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Original Articles
- HgCl2 Toxicity on Cultured Renal Tubular Cells of Rabbit.
- Jung Young Lee, Seong Beom Lee, Suk Hyung Lee, Won Sang Park, Nam Jin Yoo, Sang Ho Kim, Choo Soung Kim
- Korean J Pathol. 1995;29(5):615-623.
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Abstract
- To understand the mechanism of cell injury when exposed to HgCl2, monitoring of cytosolic ionized free Ca2+([Ca2+]i), viability test, measurement of the amount of ATP, and Ca-ATPase activity were evaluated in cultured rabbit renal tubular cells(RTC) exposed to HgCl2. The results were as follows: 1) HgCl2 was cytotoxic to rabbit RTC at all doses except 10 uM and the rate of killing displayed a dose- and time-dependent relationship. 2) The absence of extracellular Ca provided partial protection from irreversible injury induced by HgCl2. 3) The increasing pattem of [Ca2+]i varied according to the concentrations of HgCl2. At the low concentrations of HgCl2 (2.5-10 microM), the level of [Ca2+]i increased slowly over the flat 2-3 min and then achieved plateau-state. In contrast, at the high concentrations of HgCl2 (25-100 microM) the level of [Ca2+]i achieved peak within 1 min and then decreased to a plateau state under normal concentrations. 4) The level of ATP was decreased to 27.5% of that of normal control cells within 3 min by using a treatment of 100 microM HgCl2. 5) HgCl2 did not affect the Ca2+ ATPase activity by enzyme histochemical observation. These findings suggest that the elevation of [Ca2+]i in response to the HgCl2-induced injury is an important event in accelerating injury that ultimately leads to cell death. But other possibilities such as HgCl2 might have direct deleterious effects on the also should be considered.
- Synaptic Reorganization of Dentate Mossy Fibers and Expression of Calcium Binding Proteins in Hippocampal Sclerosis of Temporal Lobe Epilepsy.
- Sang Pyo Kim, Seung Pil Kim, Seung Che Cho, Young Rok Cho, Ji Min Jeon, Yu Na Kang, Kun Young Kwon, Eun Sook Chang
- Korean J Pathol. 1998;32(5):328-336.
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Abstract
- This study was designed to identify expression of calcium-binding proteins and synaptic reorganizations of dentate mossy fibers in hippocampal sclerosis of human temporal lobe epilepsy. Hippocampal neuronal density was quantitively analyzed in temporal lobe epilepsy group (n=50) to investigate the degree of hippocampal sclerosis and it was compared with that of autopsy control (n=3). To verify the distribution of calcium-binding proteins in neurons of epileptic hippocampi, the parvalbumin (PV)-immunoreactive and calbindin-D28K (CB)-immunoreactive neurons were quantitively analyzed in each area of Ammon's horn by immunohistochemical stain. Also, to clarify synaptic reorganizations of the dentate mossy fibers, a part of each hippocampus was examined under light microscopy and transmission electron microscopy using Timm sulphide silver method. In epileptic hippocampi, severity of hippocampal sclerosis (HS) was graded four, which consisted of 3 cases with no HS, 6 mild HS, 12 moderate HS, and 29 severe HS. The hippocampal neuronal loss was most prominent in CA1, followed by CA4 and CA2. Expression of calcium-binding proteins was more prevalent in CA2 of all groups. The proportion of PV-immunoreactive neurons in CA1 and CA4 significantly increased in the moderate and severe HS group, whereas the proportion of CB-immunoreactive neurons did not correlated with the severity of HS. Timm granules were noted in inner molecular supragranular layer of dentate gyrus of epileptic hippocampi and they tended to increase in proportion along with the severity of hippocampal sclerosis. Transmission electron microscopy showed that supragranular Timm granules corresponded to synaptic terminals of mossy fibers. These results suggest that parvalbumin appears to have more protective effect against neuronal loss and that mossy fiber synaptic reorganization seems to play a major role in pathogenesis of hippocampal sclerosis of human temporal lobe epilepsy.
- Inhibitory Effect of Tetrandrine on Extracellular Matrix Deposition in Rat Hepatic Fibrosis.
- Won Young Choi, Hyo Jeong Chae, Sun Kyung Lee
- Korean J Pathol. 1999;33(5):319-325.
