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Ito, T., N. Udaka, T. Yazawa, K. Okudela, H. Hayashi, T. Sudo, F. Guillemot, R. Kageyama, and H. Kitamura. "Basic helix-loop-helix transcription factors regulate the neuroendocrine differentiation of fetal mouse pulmonary epithelium." Development 127, no. 18 (September 15, 2000): 3913–21. http://dx.doi.org/10.1242/dev.127.18.3913.
To clarify the mechanisms that regulate neuroendocrine differentiation of fetal lung epithelia, we have studied the expression of the mammalian homologs of achaete-scute complex (Mash1) (Ascl1 - Mouse Genome Informatics); hairy and enhancer of split1 (Hes1); and the expression of Notch/Notch-ligand system in the fetal and adult mouse lungs, and in the lungs of Mash1- or Hes1-deficient mice. Immunohistochemical studies revealed that Mash1-positive cells seemed to belong to pulmonary neuroendocrine cells (PNEC) and their precursors. In mice deficient for Mash1, no PNEC were detected. Hes1-positive cells belong to non-neuroendocrine cells. In the mice deficient in Hes1, in which Mash1 mRNA was upregulated, PNEC appeared precociously, and the number of PNEC was markedly increased. NeuroD (Neurod1 - Mouse Genome Informatics) expression in the lung was detected in the adult, and was enhanced in the fetal lungs of Hes1-null mice. Expression of Notch1, Notch2, Notch3 and Notch4 mRNAs in the mouse lung increased with age, and Notch1 mRNA was expressed in a Hes1-dependent manner. Notch1, Notch2 and Notch3 were immunohistochemically detected in non-neuroendocrine cells. Moreover, analyses of the lungs from the gene-targeted mice suggested that expression of Delta-like 1 (Dll1 - Mouse Genome Informatics) mRNA depends on Mash1. Thus, the neuroendocrine differentiation depends on basic helix-loop-helix factors, and Notch/Notch-ligand pathways may be involved in determining the cell differentiation fate in fetal airway epithelium.
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Chytil, F. "The lungs and vitamin A." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 5 (May 1, 1992): L517—L527. http://dx.doi.org/10.1152/ajplung.1992.262.5.l517.
Evidence is reviewed supporting the view that vitamin A (retinol) and its metabolite, retinoic acid, called natural retinoids, are major factors involved in differentiation and in maturation of the lungs. This conclusion is based on morphological observation that lack of this dietary micronutrient causes keratinizing squamous metaplasia of the bronchopulmonary tree that can be reversed by refeeding the animal with retinol. In addition to these observations suggesting an indirect participation of retinol and/or retinoic acid in the differentiation of this organ, more direct evidence is presented that this vitamin is involved in pulmonary gene expression. Adult as well as fetal lungs accumulate retinyl esters, the storage form of vitamin A, contain specific retinol- and retinoic acid-binding proteins and, more importantly, express several isoforms of nuclear retinoic acid receptors. These proteins are involved in activation and repression of specific genes regulated by retinoic acid. That retinol and/or retinoic acid may be involved in lung maturation is suggested by experimental results showing depletion of lung retinyl esters at birth, by significant alterations in the levels of the cellular retinoic acid-binding protein during lung maturation and, more importantly, by reduction in the morbidity of prematurely born human neonates who are given vitamin A because they are susceptible to bronchopulmonary dysplasia.
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Besnard, V., S. E. Wert, K. H. Kaestner, and J. A. Whitsett. "Stage-specific regulation of respiratory epithelial cell differentiation by Foxa1." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 5 (November 2005): L750—L759. http://dx.doi.org/10.1152/ajplung.00151.2005.
