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Статті в журналах з теми "Mesenchyme Cytology"
Vagholkar, Ketan, Isha Bhatnagar, and Suvarna Vagholkar. "Giant lipoma over the back." International Surgery Journal 9, no. 3 (February 28, 2022): 687. http://dx.doi.org/10.18203/2349-2902.isj20220646.
Повний текст джерелаPermi, Harish S., Shetty K. Padma, Supriya Rai, Lakshmi Manjeera, Neetha Poojary, and Teerthanath S. "AN UNUSUAL CYTOLOGICAL EXPERIENCE OF VIRILISING OVARIAN SERTOU-LEYDIG CELL TUMOR - A RARE CASE REPORT." Journal of Health and Allied Sciences NU 03, no. 01 (March 2013): 63–65. http://dx.doi.org/10.1055/s-0040-1703636.
Повний текст джерелаKondapalli, Ananya, Lucas Redd, Lorraine DeBlanche, and Yin Oo. "Primary angiosarcoma of thyroid." BMJ Case Reports 12, no. 6 (June 2019): e228862. http://dx.doi.org/10.1136/bcr-2018-228862.
Повний текст джерелаReardon, J. D., B. S. Hatfield, A. O. Kraft, and S. C. Smith. "Gastroblastoma: Cytologic Findings with Resection and Molecular Correlation." American Journal of Clinical Pathology 154, Supplement_1 (October 2020): S125—S126. http://dx.doi.org/10.1093/ajcp/aqaa161.275.
Повний текст джерелаRyan, Mitchell. "Cytology and Mesenchymal Pathology:How Far Will We Go?" American Journal of Clinical Pathology 106, no. 5 (November 1, 1996): 561–64. http://dx.doi.org/10.1093/ajcp/106.5.561.
Повний текст джерелаGupta, Ruchika, Sugandha Sharma, Sarika Verma, Lavleen Singh, Chhabi R. Gupta, and Sanjay Gupta. "Pediatric fine-needle aspiration cytology: An audit of 266 cases of pediatric tumors with cytologic-histologic correlation." Cytojournal 17 (November 2, 2020): 25. http://dx.doi.org/10.25259/cytojournal_101_2019.
Повний текст джерелаIpek, Volkan, I. Taci Cangul, and Ahmet Akkoc. "Comparative Evaluation of the Cytological, Histopathological and Immunohistochemical Findings of Canine Cutaneous and Subcutaneous Masses." Acta Veterinaria 71, no. 1 (March 1, 2021): 61–84. http://dx.doi.org/10.2478/acve-2021-0005.
Повний текст джерелаFriciello Teixeira, Rodrigo Hidalgo, André Luiz Mota da Costa, Nathália Diez Murollo, Paolla Nicole Franco, Daniel Angelo Felippi, and Caio Henrique Paganini Burini. "Fibrossarcoma in a jaguar (Panthera onca): thermography associated with aspiration cytology as diagnostic tools." Clínica Veterinária XXII, no. 126 (January 1, 2017): 72–78. http://dx.doi.org/10.46958/rcv.2017.xxii.n.126.p.72-78.
Повний текст джерелаShivamurthy, Archana, and Padmapriya Jaiprakash. "Role of imprint cytology in the diagnosis of ovarian neoplasms." Indian Journal of Pathology and Oncology 8, no. 3 (August 15, 2021): 320–26. http://dx.doi.org/10.18231/j.ijpo.2021.064.
Повний текст джерелаFelizzola, Cláudia Ronca, Angelo João Stopiglia, and Ney Soares de Araújo. "Oral tumors in dogs: clinical aspects, exfoliative cytology and histopathology." Ciência Rural 29, no. 3 (September 1999): 499–506. http://dx.doi.org/10.1590/s0103-84781999000300020.
Повний текст джерелаДисертації з теми "Mesenchyme Cytology"
Gaboury, Louis A. "Studies of the role of mesenchymal cells in the regulation of hemopoiesis." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28784.
