Abstract: A macroglycolipid containing galactose and N-acetylglucosamine as predominant sugar constituents was prepared together with glycophorin from rabbit erythrocyte membranes by extraction with lithium diiodosalicylate and partition in aqueous phenol. The macroglycolipid was effectively separated from the glycophorin fraction by ion-exchange chromatography in the presence of a detergent, Ammonyx LO. Its yield (ca. 4 mg/100 ml erythrocytes) was significantly higher than that of the macroglycolipids from human erythrocytes. The structure of the carbohydrate moiety in the macroglycolipid was analyzed by methylation analysis, Smith degradation, nitrous acid deamination, and chromium trioxide oxidation. Assuming one ceramide residue per molecule, the average number of sugars in the macroglycolipid was about 30. The macroglycolipid had a highly branching structure: Gal(alpha 1 leads to 3)Gal(beta 1 leads to 4)GlcNAc sequences are present at nonreducing termini and leads to 3 Gal(beta 1-4)GlcNAc repeating units are present in the inner core of the sugar chain. Some of the inner galactose residues branch at the C-6 position. Constituents of the ceramide moiety were also characterized.

Abstract: A cup of tea (containing about 0.49 mg F) containing soluble fluoride in the optimum necessary amount was recommended after every school lunch to 298 school children of Suhara in Sumon, Niigata prefecture, for about 250 days from December, 1975 to November, 1976. Increment lesions which appeared at three carious predirective sites, i. e., pits and fissures, proximal, and free gingival smooth surfaces of the children of the test school in the Suhara district were compared to the lesions found at the same sites in 185 children of three control schools in the Kamijo district of the same village. Reduction rates at each site were 52.8% for the pit and fissures and 57.2% for the proximal sites, but there was no reduction at the free gingival sites.

Abstract: 1. Alterations in troponin subunits in myocardial infarction were studied in the dog heart by the analysis of troponin-tropomyosin complex, i.e, native tropomyoin, of total structural proteins in SDS gel electrophoresis, and by the measurement of degree of activation of actomyosin-ATPase by Ca++. 2. At 12 to 24 hours after coronary ligation, reductions in TN-C and tropomyosin were observed followed by a decrease in TN-I at 48 hours. The relative contents of these subunits were the lowest at 72 hours to 7 days falling to less than 10% of those in the non-ischemic myocardium. On the contrary, TN-T was preserved through the course of myocardial infarction. 3. Actomyosin-ATPase activity was increased at 12 to 24 hours after coronary ligation and then reduced rapidly at 24 to 48 hours together with the degradation of myosin. However, the activation of actomyosin-ATPase by Ca++-troponin-tropomyosin was reduced already at 12 hours simultaneously with the reduction in TN-C, and almost completely lost at 48 hours. 4. Troponin subunits and actomyosin-ATPase activity returned to those of the control myocardium at 28 days after coronary ligation indicating the recovery of infarcted tissue.

Abstract: Individual variations in effectiveness of acupuncture analgesia(AA), morphine analgesia(MA) and dorsal periaqueduct central gray stimulation-produced analgesia(d-PAG-SPA) were parallel. Close correlation was also observed between the individual variations of AA effectiveness and morphine-like-factors(MLF) in the brain. Individual variations in effectiveness of these analgesia were diminished by D-phenylalanine (D-phe).

Abstract: Inbred male ACI/N rats were treated with an intermittent carcinogenic regimen of 2-acetylaminofluorene (2-AAF) until the development of hepatomas (40 weeks), and the activation of 2-AAF by liver S-9 and the oxidation of 2-AAF; and 2 other drugs by microsomal functions were periodically examined. The S-9 activity increased at the end of 1 feeding cycle (3 weeks 2-AAF diet and 1 week normal diet), reaching a maximum of 400% of controls after 2 or 3 feedings cycles. It then declined, but the elevated S-9 activity (300 to 250% of controls) was sustained until the development of hyperplastic nodules in the livers. The microsomal oxidation of 2-AAF to N-hydroxy-2-AAF was activated by dietary 2-AAF, but the activity of cytosol (S-105) to produce mutagen from N-hydroxy-2-AAF was not affected. Cytochrome P-450 content and microsomal oxidation of aminopyrine and aniline were gradually decreased below the normal levels by 2-AAF feeding, although microsomal p-hydroxylation of aniline was temporarily elevated to about 130% of control at the first or the second feeding cycle. These results indicate that dietary 2-AAF selectively induces microsomal 2-AAF N-hydroxylase which mediates the oxidation of 2-AAF to N-hydroxy-2-AAF, a proximate carcinogenic or mutagenic metabolite.

