectal tumour specimens. When co-cultured with tumour-associated fibroblasts, colon cancer cells showed alterations in their circadian and metabolic parameters, with decreased apoptosis, increased colon cancer cell viability, and increased resistance to chemotherapeutic agents. In conclusion, the interactions among colon cancer cells and tumour-associated fibroblasts affect the molecular clockwork and seem to aggravate malignant cell phenotypes, suggesting a detrimental effect of this interplay on cancer dynamics.
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Herrera, Mercedes, Artur Mezheyeuski, Lisa Villabona, Sara Corvigno, Carina Strell, Christian Klein, Gabriele Hölzlwimmer, et al. "Prognostic Interactions between FAP+ Fibroblasts and CD8a+ T Cells in Colon Cancer." Cancers 12, no. 11 (November 3, 2020): 3238. http://dx.doi.org/10.3390/cancers12113238.

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Анотація:
Inter-case variations in immune cell and fibroblast composition are associated with prognosis in solid tumors, including colon cancer. A series of experimental studies suggest immune-modulatory roles of marker-defined fibroblast populations, including FAP-positive fibroblasts. These studies imply that the fibroblast status of tumors might affect the prognostic significance of immune-related features. Analyses of a population-based colon cancer cohort demonstrated good prognosis associations of FAP intensity and CD8a density. Notably, a significant prognostic interaction was detected between these markers (p = 0.013 in nonadjusted analyses and p = 0.003 in analyses adjusted for cofounding factors) in a manner where the good prognosis association of CD8 density was restricted to the FAP intensity-high group. This prognostic interaction was also detected in an independent randomized trial-derived colon cancer cohort (p = 0.048 in nonadjusted analyses). In the CD8-high group, FAP intensity was significantly associated with a higher total tumor density of FoxP3-positive immune cells and a higher ratio of epithelial-to-stromal density of CD8a T cells. The study presents findings relevant for the ongoing efforts to improve the prognostic performance of CD8-related markers and should be followed by additional validation studies. Furthermore, findings support, in general, earlier model-derived studies implying fibroblast subsets as clinically relevant modulators of immune surveillance. Finally, the associations between FAP intensity and specific immune features suggest mechanisms of fibroblast-immune crosstalk with therapeutic potential.
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6

Heichler, Christina, Kristina Scheibe, Anabel Schmied, Carol I. Geppert, Benjamin Schmid, Stefan Wirtz, Oana-Maria Thoma, et al. "STAT3 activation through IL-6/IL-11 in cancer-associated fibroblasts promotes colorectal tumour development and correlates with poor prognosis." Gut 69, no. 7 (November 4, 2019): 1269–82. http://dx.doi.org/10.1136/gutjnl-2019-319200.

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ObjectiveCancer-associated fibroblasts (CAFs) influence the tumour microenvironment and tumour growth. However, the role of CAFs in colorectal cancer (CRC) development is incompletely understood.DesignWe quantified phosphorylation of STAT3 (pSTAT3) expression in CAFs of human colon cancer tissue using a tissue microarray (TMA) of 375 patients, immunofluorescence staining and digital pathology. To investigate the functional role of CAFs in CRC, we took advantage of two murine models of colorectal neoplasia and advanced imaging technologies. In loss-of-function and gain-of-function experiments, using genetically modified mice with collagen type VI (COLVI)-specific signal transducer and activator of transcription 3 (STAT3) targeting, we evaluated STAT3 signalling in fibroblasts during colorectal tumour development. We performed a comparative gene expression profiling by whole genome RNA-sequencing of fibroblast subpopulations (COLVI+ vs COLVI–) on STAT3 activation (IL-6 vs IL-11).ResultsThe analysis of pSTAT3 expression in CAFs of human TMAs revealed a negative correlation of increased stromal pSTAT3 expression with the survival of colon cancer patients. In the loss-of-function and gain-of-function approach, we found a critical role of STAT3 activation in fibroblasts in driving colorectal tumourigenesis in vivo. With different imaging technologies, we detected an expansion of activated fibroblasts in colorectal neoplasias. Comparative gene expression profiling of fibroblast subpopulations on STAT3 activation revealed the regulation of transcriptional patterns associated with angiogenesis. Finally, the blockade of proangiogenic signalling significantly reduced colorectal tumour growth in mice with constitutive STAT3 activation in COLVI+ fibroblasts.ConclusionAltogether our work demonstrates a critical role of STAT3 activation in CAFs in CRC development.
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Knowles, Jonathan P., Xu Shi-Wen, Samer-ul Haque, Ashish Bhalla, Michael R. Dashwood, Shiyu Yang, Irving Taylor, Marc C. Winslet, David J. Abraham, and Marilena Loizidou. "Endothelin-1 stimulates colon cancer adjacent fibroblasts." International Journal of Cancer 130, no. 6 (June 9, 2011): 1264–72. http://dx.doi.org/10.1002/ijc.26090.

