bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synthesis and Structure of a Pyridine Complex of Trinuclear Molybdenum Cluster [Mo3S4Cl4(py)5]
Authors: Mizutani Jun , Imoto Hideo , Saito Taro 
Published: April 2006

Abstract
A pyridine complex of trinuclear molybdenum chloro sulfido cluster [Mo3S4Cl4(py)5] has been synthesized by the excision reaction of a solid state cluster compound Mo3S7Cl4 with pyridine and triphenylphosphine. The structure has been determined by the single crystal X-ray structure analysis.
Poly(phenylenevinylene) Bearing Built-in tert-Butylnitroxide. A Polyradical Ferromagnetically Coupled in the Intrachain
Authors: Kaneko Takashi , Toriu Shuichi , Kuzumaki Yoshihiro , Nishide Hiroyuki , Tsuchida Eishun 
Published: April 2006

Abstract
Poly(1,4- or 1,2-phenylenevinylene)s bearing a 2- or 4-substituted nitroxide radical were synthesized by polymerizing [bromo[N-tert-butyl-N-(trialkylsiloxy)amino]]styrenes with a palladium catalyst. The polyradicals were chemically stable, and their ESR and SQUID measurements indicated an intramolecular and through-bond ferromagnetic coupling.
High Resolution Solid State NMR in Liquids 3. 1H NMR Study of Organic Nano-Particles
Authors: Satoh Naoki , Kimura Keisaku 
Published: April 2006

Abstract
High resolution 1H NMR spectra of terephthalic acid (TPA) ultrafine particles (UFP’s) were obtained by means of motional narrowing caused by Brownian motion of UFP’s in a liquid phase of CCl4. In the case of dispersing condition of UFP’s, highly resolved signals from benzoic protons were obtained at 6.85, 6.95, 7.08, 7.25, 7.50 and 7.65 ppm with respect to tetramethylsilane (TMS), even though only a signal at 8.15 ppm was obtained from moleculary dispersed TPA in acetone. Particle size was obtained to be ca. 15 nm by a dynamic laser scattering method.
Reaction of Lanthanum(III) and Gadolinium(III) Complexes Coordinated by Pendant-armed Macrocyclic Ligand with Salicylaldehyde
Authors: Kanesato Masatoshi , Yokoyama Toshiro , Itabashi Osamu 
Published: April 2006

Abstract
In the reaction of Lanthanum(III) and Gadolinium(III) complexes coordinated by the ligand 1,9-bis(2-aminoethyl)-1,4,6,9,12,14-hexaazacyclohexadecane with salicylaldehyde, only Gd3+ was led to an unexpected complex with the ligand tris{2-(salicylideneamino)ethyl}amine. The difference of the reactivity was applied to the separation of La3+ and Gd3+.
Reactions of Alkyl malonates with Molybdenum and Tungsten Complexes. Syntheses and Structure of Hydrido-Malonato Complexes
Authors: Minato Makoto , Kurishima Susumu , Nagai Ko-ichiro , Yamasaki Mikio , Ito Takashi 
Published: April 2006

Abstract
Molybdenum and tungsten hydrido-malonato complexes have been prepared by the photochemical or thermal reactions of [MoH4(dppe)2] or trans-[W(N2)2(dppe)2] with an excess of alkyl malonates. The structure of the complex is reported, and a possible mechanism is proposed for the reaction.
Separation of Lead(II) by Solvent Extraction and Membrane Transport with a Dibenzopolyether Dicarboxylic Acid Ionophore
Authors: Hayashita Takashi , Fujimoto Takashi , Morita Yuki , Bartsch Richard A 
Published: April 2006

Abstract
The lipophilic di-ionizable ionophore 1,5-Bis[2-(2′-carboxyheptyloxy)phenoxy]-3-oxapentane (1) provides a selective solvent extraction of Pb(II) from Cu(II). The stoicheometry of the extracted species is determined to be 1:1 by equilibrium analysis. Ionophore 1 also functions as a carrier in polymeric plasticizer membrane for separation of Pb(II) from Cu(II).
JunB as a Downstream Mediator of PTHrP Actions in Cementoblasts
Authors: Berry Janice E , Ealba Erin L , Pettway Glenda J , Datta Nabanita S , Swanson Erica C , Somerman Martha J , McCauley Laurie K 
Published: April 2006

