bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellular calcium increases mediated by a recombinant human calcitonin receptor
Authors: Stroop Steven D. , Moore Emma E. 
Published: February 2010

AbstractStable transfectants expressing a recombinant human calcitonin receptor respond to calcitonin via increased cyclic adenosine 3′,5′ monophosphate (cAMP, EC50 = 0.06 nM salmon calcitonin [sCT]) and a transient mobilization of intracellular calcium ([Ca2+]i) coincident with turnover of inositol phosphate (IP; EC50 = 6 nM sCT). Millimolar increases in extracellular calcium ([Ca2+]o, EC50 = 8 mM) cause a rapid elevation in [Ca2+]i after a calcitonin dose-dependent pretreatment of cells (pretreatment EC50 = 0.2 nM sCT). Cells exhibit persistent sensitivity to increased [Ca2+]o up to 3 h after hormone exposure and even after multiple cycles of increased [Ca2+]o followed by wash. Calcitonin pretreatment of cells also allows apparent influx of elevated extracellular strontium and manganese, but little or no effect is observed on addition of barium, cadmium, or lanthanum. Human amylin (100 nM) causes a rapid and transient increase in [Ca2+]i comparable to that of calcitonin; however, no significant response to increased [Ca2+]o is observed after amylin addition. Human calcitonin gene-related product (hCGRP) (300 nM) and forskolin do not increase [Ca2+]i or activate a sensitivity to increased [Ca2+]o. Nevertheless, human amylin and human calcitonin gene-related product (hCGRP) activate adenylate cyclase with EC50s of 0.7 nM and 8 nM, respectively. The calcium-channel drugs verapamil, BAY K 8644, diltiazem, and nifedipine have little effect on [Ca2+]i increases. The calcitonin-induced transient mobilization of calcium is inhibited by treatment of cells with cholera toxin or 8-(diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8); whereas, the response to subsequent increased [Ca2+]o is inhibited by lanthanum chloride (200 μM) and lower pH (6.0). These studies suggest that a recombinant human calcitonin receptor activates three unique signal transduction pathways in BHK cells. Subnanomolar calcitonin persistently activates adenylate cyclase and a novel pathway coupled to calcium influx while much higher calcitonin levels increase inositol phosphate turnover and generate a transient mobilization of [Ca2+]i stores.
Solar ultraviolet B radiation and photoproduction of vitamin D3 in central and southern areas of argentina
Authors: Ladizesky Marta , Lu Zhiren , Oliveri Beatriz , Roman Nemesio San , Diaz Susana , Holick Michael F. , Mautalen Carlos 
Published: February 2010

Abstract
The incidence of nutritional rickets in the southern part of Argentina is 8–12 times higher than in the rest of the country. Winter 25(OH)D serum levels in normal population of southern areas are lower than in central and northern areas. To elucidate these differences, we compared the photoconversion of provitamin D3 (7-DHC) to previtamin D3 in two cities: Ushuaia (latitude 55°S) and Buenos Aires (34°S). Ampules containing 7-DHC were exposed to sunlight one day in the middle of each month either from 10:30 a.m. to 2:30 p.m. or from 8:00 a.m. to 5:00 p.m. The percentages of photoproducts formed were determined by high performance liquid chromatography (HPLC). Previous studies have proved that this is a valid model to assess “in vitro” the photoproduction of vitamin D3 in human skin. Previtamin D3 + vitamin D3 formed in Ushuaia were less (p &lt; 0.02) than those found in Buenos Aires during all seasons: summer, (X ± SEM) 6.4 ± 0.8% vs. 13.2 ± 1.8%; autumn, 1.2 ± 0.7% vs. 63 ± 1.3%; winter, 0.8 ± 0.7% vs. 3.6 ± 0.7%; spring, 3.4 ± 0.5% vs. 9.1 ± 1.1%. The photoproducts produced from 10:30 a.m. to 2:30 p.m. were similar for each month and latitude to those formed when the ampules were exposed from 8:00 a.m. to 5:00 p.m. We conclude that in Ushuaia there is a prolonged “vitamin D winter” during which cutaneous synthesis of vitamin D is absent, leading to lower serum values of 25(OH)D and contributing to the higher incidence of rickets.
The phosphatidylinositol-glycolipid anchor on alkaline phosphatase facilitates mineralization initiation in vitro
Authors: Harrison Gerald , Shapiro Irving M. , Golub Ellis E. 
Published: February 2010

