- The Morphologic Changes of the Sinusoidal Endothelial Cells in N-diethylnitrosamine Induced Cirrhotic Rat Liver.
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Ok Ji Paik, Hee Kyung Park, Jong Min Chae, Jyung Sik Kwak, Tae Joong Sohn
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Korean J Pathol. 1996;30(7):604-615.
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- The purpose of this study is to investigate the morphologic changes of the sinusoidal endothelial cells and the associated structures of the cirrhotic rat liver induced by repeat intraperitoneal injections of N-diethylnitrosamine (DEN) (100 mg/kg/week). One day to 6 weeks later, rat livers were observed under the light, transmission and scanning electron microscopy, and immunostained with laminin antibody. Two weeks after DEN treatment, the fibrillar material in Disse's space was noted, and then a basement membrane-like structure was found at 4 weeks after treatment. Laminin was detected in perisinusoidal areas after 4 weeks. Laminin was strongly positive on the fibrous septum and in the sinusoidal wall of cirrhotic nodules after 6 weeks of treatment. The diameters and numbers of sinusoidal endothelial fenestrations did not change significantly until 2 weeks. They decreased within 4 weeks, and then the sinusoidal endothelium was poorly fenestrated at 6 weeks after DEN treatment. These results suggest that as fibrosis develops in cirrhosis, the deposit of extracellular matrix such as laminin within Disse's space is a major contributing factor in the structural alteration of sinusoidal endothelial cells, and the capillarization of the sinusoidal endothelial cells may be a contributor to impairment of the hepatic function in cirrhosis.
- Ultrastructural Study of Amiodarone-Associated Lung Injury.
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Eun Yung Kim, Sang Han Lee, Yoon Kyung Sohn, Tae Joong Sohn
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Korean J Pathol. 1995;29(1):10-23.
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- Amiodarone, an antiarrhythmic drug, may exert pulmonary toxicity in some patients but the pathogenesis is not clear.
This study was carried out to investigate the pathogenetic mechanism of pulmonary injury induced by amiodarone at dose of 100 mg/kg/day given to rats by intraperitoneal injection for 3 weeks. And the preventive effects of concomitantly injected steroid (10 mg/kg/day) on amiodarone induced pulmonary injury was also studied using bronchoalveolar lavage, light microscopy and transmission electron microscopy. The results obtained were summarized as follows: Mild lymphocytosis of bronchoalveolar lavage fluid was found in all experimental groups. Intracytoplasmic lamellar body formation was found in all types of pulmonary cells and type II pneumocytes revealed the earliest abnormal lamellar body formation. The capillary endothelial cells showed cellular swelling and detachment from underlying basement membrane at early phase of experiment and the edema of alveolar wall and interstitium were noted. Interstitial fibrosis and proliferation of type II pneumocytes were noted at late phase. The lungs of steroid injected groups revealed accumulation of lamellar bodies in all types of pulmonary cells but interstitial fibrosis was not occurred. These findings support the concept that amiodarone is responsible for a drug-induced phospholipidosis and directly toxic to pulmonary endothelial and epithelial cells. And steroid may regress the progression of amiodarone induced pulmonary injury.
- An Immunohistochemical Study for the neu and ras Oncoprotein and Epidermal Growth Factor Receptor in the Breast Carcinoma.
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Jeong Ja Park, Tae In Park, Tae Joong Sohn, In Soo Suh
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Korean J Pathol. 1994;28(2):126-134.
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- To evaluate correlation between the expression of neu and ras oncoprotein and epidermal growth factor receptor on breast carcinoma and other known prognostic factors, immunohisto-chemical studies were performed. Positive reaction for neu, which appeared as brown granular deposits along cell surface and cytoplasm of the tumor cells, was significantly correlated with the histological grade but not with other prognostic factors such as tumor size, lymph node me-tastasis, local recurrence, and estrogen and progesteron receptor status. Also granular deposits of ras were noted in the carcinoma cells in the cytoplasm, while the epithelaial cells of the normal lobule and duct showed negative reation.
But expression of ras was not significantly associated ras with other prognostic factors. The reaction for EGFR was mostly negative on epithelial cells of both the normal lobule and duct, and was not significantly associated with other prognostic factors. The results suggested that expression of the neu oncoprotein is significantly associated with the histological grade of breast carcinoma, while the ras and the EGFR do not show significant prognostic value.
- The effects of Broad Spectrum Antibiotics and Endotoxin to the Carbon Tetrachloride-induced Liver Injury.
