The infrastructure of public transportation of Seoul which has been developed in parallel with the progress of modernization receives successful performance evaluation at home and abroad, currently representing the highest transport distribution ratio. In spite of this fact, the public transportation of Seoul, which has entered into advanced phase of services, still leaves much to be desired, in particular, the mobility considering the transportation vulnerable is not well assured. It is time to provide proper supports for the efficient mobility of public transportation in accordance with the social changes present in the aging and multicultural society. This study inquired about the current status of public transportation and that of its users. In addition, the main inquiry target was oriented to the elderly and foreigners for observation and investigation, as well as for the analysis of their behavior. Furthermore, through in-depth interviews, inconvenient factors have been found according to public transportation means and its usage phase, by carrying out detailed evaluations of public transportation services. Based on this, the enhancement elements were defined and the corresponding concept was designed through a series of idea workshops, and this study intended to contribute to improving future public transportation services by proposing the improvement scheme applicable to the upcoming public transportation.
Zhen Wang ;Xueheng Xie ;Mengchen Wang ;Meng Ding ;Shengliang Gu ;Xiaoyan Xing;Xiaobo Sun
Journal of Ginseng Research
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v.47
no.4
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pp.493-505
/
2023
In recent years, an increasing number of reports have explored the wound healing mechanism of these two traditional Chinese herbal medicines- Panax ginseng and Panax notoginseng, but there is no systematic research on the related core functions and different mechanisms in the treatment of wound healing up to now. Based on network pharmacology and meta-analysis, the present work aimed to comprehensively review the commonality and diversity of P. ginseng and P. notoginseng in wound healing. In this study, a wound healing-related "ingredients-targets" network of two herbs was constructed. Thereafter, meta-analysis of the multiple target lists by Metascape showed that these two medicines significantly regulated blood vessel development, responses to cytokines and growth factors and oxygen levels, cell death, cell proliferation and differentiation, and cell adhesion. To better understand the discrepancy between these two herbs, it was found that common signaling pathways including Rap1, PI3K/AKT, MAPK, HIF-1 and Focal adhesion regulated the functions listed above. In parallel, the different pathways including renin-angiotensin system, RNA transport and circadian rhythm, autophagy, and the different metabolic pathways may also explained the discrepancies in the regulation of the above-mentioned functions, consistent with the Traditional Chinese Medicine theory about the effects of P. ginseng and P. notoginseng.
Recently, transport parameters of conservative solutes such as KCl in a porous medium have been successfully determined using time domain reflectometry (TDR) . This study was initiated to Investigate the applicability of TDR technique to monitoring the fate of a heavy metal ion in a sandy soil and the distribution of its concentration along travel distance with time. A column test was conducted in a laboratory that consists of monitoring both resident and flux concentrations of $ZnCl_2$in a sandy soil under a breakthrough condition. A tracer of $ZnCl_2$(10 g/L) was injected onto the top surface of the sample as pulse type as soon as a steady-state condition was achieved. Time-series measurements of resistance and electrical conductivity were performed at 10 cm and 20 cm of distances from the inlet boundary by horizontal-positioning of parallel TDR metallic rods and using an EC-meter for the effluent exiting the bottom boundary respectively. In addition. Zn ions of the effluent were analyzed by ICP-AES. Since the mode and position of concentration detected by TDR and effluent were different, comparison between ICP analysis and TDR-detected concentration was made by predicting flux concentration using CDE model accommodating a decay constant with the transport parameters obtained from the resident concentrations. The experimental results showed that the resident concentration resulted in earlier and higher peak than the flux concentration obtained by EC-meter, implying the homogeneity of the packed sandy soil. A close agreement was found between the predicted from the transport parameters obtained by TDR and the measured $ZnCl_2$concentration. This indicates that TDR technique can also be applied to monitoring heavy metal concentrations in the soil once that a decay constant is obtained for a given soil.
