Gotowa bibliografia na temat „Bone marrow”

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Artykuły w czasopismach na temat "Bone marrow"

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Varma, Amit, Ashok K. Rajoreya, Priyanka Kiyawat, Kamal Malukani, Shilpi Dosi i Sudarshan Gupta. "Utility of Bone Marrow Aspiration and Bone Marrow Biopsy in Haematological Disorders". Indian Journal of Pathology: Research and Practice 7, nr 4 (2018): 517–23. http://dx.doi.org/10.21088/ijprp.2278.148x.7418.20.

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Kulandaivel, Anbu Lenin, i Kumudhini Priya Gunasekaran. "A A Correlative Study on Bone Marrow Angiogenesis with Bone Marrow Fibrosis and Splenomegaly". Annals of Pathology and Laboratory Medicine 5, nr 8 (19.08.2018): A722–728. http://dx.doi.org/10.21276/apalm.2120.

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Sengupta, Dr Moumita, Dr Kaushik Saha i Dr chetna J. Mistry. "Bone Marrow Aspiration Study in Thrombocytopenia". International Journal of Scientific Research 1, nr 7 (1.06.2012): 136–39. http://dx.doi.org/10.15373/22778179/dec2012/48.

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Khatik, Dr Daleep Kumar. "A Relevance Study of Bone Marrow Aspiration and Bone Marrow Biopsy in Haematological and Non Haematological Disorders". Journal of Medical Science And clinical Research 05, nr 04 (27.04.2017): 20900–20908. http://dx.doi.org/10.18535/jmscr/v5i4.184.

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NIKOLAEVA, L. P. "pH OF BONE MARROW". Periódico Tchê Química 16, nr 32 (20.08.2019): 388–94. http://dx.doi.org/10.52571/ptq.v16.n32.2019.406_periodico32_pgs_388_394.pdf.

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The bone marrow is a “niche” for stem cells; determining the bone marrow pH value is of great importance. It is very difficult, almost impossible, to carry out the intravital determination of pH. In surgical practice, there are situations when doctors have no way to save the patient's lower limb because of the threat to life. In such cases, it is possible to extract the bone marrow from the bone marrow cavity of the amputated femur and examine it. The purpose of this research was to study the acid-base balance peculiarities of the marrow of long bones and carry out a comparative analysis of the obtained data and the indicators of flat bones. The study included 40 test samples of bone marrow. Lower limb amputations were performed because of foot gangrene. Bone marrow was extracted from the femur. The marrow of flat bones was obtained by a sternal puncture. In the pH test of the sternal puncture, the data varied within the range of the blood pH, i.e., between 7.35-7.45 and 7.8. The pH and gas composition data of the sternal puncture were identical to the blood indicators. The data of bone marrow obtained from the long bone was completely different. The acid-base balance strictly ranged from 6.7 to 6.9.
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Harness, Mary, Charlotte Bloodworth i Cath Lloyd. "Bone marrow". Cancer Nursing Practice 6, nr 6 (lipiec 2007): 14–16. http://dx.doi.org/10.7748/cnp.6.6.14.s15.

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Libby, Peter. "Bone Marrow". Circulation 108, nr 4 (29.07.2003): 378–79. http://dx.doi.org/10.1161/01.cir.0000084801.04026.7b.

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Unger, Evan C., i Thomas B. Summers. "Bone marrow". Topics in Magnetic Resonance Imaging 1, nr 4 (wrzesień 1989): 31???52. http://dx.doi.org/10.1097/00002142-198909000-00006.

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Murphy, Darra T., Michael R. Moynagh, Stephen J. Eustace i Eoin C. Kavanagh. "Bone Marrow". Magnetic Resonance Imaging Clinics of North America 18, nr 4 (listopad 2010): 727–35. http://dx.doi.org/10.1016/j.mric.2010.07.003.

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Gribben, J. G., i L. M. Nadler. "Bone Marrow Purging for Autologous Bone Marrow Transplantation". Leukemia & Lymphoma 11, sup2 (styczeń 1993): 141–48. http://dx.doi.org/10.3109/10428199309064274.

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Rozprawy doktorskie na temat "Bone marrow"

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勞錦輝 i Kam-fai Simon Lo. "Cytomegalovirus and bone marrow transplantation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31215609.

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Lo, Kam-fai Simon. "Cytomegalovirus and bone marrow transplantation /". Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19471142.

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Fadini, Gian Paolo. "Bone marrow dysfunction in diabetes". Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3422580.