Abstract: In the previous study we reported that lipid A moiety plays an important role in the activity of bacterial lipopolysaccharide (LPS) to depress hepatic microsomal drug-metabolizing enzyme activity in mice (5). Recent studies on the mechanism of its action showed that the decrease in the hepatic drug-metabolizing enzyme activity, as well as cytochrome P-450 levels seen on endotoxin administration, is closely related to metabolism of the heme moiety required for synthesis of cytochrome P-450 in the liver (2,3,8, 14). On the other hand, since various humoral factors, such as glucocorticoid antagonizing factor (GAF) (10), colony stimulating factor (CSF) (12), tumor necrosis factor (TNF) (4), and serum amyloid A mediator (SAA) (13), which mediate the host response to endotoxin have recently been found, it is also interesting to determine whether or not the effect of endotoxin on the hepatic heme metabolism and cytochrome P-450 is indirectly mediated by a humoral factor. In this study, therefore, we examined the effect of an endotoxin-induced mouse serum factor on hepatic t5-aminolevulinic acid synthetase (ALA synthetase) which is a rate-limiting enzyme for heme synthesis and cytochrome P-450 levels in mice. The endotoxin used in this study was a glycolipid preparation isolated from Salmonella minnesota R595 by the method of Galanos et al (6), and abbreviated as R595 GL or GL. Free lipid A preparation derived from the 1% acetic acid hydrolysate of R595 GL was used in a complex form with bovine serum albumin (Seikagaku-Kogyo Co., Tokyo) according to Galanos et al (7). Male, 5-weekold ddy mice (Shizuoka ]ikkendobutsu Co., Shizuoka) were used in this study and maintained on a laboratory diet (Oriental Yeast Co., Tokyo), and water which were given ad libitum throughout the experiment. Mice in each group were injected intraperitoneally with R595 GL or free lipid A suspended in saline and starved for about 24 hr prior to sacrifice. Endotoxin-induced serum factor, described as post GL serum or post lipid A serum, was prepared from mouse blood which was collected by cardiac puncture at various intervals after endotoxin administration. The serum was pooled from 5 mice per group and stored at -20 C. Normal mouse serum was prepared from control mice injected with the vehicle only. Eighteen hr after serum injection, the ALA synthetase activity was assayed

Abstract: The effect of calcitonin on the metabolism of calcium and cyclic AMP in the avian bone was examined in vitro. In the chick embryonic cortical bone, calcitonin affected neither the level of cyclic AMP nor the parathyroid hormone-induced stimulation of calcium release from bone. Also, the level of cyclic AMP in the cortical or medullary bone of Japanese quails was not increased by calcitonin. The medullary bone did not respond to calcitonin either in freshly prepared tissue or in tissue cultured for 48hr in the absence of calcitonin. The activity of renal adenylate cyclase of Japanese quails was also calcitonin-insensitive. The inability of calcitonin to increase the level of cyclic AMP and to antagonize the parathyroid hormone-induced stimulation of calcium release from bone may account for the lack of hypocalcemic effect of calcitonin in birds as reported by other investigators.

Abstract: Transrectal Ultrasonotomography was performed in 44 patients with prostatic cancer before, during, and after estramustine phosphate (Estracyt®) administration. In 75.7% of 37 previously untreated patients, the deformity of the horizontal section of the prostate with prostatic cancer was corrected considerably, while in 89.2%, prostatic weight was remarkably reduced. In 57.1% of seven previously treated patients, appreciable changes were also observed in the shape and weight of the prostate. We concluded that estramustine phosphate was effective not only for untreated prostatic cancer, but also, at least in some degree, for relapsed cases.

Abstract: The Ficoll-Urografin density gradient method was used to separate differentiated mouse myeloid cells (M1), and the properties of the fractionated cellpopulations were investigated.During differentiation in vitro, M1 cells produced large adherent cells. These adherent cells showed an increased cell size and a decreased ratio of nucleus size to cell size (N/C ratio) in comparison with untreated M1 cells and nonadherent cells. With discontinuous Ficoll-Urografin density gradient centrifugation, adherent cells could be separated into subfractions with low N/C ratios (d = 1.033-1.054, rich in macrophage-like cells); those with inter-mediate N/C ratios (d= 1.054-1.059, rich in cells in the intermediate stages of differentiation); and those with high N/C ratios (d =1.059-1.067, rich in myeloblastic cells). Almost all the untreated M1 cells and nonadherent cells were banded in the high density region (d = 1.059-1.067). Both phagocytic and lysozymic activities were highest in the lowest density band. Elevated lysosomal enzyme activity in the highest density fraction of the fractionated cells indicates that these cells may differ from M1 cells in their biological activity.

