bluuebunny/crossref_metadata_2025_split huggingface dataset:
Posture, age, menopause, and osteopenia do not influence the circadian variation in the urinary excretion of pyridinium crosslinks
Authors: Schlemmer Annette , Hassager Christian , Pedersen Brian J. , Christiansen Claus 
Published: February 2010

Abstract
This study was performed to investigate whether the circadian variation in urinary pyridinium crosslinks is related to physical activity, age, the menopause, and asymptomatic osteopenia. We measured urinary pyridinoline/creatinine (Pyr/Cr) and deoxypyridinoline/creatinine (D-Pyr/Cr) in 9 healthy premenopausal women in two 27 h studies, before and at the end of 5 days of total bed rest. Both Pyr/Cr and D-Pyr/Cr showed highly significant circadian variations, with the peak at night and the nadir during the day (p &lt; 0.001). The 5 days of complete bed rest produced no changes in the circadian pattern, but a general increase of 28% was observed in pyridinium crosslinks. A group of 12 healthy, early postmenopausal women (aged 55 + 2 years), 12 healthy, elderly postmenopausal women (aged 73 + 1 years), and 12 elderly osteopenic but otherwise healthy women (aged 73 + 1 years) were also studied for 27 h. All three groups showed highly significant (p ≤ 0.001) circadian variations in the urinary excretion of pyridinium crosslinks. As expected, both Pyr/Cr (p &lt; 0.05) and D-Pyr/Cr (p &lt; 0.001) increased at the time of menopause, but the circadian variations in Pyr/Cr and D-Pyr/Cr were similar in all groups studied. We conclude that the circadian variation in the urinary excretion of pyridinium crosslinks is independent of physical factors. Furthermore, the circadian variation in pyridinium crosslinks was not related to age, menopausal status, or asymptomatic osteopenia.
Fractal organization of trabecular bone images on calcaneus radiographs
Authors: Dr. Benhamou C.L. , Lespessailles E. , Jacquet G. , Harba R. , Jennane R. , Loussot T. , Tourliere D. , Ohley W. 
Published: February 2010

Abstract
Bone density is not the unique factor conditioning bone strength. Trabecular bone microarchitecture also plays an important role. We have developed a fractal evaluation of trabecular bone microarchitecture on calcaneus radiographs. Fractal models may provide a single numeric evaluation (the fractal dimension) of such complex structures. Our evaluation results from an analysis of images with a varying range of gray levels, without binarization of the image. It is based on the fractional brownian motion model, or more precisely on the analysis of its increment, the fractional gaussian noise (FGN). The use of this model may be considered validated if two conditions are fulfilled: the gaussian repartition and the self-similarity of our data. The gaussian repartition of intermediate lines of these images was tested on a sample of 32,800 lines from 82 images. Following a chi-square goodness-of-fit test, it was checked in 86% of these lines for α = 0.01. The self-similarity was tested on 20 images by two estimators, the variance method of Pentland and the spectrum method of Fourier. Self-similarity is defined by lined-up points in a log-log plot of the FGN spectrum or of the variance as a function of the lag. We found two self-similarity areas between scales of analysis ranging from 105 to 420 μm, then above 900 μm, where linear regression produced high mean correlation coefficients (r ≥ 0.97). Following this validation, we studied the reproducibility of this new technique. Intra- and interobserver reproducibility, influence of transferring the region of interest, and long-term reproducibility were assessed and given CV of 0.61 ± 0.15, 0.68 ± 0.47, 0.53 ± 0.16, and 2.07 ± 0.84%, respectively. These data have allowed us to validate the use of this fractal model by checking the fractal organization of our radiographic images analyzed by the model. The good reproducibility of successive x-rays in the same subject allows us to undertake population studies and to envisage longitudinal series.
Bone morphogenetic protein 2 increases insulin-like growth factor I and II transcripts and polypeptide levels in bone cell cultures
Authors: Canalis Ernesto , Gabbitas Bari 
Published: February 2010

