[A case of empty sella syndrome with panhypopituitarism following acute meningoencephalitis].
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Biomedical subjects
Publications and source records attributed to K Okada.
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Eighteen patients with malignant mesothelioma were seen at Kure Mutual Aid Hospital over a 10-year period. According to occupational history, chest x-ray manifestations, and evidence of asbestos bodies in the tissue, 13 of these cases were definitely thought to be due to exposure to asbestos as a result of two or three of these items testing positive. Kure City is one of the major ship-building cities in Japan since the 1920s. Most of the 18 patients worked in ship building before and during World War II. Malignant mesothelioma appeared about 40 years after their first exposure to asbestos. In western countries, most malignant mesotheliomas are thought to be induced by exposure to asbestos fibers (1,2). Consequently, there has been a serious effort to deal with this problem recently, including lowering rate of exposure. In Japan, however, there have been few reports that asbestos fibers caused malignant mesothelioma (3). This report suggests that an increased incidence of malignant mesotheliomas in a specific area of Japan may also be due to exposure to asbestos fibers.
Changes of cerebral white matter on computed cranial tomography related to aging were studied in 70 subjects aged 30 to 94 years. The subjects had no histories of cerebrovascular accidents and no abnormalities in the central nervous system were shown by physical examinations nd CT scans. We measured the average attenuation values (CT numbers) of each elliptical region (165 pixels, 0.39 cm2) in the bilateral thalamus and twelve areas of deep white matter. Multiple regression analysis was used to assess the effects of age, cranial size and cranial bone CT numbers on the brain CT numbers. We also studied the association between brain CT numbers and brain atrophy, hypertension, diabetes mellitus. CT numbers of frontal white matter surrounding anterior horns decreased with aging in 70 subjects aged 30 to 94 years. No significant correlation between age and brain CT numbers was found in any other region by multivariate analysis, because of the prominent effect of cranial bone CT numbers on brain CT numbers. Although no age-related changes of white matter CT numbers was found in 41 subjects aged 30 to 65 years, there were significant negative correlations between age and white matter CT numbers at all regions in 29 subjects aged 66 to 94 years. Brain atrophy was associated with brain CT numbers. No association was found for hypertension or diabetes mellitus. Brain CT numbers decreased with aging even in neurologically healthy persons in older age. Brain CT numbers also decreased as cerebral atrophy advanced.
The purpose of this study is to demonstrate the localization and distribution of keratin-positive cells (KPC) in the various pathological types of prostatic cancer, and to investigate the correlation between the basal cell and KPC. The localization of keratin was immunohistochemically investigated in 20 benign prostatic hyperplasia (BPH) and 33 human prostatic adenocarcinomas by the indirect immunoperoxidase technique, using anti human keratin rabbit serum on frozen sections. In BPH, strongly positive staining for keratin was detected in the cytoplasm of basal cells. Glandular epithelial cells were positive. In the cancer sections, no KPC was observed in all 6 cases of the large acinar type, all 10 cases of the small acinar type and all 12 cases of the column and cord type. On the other hand, KPC remained around the cancer cell populations in all 10 cases of the cribriform type. In the fused gland type, KPC was localized in 3 of 9 cases and in the medullary type 3 of 7 cases. If KPC was regarded as the marker of the basal cell as shown in BPH, it would be speculated that the absence of KPC occurred in some type of prostatic cancer showed the disappearance of basal cell. That is, KPC could not be detected in large acinar, small acinar and column and cord type, while KPC remained completely or partially in the cribriform, fused gland and medullary type. These histochemical alteration would suggest the different degree of malignancy in the various histological type of prostatic cancer.
