• Korean Journal of Applied Biomechanics
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• v.31 no.2
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• pp.133-139
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• 2021

Objective: This study aims to verify the conventional deadlift motions using by two different grips, thereby elucidating the grounds for effective training methods that can minimize the risk of injury. Method: Total of 18 healthy young adults were recruited for this study (age: 25.11±2.19 yrs., height: 175.67±5.22 cm, body mass: 78.5±8.09 kg, 1-RM: 125.75±19.48 kg). All participants were asked to perform conventional deadlift with two types of grips which are overhand grip (OG) and underhand grip (UG). In each grip, participant perform the deadlift with 50% and 80% of the pre-measured 1-RM. A 3-dimensional motion analysis with 8 infrared cameras and 3 channels of EMG was performed in this study. A two-way ANOVA (group × load) with repeated measure was used for statistical verification. The significant level was set at α=.05. Results: There were significant differences in grip type and weight on the right shoulder joint, and only significant difference in grip on the left shoulder joint (p<.05). The hip joint ROM was significantly increased as the weight increased in both types of grips on phase 1, while the ROM of hip joint was significantly decreased as the weight increased only in the case of OG on phase 2 (p<.05). In case of the OG, as the weight, increased significantly increased L1 ROM and L3 ROM were revealed on phase 1 and phase 2, respectively (p<.05). Moreover, as the weight increased, UG revealed significantly decreased L5 ROM on phase 1, while both grips showed significantly increased ROM on phase 2 (p<.05). In addition, the erector spinae and the biceps femoris, which are synergist for the motion, showed a significant difference in both types of grip according to the weight (p<.05). The muscle activity ratio of gluteus maximus/biceps femoris showed a significant difference only in the UG according to the weight (p<.05). Conclusion: In conclusion, beginners might be suggested to use the UG for maintaining the neutral state of the lumbar spine and focus on the gluteus maximus muscle, which is the main activation muscle. For the experts, it may recommend alternative use of the OG and UG according to the training purpose to minimize the compensation effect.

• Journal of the Korean BIBLIA Society for library and Information Science
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• v.33 no.4
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• pp.73-92
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• 2022

This study intends to design a model that can effectively service policy data necessary for the implementation of new national agenda in order to provide high-quality policy information services that go beyond those of the existing Policy Information Portal (POINT) of National Sejong Library. To this end, it was determined that providing an integrated search environment, in lieu of data search through individual access, was necessary. Subsequently, four possible models for a national agenda service model were presented. First, designing a computerized system for both interface and electronic information source aspects was proposed for the national agenda service system operation. Second, designing the Linked Open Data system and the time-series service system for national policy information, providing the translation service of overseas original data, and securing the researcher's desired data were presented for the national agenda service information source operation. Third, strengthening public relations for policy users, building and promoting the site brand, operating SNS channels, and reinforcing the activation of auxiliary materials and the accessibility of external services were proposed for public relations of national agenda service. Fourth, expanding the information network with Open API, cloud service, and overseas libraries was proposed for collaborating and cooperating with the agenda service.

• Molecules and Cells
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• v.46 no.9
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• pp.545-557
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• 2023

Sphingomyelinase (SMase) catalyzes ceramide production from sphingomyelin. Ceramides are critical in cellular responses such as apoptosis. They enhance mitochondrial outer membrane permeabilization (MOMP) through self-assembly in the mitochondrial outer membrane to form channels that release cytochrome c from intermembrane space (IMS) into the cytosol, triggering caspase-9 activation. However, the SMase involved in MOMP is yet to be identified. Here, we identified a mitochondrial Mg²⁺-independent SMase (mt-iSMase) from rat brain, which was purified 6,130-fold using a Percoll gradient, pulled down with biotinylated sphingomyelin, and subjected to Mono Q anion exchange. A single peak of mt-iSMase activity was eluted at a molecular mass of approximately 65 kDa using Superose 6 gel filtration. The purified enzyme showed optimal activity at pH of 6.5 and was inhibited by dithiothreitol and Mg²⁺, Mn²⁺, Ni²⁺, Cu²⁺, Zn²⁺, Fe²⁺, and Fe³⁺ ions. It was also inhibited by GW4869, which is a non-competitive inhibitor of Mg²⁺-dependent neutral SMase 2 (encoded by SMPD3), that protects against cytochrome c release-mediated cell death. Subfractionation experiments showed that mt-iSMase localizes in the IMS of the mitochondria, implying that mt-iSMase may play a critical role in generating ceramides for MOMP, cytochrome c release, and apoptosis. These data suggest that the purified enzyme in this study is a novel SMase.