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Background. Diabetes mellitus (DM) increases cardiovascular disease (CVD) and this is attributed, at least in part, to shortage of vascular regenerative cells derived from the bone marrow (BM). Indeed, the BM harbours several subsets of progenitor cells for endothelial, smooth muscle cells and cardiomyocytes, which derive from a common CD34+ ancestor. Recent data from experimental models of type 1 and type 2 diabetes highlight BM pathologies that include microangiopathy, neuropathy, altered gene expression and niche dysfunction. Aims. The set of experiments herein described aim to portray the alterations of BM function in clinical and experimental diabetes. Methods. The approaches are diversified and include: 1) A prospective trial of direct BM stimulation with human recombinant granulocyte colony stimulating factor (G-CSF) in diabetic and non diabetic patients; 2) A meta-regression analysis of trials using G-CSF to stimulate cardiovascular repair in diabetic and non diabetic patients; 3) A study of stem/progenitor cell compartmentalization in the BM and peripheral blood (PB), in relation to diabetes; 4) An animal study to dissect the role of DPP-4 dysregulation in the impaired stem/progenitor cell mobilization induced by diabetes. Results. Part 1: in response to G-CSF, levels of CD34+ cells and other progenitor cell phenotypes increased in non DM subjects. DM patients had significantly impaired mobilization of CD34+, CD133+, CD34+CD133+ hematopoietic stem cells and CD133+KDR+ endothelial progenitors, independently of potential confounders. The in vivo angiogenic capacity of circulating mononuclear cells increased after hrG-CSF in non DM controls, but not in DM patients. DM was associated with inability to upregulate CD26/DPP-4 on CD34+ cells, which is required for the mobilizing effect of G-CSF. Part 2: for the meta-regression analysis 227 articles were screened, 96 were retrieved for evaluation and 24 retained for the analysis of the primary end-point. There was a strong negative correlation between prevalence of diabetes and achieved CD34+ cell levels after G-CSF stimulation (r=-0.68; p<0.0001), while there was no correlation with other traditional risk factors. A multiple regression analysis showed that the correlation between diabetes and mobilization was independent. In 13 articles reporting pre- and post-G-CSF cell counts, the increase in CD34+ cells was also negatively correlated with prevalence of diabetes (r=-0.82; p<0.0001). Part 3. PB and BM CD34+ cell counts were directly correlated, and that most circulating CD34+ cells were viable, non-proliferating and derived from the BM. Then, PB and BM CD34+ cell levels were analyzed in a 2-compartment model in 72 patients with or without cardiovascular disease. Self organizing maps showed that disturbed compartmentalization of CD34+ cells was associated with aging and cardiovascular risk factors, especially diabetes. High activity of DPP-4, a regulator of the mobilizing chemokine SDF-1α, was associated with altered stem cell compartmentalization. The role of DPP-4 in the BM mobilization response of diabetic rats was then assessed. Diabetes differentially affected DPP-4 activity in PB and BM and impaired stem/progenitor cell mobilization after ischemia or G-CSF administration. DPP-4 activity in the BM was required for the mobilizing effect of G-CSF, while in PB it blunted ischemia-induced mobilization. Indeed, DPP-4 deficiency restored ischemia (but not G-CSF) -induced stem cell mobilization and improved vascular recovery in diabetic animals. Conclusion. Evidences from multiple clinical and experimental approaches indicate that diabetes impairs the mobilization of stem/progenitor cells from the BM to PB. This primary BM defect is related to a maladaptive and tissue-specific DPP-4 dysregulation
Presupposti. Il diabete mellito (DM) aumenta il rischio cardiovascolare e ciò viene attribuito almeno in parte alla riduzione delle cellule vasculo-rigenerative di origine midollare. Infatti il midollo osseo contiene precursori per cellule endoteliali, muscolari lisce e cardiomiociti, che derivano da un progenitore CD34+. Dati recenti ottenuti da modelli sperimentali di diabete tipo 1 e tipo 2 indicano l’esistenza di difetti midollari che includono microangiopatia, neuropatia, alterazione dell’espressione genica e disfunzione della nicchia staminale. Obiettivi. Questo set di esperimenti ha avuto l’obiettivo di descrivere in dettaglio le alterazioni della funzione midollare nel diabete clinico e sperimentale. Metodi. Gli approcci metodologici sono diversificati e comprendono: 1) un trial di stimolazione midollare diretta con G-CSF ricombinante umano in pazienti con e senza diabete; 2) un’analisi di meta-regressione dei trials in cui il G-CSF è stato somministrato per indurre rigenerazione cardiovascolare in pazienti con e senza diabete; 3) lo studio della compartimentalizzazione delle cellule staminali/progenitrici nel midollo e nel sangue periferico, in relazione al diabete; 4) un modello animale per la definizione del ruolo di DPP-4 nel difetto di mobilizzazione midollare associato al diabete. Risultati. Parte 1: in risposta al G-CSF, le cellule CD34+ circolanti aumentavano significativamente nel paziente non diabetico, ma non nel diabetico, che mostrava anche una difettosa mobilizzazione di cellule ematopoietiche CD133+ e CD34+CD133+, nonché di cellule progenitrici endoteliali CD133+KDR+, indipendentemente dai possibili fattori confondenti. La capacità angiogenica in vivo delle cellule mononucleate aumentava significativamente dopo G-CSF nei soggetti diabetici ma non nei non diabetici, rispetto al basale. Il diabete risultava associato ad una incapacità di upregolare DPP-4 sulle cellule CD34+ in risposta al G-CSF. Parte 2: per la meta-regressione sono stati individuati 227 articoli, recuperati 96 e trattenuti 24 per l’analisi primaria. È stata identificata una forte correlazione negativa tra prevalenza del diabete all’interno di ogni trial e livello delle cellule CD34+ raggiunte dopo mobilizzazione con G-CSF (r=-0.68; p<0.0001). Una analisi di regressione multipla ha confermato che il risultato era indipendente da possibili fattori confondenti. In 13 articoli contenenti dati sui livelli di cellule CD34+ pre- e post-G-CSF, la correlazione negativa tra prevalenza del diabete e mobilizzazione appariva ancora più stretta (r=-0.82; p<0.0001). Parte 3: i livelli delle cellule CD34+ nel midollo e nel sangue periferico risultano essere direttamente correlati e la maggior parte delle cellule CD34+ erano di origine midollare, non proliferanti e non apoptotiche. Lo studio della compartimentalizzazione delle cellule CD34+ in 72 pazienti con e senza malattia cardiovascolare mediante l’uso delle mappe auto-organizzanti ha permesso di rilevare alterazioni della mobilizzazione in presenza di diabete ed elevato rischio cardiovascolare. Inoltre, un’elevata attività plasmatica di DPP-4 si associava ad alterata compartimentalizzazione delle cellule CD34+. In ratti diabetici rispetto ai controlli, l’attività di DPP-4 risultava significativamente aumentata nel sangue periferico e ridotta nel midollo osseo. Lo studio di ratti geneticamente deficienti dell’enzima DPP-4 ha permesso di stabilire che l’alterazione tessuto-specifica di DPP-4 nel diabete è responsabile del difetto di mobilizzazione post-G-CSF e post-ischemia. La delezione di DPP-4 ripristinava la mobilizzazione post-ischemica di cellule staminali ematopoietiche e progenitrici endoteliali e favoriva il recupero del tessuto ischemico nel diabete. Conclusioni. Diversi tipi di evidenze sperimentali indicano chiaramente che il diabete induce un difetto nella mobilizzazione delle cellule staminali/progenitrici midollari. Questo difetto primitivo del midollo osseo nel diabete è correlato ad una disregolazione tessuto-specifica dell’attività dell’enzima DPP-4
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Fisher, Maya. "Bone marrow regeneration follwing tibial marrow ablation in rats is age dependent". Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/26526.

