Estimates of microcurie-days residence, bone dose equivalent, and (MPC)W for thorium-232 in man using a mammillary model

1973 ◽  
Vol 35 (1-2) ◽  
pp. 129-147
Author(s):  
S. R. Bernard
Keyword(s):  
Dose Equivalent ◽  
Thorium 232 ◽  
Mammillary Model

Neutron dose evaluation of Elekta Linac at two energies (10 & 18 MV) by MCNP code and comparison with experimental measurements

2014 ◽  
Vol 6 (1) ◽  
pp. 1006-1015
Author(s):  
Negin Shagholi ◽  
Hassan Ali ◽  
Mahdi Sadeghi ◽  
Arjang Shahvar ◽  
Hoda Darestani ◽  
...  
Keyword(s):  
Monte Carlo ◽  
Measurement Data ◽  
Calculated Data ◽  
High Energy ◽  
Neutron Dose ◽  
Dose Assessment ◽  
Photon Flux ◽  
Dose Equivalent ◽  
Monte Carlo Techniques ◽  
Neutron Dose Equivalent

Medical linear accelerators, besides the clinically high energy electron and photon beams, produce other secondary particles such as neutrons which escalate the delivered dose. In this study the neutron dose at 10 and 18MV Elekta linac was obtained by using TLD600 and TLD700 as well as Monte Carlo simulation. For neutron dose assessment in 2020 cm2 field, TLDs were calibrated at first. Gamma calibration was performed with 10 and 18 MV linac and neutron calibration was done with 241Am-Be neutron source. For simulation, MCNPX code was used then calculated neutron dose equivalent was compared with measurement data. Neutron dose equivalent at 18 MV was measured by using TLDs on the phantom surface and depths of 1, 2, 3.3, 4, 5 and 6 cm. Neutron dose at depths of less than 3.3cm was zero and maximized at the depth of 4 cm (44.39 mSvGy-1), whereas calculation resulted  in the maximum of 2.32 mSvGy-1 at the same depth. Neutron dose at 10 MV was measured by using TLDs on the phantom surface and depths of 1, 2, 2.5, 3.3, 4 and 5 cm. No photoneutron dose was observed at depths of less than 3.3cm and the maximum was at 4cm equal to 5.44mSvGy-1, however, the calculated data showed the maximum of 0.077mSvGy-1 at the same depth. The comparison between measured photo neutron dose and calculated data along the beam axis in different depths, shows that the measurement data were much more than the calculated data, so it seems that TLD600 and TLD700 pairs are not suitable dosimeters for neutron dosimetry in linac central axis due to high photon flux, whereas MCNPX Monte Carlo techniques still remain a valuable tool for photonuclear dose studies.

scholarly journals Personal dose equivalent conversion coefficients for neutron fluence over the energy range of 20-250 MeV

2009 ◽  
Vol 138 (3) ◽  
pp. 199-204 ◽  
Author(s):  
R. H. Olsher ◽  
T. D. McLean ◽  
A. L. Justus ◽  
R. T. Devine ◽  
M. S. Gadd
Keyword(s):  
Energy Range ◽  
Neutron Fluence ◽  
Dose Equivalent ◽  
Conversion Coefficients

scholarly journals Acute Nicotine Reduces Brain Arachidonic Acid Signaling in Unanesthetized Rats

2009 ◽  
Vol 29 (3) ◽  
pp. 648-658 ◽  
Author(s):  
Lisa Chang ◽  
Stanley I Rapoport ◽  
Henry N Nguyen ◽  
Dede Greenstein ◽  
Mei Chen ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Brain Regions ◽  
Membrane Phospholipids ◽  
Dose Equivalent ◽  
Central Effects ◽  
Postsynaptic Receptors ◽  
Cytosolic Phospholipase ◽  
Presynaptic Release

Nicotine exerts its central effects by activating pre- and postsynaptic nicotinic acetylcholine receptors (nAChRs). Presynaptic nAChRs modulate the release of many neurotransmitters that bind to postsynaptic receptors. These may be coupled to the activation of cytosolic phospholipase A2 (cPLA2), which hydrolyzes arachidonic acid (AA) from membrane phospholipids. We hypothesized that nicotine would modify brain signaling involving AA by binding to nAChRs. Nicotine (0.1 mg/kg, subcutaneously) or saline was injected 2 or 10 mins before infusing [1-14C]AA in unanesthetized rats. The AA incorporation coefficient k∗ (a marker of the AA signal) was measured in 80 brain regions by quantitative autoradiography. Nicotine, compared to saline, when administrated 2 mins before [1-14C]AA infusion, significantly decreased k∗ for AA in 26 regions, including cerebral cortex, thalamus, and habenula—interpeduncular regions, by 13% to 45%. These decreases could be entirely prevented by pretreatment with mecamylamine (1.0 mg/kg, subcutaneously). When administered 10 mins before [1-14C]AA infusion, nicotine did not alter any value of k∗. In summary, nicotine given to unanesthetized rats rapidly reduces signaling involving AA in brain regions containing nAChRs, likely by modulating the presynaptic release of neurotransmitters. The effect shows rapid desensitization and is produced at a nicotine dose equivalent to smoking one cigarette in humans.

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