bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of measles virus nucleocapsid transcripts in circulating blood cells from patients with paget disease
Authors: Reddy Sakamuri V. , Singer Frederick R. , Mallette Lawrence , Roodman G. David 
Published: February 2010

Abstract
Paget disease of bone is characterized by abnormalities in all phases of bone remodeling, but the fundamental cellular abnormality resides in the osteoclast (OCL). Osteoclasts in bone involved by Paget disease contain viral-like nuclear and cytoplasmic inclusions that react with antibodies directed against paramyxovirus nucleocapsid proteins, such as measles virus, respiratory syncytial virus, or canine distemper virus. However, the identity of the virus or the mechanisms responsible for its persistence or pathologic role in Paget disease is unclear. Furthermore, although Paget disease persists for many years, it remains a highly localized process with new lesions rarely if ever developing in previously unaffected bones. Since osteoclasts are formed by fusion of mononuclear precursors derived from colony forming unit-granulocyte macrophage (CFU-GM), the granulocyte-macrophage progenitor, we used reverse transcriptase polymerase chain reaction (RT-PCR) analysis to determine if CFU-GM, more differentiated osteoclast precursors, and peripheral blood cells derived from CFU-GM express measles virus nucleocapsid (MV-N) transcripts. We found that osteoclast precursors, as well as peripheral blood mononuclear cells, express MV transcripts in 9 of 13 patients. Sequence analysis of the PCR amplified products confirmed nucleotide identity of MV-N transcripts expressed in peripheral blood and bone marrow-derived cells from the same patient. In contrast, MV-N transcripts were not detected in OCL precursors or the peripheral blood from 10 normal subjects. In situ hybridization studies using 35S-labeled antisense riboprobes to MV-N transcripts further confirmed the expression of MV transcripts in these cells. Sequence analysis of the PCR amplified product from one of these patients also identified a novel mutation that converted lysine441 to glutamic acid441 in the MV-N transcript. These data demonstrate that OCL precursors and circulating peripheral blood cells also express MV transcripts in patients with Paget disease and suggest that the pagetic marrow microenvironment plays a critical role in maintaining the highly localized nature of the lesions in Paget disease. (J Bone Miner Res 1996;11:1602–1607)
Transforming growth factor-β stimulates bone resorption in neonatal mouse calvariae by a prostaglandin-unrelated but cell proliferation-dependent pathway
Authors: Dr. Lerner Ulf H. 
Published: February 2010

Abstract
The relationships between bone resorption, prostanoid formation, and cell proliferation in cultured neonatal mouse calvariae stimulated with transforming growth factor-β (TGF-β) have been examined. Bone resorption was assessed by analyzing the mobilization of minerals (45Ca, Ca2+, Pi) and the release of 3H from bones prelabeled with [3H] proline. Prostanoid formation was determined by analyzing the amounts of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1α (the stable breakdown product of PGI2) in culture media. Purified porcine TGF-β1 and recombinant human TGF-β2 stimulated the release of 45Ca and the formation of prostanoids. The effects were time and dose dependent. The concentrations of TGF-β1 and TGF-β2 causing half maximal stimulation of 45Ca release were 1 and 0.1 ng/ml, respectively. TGF-β1 also enhanced the release of 3H from [3H]proline labeled bones and the mobilization of Ca2+ and Pi from unlabeled bones, as well as the release of lysosomal enzymes (β-N-acetylglu-cosaminidase). The degree of stimulation of mineral mobilization and matrix degradation was less than that obtained in bones stimulated with parathyroid hormone or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). TGF-β1-induced stimulation of 45Ca release was inhibited by calcitonin, acetazolamide, and the bisphosphonate AHPrBP, three different osteoclast inhibitors. In contrast to the escape from calcitonin-induced inhibition seen in parathyroid hormone (PTH)-stimulated bones, the inhibitory effect of calcitonin in TGF-β1-stimulated bones persisted in long-term cultures (144 h). The stimulatory effect of TGF-β1 was inhibited by anti-TGF-β1 and by γ-interferon (1000 U/ml). Indometacin (1 μM), flurbiprofen (1 μM), and meclofenamic acid (1 μM) completely abolished the stimulatory effect of TGF-β1 on PGE2 and 6-keto-PGF1α formation without affecting TGF-β1-induced stimulation of 45Ca release. Similarly, the stimulatory effect of TGF-β2 on 45Ca release was unaffected by indomethacin. In bones in which prostaglandin formation was abolished by indomethacin, a 45Ca release response to TGF-β1 was obtained at 12 h. The mitotic inhibitor hydroxyurea inhibited TGF-β1 but not PTH-induced 45Ca release. These data demonstrate that TGF-β1 and TGF-β2 have the capacity to stimulate bone resorption and prostanoid formation in neonatal mouse calvariae, but that the effect of TGF-β on bone resorption is unrelated to prostanoid formation. In addition, it is shown that bone resorption stimulated by TGF-β is dependent on cell replication. (J Bone Miner Res 1996;11:1628-1639)
Na+/Ca2+ exchange in rat osteoblast-like UMR 106 cells
Authors: White Kenneth E. , Gesek Frank A. , Friedman Peter A. 
Published: February 2010