Abstract
Alkaline phosphatase (AP) is required for the proper mineralization of cartilage and bone. The enzyme is localized to the outer surface of cells through a phosphatidylinositol-glycolipid anchor, which is covalently attached to the carboxyl terminus of the protein. In calcifying cartilage, AP-rich matrix vesicles (MVs) are released into the matrix from chondrocytes, and apatite formation is initiated within and around these particles. In this paper we examine the role of the AP glycolipid anchor using an in vitro mineralization assay system. AP was purified to homogeneity, and the purified enzyme was used to drive mineral formation in vitro with and without the anchor. Mineral formation was initiated through phosphate release from β-glycerol phosphate (β-GP). The amount of PO−34 released was similar whether the anchor was present or absent. However, SEM and X-ray microanalysis revealed that the mineral produced by anchored AP was indistinguishable from that produced by MVs and that both of those minerals were more apatite-like than mineral formed by soluble AP or through spontaneous precipitation. Taken together, the data suggest that in addition to providing PO−34 to drive mineralization, AP influences the nature of the mineral formed. Further, AP containing its glycolipid anchor produces mineral comparable with that formed by tissue-derived MVs. Thus, in the absence of extracellular matrix, MV mineralization in vitro can be emulated by glycolipid-anchor containing AP.
A two-year program of aerobics and weight training enhances bone mineral density of young women
Authors: Friedlander Anne L. , Genant Harry K. , Sadowsky Steven , Byl Nancy N. , Glüer Claus-C. 
Published: February 2010

Abstract
Previous research suggests that physical activity may have a beneficial effect on bone mineral density (BMD) in women. This relationship was explored in a 2-year, randomized, intervention trial investigating the efficacy of exercise and calcium supplementation on increasing peak bone mass in young women. One hundred and twenty-seven subjects (ages of 20–35 years) were randomly assigned either to an exercise program that contained both aerobics and weight training components or to a stretching program. Calcium supplementation (up to 1500 mg/day including dietary intake) or placebo was given in a double-blinded design to all subjects. Spinal trabecular BMD was determined using quantitative computed tomography (QCT). Spinal integral, femoral neck, and trochanteric BMD were measured by dual X-ray absorptiometry (DXA) and calcaneal BMD by single photon absorptiometry (SPA). Fitness variables included maximal aerobic capacity (VO2max), and isokinetic muscle performance of the trunk and thigh. Measurements were made at baseline, 1 year, and 2 years. Sixty-three subjects (32 exercise, 31 stretching) completed the study, and all the measured bone parameters indicated a positive influence of the exercise intervention. There were significant positive differences in BMD between the exercise and stretching groups for spinal trabecular (2.5%), femoral neck (2.4%), femoral trochanteric (2.3%), and calcaneal (6.4%) measurements. The exercise group demonstrated a significant gain in BMD for spinal integral (1.3 ± 2.8%, p &lt; 0.02), femoral trochanteric (2.6 ± 6.1%, p &lt; 0.05), and calcaneal (5.6 ± 5.1, p &gt; 0.01) measurements. In contrast to exercise, the calcium intervention had no positive effect on any of the bone parameters. In regard to fitness parameters, the exercise group completed the study with significant gains in VO2max and isokinetic (peak torque) values for the knee flexion and extension and trunk extension. This study indicates that over a 2-year period, a combined regimen of aerobics and weight training has beneficial effects on BMD and fitness parameters in young women. However, the addition of daily calcium supplementation does not add significant benefit to the intervention.
Oral 1,25-dihydroxyvitamin D administration in osteoporotic women: Effects of estrogen therapy
Authors: Dr. Cosman Felicia , Nieves Jeri , Shen Victor , Lindsay Robert 
Published: February 2010

