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Moretti Luigi

contribution of steroids in patients receiving whole-brain irradiation for cerebral metastases. Clin Oncol (R Coll Radiol) 2004;16:339-44. 11. Edwards MS, Prados M. Current management of brain stem gliomas. Pediatr Neurosci 1987;13:309-15. 12. Hempen C, Weiss E, Hess CF. Dexamethasone treatment in patients with brain metastases and primary brain tumors: Do the benefits outweigh the side-effects? Support Care Cancer 2002;10:322-8. 13. Weissman DE. Glucocorticoid treatment for brain metastases and epidural spinal cord compression

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Irena Kostovska, Katerina Tosheska Trajkovska, Svetlana Cekovska, Goce Spasovski and Danica Labudovic

-936. 10. Benzing T. Signaling at the slit diaphragm. J Am Soc Nephrol 2004; 15(6): 1382-91. 11. Alain Meyrier. Mechanisms of Disease: focal segmental glomerulosclerosis. Nat Clin Pract Nephrol 2005; 1: 44-54. 12. Doyonnas R, Nielsen JS, Chelliah S, et al. Podocalyxin is a CD34-related marker of murine hematopoietic stem cells and embryonic erythroid cells. Blood 2005; 105 (11): 4170-4178. 13. Orlando RA, Takeda T, Zak B, et al. The glomerular epithelial cell anti-adhesin podocalyxin associates with the actin cytoskeleton

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Abhishek Singh and Birendra Nath Mallick

, Singh A, Khanday MA. Activation of inactivation process initiates rapid eye movement sleep. Prog Neurobiol 2012;97:259-76. 24. Mallick BN, Thankachan S, Islam F. Differential responses of brain stem neurons during spontaneous and stimulation-induced desynchronization of the cortical eeg in freely moving cats. Sleep Res Online 1998;1:132-46. 25. Chu NS, Bloom FE. Activity patterns of catecholamine-containing pontine neurons in the dorso-lateral tegmentum of unrestrained cats. J Neurobiol 1974;5:527-44. 26. Cedarbaum JM

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Ming Hong and Guangsheng He

prognosis is not identified. But MDS-RS without SF3B1 mutation might be associated with an adverse prognosis as compared to those with the mutation.[ 6 , 18 ] TP53 mutations are detected in approximately 5-20% of cases in MDS by NGS.[ 19 - 21 ] It is consistently shown that TP53 mutations are associated with the higher-risk MDS, therapy-related MDS and MDS with complex cytogenetics. It is well understood that TP53 mutational status predicts an aggressive disease in MDS and poor resistance to chemotherapy and allo-hematopoietic stem cells transplantation (allo

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Yuqiao Wang, Ying Zhou and Zhiyuan Hu

Cancer Cell Int 2017 17 6 5 Kasimir-Bauer S, Hoffmann O, Wallwiener D, Kimmig R, Fehm T. Expression of stem cell and epithelial-mesenchymal transition markers in primary breast cancer patients with circulating tumor cells. Breast Cancer Res 2012; 14: R15. 10.1186/bcr3099 Kasimir-Bauer S Hoffmann O Wallwiener D Kimmig R Fehm T. Expression of stem cell and epithelial-mesenchymal transition markers in primary breast cancer patients with circulating tumor cells Breast Cancer Res 2012 14 R15 6 Palmirotta R, Lovero D, Silvestris E, Felici C, Quaresmini D

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Shuai Wang and Guangsheng He

for clonal expansion is a very early immigrant from the bone marrow to the thymus, a cell expressing abundant T-lineage, stem-cell and myeloid-associated transcripts, and possessing both lymphoid and myeloid developmental potential [ 22 - 26 ] . The specific immunophenotype of ETP-ALL is CD1-, CD5weak, CD8-, or coexpression of stem cell and/or myeloid markers CD34, CD117, HLADR, CD13, CD33, CD11b or CD65 and its distinct molecular features are FLT3 mutations and absence of NOTCH1 mutations [ 27 , 28 ] . ETP-ALL was associated with an inferior clearance of leukemia

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Gianluca Rigatelli, Marco Zuin, Alan Fong, Truyen TTT Tai and Thach Nguyen

coronary ostia were also modelled, with particular attention to the left coronary stem. The model of ascending aorta and arch and LM was based on the dimensions obtained after analyzing transthoracic echocardiography (TTE) and coronary angiography (CA) of 80 consecutive patients (mean age 75.1 ± 6.2 years, 43 males) with significant (> 50%) luminal narrowing on quantitative coronary analysis (QCA) LM mid shaft or distal disease. These patients had no significant ascending aorta or aortic valve disease, and they had undergone percutaneous coronary intervention (PCI

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Ming Hong and Guangsheng He

is the source of the ectopic enhancer activating EVI1 in leukemia harboring inv(3)/t(3;3). Moreover, GATA2 is a critical hematopoietic stemness factor and aberrant EVI1 activation argues for a primitive HSC defect in this subtype of AML. Rewiring of parts of the GATA2 and EVI1 domains led to a reduction of GATA2 expression levels. Since primitive hematopoietic precursors will be particularly susceptible to disturbances of GATA2 homeostasis, GATA2 deficiency may provide the right spatiotemporal context for EVI1 oncogene activation, that is in the right cell at the

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Suli Wang, Chun Qiao, Yu Zhu, Wenyi Shen, Guangsheng He and Jianyong Li

. Although the T315A/F359I/M244V mutations were still positive, the quantity of BCR-ABL (P210) fusion gene was 8.98%, and the bone marrow cell chromosome was 46, XX [20]. Discussion Under the tyrosine kinase inhibitions (TKIs) therapy, there are still a number of patients with CML who progress to BC. How this leukemia transforms from a relatively indolent CP to an aggressive BC is still unclear. [ 2 ] Once BC happens, the management depends on the type of leukemia (myeloid or lymphoid) and if they successfully achieve CR or not. [ 3 ] Allogeneic stem cell

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Martin Rössle and Michael Schultheiss

or complete/occlusive, limited or extended and it may involve the extrahepatic portal system or the intrahepatic portal branches in isolation or in combination ( Figure 1 – 4 ). The great variance of thrombosis may be the result of variable flow patterns in the portal vein, portal tributaries and collaterals. For example, a large collateral flow may prevent thrombus formation in peripheral branches but induce thrombosis of the main stem of the portal vein ( Figure 1 ). On the other hand, a critical portal flow velocity may cause lining thrombosis of the main stem