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Academic literature on the topic 'Colony forming unit assay'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "Colony forming unit assay"

1

Skific, Marijana, and Mirna Golemovic. "Colony-forming unit assay as a potency test for hematopoietic stem/progenitor cell products." Molecular and experimental biology in medicine 2, no. 2 (October 5, 2019): 51–56. http://dx.doi.org/10.33602/mebm.2.2.8.

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Colony-forming unit (CFU) assay is a short-term culture assay used for the detection of functionally active hematopoietic progenitor cells (HPCs) in the in vitro setting. This potency assay enables the identification of colony-producing HPCs in any type of hematopoietic stem cell/progenitor product (HSC/P) including bone marrow (BM), cord blood (CB) and mobilized peripheral blood (MPB). It has been shown that the frequency of HPCs in BM, MPB and CB cellular products directly correlates with the engraftment of both neutrophils and platelets as well as with the overall survival of recipients following hematopoietic stem cell transplantation which makes the CFU assay a good quality parameter for the prediction of engraftment success. The aim of this article is to provide an overview of different approaches to setting up the CFU assay with an emphasis on different sample preparation techniques, cell plating density and colony identification and enumeration used by different laboratories.

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2

Powell, K., E. Kwee, B. Nutter, E. Herderick, P. Paul, D. Thut, C. Boehm, and G. Muschler. "Variability in subjective review of umbilical cord blood colony forming unit assay." Cytometry Part B: Clinical Cytometry 90, no. 6 (May 24, 2016): 517–24. http://dx.doi.org/10.1002/cyto.b.21376.

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3

Nagashima, Naho, Masaharu Hisasue, Katsumi Higashi, Rui Kano, Hajime Tsujimoto, and Atsuhiko Hasegawa. "Bone Marrow Colony-Forming Unit Assay in Cats With Naturally Occurring Myelodysplastic Syndromes." International Journal of Hematology 73, no. 4 (May 2001): 453–56. http://dx.doi.org/10.1007/bf02994006.

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4

Li, Bing, Jinqin Liu, Shiqiang Qu, Robert Peter Gale, Ruixian Xing, Tiejun Qin, Yue Zhang, et al. "Colony-Forming Unit Cell (CFU-C) Assays in Myelodysplastic Syndrome." Blood 126, no. 23 (December 3, 2015): 2874. http://dx.doi.org/10.1182/blood.v126.23.2874.2874.