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8

Brügger, Michael David, Tomas Valenta, Hassan Fazilaty, George Hausmann, and Konrad Basler. "Distinct populations of crypt-associated fibroblasts act as signaling hubs to control colon homeostasis." PLOS Biology 18, no. 12 (December 11, 2020): e3001032. http://dx.doi.org/10.1371/journal.pbio.3001032.

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Анотація:
Despite recent progress in recognizing the importance of mesenchymal cells for the homeostasis of the intestinal system, the current picture of how these cells communicate with the associated epithelial layer remains unclear. To describe the relevant cell populations in an unbiased manner, we carried out a single-cell transcriptome analysis of the adult murine colon, producing a high-quality atlas of matched colonic epithelium and mesenchyme. We identify two crypt-associated colonic fibroblast populations that are demarcated by different strengths of platelet-derived growth factor receptor A (Pdgfra) expression. Crypt-bottom fibroblasts (CBFs), close to the intestinal stem cells, express low levels of Pdgfra and secrete canonical Wnt ligands, Wnt potentiators, and bone morphogenetic protein (Bmp) inhibitors. Crypt-top fibroblasts (CTFs) exhibit high Pdgfra levels and secrete noncanonical Wnts and Bmp ligands. While the Pdgfralow cells maintain intestinal stem cell proliferation, the Pdgfrahigh cells induce differentiation of the epithelial cells. Our findings enhance our understanding of the crosstalk between various colonic epithelial cells and their associated mesenchymal signaling hubs along the crypt axis—placing differential Pdgfra expression levels in the spotlight of intestinal fibroblast identity.
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9

Kikuchi, Yoshinao, Takeshi G. Kashima, Takashi Nishiyama, Kazuhiro Shimazu, Yasuyuki Morishita, Masashi Shimazaki, Isao Kii, et al. "Periostin Is Expressed in Pericryptal Fibroblasts and Cancer-associated Fibroblasts in the Colon." Journal of Histochemistry & Cytochemistry 56, no. 8 (April 14, 2008): 753–64. http://dx.doi.org/10.1369/jhc.2008.951061.

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10

Agrawal, Khushboo, Viswanath Das, Natálie Táborská, Ján Gurský, Petr Džubák, and Marián Hajdúch. "Differential Regulation of Methylation-Regulating Enzymes by Senescent Stromal Cells Drives Colorectal Cancer Cell Response to DNA-Demethylating Epi-Drugs." Stem Cells International 2018 (August 12, 2018): 1–11. http://dx.doi.org/10.1155/2018/6013728.

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Анотація:
The advanced-stage colon cancer spreads from primary tumor site to distant organs where the colon-unassociated stromal population provides a favorable niche for the growth of tumor cells. The heterocellular interactions between colon cancer cells and colon-unassociated fibroblasts at distant metastatic sites are important, yet these cell-cell interactions for therapeutic strategies for metastatic colon cancer remain underestimated. Recent studies have shown the therapeutic potential of DNA-demethylating epi-drugs 5-azacytidine (AZA) and 5-aza-2′-deoxycytidine (DAC) for the treatment of solid tumors. While the effects of these epi-drugs alone or in combination with other anticancer therapies are well described, the influence of stromal cells and their secretome on cancer cell response to these agents remain elusive. In this study, we determined the effect of normal and senescent colon-unassociated fibroblasts and their conditioned medium on colorectal cancer (CRC) cell response to AZA and DAC using a cell-based DNA demethylation reporter system. Our data show that fibroblasts accelerate cell proliferation and differentially regulate the expression of DNA methylation-regulating enzymes, enhancing DAC-induced demethylation in CRC cells. In contrast, the conditioned medium from senescent fibroblasts that upregulated NF-κB activity altered deoxycytidine kinase levels in drug-untreated CRC cells and abrogated DAC effect on degradation of DNA methyltransferase 1. Similar to 2D cultures, senescent fibroblasts increased DNA demethylation of CRC cells in coculture spheroids, in addition to increasing the stemness of CRC cells. This study presents the first evidence of the effect of normal and senescent stromal cells and their conditioned medium on DNA demethylation by DAC. The data show an increased activity of DAC in high stromal cell cocultures and suggest the potential of the tumor-stroma ratio in predicting the outcome of DNA-demethylating epigenetic cancer therapy.
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Більше джерел

