The purpose of this study was to investigate the inhibitory role of vitamin A with respect to activation of Ito cells in fibrosis of the rat liver induced by common bile duct ligation(CBDL). The liver was examined by immunohistochemical staining for a-smooth muscle actin,the known marker of activated Ito cells, and light and electron microscopy after CBDL andCBDL with intraperitoneal injection of retinoic acid (Sigma, USA) 1 mg/Kg in 3 times per week. The results were sumrrlerized as follows: After CBDL, the bile ductules were markedly proliferated in the periportal areas extending toterminal hepatic veins. Interstitial fibrosis and inflammatory cell infiltration appeared, however,cholestasis was minimal. Retinoic acid treatment with CBDL decreased bile ductular proliferationand interstitial fibrosis compared to CBDL only. After CBDL, proliferated and activated Ito ceIs showing positive reaction in smooth muscle actin were present in the periductular andperisinusoidal areas, and areas of increased interstitial fibrosis. Activated ito cells weredecreased in number after CBDL with vitamin A treatment. Electron microscopically,intracytoplasmic fat droplets and the cytoplasmic processes of Ito cells were decreased afterCBDL. Myofibroblasts were frequently appeared in the interstitial fibrosis after CBDL. But,intracytoplasmic fat droplets of Ito cells were well preserved, and myofibroblasts were found lessfrequently after CBDL with vitamin A treatment. The results suggest that vitamin A plays an inbitory role in the activation and fibrogenesis ofIto cells after CBDL.
Rats ; Animals

Myeloid body formation is an ultrastructural feature of gentamicin induced nephrotoxicity in human being and experimental animals. The origin of the myeloid body is not satisfactorily understood and morphological verification of the developing process of this structure is not fully accomplished. We injected 100 mg/kg/12 hour of gentamicin in 20 Spraque-Dawley rats and examined the ultrastructural feature of the proximal convoluted tubular cells of the kidney every 30 minutes in the first 4 hours, and in 5 hours, 6 hours, 12 hours, 24 hours and 48 hours after injection of gentamicin, with a TEM and a SEM. Myeloid bodies were noted as concentric layers of membranous structures of degenerated endoplasmic reticulum and mitochondria in the lysosome. The number and size of the myeloid body containing lysosomes were increased with time. We can deduce from this observation that injured cell organelles by diffusible gentamicin within the cells are autophagocytosed by lysosomes which were also injured by the drug from pinocytotic vesicles, and incompletely digested organellar remnants are retained in the lysosomes as myeloid bodies. So we think that the myeloid body formation is a result of an exaggerated and a pathologic autophagocytic process due to cell injury induced by gentamicin.
Animals ; Endoplasmic Reticulum ; Gentamicins* ; Humans ; Kidney ; Lysosomes ; Mitochondria ; Organelles ; Rats*

PURPOSE: Introduction of shock wave lithotripsy has provided an avenue for dealing with many urinary stones noninvasively. Although shock wave is known to cause pathologic changes in various organ, little is k nown about its effect on the ureter and recovery after shock wave, the target organ in SWL of injury induced by shock wave and the potential protective effect of allopurinol and nifedipine against shock wave. MATERIALS AND METHODS: A total 24 rabbits were assigned to 2 groups. 12 rabbits received allopurinol(10mg.each) and nifedipine (1mg.each) that were given orally 3 times a day for 5 days starting the night before SWL. The other 12 rabbits reseived no medication. The left lower Ureter segments of 24 rabbits were removed ureter. Groups of 8 rabbits(4were medication group and 4, no medication group) were sacrificed 1, 3 and 5 days after shock wave exposure. The histomorphological alterations were examined under light and transmission electron microscopy. RESULTS: The epithelial cells disclosed no change after shock wave application. Histologically the muscular layer was the most affected part of ureter. There was interstitial and intracellular edema on light microscopy and made chromatin and mitochondrial changes at the subcellular level. The adventitial layer wes also edematous. This chanfes were prominent on day 1and 3 and returned to normal on day 5. The medication group showed less severe features of injury, compared with the no medication group. CONCLUSIONS: Electromagnetic shock waves produce reversible morphological changes in rabbit ureteric muscle and allopurinol and nifedipine may have its role in protecting the tissue injury produced by high energy shock waves.
Allopurinol* ; Chromatin ; Edema ; Epithelial Cells ; High-Energy Shock Waves ; Lithotripsy ; Magnets ; Microscopy ; Microscopy, Electron, Transmission ; Nifedipine* ; Rabbits ; Shock* ; Ureter* ; Urinary Calculi

