| 1. |
- Jensen, Norman, et al.
(author)
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Early attachment of platelets, leukocytes, and fibrinogen in endothelial cell seeded Dacron grafts
- 1996
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In: Annals of Vascular Surgery. - 1615-5947. ; 10:6, s. 530-536
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Journal article (peer-reviewed)abstract
- Endothelial cell seeding has been advocated as a method for reducing the thrombogenicity of prosthetic grafts. Principally two different techniques for endothelial cell seeding can be used: immediate seeding of grafts followed by implantation or initial growth and establishment of an endothelial cell-covered surface before subsequent late implantation. This study was designed to determine whether the immediate seeding technique altered thrombogenicity directly after graft implantation. Carotid arteries from 19 sheep were replaced with Dacron interposition grafts; one side was seeded with endothelial cells and the other side was left unseeded. The dynamics of thrombus formation involving radiolabeled platelets, leukocytes, and fibrinogen were studied for 4 hours with flow reduced to 35 ml/min. No difference in platelet uptake (approximately 6-fold increase compared to baseline values) was found between endothelial cell seeded and unseeded grafts. Likewise, there were no differences in leukocyte uptake (approximately 4-fold increase) or fibrinogen uptake (approximately 10- to 15-fold increase) between the two groups. No differences were demonstrated with regard to patency or thrombus weight. In this experimental investigation we were unable to verify any change in the uptake of platelets, white blood cells, or fibrinogen between endothelial cell seeded and unseeded Dacron grafts during the first 4 hours after graft placement. Immediate seeding does not affect the initial thrombogenicity of grafts.
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| 2. |
- Söderholm, Helena, 1969-, et al.
(author)
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Human achaete-scute homologue 1 (HASH-1) is downregulated in differentiating neuroblastoma cells
- 1999
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In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 256:3, s. 557-563
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Journal article (peer-reviewed)abstract
- The mammalian achaete-scute homologue, MASH-1, is crucial for early development of the sympathetic nervous system and is transiently expressed in sympathetic neuroblasts during embryogenesis. Here we report that the human homologue (HASH-1) was expressed in all analyzed cell lines (6/6) derived from the sympathetic nervous system tumor neuroblastoma. The majority of small-cell lung carcinoma (4/5) cell lines tested expressed HASH-1, while other nonneuronal/non-neuroendocrine cell lines were negative. Induced differentiation of neuroblastoma cells resulted in HASH-1 downregulation. This occurred concomitant with induction of neurite outgrowth and expression of the neuronal marker genes GAP-43 and neuropeptide Y. Constitutive expression of exogenous HASH-1 did not alter the capacity of the neuroblastoma cells to differentiate in response to differentiation-inducing agents. It is concluded that moderate HASH-1 expression does not compromise the capacity of these cells to differentiate.
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| 3. |
- Øra, Ingrid, et al.
(author)
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Arsenic trioxide inhibits neuroblastoma growth in vivo and promotes apoptotic cell death in vitro
- 2000
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In: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 277:1, s. 179-185
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Journal article (peer-reviewed)abstract
- Recent clinical studies have shown that inorganic arsenic trioxide (As(2)O(3)) at low concentrations induces complete remission with minimal toxicity in patients with refractory acute promyelocytic leukemia (APL). Preclinical studies suggest that As(2)O(3) induces apoptosis and possibly differentiation in APL cells. Like APL cells, neuroblastoma (NB) cells are thought to be arrested at an early stage of differentiation, and cells of highly malignant tumors fail to undergo spontaneous maturation. Both APL and NB cells can respond with differentiation to retinoic acid (RA) treatment in vitro and probably also in vivo. For that reason we investigated the effect of As(2)O(3) alone and in combination with RA on NB cell lines. In vitro, the number of viable NB cells was reduced at As(2)O(3) concentrations around 1 microM after 72 h exposure. The IC50 in six different cell lines treated for 3 days was in the 1.5 to 5 microM concentration interval, the most sensitive being SK-N-BE(2) cells derived from a chemotherapy resistant tumor. The combined treatment with RA (1 and 3 microM) showed no consistent additional effect with regard to induced cell death. The effect of As(2)O(3) on NB cell number involved As(2)O(3)-induced apoptotic pathways (decreased expression of Bcl-2 and stimulation of caspase-3 activity) with no clear evidence of induced differentiation. The in vivo effect of As(2)O(3) on NB growth was also investigated in nude mice bearing tumors of xenografted NB cells. Although tumor growth was reduced by As(2)O(3) treatment, complete remission was not achieved at the concentrations tested. We suggest that As(2)O(3), in combination with existing treatment modalities, might be a treatment approach for high risk NB patients.
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