Abstract: The intravenous olfaction test with Alinamin is a simple procedure and widely used. However, fundamentals on the test are still obscure in many respects.In the present study we measured changes with time in concentrations of an odorous substance in the expired air during the test.Measurement was made of concentrations of the odorous substance in the expired air after intravenous injection of Alinamin by subjecting a sulfur compound contained in Alinamin or its detritus to the gas chromatograph (Shimazu GC-6A). The results obtained were as follows.1) Alinamin was not detected in the expired air after intravenous injection of Alinamin. However, a product of decomposition of Alinamin was observed.2) Measurement was made of concentrations of this product with time. As a result, it was observed 20 seconds after initiation of the intravenous injection, reached its peak 40-60 seconds later and then decreased gradually.3) This product was identified as N-propyl mercaptan.4) We were able to learn changes with time in concentration of N-propyl mercaptan in the expired air after intravenous injection of Alinamin.

Abstract: Mouse myeloid leukemia cells (M1) were induced to different-iate in vitro by treatment with dexamethasone. The incorporation of [3H] thymidine into acid-insoluble materials began to decline after 10 h treatment. This reflected the differentiation-associated decline of DNA synthesis activity, since (i) the thymidine was almost exclusively incorporated into nuclear DNA, (ii) the incorporation was completely blocked by arabinofuranosylcytosine and (iii) the differentiation-associated changes of intracellular pool size and specific activity of thymidine were negligible. Cell fractionation by discontinuous Ficoll-Urografin density gradients revealed that the DNA synthesis of the differentiat-ed cells declined with the decreased density, or ratio of nucleus size to cell size (N/C ratio). Autoradiographic analysis showed that the decrease in DNA synthesis activity was due to the accumulation of "unlabeled" cells, which exhibited a much lower N/C ratio than "labeled" cells. Dexamethasone treat-ment also caused specific reduction in the proportion of S phase cells. These results indicate that M1 cell differentiation is closely coupled with the cessation of DNA synthesis.

Abstract: Scanning electron microscopy of the third ventricular wall of the arctic lamprey, Lampetra japonica, revealed the occurrence of supraependymal neurons in several regions of the ventricular surface. These neurons--as varicose fibers of various calibers--traversed among the cilia, microvilli, and bulbous protrusions of the ependymal surface. Occasionally synapse-like contact were found between these nerve fibers and the intraventricular processes of the cerebrospinal fluid (CSF)-contacting subependymal neurons in the hypothalamus. A possible function of the supraependymal neurons is discussed in relation to the hypothalamic neuroendocrine system.

Abstract: The histological and histochemical studies on hypocalcified dentin which occurred in incisor, and abnormal bone which formed in the alveolar bone, of a rat given strontium carbonate were made.The hypocalcified dentin and abnormal alveolar bone hardly reacted to hematoxylin, toluidine blue (pH.2.5), and alcian blue (pH.1.0) stains. The hypocalcified dentin reacted intensely to eosin and van Gieson stains, and showed a strong PAS reaction, compared with those in normal dentin. However, as for the PAS reaction in hypocalcified dentin, further investigation will be required.The abnormal alveolar bone reacted to eosin and van Gieson stains. The degree of PAS reaction in the abnormal alveolar bone was lower than that in normal alveolar bone.These observations, suggest that the occurrence of hypocalcified dentin and abnormal alveolar bone depends upon the disturbance of mucopolysaccharide and collagen metabolismsin the calcification process of hard tissues.

Abstract: Acupuncture afferent pathways were explored by stimulation-produced analgesia, by hypophysectomy, and by lesions which abolished acupuncture, morphine(0.5 mg/kg i.p.), and dorsal periaqueduct stimulation-produced analgesia. Lesion of the anterolateral tract(ALT) blocked morphine analgesia(0.05 μg intrathecal). Descending serotonergic and noradrenergic pain inhibitory systems mediate analgesia.