Abstract
Ca2+ efflux from osteoblasts is thought to be mediated by Na+/Ca2+ exchange and by a plasma membrane Ca2+-ATPase. The presence of plasma membrane Na+/Ca2+ exchange was determined in rat UMR 106 osteosarcoma cells by functional and molecular studies. Na+/Ca2+ exchange activity was tested by measuring changes of [Ca2+]i in single cells. After Na+ loading the cells and removing extracellular Na+, the direction of exchange was reversed and [Ca2+]i increased by 100%. Multiple isoforms of the NCX1 gene product, encoding plasma membrane Na+/Ca2+ exchangers, were cloned from UMR 106 cells and a sample of primary human osteoblasts using homology-based RT-PCR. Isoforms NACA3, NACA7, and NACA10 were found in UMR 106 cells, whereas human osteoblasts expressed NACA3 and NACA7. Transcripts for NCX2 and the Na+/Ca2+, K+ exchanger were not detected. Northern analysis of UMR 106 cells with a probe to the NCX1 gene product revealed the presence of a transcript of 7 kb, the size of the exchanger message. Western analysis of UMR 106 cell membrane preparations with a polyclonal antibody specific for the NCX1 exchanger showed the presence of reacting proteins consistent with the reported masses of the exchanger at 125 and 85 kD. These results demonstrate Na+-dependent Ca2+ efflux from UMR 106 cells and the presence of several NACA isoforms in UMR 106 and primary human osteoblasts. (J Bone Miner Res 1996;11:1666-1675)
Characteristics of NaF-induced differentiation of HL-60 cells
Authors: Kawase Tomoyuki , Oguro Akira , Orikasa Michiaki , Burns Douglas M. 
Published: February 2010

Abstract
Sodium fluoride (NaF) is known to stimulate osteoblastic bone formation, but little attention has been given to the possibility that NaF also affects bone resorption and the differentiation of osteoclastic progenitor cells. When human promyelocytic HL-60 cells were treated with NaF (0.5 mM, 0–4 days), cell proliferation was inhibited, and the addition of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) (10 nM, 0–4 days) augmented this antiproliferative effect. NaF increased cellular reduction of nitroblue tetrazolium (NBT), and this effect was strongly augmented by 1,25(OH)2D3. In addition, NaF produced marked changes in cellular morphology, increased cellular adhesion to plastic, reduced the nuclear/cytoplasmic ratio, and increased cellular expression of chloroacetate esterase, but failed to alter cellular nonspecific esterase activity. Furthermore, NaF increased expression of CD11b and CD66b, and this stimulation was enhanced by adding 1,25(OH)2D3. The sum of these changes in classical promyelocytic cellular indices suggest: (1) that NaF stimulates the early stages of HL-60 differentiation toward a granulocyte-like cell and (2) that 1,25(OH)2D3 promotes these actions of NaF. Additional experiments aimed at further understanding the NaF-induced conversion of HL-60 cells identified further changes. NaF also increased cellular production of prostaglandin E2 (PGE2) and nitric oxide (NO) and induced expression of inducible nitric oxide synthase (iNOS); 1,25(OH)2D3 once again augmented these NaF-induced effects. Similarly, NaF stimulated the production of interleukin 1α (IL-1α), IL-6, and tumor necrosis factor-α, and 1,25(OH)2D3 again strongly enhanced these effects. Indomethacin completely blocked stimulation of NBT reduction, NO production, and iNOS expression induced by NaF plus 1,25(OH)2D3; adding exogenous PGE2 (0.1-10 ng/ml) to these indomethacin-blocked cultures dose-dependently restored NO production. These additional findings together with the observed slow onset (24-48 h) of NaF and 1,25(OH)2D3 interaction strongly suggest that 1,25(OH)2D3 acts as a cofactor with NaF primarily through interaction with an endogenous NaF-induced cyclo-oxygenase product(s), quite possibly PGE2 itself. Such a mechanism for NaF and 1,25(OH)2D3 interaction would be strongly analogous to the interaction we have recently demonstrated between 1,25(OH)2D3 and PGE1 on the differentiation of HL-60 cells. (J Bone Miner Res 1996;11:1676-1687)
Inducible cyclo-oxygenase (COX-2) mediates the induction of bone formation by mechanical loading in vivo
Authors: Forwood M. R. 
Published: February 2010

