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Biomedical subjects

J Oshima

Publications and source records attributed to J Oshima.

58 records · Page 4Linked to original sources
PubMed1987

1,25(OH)2D3 increases cytosolic Ca++ concentration of osteoblastic cells, clone MC3T3-E1.

Effect of 1,25(OH)2D3 in vitro on cytosolic Ca++ concentration of osteoblastic cells (MC3T3-E1) was studied. Marked but transient increase of cytosolic Ca++ concentration of osteoblastic cells was observed following the addition of 10 pg/ml of 1,25(OH)2D3, but not with 10 pg/ml of 24,25(OH)2D3. The increase of cytosolic Ca++ concentration of osteoblastic cells by 1,25(OH)2D3 was not observed when the cells were incubated in Ca++ free medium. Therefore, it was concluded that 1,25(OH)2D3 increased cytosolic Ca++ concentration of osteoblastic cells through the increase of Ca++ influx into the cells.

24,25-Dihydroxyvitamin D 3↗
PubMed1987

High-performance liquid chromatographic assay of a new non-steroidal anti-inflammatory agent, 2-(10,11-dihydro-10-oxodibenzo[b,f]thiepin-2-yl)propionic acid, in human plasma and urine.

A high-performance liquid chromatographic method for the quantitation of a new anti-inflammatory agent, 2-(10,11-dihydro-10-oxodibenzo[b,f]thiepin-2-yl)propionic acid (CN-100; I), has been developed. The assay consists in extracting samples containing I and mefenamic acid, the internal standard, under acidic conditions and analysis by reversed-phase chromatography using ultraviolet detection at 330 nm. Preliminary plasma concentration-time and cumulative urinary excretion profiles from a healthy subject following oral administration of the tablet formulation are presented. This method is simple, sensitive and reproducible and is applicable to studies of the pharmacokinetic behaviour of I in humans.

Administration, Oral↗
PubMedDate not supplied

Comparative aspects of the Werner syndrome gene.

Werner syndrome (WS) ("Progeria of the adult"; entry *27770 (1)) was originally defined by Dr. Otto Werner in 1904 on the basis of "scleroderma-like" thin, tight skin and bilateral cataracts in a sibship (2). Among the many systemic clinical features of WS, the various progeroid features have drawn special attention. WS is caused by a mutation at the Werner syndrome gene (WRN) locus, which belongs to the family of RecQ helicases (GenBank accession number L76937)(3). This review focuses on the comparative aspects of WRN, including differential gene action within humans and the potential differences between species, particularly the mouse and human.

Animals↗