Abstract
The role of AP-1 family members in the action of PTHrP was examined in cementoblasts. PTHrP increased mRNA and protein levels of all Fos members, but only one Jun member (JunB) was increased. Overexpression of JunB in cementoblasts mimicked actions of PTHrP to support osteoclastogenesis and inhibit cementoblast differentiation, suggesting that the actions of PTHrP on mesenchymal cells operate through JunB.
Introduction: Cementoblasts are mesenchymal cells that share phenotypic features with osteoblasts in vitro; however, unlike osteoblasts, cementoblasts rarely support osteoclastogenesis in vivo. The osteoblast-mediated support of osteoclastogenesis involves PTH-induced reduction in osteoprotegerin (OPG) expression. PTH acts on osteoblastic cells through specific signaling pathways and transcription factors such as activator protein 1 (AP-1). The purpose of this study was to determine the impact of PTH-related protein (PTHrP) on AP-1 transcription factors in cementoblasts and the role of JunB in the actions of PTHrP.
Materials and Methods: Cementoblastic cells were treated with PTHrP and evaluated for mRNA and protein levels of AP-1 family members. Stable transfectants of OCCM cells overexpressing JunB were evaluated for OPG production, ability to support osteoclastogenesis, and measures of proliferation and differentiation.
Results: PTHrP treatment in vitro resulted in a time-dependent upregulation of mRNA and proteins for the Fos family members, but only JunB of the Jun family. OPG mRNA and protein levels were reduced by PTHrP in OCCM and were lower in JunB overexpressing cells than controls. In co-culture experiments, TRACP+ cells were increased with RANKL treatment in JunB overexpressing cells compared with controls. Cementoblast differentiation was reduced with overexpression of JunB as measured by a decrease in mineralized nodule formation and gene expression for bone sialoprotein and osterix. Measures of proliferation including cell number and cyclin D1 levels were increased in JunB overexpressing clones. In vivo, cementoblast implants exhibited a cementoblastoid nature with copious mineral-like matrix, whereas JunB-overexpressing implants were densely cellular with little mineralized matrix.
Conclusions: JunB was the only Jun family member increased by PTHrP, and its overexpression showed similar patterns of gene expression and OPG production as PTHrP treatment of controls. These data suggest that JunB may be a key mediator of PTHrP actions in cementoblasts.
Suppression of Adjuvant-Induced Arthritic Bone Destruction by Cyclooxygenase-2 Selective Agents With and Without Inhibitory Potency Against Carbonic Anhydrase II
Authors: Katagiri Mika , Ogasawara Toru , Hoshi Kazuto , Chikazu Daichi , Kimoto Aishi , Noguchi Masahiro , Sasamata Masao , Harada Shun-ichi , Akama Hideto , Tazaki Hatsue , Chung Ung-il , Takato Tsuyoshi , Nakamura Kozo , Kawaguchi Hiroshi 
Published: April 2006

Abstract
In vitro assays revealed that COX-2 inhibitors with CA II inhibitory potency suppressed both differentiation and activity of osteoclasts, whereas that without the potency reduced only osteoclast differentiation. However, all COX-2 inhibitors similarly suppressed bone destruction in adjuvant-induced arthritic rats, indicating that suppression of osteoclast differentiation is more effective than that of osteoclast activity for the treatment.
Introduction: Cyclooxygenase (COX)-2 and carbonic anhydrase II (CA II) are known to play important roles in the differentiation of osteoclasts and the activity of mature osteoclasts, respectively. Because several COX-2 selective agents were recently found to possess an inhibitory potency against CA II, this study compared the bone sparing effects of COX-2 selective agents with and without the CA II inhibitory potency.
Materials and Methods: Osteoclast differentiation was determined by the mouse co-culture system of osteoblasts and bone marrow cells, and mature osteoclast activity was measured by the pit area on a dentine slice resorbed by osteoclasts generated and isolated from bone marrow cells. In vivo effects on arthritic bone destruction were determined by radiological and histological analyses of hind-paws of adjuvant-induced arthritic (AIA) rats.
Results: CA II was expressed predominantly in mature osteoclasts, but not in the precursors. CA II activity was inhibited by sulfonamide-type COX-2 selective agents celecoxib and JTE-522 similarly to a CA II inhibitor acetazolamide, but not by a methylsulfone-type COX-2 inhibitor rofecoxib. In vitro assays clearly revealed that celecoxib and JTE-522 suppressed both differentiation and activity of osteoclasts, whereas rofecoxib and acetazolamide suppressed only osteoclast differentiation and activation, respectively. However, bone destruction in AIA rats was potently and similarly suppressed by all COX-2 selective agents whether with or without CA II inhibitory potency, although only moderately by acetazolamide.
Conclusions: Suppression of osteoclast differentiation by COX-2 inhibition is more effective than suppression of mature osteoclast activity by CA II inhibition for the treatment of arthritic bone destruction.
The 25-Hydroxyvitamin D 1-Alpha-Hydroxylase Gene Maps to the Pseudovitamin D-Deficiency Rickets (PDDR) Disease Locus
Authors: St-Arnaud René , Messerlian Serge , Moir Janet M. , Omdahl John L. , Glorieux Francis H. 
Published: April 2006