Foxa1 is a member of the winged helix family of transcription factors that is expressed in epithelial cells of the conducting airways and in alveolar type II cells of the lung. To determine the role of Foxa1 during lung morphogenesis, histology and gene expression were assessed in lungs from Foxa1−/− gene-targeted mice from embryonic day (E) 16.5 to postnatal day (PN) 13. Deletion of Foxa1 perturbed maturation of the respiratory epithelium at precise times during lung morphogenesis. While dilatation of peripheral lung saccules was delayed in Foxa1−/− mice at E16.5, sacculation was unperturbed later in development (E17.5–E18.5). At PN5, alveolarization was markedly delayed in Foxa1−/− mice; however, by PN13 lung histology was comparable to wild-type controls. Clara cell secretory protein (CCSP), prosurfactant protein (SP)-C, and SP-B protein content and immunostaining were decreased in Foxa1−/− mice between E16.5 and E18.5 but normalized after birth. Timing and sites of expression of thyroid transcription factor-1, Foxj1, and β-tubulin were unaltered in lungs of Foxa1−/− mice. In vitro, Foxa1 regulated the activity of CCSP and SP-A, SP-B, SP-C, and SP-D promoters as assessed by luciferase reporter assays in HeLa, H441, and MLE15 cells. Although Foxa1 regulates respiratory epithelial differentiation and structural maturation of the lung at precise developmental periods, the delay in maturation is subsequently compensated at times to enable respiratory function and restore normal lung structure after birth.
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BRODY, J. "Alveolar cell differentiation markers in human lungs." Journal of Molecular and Cellular Cardiology 21 (February 1989): 161–64. http://dx.doi.org/10.1016/0022-2828(89)90852-3.
Meierovics, Anda I., and Siobhán C. Cowley. "MAIT cells promote inflammatory monocyte differentiation into dendritic cells during pulmonary intracellular infection." Journal of Experimental Medicine 213, no. 12 (October 31, 2016): 2793–809. http://dx.doi.org/10.1084/jem.20160637.
Mucosa-associated invariant T (MAIT) cells are a unique innate T cell subset that is necessary for rapid recruitment of activated CD4+ T cells to the lungs after pulmonary F. tularensis LVS infection. Here, we investigated the mechanisms behind this effect. We provide evidence to show that MAIT cells promote early differentiation of CCR2-dependent monocytes into monocyte-derived DCs (Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection. Adoptive transfer of Mo-DCs to MAIT cell–deficient mice (MR1−/− mice) rescued their defect in the recruitment of activated CD4+ T cells to the lungs. We further demonstrate that MAIT cell–dependent GM-CSF production stimulated monocyte differentiation in vitro, and that in vivo production of GM-CSF was delayed in the lungs of MR1−/− mice. Finally, GM-CSF–deficient mice exhibited a defect in monocyte differentiation into Mo-DCs that was phenotypically similar to MR1−/− mice. Overall, our data demonstrate that MAIT cells promote early pulmonary GM-CSF production, which drives the differentiation of inflammatory monocytes into Mo-DCs. Further, this delayed differentiation of Mo-DCs in MR1−/− mice was responsible for the delayed recruitment of activated CD4+ T cells to the lungs. These findings establish a novel mechanism by which MAIT cells function to promote both innate and adaptive immune responses.
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Li, Changgong, Susan M. Smith, Neil Peinado, Feng Gao, Wei Li, Matt K. Lee, Beiyun Zhou, et al. "WNT5a-ROR Signaling Is Essential for Alveologenesis." Cells 9, no. 2 (February 7, 2020): 384. http://dx.doi.org/10.3390/cells9020384.
WNT5a is a mainly “non-canonical” WNT ligand whose dysregulation is observed in lung diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Germline deletion of Wnt5a disrupts embryonic lung development. However, the temporal-specific function of WNT5a remains unknown. In this study, we generated a conditional loss-of-function mouse model (Wnt5aCAG) and examined the specific role of Wnt5a during the saccular and alveolar phases of lung development. The lack of Wnt5a in the saccular phase blocked distal airway expansion and attenuated differentiation of endothelial and alveolar epithelial type I (AT1) cells and myofibroblasts. Postnatal Wnt5a inactivation disrupted alveologenesis, producing a phenotype resembling human bronchopulmonary dysplasia (BPD). Mutant lungs showed hypoalveolization, but endothelial and epithelial differentiation was unaffected. The major impact of Wnt5a inactivation on alveologenesis was on myofibroblast differentiation and migration, with reduced expression of key regulatory genes. These findings were validated in vitro using isolated lung fibroblasts. Conditional inactivation of the WNT5a receptors Ror1 and Ror2 in alveolar myofibroblasts recapitulated the Wnt5aCAG phenotype, demonstrating that myofibroblast defects are the major cause of arrested alveologenesis in Wnt5aCAG lungs. Finally, we show that WNT5a is reduced in human BPD lung samples, indicating the clinical relevance and potential role for WNT5a in pathogenesis of BPD.
