Publications by authors named "Y Ishiwari"

Immunosuppressant drugs are currently required by transplant recipients for the remainder of their lives, despite the many adverse effects associated with these therapies. Acute osteoporosis is one such effect, and a reproducible osteoporosis model has been established through the administration of the immunosuppressant drug FK506 in rats. The cause of this osteoporosis has been shown to be abnormal osteoclast proliferation, altering the process of bone remodeling.

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The osteosclerotic (oc/oc) mouse, a genetically distinct murine mutation that has a functional defect in its osteoclasts, also has rickets and shows an altered endochondral ossification in the epiphyseal growth plate. The disorder is morphologically characterized by an abnormal extension of hypertrophic cartilage at 10 days after birth, which is later (21 days after birth) incorporated into the metaphyseal woven bone without breakdown of the cartilage matrix following vascular invasion of chondrocyte lacunae. In situ hybridization revealed that the extending hypertrophic chondrocytes expressed type I and type II collagen mRNA, as well as that of type X collagen and that the osteoblasts in the metaphysis expressed type II and type X collagen mRNA, in addition to type I collagen mRNA.

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Abnormal amplification of epidermal growth factor receptor (EGFR) gene has been reported widely in various human tumors. However, the status of amplification of this gene in the process of carcinogenesis is not clearly defined. We used competitive polymerase chain reaction (PCR) to study whether EGFR gene is amplified and the degree of amplification in pre-malignant and malignant oral epithelial lesions, and also examined the relationship between EGFR gene aberration and the development of squamous cell carcinoma (SCC).

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We examined a patient with cleidocranial dysplasia (CCD) and cleft lip and found a new stop codon mutation in CBFA1. This mutation was a heterozygous C-to-T transition in exon 3 of CBFA1. This nucleotide change converts a CAA codon to a TAA (stop) codon at amino acid position Gln195 in the runt domain of CBFA1.

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Objective: To examine the nitric oxide (NO) production relevant to chondrocyte cell death in order to elucidate the mechanism of chondro-osteophyte formation in osteoarthrotic joints.

Design: Human chondro-osteophytes were obtained during total hip arthroplasty. Expression of inducible nitric oxide synthase (iNOS) mRNA was determined by in-situ hybridization.

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