bluuebunny/crossref_metadata_2025_split huggingface dataset:
Photochemical Reaction of (l-cysteinesulfinato-N,S){tris(2-aminoethyl)amine}cobalt(III). Formation of a Cobalt(III) Complex with an Uncoordinated Sulfinate Group
Authors: Akhter Farooque MD , Kojima Masaaki , Hirotsu Masakazu , Kashino Setsuo , Yoshikawa Yuzo 
Published: April 2006

Abstract
On photolysis of cis(t-N,S)-[Co{S(O)2CH2CH(COOH)NH2-S,N}(tren)]2+ (t-N = tertiary amine nitrogen; tren = tris(2-aminoethyl)amine) with visible light two types of linkage isomerization took place to yield cis(t-N,O(C))-[Co{NH2CH(CH2SO2)COO-N,O}(tren)]+ (O(C) = oxygen of carboxylate group) with an uncoordinated sulfinate group, and a pair of diastereomers of cis(t-N,O(S))-[Co{OS(O)CH2CH(COOH)NH2-O,N}(tren)]2+ (O(S) = oxygen of sulfinate group).
Aggregation Numbers and Shapes of Lysophosphatidylcholine and Lysophosphatidylethanolamine Micelles
Authors: Hayashi Hideko , Yamanaka Teruko , Miyajima Miyuki , Imae Toyoko 
Published: April 2006

Abstract
Aggregation numbers and shapes of 1-palmitoyl-sn-glycero-3-phosphocholine(LPPC) and 1-lauroyl-sn-glycero-3-phosphoethanolamine(LLPE) micelles have been investigated at 35 °C by static and dynamic light scattering method. The average aggregation number of LPPC micelle is 139. The LLPE micelle is rod-like shape, and grows with increasing concentration. At 5.87 mg cm−3 micelle concentration, apparent aggregation number of LLPE is 902 and average length of rigid rod is estimated to be 45–57 nm.
Alkali Metal Sensing with a Fluorescent 5,11,17,23-Tetraphenylcalix[4]arene and the Mechanism of the Fluorescence Change
Authors: Matsumoto Hitoshi , Shinkai Seiji 
Published: April 2006

Abstract
The fluorescence intensity of a tetraester derivative of the title compound increases markedly upon the Na+-binding. Hence, this is useful as a new, convenient Na+-sensing system. The mechanism of the fluorescence increase is discussed by comparing the fluorescence properties of several reference compounds.
Electrochemical Intercalation of Organic Molecules into Thin Film of Layered Oxide MoO3
Authors: Tagaya Hideyuki , Ara Kensuke , Ogata Tateaki , Matsushita Koichi , Kadokawa Jun-ichi , Karasu Masa , Chiba Koji 
Published: April 2006

Abstract
Electrochemical reduction of vacuum evaporated MoO3 thin film in organic electrolyte solution resulted in the formation of organic intercalation compounds of pyridine, 4-methylpyridine and 4-propylpyridine. Interlayer spacings of MoO3 increased to 12–19 Å by the intercalation, and reduction of MoO3 was confirmed by XPS measurement.
A Remarkably Rapid Synthesis of Ruthenium(II) Polypyridine Complexes by Microwave Irradiation
Authors: Matsumura-Inoue Takeko , Tanabe Masahiro , Minami Takayoshi , Ohashi Tomoko 
Published: April 2006

Abstract
A facile synthesis method or ruthenium(II) polypyridine complexes by microwave irradiation has been developed. This method greatly reduces reaction time from 4 hours to 20 minutes with better yield(60–90%). The procedures are simple and may be used for synthesis of a variety of metal polypyridine complexes.
The effect of serum creatinine method choice on estimated glomerular filtration rate determined by the abbreviated MDRD formula
Authors: McKillop Derek J , Cairns Brian , Duly Ellie , Van Drimmelen Marie , Ryan Michael 
Published: April 2006