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Raslan, Ahmed A., Youn Jeong Oh, Yong Ri Jin, and Jeong Kyo Yoon. "R-Spondin2, a Positive Canonical WNT Signaling Regulator, Controls the Expansion and Differentiation of Distal Lung Epithelial Stem/Progenitor Cells in Mice." International Journal of Molecular Sciences 23, no. 6 (March 13, 2022): 3089. http://dx.doi.org/10.3390/ijms23063089.
The lungs have a remarkable ability to regenerate damaged tissues caused by acute injury. Many lung diseases, especially chronic lung diseases, are associated with a reduced or disrupted regeneration potential of the lungs. Therefore, understanding the underlying mechanisms of the regenerative capacity of the lungs offers the potential to identify novel therapeutic targets for these diseases. R-spondin2, a co-activator of WNT/β-catenin signaling, plays an important role in embryonic murine lung development. However, the role of Rspo2 in adult lung homeostasis and regeneration remains unknown. The aim of this study is to determine Rspo2 function in distal lung stem/progenitor cells and adult lung regeneration. In this study, we found that robust Rspo2 expression was detected in different epithelial cells, including airway club cells and alveolar type 2 (AT2) cells in the adult lungs. However, Rspo2 expression significantly decreased during the first week after naphthalene-induced airway injury and was restored by day 14 post-injury. In ex vivo 3D organoid culture, recombinant RSPO2 promoted the colony formation and differentiation of both club and AT2 cells through the activation of canonical WNT signaling. In contrast, Rspo2 ablation in club and AT2 cells significantly disrupted their expansion capacity in the ex vivo 3D organoid culture. Furthermore, mice lacking Rspo2 showed significant defects in airway regeneration after naphthalene-induced injury. Our results strongly suggest that RSPO2 plays a key role in the adult lung epithelial stem/progenitor cells during homeostasis and regeneration, and therefore, it may be a potential therapeutic target for chronic lung diseases with reduced regenerative capability.
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Lai, Jen-Feng, Lucas J. Thompson, and Steven F. Ziegler. "TSLP drives acute TH2-cell differentiation in lungs." Journal of Allergy and Clinical Immunology 146, no. 6 (December 2020): 1406–18. http://dx.doi.org/10.1016/j.jaci.2020.03.032.
Alabed, Mashael, Asma Sultana Shaik, Narjes Saheb Sharif-Askari, Fatemeh Saheb Sharif-Askari, Shirin Hafezi, Bushra Mdkhana, Elaref Ratemi, Saleh Al-Muhsen, Qutayba Hamid, and Rabih Halwani. "Enhanced Infiltration of Central Memory T Cells to the Lung Tissue during Allergic Lung Inflammation." International Archives of Allergy and Immunology 183, no. 2 (October 20, 2021): 127–41. http://dx.doi.org/10.1159/000518835.
Memory T cells play a central role in regulating inflammatory responses during asthma. However, tissue distribution of effector memory (T<sub>EM</sub>) and central memory (T<sub>CM</sub>) T-cell subtypes, their differentiation, and their contribution to the persistence of lung tissue inflammation during asthma are not well understood. Interestingly, an increase in survival and persistence of memory T cells was reported in asthmatic lungs, which may suggest a shift toward the more persistent T<sub>CM</sub> phenotype. In this report, we investigated the differential distribution of memory T-cell subtypes during allergic lung inflammation and the mechanism regulating that. Using an OVA-sensitized asthma mouse model, we observed a significant increase in the frequency of T<sub>CM</sub> cells in inflamed lungs compared to healthy controls. Interestingly, adoptive transfer techniques confirmed substantial infiltration of T<sub>CM</sub> cells to lung tissues during allergic airway inflammation. Expression levels of T<sub>CM</sub> homing receptors, CD34 and GlyCAM-1, were also significantly upregulated in the lung tissues of OVA-sensitized mice, which may facilitate the increased T<sub>CM</sub> infiltration into inflamed lungs. Moreover, a substantial increase in the relative expression of T<sub>CM</sub> profile-associated genes (EOMES, BCL-6, ID3, TCF-7, BCL-2, BIM, and BMI-1) was noted for T<sub>EM</sub> cells during lung inflammation, suggesting a shift for T<sub>EM</sub> into the T<sub>CM</sub> state. To our knowledge, this is the first study to report an increased infiltration of T<sub>CM</sub> cells into inflamed lung tissues and to suggest differentiation of T<sub>EM</sub> to T<sub>CM</sub> cells in these tissues. Therapeutic interference at T<sub>CM</sub> infiltration or differentiations could constitute an alternative treatment approach for lung inflammation.
