Igaku kenkyu. Acta medica最新文献

To study the presence and significance of so-called "tumor cord" in human solid neoplasms, histopathological analysis was made on 69 cases of human lung carcinoma. The specimens were divided into small cell and non-small cell carcinoma, and the extent of tumor cord was determined. All cases of small cell carcinoma examined were found to have tumor cord structure, although its degree was variable. On the other hand, in non-small cell carcinoma, tumor cord was observed only in part of the cases. Small cell carcinoma responds usually well to therapies, although recurrence occurs frequently. These characteristics of small cell carcinoma could be explained by biphasic cell survival after treatment of tumors with tumor cord structure.

Forty-six heart valve prostheses were implanted in 37 patients from November 1974 to December 1982 at National Fukuoka Higashi Hospital. The patients consisted of 18 males and 19 females, with ages ranging from 14 to 66, mean 44.8 years. Bioprosthesis was used in 89.2% of the patients. There was no hospital death among the 30 single valve replacements, but one of the 7 patients receiving mitral and aortic double valve replacements died. The discharged survivors were followed up from a minimum of 8 to a maximum of 16 years (mean 9.3 years) with a cumulative follow-up period of 334.1 years with 100% completion. The actuarial survival rate at 13 years was 95 +/- 6% for mitral valve replacement (MVR), 71 +/- 17% for aortic valve replacement (AVR), and 58 +/- 19% for mitral and aortic double valve replacement (DVR), including 1 mitral and tricuspid valve replacement. This rate for overall cases was 40 +/- 29% at 17 years. Structural valve deterioration of the bioprosthesis occurred in 7 patients at the incidence of 2.4%/patient-year. The reoperation free percentage was 77 +/- 10% at 13 years in the Hancock porcine bioprosthesis (Hancock) group and 50 +/- 23% at 9 years in the Carpentier-Edwards porcine bioprosthesis (Carpentier-Edwards) group. Valve thrombosis was encountered in one case having Björk-Shiley aortic valve prosthesis with a linearized rate of 3.3%/patient-year in the group. A long-term follow-up study showed an increasing incidence of structural valve deterioration in the bioprosthesis group and thromboembolic complications in all types of prosthesis.

Usefulness of endoscopic ultrasonography (EUS) for the diagnosis of chronic pancreatitis, particularly for mild chronic pancreatitis and so-called clinically suspected chronic pancreatitis diagnosed by the criteria documented by the Committee of Japanese Society of Gastroenterology for chronic pancreatitis (CJSG criteria), is described in this paper. 89 patients with chronic pancreatitis including 43 with mild chronic pancreatitis (MIP), 29 with moderate chronic pancreatitis (MOP) and 17 with advanced chronic pancreatitis (ADP) diagnosed by Endoscopic Retrograde Cholangio-Pancreatography (ERCP) were selected for the study and following results were obtained. 1) The number of findings of wall irregularity of the main pancreatic duct and heterogeneity of the pancreatic parenchyma were more clearly shown by EUS although they had been classified as suspicious of chronic pancreatitis diagnosed by conventional US by the CJSG criteria. 2) The pancreatic parenchymal echo pattern by EUS can be divided into 6 patterns, rough-high echo, spotty-high echo, linear-high echo, rough-low echo, diffuse-high echo and diffuse-low echo. 3) Spotty high echo was observed in high rate in the patients even with MIP showing only a slight change of the main pancreatic ducts by ERCP. Therefore, this pattern could be present in early stage of chronic pancreatitis. 4) The pancreatic parenchymal change by aging detected by EUS was often seen as linear-high and/or diffuse-high echo patterns. 5) Differentiation of changes of the pancreatic parenchyma and wall of the main pancreatic duct by chronic pancreatitis from the change by aging was possible by using EUS. 6) By macro- and micro-scopic studies of the pancreatic parenchyma, pancreatic calculus, fatty change and irregular fibrosis were shown by EUS as rough-high echo accompanied by acoustic shadow, spotty-high echo and rough-low echo patterns respectively.