Дисертації з теми "Colon fibroblasts"

1

Davies, Paul Andrew. "Studies on the regulation of marrow fibroblast colony formation and differentiation." Thesis, University of Sheffield, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364241.

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2

胡, 興柏. "ACTIVATION OF FIBROBLAST-DERIVED MATRIX METALLOPROTEINASE-2 BY COLON CANCER CELLS IN NON-CONTACT CO-CULTURES." Doctoral thesis, Kyoto University, 2000. http://hdl.handle.net/2433/151419.

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Анотація:
京都大学
0048
新制・課程博士
博士(医学)
甲第8550号
医博第2272号
新制||医||747(附属図書館)
UT51-2000-M14
京都大学大学院医学研究科内科系専攻
(主査)教授 鍋島 陽一, 教授 月田 承一郎, 教授 千葉 勉
学位規則第4条第1項該当
Doctor of Medical Science
Kyoto University
DAM
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3

Bellomo, Alicia. "Contrôle de l’homéostasie des macrophages de la pulpe rouge splénique par une niche fibroblastique." Thesis, Aix-Marseille, 2020. http://www.theses.fr/2020AIXM0197.

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Situés dans les cordons de Billroth de la rate, les macrophages de la pulpe rouge (RPM) sont continuellement exposés au flux du sang. Leur fonction principale est d’éliminer les globules rouges sénescents et de recycler le fer contenu dans leur hémoglobine. Les cellules dites« stromales » sont des cellules de soutien qui constituent des niches pour les macrophages de différents organes. Au cours de mon travail de thèse, j’ai étudié les mécanismes qui régulent l'homéostasie des RPM en me focalisant sur la contribution des cellules stromales. En utilisant différentes techniques d’imagerie, j’ai révélé que les RPM sont enchâssés dans un réseau réticulaire de fibroblastes caractérisés par l'expression de la protéine de la tumeur de Wilm 1(WT1) et le facteur de stimulation des colonies de macrophages 1 (CSF1). La délétion conditionnelle du gène Csf1 dans les fibroblastes de la pulpe rouge exprimant WT1, mais pasdans les fibroblastes de la pulpe blanche, réduit drastiquement le nombre de RPM sans modifier le niveau de CSF1 circulant. Suite à la déplétion des RPM, les fibroblastes de la pulpe rougeproduisent de manière transitoire les facteurs chimiotactiques pour les monocytes CCL2 et CCL7et de fait contribuent à la reconstitution de la population de RPM. Ainsi, les fibroblastes de la pulpe rouge soutiennent et nourrissent les RPM, une fonction qui est vraisemblablement conservée chez l'homme
Located within red pulp cords, splenic red pulp macrophages (RPM) are constantly exposed tothe blood flow, clearing senescent red blood cells (RBC) and recycling iron from hemoglobin.Here, we studied the mechanisms underlying RPM homeostasis, focusing on the involvement ofstromal cells as these cells perform anchoring and nurturing macrophage niche functions inlymph nodes and liver. Microscopy revealed that RPM are embedded in a reticular meshwork ofred pulp fibroblasts characterized by the expression of Wilm’s Tumor 1 (WT1) and colonystimulating factor 1 (CSF1). Conditional deletion of Csf1 in WT1+ red pulp fibroblasts, but notwhite pulp fibroblasts, drastically altered the RPM network without altering circulating CSF1levels. Upon RPM depletion, red pulp fibroblasts transiently produced the monocytechemoattractants CCL2 and CCL7, thereby contributing to the replenishment of the RPMnetwork. Thus, red pulp fibroblasts anchor and nurture RPM, a function likely conserved inhumans
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4

Yu, Bei. "Basic fibroblast growth factor as a therapeutic target for chemosensitization in colorectal cancer." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1142882177.

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5

Dumortier, Jérôme. "Interactions épithélio-mésenchymateuses au cours du développement des tumeurs malignes digestives : étude expérimentale in vivo et in vitro." Lyon 1, 2000. http://www.theses.fr/2000LYO1T152.