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Hyun Ho Shin, O Joon Kwon, Yoon Kyung Sohn, In Soo Suh, Tae Joong Sohn
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Korean J Pathol. 1992;26(4):329-337.
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- This study was performed to investigate the effect of endotoxin to the CCl4-induced liver injury. Twelve Sprague-Dawley rats were intraperitoneally injected 1.6 g/kg CCl4 as control group. Another 24 rats were orally administrated 300 mg/kg of neomycin at 16 and 3 hours prior to CCl4 injection as experimental group. Twelve among them were intraperitoneally infected 1.0 mg/kg of endotoxin(E-Coli, 0111:B4, No L-2630, lipopolysaccharide, Sigma, USA) and CCl4 simultaneously for offsetting neomycin effect. The rats were sacrificed at 1, 4, 10, and 24 hours after CCl4 injection. The liver tissues from all experimental groups were observed by light and electron microscopy. The results obtained were summarized as follows: In the CCl4 only group, the hepatocytes revealed sweling of ER and mitochondria with many lipid droplet in the cytoplasm. Focal cellular necrosis was seen at the later phase. The Kupffer cells were activated and showed many cytoplasmic processes, secondary lysosomes, and vaculoles.
The endothelial cells were edematous. Several neutrophils, platelets, and microthrombi were scattered in the sinusoid.
In the neomycin-CCl4-endotoxin administrated group, both hepatocytic destruction and intrasinusoidal microthrombi formation were more pronounced. In the neomycin pretreated group, the hepatocytes revealed mild cellular destruction without necrosis. There is no intrasinusoidal microthrombi.
According to these results, it would be concluded that the small dosage of gastrointestinal tract-derived endotoxin affects to the liver injury caused by CCl4. The synergistic effects of CCl4 and gastrointestinal tract-derived endotoxin which can not be detoxified by damaged Kupffer cells, may be more important in the pathogenesis of CCl4-induced liver injury.
- The Effects of Proteolytic Agent on the Lung Injured by Endotoxemia.
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Chang Ho Cho, Yoon Kyung Sohn, Jyung Sik Kwak, Tae Joong Sohn
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Korean J Pathol. 1991;25(3):215-222.
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- The authors studied the lung injury induced by endotoxemia and the effects of proteolytic agent on the lung changed by endotoxemia. Sprague-Dawley rats were intraperitoneally administrated with a single dose of endotoxin (4 mg/kg, E.
coli 025 : B6 lipopolysaccharide) or with endotoxin and gabexate mesilate (200 mg/kg), a proteolytic agent, concomitantly. Rats of each group were scarificed at 9, 18, and 27 hours after injection. Light and electron microscopic examination were done. The results obtained were summarized as follows: Light microscopic exmination revealed congested capillaries and neutrophilic infiltration in both groups.
Electron microscopic findings were interstitial and alveolar neutrophilic infiltration, endothelial swelling with increased pinocytotic vesicles and cytoplasmic process formation, and interstitial edema. Decrease of osmiophilic bodies in the type II pneumocytes had appeared at 9 hours after endotoxin injection. These changes were increased in severity at 18 hours and 27 hours after endotoxin injection.
In the group of concomitant treatment of gabexate mesilated and endotoxin, there was no edema at 9 hours after injection. After 18 hours welling of endothelial cell and interstitial edema had appeared. However, the severity of the edema was markedly decreased. Type II pneumocytes showed well preserved osmiophilic bodies. According to these results, it is considered that administration of gabexate mesilate can significantly redeced the lung injury induced by endotoxemia.
- Phospholipidosis of Liver Induced by Amiodarone.
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Dong Hoon Kim, Gium Mi Jang, In Soo Suh, Tae Joong Sohn
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Korean J Pathol. 1991;25(1):1-10.
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- Ultrastructural study of the effects of amiodarone on the liver tissue was performed. Rats were fed with amiodarone containing diet and were sacrificerd at 1st, 3rd, 4th, 5th and 8th weeks of experiment. Charateristic lisosomal inclusion bodies were appeared form first week, which were more prominent and increased in size at the 5th and 8th week of experiment. These inclusion bodies were found in hepatocytes, Kupffer cells, bile duct epithelial cells and fibroblasts but most prominent in hepatocytes. The lysosomal inclusion bodies could be divided into four types; those characterized by (1) dense bodies with packed crystaloid contents, (2) multilamellated bodies, (3) irregular shaped bodies with varying electron density and 4. dense bodies containing stacks of fine membranous structures. All types were found in all experimental groups. But the type 1 and 2 were predominent at early stage, while type 3 and 4 were more prominent at later stage According to these findings, the formation of the lysosmal inclusion body was a characteristic change in derangement of phospholipid metabolism. And amiodarone could induce disturbance of phospholipid metabolism in all kinds of cells in liver tissue.
