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Biomedical subjects

M Takagi

Publications and source records attributed to M Takagi.

At least 919 records · Page 51Linked to original sources

[Laboratory and clinical studies of 6059-S in pediatric field (author's transl)].

The authors have carried out the laboratory and clinical studies of 6059-S. The results were as follows: The sensitivity was estimated by the plate dilution method on 27 strains of S. aureus, 26 strains of E. coli, K. pneumoniae and P. aeruginosa, 21 strains of Salmonella sp. and 9 strains of GM resistant P. aeruginosa isolated from patients. The distribution of sensitivity of S. aureus was 6.25-12.5 micrograms/ml and the peak of distribution was 6.25 micrograms/ml. The growth of 80.8% of E. coli was inhibited at concentration of less than 0.1 microgram/ml. The growth of 88.5% of K. pneumoniae was inhibited at concentration of less than 0.2 microgram/ml. The growth of 81.0% of Salmonella sp. was inhibited at concentration of less than 1.56 microgram/ml. The distribution of sensitivity of P. aeruginosa was 12.5- greater than 100 micrograms/ml and the peak of distribution was 25.0 micrograms/ml. The distribution of sensitivity of GM-resistance P. aeruginosa (greater than or equal to 25 micrograms/ml) was 12.5-50 microgram/ml and 5 of 8 strains were inhibited at concentration of less than 25 micrograms/ml. Phagocytosis was determined by Quie's method. Phagocytosis of E. coli, K. pneumoniae, Proteus vulgaris and Enterobacter cloacae by human polymorphonuclear neutrophil was more enhanced in the presence of 1 MIC and 1/2 MIC for 6059-S than for cefazolin at 4 and 6 hours after incubation. But phagocytosis of S. aureus did not enhanced in the presence of 6059-S. 6059-S was given by intravenous administration for 5 minutes and drip infusion for one hour at a single dose of 10 mg/kg of 6059-S to 3 and 4 children respectively. After intravenous administration of 6059-S, the mean peak serum level was 76.0 +/- 2.0 micrograms/ml at 15 minutes, 36.0 +/- 2.8 micrograms/ml at one hour, 1.5 +/- 0.4 micrograms/ml at 6 hours respectively. Half-life time was 1.3 hours. And after drip infusion of 6059-S was 39.9 +/- 9.7 micrograms/ml at one hour, 11.7 +/- 4.8 micrograms/ml at 3 hours and 1.8 +/- 1.4 micrograms/ml at 7 hours respectively. Half-life time was 1.4 hours. The mean urinary excretion rate was 90.4 +/- 6.1%, 76.5 +/- 16.0% up to 6 hours after intravenous administration and drip infusion respectively. 6059-S was effective in 17 cases out of 18 cases with bacterial infections. No side effects were observed except for 4 cases with elevation of serum transaminase, each on case of eosinophilia and of anemia.

Adolescent↗

Sialadenoma papilliferum: report of case.

A case of sialadenoma papilliferum, which occurred on the hard palate off a 61-year-old man, is reported. The tumor is considered to be a true neoplasm rather than hyperplasia of the duct cells of the salivary gland.

Adenoma↗

Intranuclear crystalloids associated with abnormal granules in eosinophilic leukocytes.

Ultrastructural evaluation of eosinophilic leukocytes from a 2-yr-old asymptomatic girl with chronic benign neutropenia (CBN) revealed a variety of morphological abnormalities. All eosinophils obtained from blood and marrow specimens contained multipole microcrystalloids in most of the mature cytoplasmic granules. An increase in crystalloid-free, immature granules in late (bilobed nuclei) eosinophils suggested a delay in granule maturation. The eosinophil granules appeared to be of normal size and demonstrated normal acid phosphatase reactivity. Eosinophilic myelocytes contained abnormal cisternae of rough endoplasmic reticulum (RER) and lacked abundant elongated RER cisternae seen in normal cells. A few eosinophilic myelocytes in specimens of bone marrow from the child contained large intranuclear crystalloids measuring up to 3 mu in length. The intranuclear crystalloid contained as cubic lattice of dense material with a periodicity similar to that described for cytoplasmic crystalloids. The ultrastructural morphology of marrow neutrophils was normal, as described in other cases of CBN. Ultrastructural examination of blood eosinophils from the father demonstrated microcrystalloids in cytoplasmic granules identical to those seen in the child. The father was asymptomatic and had normal leukocyte counts. Thus, anomalous crystalloid granule genesis occurred in the father and daughter and was not necessarily associated with neutropenia or clinical symptomatology. This anomaly is associated with the accumulation of intranuclear crystalloid material in eosinophilic myelocytes, which do not appear to be released from the marrow compartment.

Acid Phosphatase↗

Ultrastructural cytochemistry and radioautography of complex carbohydrates in secretory granules of epiphyseal chondrocytes.