Повний текст джерелаMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Lavado, Andrea Sofia Caetano das Neves. "Porphyrinic-nanoplatforms : controlled intracellular generation of reactive oxygen species in human mesenchymal stem cells." Thesis, University of Nottingham, 2014. http://eprints.nottingham.ac.uk/14200/.
Повний текст джерелаEbrahim, Neven. "Cellular and molecular mechanisms underlying extravasation of human Wharton's jelly mesenchymal stem cells across fetal and adult endothelial cell monolayers." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/33246/.
Повний текст джерелаTang, Ruizhi. "Primary cilia on colonic mesenchymal cells regulate DSS-induced colitis and inflammation associated colon carcinogenesis." Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT020/document.
Повний текст джерелаGlycylation, a posttranslational modification of microtubules, is crucial in the maintenance of PC. Our group previously identified an unexpected role of the tubulin glycylase TTLL3 in the regulation of colon homeostasis and tumorigenesis. Specifically, a decreased number of primary cilia (PC) was observed in mice deficient for the glycylase TTLL3, which is the only glycyclase expressed in the colon. TTLL3-/- mice display no obvious abnormalities in the steady state. However, when exposed to chemically induced colon carcinogenesis, TTLL3-/- mice are more susceptible to tumor formation. Importantly, TTLL3 expression levels were significantly downregulated in human primary colorectal carcinomas and metastases as compared to healthy colon tissue, suggesting a link between TTLL3 regulation of PC and colorectal cancer development.The aim of my thesis project was to explore the relation of PC and colon carcinogenesis. In fact, I could demonstrate that the number of PC decreases during chemically induced colon carcinogenesis in mice. Notably, I discovered that PC in the colon are mostly expressed by fibroblasts. To better characterize the role of PC in murine colon, I studied the consequences of a loss of PC in intestinal fibroblasts. For this, I used two independent ciliary conditional knockout mice, kinesin-3A (Kif3A) and intraflagellar transport 88 (Ift88), both essential for cilia formation. Specific deletion in intestinal fibroblasts is obtained by crossing with colVI-cre transgenic mice. Though the colVI promoter is only active in a subset of colonic mesenchymal cells I found that the decreased number of PC in colonic mesenchymal cells promotes chemically induced colitis and carcinogenesis. RNAseq on isolated colonic mesenchymal cells of mutant mice suggests a triggering of Wnt and Notch signaling in ColVIcre-Kif3aflx/flx mice. We are presently validating these findings by qPCR and immunohistochemistryTaken together, I discovered that PC are expressed by at least a subset of colonic mesenchymal cells, which has not been described before. Decreased numbers of those PC renders mice more susceptible to colitis and colitis associated carcinogenesis
Aksoy, Ceren. "Characterization And Identification Of Human Mesenchymal Stem Cells At Molecular Level." Phd thesis, METU, 2012. http://etd.lib.metu.edu.tr/upload/12614272/index.pdf.
Повний текст джерелаDostert, Gabriel. "Les nanovésicules extracellulaires sécrétées par les CSMs et les nanovésicules de synthèse issues d’agro-ressources : de leur caractérisation à leur utilisation en ingénierie tissulaire." Thesis, Université de Lorraine, 2017. http://www.theses.fr/2017LORR0097/document.