The interrelationship among localization of tumor, local extension, lymph node metastasis and various histological grades was investigated in 31 consecutive series of prostate cancer treated by radical prostatectomy. Surgical specimens were examined by step sections cut perpendicular to the urethra. Each tumor was graded histologically in accordance with WHO-Mostofi grading (evaluated by nuclear anaplasia and structural differentiation), Gleason's and M.D. Anderson's grading systems. The areas of the prostate was divided into 4 quadrants delimited vertically along the urethral axis and transversely at the level of utricle, i.e. anterior/superior, anterior/inferior, posterior/superior and posterior/inferior quadrants. Topographical localization and extension of each tumor was examined in accordance with the above area subdivision. Every tumor was growing at least in the posterior/inferior area. All cases with tumor progression to the anterior/superior area also revealed extensive tumor growth in the other two or three quadrants. Therefore, prostate cancer appears to be originated from the posterior/inferior area of the prostate and terminated in the anterior/superior area as local extension. In 31 cases examined, capsular invasion was noted in 22, seminal vesicle invasion in 16, and lymph node metastasis in 12 cases. All cases with seminal vesicle invasion also showed capsular invasion. None of the cases without capsular and/or seminal vesicle invasion had lymph node metastasis. Thus, it is inferred that prostate cancer is initially growing locally, extending to the capsule and seminal vesicle and then metastasizes to the pelvic lymph nodes. As for the histological grading, higher grade tumors tended to show higher incidence of capsular and seminal vesicle invasion and lymph node metastasis.(ABSTRACT TRUNCATED AT 250 WORDS)
The collaborate studies of clinical application of Extracorporeal Shock Wave Lithotripsy (ESWL) using Sonolith 2000, performed at Departments of Urology of Nara Medical University, the University of Tokai School of Medicine and Wakayama Medical College between March and August 1987, were reported. In total 155 ESWL sessions were carried out on 111 patients suffering from in total 119 upper urinary tract stones. The localization system using ultrasound imaging with a computer assisted multiarticulated arm were evaluated as excellent or effective in 117 cases (98.3%). The stone fragmentations were evaluated as excellent (less than or equal to 3 mm) or effective (less than or equal to 5 mm) in 101 cases (84.9%). On the X-ray film obtained six weeks after the final ESWL treatments, 61 cases (51.3%) were free from stone fragments, 20 cases (16.8%) had sand-like fragments and 18 cases (15.1%) had stone fragments less than 5 mm. 99 cases (83.2%) without stone or with stone fragments less than 5 mm were considered to be with satisfactory results. No serious adverse effect was observed, but petchia on the flanks where shock wave penetrated and mild hematuria were observed in all cases. It is concluded that ESWL treatment using Sonolith 2000 is applicable in the managements of patients with the upper urinary tract stones without serious adverse effects.
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A 69-year-old man initially came to our hospital with the chief complaint of dysuria and hematuria. On rectal examination, the prostate gland was found to be grossly enlarged and rock hard in consistency. Abnormal laboratory data included: lactate dehydrogenase, alkaline phosphatase, acid phosphatase and prostatic acid phosphatase. Chest X-ray revealed multiple nodular lesions in both lung fields. Pathologic findings of the prostate needle biopsy revealed moderately well differentiated adenocarcinoma. Early combined hormonal and chemotherapy (adriamycin, TGF, methotrexate, bleomycin) was performed. After two courses of this regimen, the pulmonary lesions vanished completely. In addition, partial disappearance of osteoblastic lesions on bone scans was recognized.
Serum prostatic specific antigen (PA), gamma-seminoprotein (gamma-Sm) and prostatic acid phosphatase (PAP) levels were measured in 113 untreated patients with prostatic cancer and in 137 patients with benign prostatic hypertrophy (BPH). We used a PA-TESTWAKO enzyme immunoassay kit, gamma-Sm enzyme immunoassay kit and PAP radioimmunoassay kit. Of the 113 patients, 81.4%, 73.5% and 69%, respectively, were detectable using a single assay. PA was more sensitive than the other two markers in all stages, especially in localized disease (stages A, B and C). Using the BPH group as a negative control, specificities of PA, gamma-Sm and PAP were 85.4%, 81.0% and 94.2%, respectively. Efficiency was, respectively, 81.2%, 79.6% and 82.8%. In the follow up period, 15 patients presented disease progression. At the time of clinical detectable progression, the sensitivities of PA and gamma-Sm were both 100% (15/15), while 67% (10/15) for PAP. Concerning the sensitivity within 6 months prior to progression, gamma-Sm and PA tended to be more sensitive than PAP in early detection of disease progression. This study shows that PA is more reliable than gamma-Sm and PAP in detecting and staging of prostatic cancer. gamma-Sm and PA appear to be more reliable in earlier prediction of disease progression.