Secretory granules of chondrocytes contain a variety of complex carbohydrates, which include glycosaminoglycans and glycoproteins necessary for the formation of the cartilage matrix. The present study has utilized ultrastructural, cytochemical, and radioautographic methods to determine the subcellular route of incorporation of sulfated and vicinal glycol-containing complex carbohydrates into secretory granules and their subsequent distribution in granules. High iron diamine specifically stained sulfated glycoconjugates in Golgi saccules, Golgi derived vacuoles, and mature secretory granules. Incubation of chondrocytes with 35SO4 resulted in significant radioautographic labeling of Golgi saccules, condensing vacuoles, intermediate granules containing moderately dense amorphous material, and mature granules containing fibrillar material. Periodic acid-thiocarbohydrazide-silver proteinate (PA-TCH-SP) staining of unosmicated thin sections localized vicinal glycol-containing glycoconjugates in cisternae of rough endoplasmic reticulum and coated vesicles, some of which appeared to be budding from rough endoplasmic reticulum. Similar coated vesicles appeared to fuse with condensing vacuoles and granules of intermediate maturity which evidenced moderate PA-TCH-SP reactivity. These vesicles were very seldom seen associated with Golgi saccules which contained 35SO4 radiolabels and high iron diamine reactivity but lacked significant PA-TCH-SP staining. The PA-TCH-SP-positive vesicles were not associated with mature secretory granules which demonstrated strong PA-TCH-SP staining. Lysosomes demonstrated moderately heavy PA-TCH-SP staining. Amylase digestion of en bloc specimens removed all PA-TCH-SP reactive cytoplasmic glycogen, however, staining of cytoplasmic organelles was not decreased. These studies indicate that sulfated glycosaminoglycans and vicinal glycol-containing glycoproteins are transported to secretory granules by Golgi saccules and coated vesicles, respectively, and are subsequently distributed differently within the maturing secretory granules.

Animals↗

Potentiation of excitatory postsynaptic potentials during and after repetitive stimulation in thin hippocampal sections.

Excitatory postsynaptic potentials (EPSPs) elicited by mossy fiber stimulation were recorded intracellularly from neurons in the CA3 region in thin hippocampal sections in vitro and potentiation of the EPSPs was examined during and after repetitive stimulation. Inhibitory postsynaptic potentials (IPSPs) and seizure discharges were blocked by bicuculline and high concentrations of Mg2+. When two shocks were applied at short intervals, the second EPSP was markedly potentiated. This potentiation declined exponentially with a time-constant of about 180 ms and was unaffected by changes in ambient temperature. The amount of potentiation during a pulse train was explained by summation of potentiation by individual pulses. Post tetanic potentiation lasted longer in media containing Ca2+ at higher concentrations and Mg2+ at lower concentrations. At high Ca2+ concentrations, tetanic stimulation induced long-term potentiation which was occasionally preceded by a long-lasting suppression. Tetanus to a bundle of mossy fibers potentiated EPSPs elicited by stimulation of a separate bundle of mossy fibers (heterosynaptic potentiation) but did not augment EPSPs elicited by fimbrial stimulation.

Animals↗

Coupling factor F1 ATPase with defective beta subunit from a mutant of Escherichia coli.

The defective coupling factor F1 ATPase from a mutant strain (KF11) of Escherichia coli was purified to a practically homogeneous form. The final specific activity of Mg2+-ATPase was 6-9 units/mg protein, which is about 10-15 times lower than that of F1 ATPase from the wild-type strain. The mutant F1 had a ratio of Ca2+-ATPase to Mg2+-ATPase of about 3.5, whereas the wild-type F1 had ratio of about 0.8. The mutant F1 was more unstable than wild-type F1: on storage at -80 degrees C for 2 weeks, about 80% of its activity (dependent on Ca2+ or Mg2+) was lost, whereas none of the activity of the wild-type F1 was lost. The following results indicate that the mutation is in the beta subunit. (i) High Mg2+-ATPase activity (about 20 units/mg protein) was reconstituted when the beta subunit from wild type F1 was added to dissociated mutant F1 and the mixture was dialyzed against buffer containing ATP and Mg2+. (ii) Low ATPase activity having the same ratio of Ca2+-ATPase to Mg2+-ATPase as the mutant F1 was reconstituted when a mixture of the beta subunit from the mutant F1 and the alpha and gamma subunits from wild-type F1 was dialyzed against the same buffer. (iii) Tryptic peptide analysis of the beta subunit of the mutant showed a difference in a single peptide compared with the wild-type strain.

Adenosine Triphosphatases↗

Effect of adenosine and adenosine 5'-monophosphate on cell division of cultured mastocytoma P-815 cells.

