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- Aust, Gabriela, et al.
(författare)
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CD97: A dedifferentiation marker in human thyroid carcinomas
- 1997
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Ingår i: Cancer Research. - 0008-5472 .- 1538-7445. ; 57:9, s. 1798-1806
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Tidskriftsartikel (refereegranskat)abstract
- CD97 is a dimeric glycoprotein of Mr 75,000-85,000 and 28,000 belonging to a novel subfamily of seven-span transmembrane region leukocyte cell surface molecules. It is expressed abundantly in cells of hematopoietic origin. This is the first report demonstrating the expression of CD97 outside the hematopoetic system. CD97 was studied in normal human and neoplastic follicular epithelium of the thyroid and anaplastic (n = 3) and papillary (n = 1) thyroid carcinoma cell lines. In normal thyroid tissue (n = 11), no immunoreactivity of CD97 could be found, whereas in differentiated thyroid carcinomas (n = 10), CD97 expression was either lacking or low. Eleven of 12 undifferentiated anaplastic carcinomas revealed high CD97 presentation. CD97 was absent or only weakly present in patients with postoperative T1 tumors but increased greatly with the progression to postoperative T4 tumors. CD97 is clearly present in thyroid carcinoma cell lines but only at a very low level in normal human thyrocytes. Quantitation of CD97 cell surface expression levels revealed that C 643 and SW 1736 cells showed a two to four times higher specific antibody-binding capacity than did 8505 C and HTh 74 cells and a nearly 20 times higher specific antibody-binding capacity than normal thyrocytes. Phorbol 12-myristate 13-acetate treatment progressively caused a decrease of CD97 antigen expression in all cell lines to about 30% of their initial levels after 48 h. Immunohistochemical staining of SW 1736 cells revealed that CD97 is located in most of the cell compartments and suggested a CD97 internalization process after phorbol 12-myristate 13-acetate treatment. Semiquantitative reverse transcription-PCR showed a correlation of CD97 mRNA and cell surface CD97 expression level in the cell lines. SW 1736, HTh 74, and 8505 C cells apparently expressed CD97 with alternative glycosylation compared to peripheral lymphocytes, whereas most of the CD97 antigen presented on thyrocytes and C 643 cells had glycosylation sites resembling those of lymphocytes. The data suggest that CD97 expression may be a sensitive marker of dedifferentiation and of lymph node involvement in human thyroid tumors.
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- Schou, Henning, et al.
(författare)
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Central and mixed venous blood oxygen correlate well during acute normovolemic hemodilution in anesthetized pigs
- 1998
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172. ; 42:2, s. 172-177
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Central venous oxygen saturation (ScvO2) and oxygen tension (PcvO2), obtained from the superior vena cava, correlate well with mixed venous (pulmonary arterial) oxygen saturation (SvO2) and tension (pvO2) when the hematocrit is normal. The present study was undertaken to assess whether extreme hemodilution affects this relation. METHODS: We compared mixed and central venous blood during graded arterial desaturation (inspired fraction of oxygen (FIO2) between 1.0 and 0.10) in 10 hemodiluted pigs, and in 10 pigs with normal hematocrit (control), during fentanyl-ketamine-pancuronium anesthesia and mechanical ventilation. RESULTS: Arterial oxygen saturation decreased from 100% at FIO2 = 1.0 to 44 +/- 12% at FIO2 = 0.10 (mean +/- SD). Venous oxygen saturation ranged from 3.5% to 97.3%. The regression coefficient between SvO2 and ScvO2 was 0.97 (R2 = 0.93, bias -2.4 +/- 5.8%) in the hemodiluted and 0.99 (R2 = 0.97, bias -3.0 +/- 5.0%) in the control group. Venous oxygen tension values ranged from 0.5 kPa to 9.5 kPa, and the regression coefficient for oxygen tension was 0.94 (R2 = 0.89, bias -0.20 +/- 0.47 kPa) in the hemodiluted and 0.99 (R2 = 0.97, bias -0.43 +/- 0.48 kPa) in the control group. The regression coefficient for pH was 0.95 in the hemodiluted and 0.98 in the control animals. CONCLUSION: The findings indicate that also during hemodilution monitoring of central venous blood oxygen may be as useful as monitoring of mixed venous blood oxygen.
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- Schou, Henning, et al.