- Ultrastructural Studies of Aortic Endothelial Injury and Regeneration.
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Gium Mi Jang, Dong Hoon Kim, Jyung Sik Kwak, Tae Joong Sohn
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Korean J Pathol. 1990;24(4):337-348.
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- Author performed this experiment to define the most important factor preventing the intimal thickening. An endothelium of abdominal aorta in the rat was denuded by two different wires having same caliver. The degree of injury was limited to the endothelial cells in one, and extended to the internal elastic lamina in another. The results showed that at 72 hours, in the case of superficial injury, the entire injury site was covered by new regenerating cells, but in the case of disruption of the internal elastic lamina, the migrating smooth muscle cell completely reached into the intima and resulted in intemal thickening. Similar findings persisted to 1 week later. Above results suggest the most important factor preventing the intimal thickening in endothelial injury is the depth of the injury which limited within the endothelial cells without extending into the internal elastic lamina and medial smooth muscle cells.
- A Study on the Pathogenesis of Renal Papillary Necrosis Induced by Endotoxin.
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Kyung Rak Sohn, Tae Joong Sohn
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Korean J Pathol. 1989;23(4):416-454.
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- The author carried out an experimentation to clarify a possible pathogenesis of renal papillary necrosis induced by an univisceral Shwartzman reaction. The experimental animals were healthy white rabbits in weighing between 1.7 kg and 3.0 kg. Under the condition of ureterostomy, animals were pretreated with 0.5 cc of 50% ethyl alcohol and followed by administration of 0.2 ~ 1.5 mg endotoxin (E. coli 026 : B6, bacto lipopolysaccharide B. Difco, U.S.A.) as preparation in the renal pelvis. And then sacrificed at 10 minutes, 30 minutes, 1 hour, 2 hours, 6 hours and 24 hours after intravenous injection of 0.2 mg or 0.6 mg endotoxin through the ear veins, subjection to examine light and electron microscopically. The obtained results were summarized as follows: Papillary necrosis was developed in 88% among 18 cases excluding 6 cases died before sacrification. There were two types of necrosis, namely papillary and medullary type, but the former and combined forms of both types were the most common findings. Initial main target site of injury in renal papilla induced by endotoxiin was the endothelium of vasa recta and then followed by the Henle's loop, interstitial cell and collecting tubule respectively.
Vascular injuries such as swelling and detachment of endothelium were observed since 10 minutes after endotoxin injection. Henle's loop showed stratification of basement membrane without consistent features with time lapses and initially observed fatty vaculoes at 1 hour after endotoxin injection were more eminent in 24 hours group. Main changes of interstitial cells were decrease of lipid droplets while increase of fatty vacuoles; the latter were initially observed in 1 hour group and more eminent in 24 hours group.
Collecting tubule showed many fatty vacuoles especially in 24 hours group. It is thought that emergence of fatty vacuoles seems to be a kind of immature lipid droplets to compensate the increased demand of PC release due to continuous ischemic condition. In conclusion, it is thought that ischemic injury due to the vascular changes is pathogenic mechanism producing renal papillary necrosis.
Endotoxin induced univisceral Shwartzman reaction in the kidney may be a good experimental model in studying renal papillary necrosis.
- An Ultrastructural Cytochemical Study on the Mechanism in the Development of Fatty Liver Induced by the Orotic Acid.
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Jae Bok Park, In Soo Suh, Tae Joong Sohn
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Korean J Pathol. 1988;22(3):244-258.
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- For the elucidation of a possible pathogenetic mechanism of fatty accumulation by the orotic acid in the liver, male Sprague-Dawley rats were fed on semisynthetic diet containing 1 per cent orotic for a week, and followed by the morphological examination on the rat livers. The experimental animals were sacrificed on the 1st, 2nd, 3rd, and the 7th days of orotic acid feeding and daily sacrifice was performed after conversion to normal diet feeding during the performed after conversion to normal diet feeding during the period of successive 7 days. The control group animals were fed on normal regular diet, or semisynthetic diet without orotic acid. The liver tissues were examined by the light ad electron microscopy, together with electron microscopic cytochemical study for glucose-6-phosphatase and thiamine pyrophosphatase. On the light microscopy, the lipid droplets began to appear in the 3rd day of orotic acid feeding and then occupy through the all hepatic lobules in the 7th day of orotic acid feeding. On the electron microscopy in the 3rd day of orotic acid administraion, the endoplasmic rdticulum were fragmented and vesiculated, and vesicles containing VLDL particles were demonstrated closely around the Golgi complex. In the 7th day, Golgi complex were increased in numbers. The limiting membrances of lipid vacuoles were regarded to originated from rough-surfaced endoplasmic reticulum of account of demonstration of glucose-6-phospatase in them. In the Golgi complex the activity of thyamine pyprophosphatase were markedly decreased in the 1st day of orotic acid feeding, and then the activity of this enzyme is failed to present afterthat.