The growth of mouse mastocytoma P-815 cells in culture (37 degrees, 42 hr) was inhibited by exogenous adenosine (0.2 to 1.0 mM) and more effectively by AMP (0.01 to 0.1 mM), but not by adenine. The inhibited growth (a 25% inhibition by 0.5 mM adenosine and a 80% inhibition by 0.25 mM AMP) was restored to a near control level by the addition of uridine (0.5 mM) to the medium. The pretreatment (37 degrees, 3 hr) of the cells with adenosine or AMP caused a 60% inhibition of incorporation (37 degrees, 2 hr) of [U-14C]aspartate into uracil nucleotides, accumulating 14C-orotate and orotidine. Both dipyridamole, an inhibitor of adenosine uptake, and exogenous adenosine deaminase suppressed the growth inhibition induced by not only adenosine but also AMP. 2-Chloroadenosine, which is resistant to the action of adenosine deaminase, was a more potent growth inhibitor, while 3'AMP and 2'-AMP, which are not hydrolyzed to adenosine by membrane 5'-nucleotidase, were ineffective. Adenosine 5'-sulfate and other 5'-substituted adenosines were also ineffective. These observations indicate that AMP inhibits the growth of mastocytoma P-815 cells as a result of its continuous conversion to adenosine and a constant exposure of the cells to a low concentration of adenosine which readily permeates the cell membrane. In addition, adenosine, AMP and their agarose-linked forms rapidly (37 degrees, 20 min) elevated cellular levels of cAMP. This effect was not suppressed by dipyridamole. Apparently adenosine and AMP also act extracellularly for growth inhibition by regulating cAMP levels.

Adenine Nucleotides↗

Effect of adenosine 3',5'-monophosphate on growth and several functions of cultured mastocytoma P-815 cells.

Growth-inhibited mouse mastocytoma P-815 cells at stationary phase contained more histamine, serotonin and adenosine 3',5'-monophosphate (cAMP), and higher activities of histidine decarboxylase and adenylate cyclase than the cells during exponential growth. The elevation of endogenous cAMP levels induced by several growth-inhibiting agents such as N6, O2'-dibutyryl cAMP (Bt2cAMP), prostaglandin E1, AMP and 2-chloroadenosine stimulated several functions characteristic of mastocytoma P-815 cells in culture, elevating the synthesis of histamine and serotonin, the activity of chymotrypsin-like protease, and the incorporation of [35S]sulfate into acidic glycosaminoglycans. 1-Methyl-3-isobutyl-xanthine (MIX), a potent inhibitor of cAMP phosphodiesterase, potentiated stimulatory effect of these agents. The results indicate that cAMP regulates the growth and functions of mastocytoma P-815 cells. [35S]-Sulfated acidic glycosaminoglycans synthesized in cells at stationary phase or in cells treated with Bt2cAMP plus MIX mainly localized in the 3000-10000 x g sedimentable fraction of cell homogenates, and had a molecular weight of 200000 to 400000 based on gel filtration. This acidic glycosaminoglycan was resistant to chondroitinase ABC and the heparin-degrading enzyme present in the 20000 x g sedimentable fraction of the cells, and was identified as a highly sulfated macromolecular heparin based on behaviors on DEAE-cellulose column and on acidic electrophoresis. Cycloheximide suppressed the stimulatory effect of Bt2cAMP on the synthesis of histamine and [35S]-sulfated acidic glycosaminoglycan.

Adenosine↗

Effect of D-glucosamine on growth and several functions of cultured mastocytoma P-815 cells.

In order to elucidate the biochemical basis for the selective cytotoxicity of D-glucosamine to neoplastic cells, the effect of glucosamine on the growth and several functions of mastocytoma P-815 cells were examined. Incubation of mastocytoma cells with 5 mM glucosamine resulted in a marked inhibition of growth and a significant reduction of cellular uptake and oxidation of glucose and of cellular levels of adenosine triphosphatase (ATP). Glucosamine also reduced the uridine nucleotide pool sizes, and accumulated uridine diphosphate (UDP)-N-acetylglucosamine. However, growth inhibition by glucosamine, which was reversed by glucose, was not prevented by exogenous uridine. In addition, glucosamine suppressed the phosphorylation of thymidine and its incorporation into deoxyribonucleic acid (DNA). The suppression of cell division by glucosamine was accompanied by the elevation of several functions of mastocytoma cells, including the accumulation of adenosine-3', 5'-monophosphate (cAMP), histamine, and serotonin. The incorporation of [(35)S]SO(4)(2-) into acidic glycosaminoglycan was also increased. Of these functional alterations, the elevation of cAMP levels was the earliest detectable change, indicating that growth and functions of mastocytoma cells are also regulated by cAMP. However, glucosamine did not affect the adenylate cyclase activity of plasma membrane in vitro, suggesting the necessity of intact membrane structure for the action of glucosamine.

Adenosine Triphosphate↗

Ultrastructural localization of phosphatases in the rat parathyroid gland.

Ultrastructural localizations of phosphatases were observed in the rat parathyroid gland. Activities of alkaline phosphatase and adenosine triphosphatase were found on the caveolae or pinocytotic vesicles of the capillary endothelia. In the parenchymal cells, they were demonstrated to be stronger both at the plasma membranes facing the pericapillary space and at their transitional portions to the lateral plasma membranes than at the remaining lateral plasma membranes including microvilli. Activities of thiamine pyrophosphatase and inosine diphosphatase were detected on one or two layers of lamellae at the inner face of the Golgi apparatus, and the localization of the latter enzyme was more restricted than that of the former. Additionally, they were sometimes observed also on the blood capillary wall. Contrasted to these enzymes, acid phosphatase activity was demonstrated on the entire Golgi lamellae besides lysosomes, but not on multivesicular bodies, vacuolar bodies and storage granules.

Acid Anhydride Hydrolases↗