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Bedoya, Felipe, Guang-Shing Cheng, Abigail Leibow, Nardine Zakhary, Katherine Weissler, Victoria Garcia, Elizabeth Kropf, et al. "Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice (P1043)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 139.11. http://dx.doi.org/10.4049/jimmunol.190.supp.139.11.
Abstract We have examined the formation, participation and functional specialization of virus-reactive Foxp3+ regulatory T cells (Tregs) in a mouse model of influenza virus infection. “Natural” Tregs generated intra-thymically based on interactions with a self-peptide proliferated in response to a homologous viral antigen in the lungs, and to a lesser extent in the lung-draining mediastinal LN (medLN), of virus-infected mice. By contrast, conventional CD4+ T cells with identical TCR specificity underwent little or no conversion to become “adaptive” Tregs. The virus-reactive Tregs in the medLN and the lungs of infected mice upregulated a variety of molecules associated with Treg activation, and also acquired expression of molecules (T-bet, Blimp-1 and IL-10) that confer functional specialization to Tregs. Notably, however, the phenotypes of the T-bet+ Tregs obtained from these sites were distinct, since Tregs isolated from the lungs expressed significantly higher levels of T-bet, Blimp-1 and IL-10 than did Tregs from the medLN. Adoptive transfer of antigen-reactive Tregs led to decreased proliferation of anti-viral CD4+ and CD8+ effector T cells in the lungs of infected hosts, while depletion of Tregs had a reciprocal effect. These studies demonstrate that thymically-generated Tregs can become activated by a pathogen-derived peptide and acquire discrete T-bet+ Treg phenotypes while participating in and modulating an antiviral immune response.
Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors highly expressed in the lung that modulate pulmonary inflammation during disease. However, the contributions of RAGE signaling are unknown during pulmonary organogenesis. In order to test the hypothesis that RAGE misexpression adversely affects lung morphogenesis, conditional transgenic mice were generated that over-express RAGE in alveolar type II cells of the lung. When RAGE is over-expressed throughout embryogenesis, severe lung hypoplasia ensues, culminating in perinatal lethality. Flow cytometry and immunohistochemistry employing cell-specific markers for various distal cell types demonstrated anomalies in key epithelial cell populations resulting from RAGE up-regulation through embryonic (E) 18.5. Electron microscopy also identified significant morphological disturbances to distal cell types including separation from the basement membrane. Possible mechanisms leading to the disappearance of pulmonary tissue by increased RAGE expression were then evaluated. A time course of lung organogenesis commencing at E12.5 demonstrated that increased RAGE expression primarily alters lung morphogenesis beginning at E16.5. TUNEL immunohistochemistry and immunoblotting for active caspase-3 confirm a shift toward apoptosis in lungs from RAGE over-expressing mice when compared to wild type controls. Assaying for NF-κB also revealed elevated nuclear translocation in lungs from transgenic mice compared to controls. An RT-PCR assessment of genes regulated by NF-κB demonstrated elevated expression of Fas ligand, suggesting increased activity of the Fas-mediated signal transduction pathway in which ligand-receptor interaction triggers cell death. These data provide evidence that RAGE expression must be tightly regulated during organogenesis. Furthermore, additional elucidation of RAGE signaling potentially involved in branching morphogenesis and cell cycle abnormalities may provide insight into the progression of RAGE-mediated lung diseases.