No abstract available.
Humans ; Token Economy*

No abstract available.
Drinking*

The athors have presented recently treated 4 cases of malignant tumors of the eye and adnexa. 1. All of them were rapidly aggrevated after previous incompleted surgical management (3 cases) or postponement 01 operation (1 case). 2. Three cases of them except adenoid cystic Ca. were recurred after orbital exenteration. 3. The authors were concluded that the poor prognosis is due to its nature of malignancy and delayed radical surgical management.
Adenoids ; Melanoma* ; Orbit ; Prognosis

Lipomas of the heart are benign neoplasms and have rarely been described. Due to the fact that they normally cause no symptoms, diagnosis is often purely accidental. Because of the rarity of these tumors, it seems worthwhile to present an example studied at autopsy. It was associated with the sudden death of a 15-year-old boy. The tumor arose from the wall of the left ventricle and occupied the pericardial cavity, measuring 13x7x6 cm in size. The tumor was whitish-yellow, translucent, and soft. Microscopically, the tumor was composed of mature adipose tissue which extended between muscle fibers. This current case, the giant cardiac lipoma is believed to produce disturbances of the conduction system and distrubances of cardiac filling.

We describe an ovarian mucinous cystadenocarcinoma with a sarcoma-like mural nodule. In the literature, rare cases of ovarian mucinous tumors have been described which contain foci of undifferentiated carcinoma, sarcoma, and sarcoma-like nodules. The distinction between these lesions is important because of poorer prognosis of true sarcoma and anaplastic carcinoma than sarcoma-like mural nodules. This case shows different results of immunohistochemical stain for anaplastic carcinoma.

No abstract available.
Holoprosencephaly*

BACKGROUND: There is considerable controversy about the exact molecular mechanisms of excitatory amino acid receptors in epileptogenesis. METHODS: We used in situ hybridization to examine the hybridization density (HD) of n-methyl- D-aspartic acid receptor type 1 (NMDAR-1) and alpha-amino-3-hydroxy -5-methyl-4-isoxazole-propionate (AMPA) receptor type 2 (GluR-2) mRNA, in the hippocampus obtained from the kainic acid (KA)-induced status epilep-ticus (SE) model. Some Sprague-Dawley rats were injected with KA (10 mg/Kg; I.p.), and others with MK-801 (4 mg/kg) 20 minutes prior to KA. The rats were allowed to have 4-hour SE and were killed at 8 hours or 4 weeks after KA or MK-801/KA injection. HD of NMDAR-1 and GluR-2 mRNA in subfields of the hippocampus was measured by an image analysis system. RESULTS: A typical neuropathological finding of hippocampal sclerosis and spontaneous repetitive seizures (SRS) were observed in the KA injected rats, but not in the MK-801 pretreated rats, killed at 4 weeks. Compared with controls, the rats killed at 8 hours after KA showed increased CA1, CA2, and CA3 NMDAR-1 HD, and stratum granulosum (SG) GluR-2 HD. The increase of NMDAR-1, not GluR-2, HD was blocked effectively by MK-801. The increase of SG GluR-2 HD remained until 4 weeks after the KA injection. CONCLUSIONS: Not only the NMDAR-1activa-tionbut also the GluR-2 activation is an important factor in delaying hippocampal neuronal loss and epileptogenesis. (J Korean Neurol Assoc 19(1):36~44, 2001
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid ; Animals ; D-Aspartic Acid ; Dizocilpine Maleate ; Epilepsy, Temporal Lobe ; Gene Expression* ; Glutamic Acid* ; Hippocampus ; In Situ Hybridization ; Kainic Acid ; N-Methylaspartate ; Neurons ; Rats ; Rats, Sprague-Dawley ; Receptors, Glutamate* ; RNA, Messenger ; Sclerosis ; Seizures ; Temporal Lobe*