Повний текст джерелаNanoscale extracellular vesicles (nEVs) derived from mesenchymal stem cells (MSCs) and synthetic nanovesicles are at the centre of many research studies for the development of new therapeutic strategies in regenerative medicine. A standardized method was used to isolate nEVs from conditioned media of CSMs and to characterize them. We focused on their size with a range of 30 to 150 nm and the presence of some of their membrane markers (CD9, CD63 and CD81). During this work, two isolation methods were tested. The results obtained by the physical (Nanosight®, transmission electron microscopy) and biological (flow cytometry) analyses of the different samples allowed to standardize the method of isolation of the nEVs by successive centrifugation and ultracentrifugation. Then, we studied the use of these nEVs derived from MSCs in cell culture. Interactions between these nEVs and endothelial cells (ECs) have been demonstrated in vitro. These interactions lead to changes in the cellular behaviour of ECs by increasing their potential to form vascular networks. In parallel of this work on nEVs, we studied the use of synthetic nanovesicles, called nanoliposomes (NLPs) prepared from agro-resource derived lecithin (salmon) as TGF-β1 transporters for applications in regenerative medicine. After their physicochemical characterization, this preliminary study showed that these NLPs do not exhibit cytotoxicity for MSCs in vitro. There is an important potential for the use of nEVs derived from MSCs as well as NLPs to develop new cell-free therapy innovative strategies in the field of regenerative medicine
Keller, Laetitia. "Ressources cellulaires mésenchymateuses pour l'ingénierie de l'organe dentaire." Phd thesis, Université de Strasbourg, 2012. http://tel.archives-ouvertes.fr/tel-00766865.
Повний текст джерелаSantos, Luis. "Cell Mechanics Regulate Mesenchymal Stem Cell Morphology and T Cell Activation." Thesis, 2014. https://doi.org/10.7916/D8K64G7T.
Повний текст джерелаWobma, Holly Michelle. "Interferon-gamma/Hypoxia Primed Mesenchymal Stem Cells for an Improved Immunosuppressive Cell Therapy." Thesis, 2018. https://doi.org/10.7916/D8ZC9K1D.
Повний текст джерела"Roles of CRBP1, N-cadherin and SOX11 in differentiation and migration of bone marrow-derived mesenchymal stem cells." 2012. http://library.cuhk.edu.hk/record=b5549603.
Повний текст джерела方法:培養的骨髓間充質幹細胞來源於6-8周大小的SD大鼠。細胞的表型經過多分化潛能測試(成骨分化,成脂分化和成軟骨分化)和流式細胞儀檢驗。克隆大鼠的CRBP1, N-cadherin和SOX11基因到慢病毒載體。而且還設計了針對CRBP1和 N-cadherin的shRNA及非特異性對照shRNA。慢病毒由暫態轉染293FT細胞產生。細胞遷移實驗採用了BD Falcon的細胞遷移系統(cell culture insert)。實驗採用了定量PCR、免疫共沉澱、western雜交和雙螢光報告檢驗。對於體內實驗,細胞經感染帶有不同基因的病毒後,種植到Si-TCP材料並移植到裸鼠皮下。8周後,收集樣品進行組織學和免疫組織學分析。最後,我們建立了大鼠的股骨開放式骨折模型,並在4天后將SOX11基因修飾的間充質幹細胞通過心臟注射打到大鼠體內。4周後,收集股骨骨折樣品並進行microCT、力學測試和組織學分析。
結果:CRBP1過表達能夠促進骨髓間充質幹細胞的成骨分化潛能,並能抑制其成脂分化。進一步的機理研究表明CRBP1可以通過與RXRα的蛋白相互作用抑制RXRα誘導的β-catenin降解,從而維持β-catenin和磷酸化-ERK1/2在較高的水準,導致間充質幹細胞成骨能力增強;N-cadherin過表達可以促進間充質幹細胞的遷移,但是卻通過下調β-catenin和磷酸化ERK1/2抑制其成骨分化。過表達SOX11可以通過增強BMP信號通路促進三系分化。SOX11還可以通過啟動CXCR4的表達來促進細胞遷移。最後,在大鼠的股骨開放骨折模型上通過系統注射,我們證明穩定過表達SOX11的間充質幹細胞遷移到骨折部位的數量明顯增加。這些細胞到達骨折部位以後可以起始骨痂的鈣化,促進骨折的修復。
結論:本研究證明CRBP1, N-cadherin 和SOX11具有調節骨髓間充質幹細胞遷移和/或分化的功能。這些基因也許會成為幹細胞治療的新靶點。系統注射SOX11基因修飾的骨髓間充質幹細胞對於骨折修復可能具有較好的療效。本研究初步研究了CRBP1, N-cadherin 和SOX11在間充質幹細胞中的作用,為探討以間充質幹細胞為基礎的組織工程的某些新臨床應用提供了一些線索。
Introduction: Mesenchymal stem cells (MSCs) can be easily harvested, expanded, and have the capability of differentiating into osteoblasts, chondrocytes and adipocytes, and they can home to various tissues in response to stimuli such as inflammation, infection and injuries. MSCs are therefore valuable cell source for musculoskeletal tissue engineering. Peripheral blood-derived MSCs (PB-MSCs) are one kind of MSCs that reside in peripheral blood, whereas the main source of MSCs is bone marrow-derived MSCs (BM-MSCs). In our previous study, we found many genes were differentially expressed in the PB-MSCs compared to their counterpart BM-MSCs demonstrated by microarray analysis, among which the effects of CRBP1, SOX11 and N-cadherin on MSCs in terms of migration and differentiation are studied.