Abstract
Insulin-like growth factors (IGF) I and II are among the most prevalent growth factors secreted by bone cells and are presumed to act as autocrine regulators of bone formation. Certain growth factors, synthesized by skeletal cells and known to stimulate the replication but not the differentiated function of cells of the osteoblastic lineage, have been shown to inhibit skeletal IGF-I and II synthesis. We postulated that growth factors with limited mitogenic activity and with differentiation-inducing properties, such as bone morphogenetic protein (BMP) 2, have the opposite effect and enhance IGF-I and II synthesis. We tested the effects of BMP-2 on IGF-I and II mRNA expression and polypeptide concentrations in cultures of osteoblast-enriched (OB) cells from 22 day fetal rat calvariae. Steady-state IGF-I and II mRNA levels were determined by northern blot analysis, and IGF-I and II concentrations were determined in acidified and fractionated culture medium by a specific radioimmunoassay. After 24-48 h of treatment, BMP-2 at 3.3 nM increased IGF-I and II transcripts by up to twofold and polypeptide levels by up to fourfold. BMP-2 was a more potent stimulator of IGF-II synthesis, and it was active at doses as low as 0.03 nM for IGF-II mRNA and 0.3 nM for IGF-II protein, whereas a dose of 3.3 nM was required to observe the effect on IGF-I synthesis. The effects of BMP-2 on IGF-I and II transcripts and polypeptide levels were dependent on protein synthesis and decreased in the presence of cycloheximide at 3.6 μM. In conclusion, BMP-2 increases skeletal IGF-I and II synthesis by increasing IGF-I and II transcript levels, and this effect may contribute to its actions on selected aspects of OB cell differentiated function.
Alterations in calcium intake on peak bone mass in the female rat
Authors: Peterson Catherine A. , Eurell Jo Ann C. , Erdman John W. 
Published: February 2010

AbstractThis study compared the effect of a calcium deficit or surfeit on bone growth and development in the early phase of peak bone mass attainment with the late phase of peak bone mass attainment using the female Sprague-Dawley rat as a model. Groups of weanling animals were fed one of three nutritionally complete but calcium-altered diets (0.25%, 0.5%, or 1.0% calcium) for 8 weeks. Animals within each diet group were then rerandomized into one of the above diets and fed until 37 weeks of age. Each group contained five rats. In addition, three groups that received the 0.25% calcium diet for the first 8 weeks remained on the diet until week 20 when they were further randomized into one of the three diet groups and fed until 37 weeks of age. Results of this experiment indicate that increasing the calcium intake after adolescence (12-weeks-old) of those female rats consuming a low calcium diet will not substantially alter the adult bone volume of the metaphyseal region of the proximal tibia. Further, low calcium intakes through adolescence retard and prolong longitudinal bone growth. In contrast, however, those rats fed a diet providing calcium either at (0.5%) or twice the National Research Council's requirement level through adolescence had greater tibial bone volume as an adult when fed diets containing 1.0% calcium after this time period. It appears that the mechanism for this increase involves both a protection from resorption and an increase in bone formation/mineralization. This study is the first to show that low calcium intakes through adolescence have a nonreversible, deleterious effect on peak bone mass, whereas higher intakes promote greater peak bone mass and provide potential protection from age-related bone loss.
AzaThioprine alone is bone sparing and does not alter cyclosporin A-induced osteopenia in the rat
Authors: Bryer Haldon P. , Isserow Jonathan A. , Armstrong Eamon C. , Mann Gary N. , Rucinski Boguslaw , Buchinsky Farrel J. , Romero David F. , Epstein Solomon 
Published: February 2010

