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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
1995-4-3
|
| pubmed:abstractText |
In order to examine the mechanism of the anabolic effect of parathyroid hormone (PTH) on bone formation, human PTH(1-34) [hPTH(1-34)] (30 micrograms/kg) was injected subcutaneously to 9-week-old rats 5 times a week for 1 or 3 weeks. Trabecular bone volume (BV/TV) in the tibial metaphysis was not significantly different between the PTH- and vehicle-treated groups, but the parameters related to bone formation, including osteoid surface (OS/BS), mineralizing surface (MS/BS), mineral apposition rate (MAR), and bone formation rate (BFR/BS), were significantly increased as early as 1 week after PTH treatment. And the parameters related to bone resorption including eroded surface (ES/BS) and osteoclast number (N.Oc/BS) were also significantly increased as early as 1 week after PTH treatment. Treatment with PTH for 1 week induced no significant increase in bone mineral density at the femoral metaphysis, whereas the same treatment for 3 weeks induced a significant increase. When bone marrow cells isolated from femora and tibiae of either PTH- or vehicle-treated rats were cultured at a high density (2 x 10(7) cells/one well of 24-multiwell plate), cellular alkaline phosphatase (ALP) activity was significantly increased in the cells isolated from PTH-treated rats compared with vehicle-treated rats. When bone marrow cells were cultured at a low density (4 x 10(6) cells/a one well of 6-multiwell plate) to generate colonies (colony forming unit-fibroblastic, CFU-F), PTH induced apparent increases in both the total number of CFU-F and the number of ALP-positive CFU-F.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:issn |
8756-3282
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
15
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
717-23
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7873302-Alkaline Phosphatase,
pubmed-meshheading:7873302-Animals,
pubmed-meshheading:7873302-Biomechanics,
pubmed-meshheading:7873302-Bone Density,
pubmed-meshheading:7873302-Bone Development,
pubmed-meshheading:7873302-Bone Marrow,
pubmed-meshheading:7873302-Bone Marrow Cells,
pubmed-meshheading:7873302-Cell Count,
pubmed-meshheading:7873302-Cell Differentiation,
pubmed-meshheading:7873302-Cell Division,
pubmed-meshheading:7873302-Cells, Cultured,
pubmed-meshheading:7873302-Colony-Forming Units Assay,
pubmed-meshheading:7873302-Female,
pubmed-meshheading:7873302-Femur,
pubmed-meshheading:7873302-Humans,
pubmed-meshheading:7873302-Injections, Subcutaneous,
pubmed-meshheading:7873302-Osteoclasts,
pubmed-meshheading:7873302-Parathyroid Hormone,
pubmed-meshheading:7873302-Peptide Fragments,
pubmed-meshheading:7873302-Rats,
pubmed-meshheading:7873302-Rats, Sprague-Dawley,
pubmed-meshheading:7873302-Stem Cells,
pubmed-meshheading:7873302-Teriparatide,
pubmed-meshheading:7873302-Tibia
|
| pubmed:articleTitle |
Increased bone formation by intermittent parathyroid hormone administration is due to the stimulation of proliferation and differentiation of osteoprogenitor cells in bone marrow.
|
| pubmed:affiliation |
Department of Orthopaedic Surgery, Niigata University School of Medicine, Japan.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|