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6

Manka, Margareta [Verfasser], and Florian [Akademischer Betreuer] Obermeier. "Modulation der Immunantwort von Colon Lamina Propria Fibroblasten bei Morbus Crohn durch Interleukin-33 / Margareta Manka. Betreuer: Florian Obermeier." Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/1037021347/34.

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7

Jordan, Grant R. "Regulation of the proliferation and osteogenic differentiation of colony forming units-fibroblastic derived from human bone marrow." Thesis, University of Bath, 1999. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323593.

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8

Mayr, Rebecca Anna [Verfasser], та Florian [Akademischer Betreuer] Obermeier. "GSK3-β – ein Modulator proinflammatorischer Prozesse in primären humanen Colon Lamina Propria Fibroblasten und in Kolonepithelzellen / Rebecca Anna Mayr. Betreuer: Florian Obermeier". Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/1037021282/34.

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9

Silva, David Ramos da [UNESP]. "Efeito do etanol na cicatrização do cólon distal do rato: estudo da força de ruptura, avaliação histológica, quantificação de fibroblastos e análise morfométrica sa área da cicatriz." Universidade Estadual Paulista (UNESP), 2001. http://hdl.handle.net/11449/88909.

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Анотація:
Made available in DSpace on 2014-06-11T19:23:40Z (GMT). No. of bitstreams: 0 Previous issue date: 2001Bitstream added on 2014-06-13T18:51:02Z : No. of bitstreams: 1 silva_dr_me_botfm.pdf: 2448429 bytes, checksum: 2109583be6db8fca687c468e5def8fe6 (MD5)
Este trabalho investigou o processo de reparação de uma ferida cirúrgica do cólon distal de ratos tratados com etanol. Foi utilizado o estudo da força de ruptura, avaliação histológica, quantificação de fibroblastos e análise morfométrica da área da cicatriz. Foram utilizados 126 ratos distribuídos por sorteio em 02 grupos: Grupo A1-controle e Grupo A2- etanol. Os animais do grupo A1 receberam ração e água “ad libitum” por 60 dias, após este período 12 animais foram sacrificados e submetidos ao estudo da força de ruptura. Os demais foram operados e submetidos a uma anastomose do cólon distal e estudados no 7o, 14o e 21o dias pósoperatório. Os animais do grupo A2 receberam ração e solução hidroalcoólica a 30% por 60 dias. Após este período foram submetidos ao mesmo procedimento do grupo controle; receberam ração e água no período pósoperatório, até o final do experimento. Verificou-se que a força de ruptura do segmento intestinal estudado foi menor em animais não operados tratados com etanol (A2M0) e, também foi menor nos animais tratados com etanol, operados e estudados no 14o dia pós-operatório (A2M2) quando comparados ao controle. A análise morfométrica da área da cicatriz demonstrou valores significantemente maiores nos animais tratados com etanol e estudados no 7o dia pós-operatório (A2M1) quando comparados ao controle...
This study investigated the healing process of a distal colon surgical wound in rats treated with ethanol. The rupture strength, histological evaluation, fibroblast quantification and morphometric analysis of the healing tissue were performed. One hundred and twenty-six rats were randomized into 2 groups: Group A1 – control group and Group A2 – ethanol group. Group A1 animals received food and water ad libidum for 60 days, after this period, 12 animals were sacrificed and underwent an evaluation of rupture strength. The remaining rats were operated and underwent distal colon anastomosis and were evaluated on the 7th /14th and 21st postoperative days. Group A2 animals received food and hydroalcoholic solution at 30% for 60 days. After this period they underwent the same procedure used for the control group. In the postoperative period they received food and water until the end of the investigation. It was observed that the rupture strength of the studied intestinal segment was lower in the animals which were not operated and treated with ethanol (A2T0). This strength was also lower in the animals which were operated and treated with ethanol evaluated on the 14th postoperative day (A2T2), when compared to the control group... (Complete abstract, click electronic access below)
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10

Silva, David Ramos da. "Efeito do etanol na cicatrização do cólon distal do rato estudo da força de ruptura, avaliação histológica, quantificação de fibroblastos e análise morfométrica sa área da cicatriz /." Botucatu : [s.n.], 2001. http://hdl.handle.net/11449/88909.

