• Journal of the Korean Society for Nondestructive Testing
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• v.27 no.5
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• pp.449-458
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• 2007

In this paper, we reconstructed the cross-sectional images of two phantoms simulating a petrochemical process from gamma radiation measurements. Three different weight functions for EM image reconstruction algorithm were built and compared with histograms representing the variance of the homogeneity of the phantom material, The radiation source, $^{137}Cs$, collimated by a lead with 5 mm diameter aperture and the measurement was made with a lead shielded 1inch NaI detector. As a result, the method taking into account the beam area in each pixel for a weight function showed the best resolution among the three methods.

• Nuclear Engineering and Technology
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• v.50 no.6
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• pp.989-995
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• 2018

Argonne National Laboratory of the United States and Kharkov Institute of Physics and Technology (KIPT) of Ukraine have cooperated on the development, design, and construction of a neutron source facility. The facility was constructed at Kharkov, Ukraine, and its commissioning process is underway. The facility will be used for researches, producing medical isotopes, and training young nuclear specialists. The neutron source facility is designed with a provision to include a cryogenically cooled moderator system-a cold neutron source (CNS). This CNS provides low-energy neutrons, which will be used in the scattering experiment and material structures analysis. Cold neutron guides, coated with reflective material for the low-energy neutrons, will be used to transport the cold neutrons to the experimental site. The cold neutron guides would keep the cold neutrons within certain energy and angular space concentrated inside, while most of the gamma rays and high-energy neutrons are not affected by the cold neutron guides. For the KIPT design, the cold neutron guides need to extend several meters outside the main shield of the facility, and curved guides will also be used to remove the gamma and high-energy neutron. The neutron guides should be installed inside a shield structure to ensure an acceptable biological dose in the facility hall. Heavy concrete is the selected shielding material because of its acceptable performance and cost. Shield design analysis was carried out for the CNS guide hall. MCNPX was used as the major computation tool for the design analysis, with neutron and gamma dose calculated separately. Weight windows variance reduction technique was also used in the shield design. The goal of the shield design is to keep the total radiation dose below the $5.0{\mu}Sv/hr$ guideline outside the shield boundary. After a series of iterative MCNPX calculations, the shield configuration and parameters of CNS guide hall were determined and presented in this article.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.603-612
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• 1999

Background : It has been documented that brief repetitive periods of ischemia and reperfusion (ischemic preconditioning, IP) enhances the recovery of post-ischemic contractile function and reduces infarct size after a longer period of ischemia. Many mechanisms have been proposed to explain this process. Recent studies have suggested that transient increase in the intracellular calcium may have triggered the activation of protein kinase C(PKC); however, there are still many controversies. Accordingly, the author performed the present study to test the hypothesis that preconditioning with high concentration of calcium before sustained subsequent ischemia(calcium preconditioning) mimics IP by PKC activation. Material and Method : The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) Method: The isolated hearts from the New Zealand White rabbits(1.5∼2.0 kg body weight) were perfused with Tyrode solution by Langendorff technique. After stabilization of baseline hemodynamics, the hearts were subjected to 45-minute global ischemia followed by a 120-minute reperfusion with IP(IP group, n=13) or without IP(ischemic control, n=10). IP was induced by single episode of 5-minute global ischemia and 10-minute reperfusion. In the Ca2+ preconditioned group, perfusate containing 10(n=10) or 20 mM(n=11) CaCl2 was perfused for 10 minutes after 5-minute ischemia followed by a 45-minute global ischemia and a 120-minute reperfusion. Baseline PKC was measured after 50-minute perfusion without any treatment(n=5). Left ventricular function including developed pressure(LVDP), dP/dt, heart rate, left ventricular end-diastolic pressure(LVEDP) and coronary flow(CF) was measured. Myo car ial cytosolic and membrane PKC activities were measured by 32P-${\gamma}$-ATP incorporation into PKC-specific pepetide. The infarct size was determined using the TTC (tetrazolium salt) staining and planimetry. Data were analyzed using one-way analysis of variance(ANOVA) variance(ANOVA) and Tukey's post-hoc test. Result: IP increased the functional recovery including LVDP, dP/dt and CF(p<0.05) and lowered the ascending range of LVEDP(p<0.05); it also reduced the infarct size from 38% to 20%(p<0.05). In both of the Ca2+ preconditioned group, functional recovery was not significantly different in comparison with the ischemic control, however, the infarct size was reduced to 19∼23%(p<0.05). In comparison with the baseline(7.31 0.31 nmol/g tissue), the activities of the cytosolic PKC tended to decrease in both the IP and Ca2+ preconditioned groups, particularly in the 10 mM Ca2+ preconditioned group(4.19 0.39 nmol/g tissue, p<0.01); the activity of membrane PKC was significantly increased in both IP and 10 mM Ca2+ preconditioned group (p<0.05; 1.84 0.21, 4.00 0.14, and 4.02 0.70 nmol/g tissue in the baseline, IP, and 10 mM Ca2+ preconditioned group, respectively). However, the activity of both PKC fractions were not significantly different between the baseline and the ischemic control. Conclusion: These results indicate that in isolated Langendorff-perfused rabbit heart model, calcium preconditioning with high concentration of calcium does not improve post-ischemic functional recovery. However, it does have an effect of limiting(reducing) the infart size by ischemic preconditioning, and this cardioprotective effect, at least in part, may have resulted from the activation of PKC by calcium which acts as a messenger(or trigger) to activate membrane PKC.