• Structural Engineering and Mechanics
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• v.50 no.5
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• pp.665-677
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• 2014

A numerical method, using a special mixed finite element associated with the virtual crack extension technique, has been developed to evaluate the energy release rate for kinking cracks. The element is two dimensional 7-node mixed finite element with 5 displacement nodes and 2 stress nodes. The mixed finite element ensures the continuity of stress and displacement vectors on the coherent part and the free edge effect. This element has been formulated starting from a parent element in a natural plane with the aim to model different types of cracks with various orientations. Example problems with kinking cracks in a homogeneous material and bimaterial are presented to assess the computational accuracies.

• Structural Engineering and Mechanics
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• v.25 no.6
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• pp.733-751
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• 2007

The metis element method (Hung 1978) has been applied to analyse free edge interlaminar stresses and delamination in composite laminates, which are subjected to extension and bending. The paper recalls Lekhnitskii's solution for generalized plane strain state of composite laminate and Wang's singular solution for determination of stress singularity order and of eigen coefficients $C_m$ for delamination problem. Then the formulae of metis displacement finite element in two-dimensional problem are established. Computation of the stress intensity factors and the energy release rates are presented in details. The energy release rate, G, is computed by Irwin's virtual crack technique using metis elements. Finally, results of interlaminar stresses, the three stress intensity factors and the energy release rates for delamination crack in composite laminates under extension and bending are illustrated and compared with the literature to demonstrate the efficiency of the present method.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2001.05a
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• pp.117-117
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• 2001

We investigated Free radical generation of endocrine disrupter, bisphenol A and alkyl esters of phthalic acid (DEP, DBP) using lipid peroxidation, enzyme assay (SOD, Catalase, Gpx-px), Cell viability and phototoxicity. Bisphenol A are monomers of various plastics including polycarbonates and epoxy resins which are used in numerous consumer products. The release of BPA from some of these materials has recently been reported. (omitted)

• Animal cells and systems
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• v.7 no.4
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• pp.309-315
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• 2003

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L-NAME. Chitosan, the linear polymer of D-glucosamine in $\beta$(1\longrightarrow4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from $HgCl_2$injury.

• Journal of Pharmaceutical Investigation
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• v.26 no.2
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• pp.105-112
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• 1996

The surface of albumin microspheres was modified with methotrexate(MTX) by using 1,3-dicyclohexylcarbodiimide (DCC). Surface-modified albumin microspheres entrapping no MTX (SAMS), free MTX (SAMSF) and MTX-bovine serum albumin(BSA) conjugates(SAMSC) were prepared. The organ-targeting ability of free $[^3H]MTX,\;[^3H]MTX-BSA$ conjugate and the above microspheres was evaluated after i.v. administration of the preparations, equivalent to 150 nCi via the tail vein of mice. The total radioactivity in the lung increased immediately in a few minutes after i.v. injection of the microspheres, and then declined for the period of 3-4 weeks. However, the radioactivity in the liver, spleen and kidney increased slowly during the rapid decrease in radioactivity in the lung. This suggested that the microspheres could be entrapped rapidly in the lung through mechanical filtration because of their large size and slowly redistributed to the liver, spleen and kidney due to either the microspheres being degraded enough for the size to allow passage through the capillary beds of the lung and/or the release of $[^3H]MTX\;or\;[^3H]MTX-BSA$ conjugates from the microspheres. The amount of $60{sim}70%$ of the dose was targeted to the liver after the i.v. injection of SAMS, SAMSF and SAMSC, and the values of $(R_e\;^*\;_{e)liver}$ from the microspheres were $5{\sim}7$ compared to free MTX. This suggested that the liver-targeting ability from surface-modified albumin microspheres could be $5{\sim}7$ times as that of free MTX. The liver-targeted drug was accumulated in the Kupffer cells at the initial stage, thereafter the drug in the Kupffer cell was slowly transferred into the hepatocytes. The value of AUQ for liver from SAMS was higher than that from SAMSF, but much lower than that from SAMSC. This suggest that MTX bound to their surface could be eliminated slower than the entrapped free MTX, and faster than the entrapped MTX-BSA conjugates. This is consistent with the in vitro release rates order in the presence of a proteolytic enzyme. Also, surface-modified MTX was scarcely released in the absence of a proteolytic enzyme. Therefore, the surface-modified MTX nay be released (or eliminated) rapidly from SAMSC at the target site, and thereafter MTX may be released (or eliminated) slowly from the entrapped MTX-BSA conjugates in SAMSC for a long period.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.2
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• pp.135-142
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• 1997