Methods: BM-MSCs and PB-MSCs were cultured from 6-8 weeks SD rats. The phenotypes of MSCs were characterized by tri-lineage (adipo-, osteo- and chondrogenic) differentiation and flow cytometry analysis. The genes encoding rat CRBP1, SOX11 and N-cadherin were cloned into lentiviral vectors respectively. shRNAs targeting CRBP1, N-cadherin, and one nonspecific shRNA were designed. Pseudo-lentivirus was produced by transient transfection of 293FT cells. Cell migration was examined using transwell insert culture system. Quantitative RT-PCR, CO-IP, western blot and dual-luciferase assay were employed in the studies. For in vivo study, MSCs transduced with different genes were seeded on Si-TCP scaffolds and implanted subcutaneously in nude mice. 8 weeks later, the samples were collected for histological and immunohistological analysis. Finally, an open femoral fracture model was established in 8-week old SD rats, SOX11-modified MSCs were injected at four days after fracture. At 4-week after MSCs injection, the femurs were collected for microCT, mechanical test and histological analysis.
Results: For CRBP1gene, our results showed that CRBP1 overexpression promoted osteogenic differentiation of BM-MSCs, while inhibited their adipogenic differentiation. We demonstrated that CRBP1 promoted osteogenic differentiation by inhibiting RXRα-induced β-catenin degradation through physical interactions, and maintaining β-catenin and pERK1/2 at higher levels. For N-cadherin gene, we found that N-cadherin overexpression promoted MSCs migration, and suppressed osteogenic potential of MSCs through inhibiting ERK and β-catenin signaling pathways. For SOX11 gene, we demonstrated that SOX11 overexpression enhanced the adipo-, osteo- and chondrogenic differentiation of BM-MSCs, through enhancing BMP signaling pathways. The migration capacity of BM-MSCs was also enhanced when Sox-11 was overexpressed, through activating CXCR4 expression. Finally, in the open femur fracture model we demonstrated that a larger number of SOX11-overexpressing BM-MSCs migrated to the fracture site, initiated earlier callus ossification and improved bone fracture healing quality.
Conclusions: This study demonstrated that CRBP1, N-cadherin and SOX11 gene can regulate the migration and/or differentiation potentials of BM-MSCs. These genes may become new therapeutic targets in stem cell therapy applications. Systemic administration of genetically modified SOX11-overexpressing BM-MSCs may be useful in promoting fracture healing. Overall, this study defined some unknown functions of CRBP1, N-cadherin and SOX11 in MSCs and shed the lights on some novel therapeutic implications for MSCs-based tissue engineering.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Xu, Liangliang.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2012.
Includes bibliographical references (leaves 128-144).
Abstract also in Chinese.