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Анотація:
Orientador: Shoiti Kobayasi
Resumo: Este trabalho investigou o processo de reparação de uma ferida cirúrgica do cólon distal de ratos tratados com etanol. Foi utilizado o estudo da força de ruptura, avaliação histológica, quantificação de fibroblastos e análise morfométrica da área da cicatriz. Foram utilizados 126 ratos distribuídos por sorteio em 02 grupos: Grupo A1-controle e Grupo A2- etanol. Os animais do grupo A1 receberam ração e água "ad libitum" por 60 dias, após este período 12 animais foram sacrificados e submetidos ao estudo da força de ruptura. Os demais foram operados e submetidos a uma anastomose do cólon distal e estudados no 7o, 14o e 21o dias pósoperatório. Os animais do grupo A2 receberam ração e solução hidroalcoólica a 30% por 60 dias. Após este período foram submetidos ao mesmo procedimento do grupo controle; receberam ração e água no período pósoperatório, até o final do experimento. Verificou-se que a força de ruptura do segmento intestinal estudado foi menor em animais não operados tratados com etanol (A2M0) e, também foi menor nos animais tratados com etanol, operados e estudados no 14o dia pós-operatório (A2M2) quando comparados ao controle. A análise morfométrica da área da cicatriz demonstrou valores significantemente maiores nos animais tratados com etanol e estudados no 7o dia pós-operatório (A2M1) quando comparados ao controle... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: This study investigated the healing process of a distal colon surgical wound in rats treated with ethanol. The rupture strength, histological evaluation, fibroblast quantification and morphometric analysis of the healing tissue were performed. One hundred and twenty-six rats were randomized into 2 groups: Group A1 - control group and Group A2 - ethanol group. Group A1 animals received food and water ad libidum for 60 days, after this period, 12 animals were sacrificed and underwent an evaluation of rupture strength. The remaining rats were operated and underwent distal colon anastomosis and were evaluated on the 7th /14th and 21st postoperative days. Group A2 animals received food and hydroalcoholic solution at 30% for 60 days. After this period they underwent the same procedure used for the control group. In the postoperative period they received food and water until the end of the investigation. It was observed that the rupture strength of the studied intestinal segment was lower in the animals which were not operated and treated with ethanol (A2T0). This strength was also lower in the animals which were operated and treated with ethanol evaluated on the 14th postoperative day (A2T2), when compared to the control group... (Complete abstract, click electronic access below)
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Частини книг з теми "Colon fibroblasts"

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Hendriks, T., K. M. L. C. Huyben, and M. F. W. C. Martens. "Regulatory Aspects of Collagen Synthesis in Fibroblasts from Human Colon and Skin." In Wound Healing and Skin Physiology, 245–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77882-7_22.

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Diecke, Sebastian, Leszek Lisowski, Nigel G. Kooreman, and Joseph C. Wu. "Second Generation Codon Optimized Minicircle (CoMiC) for Nonviral Reprogramming of Human Adult Fibroblasts." In Methods in Molecular Biology, 1–13. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1047-2_1.

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Valent, P., K. Geissler, P. Kalhs, P. Kier, and P. Bettelheim. "Fibroblast Colony Stimulating Activity of GM-CSF and IL-3 in Human Bone Marrow Cell Cultures." In Cytokines in Hemopoiesis, Oncology, and AIDS, 85–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75510-1_12.

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"Colony-Forming Fibroblastic Cells." In Encyclopedia of Systems Biology, 440. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_100227.

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Wernert, Nicolas. "15 Role of fibroblastic stroma in colon carcinoma." In Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma, 255–65. Elsevier, 2002. http://dx.doi.org/10.1016/s1874-5784(02)80031-9.

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Zielinska, Aleksandra, Magorzata Latocha, Magdalena Jurzak, and Dariusz Kusmierz. "Expression of Matrix Metalloproteinases and Theirs Tissue Inhibitors in Fibroblast Cultures and Colo-829 and SH-4 Melanoma Cultures After Photodynamic Therapy." In Recent Advances in the Biology, Therapy and Management of Melanoma. InTech, 2013. http://dx.doi.org/10.5772/54935.

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Тези доповідей конференцій з теми "Colon fibroblasts"

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FARINON, MIRIAN, PATRÍCIA GNIESLAW OLIVEIRA, MONICA GUMA, and RICARDO MACHADO XAVIER. "THE ROLE OF GASTRIN-RELEASING PEPTIDE IN MYOFIBROBLAST ACTIVATION OF COLON FIBROBLASTS." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-593.

