Journal of the Korean Society of Groundwater Environment
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v.1
no.2
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pp.100-104
/
1994
The rock matrix diffusion provides a retarding mechanism for sorbing and especially non-sorbing radionuclides. It has to be verified not only theoretically and experimentally but also from natural phenomena, before the mechanism can be incorporated fully into transport codes. The natural analogue studies, such as the concentration variation of radionuclides in profiles perpendicular to fluid-conducting fractures and to intrusive contact zones, have been believed to provide a validation. In thermal alteration zones of Naeduckri granite intruded by a pegmatite, large alkali and alkaline earth elements such as K, Rb, Sr, and Ba were moderately migrated during thermal alteration. Li, V. and Nb were also migrated about 9cm in width from the contact between the granite and the pegmatite. The concentration variation of these elements in thermally altered zones seems to be resulted from the local migration due to the re-equilibration among the elements released from the breakdown of primary minerals in the granite. Most of these natural analogue studies simply show only the concentration variation of elements without detailed informations on the diffusion time and other important data fir interpreting the behaviour of radionuclides, because of the absence of appropriate minerals for age data. Despite this problem, natural analogue studies will be needed for transport models of radionuclides in safety assessment.
Human neutrophil elastase (HNE, EC 3,4,21, 11), a mediator of tissue breakdown, was inhibited by tetracycline, oxytetracycline and demeclocycline. Among them, oxytetracycline showed the most potent inhibitory effect on the activity of HNE. IC50 of this drug at our specific condition was less than 1 mM. Tetracycline inhibited human neutrophil elastase non-competitively, and oxytetracycline inhibited competitively. Ki values of tetracycline and oxytetracycline were 4.9 mM and 0.39 mM, respectively. Structural modified tetracycline, de-dimethylaminotetracycline, which showed no antibiotic activity since the active dimethylamino radical was removed from the position #4 of the tetracycline, showed similar inhibition effect on the activity of human neutrophil elastase to that of tetracycline. Thus, we speculated that inhibition of human neutrophil elastase by tetracyclines was not depended on the dimethylamino radical which is a critical active site for antibiotic effect, rather it was depended on the hydoxyl radical of tetracyclines. Therefore, the property of inhibiting elastase may be an additional molecular biochemical mechanism of action of these drugs at the inflammatory sites.
Lee Shin-Bok;Yoo Young-Ran;Jung Ja-Young;Park Young-Bae;Kim Young-Sik;Joo Young-Chang
Journal of the Microelectronics and Packaging Society
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v.12
no.2
s.35
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pp.167-174
/
2005
Smaller size and higher integration of electronic components make smaller gap between metal conducting layers in electronic package. Under harsh environmental conditions (high temperature/humidity), electronic component respond to applied voltages by electrochemically ionization of metal and metal filament formation, which lead to short failure and this phenomenon is termed electrochemical migration(ECM). In this work, printed circuit board(PCB) is used for determination of ECM characteristics. Copper leads of PCB are soldered by eutectic solder alloys. Insulation breakdown time is measured at $85^{\circ}C,\;85{\%}RH$. CAF is the main mechanism of ECM at PCB. Pb is more susceptible to CAF rather than Sn, which corresponds well to the corrosion resistance of solder materials in aqueous environment. Polarization tests in chloride or chloride-free solutions fur pure metal and eutectic solder alloys are performed to understand ECM characteristics. Lifetime results show well defined log-normal distribution which resulted in biased voltage factor(n=2) by voltage scaling. Details on migration mechanism and lifetime statistics will be presented and discussed.
Second-order rate constants ($k_N$) have been measured spectrophotometrically for nucleophilic substitution reactions of 2-pyridyl X-substituted benzoates 8a-e with a series of alicyclic secondary amines in $H_2O$ at $25.0{\pm}0.1^{\circ}C$. The $k_N$ values for the reactions of 8a-e are slightly smaller than the corresponding reactions of 4-nitrophenyl X-substituted benzoates 1a-e (e.g., $kN^{1a-e}/k_N^{8a-e}$ = 1.1 ~ 3.1), although 2-pyridinolate in 8a-e is ca. 4.5 $pK_a$ units more basic than 4-nitrophenolate in 1a-e. The Br$\o$nsted-type plot for the aminolysis of 8c (X = H) is linear with $\beta_{nuc}$ = 0.77 and $R^2$ = 0.991 (Figure 1), which is typical for reactions reported previously to proceed through a stepwise mechanism with breakdown of a zwitterionic tetrahedral intermediate $T^{\pm}$ being the rate-determining step (RDS), e.g., aminolysis of 4-nitrophenyl benzoate 1c. The Hammett plot for the reactions of 8a-e with piperidine consists of two intersecting straight lines (Figure 2), i.e., $\rho$ = 1.71 for substrates possessing an electron-donating group (EDG) while $\rho$ = 0.86 for those bearing an electron-withdrawing group (EWG). Traditionally, such a nonlinear Hammett plot has been interpreted as a change in RDS upon changing substituent X in the benzoyl moiety. However, it has been proposed that the nonlinear Hammett is not due to a change in RDS since the corresponding Yukawa-Tsuno plot exhibits excellent linear correlation with $\rho$ = 0.85 and r = 0.62 ($R^2$ = 0.995, Figure 3). Stabilization of substrates 8a-e in the ground state has been concluded to be responsible for the nonlinear Hammett plot.