Background: The aim of this study was to measure the variability in estimated glomerular filtration rate (eGFR) calculated by laboratories in Northern Ireland where creatinine assays other than the Beckman CX3 assay used to derive the Modification of Diet in Renal Disease (MDRD) are utilized. Methods: Fifty patient samples were analysed for serum creatinine by kinetic Jaffe assays on the Roche modular P-800 (compensated assay), the Beckman LX20 and the Abbott Aeroset analysers. Results: The median (interquartile range) eGFR calculated by the abbreviated MDRD equation using the creatinine results obtained by each method were 45.4 (31.7-66.6), 49.2 (35.4-78.1) and 50.0 (35.1-71.2) mL/min/1.73 m2 for Beckman, Roche (compensated) and Abbott assays, respectively. Following mathematical alignment of creatinine methods to the Beckman method the median (interquartile range) eGFR for the Roche and Abbott methods were 44.0 (32.0-67.6) and 45.6 (31.2-64.8) mL/min/1.73 m2, respectively. Conclusion: The regression equations published in this study can be used to align creatinine methods. However, method-related biases in eGFR of up to10% are minimal in the context of the magnitude of variance reflected in the 90% confidence intervals.
Rho and Rho Kinase Are Involved in Parathyroid Hormone-Stimulated Protein Kinase C α Translocation and IL-6 Promoter Activity in Osteoblastic Cells
Authors: Radeff Julie M , Nagy Zsolt , Stern Paula H 
Published: April 2006

Abstract
The role of small G-proteins in PTH-stimulated PKC translocation and IL-6 promoter expression in UMR-106 cells was determined. The effects of PTH(1–34) and PTH(3–34) in stimulating PKCα translocation and IL-6 were inhibited by agents that interfere with the activity of small G-proteins of the Rho family and with the downstream kinase Rho kinase.
Introduction: Activation of protein kinase C (PKC) is a signaling mechanism by which parathyroid hormone (PTH) modulates interleukin-6 (IL-6) in osteoblasts, leading to osteoclastogenesis and bone resorption. PKCα and PKCβI are translocated after treatment with PTH in UMR-106 osteoblastic cells; however, the pathway leading to PKC isozyme translocation is not established. Diacylglycerol (DAG) generation from phospholipase D (PLD) is one pathway of PKC activation, and PTH-mediated PLD activity is dependent on small G-proteins of the Rho family. This study investigated whether Rho proteins modulate the PKCα translocation and IL-6 promoter activity stimulated by PTH in UMR-106 cells.
Materials and Methods: UMR-106 cells were treated with PTH(1–34) or PTH(3–34). PKC translocation was determined by immunofluorescence, Rho A activation by Rhotekin assay and by translocation assessed by Western blotting in membrane and cytosol fractions, and IL-6 promoter expression by luciferase assay.
Results and Conclusions: Inhibition of Rho proteins with Clostridium difficile toxin B or inhibition of Rho prenylation with GGTI attenuated PTH(1–34)- and PTH(3–34)-stimulated translocation of endogenous PKCα and IL-6 promoter activity. Expression of a constitutively active RhoA (RhoA63L) mimicked the effect of PTH(1–34) or PTH(3–34) to promote membrane localization of PKCα, whereas cells expressing a dominant negative RhoA (RhoA19N) did not respond to PTH(1–34) or PTH(3–34). The Rho kinase inhibitor Y27632 attenuated PTH(1–34)- and PTH(3–34)-stimulated PKCα translocation and IL-6 promoter activation. Rho seemed to be acting at a step before production of diacylglycerol (DAG), because the stimulation of PKCα translocation by the DAG mimetic phorbol 12,13 dibutyrate (PDBu) was unaffected by C. difficile toxin B or Y27632. These results indicate that Rho proteins are an important component of PTH signaling in osteoblastic cells and provide further demonstration of convergence between PKC and small G-protein signaling pathways.
Intravenous Pamidronate Prevents Femoral Bone Loss and Renal Stone Formation During 90-Day Bed Rest
Authors: Watanabe Yukiko , Ohshima Hiroshi , Mizuno Koh , Sekiguchi Chiharu , Fukunaga Masao , Kohri Kenjiro , Rittweger Jörn , Felsenberg Dieter , Matsumoto Toshio , Nakamura Toshitaka 
Published: April 2006