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Abstract Introduction: The myelodysplastic syndromes (MDS) are a group of clonal diseases derived from hematopoietic stem cells (HSC). Colony-forming unit cell (CFU-C) assay is an effective method to study the number and the function of HSC in vitro. In this study, we focus on the characteristics and the prognostic value of CFU-C in patients with MDS. Patients and Method: CFU-C assays were performed according to the protocol of MethoCultTM H4435 Enriched (STEMCELL Technologies). A colony was defined as an aggregate of >40 cells. Clusters consisted of 4 to 40 cells. 560 consecutive newly-diagnosed, untreated subjects with MDS diagnosed from March, 2001 to April, 2013 were studied. All subjects were reclassified according to the 2008 WHO criteria. 535 subjects with evaluable cytogenetics were classified using the International Prognostic Scoring System (IPSS) and the revised International Prognostic Scoring System (IPSS-R) criteria. Follow-up data were available for 470£¨84%£©subjects. Median follow-up of survivors was 26 months (range, 1-170) months. Subjects receiving an allotransplants were censored in survival analyses. Erythroid and myeloid colonies were isolated from each subject with one cytogenetic abnormality such as del(5/5q-) or +8. Cytogenetic abnormalities of each colony were analyzed by fluorescence in situ hybridization (FISH). SPSS 17.0 software was used to make statistical analysis. Results: Frequencies of burst-forming units-erythroid (BFU-E), colony forming unit-erythroid (CFU-E) and colony forming unit-granulocytes/macrophages (CFU-G/M) were significantly lower than normals (P<0.05) (Table 1). Subjects classified as lower risk in IPSS and IPSS-R had significantly higher numbers of BFU-E and CFU-E (P<0.05) but similar numbers CFU-G/M and clusters-G/M compared with higher risk subjects (Table 2). In 11 subjects with del(-5/5q-) or +8 identified by G- and/or R-banding, both normal and abnormal CFU-Cs were identified in 8 subjects studied by FISH. A high ratio of cluster- to CFU-G/M (>0.6) was associated with poor-risk cytogenetics (Table 2) and with worse overall survival in univariable (Figure 1, P=0.001) and multivariable analyses (HR 1.748, [1.01-3.0]; P=0.046) after adjusting for IPSS. Conclusions: These data suggest abnormalities of proliferation and differentiation of erythroid and myeloid precursor cells in vitro parallel the ineffective hematopoiesis typical of MDS and may be useful in predicting outcomes of patients with MDS. Table 1. CFU-C in MDS subtypes N BFU-E CFU-E CFU-G/M N Ratio of cluster- to CFU-G/M RA 21 8 (0-44) 40 (0-134) 14 (0-127)1 6 0.25 (0.40-1.00) RT 4 18 (4-55) 75 (60-90)1 30 (18-70)1 2 2 RARS 27 12 (0-33) 35 (1-140) 12 (0-70)1 10 0.45 (0.17-0.80) RCMD 275 10 (0-80) 33 (0-178) 14 (0-100) 126 0.35 (0-0.83) RAEB1 112 10 (0-258) 32 (0-312) 14 (0-89) 53 0.47 (0-1.00) RAEB2 103 9 (0-46) 25 (0-120) 13 (0-72) 42 0.37 (0-1.00) MDS-U 15 4 (0-58) 25 (0-161) 10 (0-43) 3 2 Del(5q) 3 2 (2-4) 15 (0-20) 5 (5-41)1 1 2 1No significant difference compared with normals. 2Too few cases to analyze. Table 2. Associations between CFU-C and clinical and laboratory variables N BFU-E P CFU-E P CFU-G/M P Number Ratio of cluster- to CFU-GM P IPSS 0.064 0.006 0.361 0.089 Low 30 13 (0-44) 60 (0-169) 19 (0-45) 10 0.44 (0.24-0.70) Int-1 361 10 (0-258) 33 (0-312) 14 (0-127) 150 0.33 (0-1.00) Int-2 115 9 (0-61) 30 (0-137) 14 (0-72) 52 0.45 (0-1.00) High 29 7 (0-34) 21 (0-93) 12 (0-67) 12 0.44 (0-1.00) IPSS-R 0.003 0.003 0.125 0.209 Very low 7 16 (9-25) 30 (15-120) 18 (5-33) 2 0.29 (0.10-0.49) Low 130 14 (0-80) 42 (0-178) 17 (0-70) 48 0.31 (0-0.77) Intermediate 173 10 (0-66) 34 (0-161) 13 (0-127) 81 0.37 (0-1.00) High 139 9 (0-259) 29 (0-312) 11 (0-89) 51 0.33 (0-1.00) Very high 86 8 (0-61) 25 (0-137) 14 (0-91) 42 0.47 (0-1.00) Cytogenetics (IPSS) 0.867 0.055 0.290 0.007 Good 327 10 (0-258) 36 (0-312) 15 (0-89) 133 0.33 (0-1.00) Intermediate 133 10 (0-69) 30 (0-162) 12 (0-127) 63 0.45 (0-1.00) Poor 75 10 (0-61) 25 (0-137) 14 (0-91) 28 0.42 (0-1.00) Cytogenetics (IPSS-R) 0.990 0.090 0.676 0.022 Very good 7 11 (4-20) 48 (1-110) 14 (8-28) 2 0.49 (0.43-0.56) Good 324 10 (0-258) 35 (0-312) 15 (0-89) 132 0.33 (0-1.00) Intermediate 129 10 (0-69) 30 (0-162) 12 (0-127) 62 0.45 (0-1.00) Poor 27 10 (0-61) 35 (0-137) 16 (0-48) 8 0.36 (0.15-1.00) Very poor 48 11 (0-42) 22 (0-120) 14 (0-91) 20 0.53 (0-1.00) Figure 1. Overall survival in subjects with cluster- to CFU-G/M ratios ¡Ü or > 60%. Figure 1. Overall survival in subjects with cluster- to CFU-G/M ratios ¡Ü or > 60%. Disclosures No relevant conflicts of interest to declare.