Kim, Kwang-Pyo;Lee, Won-Keun;Kim, Jong-Su;Yoon, Yeo-Chang;Yoon, Suk-Chul
Journal of Radiation Protection and Research
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v.21
no.1
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pp.41-50
/
1996
In this study, the theoretical calculation of the air kerma-to-dose equivalent conversion factors was performed with a Monte Carlo N-Particle transport code for the two types of extremity phantom of the ANSI and the KAERI, respectively. Considering the distribution of absorbed dose due to the interaction of homogeneous Parallel broad beam of monoenergetic primary photons in the range between 15keV and 1.5MeV, the air kerma-to-dose equivalent conversion factors based on the kerma approximation were calculated. It is showed that all the theoretical conversion factors of the two types of the extremity phantom for the ANSI and the KAERI agree well with the experimental values of the ANSI N13.32 draft(1995) for each energy within 5.7%, maximum difference ratio, except for 13.6%, difference ratio in the case for the energy of less than 40keV. It is due to uncertainties of experiment occurred in the low X-ray energy range and geometry considered in the MCNP code.
The inhibition/influences of adenine compounds on the heart have been described repeatedly by many investigators, since the first report by Druny and Szent-Gyorgyi [1929]. These studies have shown that adenosine and adenine nucleotides have an over-all effect similar to that of acetylcholine [ACh] by slowing and weakening the heartbeat. The basic cellular and membrane events underlying the inhibitory action of adenosine on sinus rate, however, are not well understood. Furthermore, the physiological role of adenosine in regulation of the heartbeat remains still to be elucidated. Therefore, this study was undertaken in order to examine the response of rabbit SA node to adenosine and to compare the response to that of ACh. Isolated SA node preparation, whole atrial pair, or left atrlal strip was used in each experiment. Action potentials of SA node were recorded through the intracellular glass microelectrodes, which were filled with 3M KCI and had resistance of 30-50 M. All experiments were performed in a bicarbonate-buffered Tyrode solution which was aerated with 3% $CO_2-97%$$O_2$ gas mixture and kept at $35^{\circ}C$. Spontaneous firing rate of SA node at 35C [Mean + SEM, n=16] was 154 + 3.3 beats/min. The parameters of action potentials were: maximum astolic potential [MDP], -731.7mV: overshoot [OS], 9 + 1.4mV; slope of pacemaker potential [SPP], 94 3.0mV/sec.Adenosine suppressed the firing rate of SA node in a dose dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was potentiated in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine [2mg/l] and propranolol [$5{\times}10^{-6}M$]. ACh [$10^{-6}M$] responses on action potential were similar to those of adenosine by increasing MDP and decreasing SPP. These effects of ACh disappeared by pretreatment of atropine [2mg/1]. Inhibition/effects of adenosine and ACh on sinus rate were enhanced synergistically with the simultaneous administration of adenosine and ACh. Marked decrease of overshoot potential was the most prominent feature on action potential. Dipyridamole [DPM], which is known to block the adenosine transport across cell membrane, definitely potentiated the action of adenosine . Adenosine suppressed the sinus rate and atrial contractility in the same dosage range, even in the reserpinized preparation. Above` results suggest that adenosine suppresses pacemaker activity, like ACh, by acting directly on the membrane of SA node, increasing MDP and decreasing SPP.