Abstract
The immunosuppressant agent cyclosporin A (CsA) induces a high turnover osteopenic state, while the effect on bone of the antimetabolite azathioprine, a drug often used in conjunction with CsA in transplant patients, is less clear. This study was therefore designed to investigate the outcome of azathioprine administration, with reference to CsA, on bone mineral metabolism using the rat model. Four groups of 10-week-old male Sprague-Dawley rats (12 per group) were randomly allocated to receive by daily gavage for a 28-day period: (1) no treatment (control group); (2) azathioprine 1.5 mg/kg bw; (3) CsA 15 mg/kg bw; and (4) a combination of azathioprine and CsA, as described above. Rats were weighed and blood assayed serially for osteocalcin, ionized calcium, 1,25-dihydroxyvitamin D (1,25(OH)2VitD), and parathyroid hormone (PTH). Tibiae were removed following sacrifice on day 28 after double calcein labeling for histomorphometric analysis. Immunosuppressant groups were compared with nontreated control. We confirmed our previous findings that CsA induces a state of high turnover bone loss which is accompanied by a diminished gain in body weight (p &lt; 0.01) and elevated serum osteocalcin (p &lt; 0.001) and 1,25(OH)2VitD levels (p &lt; 0.001). Azathioprine treatment alone did not alter ionized calcium, 1,25(OH)2VitD, or PTH levels. However, there was biochemical evidence of impaired osteoblastic activity as seen by decreased osteocalcin values on days 14 and 28 (p &lt; 0.001). Azathioprine caused no loss of bone volume nor any deviation from the norm in mineral apposition rate, bone formation rate, or longitudinal bone growth. All three treatment groups showed an increased recruitment of osteoclasts to the bone surface. In summary, this report demonstrates that azathioprine, despite appearing to suppress osteoblastic activity and encourage osteoclast recruitment, maintains bone volume in the rat and does not alter the osteopenic effects brought about by CsA administration.
Matrix mineralization and the differentiation of osteocyte-like cells in culture
Authors: Mikuni-Takagaki Yuko , Kakai Yoshio , Satoyoshi Masanori , Kawano Eiji , Suzuki Yoshihisa , Kawase Toshio , Saito Shigeru 
Published: February 2010

Abstract
Osteocyte-like cells were prepared by sequentially treating calvaria from newborn rats with collagenase and chelating agents. On a reconstituted gel of basement membrane components, cells from the third collagenase digest displayed a round shape and expressed the highest level of alkaline phosphatase with minimal osteocalcin deposition into the matrix. On the other hand, cells derived from the interior after EDTA treatment exhibited well-developed dendritic cell processes and expressed essentially no alkaline phosphatase. The latter population also showed quite distinct characteristics such as higher extracellular activities of casein kinase II and ecto-5′-nucleotidase and the extracellular accumulation of a large amount of osteocalcin associated with mineral. These diverse phenotypic and protein expressions as well as the sites from which each population of cells were recovered strongly suggest that we have isolated osteoblastic and osteocytic cells. Bone sialoprotein II was extracellularly phosphorylated by casein kinase II in osteocytic cells but not in osteoblastic cells. We discuss the possibility that differentiation of young osteocytes from osteoblasts may facilitate the biochemical sequence of mineral deposition in the bone matrix.
In vivo, three-dimensional microscopy of trabecular bone
Authors: Dr. Kinney J.H. , Lane N.E. , Haupt D.L. 
Published: February 2010

Abstract
Osteoporosis, which is correlated with low bone mass and increased bone fragility, is responsible for about 1.2 million fractures per year in the United States. We have used the three-dimensional (3-D), X-ray tomographic microscope to image the trabecular bone architecture of the proximal tibias of six Sprague—Dawley rats in vivo. Three of these rats were then ovariectomized to induce estrogen depletion, and three remained as controls. Five weeks later, the tibias were reimaged. The ovariectomized rats lost approximately 65% of their trabecular bone volume as compared with an insignificant change in the control rats. The connectivity density of the trabecular bone, as measured by the Euler characteristic, was linearly correlated with trabecular bone volume, even in the ovariectomized rats. Hypoestrogenemic bone loss manifested itself in greatly reduced connectivity and fewer trabecular elements, but not in thinning of trabeculae. The ability to microscopically image sequential changes in the 3-D architecture of trabecular bone in vivo will allow exploration of the earliest stages of hypoestrogenemic bone loss and to more rapidly test the effectiveness of new clinical treatments for this major public health problem.
Ethnic differences in bone density in female South African nurses
Authors: Dr. Daniels Elvis D. , Pettifor John M. , Schnitzler Christine M. , Russell Sheila W. , Patel Deepak N. 
Published: February 2010

