bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relation of fractional 47Ca retention to season and rates of bone loss in healthy postmenopausal women
Authors: Krall Elizabeth A. , Dawson-Hughes Bess 
Published: February 2010

Abstract
Fractional Whole-Body Retention Of 47Ca (retention fraction) in 58 healthy postmenopausal women participating in a calcium supplementation trial was examined for seasonal variation and for relationships to rates of bone loss and plasma vitamin D levels. Retention fraction was measured after 18 months in the trial. Bone mineral densities of the radius, femoral neck, and lumbar spine were measured at baseline, 12 months, and 24 months in the trial, and plasma 1,25-dihydroxyvitamin D [1,25-(OH)2D] and 25-hydroxyvitamin D (25-OHD) at 12, 18, and 24 months. The adjusted retention (retention fraction adjusted for total calcium intake, smoking status, and log years since menopause) was significantly higher in women evaluated in the months of August through October (mean ± SD, 19.8 ± 4.1%, n = 13) than in March through May (mean ± SD, 17.0 ± 4.7%, n = 18, p = 0.05). Plasma 25-OHD was associated with retention fraction only in women with low calcium intakes (partial r = 0.69 controlling for total calcium intake and log body mass index, n = 14, p = 0.01). Plasma 1,25-(OH)2D was not related to retention fraction. Adjusted retention, independent of total calcium intake, log years since menopause, smoking status, and season, explained 8% of the variability in the annual change in radius density (partial r = 0.29, p &lt; 0.05). No significant associations were seen at the spine and femur. These results indicate there is seasonal variation in calcium retention, that calcium retention is positively correlated with plasma 25-OHD levels in women with low calcium intakes, and that an increased level of retained calcium is associated with a lower rate of bone loss from the radius.
Journal of Bone and Mineral Research
Authors: Dr. Melton L. Joseph 
Published: February 2010

Abstract
The impact of primary hyperparathyroidism (HPT) on the population has not been well documented, and even less information is available for asymptomatic HPT. Only 57 deaths were attributed to the condition in the United States in 1986, for a reported HPT death rate of 0.24 per million per year. Many more patients were affected, however, and the incidence of hospitalization for HPT was 6.6 per 100,000 in 1986, counting all listed diagnoses, and 2.9 per 100,000 counting only first-listed diagnoses. Surgery was performed on approximately 10,000 hospitalized patients in the United States in 1986, for a parathyroidectomy rate of about 4.2 per 100,000 per year. When nonhospitalized cases are included, the rates are even higher. The estimated annual incidence of HPT was 42.1 per 100,000 in Rochester, Minnesota in 1974–1976; the prevalence of HPT was 4.3 per 1000 in a population survey in Sweden. By any of these measures, HPT is more common in women than men and increases with aging in both sexes. The potential cost of HPT could be as high as $420 million/year in the United States, but no formal estimates have been made. Disability related to HPT or its treatment has not been quantified; randomized clinical trials to determine the utility of parathyroidectomy have not been performed; and no assessment of cost benefit or cost effectiveness of any therapeutic modality has been carried out. Until patient management and cost issues are resolved, it is premature to consider an aggressive program to screen the general population for HPT.
Journal of Bone and Mineral Research
Authors: Heath Hunter 
Published: February 2010

AbstractOver the last 25 years, the perceived clinical spectrum of primary hyperparathyroidism (HPT) has changed dramatically from a disorder characterized by severe bone and renal disease to one typically manifested by few or mild symptoms and little evidence of organ damage. Reasons for this change in spectrum include changing demographics (primary HPT is primarily a disease of the middle-aged and elderly), diffusion of medical knowledge leading to a higher index of suspicion, and improved clinical laboratory technology (especially inexpensive and accurate determination of serum calcium and parathyroid hormone). In the first 343 cases of primary HPT seen at the Massachusetts General Hospital, 57% had renal stones, 23% had hyper-parathyroid bone disease, and &lt; 1% had no symptoms. By contrast, studies dating from the availability of automated serum calcium measurement found renal stones and hyperparathyroid bone disease in &lt; 5% of cases, and about half of cases had few or no symptoms. Most patients with primary HPT today have mild, nonspecific symptoms, such as weakness, fatigue, and mental depression, and such signs as arterial hypertension and osteopenia, and detection of their hypercalcemia is generally serendipitous. The mildness and slow progression seen in many cases of primary HPT has resulted in much controversy about appropriate management.
Journal of Bone and Mineral Research
Authors: Professor Ljunghall Sverker , Jakobsson Sören , Joborn Charlotte , Palmér Mats , Rastad Jonas , Åkerström Göran 
Published: February 2010

