bluuebunny/crossref_metadata_2025_split huggingface dataset:
Equivalency of various methods for estimating osteoid seam width
Authors: Quarles L. Darryl , Lobaugh Bruce 
Published: February 2010

Abstract
We compared the true osteoid seam width (TOSW) as measured by a modification of the orthogonal intercept lengths with various methods of estimating seam widths, including (1) the commonly used length measurements at four equidistant points (O.Wi/4PT), (2) osteoid area divided by the osteoid perimeter (O.Ar/O/Pm) or the bone/osteoid interface (O.Ar/B.Bd), and (3) a novel method for estimating seam width defined as the osteoid area divided by the major axis of the seam (O.Ar/Axis). All methods for approximating osteoid seam width significantly exaggerated the true osteoid seam dimension by an amount that ranged from 16 to 23%. However, the relative accuracy of all methods of estimating osteoid seam width are equivalent as evidenced by the similar mean difference from the TOSW (3.4, 4.1, 5.1, and 3.8) demonstrated by O.Wi/5PT, O.Ar/Axis, O.Ar/O.Pm, O.Ar/B.Bd, respectively. Regression analysis of the various estimates of seam width on TOSW also demonstrated the equivalency of these methods. Moreover, all estimates could be employed to discriminate seams of normal dimensions from abnormally wide seams in bone specimens derived from patients with osteomalacia.
Differences between the methods, however, were observed that may have practical importance. In this regard, the direct procedure of determining distance demonstrated less variance than the indirect estimate of width. As a result, the direct measurement required fewer samples (n = 13) to detect a significant difference to normal and could discriminate smaller deviations in seam width (1.7 μm) at a given sample size compared with O.Ar/Axis (n = 28; 2.9 μm), O.Ar/O.Pm (n = 42; 3.4 μm), and O.Ar/B.Bd (n = 42; n = 3.2). However, in spite of the differences in the various methods, all width estimates can be successfully employed to discriminate small changes in seam widths provided that adequate numbers of seams are evaluated and mean values compared.
Noninvasive axial and peripheral assessment of bone mineral content: A comparison between osteoporotic women and normal subjects
Authors: van Berkum F.N.R. , Birkenhäger J.C. , Zeelenberg J. , Pols H.A.P. , Birkenhäger-Frenkel D.H. , van Veen L.C.P. , Trouerbach W.T. , Stijnen T. 
Published: February 2010

Abstract
We compared different methods of bone densitometry in women with spinal osteoporosis and normal subjects to assess their discriminatory capability. The methods used included: quantitative computed tomography of the spine (QCT) specified as to trabecular (QCTtrab) and cortical bone (QCTcort), dual-photon absorptiometry of the spine (DPAspine), single-photon absorptiometry of the distal and proximal forearm (SPAdist and SPAprox), and quantitative roentgen microdensitometry of the phalanx (QMD). A total of 25 postmenopausal osteoporotic women and 24 healthy comparison subjects matched for age and years since menopause were studied. In the osteoporotic group an average decrement of the axial bone mineral density of −50% (p &lt; 0.001) and −20% (p &lt; 0.001) were observed for QCTtrab and QCTcort, respectively. For DPAspine, SPAdist, SPAprox, and QMD the difference between normal and osteoporotic subjects was −20% (p &lt; 0.001), −12% (p &lt; 0.05), −7% (NS), and −6% (NS), respectively. With the peripheral measurements (SPA and QMD), alone or in combination, no adequate discrimination between women with or without vertebral compression fractures could be obtained. Although QCTtrab showd the highest diagnostic sensitivity (81%), it appears not to be superior to DPAspine. Combinations of the various axial and peripheral measurements did not result in an essentially better sensitivity.
In normal women as well as in osteoporotic individuals the trabecular and cortical QCT measurements showed two opposite trends, suggesting an increase in cortical and a decrease in trabecular density from L1 to L3.
Parathyroid cell number and size in hypercalcemic rats: A stereologic study employing modern unbiased estimators
Authors: Wernerson Annika , Reinholt Finn P. , Svensson Olle 
Published: February 2010