Abstract
In the United States, the higher prevalence of osteoporosis and the higher incidence of fractures in whites than in blacks may be attributed to the finding of lower bone density (BD) in both white children and adults. In South Africa, osteoporosis and fractures also occur more frequently in whites than in blacks. Appendicular BD has been found to be similar in black and white children in South Africa, but there is little information available on BD of adults in South Africa. This cross-sectional study aimed to assess changes in BD with age in adult females in South Africa and to assess possible differences in peak BD and in the rate of postmenopausal bone loss between blacks and whites. Data for 180 black and 184 white female nurses aged 20–64 years were analyzed. The distal radius bone density (RBD) was measured by single photon absorptiometry. The lumbar spine bone density (SBD) and the femur bone density (FBD) were measured by dual-energy X-ray absorptiometry. Blacks were shorter than whites (p = 0.0001), and blacks' weight, body mass index, and skinfold thickness increased with age. Peak SBD and RBD were similar in blacks and whites, but peak FBD was higher in blacks (p = 0.0001). This ethnic difference in peak FBD became apparent in the fourth decade. Peak FBD was similar in black and white subjects with normal body mass indices (p = 0.09), but in overweight subjects peak FBD was higher in blacks than in whites (p = 0.0001). SBD (p = 0.03), RBD (p = 0.0002), and FBD (p = 0.04) in whites, but not in blacks, decreased after the menopause. Weight had a positive association with FBD in premenopausal blacks (R = 0.24, p = 0.0001) but not in whites. In the postmenopausal group, adiposity had a positive association with SBD and RBD in blacks and with FBD in both blacks and whites. These results suggest that weight-bearing is important in the attainment of peak FBD and that adiposity may be important in decreasing postmenopausal bone loss. The finding of higher FBD in blacks than in whites may explain the lower rate of femoral fractures in black South Africans. However, the similarity in SBD between blacks and whites in this study suggests that factors other than bone density might contribute to the lower vertebral fracture rate in black compared with white South Africans.
Physicochemical effects of a new slow-release potassium phosphate preparation (UroPhos-K) in absorptive hypercalciuria
Authors: Breslau Neil A. , Padalino Paulette , Kok Dirk Jan , Kim Young Gon , Pak Charles Y.C. 
Published: February 2010

Abstract
A new slow-release, neutral potassium phosphate salt (UroPhos-K) has been formulated in order to minimize gastrointestinal side effects and avoid sodium-induced calciuria. It was tested in a prospective randomized, double-blind trial in a group of 21 kidney stone patients with absorptive hypercalciuria type I (AH). Twelve patients allocated to the UroPhos-K group received four tablets twice daily with breakfast and an evening snack providing 1240 mg of phosphorus and 63.5 mEq of potassium daily. Nine patients assigned to the placebo group received placebo tablets of the same appearance containing excipient only. Subjects were studied during a 3-day period in the hospital while consuming a constant metabolic diet containing 400 mg Ca, 100 mEq Na, and 800 mg P per day before and after 3 months of treatment. Treatment with UroPhos-K did not cause any significant gastrointestinal side effects; nor did it raise fasting serum K or phosphorus, or reduce hemoglobin or creatinine clearance. It was associated with a rise in urinary K from 46 ± 7 to 98 ± 9 mEq per day and phosphorus from 744 ± 185 to 1535 ± 112 mg per day (p &lt; 0.001 each). UroPhos-K treatment reduced urinary Ca from 288 ± 63 to 171 ± 49 mg/day (p &lt; 0.001), without altering oxalate excretion. It reduced the urinary saturation of calcium oxalate without altering that of brushite. Moreover, by increasing urinary excretion of inhibitors (citrate and pyrophosphate), it reduced the propensity for spontaneous nucleation of brushite (increased formation product of brushite) and inhibited crystal agglomeration of calcium oxalate. None of these changes were seen in the placebo-treated group. It is concluded that treatment with UroPhos-K reduces urinary stone-forming potential without causing gastrointestinal side effects.
Autoregulation of inducible prostaglandin G/H synthase in osteoblastic cells by prostaglandins
Authors: Pilbeam Carol C. , Raisz Lawrence G. , Voznesensky Olga , Alander Cynthia B. , Delman Bradley N. , Kawaguchi Hiroshi 
Published: February 2010