• Progress in Medical Physics
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• v.14 no.1
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• pp.54-67
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• 2003

The voltage-dependence of N-type calcium current inactivation is U-shaped with the degree of inactivation roughly mirroring inward current. This voltage-dependence has been reported to result from a purely voltage-dependent mechanism. However, $Ca^{2＋}$-dependent inactivation of N-channels has also been reported. We have investigated the role of $Ca^{2＋}$ in N-channel inactivation by comparing the effects of $Ba^{2＋}$and $Ca^{2＋}$ on whole-cell N-current in rat superior cervical ganglion neurons. For individual cells in-activation was always larger in $Ca^{2＋}$ than in $Ba^{2＋}$ even when internal EGTA (11 mM) was replaced with BAPTA (20 mM). The inactivation vs. voltage relationship was U-shaped in both divalent cations. The enhancement of inactivation by $Ca^{2＋}$ was inversely related with the magnitude of inactivation in $Ba^{2＋}$ as if the mechanisms of inactivation were the same in both $Ba^{2＋}$ and $Ca^{2＋}$. In support of this idea we could separate fast ( ${\gamma}$ ～150 ms) and slow ( ${\gamma}$ ～ 2500 ms) components of inactivation in both $Ba^{2＋}$and $Ca^{2＋}$ using 5 sec voltage steps. Differential effects were observed on each component with $Ca^{2＋}$ enhancing the magnitude of the fast component and the speed of the slow component. The larger amplitude of fast component indicates that the more channels inactivate via this pathway with $Ca^{2＋}$ than with $Ba^{2＋}$, but the stable time constants support the idea the fast inactivation mechanism is identical in $Ba^{2＋}$and $Ca^{2＋}$. The results do not support a $Ca^{2＋}$-dependent mechanism for fast inactivation. However, the $Ca^{2＋}$-induced acceleration of the slowly inactivating component could result from a $Ca^{2＋}$-dependent process.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.357-371
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• 1996

Lithium (Li) is known to be used not only during acute manic psychosis but also acute depressive phase in manic-depression. In the present study, it was attempted to investigate the effect of lithium on catecholamine (CA) secretion from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. Replacement of $Na^+$ (118.4 mM) by lithium in the normal Krebs-bicarbonate solution used to perfuse the gland produced gradually an increased response in the spontaneous catecholamine release, which was peaked at $30{\sim}60$ min after its perfusion. Li-Krebs solution was perfused into an adrenal vein for 2 hours in every experiments. Li-Krebs-evoked CA secretory responses were depressed significantly under loading with $Ca^{++}-free$ medium. This CA secretion evoked by lithium loading was also reduced markedly by the pretreatment with nicardipine ($10^{-6}$ M), TMB-8 ($10^{-5}$ M) and chlorisondamine ($10^{-6}$ M) for 20 min, respectively, while was not affected by preloading with a pirenzepine ($2{\times}10^{-6}$ M)-containing Krebs. $Na^+$ pump inhibition by pretreatment with ouabain ($10^{-4}$ M) for 20 min did make the marked depression in Li-evoked CA secretory responses. Moreover, Li-evoked CA release was also diminished markedly by preloading with tetrodotoxin ($5{\times}10^{-7}$ M)-contaming Krebs for 20 min. All these experimental results taken together suggest that lithium enhances CA secretion in a $Ca^{++}$-dependent fashion by its accumulation in the adrenomedullary chromaffin cells of the rat, and that this secretory effect may be meidated by a dual mechanism: (i) chromaffin cell depolarization and subsequent opening of voltage-sensitive $Ca^{++}$ channels and (ii) activation of a $[Li]_i-[Ca]_0$ counter-transport system.

• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.263-274
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• 1993

Potassium $(K^+)$ channels are present in airway smooth muscle cells, and their activation results in hyperpolarization and relaxation. Because these effects may have therapeutic relevance to hypersensitivity and asthma, we examined the effect of a potassium channel activator, cromakalim (BRL 34915, CK) on the release of mediators from superfused tracheal and parenchymal strips after passive sensitization with $IgG_1$ antibody. Both tissues were superfused with CK $(2{\times}10^{-6}\;M)$ for 30 min and challenged with CK and antigen (Ox-HSA). Using monodispersed, partially purified, highly purified guinea pig lung mast cells, we also examined the effect of CK on mediator release from these cells after passive sensitization with $IgG_{1}$ antibody $({\alpha}-OA)$. Guinea pig lung mast cells were purified using enzyme digestion method, count current elutriation, and discontinuous Percoll density gradient. After CK pretreatment, passively sensitized mast cells were challenged with varying concentration of antigen (OA, immunological stimuli) or with varying concentration of calcium ionophore (CaI, non-immunological stimuli). Histamine (Hist) release was determined by spectrophotofluorometry, and leukotrienes (LT) by radioimmunoassy. CK pretreatment decreased Hist by 35% and LT release by 40% in the antigen-induced tracheal tissue after $IgG_1$ sensitization but did not decrease the contractile response. In the antigen-induced parenchymal tissue CK decreased Hist release by 25% but poorly decreased LT. Both immunologic and non-immunologic stimuli caused a dose-dependent release of Hist and LT from monodispersed, partially purified and highly purified lung mast cells. Verification of LT release was obtained by the use of 5-lipoxygenase inhibitor, A64077 (Zileuton). CK decreased Hist and LT release by 20% respectively in the OA-induced guinea pig lung mast cells after $IgG_1$ sensitization. The inhibitory effects of CK on the Hist and LT release in the Ox-HSA-induced airway smooth muscle tissues or in the OA-induced and CaI-induced mast cells after $IgG_1$ sensitization were completely blocked by TEA and GBC. These studies show that guinea pig lung mast cells seem to be an important contributor to LT release, and that CK (which has been known as an airway smooth muscle relaxant) can in part act to inhibit mediator release in the antigen-induced airway smooth muscle, and that CK may also act to inhibit mediator release in the OA-induced and CaI-induced highly purified mast cells. These results suggest that Hist and LT release evoked by mast cell activation might in part be associated with $K{^+}4 channel activity.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.39-49
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• 1996

In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$ $([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$ $K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$ $K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$ $K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.

• Journal of Chest Surgery
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• v.34 no.9
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• pp.704-710
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• 2001

Background: Extracorporeal circulation using pump-oxygenator is an inevitable process to keep vital sign during cardiac arrest for open heart surgery. However, the diversion of blood through nonendothelialized channels appears to stimulate inflammatory response, and leukocyte activation may lead to cardiopulmonary edema. Our study evaluated the effect of leukocyte-induced cardiopulmonary edema using three different pump-oxygenator priming solutions; non-hemic crystalloid solution ; leukocyte-depleted homologous blood; non leukocyte-depleted homologous blood in priming solutions. Material and Method: Each different priming solution was used on five dogs, and the effect of leukocyte-induced cardiopulmonary edema during cardiopulmonary bypass(CPB) was evaluated. For each dog after 2 hours of exracorporeal circulation and another 4 hours of post-pump period, the dog was sacrificed and its heart and lung tissues were obtained for measuring Wet/Dry ratio. Arterial $O_2$partial pressure(PaO$_2$) and $CO_2$partial pressure(Pa$CO_2$) were checked. For the evaluation of ventilatory function, $CO_2$partial pressure difference between arterial blood (Pa$CO_2$) and exhaled air(Et$CO_2$) was measured. Result: 1. No significant difference was seen in arterial PaO$_2$and Pa$CO_2$among groups. 2. Ventilatory function evaluated by Pa$CO_2$and Et$CO_2$showed no significant difference between non-hemic and blood-mixed priming solution (P<0.05). 3. Cardiac and lung Wet/Dry ratios were remarkedly lower in the leukocyte-depleted group. There was no significant difference between the non-hemic and blood-mixed groups. Conclusion: Based upon this result, we concluded that the leukocyte depletion from homologous blood of CPB priming solution has a beneficial effect in reducing cardiopulmonary edema compared with non leukocyte-depleted or crystalloid priming solutions.