AbstractLong-term bed rest has potential risks of bone loss and renal stone formation. We examined the effects of resistive exercise and intravenous pamidronate on BMD, bone turnover, urinary calcium, and renal stone formation in 25 healthy males during 90-day bed rest. Pamidronate prevented femoral bone loss and renal stone formation, but resistive exercise showed little effects.Introduction: Long-term bed rest increases the risks of bone loss and urinary stone formation. Resistive exercise increases bone formation, and bisphosphonates reduce bone resorption. However, the effects of muscle exercise and bisphosphonates have not been examined side-by-side. The objectives of this study are to compare the effects of pamidronate with resistive exercise on BMD and renal stone formation during prolonged bed rest.Materials and Methods: Twenty-five male white volunteers, 26–45 years of age, were randomly assigned to the control (n = 9), exercise (n = 9), and pamidronate (n = 7) groups and underwent 90-day 6° head-down tilt bed rest. Exercise group performed squats and heel raises on a flywheel device for 30 minutes every 3 days. Pamidronate (60 mg) was administered intravenously 14 days before bed rest. BMD of the head, forearm, lumbar spine, and proximal femur; biochemical bone markers; calcium (Ca) metabolism; and abdominal radiographs were examined during 90 days of bed rest and 360 days of reloading.Results: In controls, proximal femoral BMD decreased, and bone resorption markers and urinary Ca increased during bed rest, along with development of renal stones in two of nine subjects. Resistive exercise increased bone formation but was unable to prevent femoral BMD decrease and increases in bone resorption and urinary Ca during bed rest, with formation of renal stones in four of nine subjects. Pamidronate maintained femoral BMD, reduced bone resorption and urinary Ca, and completely prevented renal stone formation.Conclusions: Resistive exercise increased bone formation but could not reduce bone resorption and the risk of renal stones. In contrast, inhibition of bone resorption by pamidronate could preserve bone mineral and reduce the risk of renal stone formation during prolonged bed rest.
Additive Protective Effects of Estrogen and Androgen Treatment on Trabecular Bone in Ovariectomized Rats
Authors: Tivesten Åsa , Movérare-Skrtic Sofia , Chagin Andrei , Venken Katrien , Salmon Phil , Vanderschueren Dirk , Sävendahl Lars , Holmäng Agneta , Ohlsson Claes 
Published: April 2006

Abstract
Both ER and AR activation regulates trabecular bone mass. We show that combined estrogen and androgen treatment results in additive protection of trabecular bone in OVX rats. This may in part be attributable to the effect of AR activation to attenuate the inhibitory effect of ER activation on bone formation.
Introduction: Sex steroids are important regulators of trabecular bone mass. Both estrogen receptor (ER) and androgen receptor (AR) activation results in increased trabecular bone mass. The aim of this study was to investigate if combined estrogen and androgen treatment might be beneficial in the treatment of trabecular bone loss.
Materials and Methods: Twelve-week-old female rats were ovariectomized (OVX) and treated with vehicle (V), 17β-estradiol (E2; ER activation), dihydrotestosterone (DHT; AR activation), or the combination (E2 + DHT) for 6 weeks. The skeletal phenotype was analyzed by pQCT, μCT, histomorphometry of growth plates, and serum levels of biochemical bone markers.
Results: Both E2 (+121% over V) and DHT (+34%) preserved the trabecular volumetric BMD (tvBMD) in OVX rats. The effect of E2 and DHT on tvBMD was additive, resulting in a 182% increase over V in the rats given E2 + DHT. μCT analyses of the trabecular bone microstructure revealed that the effect of E2 and DHT was additive on the number of trabeculae. E2 treatment reduced serum markers of both bone resorption (collagen C-terminal telopeptide) and bone formation (osteocalcin), indicating reduced bone turnover. Addition of DHT to E2 treatment did not modulate the effects of E2 on the marker of bone resorption, whereas it attenuated the inhibitory effect of E2 on the bone formation marker, which might explain the additive protective effect of E2 and DHT on trabecular bone mass. In contrast, DHT partially counteracted the suppressive effect of E2 on longitudinal bone growth and the E2-induced alterations in growth plate morphology.
Conclusions: These findings show that combined estrogen and androgen treatment results in additive protective effects on trabecular bone in OVX rats. Our data suggest that a combined treatment with selective ER and AR modulators might be beneficial in the treatment of osteoporosis.
Sesquiterpene Lactone Parthenolide Blocks Lipopolysaccharide-Induced Osteolysis Through the Suppression of NF-κB Activity
Authors: Yip Kirk Ho Man , Zheng Ming H , Feng Hao Tian , Steer James H , Joyce David A , Xu Jiake 
Published: April 2006

