Relevant bibliographies by topics / Haematopoeitic

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'Haematopoeitic'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Haematopoeitic"

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MacMillan, Margaret L., and John E. Wagner. "Haematopoeitic cell transplantation for Fanconi anaemia - when and how?" British Journal of Haematology 149, no. 1 (April 2010): 14–21. http://dx.doi.org/10.1111/j.1365-2141.2010.08078.x.

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Yapa, H. Manisha N., Donal P. McLornan, Kavita Raj, Matthew Streetly, Majid Kazmi, Kirsty Cuthill, John Laurie, Padma A. Menon, and Eithne MacMahon. "Pneumonitis post-haematopoeitic stem cell transplant – Cytopathology clinches diagnosis." Journal of Clinical Virology 55, no. 3 (November 2012): 278–81. http://dx.doi.org/10.1016/j.jcv.2012.08.007.

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Weilbacher, K. "PL9.2. Haematopoeitic cell and growth factor – tumour cell interactions." Cancer Treatment Reviews 34 (2008): 49. http://dx.doi.org/10.1016/j.ctrv.2008.03.138.

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Chakraborty, Sohini, Shobha Badiger, Sharat Damodar, and Sunil Bhat. "Haploidentical haematopoeitic stem cell transplants (Hsct) in paediatric acute leukemia." Pediatric Hematology Oncology Journal 2, no. 2 (2017): S5. http://dx.doi.org/10.1016/j.phoj.2017.11.141.

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Oldreive, Ceri, Tatjana Stankovic, Philip J. Byrd, Grant S. Stewart, Anna Smith, Alexander J. Taylor, Peggy Fooks, et al. "PALB2 Mutational Status in Haematopoeitic Malignancies - a Potential Therapeutic Target?" Blood 128, no. 22 (December 2, 2016): 2726. http://dx.doi.org/10.1182/blood.v128.22.2726.2726.

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Abstract PALB2 protein is one of the principal components of Homologous Recombination Repair (HRR) that facilitates recruitment of other HRR proteins such as BRCA1, BRCA2 and Rad51. Biallelic PALB2 inactivation is associated with a severe form of Fanconi Anemia (FA-N), however, biallelic PALB2 mutations also occur in patients with a FA-N syndrome variant characterised by a predisposition to B-cell lymphoma development. The association of PALB2 with FA-N and FA-N variant suggests that PALB2 may play a pathogenic role in a wider range of sporadic haematopoietic malignancies. To address this possibility, the mutational status of the PALB2 gene was assessed in 30 myelodysplastic syndrome (MDS) samples, 23 acute lymphoblastic leukaemias (ALL), 171 chronic lymphocytic leukaemias (CLL) and 24 paediatric non-Hodgkin lymphomas (NHL) of T- or B-cell origin. Overall, pathogenic (truncating or splicing errors)orlikely pathogenic sequence changes (missense alterations not previously reported but predicted to alter protein function) were detected in 17 (6.7%) of these patients. PALB2 was most frequently altered in NHL (25%), followed by MDS (6%), CLL (5%) and ALL (4%). The overall incidence of changes observed for B-cell NHL was higher than the frequency detected in T-cell NHL. PALB2 sequence changes were distributed across the whole gene including the DNA binding, BRCA1-interacting and BRCA2-interacting domains. Of note, a single truncating mutation; in the BRCA1-interacting domain, c.886delA; was detected in three cases, two with progressive CLL and one with MDS and interestingly only became detectable in one of these CLL patients following ibrutinib treatment. Furthermore, a polymorphic variant (c.2993G>A), previously associated with an increased breast cancer risk, was present at higher frequency than in the general population in cohorts of both CLL and ALL patients. HRR defective tumour cells can be targeted by pharmacological inhibition of co-operating DNA repair pathways using the principal of synthetic lethality. To explore whether this concept can be utilised in the context of PALB2 deficiency, we evaluated the effectiveness of inhibition of two pathways; PARP and ATR; that co-operate with PALB2. The cytotoxicity induced by either an ATR inhibitor or a PARP inhibitor was assessed in lymphoblastoid cell lines derived from a paediatric B-cell NHL patient carrying the c.1676_1677delAAinsG and c.2586+1G>A mutations. As predicted, exposure of lymphoid cells with PALB2 mutations to either ATR or PARP inhibitor alone exerted a cytotoxic effect which was enhanced when both inhibitors were applied in combination. In conclusion, our results suggest that PALB2 is altered in a subset of patients with different haematopoietic malignancies. This potentially provides another avenue for targeted therapies utilising the concept of synthetic lethality via application of PARP and ATR inhibitors that are currently being tested in clinical trials. Disclosures Janic: Novo Nordisk: Other: Paid Instructor, Research Funding; Baxter: Other: Paid Instructor, Research Funding; Bayer: Other: Paid Instructor, Research Funding; Pfizer: Other: Paid Instructor, Research Funding; Octopharma: Research Funding.
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Foster, H., J. Davidson, E. Baildam, M. Abinun, and L. R. Wedderburn. "Autologous haematopoeitic stem cell rescue (AHSCR) for severe rheumatic disease in children." Rheumatology 45, no. 12 (October 31, 2006): 1570–71. http://dx.doi.org/10.1093/rheumatology/kel319a.