On the above findings it is assumed that orotic acid depresses the function of trans aspect of Golgi stack and the VLDL is interrupted and followed by the retrograde accumulation of VLDL. The cis aspect of Golgi stack and rough-surfaced endoplasmic reticulum were accumulated with VLDL particles, and eventually coalesced vesicles of VLDL with become lipid vacuole. The sequential alteration of endoplasmic reticulum and Golgi complex is supporting the concept of conformational change of membranes in cytocavitary net-work.
- The Formation of Giant Mitochondria in the Liver Cells Induced by Hydrazine.
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Il Hoon Kwon, Jong Gi Lee, Yoon Kyung Sohn, Tae Joong Sohn
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Korean J Pathol. 1986;20(3):288-294.
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- The authors studied the formation of giant mitochondria in liver cell. The Sprague Dawley rats were sacrificed following intervals; 5, 10, 20, 30, and 60 minutes after intraperitoneal injection of hydrazine in the amount of 200 microliter/kg. And the extracted liver tissues were examined with light and electron microscopes. The results obtained were summarized as follow; Light microscopically, there is little difference between control and experimental groups.
Electron microscopically, elongated, bizzare shaped mitochondria are appears 5 minutes after hydrazine injection. Those show attenuated portion, Y, U, or C shaped feature suggesting fusion or budding mitochondria. The number of giant mitochondria is decreased after 10 minutes group and rarely present in 60 minutes group. The results suggest in this experiment that the formation of giant mitochondria is kind of reversible change and it is different from the mitochondrial swelling of cellular injury. Intermitochondrial fusion and mitochondrial budding may be related with the formation of giant mitochondria.
- Ultrastructural Changes of Liver Cell Mitochondria in Autolysis.
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Yoon Kyung Sohn, Il Hoon Kwon, Tae Joong Sohn
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Korean J Cytopathol. 1985;19(3):290-301.
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- The authors studied the ultrastructural changes of liver cell mitochondria in autolysis. The male Sprague-Dawley rats, weighting 140~160 gm were sacrificed for extract liver tissue. The slices of the liver tissue were incubated in 37 degrees C aseptic normal saline, and those were examined by following intervals; 10, 20 and 30 minutes and 1, 2, 6, 12 and 24 hours with light and electron microscope. The results obtained by light microscopy were summerized as follow.
Several fine intracytoplasmic vacuoles were observed 1 hour after incubation. After 3 hours, focal destruction of cytoplasmic membrane with pyknosis of nuclei were observed.
More delicate intracytoplasmic architectural changes could not be detected at light microscopic studies. The cord arrangement and cellular boundaries were relatively well preserved until 24 hours after incubation.
Electronmicroscopically, mild intramitochondrial swelling with diminution of intramatrical granules were observed at 20 minutes. These were the earliest findings. Both high amplitude swelling and destruction of mitochondrial membrane were observed concurrently at 1 hour after incubation. The earlier membrane changes were observed at inner membrane with cristae and followed by degeneration of the outer membrane. The intramatrical amorphous dense deposits were observed at 30 minutes when the membranes were not destroyed. These deposits were noted in the other experimental groups which were incubated longer than 30 minutes. More electron dense deposits were observed after 1 hour at that time the membrane changes appeared. Vhe results suggest in this experiment that the earliest autolytic changes of liver cell mitochondria is loss of intramitochondrial granules and the membraneous changes led to the irreversible mitochondiral injury. The appearance of two types of intramitochondrial dense deposits would be an interesting finding needed to require further investigation for the chemical stucture and mechanism of dense deposit formation.
- Ultrastructural Changes in the Exocrine and Endocrine Cells of Rat Pancreas in Endotoxin Shock.
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Kun Young Kwon, Chai Hong Chung, Tae Joong Sohn
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Korean J Cytopathol. 1985;19(3):255-289.