Abstract
Pseudovitamin D-deficiency rickets (PDDR) is an autosomal recessive disorder that may be due to impaired activity of 25-hydroxyvitamin D-1α-hydroxylase, a renal cytochrome P450 enzyme (P4501α) of the vitamin D pathway. The disease locus for PDDR has been mapped by linkage analysis to 12q13-q14, but the molecular defect underlying the enzyme dysfunction has remained elusive due to the lack of sequence information for the P4501α gene (hereafter referred to as 1α-OHase). We have used a probe derived from the rat 25-hydroxyvitamin D-24-hydroxylase (CYP24; 24-OHase) sequence to identify and clone the 1α-OHase cDNA. The full-length 1α-OHase clone of 2.4 kb codes for a protein of predicted Mr 55 kDa. Functional activity of the cloned sequence was assessed using transient transfection, and the production of authentic 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] was confirmed using high performance liquid chromatography fractionation and time-of-flight mass spectrometry. The expression of the gene was analyzed in vitamin D–replete animals; treatment with 1α,25(OH)2D3 reduced 1α-OHase transcript levels by 70%, while administration of parathyroid hormone led to a 2-fold increase in the expression of the gene, thus confirming the hormonal regulation previously described using biochemical methods. The rat cDNA was used to obtain a human genomic clone. Interestingly, the human 1α-OHase gene mapped to 12q13.1-q13.3, providing strong evidence that a mutation in the 1α-OHase gene is responsible for the PDDR phenotype. The availability of a cloned sequence for 1α-OHase generates novel tools for the study of the molecular etiology of PDDR, and will allow the investigation of other disturbances of vitamin D metabolism.
Different Morphometric and Densitometric Parameters Predict Cervical and Trochanteric Hip Fracture: The EPIDOS Study
Authors: Duboeuf F. , Hans D. , Schott A. M. , Kotzki P. O. , Favier F. , Marcelli C. , Meunier P. J. , Delmas P. D. 
Published: April 2006

Abstract
We used an experimental software measuring the hip axis length (HAL) and bone mineral density (BMD) in specific regions of the lower and upper part of the femoral neck on dual-energy X-ray absorptiometry scans. To determine whether these parameters were significant predictors of the type of hip fracture, we measured 167 healthy women (controls), 24 women with trochanteric, and 42 women with cervical hip fractures within the EPIDOS prospective cohort. EPIDOS is a multicenter prospective study on risk factors for hip fracture performed in 7575 elderly women living at home, aged 75–95 and conducted in five French centers (Amiens, Lyon, Montpellier, Paris, Toulouse). Measurements were performed on data acquired at baseline before the occurrence of fracture. In the cervical fracture group, HAL was significantly longer than in controls (94.2 vs. 92.3, p = 0.03), and the associated odds ratio (OR) adjusted for age, weight, and total femoral neck BMD was significant (OR = 1.64, 95% confidence interval [CI] 1.06–2.55). In contrast, HAL was not significantly different from controls in the trochanteric fracture group. Femoral neck diameter was not a predictor of fracture. The upper and lower femoral neck BMD was lower in the trochanteric fracture group than in controls, and both measurements predicted trochanteric femoral neck fracture. In contrast, the prediction of cervical femoral neck fracture was enhanced by measuring only the upper part of the femoral neck (OR = 2.79 vs. 1.97 for the total femoral neck) while BMD of the lower part was not different from controls. Hip axis length is a predictor of femoral neck fracture. Femoral neck BMD distribution is different between cervical and trochanteric fractures. These results support the hypothesis of a different pathophysiological mechanism between the two types of hip fractures.
Influence of the Vitamin D Receptor Gene Alleles on Bone Mineral Density in Postmenopausal and Osteoporotic Women
Authors: Dr. Vandevyver Caroline , Wylin Tine , Cassiman Jean-Jacques , Raus Jef , Geusens Piet 
Published: April 2006