Abstract
In 1969, a health survey was offered to all inhabitants of a town district in Sweden. A clinical examination was carried out, and among other variables, a measurement was made of serum calcium. The same procedure was repeated in 1971. From these two investigations a cohort of 176 individuals (1.1%) with sustained hypercalcemia was identified who could be followed during the subsequent 15 years. Comparisons were made with an age- and sex-matched control group from the same health survey. Survival was significantly lower in the hypercalcemic cohort than in the control group. This reduction was related to the degree of hypercalcemia and apparently mainly due to diseases of the circulatory organs. There was no marked deterioration of renal function, and although there was in some patients a moderate progression of the hypercalcemia, none developed a hypercalcemic crisis during 15 years of follow-up. In consecutively referred patients with primary hyperparathyroidism, psychiatric disturbances of mainly a depressive character were found upon detailed analysis within a majority of the patients, and parathyroid surgery resulted in a clear improvement in mental health.
Effects of Gallium on Bone in the Rat
Authors: Wakley Glenn K. , Garand Joseph , Brown Daniel , Szukalski Bernard W. , Bell Norman H. , Turner Russell T. 
Published: February 2010

Abstract
Gallium nitrate lowers the serum calcium in patients with hypercalcemia caused by malignancy and is available for clinical use. The mechanism for the hypocalcemic action is unknown, however. The present studies were undertaken to determine the effects of gallium on bone metabolism. Normal male rats were implanted subcutaneously with mineralized allogeneic bone matrix. Histomorphometry of the implants and of tibiae was determined after three doses of tetracycline administered at intervals of 1 week. Gallium as nitrate was administered daily by intraperitoneal injection at doses of 0.9, 1.8, and 3.6 mg elemental gallium per kg body weight for 21 days in one study and at 3.5 mg/kg for 33 days in a second study. All the gallium-treated rats gained weight. Rats given gallium at doses of 3.5 mg/kg or more grew at a lower rate than untreated controls (-7 and -10% at doses of 3.5 and 3.6 mg/kg, respectively; p &lt; 0.05). At a dose of 0.9 mg/kg, gallium did not inhibit bone resorption or lower serum calcium but inhibited bone formation by 32% and bone apposition by 36% at the endosteal surface of the tibia. At a dose of 1.8 mg/kg, gallium produced modest hypocalcemia, prevented a rise in circulating 1,25-dihydroxyvitamin D [1,25-(OH)2D], inhibited bone resorption in implants, and inhibited bone formation by 19% and bone apposition by 18%. At a dose of 3.5 mg/kg, gallium lowered the serum calcium and serum 1,25-(OH)2D, inhibited growth, and accentuated the antiresorptive and antiformative effects seen at the two lower doses. The results indicate that gallium inhibits bone resorption, produces hypocalcemia, alters vitamin D metabolism, and inhibits bone formation at doses below those that inhibit bone resorption. The mechanism for hypocalcemia may be by direct action on bone and could involve an indirect effect on calcium metabolism mediated by changes in the metabolism of vitamin D.
Platelets contribute to circulating levels of bone sialoprotein in human
Authors: Chenu C. , Delmas P.D. 
Published: February 2010