Objectives : Intracerebral hemorrhage (ICH) is characterized by breakdown of blood vessels within the brain parenchyma. Fundamental therapeutic strategies for ICH, particularly those aimed at neuroprotection, have to be established. So in this experiment, the effects of Woowhangchongshim-won, a traditional prescription formula for treating Cerebral Apoplexy in Asian countries, were investigated. Methods : After intraperitoneal injection of chloralhydrate, rats were placed in a stereotaxic frame. ICH was induced by injection of 1 U collagenase type IV and drug was administered orally for 10 days. The molecular profile of cerebral hemorrhage in rat brain tissue was measured using micro array technique to identify up- or down- regulated genes in brain tissue. These genes induced by brain damage were mainly concerned with general metabolic process such as primary metabolic process, cellular metabolic process, macromolecule metabolic process, and biosynthetic process. Results : The number of genes increased in control and not-changed in experiment was 374, and decreased in control and not-changed in experiment was 527. We are concerned with genes that can be recovered by treatment with medicine, it is especially interesting to above types of genes. Conclusions : Upon medicine treatment to the rat having cerebral hemorrhage, expressions of some genes were restored to normal level. Further analysis using protein interaction database identified some key molecules that can be used for elucidation of therapeutical mechanism of medicine in future.
Objectives: Cancer lethality is usually the result of local invasion and metastasis of neoplastic cell from the primary tumor. Because of their ability to degrade extracellular matrix components, matrix metalloproteinases (MMPs) and basic fibroblast growth factor (bFGF) have been implicated in the breakdown of basement membrane and underlying stroma, thereby facilitating tumor growth and invasion. It has been well established that MMPs and bFGF expression correlate with cervical lymph node metastasis, but studies on expression in the metastatic cervical lymph node itself are not enough. We have analyzed matrix metalloproteinases (MMPs) and basic fibroblast growth factor (bFGF) in squamous cell carcinoma of the head and neck and metastatic cervical lymph node, and evaluated their relationship and clinicophathologic significance. Material and Methods: 20 cases of squamous cell carcinoma of the head and neck were entered on the study of immunohistochemical stains for MMP-9 and bFGF in the obtained tissue from primary tumor and metastatic cervical lymph node. We analyzed the relationship between MMP-9, bFGF expression of the primary tumor and metastatic node with age, sex, T-stage, N-stage, histologic grade, pathologic stage and disease free survival. Results: Expression of MMP-9 and bFGF in cancer cell and metastatic lymph node was higher than that in normal cell and lymph node. According to histologic differentiation, expression of MMP-9 of the metastatic cervical lymph node was higher than primary tumor. Considering to other clinicopathologic factor, no statistical significance was seen in MMP-9 and bFGF. Conclusion: We found that expression of MMP-9 is higher in the metastatic lymph node than primary tumor in the poorly differentiated squamous cell carcinoma. But we don't find out the statistical significance in relation between bFGF and clinical factors. So we guess that some different mechanism of MMP-9 and bFGF in Head & Neck squamous cell carcinoma exist. Further studies will be necessary to establish their pathogenesis in the Head and Neck cancer.
p62 is a novel cytoplsmic protein that binds to SH2 domain of p56$^{lck}$, lymphocyte-specific protein tyrosine kinase, and the expression of p62 was observed in most tissues. In addition p62 interacts with various proteins including ubiquitin and atypical PKC isoform, indicating its diverse biological role in different tissues. However, little is known about functional connection between p62 and its binding proteins. In the present study, a novel cellular protein, p62 has been shown to bind to 14-3-3 $\tau$ isoform that is specific for T cells. Moreover, overexpression of p62 in T cells caused to delay onset of UV-induced apoptosis characterized by DNA fragmentation and breakdown of poly (ADP-ribose) polymerase (PARP). Lately, 14-3-3 proteins have been shown to mediate survival signal via interacting proapoptotic Bad protein in the Iymphocyte. These results suggested the presence of p62-mediated regulatory mechanism during apoptosis in T cells, in which activation-induced apoptotic signal could be interfered by p62 and 14-3-3 protein.n.
