Sclerosing hepatic carcinoma (SHC) is composed of slender cords or small nests of tumor cells with peripheral palisading, and abundant intervening sclerosis. The tumor seems to have the histologic features of both hepatocellular carcinoma (HCC) and cholangiocarcinoma. To evaluate the phenotypic expression of SHC and to investigate its cellular origin, immunohistochemical studies on three cases of SHC were performed. In all cases, the tumor cells showed positive staining for cytokeratins AE1, AE3 and 19, carcinoembryonic antigen (CEA) and epithelial membrane antigen (EMA). The expressions of cytokeratins AE1 and 19 were stronger in the palisading cells than the interior of the cords and nests. Conversely, CEA and EMA were expressed mainly in the inner portion. Alpha-fetoprotein was expressed in only one case, mainly in the palisading cells. In summary, SHC has the histological as well as the immunohistochemical profiles intermediate between HCC and cholangiocarcinoma, and the immunohistochemical profile suggests that SHC arises from primitive hepatoblast with a tendency of differentiation to the bile duct epithelium.
Carcinoma, Hepatocellular

No abstract available.
Peritoneal Dialysis, Continuous Ambulatory*

Ichthyosis hystrix is a localized variant of Bullous Congenital Ichthyosiform Erythroderma by Broq, and also, localized form of Epidermolytic hyperkeratosis according to Frost and Van Scott's classification of ichthyosi-form dermatoses. Clinically it is generally considered to be widespread systematized epidermal nevus, and demonstrating an autosomal dominant pattem of inheritance, and characterized by verrucous scale at or shortly after birth with particular involve- ment of flexural areas. A case of 21 year old girl with ichthyosis hystrix was reported, The skin lesion showed multiple rice to pea sized linear verrucous papules on left forearm, neck, axilla and upper chest. The skin biopsy was done, the finding shows remarked laminated hyperkeratosis, acanthosis, papillomatosis, and vacuoliization on malpighian layer. Diagnosis was confirmed by clinicaI apperance and histopathologicaI finding. The method of treatment is 0. 05% Vitamin A acid ointment application and show marked improvement.
Axilla ; Biopsy ; Classification ; Diagnosis ; Female ; Forearm ; Humans ; Hyperkeratosis, Epidermolytic ; Ichthyosis* ; Neck ; Nevus ; Papilloma ; Parturition ; Peas ; Porcupines* ; Skin ; Skin Diseases ; Thorax ; Tretinoin* ; Vitamin A* ; Vitamins* ; Wills ; Young Adult

No abstract available.
Influenza, Human* ; Vaccination*

No abstract available.
Mouth Mucosa* ; Salivary Ducts*

No abstract available.
Epinephrine* ; Facial Nerve* ; Paralysis* ; Rabbits*

No abstract available.
Evoked Potentials, Auditory, Brain Stem* ; Rabbits*

No abstract available.
Lakes* ; Lip* ; Nevus, Blue*

p21 is a universal inhibitor of cyclin-dependent kinase (cdk) and of cell-cycle progression. p21 expression is variable according to the type of tissue and the pathologic condition. To study the role of p21 in the multistep hepatocarcinogenesis, the expression of p21, p53 and Ki-67 was investigated in 53 cases of inactive liver cirrhosis, 4 cases of low grade dysplastic nodules, 3 cases of high grade dysplastic nodules, 7 cases of early hepatocellular carcinomas (HCCs), 27 cases of small HCCs (< or =3 cm), and 52 cases of advanced HCCs (>3 cm). p21 expression was not detected in liver cirrhosis, low grade dysplastic nodules, high grade dysplastic nodules and early HCCs which were mitotically inactive. p21 expression was significantly increased in small HCCs and advanced HCCs which were mitotically active. p21 expression was significantly correlated with Ki-67 labelling indices. p53 protein was not expressed in liver cirrhosis, dysplastic nodules, and early HCCs. The expression of p53 protein was, however, significantly increased in small and advanced HCCs. The p21 expression was not correlated with p53 expression. Therefore, p21 is suggested to play a role in the mitotically active small and advanced HCCs, but not in the mitotically inactive lesion of dysplastic nodules and early HCC in multistep hepatocarcinogenesis. These findings suggest that homeostatic mechanism of growth control is not totally destroyed in HCC.
Carcinoma, Hepatocellular ; Cell Proliferation* ; Humans* ; Liver Cirrhosis ; Phosphotransferases

To elucidate the effect of copper on the 3'-methyl-4-dimethylaminoazobenzene(3'-MeDAB) induced hepatic carcinogenesis, Sprague-Dawley rats were divided into 4 groups according to 3'-MeDAB and copper administration: I. noraml control, II. copper only, III. 3'-MeDAB only, IV. 3'-MeDAB plus copper. The animals of groups III and IV were fed experimental diet containing 0.06% 3'-MeDAB. Copper was administrated intraperitoneally in a dose of 0.5 mg, twice a weak. Animals were sacrificed at different intervals. Liver weight, hepatic copper content and gross and microscopical changes of the liver were examined and the cell kinetics of various lesions in the hepatic carcinogenesis was studied by applying the immunohistochemical method for bromodeoxyuridine(BrdU). The hepatic copper content was significantly increased in animals given copper but returned to the normal value after cessation of adminstration. 3'-MeDAB administration caused oval cell proliferation and produced hyperplastic nodules, cholangiofibrosis and carcinoma of the liver. Simultaneous administration of copper did not alter the incidence of 3'-MeDAB induced lesions, except for carcinoma. The liver weight and the size of hepatic nodules and masses were smaller in group IV than in group III. The liver weight as well as the nodularity and the mass formation continued to increase affect cessation of 3'-MeDAB administration. Copper did not affect the BrdU labelling indices of the hepatic lesions induced by 3'-MeDAB. The oval cell proliferation and the BrdU labelling indices of the oval cell and the hyperplastic nodule were decreased, but the incidence of cholangiofibrosis and its BrdU labelling index were still elevated after cessation of 3'MeDAB administration. These findings indicate that copper could delay the developement of 3'-MeDAB induced hepatic lesions, but not suppress, since copper does not stay long enough to accumulate in the rat liver, and that copper could not affect the proliferation of 3'-MeDAB induced hepatic lesions once developed.
Rats ; Animals ; Incidence