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Thesis (M. S.)--Biology, Georgia Institute of Technology, 2009.
Committee Chair: Boyan Barbara; Committee Member: Guldberg Robert; Committee Member: Lovachev Kiril; Committee Member: Schwartz Zvi. Part of the SMARTech Electronic Thesis and Dissertation Collection.
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Jackson, G. H. "Long term bone marrow culture studies of patients with lymphoid malignancies undergoing autologous bone marrow transplantation". Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309068.

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Schmidt-Mende, Jan Georg. "Bone marrow apoptosis in myelodysplastic syndromes". [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=96939781X.

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McIntosh, Bryan James. "Regulation of thrombopoietin in bone marrow". Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3284334.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed January 9, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 50-58).
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Funaki, Hilde. "Psychological responses to bone-marrow-transplantation". Thesis, City University London, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283269.

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Sebastian, Anil. "Recreating bone marrow tissues in vitro". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528263.

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Davison, Glenda Mary. "Immune reconstitution post bone marrow transplantation". Master's thesis, University of Cape Town, 2000. http://hdl.handle.net/11427/3376.

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Bibliography: leaves 82-95.
The aims of this project were therefore: to document the immune reconstitution following T-cell depleted bone marrow and peripheral blood stem cell transplantation and to compare this with the recovery following autologous grafts. to document the cell surface expression of CD95 in an attempt to comment on the role played by FAS mediated apoptosis in the post transplant immune deficiency.
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Książki na temat "Bone marrow"

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Espéli, Marion, i Karl Balabanian, red. Bone Marrow Environment. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1425-9.