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Fénié, Nicolas, Claudine Bertrand, Aurélien Lacombe, Serge Roche, Corinne Bousquet, Valérie Gouazé-Andersson, Christine Toulas, Elizabeth Moyal, and Audrey Ferrand. "Abstract B16: Progastrin activates colon fibroblasts and participates to the dialogue between tumor epithelial cells and stromal fibroblasts in colorectal cancer." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b16.

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Cheng, KL, CC Chen, and KC Yang. "PO-299 Aberrant TXNDC5 expression in colon stromal fibroblasts promotes colorectal cancer carcinogenesis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.812.

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Modis, Katalin, Manjit Maskey, Paul Johnson, Csaba Szabo, Mark R. Hellmich, and Celia Chao. "Abstract 2980: Cystathionine-beta-synthase (CBS)-derived hydrogen sulfide (H2S) supports proliferation, migration and bioenergetics in colon cancer-associated fibroblasts (CAFs)." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2980.

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Kitagawa, H., N. Yamamoto, G. Kosaki, and H. Yamazaki. "AN IMPORTANT ROLE OF CARBOHYDRATE MOIETIES ON CANCER CELL MEMBRANE GLYCOPROTEINS IN CANCER CELL-INDUCED PLATELET AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644667.

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Platelet aggregation induced by cancer cells may be an essential process in the development of hematogenous metastasis of cancers. A mechanism in HMV-I (human vaginal melanoma cell line)-induced platelet aggregation was studied by using monoclonal antibodies against membrane proteins of cancer cells or platelets. HMV-I cells or their membrana ractions induced platelet aggregation of human heparinized PRP, to which hirudin had no inhibitory effect. The platelet aggregation by HMV-I was completely lost after the pretreatment of the cells with 0.3U/ml neuraminidase for 60 min at 37°C. Preincubation of platelets with monoclonal antibodies against platelet GP lb or GP Ilb/lIIa inhibited HMV-I induced aggregation. A monoclonal antibody MB3 (igM) against another human melanoma (HMMB) which had been transplanted in nude mice was produced by hybridoma technique. Screening studies by cell binding ELISA revealed that MB3 antibody reacted with not only HMMB cells but also many other cells including HMV-I, M7609 (colon carcinoma cell line) and normal fibroblasts. Western-blot analyses showedthat MB3 antibody reacted with multiple, more than ten, proteins with molecular weights ranging from UO to 200 kDa in unreduced SDS-PAGE of HMV-I, HMMB or M7609. In contrast, when .these cells pretreated with neuraminidase were used in Western-blot, MB3 reactivity were all lost. MB3 reacted with at least three glycoproteins of human red cell membrane in Western-blot, but it did not react with human platelets. Immune adherent asgay with trypsin-treated HMV-I or HMMB cells as target cells showed negative reactivity. MB3 antibody inhibited HMV-I-induced aggregation of platelets, but did not inhibit M7609-induced aggregation which depended on thrombin generation.These results suggest that MB3 antibody may be against sialic acid-containing carbohydrate moieties of membrane glycoproteins on these cancercells and that the carbohydrate(s) may play a critical role in' cancer cell-platelet interaction.
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Irene, Gomez, Martin Paloma, Herrera Mercedes, Martinez Esther, Herrera Alberto, garcia Vanesa, Silva javier, et al. "Abstract 1298:TWIST1is expressed by cells with fibroblastic phenotype in colon carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1298.

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Jumanov, I. I., R. A. Safarov, and O. I. Djumanov. "Error Control of Identification and Filtering of Micro-Object Images." In III All-Russian Scientific Conference with International Participation "Science, technology, society: Environmental engineering for sustainable development of territories". Krasnoyarsk Science and Technology City Hall, 2022. http://dx.doi.org/10.47813/nto.3.2022.6.109-124.