(författare)
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Hemodilution significantly decreases tolerance to isoflurane-induced cardiovascular depression
- 1997
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172. ; 41:2, s. 218-228
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Hemodilution is used to reduce the need for allogenic blood transfusion. The aim of this study was to evaluate to what extent acute extreme normovolemic hemodilution affects the circulatory response to isoflurane. METHODS: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to isoflurane at end-tidal concentrations of 0, 0.5, 1.0, 1.5 and 2%, before and after extreme normovolemic hemodilution (hematocrit 33 +/- 3% and 11 +/- 1%, respectively). Systemic and myocardial hemodynamics and oxygen delivery and consumption were measured. RESULTS: At zero end-tidal isoflurane concentration, hemodilution caused an increase in cardiac output (from 157 +/- 12 to 227 +/- 39 ml kg min-1, P < 0.01) a decrease in systemic vascular resistance (from 39 +/- 7 to 18 +/- 5 mmHg.L-1.min-1, P < 0.01) a decrease in mean arterial blood pressure (MAP) (from 130 +/- 13 to 91 +/- 13 mmHg, P < 0.01) and a decrease in systemic oxygen delivery (from 23.1 +/- 2.7 to 11.8 +/- 1.7 ml.kg-1.min-1, P < 0.01). When the end-tidal isoflurane concentration was increased from 0 to 2% after hemodilution, cardiac output decreased by 86 +/- 37 ml.kg-1.min-1, as compared with 36 +/- 20 ml.kg-1.min-1 (P < 0.01) before hemodilution. Likewise, systemic vascular resistance decreased with increasing isoflurane concentrations; at 2%, the decrease was 7 +/- 4 mmHg.L-1.min-1 after hemodilution and 18 +/- 5 mmHg.L-1.min-1 before hemodilution (P < 0.01). At an end-tidal isoflurane concentration of 2%, MAP had decreased to 43 +/- 6 mmHg after hemodilution, and to 61 +/- 15 mmHg before hemodilution (P < 0.01). After hemodilution, isoflurane concentrations above 1% decreased systemic oxygen delivery enough to cause delivery-dependent oxygen consumption and hyperlactemia; and at 2% isoflurane, myocardial blood flow became insufficient, as indicated by myocardial lactate production. CONCLUSIONS: isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.
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| 5. |
- Schou, Henning, et al.
(författare)
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Nitrous oxide reduces inspired oxygen fraction but does not compromise circulation and oxygenation during hemodilution in pigs
- 1997
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172. ; 41:7, s. 923-930
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The use of nitrous oxide (N2O) during hemodilution has been questioned. Nitrous oxide reduces the inspired oxygen fraction (F1O2), depresses myocardial function and may reduce cardiac output (CO) and systemic oxygen delivery (DO2SY). The aim of this study was to evaluate the importance of the effects of nitrous oxide on systemic and myocardial circulation and oxygenation during extreme, acute, normovolemic hemodilution. METHODS: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to 65% N2O before and after extreme isovolemic hemodilution (hematocrit 33 +/- 1% and 10 +/- 1%, respectively). Systemic and myocardial hemodynamics, oxygen delivery and consumption and blood lactate were measured before (at F1O2 1.0 and 0.35) and during N2O exposure. RESULTS: Hemodilution caused an increase in CO from 137 +/- 43 to 229 +/- 32 ml.kg-1.min-1 (P < 0.01), a decrease in systemic vascular resistance (from 42 +/- 14 to 20 +/- 4 mmHg.L-1.min-1, P < 0.05), a decrease in mean arterial blood pressure (from 119 +/- 19 to 100 +/- 26 mmHg, P < 0.05) and a decrease in DO2SY from 21.1 +/- 6.9 to 13.7 +/- 2.1 ml.kg-1.min-1 (P < 0.01). Cardiac venous blood flow increased by 135% (P < 0.01) and cardiac venous saturation from 25 +/- 6 to 41 +/- 5% (P < 0.05). After hemodilution, changing F1O2 from 1.0 to 0.35 reduced arterial blood oxygen content from 59.4 +/- 3.7 to 52.3 +/- 5.1 ml.L-1 (P < 0.01), mixed venous saturation (SvO2) from 75 +/- 9 to 47 +/- 7% (P < 0.05) and DO2SY from 13.7 +/- 2.1 to 11.9 +/- 2.3 ml.kg-1.min-1 (P < 0.05). Dissolved oxygen at F1O2 = 1.0 and F1O2 = 0.35 constituted 25.4 +/- 3.1% and 10.1 +/- 1.5%, respectively, of systemic oxygen delivery after hemodilution, compared with 10.7 +/- 1.2% and 3.9 +/- 0.5% before hemodilution (P < 0.01). Left ventricular oxygen delivery and consumption were unchanged. Exposure to N2O did not affect mean arterial blood pressure or systemic vascular resistance before or after hemodilution. After hemodilution during N2O-exposure, CO and DO2SY decreased by 9% (P < 0.01 and P < 0.05, respectively), but no changes in SvO2, systemic oxygen uptake or arterial lactate were observed. The effect of N2O on myocardial oxygenation was similar before and after hemodilution; cardiac venous blood flow, left ventricular oxygen delivery and uptake decreased, but no animals showed left ventricular lactate production. CONCLUSION: Nitrous oxide did not compromise systemic and myocardial circulation and oxygenation during acute normovolemic hemodilution in pigs. Possible adverse effects from the use of nitrous oxide during hemodilution seem to be related to a reduced F1O2, reducing the safety margin for systemic oxygen delivery.
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