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Biomedical subjects

S Seyedin

Publications and source records attributed to S Seyedin.

6 recordsLinked to original sources
PubMed1998

Effect of minocycline on osteoporosis.

The effect of oral minocycline on osteopenia in ovariectomized (OVX) old rats was examined in this study. Rats were divided into 4 groups: sham-operated, OVX followed by treatment with vehicle, minocycline, or 17 beta-estradiol. The treatment was initiated one day after OVX and proceeded for 8 wks. OVX reduced bone mineral density (BMD) in the whole femur and in the femoral regions that are enriched in trabecular bone. Treatment with minocycline or estrogen prevented a decrease in BMD. Femoral trabecular bone area, trabecular number, and trabecular thickness were reduced, and trabecular separation was increased by OVX. Treatment with minocycline or estrogen abolished the detrimental effects induced by OVX. OVX also reduced indices that reflect the interconnectivity of trabecular bone, and the loss of trabecular connectivity was prevented by treatment with minocycline or estrogen. Based on the levels of urinary pyridinoline, we showed that the effect of estrogen, but not minocycline, was primarily through its inhibitory effect on bone resorption. Analysis of bone turnover activity suggests that OVX increased parameters associated with bone resorption (eroded surface) and formation (osteoid surface, mineralizing surface, mineral apposition rate, and bone formation rate). Treatment with minocycline reduced bone resorption modestly and stimulated bone formation substantially. In contrast, treatment with estrogen drastically reduced parameters associated with both bone resorption and formation. We have concluded that oral minocycline can effectively prevent the decrease in BMD and trabecular bone through its dual effects on bone resorption and formation.

Amino Acids↗
PubMed1994

Direct, enzyme-linked immunoassay for urinary deoxypyridinoline as a specific marker for measuring bone resorption.

Several studies in recent years have shown that the pyridinium crosslinks of collagen provide good urinary markers of collagen degradation, primarily reflecting bone resorption. Most studies, however, were based on time-consuming HPLC assays of the crosslinks. We now describe the development of an immunoassay (ELISA) based on a monoclonal antibody for free deoxypyridinoline (Dpd) and its use in healthy individuals and patients with bone-related disorders to measure the urinary excretion of Dpd as an improved assessment of bone resorption rate. The Dpd antibody exhibited less than 1% cross-reaction with free pyridinoline and was shown to react only with free Dpd in urine, having no significant interaction with peptide forms of the crosslinks. The intra- and interassay variations were less than 10 and 15%, respectively. A total of 402 urine samples from patients and healthy volunteers were analyzed by both the immunoassay and HPLC. The ELISA results were highly correlated with those for total Dpd measured by HPLC over the full range of sample groups (r = 0.95). In normal adults, the excretion of Dpd (mean +/- SD) was 4.7 +/- 1.6 nmol/mmol creatinine, with about fivefold higher excretion rates in children. For 31 osteoporotic patients, the ELISA Dpd values (median 6.7; range 3.0-13.5 nmol/mmol Cr) were significantly higher (p < 0.0001) than the corresponding values for age- and sex-matched controls (median 4.0; range 1.8-7.4). The difference between the groups was similar for total Dpd by HPLC (osteoporotic: mean 12.8, range 4.8-30.7; controls: 6.6, range 3.0-18.1; p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Increased urinary excretion of pyridinium cross-links in cancer patients.

Pyridinoline (PYD) and deoxypyridinoline (DPD), two collagen-based cross-links found in bone, were measured by high-performance liquid chromatography in urine samples from 65 control subjects and 97 patients with either untreated or progressive cancer. Patients with cancer had significantly (P < 0.001) higher urine concentrations of PYD and DPD than did control subjects. Both cross-links were increased in cancer patients with and without clinically detectable bone metastases, although patients with bone and liver involvement had higher mean concentrations. The mean concentrations of both cross-links were also significantly higher in the urine samples of inpatients than in an outpatient ambulatory population. These findings suggest that the measurement of PYD and DPD in urine may be useful in assessing bone metastases and bone resorption in cancer patients.

Adult↗
PubMed1990

Osteoinductive factor inhibits formation of human osteoclast-like cells.

Osteoinductive factor (OIF) is a glycoprotein in bone that induces ectopic bone formation. Implantation of OIF plus transforming growth factor beta (TGF-beta) type 1 or 2 into subcutaneous tissues of rats induces formation of bone at the implantation site. Since TGF-beta is also present in bone matrix and inhibits formation of multinucleated cells that express an osteoclast phenotype in long-term human marrow cultures, we tested the effects of OIF on formation of these osteoclast-like cells to determine the effects of OIF on cells in the osteoclast lineage. We found that OIF inhibited total multinucleated cell (MNC) formation in a dose-dependent fashion and preferentially inhibited formation of MNCs that react with monoclonal antibody 23c6 (23c6-positive MNCs), an antibody that identifies osteoclasts. In addition, low concentrations of OIF in combination with low concentrations of TGF-beta acted synergistically to inhibit 23c6-positive MNC formation. The inhibition of 23c6-positive MNC formation by OIF was not mediated by prostaglandin synthesis. These data suggest that regulatory growth factors, such as OIF or TGF-beta, that are stored within the bone matrix and released when bone is resorbed can serve as natural inhibitors of osteoclast activity by inhibiting osteoclast formation.

Alprostadil↗
PubMedDate not supplied

Transforming growth factor-beta 2: cDNA cloning and sequence analysis.

We have obtained a cDNA clone coding for human transforming growth factor (TGF)-beta 2. The clone was isolated from a tamoxifen-treated human prostatic adenocarcinoma cell line (PC-3) using oligonucleotide probes based on the partial amino acid sequence of purified TGF-beta 2. The cDNA sequence predicts that TGF-beta 2 is synthesized as a 442-amino-acid polypeptide precursor from which the mature 112-amino-acid TGF-beta 2 subunit is derived by proteolytic cleavage. The proteins coded for by the human TGF-beta 1 and TGF-beta 2 cDNAs show an overall homology of 41%. The mature and amino-terminal precursor regions show 71% and 31% homology, respectively. Northern blot analysis identified TGF-beta 2 transcripts of 4.1, 5.1, and 6.5 kb using mRNA from several different sources. Analysis of polyadenylated RNA from tamoxifen-treated PC-3 cells showed that these cells contain higher numbers of transcripts for TGF-beta 1 than for TGF-beta 2, although they produce more TGF-beta 2 protein than TGF-beta 1. This suggests that there is a post-transcriptional level of regulation for the production of these proteins.

Amino Acid Sequence↗