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- This study was carried out to investigate the morphological changes in the exocrine and endocrine glands of rat pancreas treated with endotoxin. Thirty-five male Sprague-Dawley rats, maintained on a stock diet, weight 200.0 gm. average.
were divided into two experimental groups. Group 1. Control group. Five rats. Intraperitoneal infections of 0.3 ml normal saline only. Group 2. Endotoxin-treated group. Thirty rats. 7.6 mg of endotoxin per kg. of body weight was administered intraperitoneally. Each of 5 experimental animal was sacrificed 30 minutes, 1, 2, 4, 6 and 8 hours after endotoxin treatment, followed by examinations of histochemical, light and electron microscopy of both transmission and scanning modes. The results were as follows: A. Light microscopic findings: A mild interstitial edema and hyperemia were noted 1-hour after endotoxin treatment. Cytoplasmic vacuolization at 2-hour level(2-hours after endotoxin administration), diminished staining quality of both endocrine and exocrine cells at 6-hour level. B.
Electron microscopic examination: a. Transmission electron microscopy. The acinar cells of pancreas showed a mildly increased pre-lysosome at 30-minute level. At 1-hour level, appearance of secondary lysosome was noted in addition to the findings of mitochondrial swelling and decreased cristae; disarray and vacuolization of the RER; vacuolar change of Golgi apparatus. At 6-hour level, post-lysosomes.
The changes in the endocrine glands were similar to the findings of exocrine glands just described with time lag of 1 to 2 hours. The endothelial cells of capillaries show swelling and pinocytotic vesicle formation, protrusion of the cytoplasmic processes into the capillary lumen and increased heterochromatin at 1-hour level. These findings became more prominent as time lapses. The lumen of the endothelium tends to be narrowed, filled with fibrin and other blood cell components which later terminated with occasional complete occlusion by the formation of thrombi.
b. Histochemical study: Primary lysosomes of the control group revealed a strong reaction of the acid phosphatase whereas the endotoxin treated group with less reactivity limited in the peripheral zones of the lysosomes. Secondary lysosomes with partial reactions. However, the pre-lysosomes and post-lysosomes failed to demonstrate any acid phosphatase activity at all. c. Scanning electron microscopy. The endothelial cells of the capillaries, arterioles and venules demonstrated increased microvillous activity, broad bled formation, cytoplasmic protrusion into the luminal spaces and microthrombi formation at 1-hour level. Six-hour level onward there noted a junctional disruption and partial detachment from the subendothelium of the wall. It can be concluded, therefore: When the endotoxin enters the blood stream, it elicits endothelial injury followed by both exudation with resultant edema of the surrounding tissue and concomitant vascular occlusions due to thrombosis. This vascular occlusion, in turn, causes ischemic degenerative change of the cells of exocrine and endocrine glands of the pancreas which are followed by digestions of degradational materials from the injured cells through the lysosomal phagocytic system. Besides the above pathogenetic pathway, one can not rule out the possibility of the direct effects of the endotoxin to the cells of exocrine and endocrine cells of the pancreas also so rendered.
- Ultrastructure of Adenocarcinoma of the Stomach by Scanning Electron Microscope.
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Kyung Rak Sohn, Jyung Sik Kwak, Tae Joong Sohn
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Korean J Cytopathol. 1985;19(1):13-26.
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- The author studied 11-cases of adenocarcinoma of the stomach confirmed by gastrofiberscopic biopsy before in order to differentiate between differentiated and undifferentiated adenocarcinoma by scanning electron microscope. Light and transmission electron microscopie examination were done, too. Seven of them are differentiated accompanied by severe intestinal metaplasia and four of them are undifferentiated with rearly focal intestinal metaplasia. Two of the undifferentiated cases shows focal tubular differentiation on the superficial region of the mucosa. Microvilli on the free border are long, regular on the differentiated type but in state of variable loss of microvilli under the transmission electron microscope. Number and density of the mucous granules are variable. Scanning electron microscopic examination shows prominent disorganization of the folds, cellular pleomorphism and pleomorphic microvilli are suggestive of early marker of neoplastic transformation. The size of them are 0.6 micrometer and 1.2 micrometer on the differentiated type respectively. Disorganization of the folds is an important differential point between differentiated and undifferentiated type on the lower power examination. Development of folds, furrow, and hemispheric colliculi are more porminent on the differentiated adenocarcinoma. Presence of striated border, partial or complete loss of microvilli and intestinal metaplasia on the undifferentiated and differentiated adenocarcinomas are consisent with origin from common precursor cells.
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