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Štefková, Kateřina, Markéta Hanáčková, Jan Kučera, Katarzyna Anna Radaszkiewicz, Barbora Ambrůžová, Lukáš Kubala, and Jiří Pacherník. "MAPK p38alpha Kinase Influences Haematopoiesis in Embryonic Stem Cells." Stem Cells International 2019 (June 2, 2019): 1–16. http://dx.doi.org/10.1155/2019/5128135.

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The activation of p38alpha kinase mediates cell response to various extracellular factors including many interleukins and growth factors important for haematopoiesis. The role of p38alpha kinase was previously analysed in particular haematopoietic cells. In this study and for the first time, the role of p38alpha kinase in haematopoiesis was studied using a model of continuous haematopoietic development in pluripotent embryonic stem cellsin vitro. The expression of transcripts associated with haematopoiesis and the potential for the formation of specific haematopoietic cell colonies were compared between wild-type and mutant p38alpha gene-depleted cells. The absence of p38alpha kinase led to the inhibition of hemangioblast formation during the first step of haematopoiesis. Later, during differentiation, due to the lack of p38alpha kinase, erythrocyte maturation was impaired. Mutant p38α−/−cells also exhibited decreased potential with respect to the expansion of granulocyte colony-forming units. This effect was reversed in the absence of erythropoietin as shown by colony-forming unit assay in media for colony-forming unit granulocytes/macrophages. p38alpha kinase thus plays an important role in the differentiation of common myeloid precursor cells into granulocyte lineages.

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6

Terpstra, Wim, Henk Rozemuller, Dimitri A. Breems, Elwin J. C. Rombouts, Arie Prins, David J. P. FitzGerald, Robert J. Kreitman, et al. "Diphtheria Toxin Fused to Granulocyte-Macrophage Colony-Stimulating Factor Eliminates Acute Myeloid Leukemia Cells With the Potential to Initiate Leukemia in Immunodeficient Mice, But Spares Normal Hemopoietic Stem Cells." Blood 90, no. 9 (November 1, 1997): 3735–42. http://dx.doi.org/10.1182/blood.v90.9.3735.

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Abstract We studied the cell kill induced by granulocyte-macrophage colony-stimulating factor (GM-CSF ) fused to Diphtheria Toxin (DT-GM-CSF ) in acute myeloid leukemia (AML) samples and in populations of normal primitive hemopoietic progenitor cells. AML samples from three patients were incubated in vitro with 100 ng/mL DT-GM-CSF for 48 hours, and AML cell kill was determined in a proliferation assay, a clonogenic assay colony-forming unit-AML (CFU-AML) and a quantitative long-term bone marrow (BM) culture ie, the leukemic-cobblestone area forming cell assay (L-CAFC). To measure an effect on cells with in vivo leukemia initiating potential DT-GM-CSF exposed AML cells were transplanted into immunodeficient mice. In two out of three samples it was shown that all AML subsets, including those with long-term abilities in vivo (severe combined immunodeficient mice) and in vitro (L-CAFC assay) were reduced in number by DT-GM-CSF. Cell kill induced by DT-GM-CSF could be prevented by coincubation with an excess of GM-CSF, demonstrating that sensitivity to DT-GM-CSF is specifically mediated by the GM-CSF receptor. Therefore, binding and internalization of GM-CSF probably occur in immature AML precursors of these two cases of AML. The third AML sample was not responsive to either GM-CSF or DT-GM-CSF. The number of committed progenitors of normal bone marrow (burst-forming unit-erythroid, colony-forming unit granulocyte- macrophage, and cobble stone area forming cell [CAFC] week 2) and also the number of cells with long-term repopulating ability, assayed as week 6 CAFC, were unchanged after exposure to DT-GM-CSF (100 ng/mL, 48 hours). These studies show that DT-GM-CSF may be used to eliminate myeloid leukemic cells with long-term potential in vitro and in immunodeficient mice, whereas normal hemopoietic stem cells are spared.