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Abstract
PDF - No effective therapy has yet developed for liver fibrosis/cirrhosis by directly inhibiting the accumulation of extracellular matrix. This study was undertaken to determine the effect of tetrandrine in rat model of liver fibrosis induced by carborn tetrachloride (CCl4) administration intraorally. Tetrandrine, a calcium channel blocker, is anti-inflammatory constituent of the families Menispermaceae and Ranunculaceae, which have been used as folk remedies in China. Repeated administration of CCl4 for 14 weeks to rats induced liver fibrosis with steatosis. Rats were killed after 4, 8 or 14 weeks of treatment with CCl4, CCl4 tetrandrine (30 mg/kg) or CCl4 tetrandrine (50 mg/kg). The histopathological findings of liver were observed semi-quantitatively by light microscopy and volume percentage of the collagen deposition was determined by image analyzer. Tetrandrine inhibited collagen deposition induced by CCl4 administration, as shown by less severe steatosis and fibrosis and significantly decreased volume percentage of collagen fibers in CCl4 tetrandrine treated animals compared with CCl4 only group. Thus, the administration of tetrandrine holds great promise for treating subjects with liver fibrosis/cirrhosis as a result of chronic hepatic injury.
Case Report
- Pulmonary Aspergillus niger Fungus Ball Associated with Calcium Oxalate Crystal: A Case Report.
- Eunhee Lee, Heejung Kim, Eundeok Chang, Kyo Young Lee, Byung Kee Kim
- Korean J Pathol. 2001;35(2):165-167.
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Abstract
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- Pulmonary aspergillomas are considered to represent saprophytic growth of hyphae within the preexisting lung cavity. Causative Aspergillus species are mostly composed of A. fumigatus and A. flavus and, occasionally, A. niger. It is difficult to identify these species using histopathologic evaluation without a culture of sputum and bronchoalveolar lavage. We recently experienced a case of pulmonary Aspergillus niger infection associated with characteristic calcium oxalate crystal formation. A large cavity contained hyphae with a typical conidial head, conidiophore, and conidia. Characteristic birefrigent calcium oxalate crystals were demonstrated in the cavity wall.
Original Article
- The Study of Cell Killing Mechanism by Membrane Attack Complexes of Complement in the Nucleated Cells.
- Sang Ho Kim, Sung Hak Park, Myung Hoon Chun
- Korean J Pathol. 1992;26(3):253-269.
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Abstract
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- The mechanism of cytolysis by complement attack of nucleated cells(NC) is of special interest in comparison to that of red blood cells. It is known that NC death by membrane attack comples, C5b-9, is caused by many factors, i.e., efficiency of complex assembly, activation of intrinsic metabolic pathway by signal transduction, cytotoxic effect of the channel itself and natural repair ability. These factors suggest that colloid osmotic lysis, known in red blood cells, does not fully explain the complement-mediated cell death of NC. In this study, the authors investigated correlation between biochemical and morphological changes to prove "Ca2+-mediated metabolic death"8~13) representing a mechanism of NC death caused by C5b-9 attack. The L1210 cells, mouse leukemic cell line carrying small complement channel(TAC5b-91) were used in the experiments. The amounts of intracellular adenine nucleotides to extracellular Ca2+, ouabain, KC1 and dextran were analyzed by bioluminescence method using luminometer. Cell viability was checked by 0.4% trypan blue dye and LDH release. Morphological observation of TAC5b-91 was done by immunocytochemical staining and electron microscope. The results were as follows: 1) The release of ATP, ADP and AMP followed by cell death was rapid and progressive along the incubation time at 37 degrees C and it was accelerated in 1.5 mM of [Ca2+]0. 2) There was no evidence of ATP repairment in the TAC5b-91. 3) Extracellular KC1(150 mM), dextran(0.66 mM) and ATP supplement(0.2 microM) could not effectively inhibit ATP depletion and cell death. Ouabain(27 and 100 microM) enhanced cell death and could not completely prevent ATP loss. 4) Most of the mitochondria showed swelling, loss of cristae and Ca2+ deposit in matrix in the electron microscopic observation. Rapid, sustained and irreversible depletion of adenine nucleotides was due to Ca2+ deposit with destruction of mitochondria and also the leakage through transmembrane channels. Moreover this energy depletion was accelerated by high extracellular Ca2+ concentration. These results indicate that Ca2+-mediated, energy exhaustion is one of the mechanisms of the metabolic cell death by C5b-9 attack of NC.
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