Abstract
Bone sialoprotein (BSP) is a major bone-related protein. Although a few other tissues contain trace amounts of BSP message, bone cells and bone matrix are the major sources of BSP, suggesting that this protein could be a potential marker of bone metabolism. Purified bovine BSP showed a 70% homology of its first 13 amino acid N-terminal sequence with human BSP and was used to raise antibodies in rabbit and to develop a specific radioimmunoassay (RIA). Using this RIA, we have shown that BSP is present in serum with values in the range of 10–30 ngEq/ml in the serum of normal adults. Values obtained in plasma prepared without platelet activation are about one-half of those in matched sera, suggesting that BSP present in serum is in part derived from platelets during the activation process. Using Western blot and RIA techniques, we confirmed that platelets contain immunoreactive BSP and that the protein is released after thrombin stimulation of these cells. In addition to BSP, platelets contain a 45 kD immunoreactive material that has not been precisely identified. Available evidence indicates that this material is not osteonectin or osteopontin and that it may be a BSP-like protein rather than a degradation product of BSP. Platelets from a patient having a gray platelet syndrome, characterized by a deficiency in platelet α-granules and in the α-granule secretory proteins, did not show any deficiency of BSP, suggesting that immunoreactive BSP present in platelets is not endogenously synthesized by megakaryocytes but rather originates from plasma by endocytosis.
Composite index of skeletal mass: Principal components analysis of regional bone mineral densities
Authors: Feingold Marcia , Nelson Dorothy A. , Parfitt A. Michael 
Published: February 2010

Abstract
Principal components analysis is a statistical method that is used to reduce and explore data to facilitate further analyses. This method was applied to bone mineral densities measured at seven sites in 109 black and 44 white women, ages 22–80, at an internal medicine clinic in urban Detroit. We excluded subjects with a history of diseases or drugs known to affect bone metabolism. Principal components analysis was used to summarize the interrelationship of the densities and yielded two major results. First, the seven site measurements were reduced to a single, composite index (PC1) of skeletal mass that accounted for 73% of the variation in density among subjects. PC1 had roughly equal weights among the sites. A second combination of the seven sites indicated that the contrast between axial and appendicular regional densities accounted for another 10% of the variation among subjects. In investigating the relationship of density to age, body mass index, and ethnic group, we found that the principal components composite index had a stronger correlation with age (r = -0.58) and with body mass index (r = 0.34) than almost all of the regional densities. Black-white differences were larger for the composite index than for any single site density. A multiple regression of the composite index on ethnicity, body mass index, and age yielded a larger R2 (0.46) than any of the individual site densities. The second principal component, although of theoretical interest, showed a minimal ability to discriminate among subjects using the three independent variables of this study.
Weight-training effects on bone mineral density in early postmenopausal women
Authors: Pruitt Leslie A. , Jackson Rebecca D. , Bartels Robert L. , Lehnhard Holly J. 
Published: February 2010

Abstract
We tested the hypothesis that weight training would be an effective modality in maintaining or increasing bone mineral density (BMD) at the lumbar spine, femoral neck, and bone mineral content (BMC) at the distal wrist in early postmenopausal women. A total of 17 women completed a 9 month weight-training program, and 9 women served as a control group. Resistance training occurred three times per week using exercises designed to increase muscular strength. Mean change in lumbar BMD in the weight-trained group (1.6 ± 1.2%, mean ± SEM) was significantly different from the change in the control group (-3.6 ± 1.5%, p &lt; 0.01) over the 9 month period. No significant weight-training effect was detected at the femoral neck or distal wrist site. We conclude that weight training may be a useful exercise modality for maintaining lumbar BMD in early postmenopausal women.
Incidence of clinically diagnosed vertebral fractures: A population-based study in rochester, minnesota, 1985-1989
Authors: Cooper Cyrus , Atkinson Elizabeth J. , MichaelO'Fallon W. , Dr. Melton Joseph L. 
Published: February 2010

Abstract
Vertebral fractures are the classic hallmark of osteoporosis, yet little is known of their epidemiology. The incidence of clinically diagnosed vertebral fractures was therefore directly assessed in the predominantly white (European descent) population of Rochester, Minnesota. Altogether, 341 Rochester residents were radiologically diagnosed for the first time with one or more vertebral fractures in the 5 year study period, 1985–1989. The overall age- and sex-adjusted incidence rate was 117 per 100,000 person-years (95% CI, 105 to 130). The age-adjusted rate in women (145 per 100,000 person-years) was almost twice that in men (73 per 100,000 person-years). Of all fractures, 47 (14%) followed severe trauma, 282 (83%) followed moderate or no trauma, and 12 (3%) were pathologic. Incidence rates for fractures following moderate trauma were higher in women than in men and rose steeply with age in both genders. In contrast, fractures following severe trauma were more frequent in men, and their incidence increased less with age. These Rochester rates are greater than those previously reported from studies in Britain and Sweden but lower than the incidence rates extrapolated from a prevalence study in this population.
Perspectives: The role of changes in mechanical usage set points in the pathogenesis of osteoporosis
Authors: Frost Harold M. 
Published: February 2010