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Rich, IN. "The effect of 5-fluorouracil on erythropoiesis." Blood 77, no. 6 (March 15, 1991): 1164–70. http://dx.doi.org/10.1182/blood.v77.6.1164.1164.

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Abstract The effects of a single dose (150 mg/kg) of 5-fluorouracil on mature erythroid and erythropoietic and multipotential in vitro precursor populations in the bone marrow and spleen and circulating biologically (erythroid colony forming unit [CFU-E] assay) and immunologically active (enzyme-linked immunosorbent assay) erythropoietin (Epo) are described. All mature erythroid (reticulocytes, erythrocytes) and in vitro erythropoietic precursors (CFU-E, erythroid burst-forming unit [BFU-E]) are severely reduced, if not eradicated. Transient repopulation of the pure BFU-E and CFU-E populations on days 6 and 7, respectively, produces a marked reticulocytosis after day 9. Circulating Epo increases to above normal values by day 2. However, whereas biologically active Epo remains constant at this level until day 9, immunologically active Epo continually increases; by day 12, however, both assays detect circulating Epo levels of about 400 mU/mL. In vitro multipotential stem cells (BFU-E mix) are reduced to 32% on day 1, 7.6% on day 2, and return to normal values between days 4 and 5. The survival and repopulation kinetics of the BFU-E mix imply a stem cell population more mature than the high proliferative potential colony-forming cells. However, the BFU-E mix may be responsible for erythropoiesis repopulating ability.

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Rich, IN. "The effect of 5-fluorouracil on erythropoiesis." Blood 77, no. 6 (March 15, 1991): 1164–70. http://dx.doi.org/10.1182/blood.v77.6.1164.bloodjournal7761164.

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The effects of a single dose (150 mg/kg) of 5-fluorouracil on mature erythroid and erythropoietic and multipotential in vitro precursor populations in the bone marrow and spleen and circulating biologically (erythroid colony forming unit [CFU-E] assay) and immunologically active (enzyme-linked immunosorbent assay) erythropoietin (Epo) are described. All mature erythroid (reticulocytes, erythrocytes) and in vitro erythropoietic precursors (CFU-E, erythroid burst-forming unit [BFU-E]) are severely reduced, if not eradicated. Transient repopulation of the pure BFU-E and CFU-E populations on days 6 and 7, respectively, produces a marked reticulocytosis after day 9. Circulating Epo increases to above normal values by day 2. However, whereas biologically active Epo remains constant at this level until day 9, immunologically active Epo continually increases; by day 12, however, both assays detect circulating Epo levels of about 400 mU/mL. In vitro multipotential stem cells (BFU-E mix) are reduced to 32% on day 1, 7.6% on day 2, and return to normal values between days 4 and 5. The survival and repopulation kinetics of the BFU-E mix imply a stem cell population more mature than the high proliferative potential colony-forming cells. However, the BFU-E mix may be responsible for erythropoiesis repopulating ability.

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9

Zsebo, KM, J. Wypych, VN Yuschenkoff, H. Lu, P. Hunt, PP Dukes, and KE Langley. "Effects of hematopoietin-1 and interleukin 1 activities on early hematopoietic cells of the bone marrow." Blood 71, no. 4 (April 1, 1988): 962–68. http://dx.doi.org/10.1182/blood.v71.4.962.962.