Abstract
Estrogen has been shown to modify calcium and skeletal homeostasis. In this study, we tested the ability of estrogen to influence the effects of short-term 1,25(OH)2D administration on biochemical indices of bone formation and resorption in a cross-sectional analysis of untreated (n = 10) and estrogen-treated (n = 14) osteoporotic women. Patients were given oral 1,25(OH)2D (Rocaltrol) 0.5 μg twice a day for 5 days. Serum and urine were sampled at baseline and then 1 h after the first daily Rocaltrol dose for the 5 days of the study. 1,25(OH)2D levels rose similarly in both groups with plateaus reached by the third day of the investigation. Serum PTH levels decreased by the first sampling period (1 h after first Rocaltrol dose; p &lt; 0.008 both groups) and continued to fall gradually in both groups. There were no changes in serum calcium but serum phosphorus rose by the second day (p &lt; 0.05 both groups) and remained elevated throughout the remainder of the protocol. Serum bone GIa protein increased approximately 40% (p &lt; 0.05) with no group differences. In contrast, total alkaline phosphatase and carboxy-terminal propeptide of type I collagen did not increase in either group. Furthermore, there were no significant increments in any bone resorption indicators, including serum tartrate-resistant acid phosphatase and cross-linked carboxy-terminal telopeptide of type I collagen, as well as urine hydroxyproline and pyridinoline. Serum IGF-1 levels also remained unchanged in both groups. We conclude that oral 1,25(OH)2D administration decreased 1–84PTH levels, probably due to a suppression of parathyroid production, and did not stimulate bone resorption. Since only bone GIa protein increased, it is unclear whether or not bone formation was actually stimulated. Estrogen treatment did not modify the skeletal response to low levels of oral 1,25(OH)2D stimulation in osteoporotic women.
Different effects of bisphosphonate and estrogen therapy on free and peptide-bound bone cross-links excretion
Authors: Garnero Patrick , Gineyts Evelyne , Arbault Patrice , Christiansen Claus , Delmas Pierre D. 
Published: February 2010

Abstract
We have measured the free and peptide-bound type I collagen cross-link excretions in normal women and in patients with metabolic bone disease using the HPLC technique and immunoassays recognizing specifically the free or peptide-bound forms of pyridinoline (Pyr). After menopause, free deoxypyridinoline (free D-Pyr) excretion measured by HPLC without urine hydrolysis and expressed as a fraction of the total excretion was lower than in premenopausal women (45 ± 15% vs. 59 ± 12%, p &gt; 0.005), whereas the fraction of free Pyr was not changed. In normal pre- and postmenopausal women (n = 43), the fraction of free D-Pyr was negatively correlated with bone turnover rate as assessed by the total urinary excretion of Pyr (r = –0.64, p &gt; 0.001). In patients with a variety of metabolic bone diseases characterized by increased bone turnover (osteoporosis, Paget's disease, and hyperthyroidism), the fractions of free Pyr and free D-Pyr were significantly lower than in premenopausal controls (p &gt; 0.001 for all diseases). After 3 days of intravenous (iv) treatment with the bisphosphonate pamidronate in patients with Paget's disease and osteoporosis, the urinary excretion of cross-linked peptides measured by high performance liquid chromatography (HPLC) or enzyme-linked immunoassay (ELISA) (NTX and CrossLaps) was markedly decreased (–52% and –85% for NTX, –71% and –93% for CrossLaps™ in Paget's disease and osteoporosis, respectively). The excretion of total cross-links was decreased to a lesser extent after treatment (–25% and –25% for total Pyr, –37% and –45% for total D-Pyr) and, surprisingly, free cross-links measured either by HPLC without urine hydrolysis or with an ELISA specific for free D-Pyr were unchanged after treatment. In contrast to bisphosphonate therapy, estrogen treatment of postmenopausal women decreased not only total and cross-linked peptides but also the free cross-link excretion that was reduced by about 30–40%. The different effects of bisphosphonate and estrogen therapy on the excretion of peptide-bound and free cross-link excretion were confirmed by gel filtration of the urine on Sephadex G 25 before and after treatment. In conclusion, we have shown that increased bone turnover in patients with metabolic bone disease could result in a larger increase of the urinary excretion of cross-linked peptides over the increase of free cross-links. Bisphosphonate therapy decreased markedly cross-linked peptides without significant change in free cross-link excretion contrasting with a decrease of both free and peptide-bound cross-links after estrogen therapy. These data suggest that these two antiresorptive therapies may affect differently the pattern of bone collagen degradation, an intriguing possibility that should be further investigated in vitro.
Cyclical clodronate is effective in preventing postmenopausal bone loss: A comparative study with transcutaneous hormone replacement therapy
Authors: Prof. Filipponi Paolo , Pedetti Mariano , Fedeli Leone , Cini Luisella , Palumbo Renato , Boldrini Stefano , Massoni Cristina , Cristallini Sonia 
Published: February 2010