Abstract
Recently developed stereologic methods for unbiased estimations of particle number and size were employed to study parathyroid growth in normal and hypercalcemic young rats. Thus, the parathyroid cell number and size of parathyroid secretory cells were estimated by both the disector method and the volume-weighted mean volume method. The glandular volume was calculated from serial sections, and the volume density of secretory cells was estimated by conventional sterologic techniques. Three groups of animals were studied: normal rats at 3 weeks of age, hypercalcemic rats at 7 weeks of age, and age-matched controls. Hypercalcemia was induced by feeding the animals a purified diet that was nutritionally adequate except for low amounts of phosphate (0.02%) from 3 weeks of age. During the period from 3 to 7 weeks of age, the number of parathyroid secretory cells increased by 100%, whereas the mean cell volume increased by 20%. However, when calculated per gram body weight the volume and number of cells were larger in the younger animals. The phosphate-depleted animals grew slowly and developed severe hypercalcemia. Their parathyroid secretory cells were smaller, and each gland contained fewer cells than in age-matched controls. The lower cell number and cell volume, however, were proportional to the reduced body weight. Data from the 3-week-old animals indicate that the reduced cell number and size in hypercalcemic rats reflected growth arrest rather than atrophy.
Structure-activity relationships of parathyroid hormone analogs in the opossum kidney cell line
Authors: Carnes David L. , Cole Judith A. , Forte Leonard R. , Poelling Richard E. , Thorne Pamela K. , Eber Sammy 
Published: February 2010

Abstract
Structural alterations in the parathyroid hormone (PTH) molecule produce marked changes in biologic activity. We examined the relative sensitivity of PTH-stimulated cAMP formation and PTH-inhibitable Na+- dependent phosphate transport responses to bovine PTH analogs [bPTH-(1–34), bPTH-(1–84), 8,18-norleucine-34-tyrosinamide bPTH-(1-34), bPTH-(7–34)-amide, 8,18-norleucine-34-tyrosinamide bPTH-(3–34), transaminated bPTH-(1–34)] and the human PTH-related peptide of malignancy (1–34) in cultured opossum kidney cells. The rank order of potency for stimulation of cAMP formation was bPTH-(1–34) = hPTHrP-(1–34) &gt; nle bPTH-(1–34) &gt; bPTH-(1–84) ≥ TAbPTH-(1–34). Nle bPTH-(3–34) and bPTH-(7–34) did not affect cAMP formation in intact cells at concentrations up to 10 μM. The rank order of potency for the inhibition of phosphate transport was bPTH-(1–34) = hPTHrP-(1–34) &gt; nle bPTH-(1–34) &gt; bPTH-(1–84) = TAbPTH-(1–34) &gt; nle bPTH-(3–34). TAbPTH-(1–34) was a full agonist and inhibited phosphate transport at concentrations that did not increase cAMP formation, but nle bPTH-(3–34) was a partial agonist in spite of its inability to stimulate cAMP formation. Bovine PTH-(7–34) had no effect on phosphate transport. This study indicates that changes in the PTH molecule produce analogs that apparently discriminate between the cAMP-stimulating activity and phosphate transport-inhibiting activities of the native hormone. These analogs may prove useful in defining PTH receptor subtypes based on differences in their pharmacologic properties in the regulation of physiologic responses in PTH target cells.
Early strain-related changes in enzyme activity in osteocytes following bone loading in vivo
Authors: Skerry Timothy M. , Lanyon Lance E. , Bitensky Lucille , Chayen Jo 
Published: February 2010

Abstract
The skeleton's architecture is matched to the changing loads to which it is subjected because mechanical loading directly or indirectly influences the activity of cell populations to deposit, maintain, or remove bone tissue as appropriate. This responsiveness to load bearing presupposes that certain cells are sensitive to load itself or to its consequences within the tissue. The nature of this effect and the cells concerned have not yet been determined.
In this series of experiments, bones were exposed in vivo to a single short period of dynamic loading, which if repeated daily had been shown to result in increased new bone formation. There was an increase in the activity of glucose 6-phosphate dehydrogenase (G6PD) in the periosteal cells adjacent to the bone surface 6 min after this single period of loading. This increase was proportional to the strain magnitude in the bone tissue in the immediate vicinity of the cells. In osteocytes, although the G6PD activity in each individual cell was unchanged by loading, the number of cells displaying activity was increased. This increase was also directly proportional to the applied strain in that area of the cortex (52% compared with 26% active osteocytes at a strain of 0.002). Activation of G6PD was unaccompanied by any equivalent changes in the activities of either glyceraldehyde 3-phosphate dehydrogenase (GA3PD) or lactate dehydrogenase (LDH). This finding is consistent with loading increasing the activity of the oxidative part of the pentose monophosphate shunt pathway. It is also consistent with stimulation of a synthetic process, such as the production of RNA from ribose 5-phosphate.
These results show that intermittent loading of bone tissue produces rapid strain-related effects on the metabolism of both osteocytes and periosteal cells. This change is consistent with an increase in their synthetic activity.
The characterization, regulation, and function of insulin receptors on osteoblast-like clonal osteosarcoma cell line
Authors: Dr. Pun K. K. , Lau P. , Ho P. W. M. 
Published: February 2010