The sufficient myoplasmic $Ca^{++}$ to react with the contractile proteins is necessary to induce contraction of a cardiac muscle. These $Ca^{++}$ for the production of muscle contraction are supplied from the three recognized $Ca^{++}$ sources; internal $Ca^{++}$ release via the sarcoplasmic reticulum(SR), $Ca^{++}$ influx through a gated Ca-channel in the membrane as a Isi, and $Ca^{++}$ transport by the mechanism of Na/ca exchange. However, it is still controversial which $Ca^{++}$ sources act as a main contributor for myoplasmic $Ca^{++}$, Therefore, this study was undertaken in order to examine the $Ca^{++}$ sources for the contraction of frog ventricle. There is evidence that the SR is sparse in frog ventricular fibers, and that T-tubules are absent. Isolated ventricular strips of frog, Rana nigromaculata, were used in this experiment. Isometric tension was recorded by force transducer, and membrane potentials of ventricular muscles were measured through the intracellular glass microelectrodes, which were filled with 3M KCI and had resistance of $30{\pm}50M{\Omega}$. All experiments were performed at room temperature in a tris·buffered Ringer solution which was aerated with 100% $O_2$. Isotonic high K, low Na solution was used to induce K-contracture, K-contracture appeared at the concentration of 20 to 30mM-KCI and was potentiated in parallel with the increase in KCI concentration. The contracture had two components: an initial rapid phasic and a subsequent slow tonic contractile responses. Membrane Potentials measured at normal Ringer solution(2.5mM KCI) was -90 to -100 mV, and decreased linearly as the KCI concentration increased; -55mV at 20mM.KCI, -45mV at 30 mM.KCI, -30 mY at 50 mM.KCI, and -12 mV at 100 mM.KCI. K-contracture was evoked firstly at the membrane potential of -45 mV. The contracture was potentiated by the increase of bathing extracellular $Ca^{++}$ concentration. However, in the absence of $Ca^{++}$ the contracture was almost not induced by 50 mM.KCI solution. Caffeine(20mM) in normal Ringer solution, which is known to release $Ca^{++}$ from SR without substantial effects on the $Ca^{++}$ fluxes across the surface membrane, did not affect membrane potential and also not initiate contracture, but the caffeine in 20 mM-KCI Ringer solution produced a contracture. Above results suggest that the main $Ca^{++}$ source for the K·contracture of frog ventricle is $Ca^{++}$ influx through the voltage-dependent Ca-channel, and that in the K-contracture at the concentration of 100 mM-KCI, the mechanism of Na/ca exchange also partly contributs, in addition to the $Ca^{++}$ influx.
Journal of the Korea Academia-Industrial cooperation Society
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v.20
no.4
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pp.497-502
/
2019
Metal oxide nanostructures are promising materials for advanced applications, such as high sensitive gas sensors, and high capacitance lithium-ion batteries. In this study, tin oxide (SnO) nanostructures were grown on a Si wafer substrate using a two-zone horizontal furnace system for a various substrate temperatures. The raw material of tin dioxide ($SnO_2$) powder was vaporized at $1070^{\circ}C$ in an alumina crucible. High purity Ar gas, as a carrier gas, was flown with a flow rate of 1000 standard cubic centimeters per minute. The SnO nanostructures were grown on a Si substrate at $350{\sim}450^{\circ}C$ under 545 Pa for 30 minutes. The surface morphology of the as-grown SnO nanostructures on Si substrate was characterized by field-emission scanning electron microscopy (FE-SEM) and atomic force microscopy (AFM). Raman spectroscopy was used to confirm the phase of the as-grown SnO nanostructures. As the results, the as-grown tin oxide nanostructures exhibited a pure tin monoxide phase. As the substrate temperature was increased from $350^{\circ}C$ to $424^{\circ}C$, the thickness and grain size of the SnO nanostructures were increased. The SnO nanostructures grown at $450^{\circ}C$ exhibited complex polycrystalline structures, whereas the SnO nanostructures grown at $350^{\circ}C$ to $424^{\circ}C$ exhibited simple grain structures parallel to the substrate.
