• Journal of Hydrogen and New Energy
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• v.27 no.4
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• pp.349-356
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• 2016

Volumetric capacity metrics at cryogenic condition are critical for technological and commercial development. It must be calculated and reported in a uniform and consistent manner to allow comparisons among different materials. In this paper, we propose a simple and universal protocol for the determination of volumetric capacity of sorbent materials at cryogenic condition. Usually, the sample container volume containing porous sample at RT can be directly determined by a helium expansion test. At cryogenic temperatures, however, this direct helium expansion test results in inaccurate values of the sample container volume for microporous materials due to a significant helium adsorption, resulting significant errors in hydrogen uptake. For reducing this container volume error, therefore, we introduced and applied the indirect method such as 'volume correction using a non-porous material', showing a reliable cold volume correction.

• The Korean Journal of Nuclear Medicine
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• v.38 no.1
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• pp.21-29
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• 2004

Purpose: Much evidence suggests long-term cigarette smoking alters coronary vascular endothelial response. On this study, we applied nonnegative matrix factorization (NMF), an unsupervised learning algorithm, to CO-less $H_2^{15}O-PET$ to investigate coronary endothelial dysfunction caused by smoking noninvasively. Materials and methods: This study enrolled eighteen young male volunteers consisting of 9 smokers $(23.8{\pm}1.1\;yr;\;6.5{\pm}2.5$ pack-years) and 9 nonsmokers $(23.8{\pm}2.9 yr)$. They do not have any cardiovascular risk factor or disease history. Myocardial $H_2^{15}O-PET$ was performed at rest, during cold ($5^{\circ}C$) pressor stimulation and during adenosine infusion. Left ventricular blood pool and myocardium were segmented on dynamic PET data by NMF method. Myocardial blood flow (MBF) was calculated from input and tissue functions by a single compartmental model with correction of partial volume and spillover effects. Results: There were no significant difference in resting MBF between the two groups (Smokers: 1.43 0.41 ml/g/min and non-smokers: $1.37{\pm}0.41$ ml/g/min p=NS). during cold pressor stimulation, MBF in smokers was significantly lower than 4hat in non-smokers ($1.25{\pm}0.34$ ml/g/min vs $1.59{\pm}0.29$ ml/gmin; p=0.019). The difference in the ratio of cold pressor MBF to resting MBF between the two groups was also significant (p=0.024; $90{\pm}24%$ in smokers and $122{\pm}28%$ in non-smokers.). During adenosine infusion, however, hyperemic MBF did not differ significantly between smokers and non-smokers ($5.81{\pm}1.99$ ml/g/min vs $5.11{\pm}1.31$ ml/g/min ; p=NS). Conclusion: in smokers, MBF during cold pressor stimulation was significantly lower compared wi4h nonsmokers, reflecting smoking-Induced endothelial dysfunction. However, there was no significant difference in MBF during adenosine-induced hyperemia between the two groups.