bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of bendiocarb on development of the chick embryo
Authors: Petrovová Eva , Maženský Dávid , Vdoviaková Katarína , Massanyi Peter , Luptáková Lenka , Smrčo Peter 
Published: February 2010

AbstractAgrochemicals, including pesticides, are being used in increasing amounts in agriculture and are therefore potential environmental contaminants which may affect a variety of biological systems. The pesticide residues directly affect the embryos, disturbing their normal development and causing pathophysiological and morphological changes. We have observed embryotoxicity of cholinesterase inhibitor bendiocarb in the chick embryo. The pesticide dissolved in 10% acetone in water for injection was applied in a volume of 200 μl over the embryo through membrana papyracea at embryonic days (ED) 2, 3, 4, 5 and 10. The toxicity of bendiocarb was rather low, and lethal dose (LD50) decreased with advancing development from 0.97 mg per egg at ED 2 to 28.6 mg on ED 5. The malformations in surviving embryos were observed rarely (<2%) and occurred in both control and experimental groups. In the treatment at ED 5 and 10 there was a statistically significant reduction in body weight, but the maximum difference from controls was below 14%. In treated chick embryos on ED 3 and 4 was observed a small but not significant increase in number of dead cells using supravital staining. We conclude that bendiocarb possesses no significant toxicity in the avian embryo. Our analysis of bendiocarb embryotoxic potential in the chick embryo supports the earlier observations in other animal models, testifying to the relative safety of bendiocarb for the embryo or fetus. Copyright © 2010 John Wiley & Sons, Ltd.
Men with metabolic syndrome have lower bone mineral density but lower fracture risk—the MINOS study
Authors: Szulc Pawel , Varennes Annie , Delmas Pierre D , Goudable Joëlle , Chapurlat Roland 
Published: February 2010

Abstract
Data on the association of the metabolic syndrome (MetS) with bone mineral density (BMD) and fracture risk in men are inconsistent. We studied the association between MetS and bone status in 762 older men followed up for 10 years. After adjustment for age, body mass index, height, physical activity, smoking, alcohol intake, and serum 25-hydroxycholecalciferol D and 17β-estradiol levels, men with MetS had lower BMD at the hip, whole body, and distal forearm (2.2% to 3.2%, 0.24 to 0.27 SD, p &lt; .05 to .005). This difference was related to abdominal obesity (assessed by waist circumference, waist-hip ratio, or central fat mass) but not other MetS components. Men with MetS had lower bone mineral content (3.1% to 4.5%, 0.22 to 0.29 SD, p &lt; .05 to 0.001), whereas differences in bone size were milder. Men with MetS had a lower incidence of vertebral and peripheral fractures (6.7% versus 12.0%, p &lt; .05). After adjustment for confounders, MetS was associated with a lower fracture incidence [odds ratio (OR) = 0.33, 95% confidence interval (CI) 0.15–0.76, p &lt; .01]. Among the MetS components, hypertriglyceridemia was most predictive of the lower fracture risk (OR = 0.25, 95%CI 0.10–0.62, p &lt; .005). Lower fracture risk in men with MetS cannot be explained by differences in bone size, rate of bone turnover rate and bone loss, or history of falls or fractures. Thus older men with MetS have a lower BMD related to the abdominal obesity and a lower risk of fracture related to hypertriglyceridemia. MetS probably is not a meaningful concept in the context of bone metabolism. Analysis of its association with bone-related variables may obscure the pathophysiologic links of its components with bone status. © 2010 American Society for Bone and Mineral Research
Two doses of sclerostin antibody in cynomolgus monkeys increases bone formation, bone mineral density, and bone strength
Authors: Ominsky Michael S , Vlasseros Fay , Jolette Jacquelin , Smith Susan Y , Stouch Brian , Doellgast George , Gong Jianhua , Gao Yongming , Cao Jin , Graham Kevin , Tipton Barbara , Cai Jill , Deshpande Rohini , Zhou Lei , Hale Michael D , Lightwood Daniel J , Henry Alistair J , Popplewell Andrew G , Moore Adrian R , Robinson Martyn K , Lacey David L , Simonet W Scott , Paszty Chris 
Published: February 2010