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Lal, Arpita. "Relationship among differentiation of self, relationship satisfaction, partner support, depression, monitoring/blunting style, adherence to treatment and quality of life in patients with chronic lung disease." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1164037503.
Ansari, Naser A. (Naser Awni). "Purification and Characterization of a Differentiation Factor From Rat Lung Conditioned Medium." Thesis, North Texas State University, 1988. https://digital.library.unt.edu/ark:/67531/metadc798062/.
A Differentiation Factor (DF) was purified from rat lung conditioned medium by a four-steps procedure. The DF has a molecular weight of 27000, and an isoelectric point of 4.70. Although DF is stable up to 60°C, it is sensitive to digestion by trypsin, chymotrypsin and subtilisin. DF forms granulocyte colonies in soft agar. Studies using anti-NRK CSF antibody demonstrated that DF is distinct from GM-CSF.
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Ansari, Naser A. (Naser Awni). "Mechanism of myeloid differentiation induced by a differentiation factor isolated from rat lung conditioned medium." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc798429/.
Berg, Tove. "C/EBP transcription factors in lung cellular differentiation and development /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-586-0/.
Tompkins, David H. "Sox2 is a Master Regulator of Differentiation in Respiratory Epithelium." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307985600.
Alaqel, Abdullah. "The directed differentiation of human embryonic stem cells to lung cell lineages." Thesis, University of Bath, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760955.
Human embryonic stem cells (hESCs) show significant therapeutic potential in treating degenerative disorders. This is in part because of their ability to produce a limitless supply of starting cells and their potential to differentiate into more than 200 different cell types. The aim of the current research was to generate a robust stage wise protocol for the differentiation of hESCs to respiratory epithelial cells. The epithelial cells could then be used either for transplantation studies or, as an in vitro model for drug toxicity testing. In order to achieve this goal, we must identify the key steps in lung development and apply these to the differentiation protocol. In this study, we maintained Shef3 hESCs in their undifferentiated pluripotent state to expand the cells prior to the differentiated towards the definitive endoderm (DE) lineage. I used a two-stage protocol based on culture with a novel glycogen synthase kinase-3 (GSK-3) inhibitor (termed 1m), along with Activin-A. We confirmed the status of the cells by a combination of immunostaining and PCR. We showed loss of the pluripotency markers (Sox2 and Oct3/4) and gain of DE markers (Sox17, FoxA2 and CXCR4). After the induction of DE from hESCs, we then treated the cells with transforming growth factor (TGF)-β and bone morphogenetic protein (BMP) pathway inhibitors (SB431542 and Noggin respectively). This combinatorial treatment resulted in the differentiation into the anterior foregut endoderm (AFE) lineage based on expression of Pax9 and FoxA2 plus the up-regulation of Sox2. Further differentiation of AFE derivatives into more mature epithelial cells, termed lung progenitor cells (LPCs), was achieved following the treatment of AFE cells with a cocktail of trophic factors (BMP4, EGF, bFGF, FGF10, KGF and Wnt3a) yielded a population of NKX2.1-positive and FoxA2-positive cells that potentially corresponded to the lung lineage. Finally, prolonged treatment with FGF10 and FGF2 on LPC derived hESCs induced proximal (CC10, MUC5AC) and distal (SPB, SPC) airway epithelial cells. In addition, we also utilised the ectopic expression of an adenovirus expressing NKX2.1 to promote lung maturation. In conclusion, we have generated a protocol for the differentiation of hESCs into mature lung-like cells. The generation of these cells in vitro could potentially lead to a better in vitro model for toxicity testing and the development of novel therapies for promoting regeneration of lungs in patients with severe lung disorders.
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METZGER, DAVID EDWARD. "THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589.
Senden, Nicole Hubertina Maria. "NSP-reticulons characterization and use for the detection of neuroendocrine differentiation in lung cancer /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=8353.
Soh, Boon Seng. "Optimization of Human Embryonic Stem Cells Culture and their Differentiation towards the Lung Lineage." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516176.