A fifty four years old hepatoma patient admitted to the hospital for a surgical operation. Preoperative laboratory examination demonstrated that his serum IRI level was very high (423 microU/ml) when measured with a beads method, however RIA or a microplate method demonstrated normal values. We studied the mechanism of the discrepancy of IRI values. 1) Both the beads and microplate methods demonstrated the same IRI values when the patient's serum insulin was roughly purified with Sep-Pak. The beads method showed high IRI values in serum which passed through Sep-Pak, therefore contained no insulin. 2) The similar results were observed when the patient's serum fractionated by a gel-chromatography (Biogel P-30). The beads method demonstrated high IRI values in both insulin fractions and the fractions containing serum proteins bigger than 40,000 molecular weight. The microplate method demonstrated only one large peak of insulin. 3) When non-specific IgG of guinea pig was used as a fixed antibody instead of human insulin antibody of guinea pig that was used in the beads method, the patient's serum showed the similar values as that obtained with the beads method. We thereby concluded that the abnormal level of IRI by the beads method was derived from the unknown substance reacting with IgG of guinea pig in the patient's serum. After the surgical resection of hepatoma, the levels of IRI measured by the beads method decreased significantly, suggesting that the substance is related to hepatoma cells.

A sixteen year old woman came to the hospital for glucosuria and amenorrhea. Physical examination demonstrated that she had hirsutism, deepening of voice, and pigmented skin in her axillary lesion which was histologically diagnosed as acanthosis nigricans. Ultrasonography showed polycystic ovaries. A diabetic pattern of 75 g oral glucose tolerance test, very high levels of serum insulin (fasting: 320, peak: 1,220 microU/ml), and hyperandrogenism characterized by increases of urine 17-KS, serum testosterone and DHEA-S were found. Both serum insulin and insulin-receptor antibodies were found to be negative. Insulin binding to both erythrocytes and cultured skin fibroblasts were significantly decreased (about 30% of normal controls). Scatchard plot analysis demonstrated decreased number of insulin receptors to about 30% of the normal controls. We therefore diagnosed that she had insulin receptor abnormality, Type A in Kahn's classification.

At the treatment of a bedsore of which had been resistant to various sorts of antibiotics, the mixture of several drugs was used for the treatment of its bedsore. Those drugs from which were used as the drugs-mixture, are 1% liquid of Pioctanin (C24H28N3Cl). 600 mg of Ascorbic acid, 9 mg of Pantothenic calcium and 20mg of hydrochloric Amitriptyline, respectively. The drugs-mixture, as mentioned above, has been scattered over its bedsore before the usual traditional treatment. After that, the bedsore has been treated by Gebencream (1% Cream of Sulfadiazine silver) as usually. Since a few days after that, Pseudomonas aeruginosa has never been able to be found on its bedsore at all. After a month, Staphylococcus aureus, Enterococcus faecalis and Serratia marcescens, which had been resistant to many antibioticus till that, cannot be found at all, too.

A human monoclonal antibody, ll-50 (IgM, lambda), was generated, which reacted specifically with a major of glycolipid present in LS174T colon cancer cells. The glycolipid antigen which reacted with the ll-50 antibody was expected to four sugar residues from its TLC mobility, and it was ascertained that the glycolipid antigen which reacted with ll-50 antibody might be Lc4 antigen [Gal beta 1----3 GLcNAc beta 1----3 Gal beta 1----4 Glc beta 1----1 Cer] judging from TLC immunostaining and ELISA when the reactivity of ll-50 antibody was tested using various pure glycolipids in 3-5 sugar residues as an antigen. Sera in patients with malignant disorders and healthy individuals were analyzed by Sandwich assay of immobilized and biotinylated ll-50 antibody. The serum of the Lc4 antigen recognized by ll-50 antibody was significantly higher in patients with malignant disorders than that in healthy individuals (p less than 0.05). Three mouse monoclonal anti-idiotype antibodies, G3, B3 and C5 (all IgG1), were generated by the immunization of BALB/c mice with ll-50 antibody. These anti-idiotype antibodies specifically bound to to human monoclonal antibody, ll-50 and had a significant inhibitory activity towards the binding of ll-50 antibody to the Lc4 antigen. This indicated that these anti-idiotype antibodies, G3, B3, and C5, were paratope-related anti-idiotype antibodies. G3, B3, and C5 were expected to define the nearest idiotope because they could mutually inhibit ll-50 antibody. Sera in patients with malignant disorders and healthy individuals were analyzed by Sandwich assay of immobilized and biotinylated anti-idiotype antibodies, G3, B3, and C5. As to the ll-50 like antibodies defined by C5 (Id-C5+), the mean serum level in patients with malignant disorders was significantly higher than that in healthy individuals (p less than 0.05). As to the ll-50 like antibodies defined by B3 (Id-B3+), the mean serum level in patients with malignant disorders was significantly higher than that in healthy individuals.(ABSTRACT TRUNCATED AT 400 WORDS)