Abstract
The properties and regulation of insulin receptors on monolayers of cultured clonal osteoblastic rat osteosarcoma UMR-106 cells and human osteosarcoma U20S cells were studied. Confluent cultures of UMR-106 cells bound lactoperoxidase-labeled, HPLC-purified [125I]A-14-monoiodinated insulin in a reversible, saturable, and specific manner. Binding was related inversely to the incubation temperature. Prolonged period of steady-state binding was achieved at all temperatures studied. Competition curves demonstrated half-maximal inhibition of [125I]insulin binding at an unlabeled insulin concentration of about 1 nM. Scatchard analysis of the binding data was curvilinear, suggesting negative cooperativity, and revealed that UMR-106 osteoblasts contained about 87,000 receptor sites per cell according to a two-site model. Bound [125I]insulin dissociated from osteoblasts with a t1/2 of about 15 minutes at 22°C. The dissociation curve was multiexponential, and the addition of native insulin accelerated the dissociation of intact but not degraded [125I]insulin. Preincubation with 125 nM insulin for 1 h induced 70% loss of binding sites and reduced the total insulin bound by 30%. When monolayers were treated with the lysosomotropic agent chloroquine, a 40% increase in cell-associated radioactivity that could not be dissociable in fresh buffer was observed. The use of an energy depleter, sodium fluoride, completely inhibited the effects of chloroquine. Similar results were obtained for human osteosarcoma U20S cells except that the number of receptor sites was far less than that of UMR-106 cells. Insulin increased collagen synthesis at a half-maximal concentration of 1 nM. To conclude, cultured rat and human osteoblasts possess insulin receptors that exhibit kinetic properties and specificity similar to those of other insulin target cells. Receptor-bound insulin is internalized and degraded by a chloroquine-sensitive, energy-requiring reaction. Insulin receptor on bone cells modulates the synthesis of collagen and this role may be important in bone homeostasis.
Regulation of 1,25-dihydroxyvitamin d3 by calcium in the parathyroidectomized, parathyroid hormone-replete rat
Authors: Weisinger Jose R. , Favus Murray J. , Langman Craig B. , Dr. Bushinsky David A. 
Published: February 2010

AbstractParathyroid hormone (PTH) is a major stimulus for the renal production of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Elevated arterial blood ionized calcium ([Ca2+]) depresses serum 1,25-(OH)2D3 in nonparathyroidectomized rats even when serum PTH is maintained at high levels by infusion. However, suppression by [Ca2+] of endogenous PTH, causing the fall in 1,25-(OH)2D3, cannot be excluded. To determine whether [Ca2+] regulates 1,25-(OH)2D3 in the absence of a variation in PTH, we parathyroidectomized (PTX) rats (post-PTX calcium levels &lt;7.0 mg/dl), inserted arterial and venous catheters, and then replaced PTH using an osmotic pump. We varied [Ca2+] by infusing either 75 mM sodium chloride (control), 0.61 μmol/min of EGTA (EGTA), or calcium chloride at 0.61 μmol/min (low calcium) or 1.22 μmol/min (high calcium) for 24 h 5 days after surgery. Blood was then drawn from the rat through the arterial catheter. Compared with the control, [Ca2+] fell with EGTA, remained constant with the low-calcium infusion, and rose with the high-calcium infusion. 1,25-(OH)2D3 was correlated inversely with [Ca2+] in all four groups together (r = −0.635, n = 34, p &lt; 0.001), within the control group alone (r = −0.769, n = 11, p &lt; 0.002), and within the EGTA group alone (r = −0.774, n = 10, p &lt; 0.003). Serum phosphorus, PTH, and arterial blood pH were not different in any group, and none correlated with serum 1,25-(OH)2D3. We conclude that 1,25-(OH)2D3 levels are regulated by [Ca2+] independently of serum PTH, phosphorus, and acid-base status, all of which support the hypothesis that [Ca2+] is a principal regulator of serum 1,25-(OH)2D3 in the rat.
Trabecular bone remodeling and bone mineral density in the adult cat during chronic dietary acidification with ammonium chloride
Authors: Ching Shelley V. , Norrdin Robert W. , Dr. Fettman Martin J. , LeCouteur Richard A. 
Published: February 2010