Abstract
The development of bone-rebuilding anabolic agents for treating bone-related conditions has been a long-standing goal. Genetic studies in humans and mice have shown that the secreted protein sclerostin is a key negative regulator of bone formation. More recently, administration of sclerostin-neutralizing monoclonal antibodies in rodent studies has shown that pharmacologic inhibition of sclerostin results in increased bone formation, bone mass, and bone strength. To explore the effects of sclerostin inhibition in primates, we administered a humanized sclerostin-neutralizing monoclonal antibody (Scl-AbIV) to gonad-intact female cynomolgus monkeys. Two once-monthly subcutaneous injections of Scl-AbIV were administered at three dose levels (3, 10, and 30 mg/kg), with study termination at 2 months. Scl-AbIV treatment had clear anabolic effects, with marked dose-dependent increases in bone formation on trabecular, periosteal, endocortical, and intracortical surfaces. Bone densitometry showed that the increases in bone formation with Scl-AbIV treatment resulted in significant increases in bone mineral content (BMC) and/or bone mineral density (BMD) at several skeletal sites (ie, femoral neck, radial metaphysis, and tibial metaphysis). These increases, expressed as percent changes from baseline were 11 to 29 percentage points higher than those found in the vehicle-treated group. Additionally, significant increases in trabecular thickness and bone strength were found at the lumbar vertebrae in the highest-dose group. Taken together, the marked bone-building effects achieved in this short-term monkey study suggest that sclerostin inhibition represents a promising new therapeutic approach for medical conditions where increases in bone formation might be desirable, such as in fracture healing and osteoporosis. © 2010 American Society for Bone and Mineral Research
A patient with severe hypercalcemia in multiple organ dysfunction syndrome: Role of elevated circulating 1α,25(OH)2vitamin D levels
Authors: Kazama Junichiro James , Yamamoto Takashi , Oya Hiroshi , Yamamoto Satoshi , Sato Yoshinobu , Sakurada Junko , Honda Tadayuki , Endoh Hiroshi , Narita Ichiei 
Published: February 2010

Abstract
A 54-year-old man was transferred to our ICU because of systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS). He died after 38 days of intensive care. During treatment, his serum calcium (Ca) levels continued to increase and reached 3.95 mmol/L, while the ionized Ca levels reached 2.30 mmol/L before his death. He presented with severe kidney injury, pancreatitis, and hemorrhagic gastric erosion that worsened his prognosis; these were possibly associated with the hypercalcemia. His circulating 1α,25-dihydroxyvitamin D [1,25(OH)2D] level was elevated (75.7 to 204 pg/mL), whereas the levels of 25-hydroxyvitamin D, parathyroid hormone, and parathyroid hormone–related peptide were not. Liver histology revealed immunoreactivity for 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) in some of the hepatocytes, in which the localization pattern was similar to that of lysozyme-positive hepatocytes. Our ICU has previously encountered 22 similar MODS patients who presented with hypercalcemia over the last 8 years. SIRS with severe kidney and liver injuries are common clinical findings in hypercalcemic patients with MODS. Of the 23 hypercalcemic MODS patients, including the present patient, 17 had circulating 1,25(OH)2D levels exceeding 70 pg/mL despite severe kidney injury. Extrarenal activation of CYP27B1 seems to play a role in the development of hypercalcemia in this disease condition. Clinicians need to be aware that severe hypercalcemia may occur in MODS patients. © 2010 American Society for Bone and Mineral Research
Estimates of the proportion of older white men who would be recommended for pharmacologic treatment by the new US national osteoporosis foundation guidelines
Authors: Donaldson Meghan G , Cawthon Peggy M , Lui Lily Y , Schousboe John T , Ensrud Kristine E , Taylor Brent C , Cauley Jane A , Hillier Teresa A , Dam Thuy T , Curtis Jeff R , Black Dennis M , Bauer Douglas C , Orwoll Eric S , Cummings Steven R 
Published: February 2010

Abstract
The new US National Osteoporosis Foundation's (NOF's) Clinician's Guide to Prevention and Treatment of Osteoporosis includes criteria for recommending pharmacologic treatment based on history of hip or vertebral fracture, femoral neck or spine bone mineral density (BMD) T-scores of −2.5 or less, and presence of low bone mass at the femoral neck or spine plus a 10-year risk of hip fracture of 3% or greater or of major osteoporotic fracture of 20% or greater. The proportion of men who would be recommended for treatment by these guidelines is not known. We applied the NOF criteria for treatment to men participating in the Osteoporotic Fractures in Men Study (MrOS). To determine how the MrOS population differs from the general US population of Caucasian men aged 65 years and older, we compared men in MrOS with men who participated in the National Health and Nutrition Examination Survey (NHANES) III on criteria included in the NOF treatment guidelines that were common to both cohorts. Compared with NHANES III, men in MrOS had higher femoral neck BMD values. Application of NOF guidelines to MrOS data estimated that at least 34% of US white men aged 65 years and older and 49% of those aged 75 years and older would be recommended for drug treatment. Application of the new NOF guidelines would result in recommending a very large proportion of white men in the United States for pharmacologic treatment of osteoporosis, for many of whom the efficacy of treatment is unknown. © 2010 American Society for Bone and Mineral Research
Phosphoproteome reveals an atlas of protein signaling networks during osteoblast adhesion
Authors: Milani Renato , Ferreira Carmen V. , Granjeiro José M. , Paredes‐Gamero Edgar J. , Silva Rodrigo A. , Justo Giselle Z. , Nader Helena B. , Galembeck Eduardo , Peppelenbosch Maikel P. , Aoyama Hiroshi , Zambuzzi Willian F. 
Published: February 2010