Declaration --- p.i
Abstract --- p.ii
摘要 --- p.v
Acknowledgements --- p.vii
Chapter 1 --- p.1
Introduction --- p.1
Chapter 1.1 --- Mesenchymal stem cells --- p.2
Chapter 1.1.1 --- Characteristics of mesenchymal stem cells --- p.2
Chapter 1.1.2 --- Bone marrow- and peripheral blood-derived MSCs --- p.4
Chapter 1.1.3 --- Other tissue-derived MSCs --- p.5
Chapter 1.2 --- Adipogenesis of MSCs --- p.6
Chapter 1.3 --- Chondrogenesis of MSCs --- p.7
Chapter 1.4 --- Osteogenesis of MSCs --- p.8
Chapter 1.4.1 --- Regulators of osteogenesis --- p.9
Chapter 1.4.2 --- Stratergies for improving bone tissue engineering --- p.11
Chapter 1.5 --- Signaling pathways involved in osteogenesis --- p.13
Chapter 1.5.1 --- ERK signaling pathway --- p.14
Chapter 1.5.2 --- Wnt signaling pathway --- p.15
Chapter 1.5.3 --- BMP signaling pathway --- p.17
Chapter 1.6 --- Migration of MSCs --- p.20
Chapter 1.7 --- Fracture healing --- p.22
Chapter 1.8 --- Clinical application of MSCs --- p.23
Chapter 1.8.1 --- BM-MSCs vs. PB-MSCs --- p.24
Chapter 1.8.2 --- Autologous vs. Allogeneic MSCs transplantation --- p.25
Chapter 1.9 --- Scope of the present study --- p.26
Chapter 1.9.1 --- CRBP1 --- p.26
Chapter 1.9.2 --- N-cadherin --- p.27
Chapter 1.9.3 --- SOX11 --- p.27
Chapter 1.10 --- Experimental scheme --- p.29
Chapter 2 --- p.31
Comparison between PB-MSCs and BM-MSCs --- p.31
Chapter 2.1 --- Chapter introduction --- p.32
Chapter 2.2 --- Materials and methods --- p.33
Chapter 2.2.1 --- Cell culture --- p.33
Chapter 2.2.2 --- Flow cytometry --- p.33
Chapter 2.2.3 --- Adipogenic differentiation --- p.34
Chapter 2.2.4 --- Osteogenic differentiation --- p.34
Chapter 2.2.5 --- RNA Extraction and Real-time PCR --- p.34
Chapter 2.3 --- Results --- p.35
Chapter 2.3.1 --- Morphology of PB-MSCs --- p.35
Chapter 2.3.2 --- Cellular surface markers of BM-MSCs and PB-MSCs --- p.36
Chapter 2.3.3 --- Multi-differentiation potential of BM-MSCs and PB-MSCs --- p.38
Chapter 2.3.4 --- Target genes expression in BM-MSCs and PB-MSCs --- p.39
Chapter 2.4 --- Discussion and future work --- p.40
Chapter 3 --- p.41
Role of CRBP1 in Differentiation and Migration of MSCs --- p.41
Chapter 3.1 --- Chapter introduction --- p.42
Chapter 3.2 --- Materials and methods --- p.46
Chapter 3.2.1 --- Chemicals --- p.46
Chapter 3.2.2 --- Isolation and culture of BM-MSCs --- p.46
Chapter 3.2.3 --- RNA Extraction and Real-time PCR --- p.47
Chapter 3.2.4 --- Plasmid construction, transfection, production of lentivirus and infection --- p.48
Chapter 3.2.5 --- Osteogenic differentiation --- p.50
Chapter 3.2.6 --- Adipogenic differentiation --- p.50
Chapter 3.2.7 --- Western blot --- p.51
Chapter 3.2.8 --- Immunofluorescence labeling and fluorescence microscopy --- p.52
Chapter 3.2.9 --- Cell migration assay --- p.52
Chapter 3.2.10 --- Ectopic bone formation assay --- p.52
Chapter 3.2.11 --- Statistical analysis --- p.53
Chapter 3.3 --- Results --- p.53
Chapter 3.3.1 --- Transducing BM-MSCs with lentivirus carrying CRBP1 or shRNAs --- p.53
Chapter 3.3.2 --- CRBP1 accelerates osteogenesis of BM-MSCs via enhancing ERK1/2 and β-catenin pathways --- p.56
Chapter 3.3.3 --- CRBP1 stabilizes β-catenin by inhibiting RXRα-induced degradation --- p.58
Chapter 3.3.4 --- CRBP1 inhibits adipogenesis of BM-MSCs --- p.61