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Din, Nazzlin Dizana. "Thalassaemia Care in Terengganu – A Local Report." Malaysian Journal of Paediatrics and Child Health 26, no. 2 (July 28, 2020): 1–5. http://dx.doi.org/10.51407/mjpch.v26i2.79.

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Inherited thalassaemia disease is commonly found in many countries of the world. Care of the disease requires comprehensive management strategies comprising of clinical management of both transfusion dependant thalassaemia (TDT) and non-transfusion dependant thalassaemia (NTDT). It also includes preventive measures such as screening programmes and genetic counseling in order to contain the genetic transmission. At the moment, the only cure is through haematopoeitic stem cell transplant (HSCT). This report illustrates thalassaemia disease prevalence in the Terengganu state and the evolution of care since National Thalassaemia Programme was launched in 2009.
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Zhu, Grace G., Benjamin L. Witt, Thomas C. Winter III, and Douglas M. Rogers. "Multiple enlarging hepatic and retroperitoneal myelolipomas in the setting of Cushing disease." BMJ Case Reports 14, no. 2 (February 2021): e239107. http://dx.doi.org/10.1136/bcr-2020-239107.

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Myelolipomas are benign tumours typically occurring in the adrenal glands, made up of fat and trilineage haematopoeitic cells resembling bone marrow. Their aetiology is not well understood; however, they have a clear association with elevated serum adrenocorticotropic hormone (ACTH). Extra-adrenal myelolipomas are rare, and to our knowledge there are no previously reported cases of multiple enlarging hepatic and retroperitoneal myelolipomas in the setting of Cushing disease. We present the case of a patient with an ACTH-producing pituitary adenoma who developed multiple enlarging fat containing lesions in the liver and retroperitoneum, which were histologically proven multifocal myelolipomas.
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Robenshtok, E., A. Gafter-Gvili, M. Paul, E. Goldberg, L. Vidal, and L. Leibovici. "P964 Antifungal prophylaxis for patients undergoing chemotherapy or haematopoeitic stem cell transplantation-meta-analysis." International Journal of Antimicrobial Agents 29 (March 2007): S254. http://dx.doi.org/10.1016/s0924-8579(07)70805-1.

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H, Ariffin, Daud SS, and Ibrahim K. "QUANTITATIVE EVALUATION OF CHIMERISM STATUS FOLLOWING HAEMATOPOEITIC STEM CELL TRANSPLANTATION USING A MICROCHIP ELECTROPHORESIS SYSTEM." Journal of Health and Translational Medicine 10, no. 1 (June 25, 2007): 11–16. http://dx.doi.org/10.22452/jummec.vol10no1.3.

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Dissertations / Theses on the topic "Haematopoeitic"

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Yemm, Adrian Ian. "Enhancing haematopoeitic stem cell recruitment to injured murine colon." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/4859/.

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Haematopoietic stem cells (HSCs) have been described as potential therapeutic agents for the repair of several inflammatory injuries including inflammatory bowel diseases (IBDs). However, their efficacy within clinics has been poor. This has been partially attributed to poor recruitment to sites of injury. Thus identifying the mechanisms by which HSCs are recruited to inflamed bowel, and developing strategies to enhance this recruitment, may increase their clinical efficacy. Critical adhesive mechanisms and several pre-treatment strategies to enhance adhesion to chronically (DSS induced colitis) and acutely (IR) injured murine colon were investigated in vitro and in vivo. It was found that recruitment to IR injured colon was mediated by CD49d, whereas recruitment to colitic colon was mediated by both CD18 and CD49d. In vitro investigation revealed that both hydrogen peroxide (H2O2) and platelet derived pre-treatments, such as coating HSCs with platelet microparticles (PMPs), could enhance adhesion to colon endothelial cells, immobilised endothelial counterligands ICAM-1 and VCAM-1 and frozen tissue sections. Furthermore, pre-treatment of HSCs with PMPs significantly enhanced their adhesion to chronically injured colon in vivo. These increases in adhesion were likely to be attributed to the altered distribution of integrins on the HSC surface as determined confocally. Furthermore, electron micrscopy showed that pre-treatment also resulted in overt HSC morphological changes reminiscent of activated macrophages. Overall, these investigations describe a two-component recruitment mechanism for pre-treated cells in which enhanced recruitment is dependent on both activation of stem cells and also vascular endothelium. These studies provide novel evidence that pre-treatment of HSCs can result in their increased recruitment to injured colon, a finding that may allow for stem cell therapy for IBDs to be fully realised.
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Byrne, Eilis Mary. "Structural and functional analysis of SHP1, an SH2 domain containing protein tyrosine." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365723.