Cajanus indicus is a herb with medicinal properties and is traditionally used to treat various forms of liver disorders. Present study aimed to evaluate the effect of a 43 kD protein isolated from the leaves of this herb against chloroform induced hepatotoxicity. Male albino mice were intraperitoneally treated with 2mg/kg body weight of the protein for 5 days followed by oral application of chloroform (0.75ml/kg body weight) for 2 days. Different biochemical parameters related to physiology and pathophysiology of liver, such as, serum glutamate pyruvate transaminase and alkaline phosphatase were determined in the murine sera under various experimental conditions. Direct antioxidant role of the protein was also determined from its reaction with Diphenyl picryl hydraxyl radical, superoxide radical and hydrogen peroxide. To find out the mode of action of this protein against chloroform induced liver damage, levels of antioxidant enzymes catalase, superoxide dismutase and glutathione-S-transferase were measured from liver homogenates. Peroxidation of membrane lipids both in vivo and in vitro were also measured as malonaldialdehyde. Finally, histopathological analyses were done from liver sections of control, toxin treated and protein pre- and post-treated (along with the toxin) mice. Levels of serum glutamate pyruvate transaminase and alkaline phosphatase, which showed an elevation in chloroform induced hepatic damage, were brought down near to the normal levels with the protein pretreatment. On the contrary, the levels of anti-oxidant enzymes such as catalase, superoxide dismutase and glutathione-S-transferase that had gone down in mice orally fed with chloroform were significantly elevated in protein pretreated ones. Besides, chloroform induced lipid peroxidation was effectively reduced by protein treatment both in vivo and in vitro. In cell free system the protein effectively quenched diphenyl picryl hydrazyl radical and superoxide radical, though it could not catalyse the breakdown of hydrogen peroxide. Post treatment with the protein for 3 days after 2 days of chloroform administration showed similar results. Histopathological studies indicated that chloroform induced extensive tissue damage was less severe in the mice livers treated with the 43 kD protein prior and post to the toxin administration. Results from all these data suggest that the protein possesses both preventive and curative role against chloroform induced hepatotoxicity and probably acts by an anti-oxidative defense mechanism.
Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Bong-Ha;Ryu, Ki-Won;Jung, Myung-Chai
The Journal of Internal Korean Medicine
/
v.25
no.2
/
pp.202-213
/
2004
Object : Objective: This study was conducted to investigate the anti-cancer effects of Mylabris phalerata (반모) in some kinds of cancer cells. Materials and Methods: Some kinds of cancer cells lines were treated. We used nine kinds of cancer cell lines, such as stomach cancer cells (Kato), lung cancer cells (Calu-1, NCI-H 1395), urinary bladder cancer cells (HS789T), bone cancer cells (Saos-2), brain cancer cells (SK-N-MC), liver cancer cells (Hep-G2), skin cancer cells (Mo-1) and prostate cancer cells (PC-3) with the water decoction of Mylabris phalerata. The histological changes of all cell lines in the media (RPMI-1640) containing the decoction of Mylabris phalerata were observed and we examined cell death assay by trypan blue exclusion testing was examined. Finally, the change of mitochondrial membrane potential was measurd and the inhibitory effect of Mylabris phalerata on cell increase was examined by analyzing the cell cycle. Results: In histologic change all cancer cell lines showed withdrawn and floating appearance that is typical in cellular impairment. Most of the cell lines showed over 50% death rate after 24 hours in trypan blue exclusion tests. Especially the stomach, urinary bladder. brain and liver cell lines showed over 30% death rate after 12 hours. All cell lines treated with Mylabris phalerata were less stained than the control group and the mitochondrial membrane potential in the Mylabris phalerata treated cell lines was markedly lower than that in the control group. The measurement of DNA quantity in all cell lines showed the disappearance of the peak and the thickened left axis, which suggests that all cellular DNA degraded. Conclusion: Mylabris phalerata had cytotoxicity on various kinds of cancer cell lines and the mechanism of that was the impairment of mitochondria by the breakdown of the mitochondrial cell membrane. We propose that this is in part attributable to the destruction of DNA in cancer cells.
The cells associated with normal defense mechanism in inflammation release free oxygen radicals, hydroxy radicals, and various protease, all of which can damage the surrounding cells(fibroblasts) and matrix molecules(collagen). The objective of this study was to evaluate the effects of "scavenger" enzyme, superoxide dismutase(SOD). to periodontal ligament (PDL) cells. Human PDL cells were cultured from the teeth extracted for non-periodontal reason. Cultured PDL cells in vitro were treated with SOD and LPS according to dosage and culture times. Cellular activity was exaimed by Microtitration(MTT) assay. The quantitative expression of cellular proliferation by proliferating cell nuclear antigen(PCNA), collagen type I and fibronectin by indirect immunocytochemically stain in PDL cells were done. The results were as follows: 1. As only SOD treated group at 2 and 3 days, PDL cell activity was significantly increased at more than 150U(P<0.05). 2. When LPS(0.5, $5{\mu}g/m{\ell}$) and SOD(more than 150U) were added together, it was significantly increased than LPS only treated and control groups at 2 days(P<0.05). 3. When LPS($5{\mu}g/m{\ell}$) and SOD(150, 300U) were added together, PCNA index was significantly increased than LPS only treated and control groups at 2 and 3 days(P<0.05). 4. When LPS($5{\mu}g/m{\ell}$) and SOD(150U) were added together, collagen type I was significantly increased than LPS only treated and control groups at 3 days(P<0.05). 5.When LPS($5{\mu}g/m{\ell}$) and SOD(300U) were added together, fibronectin was significantly increased than LPS only treated and control groups at 3 days(P<0.05). On the above the results, the SOD in association with collagen type I, fibonectin, and PCNA may afford biological protection to oxy-radicals that were typically liberated during normal inflammatory response. Thus, the exogenous application of SOD may be effective in sthe treatment of the localized breakdown associated with chronic periodontal disease.
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