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Abstract Hematopoietin-1 (H-1) was purified from the human cell line 5637 and two amino acid sequences were observed in the preparation. One sequence was identical to that of interleukin 1 alpha (IL 1 alpha) and the other to that of IL 1 beta. The action of recombinant IL 1 alpha and other hematopoietic growth factors was studied using (a) a high proliferative potential colony-forming cell assay that uses primitive hematopoietic precursors from bone marrow, and (b) a spleen colony-forming unit assay. The results indicate that the IL 1 alpha target cell population is different than the target cell populations of IL 3, granulocyte- macrophage colony-stimulating factor; that IL 1 alpha in combination with mononuclear phagocyte colony-stimulating factor provides a proliferative stimulus; and that IL 1 alpha has at least a survival- enhancing and possibly proliferation-inducing effect on primitive hematopoietic stem cells.

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Zsebo, KM, J. Wypych, VN Yuschenkoff, H. Lu, P. Hunt, PP Dukes, and KE Langley. "Effects of hematopoietin-1 and interleukin 1 activities on early hematopoietic cells of the bone marrow." Blood 71, no. 4 (April 1, 1988): 962–68. http://dx.doi.org/10.1182/blood.v71.4.962.bloodjournal714962.

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Hematopoietin-1 (H-1) was purified from the human cell line 5637 and two amino acid sequences were observed in the preparation. One sequence was identical to that of interleukin 1 alpha (IL 1 alpha) and the other to that of IL 1 beta. The action of recombinant IL 1 alpha and other hematopoietic growth factors was studied using (a) a high proliferative potential colony-forming cell assay that uses primitive hematopoietic precursors from bone marrow, and (b) a spleen colony-forming unit assay. The results indicate that the IL 1 alpha target cell population is different than the target cell populations of IL 3, granulocyte- macrophage colony-stimulating factor; that IL 1 alpha in combination with mononuclear phagocyte colony-stimulating factor provides a proliferative stimulus; and that IL 1 alpha has at least a survival- enhancing and possibly proliferation-inducing effect on primitive hematopoietic stem cells.

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Dissertations / Theses on the topic "Colony forming unit assay"

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Casati, Silvia. "Development of in vitro tests to predict thrombocytopenia : standardisation of the colony-forming unit-megakaryocyte (CFU-MK) assay." Thesis, University of Nottingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395459.

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Buchanan, Sandhya S. "Preservation of two therapeutic biopharmaceuticals using sugars and polymers : hematopoietic stem and progenitor cells and a live attenuated viral vaccine /." Connect to full text via ProQuest. IP filtered, 2006.

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Thesis (Ph.D. in Pharmaceutical Sciences) -- University of Colorado, 2006.
Typescript. Includes bibliographical references (leaves 191-216). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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Lindton, Bim. "Experimental studies of human fetal liver cells : in regard to in utero hematopoietic stem cell transplantation /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-134-9.

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Qadan, Maha Ahmad. "Sourcing and Modulation of the Fate of Connective Tissue Progenitors." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1479416651140376.

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Raut, Vivek P. "METHODS TO QUANTITATIVELY ASSESS THE PERFORMANCE OF CONNECTIVE TISSUE PROGENITOR CELLS IN RESPONSE TO SURFACE MODIFIED BIOMATERIALS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1372334668.

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SOO, CAROL. "MECHANISMS OF OZONE TOXICITY." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1020710528.

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Lauret, Evelyne. "Contribution à l'étude du contrôle humoral de la détermination de la différenciation des cellules souches hématopoiétiques pluripotentes (CFU-s) chez la souris." Paris 11, 1985. http://www.theses.fr/1985PA112310.