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Krishnan, Jaya. "The role of vascular endothelial growth factor receptor 3, and its ligands vascular endothelial growth factor C and vascular endothelial growth factor D in tumour metastasis and haematopoeisis." Thesis, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270576.

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Largeot, Anne. "Contrôle de l'expression du gène HOXA9 dans les cellules souches/progénitrices hématopoïétiques : rôle des enzymes épigénétiques MOZ et MLL, et du facteur de polyadénylation Symplekin." Thesis, Dijon, 2013. http://www.theses.fr/2013DIJOS080/document.

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Mon travail de thèse porte sur l’étude du rôle de l’histone acétyl-transférase MOZ et de l’histone méthyle-transférase MLL dans l’hématopoïèse. Elles contrôlent l’expression de nombreux gènes, nottament des gènes HOX, des facteurs de transcription connus pour leur rôle dans l’hématopoïèse normale et pathologique. Les deux protéines ont des gènes cibles communs tel qu'HOXA9. Ces observations nous ont conduit à rechercher une coopération fonctionnelle entre MOZ et MLL. Nous avons montré que MOZ était associée avec MLL dans les cellules souches/progénitrices humaines CD34+ afin d’activer la transcription des gènes HOXA5, HOXA7 et HOXA9. En effet, les deux protéines interagissent et sont recrutées au niveau de leur promoteur. Nous avons mis en évidence une interférence fonctionnelle entre ces deux facteurs épigénétiques, puisque MOZ est nécessaire au recrutement et à l’activité enzymatique de MLL au niveau des gènes HOXA5, HOXA7 et HOXA9 et réciproquement.Afin de caractériser le mécanisme d’action impliquant la coopération entre MOZ et MLL, nous avons recherché d’autres partenaires associés à ce duo. Nous avons identifié la Symplekin, un membre de la machinerie de polyadénylation. Nous avons mis en évidence l’interaction de la Symplekin avec MOZ et MLL dans les cellules de la lignée hématopoïétique humaine KG1. Les trois protéines sont co-recrutées sur le promoteur du gène HOXA9. Nous avons démontré le rôle ambivalent de la Symplekin. Bien qu’elle soit importante pour la polyadénylation et par conséquent pour la stabilité de l’ARN Hoxa9, la Symplekin empêche le recrutement de MOZ et de MLL au niveau du gène HOXA9, conduisant ainsi à une diminution de sa transcription
My thesis project has consisted of the study of MOZ, and MLL. They are epigenetic regulators. MOZ and MLL activate transcription of HOX genes, which are transcription factors essential during haematopoiesis. MOZ and MLL have some target genes in common. In our study, we characterised a cooperation between MOZ and MLL in human haematopoietic stem/progenitor cells CD34+. They are both recruited onto HOX promoters. MOZ is essential for MLL recruitment, and this is reciprocal. In conclusion, we provided an example of a mechanism involving a direct cross-talk between two histone modifying enzymes.In order to dissect the mechanism of action of this complex, we decided to identify novel proteins interacting with both MOZ and MLL. A member of the RNA polyadenylation machinery has been isolated: Symplekin. We confirmed the interaction between MOZ, MLL and Symplekin in the human haematopoietic immature cell line KG1. We showed that Symplekin is co-recruited to HOXA9 promoter along with MOZ and MLL. We demonstrated the dual role of this member of the polyadenylation machinery. Indeed, besides the fact that Symplekin is important for Hoxa9 polyadenylation, thus its stability, it prevents MOZ and MLL recruitment onto HOXA9 promoter, leading to a decrease of HOXA9 transcription.Our work improved the understanding of the mechanism of action of MOZ and MLL in HOX control
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Chen, Linping [Verfasser]. "Selective expansion of GP 91phox gene-modified murine haematopoeitic stem cells / by Linping Chen." 2006. http://d-nb.info/979969387/34.

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Conference papers on the topic "Haematopoeitic"

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Ramesh, Nisha, Mohamed E. Salama, and Tolga Tasdizen. "Segmentation of haematopoeitic cells in bone marrow using circle detection and splitting techniques." In 2012 IEEE 9th International Symposium on Biomedical Imaging (ISBI 2012). IEEE, 2012. http://dx.doi.org/10.1109/isbi.2012.6235520.

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Lane, Matthew A., Venetia Bigley, Matt Collin, Cliff Morgan, and Jim L. Lordan. "Pulmonary Alveolar Proteinosis Due To Monocytopenia: Lung Transplant Or Haematopoeitic Stem Cell Transplant?" 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.a1141.

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