AbstractIn vivo, indomethacin blockade of bone formation has been used to illustrate the role of prostaglandins. Indomethacin blocks the constitutive (COX-1) and inducible (COX-2) forms of cyclo-oxygenase, and is therefore nonspecific in its action. To test the hypothesis that COX-2 mediates the bone formation response to loading, rats were treated with vehicle, NS-398 (a specific COX-2 inhibitor) or indomethacin at 0.02, 0.2, or 2.0 mg/kg p.o. 3 h before loading the right tibia in four-point bending. Bending or sham loads of 65 N were applied for one bout of 300 cycles and bone formation assessed 5–8 days after loading. Mechanically induced bone formation at the endocortical surface was calculated by subtracting formation indices of the left leg (control) from those of the right (loaded), and woven bone surface and area were measured at the periosteal surface. Endocortical bone formation was significantly increased by bending but not sham loading (p &lt; 0.05). The increase in the endocortical bone formation rate and mineralizing surface caused by bending was only partially inhibited by indomethacin, even at the highest dose, whereas NS-398 completely blocked bone formation at all doses (p &lt; 0.05). The mineral apposition rate was depressed in a dose-response fashion by NS-398 (p &lt; 0.05), but not by indomethacin. Woven bone formation at the periosteal surface was not prevented by treatment with indomethacin nor NS-398, suggesting that its formation is not dependent on prostaglandin production. These data suggest that induction of COX-2 is important for lamellar bone formation elicited by mechanical strain. (J Bone Miner Res 1996;11:1688-1693)
Demineralized bone matrix mediates differentiation of bone marrow stromal cells in vitro: Effect of age of cell donor
Authors: José Becerra , Andrades José A. , Ertl Delia C. , Sorgente Nino , Nimni Marcel E. 
Published: February 2010

Abstract
Bone maintenance requires a continuous source of osteoblasts throughout life. Its remodeling and regeneration during fracture repair is ensured by osteoprogenitor stem cells which are part of the stroma of the bone marrow (BM). Many investigators have reported that in cultured BM stromal cells there is a cell population that will differentiate along an osteogenic lineage if stimulated by the addition of osteogenic inducers, such as dexamethasone (dex), beta-glycerophosphate (β-GP), transforming growth factor beta-1 (TGF-β1) and bone morphogenetic protein-2 (BMP-2). Here we report the effects of demineralized bone matrix (DBM) on the osteogenic differentiation of BM stromal cells in vitro, using morphological criteria, alkaline phosphatase (AP) activity, and calcium accumulation. DBM and DBM-conditioned medium (DBMcm) enhanced bone formation in the presence of dex and β-GP, whereas DBM particles caused changes in the cell phenotype. Temporal expression of total and skeletal AP by BM stromal cells from 4-week-old rats showed a biphasic pattern enhanced by DBM and suggesting the presence of two cell populations. In one population, AP synthesis reaches a maximum during the first week in culture, following which cells either die or loose their ability to synthesize AP. A second, less abundant population begins to proliferate and synthesize AP during the second and third weeks. The synthesis of AP, which often decreases by the third week, can be maintained at high levels only if DBM is added to the cultures. BM stromal cells isolated from 24- and 48-week-old rats showed a decrease or loss of this biphasic AP expression pattern compared with cells isolated from 4-week-old rats. The addition of DBM to cultures derived from 24- and 48-week-old rats stimulated mostly the second cell population to synthesize AP, suggesting that DBM contains a factor(s) that acts on a specific bone marrow cell population by increasing the proliferation of active cells or inducing the differentiation of dormant cells. (J Bone Miner Res 1996;11:1703-1714)
Effects of recombinant human growth hormone and insulin-like growth factor-I, with or without 17β-estradiol, on bone and mineral homeostasis of aged ovariectomized rats
Authors: Verhaeghe J. , van Bree R. , van Herck E. , Thomas H. , Skottner A. , Dequeker J. , Mosekilde L. I. , Einhorn T. A. , Bouillon R. 
Published: February 2010

