Biomedical subjects

Kaoru Oikawa

Publications and source records attributed to Kaoru Oikawa.

4 recordsLinked to original sources

PubMed2006

A crucial role for matrix metalloproteinase 2 in osteocytic canalicular formation and bone metabolism.

Extracellular matrix production and degradation by bone cells are critical steps in bone metabolism. Mutations of the gene encoding MMP-2, an extracellular matrix-degrading enzyme, are associated with a human genetic disorder characterized by subcutaneous nodules, arthropathy, and focal osteolysis. It is not known how the loss of MMP-2 function results in the pathology. Here, we show that Mmp2(-/-) mice exhibited opposing bone phenotypes caused by an impaired osteocytic canalicular network. Mmp2(-/-) mice showed decreased bone mineral density in the limb and trunk bones but increased bone volume in the calvariae. In the long bones, there was moderate disruption of the osteocytic networks and reduced bone density throughout life, whereas osteoblast and osteoclast function was normal. In contrast, aged but not young Mmp2(-/-) mice had calvarial sclerosis with osteocyte death. Severe disruption of the osteocytic networks preceded osteocyte loss in Mmp2(-/-) calvariae. Successful transplantation of wild-type periosteum restored the osteocytic canalicular networks in the Mmp2(-/-) calvariae, suggesting local roles of MMP-2 in determining bone phenotypes. Our results indicate that MMP-2 plays a crucial role in forming and maintaining the osteocytic canalicular network, and we propose that osteocytic network formation is a determinant of bone remodeling and mineralization.

Animals↗

PubMed2006

[Cost-effectiveness analysis of routine immunization for varicella in Japan].

OBJECTIVE: Immunization for varicella is not currently included in routine immunizations in Japan. This study was conducted to assess test its cost-effectiveness when it becomes a routine. METHODS: We surveyed and collected information for the year beginning 15th June 2004 in one area. Almost all 11 pediatric clinics or hospitals in the area cooperated in this survey. There was a questionnaire form for families and for doctors. Absent days from routine tasks, i.e., job, housekeeping or study, for family nursing and others were asked on family form. Medical costs and other costs were asked on doctor form. Neither form included the patient's name or name of the medical institution. Doctors explained this survey to patients' family on their first visiting day and asked to cooperate. If they refused the doctor form was also discarded. Since family form was written after recovery and mailed, cooperation in this survey was voluntary. Opportunity cost for family nursing is estimated as opportunity cost based on the 2002 Basic Surveillance of Wage Structure. The burden of sequel cases was estimated assuming six million yen per Quality-adjusted Life Years (QALY). Total number of patients was estimated to be 0.84 million, which includes unvaccinated people in a birth cohort. We adopted incremental benefit cost ratios form societal viewpoint as a measure. RESULTS: We collected 402 data from the doctor form and 265 from the family form. Total disease burden in all of Japan is estimated to be 52.2 billion yen, but opportunity cost accounted for 80%. The incremental benefit cost rations averaged more than 4 when vaccination cost is assumed to be five to twelve thousand yen. The lower limit of the confidence intervals is about 1.5. DISCUSSION AND CONCLUSION: The disease burden of varicella was greater than measles in 2000, when there were measles 0.2 million patients. The incremental benefit cost ratio showed that there will almost surely be an additional benefit due to routine immunization is greater than the additional cost. Therefore, we found strong evidence for routine immunization for varicella.

Chickenpox↗

PubMed2005

[Bone mass regulation].

Explore the source record for details and available documents.

Adaptor Proteins, Signal Transducing↗

PubMed2004

Tob deficiency superenhances osteoblastic activity after ovariectomy to block estrogen deficiency-induced osteoporosis.

Tob (transducer of erbB2) is a member of antiproliferative family proteins and acts as a bone morphogenic protein inhibitor as well as a suppressor of proliferation in T cells, which have been implicated in postmenopausal bone loss. To determine the effect of Tob deficiency on estrogen deficiency-induced bone loss, we analyzed bone metabolism after ovariectomy or sham operation in Tob-deficient mice. Ovariectomy in WT mice decreased trabecular bone volume and bone mineral density (BMD) as expected. In Tob-deficient mice, ovariectomy reduced bone volume and BMD. However, even after ovariectomy, both trabecular bone volume and BMD levels in Tob-deficient bone were comparable to those in sham-operated WT bones. Bone formation parameters (mineral apposition rate and bone formation rate) in the ovariectomized Tob-deficient mice were significantly higher than those in the ovariectomized WT mice. In contrast, the ovariectomy-induced increase in the bone resorption parameters, osteoclast surface, and osteoclast number was similar between Tob-deficient mice and WT mice. Furthermore, in ex vivo nodule formation assay, ovariectomy-induced enhancement of nodule formation was significantly higher in the bone marrow cells from Tob-deficient mice than in the bone marrow cells from ovariectomized WT mice. Both Tob and estrogen signalings converge at bone morphogenic protein activation of alkaline phosphatase and GCCG-reporter gene expression in osteoblasts, revealing interaction between the two signals. These data indicate that Tob deficiency prevents ovariectomy-induced bone loss through the superenhancement of osteoblastic activities in bone and that this results in further augmentation in the bone formation rate and the mineral apposition rate after ovariectomy in vivo.

3T3 Cells↗