1949-, Bernal Samuel D., Hesketh Paul J. 1952-, and International Conference on Lung Cancer (1990), eds. Lung cancer differentiation: Implications for diagnosis and treatment. New York: Marcel Dekker, Inc., 1992.
International IASLC Workshop on Lung Tumor and Differentiation Antigens (3rd 1993 Zurich, Switzerland). Third International IASLC Workshop on Lung Tumor and Differentiation Antigens: University Hospital, Zurich, Switzerland, September 8-11, 1993. [New York]: Published for the UICC by Wiley-Liss, 1994.
Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
Частини книг з теми "Lungs Differentiation":
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Marin, L. "Lung Embryogenesis and Differentiation." In Physiology of the Fetal and Neonatal Lung, 1–15. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-4155-7_1.
Smith, B. T., M. Post, and J. Floros. "Differentiation of the Pulmonary Epithelium." In Physiology of the Fetal and Neonatal Lung, 17–24. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-4155-7_2.
Gaillard, Dominique, and Edith Puchelle. "Differentiation and Maturation of Airway Epithelial Cells: Role of Extracellular Matrix and Growth Factors." In Lung Development, 46–76. New York, NY: Springer New York, 1999. http://dx.doi.org/10.1007/978-1-4614-7537-8_3.
Snoeck, Hans-Willem. "Directed Differentiation of Human Pluripotent Stem Cells into Lung and Airway Epithelial Cells." In Stem Cells in the Lung, 265–85. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21082-7_16.
Alizadeh, Javad, Shahla Shojaei, Adel Sepanjnia, Mohammad Hashemi, Eftekhar Eftekharpour, and Saeid Ghavami. "Simultaneous Detection of Autophagy and Epithelial to Mesenchymal Transition in the Non-small Cell Lung Cancer Cells." In Autophagy in Differentiation and Tissue Maintenance, 87–103. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/7651_2017_84.
Zheng, Dahai, and Jianzhu Chen. "Culture and Differentiation of Lung Bronchiolar Epithelial Cells In Vitro." In Methods in Molecular Biology, 33–40. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8600-2_4.
Meleady, Paula, Finbar O’ Sullivan, Shirley McBride, and Martin Clynes. "Isolation, Cultivation and Differentiation of Lung Type II Epithelial Cells." In Animal Cell Culture Techniques, 357–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80412-0_19.
Ray Banerjee, Ena. "Tissue Differentiation of ESC into Lung Cells and Functional Validation." In Perspectives in Regenerative Medicine, 39–65. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-2053-4_4.
Cintrón, Rosa Vélez, Andrés J. Martínez, Jo Ann Jusino, María Conte-Miller, and Adalberto Mendoza. "Automated TTF-1 Immunohistochemistry Assay for the Differentiation of Lung Adenocarcinoma Versus Lung Squamous Cell Carcinoma." In Methods in Molecular Biology, 1–12. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1278-1_1.
Тези доповідей конференцій з теми "Lungs Differentiation":
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Pandit, Kusum, Jadranka Milosevic, Panayiotis Benos, Claudia Coronello, Ahmi Ben-Yehudah, James Hagood, Namasivayam Ambalavanan, and Naftali Kaminski. "Global Microrna Profiles Of Idiopathic Pulmonary Fibrosis Lungs Indicate Reversal Of Lung Differentiation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5528.
Danopoulos, S., S. Bhattacharya, C. Cherry, G. Deutsch, T. Mariani, and D. Al Alam. "Transcriptional characterization suggests accelerated epithelial differentiation in Trisomy 21 Lungs." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4105.
Danopoulos, S., S. Bhattacharya, C. Cherry, G. Deutsch, T. J. Mariani, and D. Al Alam. "Transcriptional Characterization Suggests Accelerated Epithelial Differentiation in Trisomy 21 Lungs." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5294.
Luo, Y., H. Chen, J. Chiu, and W. Shi. "Epithelial Differentiation and the Proximal-Distal Axis Are Disrupted in MesenchymeBmpr1a Knockout Fetal Lungs." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3261.
Hecker, L., T. Jones, JC Horowitz, VN Lama, and VJ Thannickal. "Multipotent Differentiation of Mesenchymal Stem/Progenitor Cells Isolated from Lungs of Patients with Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2004.