Abstract
It is well established that genetic factors contribute to bone turnover and bone density. Evidence exists suggesting that a major part of this genetic influence may be due to polymorphisms in the vitamin D receptor (VDR) gene. However, it is not clear whether the VDR genotype effect persists in elderly women. In the present study, the relationship between the BsmI, ApaI, and TaqI polymorphisms in the VDR gene, and the bone mineral density (BMD) at the lumbar spine, the femoral neck (FN), and the proximal radius was investigated in a large group of elderly women (75.5 ± 5.0 years) of Caucasian origin and in 84 Type I osteoporotic women (66.6 ± 8.4 years). We did not find a correlation between the VDR genotypes and BMD in elderly women. However, a significantly higher FN-BMD was observed in obese (body mass index [BMI] &gt; 30 kg/m2) versus nonobese (BMI &lt; 30 kg/m2) women (p &lt; 0.01). This relationship was observed for all BsmI genotypes. Furthermore, the FN-BMD of nonobese women with bb BsmI genotype was 5% higher than that of women with the BB genotype (p = 0.04). We conclude that the VDR gene polymorphisms influence the FN-BMD in nonobese postmenopausal women. In a second part of the study, possible correlations between the VDR gene polymorphisms and osteoporosis Type I were analyzed. Our data could not reveal any association between these parameters.
Three-Fold Induction of Renal 25-Hydroxyvitamin D3-24-Hydroxylase Activity and Increased Serum 24,25-Dihydroxyvitamin D3 Levels Are Correlated with the Healing Process After Chick Tibial Fracture
Authors: Seo Eun-Gyoung , Prof. Norman Anthony W. 
Published: April 2006

Abstract
To investigate the possible biological actions of 24,25-dihydroxyvitamin D3 (24,25(OH)2D3), a tibial fracture-healing model was established in White Leghorn chicks. Three-week-old White Leghorn chicks fed a vitamin D3–replete diet were divided into four groups (control, anesthetized, sham, and fractured). On varying days after tibial fracture (F) or sham manipulation (S), renal 25(OH)D3-1α-hydroxylase and 25(OH)D3-24-hydroxylase (24-hydroxylase) activities and serum Ca2+ concentrations were measured. Metofane anesthesia was found to have no effect on the activity of either of the hydroxylases; the activities of the hydroxylases in the control, anesthetized, and sham-operated birds were similar. By 10 days after tibial fracture, the renal 24-hydroxylase activity increased more than 3-fold in F (1.33 ± 0.07 pmol/mg of protein) as compared with S (0.42 ± 0.03 pmol/mg of protein) (p &lt; 0.0001). A time-dependent study of the renal 24-hydroxylase activity during the fracture repair process revealed a slow increase from the first day after fracture, a higher activity at 8 days, which peaked at 10–11 days, which is consistent with the formation of the callus. The 24-hydroxylase activity then returned to the same level as the sham group 14 days after fracture. There was no significant difference in serum Ca2+ levels between the F and S groups over the 3-week postfracture period. Serum levels of vitamin D3 metabolites were also measured during the fracture healing process: a 3.4× increase of the 24,25(OH)2D3 level in the fractured group (3.64 ± 1.16 nM) was observed as compared with the control groups (1.08 ± 0.49 nM) at 10 days after fracture (p = 0.068). No significant differences were observed in the plasma levels of 25(OH)D3 or 1α,25(OH)2D3 between the group with a fracture and the controls. Exposure of primary chick kidney cells in culture to serum obtained from chicks with a tibial fracture for 20 h resulted in an ∼40% increase in the activity of the 24-hydroxylase as compared with cells exposed to serum from control birds. These results suggest that 24,25(OH)2D3 is involved in the early process of fracture repair and that there is some form of physiological communication between the fractured bone and the kidney so as to increase the renal 24-hydroxylase and the circulating concentration of this metabolite.
Quantitative Ultrasound of the Calcaneus Reflects the Mechanical Properties of Calcaneal Trabecular Bone
Authors: Bouxsein M. L. , Radloff S. E. 
Published: April 2006