Abstract
This study aimed to evaluate whether recombinant human growth hormone (rhGH) or insulin-like growth factor-I (rhIGF-I) can reverse or prevent further bone loss in aged osteopenic ovariectomized (OVX) rats and to compare their effects with those of 17β-estradiol (E2). Twelve-month-old rats were OVX, remained untreated for 8 weeks, and subsequently received daily subcutaneous (SC) injections of rhGH (75 μ/day), rhIGF-I (250 μg/day), E2 (1.5 μg/day), and their respective combinations during 8 weeks, and were then compared with sham-operated, pretreatment OVX, and saline-treated OVX rats. A single sc injection of rhGH resulted in peak hGH concentrations after 90 minutes, with a half-life of 124 minutes; the highest plasma IGF-I concentrations were reached 45 minutes after rhIGF-I injection (+57% vs. baseline) with a gradual decline thereafter. Measurements included: biochemical parameters of bone remodeling (plasma osteocalcin and urinary pyridinolines); histomorphometry of proximal tibial metaphysis; DXA of femur; biomechanical analysis of femur and fifth lumbar vertebra (L5); plasma 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), and calbindin-D9K in duodenal mucosa. Whereas all E2-treated OVX rats had much suppressed bone remodeling, rhGH or rhIGF-I had no effect on any biochemical or histomorphometrical parameter of remodeling. The bone mineral density (BMD) at the distal femoral metaphysis as well as parameters of strength at L5 were maintained at pretreatment values in OVX rats treated with E2, GH, or IGF-I, but not in saline-treated OVX rats; their effects were not additive, however. Trabecular bone volume in the tibial metaphysis was also higher in rats treated with these agents than in saline-treated rats, but this was more apparent at the primary than at the secondary spongiosa, suggesting that their mechanism of action is on primary spongiosa formation or breakdown. E2 alone was ineffective to augment the BMD at the femoral diaphysis; however, the diaphyseal BMD was 12–14% higher (p &lt; 0.01) after 8 weeks of GH treatment than in pretreatment or saline-treated OVX rats and sham-operated rats, while IGF-I was less effective than GH. GH or IGF-I treatment had no effect on plasma 1,25(OH)2D3 or duodenal calbindin-D9K concentrations, but the combination of GH or IGF-I with E2 potentiated the effect of E2 to stimulate calbindin-D9K concentrations and urinary calcium excretion, indicating “hyperabsorption hypercalciuria”. In conclusion, the administration of rhGH and rhIGF-I, like that of E2, into aged OVX rats prevents further loss of bone mass and strength at sites containing trabecular bone. In addition, rhGH increases cortical bone mass above pretreatment values. (J Bone Miner Res 1996;11:1723-1735)
The effect of androgen treatment on bone metabolism in female-to-male transsexuals
Authors: Lips Paul , van Kesteren Paul J. M. , Asscheman Henk , Gooren Louis J. G. 
Published: February 2010

Abstract
Histomorphometry was performed in iliac crest biopsies from 15 female-to-male (F-M) transsexuals with a mean age of 30 ± 6.1 (SD) years. At the time of study, they had been treated with parenteral testosterone esters (250 mg/2 weeks) or oral testosterone undecanoate (160 mg/day). The median androgen treatment duration was 39 months. The patients had undergone hysterectomy and bilateral ovariectomy. The bone biopsy was obtained after double tetracycline labeling. Histomorphometric results were compared with data from 8 postmenopausal women and with data from 11 healthy men who had died suddenly. Dynamic parameters were compared with data from the literature. The biochemical picture was characterized by serum testosterone concentrations lower than in eugo-nadal men and estradiol concentrations lower than in eugonadal women and elevated gonadotrophin levels. The bone mineral density in the F-M transsexuals was as expected for age (Z-score −0.31 ± 1.49). Cortical thickness was significantly higher in F-M transsexuals than in both control groups. Trabecular bone structure was similar in F-M transsexuals and both control groups. The bone formation parameters were generally lower in F-M transsexuals than in the control groups. The eroded surface was lower in F-M transsexuals than in postmenopausal women. The low bone turnover and preservation of trabecular bone is consistent with the assumption that testosterone treatment protects the bone in these F-M transsexuals from the deleterious effects of estrogen deficiency. The increased cortical thickness suggests an anabolic effect of the testosterone treatment. (J Bone Miner Res 1996;11:1769–1773)
Serum N-terminal osteocalcin is a good indicator for estimating responders to hormone replacement therapy in postmenopausal women
Authors: Chen Jui-Tung , Hosoda Kenji , Hasumi Katsuhiko , Ogata Etsuro , Shiraki Masataka 
Published: February 2010

