Comparison of Measured and Monte Carlo Calculated Dose Distributions from Indigenously Developed 6 MV Flattening Filter Free Medical Linear Accelerator.

PURPOSE: Monte Carlo simulation was carried out for a 6 MV flattening filter-free (FFF) indigenously developed linear accelerator (linac) using the BEAMnrc user-code of the EGSnrc code system. The model was benchmarked against the measurements. A Gaussian distributed electron beam of kinetic energy 6.2 MeV with full-width half maximum of 1 mm was used in this study. METHODS: The simulation of indigenously developed linac unit has been carried out by using the Monte Carlo-based BEAMnrc user-code of the EGSnrc code system. Using the simulated model, depth and lateral dose profiles were studied using the DOSXYZnrc user-code. The calculated dose data were compared against the measurements using an RFA dosimertic system made by PTW, Germany (water tank MP3-M and 0.125 cm3 ion chamber). RESULTS: The BEAMDP code was used to analyze photon fluence spectra, mean energy distribution, and electron contamination fluence spectra. Percentage depth dose (PDD) and beam profiles (along both X and Y directions) were calculated for the field sizes 5 cm × 5 cm - 25 cm × 25 cm. The dose difference between the calculated and measured PDD and profile values were under 1%, except for the penumbra region where the maximum deviation was found to be around 3%. CONCLUSIONS: A Monte Carlo model of indigenous FFF linac (6 MV) has been developed and benchmarked against the measured data.

Monte Carlo based investigations of electron contamination from telecobalt unit head in build up region and its impact on surface dose.

A Telecobalt unit has wide range of applications in cancer treatments and is used widely in many countries all around the world. Estimation of surface dose in Cobalt-60 teletherapy machine becomes important since clinically useful photon beam consist of contaminated electrons during the patient treatment. EGSnrc along with the BEAMnrc user code was used to model the Theratron 780E telecobalt unit. Central axis depth dose profiles including surface doses have been estimated for the field sizes of 0×0, 6×6, 10×10, 15×15, 20×20, 25×25, 30×30cm2 and at Source-to-surface distance (SSD) of 60 and 80cm. Surface dose was measured experimentally by the Gafchromic RTQA2 films and are in good agreement with the simulation results. The central axis depth dose data are compared with the data available from the British Journal of Radiology report no. 25. Contribution of contaminated electrons has also been calculated using Monte Carlo simulation by the different parts of the Cobalt-60 head for different field size and SSD's. Moreover, depth dose curve in zero area field size is calculated by extrapolation method and compared with the already published data. They are found in good agreement.

Design of 6Mev linear accelerator based pulsed thermal neutron source: FLUKA simulation and experiment.

The 6MeV LINAC based pulsed thermal neutron source has been designed for bulk materials analysis. The design was optimized by varying different parameters of the target and materials for each region using FLUKA code. The optimized design of thermal neutron source gives flux of 3×10(6)ncm(-2)s(-1) with more than 80% of thermal neutrons and neutron to gamma ratio was 1×10(4)ncm(-2)mR(-1). The results of prototype experiment and simulation are found to be in good agreement with each other.

Measurement of angular distribution of neutron flux for the 6MeV race-track microtron based pulsed neutron source.

The 6MeV race track microtron based pulsed neutron source has been designed specifically for the elemental analysis of short lived activation products, where the low neutron flux requirement is desirable. Electrons impinges on a e-gamma target to generate bremsstrahlung radiations, which further produces neutrons by photonuclear reaction in gamma-n target. The optimisation of these targets along with their spectra were estimated using FLUKA code. The measurement of neutron flux was carried out by activation of vanadium at different scattering angles. Angular distribution of neutron flux indicates that the flux decreases with increase in the angle and are in good agreement with the FLUKA simulation.

Mechanistic and metabolic inferences from the binding of substrate analogues and products to arginase.

Arginase is a binuclear Mn(2+) metalloenzyme that catalyzes the hydrolysis of L-arginine to L-ornithine and urea. X-ray crystal structures of arginase complexed to substrate analogues N(omega)-hydroxy-L-arginine and N(omega)-hydroxy-nor-L-arginine, as well as the products L-ornithine and urea, complete a set of structural "snapshots" along the reaction coordinate of arginase catalysis when interpreted along with the X-ray crystal structure of the arginase-transition-state analogue complex described in Kim et al. [Kim, N. N., Cox, J. D., Baggio, R. F., Emig, F. A., Mistry, S., Harper, S. L., Speicher, D. W., Morris, Jr., S. M., Ash, D. E., Traish, A. M., and Christianson, D. W. (2001) Biochemistry 40, 2678-2688]. Taken together, these structures render important insight on the structural determinants of tight binding inhibitors. Furthermore, we demonstrate for the first time the structural mechanistic link between arginase and NO synthase through their respective complexes with N(omega)-hydroxy-L-arginine. That N(omega)-hydroxy-L-arginine is a catalytic intermediate for NO synthase and an inhibitor of arginase reflects the reciprocal metabolic relationship between these two critical enzymes of L-arginine catabolism.

Modulation of cholinergic airway reactivity and nitric oxide production by endogenous arginase activity.

Cholinergic airway constriction is functionally antagonized by agonist-induced constitutive nitric oxide synthase (cNOS)-derived nitric oxide (NO). Since cNOS and arginase, which hydrolyzes L-arginine to L-ornithine and urea, use L-arginine as a common substrate, competition between both enzymes for the substrate could be involved in the regulation of cholinergic airway reactivity. Using a perfused guinea-pig tracheal tube preparation, we investigated the modulation of methacholine-induced airway constriction by the recently developed, potent and specific arginase inhibitor N(Omega)-hydroxy-nor-L-arginine (nor-NOHA). Intraluminal (IL) administration of nor-NOHA caused a concentration-dependent inhibition of the maximal effect (E(max)) in response to IL methacholine, which was maximal in the presence of 5 microM nor-NOHA (E(max)=31.2+/-1.6% of extraluminal (EL) 40 mM KCl-induced constriction versus 51.6+/-2.1% in controls, P<0.001). In addition, the pEC(50) (-log(10) EC(50)) was slightly but significantly reduced in the presence of 5 microM nor-NOHA. The inhibition of E(max) by 5 microM nor-NOHA was concentration-dependently reversed by the NOS inhibitor N(Omega)-nitro-L-arginine methyl ester (L-NAME), reaching an E(max) of 89.4+/-7.7% in the presence of 0.5 mM L-NAME (P<0.01). A similar E(max) in the presence of 0.5 mM L-NAME was obtained in control preparations (85.2+/-9.7%, n.s.). In the presence of excess of exogenously applied L-arginine (5 mM), 5 microM nor-NOHA was ineffective (E(max)=33.1+/-5.8 versus 31.1+/-7.5% in controls, n.s.). The results indicate that endogenous arginase activity potentiates methacholine-induced airway constriction by inhibition of NO production, presumably by competition with cNOS for the common substrate, L-arginine. This finding may represent an important novel regulation mechanism of airway reactivity.