As it has been reported that the depolarization-induced norepinephrine (NE) release is modulated by activation of presynaptic $A_1$-adenosine heteroreceptor and various lines of evidence indicate that $A_2$-adenosine receptor also presents in hippocampus, and that the adenosine effect is magnesium dependent, the present study was undertaken to delineate the role of adenosine receptors in the modulation of hippocampal NE release. Slices from the rat hippocampus were equilibrated with $[^3H]-NE$ and the release of the labelled product, $[^3H]-NE$, was evoked by electrical stimulation (3 Hz, 5 V $cm^{-1}$, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium outflow was investigated. $N^6-cyclo-pentyladenosine$ (CPA), in concentrations ranging from 0.1 to 10 ${\mu}M$, decreased the $[^3H]-NE$ release in a dose-dependent manner without changing the basal rate of release, and these effects were significantly inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 2 ${\mu}M$) treatment. When the magnesium concentration was reduced to 0.4 mM or completely removed, the evoked NE release increased along with decreased basal rate of release. In contrast, increasing the magnesium concentrations to 2.4 and 4 mM, decreased the evoked NE release. The CPA effects on evoked NE release were reducedby magnesium removal, but potentiated by 2.4 mM magnesium in the medium. 5-(N-cyclopropyl)-carboxamodiadenosine (CPCA, 1 & 10 ${\mu}M$), an $A_2$-agonist, decreased the evoked tritium outflow, and this effect was also abolished by DPCPX pretreatment. CGS, a powerful $A_2$-agonist, did not affect the evoked NE release. However, the effects of CPCA and CGS on evoked NE release were significantly increased by pretreatment of DPCPX in the magnesium-free medium. These results indicate that inhibitory effect of $A_1$-adenosine receptor on NE release is magnesium-dependent, and $A_2$-receptor may be present in the rat hippocampus.

• Archives of Pharmacal Research
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• v.25 no.6
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• pp.932-939
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• 2002

The aim of the present study was to determine the characteristics of cytisine on the secretion of catecholamines (CA) in isolated perfused rat adrenal glands, and to clarify its mechanism of action. The release of CA evoked by the continuous infusion of cytisine ($1.5{\times}10^{-5} M$) was time-dependently reduced from 15 min following the initiation of cytisine infusion. Furthermore, upon the repeated injection of cytisine ($5{\times}10^{-5}$), at 30 min intervals into an adrenal vein, the secretion of CA was rapidly decreased following the second injection. Tachyphylaxis to the release of CA was observed by the repeated administration of cytisine. The cytisine-induced secretion of CA was markedly inhibited by pretreatment with chlorisondamine, nicardipine, TMB-8, and the perfusion of $Ca^{2+}$-free Krebs solution, while it was not affected by pirenzepine or diphenhydramine. Moreover, the secretion of CA evoked by ACh was time-dependently inhibited by the prior perfusion of cytisine ($5{\times}10^{-6} M$). Taken together, these experimental data suggest that cytisine causes secretion of catecholamines from the perfused rat adrenal glands in a calcium-dependent fashion through the activation of neuronal nicotinic ACh receptors located in adrenomedullary chromaffin cells. It also seems that the cytisine-evoked release of catecholamine is not relevant to the activation of cholinergic M$_1$-muscarinic or histaminergic receptors.

• The Journal of Korean Physical Therapy
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• v.13 no.1
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• pp.237-243
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• 2001

Skeletal muscle cells are activated by ${\alpha}$-motorneurons which release acetylcholine at the neuromuscular junction. This results in a local depolarization of surface membrane which triggers an action potential. The action potential propagates along the surface membrane and also into the T-tubule system. In the triads T-tubules are in close connection with the terminal cisternae of the sarcoplasmic reticulum(SR). The action potential activaies T-tubule voltage sensors(DHP receptors). which activates SR Ca$^{2+}$ release channels(ryanodinc receptors). Ca$^{2+}$ have a key role in skeletal muscle in that an increase of free myoplasmic Ca$^{2+}$ concentration. The process of coupling chemical and electrical signals at the cell surface to the intracellular release of Ca$^{2+}$and ultimate contraction of muscle fibers is termed excitation-contraction coupling(ECC). Coupling of cel1 surface signals to intracellular Ca$^{2+}$ release proceeds by several mechanisms in skeletal muscle cells. This review focus on sarcopiasmic reticulum(SR) Ca$^{2+}$ releasing mechanisms from sarcoplasmic reticulum in the skeletal muscle. The mechanisms include DCCR, CICR, and HCR.

• Macromolecular Research
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• v.16 no.3
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• pp.189-193
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• 2008

Thermal cross-linking method of poly(vinyl alcohol) (PVA) using poly(acrylic acid) (PAA) was carried out on PVA/PAA hydrogels. The level of gelation was measured in the PVA/PAA hydrogels with various PAA contents. The swelling behavior at various pHs showed that the swelling kinetics and water contents of the PVA/PAA hydrogels reached equilibrium after 30 h, and the time to reach the equilibrium state decreased with increasing PAA content in the hydrogel. The water content increased with increasing pH of the buffer solution. The permeation and release of the drug were tested using indomethacin as a model drug. The permeated and released amounts of the drug increased with decreasing the PAA content because of the low free volume in the hydrogel due to the higher cross-linking density. The kinetic profile of drug release at various pHs showed that all samples reached the equilibrium state within the 5 h.

• Journal of the Korean Society of Clothing and Textiles
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• v.5 no.1
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• pp.23-26
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• 1981

In this paper, the extraction mechanism of free formaldehyde in the urea formaldehyde resin finished cotton fabric is discussed. An empirical equation for formaldehyde release has been formulated. $$F=3.7\times10^{-3}\;H\;T^{2.2326}+440$$ in which, F: the amount of free formaldehyde extracted ($\mu$g/g) H: extraction time (min) T: extraction temperature ($^{\circ}C$)