We report a rare case of adreno-hepatic fusion in a 63-year-old man with a traumatic hepatic rupture. The adrenal tissue was located beneath the Glisson's capsule of the liver, and measured 3.5x2x0.3 cm. On histologic examination, the ectopic tissue was composed of both adrenal cortex and medulla surrounded by a delicate capsule of connective tissue.
Adrenal Cortex ; Choristoma ; Connective Tissue ; Humans ; Liver ; Middle Aged ; Rupture

This study examined the expression of the bcl-2 protein in 59 cases of transitional cell carcinomas (TCCs) of the bladder and evaluated the relationship of bcl-2 and p53 with apoptosis. The cases were divided into 41 low-grade TCCs, 18 high-grade TCCs, 32 superficial TCCs, and 27 invasive TCCs. p53 and bcl-2 protein were detected by the immunohistochemical method and apoptosis was analysed by using hematoxylin-eosin stained slide. The results were as follows: bcl-2 protein was detected in 8 (14%) TCCs and all of these cases were low grade TCCs. Expression of bcl-2 protein was not correlated with clinical stage. There was no correlation between bcl-2 and p53 protein. According to the immunohistochemical results of bcl-2 and p53 protein, the cases were divided 4 groups. Apoptotic index (AI) was higher in p53 positive/ bcl-2 negative group than other groups but the significance was recognized only between p53 positive/bcl-2 negative group and p53 negative/bcl-2 negative group (p<0.05). p53 protein was detected in 20 (36%) TCCs and its expression was correlated positively with histologic grade and clinical stage (p<0.05). AI correlated positively with histologic grade and clinical stage (p<0.01). These data indicate that overexpression of bcl-2 protein is rare in TCC of the bladder and associated with low grade TCCs. Overexpression of p53 is associated with the tumor progression in the TCCs. AI correlates with p53 positivity but does not correlate with bcl-2 positivity.
Apoptosis* ; Carcinoma, Transitional Cell* ; Urinary Bladder*

No abstract available.
Humans ; Muramidase*

No abstract available.
Humans ; Muramidase*

No abstract available.
Humans ; Muramidase*

To investigate the effect of tumor removal and administration of OK432 on the splenic natural killer (NK) cell activity in the subcutaneous tumor bearing rats, NK cell activity assay using a 4-hour 51Cr release assay and flow cytometric analysis for NK cell population were performed. The results were as follows: 1. Splenic NK cell activity and population in the subcutaneous tumor bearing rats decreased along with the growth of the tumor. 2. The rats with subcutaneous tumor removal showed decrease of splenic NK cell activity, but splenic NK cell population was not decreased. 3. In the rats with subcutaneous tumor removal and OK432 administration, splenic NK cell activity was significantly increased 1 week after administration of OK432 and then gradually returned to normal, whereas increase of NK cell population was not significant. In the present study, splenic NK cell activity was significantly decreased despite removal of subcutaneous tumor. But with the administration of OK432, splenic NK cell activity returned to normal. Considering the role of NK cells on the first line of defense against the metastatic implantation of circulating tumor emboli, we suggest that perioperative administration of immunopotentiator such as OK432 may improve the patient's outcome after surgery of human neoplasm.
Animals ; Humans ; Killer Cells, Natural* ; Picibanil* ; Rats* ; Spleen

No abstract available.
Thumb*

Primary meningeal melanocytoma of the central nervous system is extremely rare. We report a case of meningeal melanocytoma associated with Ota's nevus as a recurrent form in a 53-year old male. The meningeal melanocytoma was removed from right parietooccipital lobe 4 years ago and recurred in right parietal, occipital and left frontal lobes. Ultrastructurally, the tumor cells were characterized by the presence of numerous melanosomes and premelanosomes in their cytoplasm. Moreover, the tumor was lacking in histologic and ultrastructural features of pigmented meningioma, melanotic schwannoma and prolonged clinical course was different from primary meningeal melanoma or metastatic malignant melanoma.
Neoplasm Metastasis

No abstract available.
Animals ; Doxorubicin* ; Mononuclear Phagocyte System* ; Rats* ; Vincristine*

BACKGROUND/AIMS: This study was aimed to examine if FB1 induced-hepatotoxicity involves apoptosis, and cholesteryl hemisuccinate (CS) pre-treatment would selectively interfere with FB1 induced-apoptosis of hepatocytes. METHODS: Sprague-Dawley rats were intravenousely injected with FB1 (1.25 mg/kg/day) for two days, and were sacrificed at 3, 6, 12, 24 and 48 hours after injection. Another experiment group was composed of rats with pretreatment of CS (100 mg/kg/day, i.p.) before FB1 injection. RESULTS: This study demonstrated that administration of hepatotoxic dose of FB1 to Sprague-Dawley rats resulted in liver injury leading to cell death by apoptosis. FB1-induced apoptosis was preceded by early elevation in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol, and appearance of injured pre-apoptotic cells at 12 hours was followed by massive fragmentation and margination of heterochromatin at 24 hours. CS pre-treatment prior to FB1 injection ameliorated serum biochemistry and hepatic injury with apoptosis, demonstrated by histological, ultrastructural and TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling) methods. In addition, there was remarkable decrease in number of PCNA (proliferative cell nuclear antigen)-positive proliferating hepatocytes compared to that of FB1 treated group. CONCLUSION: This study suggests that apoptosis significantly contributes to FB1-induced hepatotoxicity in vivo, and pre-exposure of rat to CS prevents FB1-induced hepatic apoptosis and proliferation.
Alanine Transaminase ; Animals ; Apoptosis* ; Aspartate Aminotransferases ; Biochemistry ; Cell Death ; Cholesterol ; Hepatocytes* ; Heterochromatin ; In Situ Nick-End Labeling ; Liver* ; Proliferating Cell Nuclear Antigen ; Rats* ; Rats, Sprague-Dawley