Abstract
Mechanical usage (MU) effects on modeling drifts and BMU-based remodeling affect bone mass in defined ways. Decreased MU stops additions of bone by modeling and increases removal of bone next to marrow by remodeling. The latter effect thins cortices and reduces trabecular number, thickness, and connectivity. Return to normal MU makes remodeling begin conserving existing bone and leaves modeling still off. Hypervigorous MU can make modeling increase bone mass during growth and makes remodeling keep conserving it in children and adults. These effects can be said to begin when typical bone strains rise through two threshold ranges, one for remodeling and a higher one for modeling. Raising the thresholds while normal MU continues should give bone a spurious disuse message, whereupon disuse effects would begin. The bone anatomic and tissue dynamic patterns in acute and chronic disuse resemble those seen in developing and acquired postmenopausal osteoporosis and in other forms of osteoporosis, too. If some hormones, drugs, and other agents increase those thresholds, this could explain such similarities.
The effect of ethnic group on appendicular bone mass in children
Authors: Patel Deepak N. , Pettifor John M. , Becker Pieter J. , Grieve Cathryn , Leschner Klaus 
Published: February 2010

Abstract
The prevalence of senile and postmenopausal osteoporotic fractures is considerably higher in white than black women. Although the reasons for the genetic difference have not been elucidated, it has been suggested that ethnic differences in peak bone mass may be partially responsible. The present study examined appendicular bone mass (single-photon absorptiometry, SPA) in black and white children between the ages of 6 and 20 years. The sample was stratified for ethnic group, age, and sex. The effect of weight, height, puberty, and skinfold thickness on bone mass was also assessed. The bone width (BW) and bone mineral content (BMC) of males were significantly higher than those of females (p &lt; 0.0001). There were no statistically significant differences in bone mineral content normalized for bone width (BMC/BW) between the sexes (p = 0.1743 for whites and p = 0.5456 for blacks). The bone mass parameters of black girls were generally lower than those of white girls. After adjusting for height, BMC and BMC/BW of black girls tended to be greater than those of white girls (unadjusted p = 0.0258 for BMC and p = 0.0340 for BMC/BW). White boys tended to have greater bone mass parameters than black boys. After adjusting for height the trends disappeared. Thus, unlike the studies of bone mass in adults from the United States, we were unable to show that age-matched black children have higher bone mass than whites. After adjusting for height, however, the bone mass of black children (especially black girls) was marginally, but not significantly, greater than that of white girls.
Human cystatin C, a cysteine proteinase inhibitor, inhibits bone resorption in vitro stimulated by parathyroid hormone and parathyroid hormone-related peptide of malignancy
Authors: Dr. Lerner Ulf H. , Grubb Anders 
Published: February 2010

Abstract
The effect of human recombinant cystatin C, a cysteine proteinase inhibitor, on bone resorption in vitro was evaluated. Bone resorption was assessed by analyzing the release of 45Ca and 3H from mouse calvarial bones prelabeled in vivo by injections with 45Ca or [3H]proline, respectively. In 24 h cultures, cystatin C (50 μg/ml) significantly inhibited the release of 45Ca and 3H stimulated by parathyroid hormone (PTH, 15 nmol/liter) or parathyroid hormone-related peptide of malignancy (PTHrP, 15 nmol/liter). The degree of inhibition caused by cystatin C in these 24 h cultures was similar to that caused by calcitonin (30 ng/ml). The inhibitory effect of cystatin C on 45Ca release induced by PTH was sustained in 96 h cultures, whereas the initial inhibition caused by calcitonin was transient. Cystatin C, 10–100 μg/ml, caused a dose-dependent inhibition of PTH (15 nmol/liter), and PTHrP (15 nmol/liter) stimulated 45Ca release. Addition of 50 μg/ml of cystatin C to mouse bone cultures inhibited the release of 45Ca induced by PTH and PTHrP at a wide range of submaximal and maximal concentrations of hormones (0.01–10 nmol/liter). No effect of cystatin C on 45Ca release in dead bones could be observed, nor did the inhibitor decrease the release of calcium in control bones. The inhibition by cystatin C on PTH-induced mineral mobilization was reversible. Cystatin C (1–100 μg/ml) did not affect protein synthesis or mitotic activities in mouse calvarial bones as assessed by the incorporation of I'HIproline and [3H]thymidine, respectively. These data show that cystatin C is a potent inhibitor of mineral mobilization and matrix degradation in cultured bones stimulated to resorb by PTH and PTHrP and that this effect is not due to general cytotoxicity.
1,25-Dihydroxyvitamin D3 analog structure-function assessment of the rapid stimulation of intestinal calcium absorption (transcaltachia)
Authors: Zhou Li-Xin , Nemere Ilka , Professor Norman Anthony W. 
Published: February 2010