AbstractAn investigative study was carried out for 2 years involving 124 randomly selected early postmenopausal women with spine bone mineral density (BMD) below the mean value of a normal premenopausal subject. After random division into three groups, the first 42 patients were treated with transcutaneous 17-β-estradiol (50 μg daily), the second 42 were treated with cyclical intravenous clodronate (200 mg/month iv infusion), and the third group of 40 (controls) was left untreated. After 2 years, the total drop in BMD within the control group was more than 7% as opposed to the values of –0.14% ± 0.93 in the estradiol group and 0.67% ± 0.84 in the clodronate group. A change in BMD of &lt; 1% was considered satisfactory, and this result was obtained in 32% of the controls, in 79% of the estradiol group where the percentage change in BMD moderately correlated with serum estradiol levels (r = 0.399), and in 90% of the clodronate-treated patients, in whom the percentage change in BMD inversely correlated with basal values of markers of bone turnover. Both estrogen and clodronate prevent postmenopausal bone loss. The response to transcutaneous hormone replacement therapy may be influenced by transcutaneous absorption and by a lower sensitivity to estrogen. Response to cyclical clodronate seems to be influenced by the rate of bone turnover. An interdosage interval ranging from 2–4 weeks appears suitable for most patients.
Inhibitory effects of basic fibroblast growth factor on chondrocyte differentiation
Authors: Dr. Wroblewski J. , Edwall-Arvidsson C. 
Published: February 2010

Abstract
The role of basic fibroblast growth factor (bFGF) and insulin-like growth factor I (IGF-I) in cartilage growth was studied in primary cultures of rat rib growth plate chondrocytes. Growth factors effects on expression of the proto-oncogene c-fos, DNA synthesis, differentiation, and morphological changes were analyzed by in situ hybridization, 3H-thymidine incorporation, and light and fluorescence microscopy. In serum-deprived cells, bFGF induced a transient expression of c-fos with a maximal effect 15–30 minutes after stimulation. After 24 h of culture it had a slightly lower stimulatory effect on DNA synthesis than IGF-I, but became a significantly more potent mitogen than IGF-I after 48 and 72 h. The stimulatory effect of bFGF on DNA synthesis coincided with a decrease in collagen type II and IGF-II expression. In contrast, IGF-I alone stimulated expression of these genes. In bFGF-treated cultures, cell morphology and the appearance of actin filaments was changed. Polygonal chondrocytes became elongated, fibroblast-like, and the smooth actin filaments were brush-like and disrupted. Addition of IGF-I reduced these changes without affecting c-fos expression induced by bFGF. Our results suggest that bFGF stimulates cell proliferation by preventing terminal differentiation of chondrocytes. This effect is mediated by induction of c-fos expression and a decrease in the steady-state levels of transcripts for collagen II and IGF-II.
Prevalence of low femoral bone density in older U.S. women from NHANES III
Authors: Looker Anne C. , Johnston Conrad C. , Wahner Heinz W. , Dunn William L. , Calvo Mona S. , Harris Tamara B. , Heyse Stephen P. , Lindsay Robert L. 
Published: February 2010

Abstract
Data on the number of U.S. women with low femoral bone mineral density (BMD) are currently available only from indirect estimates. We used dual-energy X-ray absorptiometry (DXA) measurements of femoral BMD from phase 1 of the third National Health and Nutrition Examination Survey (NHANES III, 1988–1991) to estimate prevalences of low femoral BMD in women ages 50 years and older using an approach proposed recently by an expert panel of the World Health Organization (WHO). Cutpoints for low BMD were derived from BMD data of 194 non-Hispanic white (NHW) women aged 20–29 years from the NHANES III dataset. The prevalence of older U.S. women with femoral osteopenia (BMD between 1 standard deviation [SD] and 2.5 SD below the mean of young NHW women) ranged from 34–50% in four different femur regions, which corresponds to ∼12–17 million women. The prevalence with osteoporosis (BMD &gt;2.5 SD below the mean of young NHW women) ranged from 17–20%, or ∼6–7 million women. Prevalences were 1.3–2.4 times higher in NHW women than non-Hispanic black women (NHB), and 0.8–1.2 times higher in NHW versus Mexican American (MA) women. The estimated numbers of NHW, NHB, and MA women with osteopenia were 10–15 million, 800,000–1.2 million, and 300,000–400,000, respectively; corresponding figures for osteoporosis were 5–6 million, 200,000–300,000, and 100,000 respectively. Thus, the first data on BMD from a nationally representative sample of older women show a substantial number with low femoral BMD. The majority of these women are white, but the number of minority women with low BMD is not trivial.
Quantitative analysis of trabecular microstructure by 400 MHz nuclear magnetic resonance imaging
Authors: Chung Hsiao-Wen , Wehrli Felix W. , Williams John L. , Kugelmass Steven D. , Wehrli Suzanne L. 
Published: February 2010