Recently many new knowledge about the LDL receptors and LDL-receptor mediated endocytosis of cholesterol have been reported (Goldstein et al. 1979). This phenomenon is also observed in keratinocyte. The use of low density lipoprotein-gold (LDL-gold) technique in electron microscopy demonstrated a reciprocal correlation between cell differentiation and LDL-receptor expression in normal and psoriatic skin which is characterized by keratotic disorder and epidermal hyperproliferation. (Mommaas-Kienhuis et al. 1987). In order to study the interaction between normal skin and lipid, and the affect of lipid to psoriatic skin, we investigated the localization of apolipoprotein AI, B100 and E in epidermis. Six normal skins, ten psoriatic skins and three skins of seborrheic dermatitis were obtained. In normal epidermis, apolipoprotein B100 was markedly detected intercellularly, and apolipoprotein E was observed intracellularly. In contrast, apolipoprotein AI was not detected in epidermis. This result showed that keratinocytes expressed B and E receptors on their surface membrane, connecting with apolipoprotein B100 and apolipoprotein E respectively. But this finding that positive reaction sites were found in all layer of epidermis also suggested that anti-apolipoprotein B100 antibody reacted extracellular cholesterol excreted outside from keratinocytes. In psoriatic skin, the basement membrane of dermo-epidermal junction, the vascular walls and perivascular regions in papillary dermis were stained positively by anti-apolipoprotein AI antibody. But the localization of apolipoprotein B100 and E were similar to normal skin, and they were also detected in the parakeratotic regions in horny layer. These results did not show the relationship between cell differentiation and B, E receptor expression on keratinocyte. And it is suggested that cholesterol metabolism in keratinocyte affected the pathogenesis of psoriasis.

Several reports showed that abnormality of mitochondrial DNA (mt DNA) can be an etiology of cardiomyopathy in recent years. Cardiac involvement in mitochondrial disease other than Kearns-Sayre syndrome (KSS), however, has not been documented clearly. Therefore, cardiac involvement, abnormality of mt DNA and defects of the respiratory chain in mitochondrial disease were studied. Thirty-eight patients with mitochondrial disease were studied. The patients were consisted of 2 patients with KSS, 1 patient with probable KSS, 15 patients with ocular myopathy, 1 patient with myoclonus epilepsy with ragged-red fibers (MERRF), 6 patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), 5 patients with undefined mitochondrial encephalomyopathy and 8 patients with mitochondrial myopathy. Cardiac involvement was evaluated by electrocardiogram (ECG), chest roentgenogram and echocardiogram. Abnormality of mt DNA was examined using Southern blotting and polymerase chain reaction method in 25 patients. Defects of the respiratory chain were examined in 27 patients. All of the KSS and probable KSS showed heart block, and 2 of the 3 patients showed abnormalities on echocardiogram. Five of the 15 patients with ocular myopathy showed abnormalities on EGG. Four of the 6 patients with MELAS showed abnormalities on ECG, 1 showed cardiomegaly, and 3 showed left ventricular hypertrophy on echocardiogram. Three of the 5 patients with undefined mitochondrial encephalomyopathy showed abnormalities on ECG, 2 showed cardiomegaly and 2 showed asymmetric septal hypertrophy and wall motion abnormalities on echocardiogram. Large-scale deletions of mt DNA were detected in all of the KSS and probable KSS, and 7 patients with ocular myopathy. Deletions of mt DNA in the skeletal and cardiac muscles were proved to be identical in a case of KSS. A point mutation in mt DNA was detected in 5 patients with MELAS. Defects of the respiratory chain were detected in 22 patients. In conclusion, cardiac involvement is frequently seen in mitochondrial disease. Abnormality of ECG, especially heart block, is characteristic of KSS. Left ventricular hypertrophy is characteristic of mitochondrial encephalomyopathy.

Physicians and investigators, engaging in the treatment of epilepsy, have expected much help of plasma level determination of antiepileptic drugs in order to manage the patients successfully and safely. However, with the lapse of time and with the cumulation of many experiences, they have known that it can not be gotten so exactly and easily as they expected at beginning of research. The author has been repeatedly pointing out the methodological errors of its measurement, since the usefulness of plasma level determination of antiepileptic drugs began to be emphasized. Recently, Krämmer described that uncritical measurement of its plasma level as a routine method was not only nonsense but also harmful. However his opinion is based on the clinical data, too. This paper explains about the methodological errors, relating to measurement for antiepileptic drugs in blood, from the standpoint of physical chemistry.