No abstract available.
Gastritis*

No abstract available.

No abstract available.

Aggressive angiomyxoma is a rare, locally aggressive tumor and occurs exclusively in the pelvic and perineal regions of women. But this tumor can occur in men, and the ratio of man to woman is about 1:6. We report a case of aggressive angiomyxoma of the scrotum in a 75-year-old man. The resected mass measured 23 21 10 cm and weighed 1,150 g, and was covered with thick but intact scrotal skin. The cut surface of the mass showed pale yellow to grayish white loose and edematous fibrous tissue with focal cystic degeneration. Microscopically, the mass was composed of loosely arranged bland-looking spindle or stellate cells and variable sized blood vessels with thickened and hyalinized wall. The spindle cells were strong positive for vimentin, focal, weak positive for desmin and smooth muscle actin but negative for S-100 protein. The spindle cells were also positive for estrogen and progesterone receptors.
Actins ; Aged ; Blood Vessels ; Desmin ; Estrogens ; Female ; Humans ; Hyalin ; Male ; Muscle, Smooth ; Myxoma* ; Receptors, Progesterone ; S100 Proteins ; Scrotum* ; Skin ; Vimentin

OBJECTIVE: Human papillomavirus (HPV) is strongly implicated as a causative agent in the etiology of cervical cancer. Of its gene products, E6 and E7 oncoproteins play major roles by inactivation of cellular p53 and pRb tumor suppressor proteins, respectively. However, it has been recently suggested that p53 and/or pRb-independent functions of E6 and E7 are involved in cervical carcinogenesis. The purpose of this study is to identify novel a cellular target, p73, of E6 and to determine how E6 inactivates p73 function, METHODS: The interaction between E6 and p73 were identified by the yeast two-hybrid assay in vivo and the GST pull-down assay in vitro. The function of the interaction was determined by transient transfections using p21 promoter-CAT reporter plasmid. The molecular mechanism underlying the functional significance of the interaction was further assessed by in vivo and in vitro protein degradation assays, and gel mobility shift assays. RESULTS: Yeast two-hybrid and GST pull-down assays indicate a physical interaction between p73 and either HPV-16 or HPV-11 E6 proteins in vivo and in vitro, respectively. Transactivation domain (amino acid residues 1-49) is found to be absolutely required for this interaction. Transient co-expression of E6 significantly inhibits the p73-mediated activation of p21WAF1 promoter in a p53-defective C33A cell line. Using Ga14-p73 fusion protein, we demonstrate that E6 inhibition of p73 transactivation function is independent of sequence-specific DNA binding, which is confirmed by direct electrophoretic mobility shift assay. Moreover, E6 inhibits p73 function by interfering with the activity of the amino-terminal activation domain. The protein degradation assays in vivo and in vitro indicate that p73, unlike p53, is not susceptible to E6-dependent proteolysis. CONCLUSION: Throughout this study, we identified p73 as a novel cellular target of HPV-E6 protein and found that E6 binds p73 through the amino-terminal transactivation domain, and inhibits its transactivation function independent of the protein degradation and DNA binding. These overall results, consequently, suggest that in addition to the inactivation of p53, the functional interference of p73 by HPV-E6 may, at least in part, contribute to E6-mediated cellular transformation.
Carcinogenesis ; Cell Line ; DNA ; Electrophoretic Mobility Shift Assay ; Human papillomavirus 11 ; Human papillomavirus 16 ; Humans ; Oncogene Proteins ; Plasmids ; Proteolysis ; Transcriptional Activation ; Transfection ; Tumor Suppressor Proteins ; Two-Hybrid System Techniques ; Uterine Cervical Neoplasms ; Yeasts