Abstract
Prostaglandins (PGs) have been postulated to amplify their own production by stimulating cyclic adenosine monophosphate activity, which in turn stimulates PG production. We examined regulation of messenger RNA levels for the inducible and constitutive prostaglandin G/H synthases, PGHS-2 and PGHS-1, in murine osteoblastic MC3T3-E1 cells, which express both PGHS-1 and PGHS-2, and in rat osteoblastic Py1a cells, which express only PGHS-2. Prostaglandins E2, F2α, and D2 induced PGHS-2 mRNA in both cell lines under serum-free conditions and stimulated small increases in PGHS-1 mRNA levels in MC3T3-E1 cells. PGE2 (1 μM) increased the transcription rate of PGHS-2 mRNA 9-fold at 2 h in serum-free cells and also induced PGHS-2 protein. In the presence of arachidonic acid or serum, PGs also increased medium PGE2. Both forskolin, a protein kinase A activator, and phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, have previously been shown to induce PGHS-2 mRNA in MC3T3-E1 cells, but in the present study only PMA induced PGHS-2 expression in Pyla cells. The induction of PGHS-2 mRNA in Py1a cells by PGs was inhibited by chelerythrine, a PKC inhibitor, and blocked by 24 h of pretreatment with PMA. The 2 h serum stimulation of PGHS-2 mRNA in MC3T3-E1 cells was inhibited 40–50% by three structurally unrelated nonsteroidal anti-inflammatory drugs (NSAIDs), suggesting that endogenous PGs also amplify PG production through induction of PGHS-2. We conclude that the mechanism for autoamplification is in part transcriptional and may involve multiple pathways. We speculate that the induction of PGHS-2 by PGs may be the means for expanding PG responses to small and intermittent signals, such as mechanical strains.
Zinc is a potent inhibitor of osteoclastic bone resorption in vitro
Authors: Moonga Baljit S. , Dempster David W. 
Published: February 2010

Abstract
It is well established that zinc, an essential trace element, plays an important role in growth and stimulates bone formation. However, the effects of zinc on bone resorption have received little attention. We studied its effects on isolated rat osteoclasts. Unexpectedly, osteoclasts were exquisitely sensitive to zinc, with a significant decrease in bone resorption occurring at concentrations as low as 10−14 M. This effect was specific for zinc and was not observed with the other transitional or alkaline metals studied. There was no evidence of toxicity at concentrations up to 10−4 M. Zinc also completely abolished the stimulatory effect of parathyroid hormone. Zinc is therefore a highly potent and selective inhibitor of osteoclastic bone resorption in vitro. The mode of action remains to be established and may represent a novel inhibitory mechanism in the osteoclast.
Morphologie stages in lamellar bone formation stimulated by a potent mechanical stimulus
Authors: Rubin Clinton T. , Gross Ted S. , McLeod Kenneth J. , Bain Steven D. 
Published: February 2010

Abstract
The temporal stages of lamellar bone formation were studied using an animal model subject to up to 16 weeks of a controlled, externally applied load. The left ulnae of 15 adult male turkeys were functionally isolated via transverse metaphyseal osteotomies, while transcutaneous Steinmann pins permitted in vivo loading of the preparation via a servo-hydraulic actuator. For 5 days per week, the ulnae were exposed to 100 cycles per day of an applied load sufficient to cause a peak strain normal to the bone's longitudinal axis of 2000 microstrain (με). The contralateral limb was left surgically undisturbed and served as a baseline control. Following a loading period of 4, 8, or 16 weeks, ulnae were harvested and prepared for quantitative bone histomorphometry. Compared with each animal's contralateral ulna, the area of the experimental ulnae increased by 12.5% (±5.6%) at 16 weeks. Periosteal mineral apposition rates in the loaded ulnae were significantly increased compared with control values, with a maximum rate of 6.0 ± 3.4 μm/day at 5 weeks, slowing to 2.0 ± 0.3 μm/day by 15 weeks. At 16 weeks, new bone was composed of primary and secondary osteons as well as circumferential lamellae, with osteocyte density and organization indistinguishable from that of the original cortex. Remnants of the initial woven bone response seen at 4 weeks remained clearly visible at both 8 and 16 weeks as diffusely labeled interstitial elements within the newly formed lamellar construct. The presence of secondary osteons, circumferential lamellae, and an osteocyte density and organization similar to that seen in controls suggests that the presence of woven bone in the initial stages of the adaptive process is not necessarily a pathologic or transient reaction to injury, but instead may be a normal stage in response to a potent mechanical stimulus.