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- Abul-Kasim, Kasim, et al.
(författare)
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Spinal Cord Injuries
- 2010
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Ingår i: Trauma to the spinal cord.. - 9781608760022 ; , s. 483-499
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Bokkapitel (refereegranskat)abstract
- Spinal cord injury can be classified as traumatic and non-traumatic. The traumatic spinal cord injuries (SCI) are caused by motor vehicle accidents (56 %), falls (14 %), firearm and violence-related (16.6 %) and sports injuries (7 %) [1]. Injuries after falls and minor trauma are more commonly seen in elderly patients as they more often have spondylosis and osteoporosis. Violence is more common in urban populations while sports injuries are common in young individuals. About 68 % of children involved in spinal cord injuries caused by motor vehicle accidents were not wearing a seatbelt. Almost 80% of patients with spinal cord injury had multiple injuries [2]. Associated injuries include other bone fractures(29.3 %) and brain injury (11.5 %) [3]. Other causes of spinal cord injuries are non-traumatic and include the following: vascular disorders, degenerative disorders, spinal tumors, infectious and inflammatory conditions of the vertebral column with secondary SCI as well as iatrogenic injuries after spinal injections and epidural catheter. Three possible mechanisms are believed to be involved in the development of spinal cord injuries [4]: (a) damage from direct trauma, (b) compression or transaction of neural elements by bone fragments, intraspinal hematoma, foreign bodies, or protruded disk, or (c) ischemia from damage of the spinal arteries or from venous congestion. As small arteries are disrupted by trauma, spinal cord swelling occurs within minutes after the trauma with resultant venous congestion and secondary ischemia. Cell death occurs days to weeks after the injury with involvement of the oligodendrocytes not only at the site of injury but also at several levels away from the injury site [5]. Following the primary spinal cord injury, a cascade of secondary injuries usually are initiated [6] resulting in: (a) vascular changes—ischemia, hemorrhage, and thrombosis [7], (b) Disturbance of electrolyte balance with accumulation of intracellular sodium resulting in edema [8], (c) accumulation of neurotransmitters and toxins edema [8], (d) inflammation [9], and (e) apoptosis.
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| 2. |
- Andersson, A., et al.
(författare)
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FLT3 mutations in a 10 year consecutive series of 177 childhood acute leukemias and their impact on global gene expression patterns
- 2008
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Ingår i: Genes, Chromosomes and Cancer. - : Wiley. - 1045-2257 .- 1098-2264. ; 47:1, s. 64-70
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Tidskriftsartikel (refereegranskat)abstract
- During 1995-2004, 209 children/adolescents were diagnosed with acute lymphoblastic or myeloid leukemia (ALL, AML) in Southern Sweden, of which 177 (85%), comprising 128 B-lineage ALL, 34 AML, and 15 T-cell ALL, could be analyzed for internal tandem duplications (ITD) and activating point mutations in the second tyrosine kinase domain (ATKD) of FLT3. Seventeen (10%) FLT3 mutations (6 ITD, 11 ATKD, mutually exclusive) were detected. None of the T-cell ALL harbored any mutations. ITD and ATKD were found in 2% and 6% of the B-lineage ALL and in 12% and 9% of the AML, being particularly common in high hyperdiploid ALL (14%), ALL (20%), and AML (23%) with 11q23/MLL rearrangements, and in AML with a normal karyotype (60%). All ATKD-positive AML with MLL rearrangements harbored the t(9,11)(p21,q23). Global gene expression data were available for 76 of the B-lineage ALL and 19 of the AML, of which 6 (8%) and 3 (16%) had FLT3 mutations, respectively. No distinct expression pattern associated with FLT3 mutations was identified. © 2007 Wiley-Liss, Inc.
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