Abstract
Effective treatment for bacteria-induced bone lytic diseases is not yet available. In this study, we showed that PAR, an NF-κB inhibitor found in medicinal herbs, can block LPS-induced osteolysis. PAR does this by inhibiting osteoclastogenesis and bone resorption and promoting apoptosis of osteoclasts through the suppression of NF-κB activity.
Introduction: Osteolysis induced by chronic gram-negative bacterial infection underlies many bone diseases such as osteomyelitis, septic arthritis, and periodontitis. Drugs that inhibit lipopolysaccharide (LPS)-induced osteolysis are critically needed for the prevention of bone destruction in infective bone diseases. In this study, we investigated the effect of parthenolide (PAR) on LPS-induced osteolysis in vivo and studied its role in osteoclastogenesis, bone resorption, apoptosis, and NF-κB activity.
Materials and Methods: The LPS-induced osteolysis in the mouse calvarium model was used to examine the effect of PAR in vivo. RANKL-induced osteoclast differentiation from RAW264.7 cells and bone resorption assays were used to assess the effect of PAR in vitro. Assays for NF-κB activation, p65 translocation, and IκB-α degradation were used to determine the mechanism of action of PAR in osteoclasts and their precursors. Flow cytometry and confocal microscopic analysis were used to examine cell apoptosis. Semiquantitative RT-PCR was performed to examine the effect of PAR on gene expression of RANK and TRAF6.
Results: We found that PAR (0.5 and 1 mg/kg), injected simultaneously with LPS (25 mg/kg) or 3 days later, blocked the LPS-induced osteolysis in the mouse calvarium model. In vitro studies showed that low concentrations of PAR (&lt;1 μM) inhibited in vitro osteoclastogenesis and osteoclastic bone resorption, whereas higher concentrations (&gt;5 μM) triggered apoptotic cell death of osteoclasts and their precursor cells in a dose-dependent manner. Furthermore, PAR inhibited LPS-induced NF-κB activation, p65 translocation, and IκB-α degradation both in mature osteoclasts and their precursors in a time- and dose-dependent manner. In addition, PAR inhibited NF-κB activation induced by osteoclastogenic factors RANKL, interleukin (IL)-1β, or TNF-α to varying degrees and reduced the gene expression of RANK and TRAF6.
Conclusion: The NF-κB pathway is known to mediate both osteoclast differentiation and survival. These findings indicate that PAR blocks LPS-induced osteolysis through the suppression of NF-κB activity and suggest that it might have therapeutic value in bacteria-induced bone destruction.
Multiple Genetic Loci From CAST/EiJ Chromosome 1 Affect vBMD Either Positively or Negatively in a C57BL/6J Background
Authors: Edderkaoui Bouchra , Baylink David J , Beamer Wesley G , Wergedal Jon E , Dunn Nancy R , Shultz Kathryn L , Mohan Subburaman 
Published: April 2006

Abstract
Skeletal phenotype analyses of 10 B6.CAST-1 congenic sublines of mice have revealed evidence for the presence of three closely linked QTLs in Chr 1 that influence femoral vBMD both positively and negatively.
Introduction: BMD is an important component of bone strength and a recognized predictor of risk for osteoporotic fracture. Our goal in this study was to fine map the chromosomal location of volumetric BMD (vBMD) quantitative trait loci (QTLs) in mouse distal chromosome 1 (Chr 1).
Materials and Methods: After several backcrosses of the B6.CAST-1T congenic strain, which carried the initial BMD QTL in Chr 1 with B6 mice, the N10F1 generation mice were intercrossed to obtain recombinations that yielded different regions of the QTL. Thirty-eight polymorphic markers were used to fine map the initial 1T QTL region (100-192 Mb). Different skeletal parameters were compared between the 10 sublines and B6 female mice at 16 weeks of age. A t-test was used to determine the significant difference between sublines and B6 control mice, whereas one-way ANOVA and posthoc (Newman-Keuls) tests were performed to compare the phenotype between the sublines.
Results: Significantly higher femur vBMD was found in sublines that carried cast alleles from 100 to 169 and 172 to 185 Mb of the centromere compared with the B6 control mice (10-12%, p &lt; 0.001). However, sublines that carried cast alleles from 185 to 192 Mb showed significantly lower femur vBMD compared with the control mice (−6%, p &lt; 0.05). Furthermore, femur vBMD phenotype showed a negative correlation with endosteal circumference (r = −0.8, p = 0.003), and a strong correlation with cortical thickness for combined data from the 10 sublines (r = 0.97, p &lt; 0.001). Moreover, a high correlation was found between body weight and both periosteal and endosteal circumferences for sublines carrying cast alleles from 167 to 175, 168 to 185, and 169 to 185 Mb, whereas no significant correlation was found between these parameters for sublines carrying cast alleles from 172 to 185 Mb.
Conclusions: Genetic analysis using congenic sublines revealed that the initial BMD QTL on Chr 1 is a complex site with multiple loci affecting bone phenotypes, showing the value of the congenic approach in clearly identifying loci that control specific traits.
Effects of Cyclic Versus Daily hPTH(1-34) Regimens on Bone Strength in Association With BMD, Biochemical Markers, and Bone Structure in Mice
Authors: Iida-Klein Akiko , Hughes Christine , Lu Shi Shou , Moreno Annette , Shen Victor , Dempster David W , Cosman Felicia , Lindsay Robert 
Published: April 2006