AbstractCell adhesion on surfaces is a fundamental process in the emerging biomaterials field and developmental events as well. However, the mechanisms regulating this biological process in osteoblasts are not fully understood. Reversible phosphorylation catalyzed by kinases is probably the most important regulatory mechanism in eukaryotes. Therefore, the goal of this study is to assess osteoblast adhesion through a molecular prism under a peptide array technology, revealing essential signaling proteins governing adhesion‐related events. First, we showed that there are main morphological changes on osteoblast shape during adhesion up to 3 h. Second, besides classical proteins activated upon integrin activation, our results showed a novel network involving signaling proteins such as Rap1A, PKA, PKC, and GSK3β during osteoblast adhesion on polystyrene. Third, these proteins were grouped in different signaling cascades including focal adhesion establishment, cytoskeleton rearrangement, and cell‐cycle arrest. We have thus provided evidence that a global phosphorylation screening is able to yield a systems‐oriented look at osteoblast adhesion, providing new insights for understanding of bone formation and improvement of cell–substratum interactions. Altogether, these statements are necessary means for further intervention and development of new approaches for the progress of tissue engineering. J. Cell. Biochem. 109: 957–966, 2010. © 2010 Wiley‐Liss, Inc.
Intact T cell receptor signaling by CD4+ T cells cultured in the rotating wall‐vessel bioreactor
Authors: Simons D.M. , Gardner E.M. , Lelkes P.I. 
Published: February 2010

AbstractT lymphocytes fail to proliferate or secrete cytokines in response to T cell receptor (TCR) agonists during culture in spaceflight or ground‐based microgravity analogs such as rotating wall‐vessel (RWV) bioreactors. In RWVs, these responses can be rescued by co‐stimulation with sub‐mitogenic doses of the diacyl glycerol (DAG) mimetic phorbol myristate acetate. Based on this result we hypothesized that TCR activation is abrogated in the RWV due to impaired DAG signaling downstream of the TCR. To test this hypothesis we compared TCR‐induced signal transduction by primary, human, CD4+ T cells in RWV, and static culture. Surprisingly, we found little evidence of impaired DAG signaling in the RWV. Upstream of DAG, the tyrosine phosphorylation of several key components of the TCR‐proximal signal was not affected by culture in the RWV. Similarly, the phosphorylation and compartmentalization of ERK and the degradation of IκB were unchanged by culture in the RWV indicating that RAS‐ and PKC‐mediated signaling downstream of DAG are also unaffected by simulated microgravity. We conclude from these data that TCR signaling through DAG remains intact during culture in the RWV, and that the loss of functional T cell activation in this venue derives from the affect of simulated microgravity on cellular processes that are independent of the canonical TCR pathway. J. Cell. Biochem. 109: 1201–1209, 2010. © 2010 Wiley‐Liss, Inc.
Integrin‐linked kinase is involved in TNF‐α‐induced inducible nitric‐oxide synthase expression in myoblasts
Authors: Tsou Hsi‐Kai , Su Chen‐Ming , Chen Hsien‐Te , Hsieh Ming‐Han , Lin Cheng‐Jyh , Lu Dah‐Yuu , Tang Chih‐Hsin , Chen Yi‐Hung 
Published: February 2010