Oxygen is the final acceptor of electron transport from fat and carbohydrate oxidation, which is the rate-limiting factor for cellular ATP production. Under altitude hypoxia condition, energy reliance on anaerobic glycolysis increases to compensate for the shortfall caused by reduced fatty acid oxidation [1]. Therefore, training at altitude is expected to strongly influence the human metabolic system, and has the potential to be designed as a non-pharmacological or recreational intervention regimen for correcting diabetes or related metabolic problems. However, most people cannot accommodate high altitude exposure above 4500 M due to acute mountain sickness (AMS) and insulin resistance corresponding to a increased levels of the stress hormones cortisol and catecholamine [2]. Thus, less stringent conditions were evaluated to determine whether glucose tolerance and insulin sensitivity could be improved by moderate altitude exposure (below 4000 M). In 2003, we and another group in Austria reported that short-term moderate altitude exposure plus endurance-related physical activity significantly improves glucose tolerance (not fasting glucose) in humans [3,4], which is associated with the improvement in the whole-body insulin sensitivity [5]. With daily hiking at an altitude of approximately 4000 M, glucose tolerance can still be improved but fasting glucose was slightly elevated. Individuals vary widely in their response to altitude challenge. In particular, the improvement in glucose tolerance and insulin sensitivity by prolonged altitude hiking activity is not apparent in those individuals with low baseline DHEA-S concentration [6]. In addition, hematopoietic adaptation against altitude hypoxia can also be impaired in individuals with low DHEA-S. In short-lived mammals like rodents, the DHEA-S level is barely detectable since their adrenal cortex does not appear to produce this steroid [7]. In this model, exercise training recovery under prolonged hypoxia exposure (14-15% oxygen, 8 h per day for 6 weeks) can still improve insulin sensitivity, secondary to an effective suppression of adiposity [8]. Genetically obese rats exhibit hyperinsulinemia (sign of insulin resistance) with up-regulated baseline levels of AMP-activated protein kinase and AS160 phosphorylation in skeletal muscle compared to lean rats. After prolonged hypoxia training, this abnormality can be reversed concomitant with an approximately 50% increase in GLUT4 protein expression. Additionally, prolonged moderate hypoxia training results in decreased diffusion distance of muscle fiber (reduced cross-sectional area) without affecting muscle weight. In humans, moderate hypoxia increases postprandial blood distribution towards skeletal muscle during a training recovery. This physiological response plays a role in the redistribution of fuel storage among important energy storage sites and may explain its potent effect on changing body composition. Conclusion: Prolonged moderate altitude hypoxia (rangingfrom 1700 to 2400 M), but not acute high attitude hypoxia (above 4000 M), can effectively improve insulin sensitivity and glucose tolerance for humans and antagonizes the obese phenotype in animals with a genetic defect. In humans, the magnitude of the improvementvaries widely and correlates with baseline plasma DHEA-S levels. Compared to training at sea-level, training at altitude effectively decreases fat mass in parallel with increased muscle mass. This change may be associated with increased perfusion of insulin and fuel towards skeletal muscle that favors muscle competing postprandial fuel in circulation against adipose tissues.
Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.
Recent advances in radiation transport algorithms, computer hardware performance, and parallel computing make the clinical use of Monte Carlo based dose calculations possible. To compare the speed and accuracies of dose calculations between different developed codes, a benchmark tests were proposed at the XIIth ICCR (International Conference on the use of Computers in Radiation Therapy, Heidelberg, Germany 2000). A Monte Carlo treatment planning comprised of 28 various Intel Pentium CPUs was implemented for routine clinical use. The purpose of this study was to evaluate the performance of our system using the above benchmark tests. The benchmark procedures are comprised of three parts. a) speed of photon beams dose calculation inside a given phantom of 30.5 cm$\times$39.5 cm $\times$ 30 cm deep and filled with 5 ㎣ voxels within 2% statistical uncertainty. b) speed of electron beams dose calculation inside the same phantom as that of the photon beams. c) accuracy of photon and electron beam calculation inside heterogeneous slab phantom compared with the reference results of EGS4/PRESTA calculation. As results of the speed benchmark tests, it took 5.5 minutes to achieve less than 2% statistical uncertainty for 18 MV photon beams. Though the net calculation for electron beams was an order of faster than the photon beam, the overall calculation time was similar to that of photon beam case due to the overhead time to maintain parallel processing. Since our Monte Carlo code is EGSnrc, which is an improved version of EGS4, the accuracy tests of our system showed, as expected, very good agreement with the reference data. In conclusion, our Monte Carlo treatment planning system shows clinically meaningful results. Though other more efficient codes are developed such like MCDOSE and VMC++, BEAMnrc based on EGSnrc code system may be used for routine clinical Monte Carlo treatment planning in conjunction with clustering technique.
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