No abstract available.
Genetic Loci* ; Loss of Heterozygosity* ; Stomach Neoplasms*

No abstract available.
Digestion* ; Exons* ; Humans* ; Polymerase Chain Reaction* ; Stomach Neoplasms*

Primary leiomyosarcoma is a rare tumor of the ovary. We experienced a case of primary ovarian leiomyosarcoma in a 68 year old woman. Microscopically, the tumor was characterized by interlacing bundles of plump spindle cells that showed immunoreactivity for alpha-smooth muscle actin, pleomorphic multinucleated giant cells and an increased mitotic rate. Ultrastructural features included abundant smooth muscle type filaments and irregular bodies. Consequently, this case has led us to propose ultrastructural and immunohistochemical criteria for primary ovarian leiomyosarcoma.
Female ; Humans

This experiment is designed to find differentially expressed genes in p388D1 cells that are specific for the serum deprived state. Serum starvation induces cells to enter the quiscent state in the cell cycle and is used to arrest cell growth or synchronize the cell cycle. Differential display and ribonuclease protection assay were used to identify quantitative change in gene expression. Nineteen genes that showed a differential expression in the differential display were cloned and 7 clones were verified by a ribonuclease protection assay. Among the 7 clones clone-16 showed same expression pattern in comparison with the differential display. Deduced amino acid sequences of clone-16 had N-glycosylation motif and seems to be a secretory protein. Getting a full sequence of clone-16 is critical for the characterization of it.
Amino Acid Sequence ; Cell Cycle ; Clone Cells ; Gene Expression ; Ribonucleases ; Starvation

Recently the adenomaatous polyposis coli(APC) gene, a tumor suppressor gene, was identified and the cDNA was cloned from chromosome 5q21. Allelic deletion or point mutation of tumor suppressor genes(TSGs) has been considered as an important mechanism in development of human tumor. Point mutations affecting APC gene are seen in the hereditary syndrome, adenomatous polyposis and spordic colon cancer. However, the mutation of APC gene and other TSGs have not been described in gastric cancer. In order to identify the mutation of exon 11 of APC gene for gastric cancer, we amplified DNA extracted from paraffin-embedded tissues by polymerase chain reaction(PCR) and digested the PCR products with restriction enzyme Rsa I. We examined the DNA extracted from paraffin-embedded 44 gastric cancer tissues with lymph nodes. Eighteen(41%) among 44 were informative for the study exon 11 of the APC gene, and we found loss of heterozygosity(LOH) for APC in 6/18(33.3%). These data suggest that the point mutation or the base change of APC gene commonly occurs in gastric cancer. We conclude that the mutation of APC gene is strongly connected with development of human gastric cancer.
Humans ; Genes, Tumor Suppressor ; Stomach Neoplasms

The acardiac fetus is a rare type of fetal monster in which, as the name implies, the heart is completely absent. Acardius occurs only in a pair monozygotic twin, and shows various other defects in addition to the absence of the heart. Our autopsy case is acardiac anceps. He weighed 1,980 gm and the height was 33 cm. The brain is poorly developed, 60 gm in weight and similar to reversed snowman (3.5x2.8x2.8, 1.5x1.5x1.3 cm). Encephalocele, 6 cm in diameter, was communicated with the brain by a tract which contains nervous tissue and primitive choroid plexus. The upper extremities were absent, while the vertebrae and lower extremities were relatively well developed. The heart, lungs, stomach, liver, and spleen were absent, but the kidney, genital organs and urinary bladder were present. The intestine was seperated into two segments which were blindly ended, 32 cm and 15 cm in length, respectively.

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.
Rabbits ; Animals

BACKGROUNDS: Recently, the cases with transient neurologic deficit and brain MRI abnormalities similar to hypertensive encephalopathy or eclampsia were reported in the organ transplanted patients, during the administration of cyclosporine with the hypothesis as "capillary lack syndrome". But in addition to cyclosporine, other immunosuppressive agents as cytabine and ant-lymphocyte globulin(ALG) may induce similar transient neurologic manifestations such headache, seizure, altered mental state and change of signal intensities in brain MRI. METHODS AND CASES: 11 patients who had suffered form hematologic disorder were included in the study. The patients were presented with a reversible transient neurologic manifestations and brain MRI abnormalities during administration of various immunosuppressant,. We analysed neourologic symptoms and signs, anatomic localizations and laboratory findings. RESULTS: The underlying hematologic disorder were severe aplastic anemia acute lymphocyte leukemia, multiple myeloma, chronic myelocytic leukemia and acute myelocytic leukemia. The cyclosporine was prescribed in six. ALG in three, idarubicin in two and prednisolone in one patient. The accompanied neurologic symptoms and sign were seizure(11/11), visual disturbance or cortical blindness(5/11) and mental status change(3/11). All the symptoms were spontaneously improved by conservative management. The insidious increase on blood pressure, hepato-renal impairment, sepsis, and hepatopathy were noted in some cases just before and after the neurologic manifestation. The ESR was elevated in all examined cases and the cholesterol level was normal. Serum cyclosporine was elevated in 2/6 cases. They showed typical MRI findings which were high signal intensity an T2WI and iso- to low signal intensity on TIWI with blunding of cortical sulci and with no enhancement. The involved lesions were the parieto-occipital area, frontal lobe, temporal lobe, and basal ganglia in series. One patient showed a petechial hemorrhage in the occipital area on both CT and MRI. In six cases, follow-up MRI showed nearly complete resolution of the lesions correlated with the clinical symptoms. CONCLUSION: We can't explain the exact mechanisms of the neurologic complication of immunosuppressants, but the characterstics of transient neurologic deficits and the corresponding reversible brain image are similar to those of hypertensive encephalopathy or eclampsia. It is suggested that the mechanism of clinical syndrome maybe a capiliary leak due to the cytokine-induced vasculopathy but future studies are warranted.
Anemia, Aplastic ; Basal Ganglia ; Blood Pressure ; Brain ; Capillaries* ; Capillary Leak Syndrome* ; Cholesterol ; Cyclosporine ; Eclampsia ; Female ; Follow-Up Studies ; Frontal Lobe ; Headache ; Hemorrhage ; Humans ; Hypertensive Encephalopathy ; Idarubicin ; Immunosuppressive Agents* ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; Leukemia, Myeloid, Acute ; Lymphocytes ; Magnetic Resonance Imaging ; Multiple Myeloma ; Neurologic Manifestations ; Prednisolone ; Pregnancy ; Seizures ; Sepsis ; Temporal Lobe

BACKGROUND: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites produced by macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. METHODS: In order to investigate the relationship between the activity of alveolar macrophage and the production of PGE2 from activated alveolar macrophage, the authors measured hydrogen peroxide and PGE2 from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica(SiO2) suspended in saline (50 mg/ml) in Sprague-Dawley rats. RESULTS: 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica. 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05) and PGE2(p>0.05) release from alveolar macrophages. Alveolar macrophages from rats with silicotic nodules released more hydrogen peroxide and PGE2 than those of control group(p<0.05). CONCLUSION: These results suggest that silica particle could activate macrophage directly and enhanced the release of PGE2 and hydrogen peroxide from the alveolar macrophage.
Animals ; Arachidonic Acid ; Collagen ; Dinoprostone* ; Fibroblasts ; Fibrosis ; Hydrogen ; Hydrogen Peroxide ; Lung ; Macrophages ; Macrophages, Alveolar* ; Monokines ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide* ; Silicosis