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Researched and developed scientifically and methodologically foundations for optimal identification of micro-objects using traditional and Gaussian filtering, median filter, filters based on fast Fourier transform, wavelet transforms, shift transforms, mechanisms using geometric, specific features, statistical, dynamic properties of image information. Mechanisms for optimizing the identification of micro-objects are proposed that have advantages in reducing the complexity and laboriousness of analyzing the structure and processing information, identifying and segmentation of the image contour, using the dynamics of growth, visual differentiation, extracting internal features and properties, approximation, smoothing, and interpretation of objects. A mechanism has been investigated and implemented that performs the following functions: aligns histology slices; finds contours of objects, a set of levels, thresholds, combines segmentation, conducts registrations, forms a search graph, performs approximations based on a wavelet, shear, and other transformations, determines parameters, performs color coding and color visualization of micro-objects. The implementations of algorithms and software modules of the software complex for identification, recognition and classification of micro-objects, in particular, cellular elements of the inflammatory series (fibroblasts, fibrocytes) of lung disease, have been tested. The signs of chronic inflammation were assessed - the presence of giant cells. A software package for visualization, recognition, classification of images of pollen grains has been developed, the implementations of which have been tested taking into account the conditions of a priori insufficiency, parametric uncertainty and nonstationarity of processes.
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McCorry, Amy M., Niamh A. Leonard, Rene Jackstadt, Dustin J. Flanagan, Owen J. Sansom, Tim Maughan, Simon Leedham, et al. "Abstract 3867: STAT1-related antigen processing and presentation dictates prognosis in the fibroblast-rich subtype of stage II/III colon cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3867.

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Woo, Jong Kyu, Ju-Hee Kang, Keumju Shin, Seong-Won Song, Jung Ju Kim, Sang-Jin Lee, and Seung Hyun Oh. "Abstract A15: Humanized anti-hepatocyte growth factor (HGF) antibody, suppresses innate irinotecan resistance induced by fibroblast-derived HGF in colon cancer cells." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a15.

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Suetsugu, Atsushi, Masashi Momiyama, Yosuke Osawa, Hisataka Moriwaki, Michael Bouvet, Shigetoyo Saji, and Robert M. Hoffman. "Abstract 2688: Color-coded imaging of the pre-metastatic niche in the lung and liver indicates the involvement of cancer-associated fibroblasts." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2688.

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Звіти організацій з теми "Colon fibroblasts"

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Sadot, Einat, Christopher Staiger, and Zvi Kam Weizmann. functional genomic screen for new plant cytoskeletal proteins and the determination of their role in actin mediated functions and guard cells regulation. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7587725.bard.

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Анотація:
The original objectives of the approved proposal were: 1. To construct a YFP fused Arabidopsis cDNA library in a mammalian expression vector. 2. To infect the library into a host fibroblast cell line and to screen for new cytoskeletal associated proteins using an automated microscope. 3. Isolate the new genes. 4. Characterize their role in plants. The project was approved as a feasibility study to allow proof of concept that would entail building the YFP library and picking up a couple of positive clones using the fluorescent screen. We report here on the construction of the YFP library, the development of the automatic microscope, the establishment of the screen and the isolation of positive clones that are plant cDNAs encoding cytoskeleton associated proteins. The rational underling a screen of plant library in fibroblasts is based on the high conservation of the cytoskeleton building blocks, actin and tubulin, between the two kingdoms (80-90% homology at the level of amino acids sequence). In addition, several publications demonstrated the recognition of mammalian cytoskeleton by plant cytoskeletal binding proteins and vice versa. The major achievements described here are: 1. The development of an automated microscope equipped with fast laser auto-focusing for high magnification and a software controlling 6 dimensions; X, Y position, auto focus, time, color, and the distribution and density of the fields acquired. This system is essential for the high throughput screen. 2. The construction of an extremely competent YFP library efficiently cloned (tens of thousands of clones collected, no empty vectors detected) with all inserts oriented 5't03'. These parameters render it well representative of the whole transcriptome and efficient in "in-frame" fusion to YFP. 3. The strategy developed for the screen allowing the isolation of individual positive cDNA clones following three rounds of microscopic scans. The major conclusion accomplished from the work described here is that the concept of using mammalian host cells for fishing new plant cytoskeletal proteins is feasible and that screening system developed is complete for addressing one of the major bottlenecks of the plant cytoskeleton field: the need for high throughput identification of functionally active cytoskeletal proteins. The new identified plant cytoskeletal proteins isolated in the pilot screen and additional new proteins which will be isolated in a comprehensive screen will shed light on cytoskeletal mediated processes playing a major role in cellular activities such as cell division, morphogenesis, and functioning such as chloroplast positioning, pollen tube and root hair elongation and the movement of guard cells. Therefore, in the long run the screen described here has clear agricultural implications.
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