Chapter 3.3.5 --- CRBP1 overexpression has no effect on MSCs migration potential --- p.63
Chapter 3.3.6 --- CRBP1 promotes ectopic bone formation in vivo --- p.64
Chapter 3.4 --- Discussion --- p.66
Chapter 3.5 --- Future work --- p.73
Chapter 4 --- p.74
Role of N-cadherin in Differentiation and Migration of MSCs --- p.74
Chapter 4.1 --- Chapter introduction --- p.75
Chapter 4.2 --- Materials and methods --- p.78
Chapter 4.2.1 --- Chemicals --- p.78
Chapter 4.2.2 --- Isolation and culture of BM-MSCs --- p.78
Chapter 4.2.3 --- Plasmid construction, transfection, production of lentivirus and infection --- p.79
Chapter 4.2.4 --- Osteogenic differentiation and ALP activity assay --- p.81
Chapter 4.2.5 --- Western blot --- p.81
Chapter 4.2.6 --- Ectopic bone formation assay --- p.82
Chapter 4.2.7 --- Statistical analysis --- p.82
Chapter 4.3 --- Results --- p.83
Chapter 4.3.1 --- Expression of N-cadherin during osteogenesis in MSCs --- p.83
Chapter 4.3.2 --- N-cadherin overexpression inhibits osteogenesis through suppressing β-catein and ERK1/2 signaling pathways --- p.84
Chapter 4.3.3 --- N-cadherin silencing increases osteogenesis through enhancing β-catenin and ERK1/2 signaling pathways --- p.86
Chapter 4.3.4 --- N-cadherin promotes migration of MSCs --- p.87
Chapter 4.3.5 --- Cellular surface markers of SV40-immortalized MSCs --- p.89
Chapter 4.3.6 --- N-cadherin inhibits ectopic bone formation in vivo --- p.89
Chapter 4.4 --- Discussion --- p.91
Chapter 4.5 --- Future work --- p.94
Chapter 5 --- p.96
Role of SOX11 in Differentiation and Migration of MSCs --- p.96
Chapter 5.1 --- Chapter introduction --- p.97
Chapter 5.2 --- Materials and methods --- p.105
Chapter 5.2.1 --- Plasmid construction, transfection, production of lentivirus and infection --- p.105
Chapter 5.2.2 --- Cell culture --- p.106
Chapter 5.2.3 --- Luciferase reporter gene assay --- p.106
Chapter 5.2.4 --- Osteogenic differentiation and ALP activity assay --- p.106
Chapter 5.2.5 --- Adipogenic differentiation --- p.107
Chapter 5.2.5 --- Chondrogenic diffferentiation --- p.107
Chapter 5.2.6 --- Western blot --- p.108
Chapter 5.2.7 --- RNA Extraction and Real-time PCR --- p.108
Chapter 5.2.8 --- Cell migration --- p.110
Chapter 5.2.9 --- Ectopic bone formation --- p.110
Chapter 5.2.10 --- Fracture healing model and analysis --- p.111
Chapter 5.2.11 --- Statistical Analysis --- p.112
Chapter 5.3 --- Results --- p.112
Chapter 5.3.1 --- SOX11 is upregulated during osteogenesis of BM-MSCs --- p.112
Chapter 5.3.2 --- SOX11 promotes adipogenesis in BM-MSCs --- p.113
Chapter 5.3.3 --- SOX11 promotes migration of BM-MSCs --- p.114
Chapter 5.3.4 --- SOX11 promotes osteogenesis in BM-MSCs --- p.115
Chapter 5.3.5 --- SOX11 promotes chondrogenesis of MSCs --- p.117
Chapter 5.3.6 --- Mechanisms of how SOX11 regulates differentiation and migration of MSCs --- p.118
Chapter 5.3.7 --- SOX11-modified MSCs promote bone fracture healing in an open femur fracture rat model --- p.122
Chapter 5.4 --- Discussion --- p.126
Chapter 5.5 --- Future work --- p.131
Appendix --- p.153
Книги з теми "Mesenchyme Cytology"
Pierre, Savagner, ed. Rise and fall of epithelial phenotype: Concepts of epithelial-mesenchymal transition. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2005.
