No abstract available.
Congenital Abnormalities*

No abstract available.
Liver*

Pleomorphic xanthoastrocytoma is histologically characterized by marked cellular pleomorphism of lipid-laden neoplastic astrocytes and bizarre giant cells showing mitotic figures and high cellularity. Inspite of its ominous-looking microscopic features, howerver, the prognosis is usually favorable. This tumor develops mainly in the supratentorial area of young people and frequently involves the leptomeninges. We experienced a case of pleomorphic xanthoastrocytoma in 18 year-old-male. In addition to the cellular pleomophism, the prominent reticulin fibers surround the individual tumor cells or the tumor cells nests. Immunohistochemical staining and electron microscopy revealed glial fibrillary acidic protein(GFAP) expression and pericytoplasmic basal lamina in the tumor cells.

Hemangiopericytoma was first described by Stout & Murray in 1942 and was an uncommon soft tissue tumor thought to be derived from vascular pericytes. Approximately 10-15% of the cases occur in children have a propensity to develop in the region of head, neck and lower extremities. We experienced a case of congenital hemangiopericytoma of small bowel in a male neonate who showed vomiting and abdorninal distension. We reported a case of congenital hemangiopericytoma of small bowel with brief review of related literature.
Child ; Head ; Hemangiopericytoma* ; Humans ; Infant, Newborn ; Intestinal Obstruction* ; Intestine, Small ; Lower Extremity ; Male ; Neck ; Pericytes ; Vomiting

PURPOSE: We measured pulmonary epithelial permeability by Tc-DTPA radioaerosol clearance in patients with diabetes and correlated with the presence of microangiopathy to understand the pathophysiology of pulmonary microangiopathy and evaluate Tc-DTPA radioaerosol clearance as a diagnostic test to assess pulmonary microangiopathy. MATERIALS AND METHODS: We performed ' Tc-DTPA radioaerosol scan in 10 normal subjects, 10 asym-ptomatic smokers, 20 diabetic patients without history of smoking (10 with microangiopathy, 10 without microangiopathy). Tc-DTPA clearance half-time (T1/2) was calculated, then compared with the result of chest radiography and pulmonary function test. RESULTS: Chest radiography and pulmonary function test were normal in all subjects. There were no significant difference of clinical or laboratory characteristics between these groups except age. The diabetic patients with micraangiopathy were significantly older (p<0.05). The T1/2of normal subjects and asyrnptomatic smokers were significantly different (65.2+23.7min vs 39.6+9.8min, p<0.05). For diabetic patients with microangiopathy, the T, was 90 5+46.5min and significantly delayed when compared with those of normals and asymptomatic smokers (p<0.05). However, the T1/2of diabetic patients without microangiopathy, 70.0+12.7 min, was not significantly different from those of normals or asyrnptomatic smokers (p>0.05). No significant correlation was found between the T1/2and spirometric parameters including DLcc>, FVC, FEV>, FEV(/FVC (%) and FEF)5-75g in all subjects, and between the T1/2 and duration of diabetes in diabetic patients. CONCLUSION: Eventhough the influence of age cant be excluded, delayed Tc-DTPA clearance half-time (T1/2)in diabetic patients with microangiopathy indicates decreased pulmonary cspillary permeability as one of the pathophysiologic results of pulmonary microangiopaththy. Further studies are needed in larger number of age matched control and diabetic patients to evaluate the diagnostic efficacy.
Diabetes Mellitus ; Diagnostic Tests, Routine ; Humans ; Permeability ; Radiography ; Respiratory Function Tests ; Smoke ; Smoking ; Technetium Tc 99m Pentetate ; Thorax

Cancer is considered to occur through abnormal growth and differentiation processes, in which oncogenes and tumor suppressor genes are deeply related. Cellular responses to DNA-damaging agents are believed to be critical determinants of human tumorigenesis. Cell cycle arrests and DNA repair following DNA damage require the coordination of multiple gene products that, as a whole, serve to maintain the integrity of the genome. Within the cell cycle, both G1-S and G2-M phase transitions are under constant surveillance by checkpoint genes for the protection of cells from either exogenous or endogenous DNA-damaging agents. p53 tumor suppressor gene mediates cell cycle perturbations in response to DNA damage, and play a role in cell death, genetic stability, and cancer susceptibility. Recently, gene therapy with p53 tumor suppressor gene is expected as a new effective therapeutic strategy in many kinds of cancer. By using retroviral vector system, we transduced p53 tumor suppressor gene into human osteosarcoma cells, and analysed its growth suppression and apoptosis inducing effects. Combined effects of p53 gene therapy with chemotherapeutic agent or radiation were also analysed. Titer of ecotrophic p53 retrovirus was 5.0x10/ml, and that of amphotrophic p53 retrovirus was 2.0x10/ml when NIH3T3 cells were used as target cells. Human osteosarcoma cells infected with amphotrophic p53 retroviruses showed increased p21waf1 gene expression, which acts as a major cyclin-dependent kinase inhibitor in DNA damage responses. In normal DMEM media, human skin fibroblasts infected with amphotrophic p53wt retroviruses showed very slow growing (1.7 fold increase in doubling time) and very low saturation density (50% decrease in cell density). In media containing chemotherapeutic agent, human osteosarcoma cells infected with p53wt retroviruses died rapidly; 75% of them died within 4 days and all of them died within 10 days of incubation with chemotherapeutic agent. Their DNAs were extracted and electrophoresed in agarose gel, and we identified DNA ladders characteristic of apoptotic cell death. When human osteosarcoma cells infected with p53 retroviruses were irradiated with ultraviolet light, more than 95% of cancer cells died within 1 day; whereas mock infected cells showed only less than 5% of cell death. These findings suggest that retroviral vector mediated p53 tumor suppressor gene transfer into cancer cells can suppress tumor cell growth and decrease tumor cell density effectively. These findings also suggest that effective induction of tumor cell apoptosis can be obtained when p53 gene therapy is used in combination with chemotherapy or radiotherapy.
Apoptosis ; Carcinogenesis ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Death ; DNA ; DNA Damage ; DNA Repair ; Drug Therapy ; Fibroblasts ; Gene Expression ; Genes, p53 ; Genes, Tumor Suppressor* ; Genetic Therapy* ; Genome ; Humans ; Oncogenes ; Osteosarcoma ; Phase Transition ; Phosphotransferases ; Radiotherapy ; Retroviridae* ; Sepharose ; Skin ; Ultraviolet Rays ; Zidovudine

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

No abstract available.
Emphysema* ; Tuberculosis*

No abstract available.
Citrobacter* ; Enterobacter*