Abstract
We developed a cyclic PTH regimen with repeated cycles of 1-week on and off daily PTH injection and explored its effects on bone strength, BMD, bone markers, and bone structure in mice. Cyclic protocols produced 60–85% of the effects achieved by daily protocols with 57% of the total PTH given, indicating more economic use of PTH. The study supports further exploration of cyclic PTH regimens for the treatment of osteoporosis.
Introduction: To minimize the cost and the catabolic action of hPTH(1-34), a cyclic PTH regimen with repeated 3-month cycles of on-and-off daily injection of hPTH(1-34) was developed in humans and shown to be as effective as a daily regimen in increasing vertebral BMD. However, changes in BMD may not adequately predict changes in bone strength. A murine model was developed to explore the efficacy of a cyclic PTH regimen on bone strength in association with other bone variables.
Materials and Methods: Twenty-week-old, intact, female C57BL/J6 mice (n = 7/group) were treated with (1) daily injection with vehicle for 7 weeks (control); (2) daily injection with hPTH(1-34) (40 μg/kg/day) for 7 weeks (daily PTH); and (3) daily injection with hPTH(1-34) and vehicle alternating weekly for 7 weeks (cyclic PTH). BMD was measured weekly by DXA, and serum bone markers, bone structure, and strength were measured at 7 weeks.
Results: Daily and cyclic PTH regimens increased BMD at all sites by 16–17% and 9–12%, respectively (all p &lt; 0.01). The most dramatic effect of cyclic PTH occurred during the second week of treatment when PTH was off, with femoral and tibial BMD continuing to increase to the same extent as that produced by daily PTH. Both daily and cyclic PTH regimens significantly increased osteocalcin (daily, 330%; cyclic, 260%), mTRACP (daily, 145%; cyclic, 70%), femoral cortical width (daily, 23%; cyclic, 13%), periosteal circumference (daily, 5%; cyclic, 3.5%), and bone strength (max load: daily, 48%; cyclic, 28%; energy absorbed: daily, 103%; cyclic, 61%), respectively. Femoral bone strength was positively correlated with BMD, bone markers, and cortical structure. Neither regimen had an effect on vertebral bone strength. Although actual effects of cyclic PTH were 60–85% of those produced by daily PTH, the effects of cyclic PTH per unit amount administered were slightly greater than those of daily PTH for most measures.
Conclusions: PTH-enhanced femoral bone strength is positively correlated with its effects on femoral BMD, bone markers, and bone structure. Cyclic PTH regimens represent a potential economic use of PTH and warrant further study.
Pharmacological Sequestration of Intracellular Cholesterol in Late Endosomes Disrupts Ruffled Border Formation in Osteoclasts
Authors: Zhao Haibo , Väänänen H Kalervo 
Published: April 2006

Abstract
We showed that the ruffled border lacks a late endosomal lipid, LBPA, but is enriched in cholesterol. A hydrophobic amine, U18666A, causes cholesterol accumulation in LBPA+ late endosomes in osteoclasts. Specific targeting of cathepsin K and the vacuolar H+-ATPase at the ruffled border is blocked by U18666A. A membrane trafficking pathway from baso-lateral membrane toward the resorptive organelle is also arrested by the inhibitor. These results indicate cholesterol homeostasis regulates late endosomal/lysosomal trafficking and polarized secretion in resorbing osteoclasts.
Introduction: Protons and acidic proteases are secreted into the resorption lacuna through the ruffled border to solubilize bone mineral and digest the organic bone matrix, respectively. Whereas evidence suggests this event occurs through a vesicular trafficking mechanism, this issue remains unresolved.
Materials and Methods: The distribution of lysobisphosphatidic acid (LBPA) and cholesterol in resorbing osteoclasts was examined by laser scanning confocal microscopy. The effects of U18666A on ruffled border formation were observed by electron microscopy.
Results and Conclusions: The ruffled border does not contain LBPA but is enriched in cholesterol. We found a hydrophobic amine, U18666A, which blocks the efflux of cholesterol from late endosomes in other cells, causes cholesterol accumulation in LBPA-containing late endosomes in osteoclasts, leading to diminished cholesterol at the ruffled border. Reflecting the U18666A-mediated inhibition of late endosome/lysosome transport, the resorptive membrane is disrupted and contains a paucity of cathepsin K and the vacuolar H+-ATPase. These results indicate that the ruffled border is formed by the fusion of lysosomes with the plasma membrane in osteoclasts through a process that is cholesterol regulated.