Знайти повний текст джерелаPham, Phuc Van. Liver, lung and heart regeneration. Cham: Springer, 2017.
Знайти повний текст джерелаGarcía, Mariana, and Marcela Bolontrade. Mesenchymal Stromal Cells As Tumor Stromal Modulators. Elsevier Science & Technology Books, 2016.
Знайти повний текст джерелаGarcía, Mariana, and Marcela Bolontrade. Mesenchymal Stromal Cells As Tumor Stromal Modulators. Elsevier Science & Technology Books, 2016.
Знайти повний текст джерелаSavagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer London, Limited, 2008.
Знайти повний текст джерелаSavagner, Pierre. Rise and Fall of Epithelial Phenotype: Concepts of Epithelial-Mesenchymal Transition. Springer, 2010.
Знайти повний текст джерелаViswanathan, Sowmya, and Hematti Peiman. Mesenchymal Stromal Cells: Translational Pathways to Clinical Adoption. Elsevier Science & Technology Books, 2016.
Знайти повний текст джерелаViswanathan, Sowmya, and Hematti Peiman. Mesenchymal Stromal Cells: Translational Pathways to Clinical Adoption. Elsevier Science & Technology Books, 2016.
Знайти повний текст джерелаJ, Prockop Darwin, Phinney Donald G, and Bunnell Bruce A, eds. Mesenchymal stem cells: Methods and protocols. Totowa, NJ: Humana Press, 2008.
Знайти повний текст джерелаBunnell, Bruce A., Darwin J. Prockop, and Donald G. Phinney. Mesenchymal Stem Cells: Methods and Protocols. Humana Press, 2010.
Знайти повний текст джерелаЧастини книг з теми "Mesenchyme Cytology"
Cian, F., and P. Monti. "Mesenchymal tumours and other neoplasms." In Differential diagnosis in small animal cytology: the skin and subcutis, 124–67. Wallingford: CABI, 2019. http://dx.doi.org/10.1079/9781786392251.0124.
Повний текст джерела"Mesenchymal, Non-Meningothelial Tumors." In Atlas of CSF Cytology, edited by Harald Kluge, Valentin Wieczorek, Ernst Linke, Klaus Zimmermann, Stefan Isenmann, and Otto W. Witte. Stuttgart: Georg Thieme Verlag, 2007. http://dx.doi.org/10.1055/b-0034-62572.
Повний текст джерела"Benign and Malignant Mesenchymal Tumours and Miscellaneous Lesions." In Monographs in Clinical Cytology, 106–14. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000061546.
Повний текст джерелаYoshizato, Katsutoshi. "Molecular Mechanism and Evolutional Significance of Epithelial–Mesenchymal Interactions in the Body‐ and Tail‐Dependent Metamorphic Transformation of Anuran Larval Skin." In International Review of Cytology, 213–60. Elsevier, 2007. http://dx.doi.org/10.1016/s0074-7696(06)60005-3.
Повний текст джерела