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Le système murin est utilisé pour étudier les mécanismes de régulation du choix de différenciation que fait la cellule souche pluripotente hématopoïétique (CFU-S) vers l’une ou l’autre des lignées sanguines. La méthode employée pour cette étude est basée sur l’analyse histologique des nodules spléniques formés par le développement des clones de CFU-S dans la rate de souris irradiée ayant reçu de la moelle 10 jours auparavant. Les proportions de chaque catégorie histologique étant définies et constantes pour une souche de souris donnée, il apparait que tout changement des proportions des différentes catégories histologiques à la suite d’une agression infligée au système hématopoïétique reflète nécessairement une modification de la détermination des cellules souches pluripotentes. L’étude des effets de cytosine arabinoside, administrée sous forme fractionnée à une souris, montre que ce protocole de traitement, in vivo, oriente préférentiellement la détermination des CFU-S médullaires et spléniques vers la granulopoïèse et la mégacaryocytopoïèse au détriment de l’érythropoïèse. De plus, le sérum de souris ainsi traité contient des facteurs humoraux capables d’orienter, in vitro, la détermination de CFU-S réceptrices de moelle de souris normale vers la lignée granulocytaire : ces facteurs, appelés pluripoïétines G, sont sécrétés par la rate et probablement par d’autres tissus. Ces résultats confirment l’hypothèse d’un contrôle humoral de la détermination des CFU-S, notion déjà établie pour la lignée érythrocytaire dans notre laboratoire. La sécrétion des pluripoïétines spécifiques des lignées érythrocytaire et granulocytaire est soumise à un mécanisme de rétrocontrôle qui dépend, tout au moins en partie, des proportions relatives des précurseurs unipotents de chacune de ces lignées
Studies have been carried out in mice to investigate mechanisms of cell differenciation, in particular the determination of the pluripotent haemopoietic stem cell (CFU-S) towards one cell lineage. The method employed is the histological analysis of spleen colonies formed by stem cells 10 days after injection into irradiated mice. Changes in the proportions of colonies of different types as the result of perturbation of haemopoiesis must necessarily reflect a change in the determination of the pluripotent stem cells. A study of the effect of repeated administration of cytosine arabinoside demonstrated a preferential shift in CFU-S determination towards granulopoiesis and megakaryocytopoiesis. In addition, the serum of mice treated in this way contains humoral factors capable, in vitro, of alter determination toward granulopoiesis. These factors have been called pluripoietis G and have been shown to be secreted by the spleen and probably other tissues. These results support the suggestion for a humoral control of CFU-S determination which has been proposed for erythropoiesis in our laboratory. The production of specific pluripoietis for erythroid and granulocytic cell lineages would appear to be under a feedback control at least in part on the relative proportions of unipotents cells in each line of differentiation

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Phillips, Roger. "The predictive value of in vitro chemosensitivity tests of anticancer drugs : in vitro chemosensitivity of a panel of murine colon tumours determined by a colony forming assay at drug exposure parameters measured in vivo." Thesis, University of Bradford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329305.

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Frühauf, Patrik. "Zařízení vzduchotechniky a kvalita vzduchu v budovách." Master's thesis, Vysoké učení technické v Brně. Fakulta stavební, 2015. http://www.nusl.cz/ntk/nusl-227751.

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This thesis deals with the relationship between HVAC systems and internal microclimate of buildings. The work discusses briefly about different components which are formulating internal microclimate. More details are then focused on the issue of microbial microclimate.

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Wendisch, Maria. "Nachweis der adaptiven Antwort nach Bestrahlung von Schilddrüsenzellen mit offenen Radionukliden." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-62681.

