39 research outputs found
遊離回腸を利用した膀胱拡張術後に発生した膀胱腺癌の1例
47歳男子にみられた, 結核性萎縮膀胱に対するU字型遊離回腸移植膀胱拡張術後20年目に同移植回腸上皮より発生したと考えられる膀胱低分化腺癌の1例を報告し, 若干の文献的考察を加えた.This is a report of a case of poorly differentiated adenocarcinoma found 20 years after bladder augmentation ileoplasty. The origin of this tumor was proved to be the ileal part of bladder augmentation. Autopsy revealed metastatic lesions in the stoma (sigmoid conduit), lungs, liver, left femur, adrenal glands and lymph nodes. A review of the literature revealed only one other such case. This is a rare case of adenocarcinoma in the ileal part of bladder augmentation
孤立性後腹膜神経線維腫の1例
後腹膜に原発し, vonRecklinghausen氏病の徴候のない孤立性神経線維腫の1例を報告する.診断上, もう一つの神経鞘由来の神経鞘腫との鑑別が問題で, 腫瘍の組織化学染色および免疫組織化学染色が孤立性神経線維腫の診断に有用であった,A solitary neurofibroma arising in the retroperitoneal space without any other stagma of von Recklinghausen's disease is reported. Confusion with another nerve sheath tumor, a schwannoma is a diagnostic pitfall. Histochemical and immunohistochemical stainings of the tumor are useful for the diagnosis of solitary neurofibroma
腎摘後14年目に孤立性脳転移をきたした腎細胞癌の1例
46歳の女性にみられた腎摘後14年目に孤立性脳転移をきたした腎細胞癌の1例を報告する.患者は突然, 頭痛, 失語, 歩行障害, 右片麻輝をきした.脳CTでは左側頭部に嚢胞性腫瘍を認め, これは外科的に完全に切除された, 脳腫瘍の顕微鏡的所見は, 腎細胞癌の原発巣と類似していた, 脳腫瘍は免疫組織学的にEMAとケラチン陽性で, 転移性腎細胞癌の診断が確認された.本症例は腎摘後10年以上へて孤立性脳転移をきたした第2例目の症例である,We report a case of solitary brain metastasis from renal cell carcinoma (RCC) 14 years after nephrectomy. A 46-year-old female had sudden onset of headaches, aphasia, gait disturbance and right hemiparesis. A brain CT revealed a cystic tumor in the left parietal area, which was surgically removed completely. Microscopic appearances of the brain tumor were similar to those of the primary RCC. Positive immunoreaction for epithelial membrane antigen (EMA) and keratin confirmed the diagnosis of metastatic RCC. This is the second case of solitary brain metastasis from RCC occurring more than 10 years after nephrectomy
T-138C Polymorphism of Matrix Gla Protein Promoter Alters Its Expression but is not Directly Associated with Atherosclerotic Vascular Calcification
Matrix Gla protein (MGP) is a crucial inhibitor of vessel and cartilage calcification. We investigated the association of T-138C MGP promoter polymorphism with the degree of atherosclerosis, vascular calcification and patients' clinical background including calcification of the trachea and costal cartilage. Analysis of 108 autopsy cases was carried out by polymorphism-specific PCR on formalin-fixed paraffin-embedded samples. Statistical correlations among eight risk factors and five markers related to atherosclerosis and extra-bone tissue calcification were multivariantly analyzed. We found very high canonical correlations between the factors and the markers, and Pearson's correlation analysis revealed six significant correlations between age and the Gore index; age and costal cartilage calcification; sex and costal cartilage calcification; hypertension and the Gore index; hypertension and the calcification factor of the Gore index; and hyperlipidemia and costal cartilage calcification. The promoter activity of the -138T allele was significantly higher than that of the –138C allele; treatment with 12-O-tetradecanonylphorbol 13-acetate (TPA) significantly activated the former, but had almost no effect on the latter. The C genotype was significantly common among Japanese subjects, (TT 45.5%, TC 37.6% and CC 16.8%) compared with that reported in the Netherlands, Northern Ireland and France. No significant correlation was observed, however, between T-138C MGP promoter polymorphism and the markers. Although the C genotype (TC+CC) tended to show a higher calcification factor than the TT genotype, no significant difference was observed among the genotypes in the Gore index or in the calcification factor. Although MGP promoter activity and the binding of the AP-1 transcription factor were clearly different between T-138 and C-138 MGP promoter polymorphism in vitro, T-138C polymorphism was, statistically, not an independent factor of atherosclerosis or atherosclerotic vascular calcification in the abdominal aorta