Abstract
A new approach for the quantitative analysis of trabecular microstructure, based on high-field proton nuclear magnetic resonance (NMR) imaging, is presented. NMR is ideal because it provides high contrast between the marrow proton signal and the bone, which appears with background intensity. Images from 1 cm3 defatted specimens of trabecular bone, suspended in water doped with 1 mM Gd(DTPA) to shorten T1 to about 300 ms, can be obtained at a resolution on the order of 30–50 μm and slice thickness of 150 μm, in 10 minutes at 400 MHz proton frequency. Digital image processing algorithms were designed and evaluated for the measurement of bone area fraction, perimeter length, mean trabecular thickness, and separation. Bone area fraction derived from the NMR images was found to be in excellent agreement with bone volume fraction measured independently (slope = 0.96, r2 = 0.924, p &lt; 0.0001). Errors in the mean trabecular thickness and separation were &lt;6%. The effects of finite imaging slice thickness and signal-to-noise ratio (SNR) were also evaluated. The data suggest a resolution of 50 × 50 × 200 μm3 and an SNR on the order of 10 to provide safe margins for precise and accurate structural analysis by means of the algorithms presented in this paper. The method allows simultaneous measurement at multiple locations within the specimen volume without the need for physical sectioning.
The effects of menopause and age on calcitropic hormones: A cross-sectional study of 655 healthy women aged 35 to 90
Authors: Assoc. Prof. Prince Richard L. , Dick Ian , Devine Amanda , Price Roger I. , Gutteridge Donald H. , Kerr Deborah , Criddle Arthur , Garcia-Webb Peter , John Andrew St. 
Published: February 2010

Abstract
Although women lose 30% of their skeletal mass after the menopause, the mechanism of this loss is uncertain. Clearly estrogen deficiency is important but whether this works only through direct effects on the skeleton is uncertain. To examine these mechanisms further we have evaluated calcium-related metabolic factors in 655 healthy women. Fasting blood samples were collected from all subjects who were up to 35 years past the menopause, and fasting urine and 24-h urine samples were collected in 365 women who were up to 25 years past the menopause. In the first 15 years postmenopause, there was a rise in total plasma calcium due to a rise in albumin. Bone resorption (hydroxyproline creatinine ratio), bone formation (alkaline phosphatase), and the urine calcium creatinine ratio all rose at menopause and remained elevated for the next 25 years. There was a transient further rise in bone resorption for the 10 years following menopause. Neither PTH nor the free calcitriol index changed for the first 10 years following menopause. Ten years past the menopause, although total calcitriol rose, the free calcitriol index fell due to a rise in vitamin D binding protein. PTH began to rise at 15 years past menopause. GFR fell gradually over the 25 years following menopause. Thus following menopause there is an increase in bone turnover and increased urine calcium loss independent of any effect of PTH or calcitriol, suggesting a direct effect of estrogen deficiency on bone and kidney. At 10 years postmenopause, the free calcitriol index fell and PTH began to rise, these changes being associated with persistent elevation of bone resorption perhaps due to increased PTH action on the bone. The cause of the fall in the free calcitriol ratio may be due to progressive renal deterioration and phosphate retention. The cause of the rise in PTH may be due to a negative external calcium balance due to a reduction in gut calcium absorption, a consequence of relative deficiency of 25 hydroxyvitamin D and the fall in calcitriol together with persistent renal calcium loss.