Plasma fibrinopeptide B beta 15-42 was significantly high in undialyzed and hemodialyzed chronic renal failure (CRF) patients, indicating that the fibrinolytic system as well as the coagulation system is stimulated. There are two kinds of plasminogen activators (PA) for the fibrinolytic system: urokinase (UK) and tissue-type PA (t-PA). PA activity of peripheral leukocytes from healthy volunteers, continuous ambulatory peritoneal dialysis (CAPD) patients and hemodialysis (HD) patients was measured and compared. Peripheral leukocyte PA in the euglobulin fraction was purified using zinc-chelate-Sepharose 6B column and Concanavalin A-Sepharose column chromatography. The different PA activity was quantitatively identified by electrophoretic enzymography and was confirmed using antibody against UK and t-PA. PA activity of peripheral leukocytes was significantly higher in HD patients on the cupro-ammonium processing membrane dialyzer than in CAPD patients and healthy volunteers. All PA activity in the three groups was UK, and t-PA was not detected. This suggested that the inflammatory response was continuously induced in HD patients, resulting in the induction of PA activity of the leukocytes and plasma, and that different mechanisms were involved for the synthesis or secretion of UK and t-PA.
A 54-year-old female with bronchial asthma and PIE syndrome induced by disodium cromoglycate (DSCG) was reported. She was referred to our hospital for further examination of the abnormal chest shadows and eosinophilia. She had been treated with DSCG, Cefaclor. Bromhexine and bronchodilator for bronchial asthma and bronchitis. Withdrawal of the drugs except for the bronchodilators alleviated her symptoms. Therefore, drug induced lymphocytes stimulation tests (DLST) were performed for those three drugs. Only DLST for DSCG showed a positive result. She had been asthmatic for ten years and treated by the drug for 18 months prior to admission. The skin test for the drug was negative and a precipitating antibody for the drug could not be found. To obtain a definite diagnosis, bronchial challenge by DSCG was performed, after her symptoms were under control. Severe asthmatic responses were provoked in 6 and 24 hours after the inhalation of DSCG. Bronchoalveolar lavage, performed 8 days after the provocation, revealed increased eosinophils and lymphocytes in BAL fluid. Although several cases of PIE syndrome induced by DSCG have been reported, this seems to be the first report of late and delayed type bronchial response and pulmonary infiltration with eosinophilia provoked by DSCG. The bronchial response to the drug was a late and delayed type reaction and sustained for a long period. This might indicate that PIE syndrome induced by the drug may be caused by a same mechanism as the provoked asthmatic response.
A new assay method for measuring single-chain urokinase-type plasminogen activator (scu-PA) activity by quantitative calorimetric assay method is described. The serine enzyme u-PA activates plasminogen to plasmin, and scu-PA is a precursor protein obtained from a tissue culture of human kidney cells. The scu-PA solution was activated by plasmin to two-chain u-PA, which releases p-nitroaniline from pyro-Glu-Gly-Arg-pNA, and the optical density at 405 nm was measured. One unit of scu-PA was defined on the basis of 1 nmol of p-nitroaniline released from the substrate per second. One unit of scu-PA was found to be equivalent to 335 u-PA (two-chain) units (IU).
Since the discovery of several potent anticancer agents which are specific inhibitors of DNA topoisomerases, the key enzymes in the DNA metabolism, efforts to elucidate the mechanism of acquired resistance to these agents and to overcome them have been focused on these enzymes, the cellular targets of the anticancer agents. These trends were briefly reviewed.
Discussed is a deceased patient, a 54-year-old male, who was admitted to hospital with the chief complaint of motor aphasia. Computed assisted tomography in the cranium showed a massive lesion in the left brain. Further, chest X-ray showed an abnormal tumorous shadow with a pleural indentation in the left middle lung field. In spite of a negativity of cancer cells in a bronchial biopsy and a brushing, we decided that this case reflected a lung cancer with brain metastasis. However, on autopsy, the tumor in the lung histologically was determined as being an (adenocarcinoma alveolar cell type) and the brain tumor was found to be a malignant astrocytoma. We have reported on this case because a double primary neoplasm, a malignant astrocytoma and lung cancer, is rare in the literature.