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Nagasawa, Takashi, red. Bone Marrow Niche. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-86016-5.

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Bain, Barbara J., David M. Clark i Bridget S. Wilkins. Bone Marrow Pathology. Chichester, UK: John Wiley & Sons, Ltd, 2019. http://dx.doi.org/10.1002/9781119398929.

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Gatter, Kevin, i David Brown, red. Bone Marrow Diagnosis. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118952061.

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Ikehara, Susumu, Fumimaro Takaku i Robert A. Good, red. Bone Marrow Transplantation. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68320-9.

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Penchansky, Lila. Pediatric Bone Marrow. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18799-5.

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Moulopoulos, Lia Angela, i Vassilis Koutoulidis. Bone Marrow MRI. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5316-8.

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Bain, Barbara J., David M. Clark, Irvin A. Lampert i Bridget S. Wilkins, red. Bone Marrow Pathology. Oxford, UK: Blackwell Science Ltd, 2001. http://dx.doi.org/10.1002/9780470757130.

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Kupfer, Gary M., Gregory H. Reaman i Franklin O. Smith, red. Bone Marrow Failure. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-61421-2.

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Champlin, Richard, red. Bone Marrow Transplantation. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1493-6.

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Części książek na temat "Bone marrow"

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O’Malley, Dennis P. "Bone Marrow". W Essentials of Anatomic Pathology, 493–532. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-60327-173-8_11.

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Bain, B. J. "Bone marrow". W Reporting Histopathology Sections, 263–79. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-7132-6_17.

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Hruban, Ralph H., William H. Westra, Timothy H. Phelps i Christina Isacson. "Bone Marrow". W Surgical Pathology Dissection, 200–202. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4757-2548-3_40.

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Bruneau, Julie, Chantal Brouzes, Vahid Asnafi i Thierry J. Molina. "Bone Marrow". W Encyclopedia of Pathology, 73–87. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-95309-0_3875.

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O’Malley, Dennis P., i Yuri Fedoriw. "Bone Marrow". W Essentials of Anatomic Pathology, 821–68. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23380-2_17.

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Brown, Geoff. "Bone Marrow". W Atlas of Comparative Diagnostic and Experimental Hematology, 115–20. West Sussex, UK: John Wiley & Sons, Ltd., 2013. http://dx.doi.org/10.1002/9781118785072.ch9.

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Babyn, Paul, i Jennifer Stimec. "Bone Marrow". W Pediatric Orthopedic Imaging, 873–901. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-45381-6_25.

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Bruneau, Julie, Chantal Brouzes, Vahid Asnafi i Thierry Jo Molina. "Bone Marrow". W Encyclopedia of Pathology, 1–15. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-28845-1_3875-1.

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Nothdurft, W. "Bone Marrow". W Medical Radiology, 113–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-83416-5_4.

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Vilanova, Joan C., Mercedes Roca i Sandra Baleato. "Bone Marrow". W Learning Musculoskeletal Imaging, 67–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-88000-4_4.

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Streszczenia konferencji na temat "Bone marrow"

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"1ST BONE MARROW ADIPOSITY SOCIETY (BMAS) SUMMER SCHOOL". W 1ST BONE MARROW ADIPOSITY SOCIETY (BMAS) SUMMER SCHOOL. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-006-5.

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Sayo, Kanae, Shigehisa Aoki i Nobuhiko Kojima. "A method to reorganize the bone marrow-like tissue with suspension of bone marrow cells". W 2015 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2015. http://dx.doi.org/10.1109/mhs.2015.7438268.

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Sieber, Fritz. "Photodynamic therapy and bone marrow transplantation". W SPIE Institutes for Advanced Optical Technologies 6, redaktor Charles J. Gomer. SPIE, 1990. http://dx.doi.org/10.1117/12.2283678.

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Nguyen, Chuong T., Joseph P. Havlicek, Jennifer Holter Chakrabarty, Quyen Duong i Sara K. Vesely. "Towards automatic 3D bone marrow segmentation". W 2016 IEEE Southwest Symposium on Image Analysis and Interpretation (SSIAI). IEEE, 2016. http://dx.doi.org/10.1109/ssiai.2016.7459162.

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Büyüktür, Ayşe G., i Mark S. Ackerman. "Information Work in Bone Marrow Transplant". W CSCW '17: Computer Supported Cooperative Work and Social Computing. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/2998181.2998361.

