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S Nakakita

Publications and source records attributed to S Nakakita.

4 recordsLinked to original sources
PubMed2006

Electron microscopic investigation on the osteogenesis at titanium implant/bone marrow interface under masticatory loading.

Electron microscopic investigation on osteogenetic process at the implant surface of threadless rod-type titanium implants with different surface roughness of Ra 0.4 +/- 0.01 microm, Sm 2.6 +/- 0.3 microm and Ra 2.0 +/- 0.12 microm, Sm 36 +/- 9.1 microm was performed at the early stage of 21 and 42 days post implantation into the jawbones of four beagles under the load bearing condition of functional mastication. The implant surfaces were covered with a blood clot and haematopoietic stem cells (HSC) including phagocytic monocytes immediately after the implantation. Successively, osteogenic stem cells (OSC) migrated from cortical and/or trabecular endosteum to the HSC-layer on the implant surface. The new bone formation at the implant/bone marrow interface was developed by collaboration of osteomediator cells (OMC) differentiated from monocytes of HSC and osteoblast phenotype cells of OSC derived from endosteum of cortical bone and/or trabecular. The new bone layer at the implant surface consisted of two layers, solution-mediated calcification layer of pseudo bone and cell (osteoblast) -mediated calcification layer of true bone. The pseudo bone was produced by solution-mediated calcification of OMC- and HSC-remnants near by the implant surface. The bone healing process at the implant/bone marrow interface depended upon two factors; the migration of OSC from cortical and/or trabecular endosteum to the implant surface and the healing potentiality. Topographic dependency upon the bone healing potential at implant/bone marrow interface was not confirmed in this experiment under the load bearing condition of functional mastication.

Animals↗
PubMed1998

Development-dependent expression of complex-type sugar chains specific to mouse brain.

We previously detected a fucosylagalactobiantenna with a bisecting GlcNAc residue (BA-2) and one lacking the GlcNAc residue linked to the Manalpha1-3 residue of BA-2 (BA-1), which were enriched specifically in mouse brain [Shimizu, H., Ochiai, K., Ikenaka, K., Mikoshiba, K., and Hase, S. (1993) J. Biochem. 114, 334-338]. Pyridylamino sugar chains were prepared from mouse brains of various ages, and BA-1 and BA-2 were quantified after separation by HPLC. In cerebrum, BA-1 was scarcely expressed in newborn brain but gradually increased in amount during development, while expression of BA-2 reached a maximum 1 week after birth followed by a rapid decrease; in adult mice, the amount of BA-1 was almost the same as that of BA-2. In cerebellum, expression of BA-1 was lower than that of BA-2 at all stages. Glycoproteins with the BA-1 and BA-2 structures were enriched in the membrane fraction, and the glycoproteins solubilized were purified by lectin-affinity chromatography and gel filtration. The results indicated that BA-1 and BA-2 occurred in glycoproteins of more than 20 kDa in cerebellum, but most BA-1 and BA-2 were found in a 80-200 kDa fraction in cerebrum. These results show that the two brain-specific sugar chains are developmentally regulated and linked to the membrane-associated glycoproteins of subcellular organellas.

Animals↗
PubMed1998

NAD+ biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes--effect of clofibrate-feeding.

NAD+ biosynthesis from tryptophan in the presence of nicotinic acid or vice versa by rat hepatocytes was investigated. In the control hepatocytes, NAD+ synthesis from tryptophan was not affected by nicotinic acid from 0.026 to 0.26 mM. NAD+ synthesis from nicotinic acid was slightly inhibited with varying concentrations of tryptophan from 0.1 to 1.0 mM. In the clofibrate-treated hepatocytes, NAD+ synthesis from tryptophan was greatly increased (234% of the control), while that from nicotinic acid was decreased (71.2% of the control). Both, NAD+ synthesis from tryptophan and that from nicotinic acid were decreased by the coexisting nicotinic acid or tryptophan. Total amount of NAD+ synthesized from tryptophan and nicotinic acid at their physiological concentrations was significantly higher than that in the control hepatocytes as a result of a large increase of NAD+ synthesized from tryptophan. When the metabolic flux of 0.1 or 0.5mM tryptophan was investigated, the glutarate pathway was suppressed in the clofibrate-treated hepatocytes, the quinolinic acid-NAD+ flux being elevated. Similarly to clofibrate, DEHP and CPP revealed an increase in NAD+ synthesis from tryptophan. Mutual relationship of NAD+ biosyntheses from tryptophan and nicotinic acid in rat hepatocytes is discussed and the relevance with peroxisomal proliferation is suggested.

Animals↗