Abstract
The possibility is now emerging that 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] can mediate biologic responses via both genomic and nongenomic pathways. To understand the molecular basis of the nongenomic response of transcaltachia, defined as the 1,25-(OH)2D3-mediated rapid (2–10 minutes) stimulation of calcium transport from the brush border to the basal lateral membrane of the epithelial cell in vitamin D-replete chick intestine, and to address the issue of whether the same receptor for the secosteroid serves as the signal transducer for both genomic and nongenomic pathways, we carried out structure-function studies using seven analogs of 1,25-(OH)2D3 with different affinities for the classic nuclear 1,25-(OH)2D3 receptor as measured by determination in a steroid competition assay of the relative competitive index (RCI). The RCI of 1,25-(OH)2D3 is by definition 100. 1,25-(OH)2D3 initiates transcaltachia within 2–10 minutes of vascular perfusion and yields a biphase response curve. Dose-dependent stimulations of Ca2+ transport by the seven analogs indicates that different structural features are essential for initiating the transcaltachic response as contrasted with binding to the classic nuclear receptor. Vascular perfusion with analogs AT (25-OH-16-ene-23-yne-D3) and Y (25-OH-23-yne-D3), which are known to activate Ca2+ channels but bind very poorly to the classic receptor (RCI &lt; 0.5), are efficient in stimulating Ca2+ transport. By comparison, compounds BT [1α,24S-(OH)2-22-en-26,27-dehydrovitamin D3] and V (1,25-(OH)2-16-ene-23-yne-D3], which bind very well to the classic nuclear receptor (RCI 75–111) but do not activate Ca2+ channels, are inefficient in stimulating Ca2+ transport. These results indicate that the membrane components that respond to the analogs of 1,25-(OH)2D, with activation of Ca2+ channels have a different ligand specificity than the classic nuclear receptor.
Is caffeine consumption a risk factor for osteoporosis?
Authors: Cooper Cyrus , Atkinson Elizabeth J. , Wahner Heinz W. , O'Fallon W. Michael , Riggs B. Lawrence , Judd Howard L. , Dr. Melton L. Joseph 
Published: February 2010

Abstract
High caffeine consumption has been proposed as a risk factor for osteoporotic fracture, but the evidence associating high caffeine intake with low bone density is inconsistent. We therefore examined the influence of caffeine consumption on bone mineral at six skeletal sites in an age-stratified random sample of white women residing in Rochester, Minnesota. After age adjustment, there was no association between overall caffeine consumption and bone mineral at five of the six sites. In the femoral shaft, however, there was a statistically significant interaction between age and caffeine consumption so that high caffeine intake was associated with slight reductions in bone mineral among elderly subjects but with modestly increased bone mineral at younger ages. When caffeine intake was categorized by source, no consistent influence of coffee, tea, or other caffeinated beverage consumption could be detected on bone mineral. Caffeine intake was, however, positively associated with cigarette smoking and alcohol consumption. After adjusting for age, caffeine consumption was not correlated with biochemical indices of bone turnover, circulating concentrations of estradiol and estrone, or other dietary and musculoskeletal variables. These data suggest that caffeine intake in the range consumed by a representative sample of white women is not an important risk factor for osteoporosis. Among elderly women, however, in whom calcium balance performance is impaired, high caffeine intake may predispose to cortical bone loss from the proximal femur.