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Zhang, Xiwen, Yanxuan Xu, Hang Xu, Nan Li, Miaohui Li, Zanzhou Bai, Bing Chen, Jie Yang i Yu Qiao. "Probability Based Bone Marrow Cell Detection". W 2022 5th International Conference on Data Science and Information Technology (DSIT). IEEE, 2022. http://dx.doi.org/10.1109/dsit55514.2022.9943845.

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Zhu, Jun, Heather T. Ma, Xinxin Zhao, Rong Ren, Xu Xing, James F. Griffth i Ping-Chung Leung. "Finite element analysis of trabecular bone with bone marrow fat". W TENCON 2013 - 2013 IEEE Region 10 Conference. IEEE, 2013. http://dx.doi.org/10.1109/tencon.2013.6718957.

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Lin, Charles P. "Optical Techniques for Studying Bone Regeneration and Bone Marrow Transplantation". W Biomedical Optics. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/biomed.2014.bw1a.1.

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Pindur, G., E. Seifried i H. Rasche. "FIBRIN DEPOSITS IN BONE MARROW AND CHANGES IN HAEMOPOIESIS AFTER ENDOTOXIN ADMINISTRATION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644256.

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Thrombotic occlusion of microcirculation during DIC has already been studied in numerous organs, but little is known about analogous findings in the bone marrow. Therefore in rats under the influence of endotoxin the defibrination was examined for its relationship to changes inthe bone marrow and haemopoiesis. Bone marrow specimens were studied histologically by fibrin staining methods. Blood cells were measured automatically on the Coulter counter, fibrinogen by clotting assay. A fall in the thrombocyte and fibrinogen level was induced through a single injection of endotoxin with a maximum after 24 hours and 48 hours. In the same phase, after a short-term drop, a marked rise in the leukocyte count in the peripheral blood was observed. Following an initial increase the erythrocytes dropped and reached their lowest level after 48 hours. In the bone marrow 24 hours after endotoxin administration a large amount of fibrin deposits were observed in the small vessels. At the same time a clear reduction in all three haemopoietic cell lines was noticed. Between days five and ten the parameters of the peripheral blood normalized. Fibrin deposits in the bone marrow were no longer evident after three days. After 28 days an increase in the granulocytopoiesis and a continuing reduction in the megakaryopoiesis was observed.lt is concluded, due to the existence of fibrin deposits in the bone marrow in the beginning phase, that the observed haematologic alterations can not only be explained by the direct effect of endotoxin, but possibly also by the temporary microcircu-latory disturbances of the bone marrow during defibrination with its adverse effects on the haemopoiesis.
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Cao, Danfeng, Jose G. Martinez, Laetitia Skalla, Erik Hultin, Jan-Ingvar Jönsson, Risa Anada, Hiroshi Kamioka, Edwin W. H. Jager i Emilio Satoshi Hara. "Tunable electroactive biomimetic bone-like surfaces for bone marrow-on-chips". W 2023 IEEE BioSensors Conference (BioSensors). IEEE, 2023. http://dx.doi.org/10.1109/biosensors58001.2023.10281047.

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Raporty organizacyjne na temat "Bone marrow"

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Pan, Shi. Redox Regulation in Bone Marrow Failure. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2012. http://dx.doi.org/10.21236/ada566819.

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Horwitz, Marshall S. Translational Control in Bone Marrow Failure. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2014. http://dx.doi.org/10.21236/ada605027.

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Coppo, Patricia A., Judy W. Davis i Steve M. Spellman. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2007. http://dx.doi.org/10.21236/ada462775.

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Spellman, Stephen. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2011. http://dx.doi.org/10.21236/ada546709.

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Setterholm, Michelle, Judy W. Davis i Steve M. Spellman. HLA Typing for Bone Marrow Transplantation. Fort Belvoir, VA: Defense Technical Information Center, październik 2007. http://dx.doi.org/10.21236/ada473611.

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Knudsen, Beatrice. Androgen, Estrogen, and the Bone Marrow Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2006. http://dx.doi.org/10.21236/ada484320.

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Knudsen, Beatrice. Androgen, Estrogen, and the Bone Marrow Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2008. http://dx.doi.org/10.21236/ada502772.

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Knudsen, Beatrice. Androgen, Estrogen and the Bone Marrow Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2009. http://dx.doi.org/10.21236/ada526009.

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Knudsen, Beatrice. Androgen, Estrogen and the Bone Marrow Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2009. http://dx.doi.org/10.21236/ada525230.

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Knudsen, Beatrice. Androgen, Estrogen, and the Bone Marrow Microenvironment. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2007. http://dx.doi.org/10.21236/ada479437.

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