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Biologische Systeme sind in der Lage sich an eine Niedrig-Dosis-Bestrahlung anzupassen und eine geringere Sensitivität gegenüber einer nachfolgenden Hoch-Dosis-Bestrahlung zu entwickeln. Dieses Phänomen wird als adaptive Antwort bezeichnet und wurde nach der Bestrahlung mit externen Strahlungsquellen wiederholt in vivo und in vitro untersucht. Im Gegensatz dazu gibt es für die Bestrahlung mit offenen Radionukliden keine systematischen und vergleichenden Untersuchungen. Im Mittelpunkt dieser Arbeit standen der Nachweis sowie die Analyse der adaptiven Antwort an PC Cl3-Zellen nach Bestrahlung mit den offenen Radionukliden Re-188 und Tc-99m. Die Zellschädigung wurde mit dem alkalischen Komet-Assay, zur Bestimmung des initialen DNA-Schadens und dem Koloniebildungstest, zur Ermittlung des klonogenen Überlebens, untersucht. Zur Aufklärung von möglichen Regulationsmechanismen der adaptiven Antwort wurde die Induktion und Reparatur von DSB mit dem gamma-H2AX-Immunfluoreszenz-Assay und die intrazelluläre Radionuklidaufnahme betrachtet. In dieser Arbeit erfolgte erstmals eine systematische Untersuchung der adaptiven Antwort nach Bestrahlung mit offenen Radionukliden in vitro. Insgesamt zeigen diese Ergebnisse, dass nach Bestrahlung mit offenen Radionukliden eine adaptive Antwort ausgebildet wird. Diese ist von der Strahlenqualität während Vor- und Folgebestrahlung sowie der Art der DNA-Schädigung und den initiierten Reparaturprozessen abhängig. Weiter Einflussfaktoren sind die Erholungszeit, die Vorbestrahlung (Dosis, Strahlenqualität) und die Art des Schadensnachweises. Neben den bekannten Regulationsmechanismen wurde erstmals die Reduktion der intrazellulären Radionuklidaufnahme als weitere mögliche adaptive Antwort beschrieben.

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Books on the topic "Colony forming unit assay"

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Stem Cell Assays. Humana Press, 2007.

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Stem cell assays. Totowa, NJ: Humana Press, 2007.

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Book chapters on the topic "Colony forming unit assay"

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Penfornis, Patrice, and Radhika Pochampally. "Colony Forming Unit Assays." In Mesenchymal Stem Cells, 159–69. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3584-0_9.

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Avraham, Hava Karsenty, Byeong-Chel Lee, and Shalom Avraham. "Colony-Forming Unit Assay: Methods and Implications." In Encyclopedia of Immunotoxicology, 190–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_279.

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Pessina, Augusto. "The Granulocyte/Macrophage Colony-Forming Unit Assay." In Animal Cell Culture Techniques, 217–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80412-0_13.

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Spangrude, G. J. "The Pre-Spleen Colony-Forming Unit Assay: Measurement of Spleen Colony-Forming Unit Regeneration." In Current Topics in Microbiology and Immunology, 31–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76912-2_3.

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Pochampally, Radhika. "Colony Forming Unit Assays for MSCs." In Mesenchymal Stem Cells, 83–91. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-169-1_6.

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Rajendran, Vijayalakshmi, and Mayur Vilas Jain. "In Vitro Tumorigenic Assay: Colony Forming Assay for Cancer Stem Cells." In Methods in Molecular Biology, 89–95. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7401-6_8.

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Jones, R. J. "Spleen Colony-Forming Unit: A Myeloid Stem Cell." In Current Topics in Microbiology and Immunology, 75–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76912-2_6.

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Louis, Sharon A., and Carmen K. H. Mak. "Enumerating Stem Cell Frequency: Neural Colony Forming Cell Assay." In Methods in Molecular Biology, 117–32. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-574-3_11.

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Schellenberg, Anne, Hatim Hemeda, and Wolfgang Wagner. "Tracking of Replicative Senescence in Mesenchymal Stem Cells by Colony-Forming Unit Frequency." In Stem Cells and Aging, 143–54. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-317-6_11.

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Jones, F. T., and M. J. Wineland. "Efficacy of Colony Forming Unit Data in Detection of a Fusarotoxicosis Problem Associated with Post-Manufacturing Growth of Fusarium Spp. In Poultry Feeds." In Mycotoxins, Wood Decay, Plant Stress, Biocorrosion, and General Biodeterioration, 93–103. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9450-2_7.

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