AbstractAmmonium chloride (NH4CI) is used as a urinary acidifier in the treatment and prevention of feline urologic syndrome. It is reported to cause alterations in calcium and bone metabolism in humans, dogs, and rats. Adult cats with normal renal function were fed 1.5% NH4CI for 6 months to study the effects of chronic dietary acidification on trabecular bone remodeling of the iliac crest and bone mineral density (BMD) of lumbar vertebral trabecular bone and femoral cortex. Histomorphometric analyses of iliac crest biopsies were performed before and after treatment. Static and dynamic parameters of bone resorption and formation were determined. Single-energy quantitative computed tomography (SEQCT) was used to measure lumbar trabecular and femoral cortical BMD. There were no significant treatment effects in iliac crest trabecular bone remodeling or BMD of the vertebrae and femora. Bone remodeling activity decreased with time in both acidotic and control cats. Vertebral BMD increased with time in both groups of cats, whereas no change was seen in the femora. Thus, chronic dietary acidification for 6 months with therapeutic levels of NH4CI produced no significant changes in trabecular bone remodeling or bone mineral density in adult cats.
Mechanism of amphotericin B stimulation of net calcium efflux from neonatal mouse calvariae
Authors: Blair Neil F. , Krieger Nancy S. , Bushinsky David A. 
Published: February 2010

AbstractAmphotericin B is a polyene antifungal agent that binds to membrane sterols, creating aqueous pores that permit ion fluxes sufficient to cause cell lysis. It has also been shown to alter ion transport in mammalian cells, including proton secretion from renal tubular cells. The latter effect can lead to distal renal tubular acidosis in patients treated for systemic fungal infections. Based on the understanding that osteoclast-mediated bone resorption is dependent on proton secretion, we examined the effect of amphotericin B on calcium efflux from neonatal mouse calvariae in organ culture. Amphotericin B (5 μg/ml) stimulated net calcium efflux from calvariae within 24 h to a level almost as great as that produced by a maximally effective concentration of parathyroid hormone. The stimulated calcium efflux was completely inhibited by both 10 ng/ml salmon calcitonin, a physiologic inhibitor of osteoclast activity, and 4 × 10−4 M acetazolamide, a specific inhibitor of carbonic anhydrase, the enzyme necessary for substantial proton generation by osteoclasts. These results indicate a direct effect of amphotericin B on bone in vitro to stimulate osteoclast-mediated calcium efflux.
Rapid publication: Impairment of macrophage colony-stimulating factor production and lack of resident bone marrow macrophages in the osteopetrotic op/op Mouse
Authors: Dr. Felix R. , Cecchini M.G. , Hofstetter W. , Elford P.R. , Stutzer A. , Fleisch H. 
Published: February 2010

Abstract
Mouse calvaria-derived osteoblastlike cells have been shown to produce macrophage colony-stimulating factor (M-CSF). This factor may be involved in osteoclastogenesis and thus in bone resorption. In the present study we investigated whether the production of M-CSF was altered in the osteopetrotic mouse mutant strain op/op, characterized by a decrease in osteoclast number and an impairment of bone resorption. Whole calvariae and cells, as well as skin and lung fibroblasts, of the op/op mouse were found to produce no measurable M-CSF, in contrast to tissue and cells derived from normal littermates. M-CSF was identified by colony assay in semisolid media and by inhibition of the biologic activity with antiserum against M-CSF. Furthermore, the number of resident macrophages, identified by F4/80 antigen (F4/80 Ag) immunohistochemistry, was drastically decreased in bone and bone marrow of the op/op mouse, but in skin these cells were normal in number and morphology. These findings suggest that both M-CSF and resident macrophages play a role in the mechanism of bone resorption. The op/op mouse appears to be a valuable model to further investigate such a hypothesis.
Chemotactic response of osteoblastlike cells to transforming growth factorβ
Authors: Pfeilschifter Johannes , Wolf Oliver , Naumann Antje , Minne Helmut W. , Mundy Gregory R. , Ziegler Reinhard 
Published: February 2010