Abstract
To provide new information about the potential role of quantitative ultrasound (QUS) in fracture risk prediction, we assessed whether QUS and densitometric variables derived from measurements of intact cadaveric feet were associated with the mechanical properties of calcaneal trabecular bone. We obtained 31 intact cadaveric feet from the local anatomic gifts program, including 13 men and 18 women, with a mean age of 77 years (range 50–91 years). Broadband ultrasound attenuation (BUA) and ultrasound transit velocity (SOS) were assessed in the intact cadaveric feet using a water-based ultrasound system. In addition, we measured the bone mineral density (BMD) of the posterior calcaneus using dual-energy X-ray absorptiometry. Cubes of trabecular bone were then removed from the calcaneus at approximately the same location as the QUS measurements were obtained, and the elastic modulus and ultimate strength of the trabecular bone specimens were measured by compressing them in the mediolateral direction. We found that QUS variables were moderately to strongly correlated with the mechanical properties of calcaneal trabecular bone (r2 = 0.48–0.63, p &lt; 0.001 for all). However, the strongest associations with the mechanical properties trabecular bone were provided by calcaneus BMD and trabecular bone apparent density (r2 = 0.66–0.88). BUA and densitometric measurements were independently associated with elastic modulus, but not with ultimate strength. Our results indicate that QUS measurements of the intact heel are associated with the mechanical properties of calcaneal trabecular bone and, in some cases, provide information in addition to that provided by BMD or density measurements.
Characterization of Native and Recombinant Bone Sialoprotein: Delineation of the Mineral-Binding and Cell Adhesion Domains and Structural Analysis of the RGD Domain
Authors: Stubbs John T. , Mintz Keith P. , Eanes Edward D. , Torchia Dennis A. , Fisher Larry W. 
Published: April 2006

Abstract
Bone sialoprotein is a small, sulfated, and phosphorylated integrin-binding glycoprotein apparently found only in tissues that eventually mineralize. Nondenatured bone sialoprotein (BSP) purified from rat osteosarcoma cell line (UMR 106–01 BSP) culture media is shown to have a hydroxyapatite Kd ≈ 2.6 × 10−9 M, perhaps the strongest affinity for this mineral of any of the matrix proteins. Both native BSP and a 47 kD fragment of UMR-BSP (Fragment 1 ∼133A–∼265Y) are more potent inhibitors of seeded hydroxyapatite crystal growth than recombinant human BSP fragments lacking post-translational modifications. The recombinant proteins, however, do show reproducible inhibitory activity, suggesting that at least some of the strong mineral-binding properties are encoded directly within the protein sequence itself. BSP facilitates the adhesion of several cell types through its integrin binding (RGD) tripeptide sequence. Nuclear magnetic resonance (NMR) analysis of a15N-enriched 59 amino acid recombinant domain containing the RGD tripeptide shows that the structure of this isolated domain is highly flexible with or without 5 mM calcium. Previous work has also shown that an endogenous fragment of UMR-BSP (Fragment 1) supports cell adhesion in the absence of the RGD sequence. In this report, non-RGD cell adhesion sites are localized within conserved amino- and carboxy-terminal tyrosine-rich domains of recombinant human BSP. Given the proximity of the latter non-RGD cell adhesion site to the RGD tripeptide, a model of BSP-receptor interactions is presented.
Clodronate and Liposome-Encapsulated Clodronate Are Metabolized to a Toxic ATP Analog, Adenosine 5′-(β,γ-Dichloromethylene) Triphosphate, by Mammalian Cells In Vitro
Authors: Frith Julie C. , Mönkkönen Jukka , Blackburn G. Michael , Russell R. Graham G. , Rogers Michael J. 
Published: April 2006

Abstract
Clodronate, alendronate, and other bisphosphonates are widely used in the treatment of bone diseases characterized by excessive osteoclastic bone resorption. The exact mechanisms of action of bisphosphonates have not been identified but may involve a toxic effect on mature osteoclasts due to the induction of apoptosis. Clodronate encapsulated in liposomes is also toxic to macrophages in vivo and may therefore be of use in the treatment of inflammatory diseases. It is generally believed that bisphosphonates are not metabolized. However, we have found that mammalian cells in vitro (murine J774 macrophage-like cells and human MG63 osteosarcoma cells) can metabolize clodronate (dichloromethylenebisphosphonate) to a nonhydrolyzable adenosine triphosphate (ATP) analog, adenosine 5′-(β,γ-dichloromethylene) triphosphate, which could be detected in cell extracts by using fast protein liquid chromatography. J774 cells could also metabolize liposome-encapsulated clodronate to the same ATP analog. Liposome-encapsulated adenosine 5′-(β,γ-dichloromethylene) triphosphate was more potent than liposome-encapsulated clodronate at reducing the viability of cultures of J774 cells and caused both necrotic and apoptotic cell death. Neither alendronate nor liposome-encapsulated alendronate were metabolized. These results demonstrate that the toxic effect of clodronate on J774 macrophages, and probably on osteoclasts, is due to the metabolism of clodronate to a nonhydrolyzable ATP analog. Alendronate appears to act by a different mechanism.