Karnati, Srikanth, and Eveline Baumgart-Vogt. "Alteration Of ROS Metabolism And Cell Type-Specific Differentiation Markers In The Lungs Of Pex11ß (-/-) Mice, A Mouse Model Deficient In Peroxisome Proliferation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4950.
Ritzmann, F., R. Sprott, F. Langer, C. Herr, C. Lehr, T. Tschernig, R. Bals, and C. Beisswenger. "Toll-like receptor signaling regulates the differentiation of 3D bronchospheres." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.92.
Goossens, Janne, Toon Ieven, Ellen Dilissen, Anne-Charlotte Jonckheere, Jonathan Cremer, Lieven Dupont, and Dominique Bullens. "Human mast cell differentiation optimization to study MRGPRX2-induced activation in vitro." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.63.
yao, yiwen, Felix Ritzmann, Alex Zimmer, Robert Bals, and Christoph Beisswenger. "Fibroblasts drive the differentiation of murine pneumocytes in air-liquid interface cultures." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.121.
Zahavi, J., S. Zaltzman, E. Firsteter, and E. Avrahami. "SEMI-QUANTITATIVE RADIONUCLIDE PHLEBOGRAPHIC (RNP) ASSESSMENT OF DEEP VEIN THROMBOSIS (DVT) AND CHRONIC VENOUS INSUFFICIENCY (CVI)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642895.
A semi-quantitative RNP using 99Technetium macroaggregated albumin for the evaluation and follow-up of DVT and CVI has been developed. Values were assigned to the deep veins of the calf, knee, tigh and pelvis based upon the localization and the characteristics of the images obtained: stasis, hot spots and collateral circulation. A maximum score of 18 reflected complete thrombosis of all 4 segments. 208 patients (mean age 53.7 years, range 18-92), 161 of whom had a proven risk factor for DVT were studied. 99Technetium was injected into the dorsal foot vein of 407 limbs with appropriate tourniquets and early and late imaging of the limbs, pelvis and lungs was performed. In 48 patients, 83 limbs, X-ray contrast phlebography (CP) was also done. The mean RNP score was 4.1 units (range 0.4-18) and higher in the left than the right lower limb. It was mostly high in patients with proximal recurrent DVT or in DVT superimposed on CVI. The score was easy to follow and helpful in the assessment of the extent of DVT. It was particularly helpful in 3 instances. 1) Assessment of venous patency following anticoagulant therapy. 2) Estimation of recurrent DVT. 3) Differentiation of recent DVT from venous insufficiency. Overall RNP method had a sensitivity of 87.6%, a specificity of 54% and an accuracy of 64.8%. The sensitivity was similar in above & below-knee thrombi. Yet the specificity was higher in above-knee thrombi. The highest accuracy (87.3%) was observed in pelvic and groin thrombi. The distribution of thrombi on CP was 19% below the knee, 31% above it and 50% both above and below the knee. Pulmonary embolism (PE) was initially observed in 54 patients (26%) with no clinical evidence of DVT and therefore untreated. This high level is most probably related to the high incidence of proximal DVT in the patients. 181 patients were treated with heparin & coumadin and the RNP score was decreased to 3.6 units (range 0.4-8.8). PE occurred during treatment in 11 (6.1%) and recurrent DVT in 16 (8.8%) patients. CVI was observed in 23 patients before treatment and in another 24 patients (13.2%) after treatment. These results indicate that the RNP method is a simple, semi-quantitative and useful technique for the evaluation and follow-up of DVT and CVI. It is most helpful in the assessment of the extent of DVT. It is also a rapid, noninvasive and cost effective techniaue.
Звіти організацій з теми "Lungs Differentiation":
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Dooner, Mark, Jason M. Aliotta, Jeffrey Pimental, Gerri J. Dooner, Mehrdad Abedi, Gerald Colvin, Qin Liu, Heinz-Ulli Weier, Mark S. Dooner, and Peter J. Quesenberry. Cell Cycle Related Differentiation of Bone Marrow Cells into Lung Cells. Office of Scientific and Technical Information (OSTI), December 2007. http://dx.doi.org/10.2172/936517.
