Spin-Lattice Relaxation Time of Inorganic Phosphate in Human Tumor Xenografts Measured in Vivo by31P-Magnetic Resonance Spectroscopy Influence of oxygen tension

1995 ◽  
Vol 34 (3) ◽  
pp. 339-343 ◽  
Author(s):  
Dag R. Olsen ◽  
Heidi Lyng ◽  
Steffen Petersen ◽  
Einar K. Rofstad
Keyword(s):  
Inorganic Phosphate ◽  
Human Tumor ◽  
Lattice Relaxation ◽  
Lattice Relaxation Time ◽  
Spin Lattice Relaxation ◽  
Resonance Spectroscopy ◽  
Human Tumor Xenografts ◽  
Tumor Xenografts ◽  
Spin Lattice

A new approach to cancer treatment

2014 ◽  
Vol 14 (1) ◽  
pp. 99-101 ◽  
Author(s):  
Syed F. Akber
Keyword(s):  
Radiation Treatment ◽  
Lattice Relaxation ◽  
Lattice Relaxation Time ◽  
Proton Spin ◽  
Ionising Radiation ◽  
Spin Lattice Relaxation ◽  
Water Proton ◽  
New Approach ◽  
Spin Lattice

AbstractA new approach is applied to correlate different phases of the HeLa cell S-3 with mean lethal ionising radiation dose (Do) along with nuclear magnetic resonance water-proton spin-lattice relaxation time (T1). This information can be used to pin-point the mitotic phase of the cells in vivo. This enables us to apply ionising radiation treatment at that particular time. This will increase the efficacy of radiation treatment in cancer patients.

Na(+)-K(+)-ATPase in endothelial cell energetics: 23Na nuclear magnetic resonance and calorimetry study

1995 ◽  
Vol 268 (1) ◽  
pp. H351-H358 ◽  
Author(s):  
M. L. Gruwel ◽  
C. Alves ◽  
J. Schrader
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Vascular Endothelial Cells ◽  
Lattice Relaxation ◽  
Lattice Relaxation Time ◽  
Shift Reagent ◽  
Spin Lattice Relaxation ◽  
Resonance Spectroscopy ◽  
Spin Lattice ◽  
Nuclear Magnetic

Sodium flux rate and energy consumption of the Na(+)-K+ pump in vascular endothelial cells of porcine aorta grown on micro-carrier beads were studied using a combination of nuclear magnetic resonance spectroscopy of intracellular 23Na and microcalorimetry. The Na+ flux into the cells was determined in the presence of the shift reagent Dy(P3O10)2(7-), while the Na(+)-K+ pump was inhibited with ouabain. Basal Na+ influx was 17 +/- 3 nmol.min-1.mg protein-1, and intracellular Na+ concentration was 23.5 +/- 3.8 mM, resulting in a complete exchange of intracellular Na+ within 5–6 min. Spin-lattice relaxation time (T1) measurements of intracellular Na+ showed a T1 of 19 +/- 1 ms under basal conditions and a T1 of 26.2 +/- 1.6 ms after pump inhibition with 50 microM ouabain. Such an increase is typical for a system in which the total amount of Na+ increases but where the amount of bound Na+ remains constant. The Na+ ionophore nystatin maximally increased the Na(+)-K+ pump rate about twofold, whereas the amount of intracellular Na+ only increased 14%. With microcalorimetry a cellular heat flux of 183 +/- 18 microW per mg endothelial protein was determined, which relates to 7.6 microW/mg endothelial protein generated by the Na(+)-K(+)-adenosinetriphosphatase. Our data demonstrate that small intracellular changes of Na+ can stimulate the endothelial Na(+)-K+ pump activity. The contribution of the Na(+)-K+ pump to total endothelial energy expenditure is approximately 4-5%.

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