During the clinical course of chronic pleuritis and pyothorax, we frequently have found abnormal clinical signs such as increased abnormal chest shadows, subjective symptoms, such as chest pain and bloody sputum, and the appearance of atypical cells in the pleural effusion. It is very difficult and important to diagnose differentially worsening of chronic inflammation and occurrence of malignant tumors. We have surgically treated six patients with malignant tumors arising from chronic pleuritis and pyothorax, who had the above abnormal signs. All of them were made, and their average age was fifty three years. Two patients exhibited increased abnormal chest shadows, 5 had subjective symptoms (5 with chest pain, 2 with bloody sputum and 2 with fever), and 1 had atypical cells in the pleural effusion. Two patients had suffered from chronic pleuritis, who both had received artificial pneumothorax therapy for pulmonary tuberculosis, and the other 4 patients had suffered from chronic pyothorax, with mean duration of thirty years. The pathological diagnoses were 2 cases each of malignant pleural mesothelioma, squamous cell carcinoma, and malignant fibrous histiocytoma. The two patients with squamous cell carcinoma had pleurocutaneous and bronchopleural fistula. The operative methods were tumor resections with pleuropneumonectomy performed in 2 patients and pneumonectomy in 1. Absolute non-curative operation was performed in 1 patient, and postoperative radiotherapy in 3 patients. All patients died of tumor recurrence, although five of them underwent reoperation, chemotherapy and radiotherapy. Their duration of survival ranged from 3 to 15 months with a mean of 9 months after appearance of malignant tumor signs.(ABSTRACT TRUNCATED AT 250 WORDS)
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To determine the phenotype of target cells for bovine leukemia virus (BLV) infection in sheep, we analyzed blood lymphocytes from BLV-infected clinically healthy and leukemic sheep by use of monoclonal antibodies. In clinically healthy and leukemic sheep that were BLV-infected, the blood concentration of T lymphocytes was within normal values, but the number of B lymphocytes was increased in several cases. In addition, the number of blood lymphocytes expressing the BLV antigen correlated well with that of B lymphocytes. Double immunofluorescence staining demonstrated that lymphocytes expressing BLV antigens bore B-cell but not T-cell surface markers. Moreover, neoplastic cells in the lymph nodes of leukemic sheep were stained immunohistochemically with an anti-B monoclonal antibody but not with any of anti-T monoclonal antibody tested, indicating that tumor cells are of B-lymphocyte origin. Collectively, these results show that BLV antigen-positive cells obtained from BLV-infected sheep that have no clinical signs and BLV-induced lymphosarcoma cells belong to the B-lymphocyte lineage.
Hepatocellular carcinoma (HCC) possessed the ability of vascular invasiveness toward hepatic portal vein on the process of progression. This biological character of HCC can influence the patients survival on clinically. In this paper, we tried to establish the in vitro portal invasion model with human materials. The hepatic portal vein endothelial cell (HPVEC) derived from intrahepatic portal veins by surgically, have been propagated, as outgrowth cultures in RPMI-1640 medium with 10% fetal bovine serum, on permeable collagen membranes (KOKEN, Tokyo) containing mainly type I collagen, covered with a solubilized tissue basement membrane (MATRIGEL, Collaborate Res., Inc., Bedford MA) involving type IV collagen, laminin and proteoglycan. The primary cultured HPVEC with polygonal shaped cells forming a pavement stone sheet, were positively stained with Factor VIII related antigen and synthesized both prostacyclin and collagenase inhibitor. Co-culture of primary human HPVEC and HuH-7 (human HCC cell line obtained from Prof. Satoh, Okayama Univ.,) cells were inoculated onto reverse side between collagen membrane and gell formed basement membrane. Morphological alterations on the side of HPVEC can be obtained such as polylayered cells and different cytoplasmic cells among HPVEC. These results indicate that this experimental model can provide an useful in vitro model for the study of HCC portal invasion.