Abstract
Transforming growth factor β (TGF-β) has multiple effects on bone cell metabolism in vitro but its exact role in bone remodeling still needs to be defined. Here we demonstrate that TGF-β is chemotactic for osteoblastlike cells from fetal rat calvariae and osteoblastlike ROS 17/2.8 osteosarcoma cells. Maximal chemotaxis occurred at 5-15 pg/ml of TGF-β and was observed with TGF-β1 and TGF-β2 at equivalent concentrations. Conditioned medium from osteoblastlike cells containing latent TGF-β failed to stimulate chemotactic migration. However, chemotactic activity was observed in conditioned medium that had been transiently acidified. Since acidification is known to activate TGF-β, these results suggest that only active TGF-β is capable of inducing a chemotactic response. Preincubation of osteoblastlike cells with TGF-β in concentrations from 10 pg/ml to 1 ng/ml for 48 h abolished a subsequent chemotactic response of these cells to TGF-β, indicating that TGF-β-induced chemotaxis is a transient phenomenon. Since TGF-β may be released from the bone matrix and/or activated during bone resorption, the chemotactic activity of TGF-β for osteoblastlike cells may be important for the recruitment of osteoblastlike cells to sites of bone remodeling.
Fluoride bioavailability from slow-release sodium fluoride given with calcium citrate
Authors: Dr. Pak Charles Y. C. , Sakhaee Khashayar , Parcel Carol , Poindexter John , Adams Beverley , Bahar Abdillahi , Beckley Robert 
Published: February 2010

Abstract
Clinical pharmacology of slow-release sodium fluoride given with calcium citrate was examined in acute and long-term studies. Following a single oral administration of 50 mg slow-release sodium fluoride, a peak serum fluoride concentration (Cmax) of 184 ng/ml was reached in 2 h; thereafter, serum fluoride concentration declined with a T1/2 of 5.9 h. The concurrent administration of calcium citrate (400 mg calcium) gave an equivalent Tmax (time required to attain Cmax) and T1/2, but a lower Cmax of 135 ng/ml. The coadministration of a meal with fluoride also reduced Cmax but increased Tmax. The area under the serum concentration curve of slow-release sodium fluoride was reduced 17-27% by a meal or calcium citrate. Thus, calcium citrate reduced fluoride absorption and peak fluoride concentration in serum of slow-release sodium fluoride but did not affect the time required to reach peak concentration or the rate of subsequent decline. The effect of a meal was similar, except for a longer period required to reach peak serum concentration. During long-term administration of 25 mg slow-release sodium fluoride coadministered with 400 mg calcium as calcium citrate on a twice daily schedule, the trough level of serum fluoride could be kept between 95 and 190 ng/ml, believed to be the therapeutic window.
Osteoporosis as the sole presentation of bone marrow mastocytosis
Authors: Lidor Cobi , Frisch Bertha , Gazit Dan , Gepstein Reuven , Hallel Tom , Mekori Yoseph A. 
Published: February 2010

Abstract
Three (young) adults with severe generalized osteopenia and vertebral compression fractures were studied. Extensive clinical and laboratory investigations were not contributory. Undecalcified bone biopsies demonstrated multiple mast cell granulomas in the marrow in two patients and numerous mast cells diffusely distributed throughout the bone marrow in the third patient. Mast cells may serve as a pathogenic agent in osteoporosis. Therefore, we conclude that isolated skeletal mastocytosis without clinical evidence of mast cell mediator release should be sought in the evaluation of a patient with unexplained severe bone loss.
Heterogeneity of human bone
Authors: Ninomiya James T. , Tracy Russell P. , Calore James D. , Gendreau Mark A. , Kelm Robert J. , Mann Kenneth G. 
Published: February 2010

Abstract
Matched samples of bone from the lumbar spine and tibia were obtained at autopsy from three adult males who had no known evidence of metabolic bone disease at the time of their demise. The soluble noncollagenous bone proteins were quantitatively extracted from these samples and assayed for the relative content of two bone-associated proteins, osteocalcin and osteonectin. When compared to trabecular bone, cortical bone had higher levels of osteocalcin and much lower levels of osteonectin. When concentration is expressed per gram of dried bone, the osteocalcin excess in cortical bone ranged from 30- to 32-fold, and the osteonectin excess in trabecular bone ranged from 21- to 47-fold. These differences were significant (P &lt; 0.01) using analysis of variance. We conclude that the human skeleton is not homogeneous with regard to these biochemical markers and that cortical and trabecular bone are biochemically quite distinct. This implies that these two types of bone may be subject to distinct regulatory mechanisms and that global assessments of skeletal function and bone quality based upon soluble markers should be applied with caution. The data also imply that a differential assessment of skeletal performance may be possible using biochemical serum markers.