Abstract
To estimate the response to hormone replacement therapy (HRT) by bone metabolic markers, 36 patients with postmenopausal osteoporosis or osteopenia were studied to assess the correlation between percent baseline changes in lumbar bone mineral density (BMD) after 12 months and those in various bone metabolic markers after 3, 6, and 12 months of HRT. All the patients were treated with 0.625 mg of conjugated estrogen and 2.5 mg of medroxyprogesterone per day and continued for 12 months. BMD was significantly increased up to 4.19 ± 0.87% after 6 months and 4.93 ± 1.27% after 12 months of HRT (p = 0.0001 by analysis of variance). In accordance with this, changes in the levels of osteocalcin (p = 0.041), alkaline phosphatase (p = 0.0001), N-terminal osteocalcin (p = 0.0001), urinary excretion of pyridinoline/Cr (p = 0.0001), and deoxypyridinoline/Cr (p = 0.0001) were significantly decreased, respectively. Among these bone metabolic markers, only the change in the serum N-terminal osteocalcin at 3 months (r = 0.557, p = 0.0022), at 6 months (r = 0.470, p = 0.0184), and at 12 months (r = 0.545, p = 0.0061) significantly correlated with the change in BMD 12 months after HRT. The elution profiles of immunoreactive osteocalcin-related molecules in serum fractionated by reverse-phase high performance liquid chromatography revealed that the N-terminal fragment as well as the intact osteocalcin molecule decreased after 3 months of HRT. These results demonstrate that N-terminal osteocalcin is a suitable predictor for estimating good responders to HRT in postmenopausal women. (J Bone Miner Res 1996;11:1784–1792)
The hepatocytes of the brown trout (Salmo trutta fario): A stereological study of some cytoplasmic components with the breeding cycle
Authors: Rocha Eduardo , Rocha Maria J. , Lobo‐Da‐Cunha Alexandre , Galante Maria H. , Monteiro Rogério A.F. 
Published: February 2010

AbstractSex differences exist in fish hepatocytes, but studies for characterizing their cytology throughout the breeding cycle are still scarce; suggesting changes, but most lacking quantitative data. To address this limitation, to complement baseline data generated from the brown trout model, and to prove that sex‐specific seasonal changes exist, we made an unbiased stereological evaluation of the hepatocytic cytoplasm. Unprecedentedly for fish liver, the stereological design was exempt from model (biased) assumptions. Five (3 years old) animals per sex were studied in endogenous vitellogenesis, exogenous vitellogenesis, and spawning season end. Liver pieces for analysis were systematically sampled. Stereology was done in transmission electron microscopy (TEM) micrographs. Primary data generated relative volume estimates of the major cytoplasmic components. Such values were used for deriving absolute volumes (per cell and per liver). Lipid droplets did not show changes. As to other targets, trends at cell and liver levels were not always equal. If the hepatocyte was the reference space, the contents in mitochondria, dense bodies, glycogen, and cytosol changed seasonally, in both sexes. If taking the liver as the reference, changes attained the Golgi apparatus and rough endoplasmic reticulum (RER), besides dense bodies, glycogen (in females), and cytosol. The components volumes (namely per liver) were often positively (negatively for glycogen) correlated with the ovary weight, disclosing new associations and implications in fish. While also offering gold‐standard data for backing morphofunctional correlations and pathology, we revealed a new process by which females increase the amount of RER and Golgi throughout vitellogenesis, breaking from the idea on how this event happens in fish. Microsc. Res. Tech. 73:766–778, 2010. © 2010 Wiley‐Liss, Inc.
Gorham‐Stout disease of the temporal bone
Authors: Mowry Sarah , Canalis Rinaldo 
Published: February 2010

AbstractGorham‐Stout (GS) disease is a rare disease of the bone and is also known as massive osteolysis. Less than 200 cases have been reported in the world literature. A 29‐year‐old female with a diagnosis of GS disease was identified. She complained of aural fullness and tinnitus bilaterally. Demineralization and moth‐eaten changes of the osseous structures of the skull base and posterior fossa were prominent. The left mastoid air cells were opacified and erosion extended to the left jugular foramen, left hypoglossal canal, left stylomastoid process, and left eustachian tube. The radiographic findings and brief literature review are presented. Laryngoscope, 2010