PURPOSE: Cerebral cortical dysplasias are one of the important causes for epileptic seizures and developmental disabilities in children, particularly in diffuse or bilateral cases. These developmental malformations are generally regarded as a group of neuronal migration disorders, however, the classification system and pathogenetic mechanisms of cortical dysplasias are not yet entirely clear. Even a novel entity, congenital bilateral perisylvian syndrome, characterized by speech delay, pseudobulbar Palsy, intractable seizures, and bilateral perisylvian abnormalities on imaging studies, have rather diverse figures on morphology and symptomatology than initially considered. We have studied the clinical features and correlations of clinical outcomes 3nd magnetic resonance imaging(MRI) findings of bilaterally involved cortical dysplasias. METHODS: 20 cases of bilateral cortical dyspalsias were grouped into three categories on the basis of MRI findings; centroparietal dysplasias(6 cases), diffuse dysplasias with (5) or without white matter lesions(4), and schizencephaly(5). EEGs, motor and language development, epilepsy, and outcomes were reviewed in each groups. RESULTS: Language delay(100%), motor developmental delay(94.7%), motor deficit(65%), epilepsy(40%) were the main reasons for their initial hospital visits. A meaningful word expression was possible at the mean age of 2 years and 2 months(1 to 4 years of age). Hypotonia and spastic motor paralysis were evident in all the cases of diffuse dysplasia with white matter lesions and the schizencephaly groups. All but one case of centroparietal dysplasia showed motor developmental delay. Epilepsies were developed in 8 cases at the mean age of 5 years and 5 months(2 months to 12 years of age) and the seizures were relatively well controlled with anticonvulsants. EEG findings were variable; normal, focal or diffuse abnormalities. High amplitude diffuse fast activities were only noted in the diffuse dysplasia group. CONCLUSION: The severity of neurological deficits and developmental delay had correlated to the size of cortical abnormalities. The epilepsies were relatively well controlled during childhood and the EEG finding of high amplitude diffuse fast activities was specific for the diffuse cortical dysplasias. Bilateral centroparietal dysplasias should be included on consideration of the causes for developmental aphasia.
Anticonvulsants ; Aphasia ; Child ; Classification ; Developmental Disabilities ; Electroencephalography ; Epilepsy ; Humans ; Language Development ; Language Development Disorders ; Magnetic Resonance Imaging* ; Malformations of Cortical Development* ; Muscle Hypotonia ; Muscle Spasticity ; Neuronal Migration Disorders ; Paralysis ; Pseudobulbar Palsy ; Seizures

PURPOSE: The purpose of this study was to analyze the results of treatment and prognosis of Marjolin's ulcer compared with primary squamous cell carcinoma. MATERIALS AND METHODS: Fourteen patients treated for Marjolin's ulcer were analyzed. Twenty patients with primary squamous cell carcinoma treated during the same time period was the control group. Mean age was 61.2 years. There were 24 males and 10 females. The locations, TNM stages, histological grades, recurrence, metastasis, and survival rate were analyzed and compared between two groups. RESULTS: The mean follow-up period was 54.8 months (range, 12-168 months). Local recurrences were found in 6 cases, 5 ones in Marjolin's ulcer patients, and one case in primary squamous cell carcinoma patients. The mean time interval between the initial presentation and occurrence of local recurrences was 9 months (range, 2-20 months). There were 6 metastases. 2 (14.3%) metastases were found in Marjolin's ulcer patients, and 4 (20.0%) metastases in primary squamous cell carcinoma patients. Total events (metastasis or local recurrence) were found in 10 pateients, 6 of them in Marjolin's ulcer group, and the remaining four in primary group. 5-year disease-free survival rate was 64.3% in Marjolin's ulcer group and 95.0% in primary squamous cell carcinoma group. CONCLUSION: Squamous cell carcinomas originating as Marjolin's ulcers revealed higher recurrence rate and lower survival rate despite of aggressive treatment. Therefore, new treatment modalities should be developed for improving outcomes.
Carcinoma, Squamous Cell ; Disease-Free Survival ; Female ; Follow-Up Studies ; Humans ; Male ; Neoplasm Metastasis ; Prognosis ; Recurrence ; Survival Rate ; Ulcer

The 26 year old male with the hypertrophic cardiomyopathy confirmed by M-mode and 2-D echocardiography is reported with the review of the literatures.
Adult ; Cardiomyopathy, Hypertrophic* ; Echocardiography ; Humans ; Male

No abstract available.
Solvents*

Granulocytic sarcoma is a rare localized tumor composed of granulocytic precusor cells. Granu-locytic sarcoma occurs in a variety of clinical conditions and it is often misdiagnosed histologically. Differential diagnosis frorh lymphoma or nonhematopoietic malignancies such as undifferentiated carcinoma or sarcoma is difficult in the routing histologic examination. An evaluation of clinical and histopathologic features was done on 4 cases of granulocytic sarcoma which were diagnosed at Pusan Paik Hospital from 1988 to 1992. During the period, 282 cases of myelogenous leukemia were diagnosed. Immunohistochemical reaction for lysozyme, myelopero-xidase, leukocyte common antigen, epthelial membrane antigen and cytokeratin was assessed comparing to lymphoma and undifferentiated carcinoma. The histologic features of the granulocytic sarcoma revealed thin nuclear membrane, fine chromatin pattern and one or two small nucleoli. It also often involved the vascular wall and infiltrated the native structures without destruction. Immunohistochemical stain revealed that all(4 cases) of granulocytic sarcoma showed diffuse and strong positivity for myeloperoxidase, and partial but strong positivity for lysozyme. One case of granulocytic sarcoma was negative and 3 cases revealed focal positive reaction for LCA, and all 4 cases was negative for cytokeratin and EMA. In summary, careful observation under light microscopy with immunohistochemical stain for myeloperoxidase, lysozyme, and LCA is helpful in the differential diagnosis of granulocytic sarcoma from malignant lymphoma and cytokeratin and EMA is useful for differential diagnosis from undifferentiated carcinoma.
Diagnosis, Differential