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- Gardeback, M., et al.
(författare)
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Splanchnic blood flow and oxygen uptake during cardiopulmonary bypass
- 2002
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Ingår i: Journal of Cardiothoracic and Vascular Anesthesia. - : Elsevier BV. - 1053-0770 .- 1532-8422. ; 16:3, s. 308-315
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To measure splanchnic blood flow (SBF) with 2 indicator dilution techniques during and after cardiopulmonary bypass (CPB), to compare the results with transesophageal echocardiography Doppler-measured right hepatic vein (RHV) flow, and to study gastric tonometry data in the same patients. Design: Single-arm prospective study. Setting: University hospital operating room and intensive care unit. Participants: Ten adult patients undergoing cardiac surgery. Interventions: SBF was measured using constant rate in fusion of indocyanine green dye and low-dose ethanol from induction of anesthesia until end of hypothermic CPB. The infusion of ethanol was continued, and SBF was measured postoperatively at 2, 3, and 4 hours after CPB. Simultaneously, RHV flow, splanchnic oxygen delivery and uptake, and gastric mucosal pH were calculated. Measurements and Main Results: SBF, RHV flow, and gastric mucosal pH remained unchanged during the study period. SBF measured with indocyanine green was 765 +/- 88 (SEM) mL/min after induction of anesthesia. SBF before CPB measured with ethanol was 985 +/- 218 mL/min. There was no significant difference between the methods. RHV flow was 450 +/- 87 mL/min after induction of anesthesia. There was no correlation between individual values of RHV flow and SBF. Splanchnic oxygen uptake was 52 +/- 7.8 mL/min after induction of anesthesia and decreased to 28 +/- 2.6 mL/min during CPB. Gastric mucosal pH was 7.32 +/- 0.02 after induction of anesthesia and showed no correlation to SBF or to splanchnic oxygen uptake. Conclusion: SBT did-not decrease during CPB. SBF could be measured with ethanol with reasonable accuracy. Transesophageal echocardiography assessment of RHV flow was not suitable to quantify SBF in the individual patient, but could be used to follow relative changes.
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- Girnita, L., et al.
(författare)
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Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact
- 2000
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Ingår i: Cancer Research. - 0008-5472 .- 1538-7445. ; 60:18, s. 5278-5283
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the functional impact of p53 on insulin-like growth factor I receptor (IGF-IR) expression in malignant cells. Using the BL-41tsp53-2 cell line, a transfectant carrying temperature-sensitive (ts) p53 and endogenous mutant p53 (codon 248), we demonstrated a drastic down-regulation of plasma membrane-bound IGF-IRs on induction of wild-type p53, However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide. Thus, even if the negative effect of wild-type p53 predominates under a competitive condition, these data indicate that mutant p53 may be important for up-regulation of IGF-IR, To further elucidate this issue, three melanoma cell lines (BE, SK-MEL-5, and SK-MEL-28) that over expressed p53 were investigated. The BE cell line has a hot spot mutation (codon 248) and expresses only codon 248-mutant p53, SK-MEL-28 has a point mutation at codon 145. SK-MEL-5 cells did not exhibit any p53 mutations, but the absence of p21(Waf1) expression suggested functionally aberrant p53. Our data suggest that interaction with Mdm-2 may underlie p53 inactivation in these cells, Using p53 antisense oligonucleotides, we demonstrated a substantial down-regulation of cell surface expression of IGF-IR proteins in all melanoma cell lines after 24 h, This was paralleled by decreased tyrosine phosphorylation of IGF-IR and growth arrest, and, subsequently, massive cell death was observed (this was also seen in BL-41tsp53-2 cells with mutant conformation of ts p53). Taken together, our results suggest that up-regulation of IGF-IR as a result of expression of aberrant p53 may be important for the growth and survival of malignant cells.
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