AbstractTumor necrosis factor‐α (TNF‐α) is a pleiotropic cytokine produced by activated macrophages. Nitric oxide (NO) is a highly reactive nitrogen radical implicated in inflammatory responses. We investigated the signaling pathway involved in inducible nitric oxide synthase (iNOS) expression and NO production stimulated by TNF‐α in cultured myoblasts. TNF‐α stimulation caused iNOS expression and NO production in myoblasts (G7 cells). TNF‐α‐mediated iNOS expression was attenuated by integrin‐linked kinase (ILK) inhibitor (KP392) and siRNA. Pretreatment with Akt inhibitor, mammalian target of rapamycin (mTOR) inhibitor (rapamycin), NF‐κB inhibitor (PDTC), and IκB protease inhibitor (TPCK) also inhibited the potentiating action of TNF‐α. Stimulation of cells with TNF‐α increased ILK kinase activity. TNF‐α also increased the Akt and mTOR phosphorylation. TNF‐α mediated an increase of NF‐κB‐specific DNA–protein complex formation, p65 translocation into nucleus, NF‐κB‐luciferase activity was inhibited by KP392, Akt inhibitor, and rapamycin. Our results suggest that TNF‐α increased iNOS expression and NO production in myoblasts via the ILK/Akt/mTOR and NF‐κB signaling pathway. J. Cell. Biochem. 109: 1244–1253, 2010. © 2010 Wiley‐Liss, Inc.
Global minimum geometries of acetylene clusters (HCCH)n with n ≤ 55 obtained by a heuristic method combined with geometrical perturbations
Authors: Takeuchi Hiroshi 
Published: February 2010

AbstractGeometry optimization of acetylene clusters (HCCH)n in the range of n ≤ 55 was carried out with a recently proposed intermolecular potential consisting of Morse potentials, damped dispersion terms, and damped Coulomb terms. The heuristic method developed by the present author was used in the optimization: optimal geometries were searched by using geometry perturbations and subsequent local optimizations. The calculations were repeated until the global minimum was found for each cluster at least three times. The obtained results were analyzed to examine structural evolution of the clusters. The geometries of the clusters with n ≥ 25 were similar to the geometry in the cubic crystal of acetylene whereas smaller clusters take icosahedron‐based geometries. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Thermodynamic stability of hydrogen‐bonded systems in polar and nonpolar environments
Authors: Pašalić Hasan , Aquino Adélia J. A. , Tunega Daniel , Haberhauer Georg , Gerzabek Martin H. , Georg Herbert C. , Moraes Tatiane F. , Coutinho Kaline , Canuto Sylvio , Lischka Hans 
Published: February 2010

AbstractThe thermodynamic properties of a selected set of benchmark hydrogen‐bonded systems (acetic acid dimer and the complexes of acetic acid with acetamide and methanol) was studied with the goal of obtaining detailed information on solvent effects on the hydrogen‐bonded interactions using water, chloroform, and n‐heptane as representatives for a wide range in the dielectric constant. Solvent effects were investigated using both explicit and implicit solvation models. For the explicit description of the solvent, molecular dynamics and Monte Carlo simulations in the isothermal–isobaric (NpT) ensemble combined with the free energy perturbation technique were performed to determine solvation free energies. Within the implicit solvation approach, the polarizable continuum model and the conductor‐like screening model were applied. Combination of gas phase results with the results obtained from the different solvation models through an appropriate thermodynamic cycle allows estimation of complexation free energies, enthalpies, and the respective entropic contributions in solution. Owing to the strong solvation effects of water the cyclic acetic acid dimer is not stable in aqueous solution. In less polar solvents the double hydrogen bond structure of the acetic acid dimer remains stable. This finding is in agreement with previous theoretical and experimental results. A similar trend as for the acetic acid dimer is also observed for the acetamide complex. The methanol complex was found to be thermodynamically unstable in gas phase as well as in any of the three solvents. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Evaluation of the performance of four molecular docking programs on a diverse set of protein‐ligand complexes
Authors: Li Xun , Li Yan , Cheng Tiejun , Liu Zhihai , Wang Renxiao 
Published: February 2010

AbstractMany molecular docking programs are available nowadays, and thus it is of great practical value to evaluate and compare their performance. We have conducted an extensive evaluation of four popular commercial molecular docking programs, including Glide, GOLD, LigandFit, and Surflex. Our test set consists of 195 protein‐ligand complexes with high‐resolution crystal structures (resolution ≤2.5 Å) and reliable binding data [dissociation constant (Kd) or inhibition constant (Ki)], which are selected from the PDBbind database with an emphasis on diversity. The top‐ranked solutions produced by these programs are compared to the native ligand binding poses observed in crystal structures. Glide and GOLD demonstrate better accuracy than the other two on the entire test set. Their results are also less sensitive to the starting structures for docking. Comparison of the results produced by these programs at three different computation levels reveal that their accuracy are not always proportional to CPU cost as one may expect. The binding scores of the top‐ranked solutions produced by these programs are in low to moderate correlations with experimentally measured binding data. Further analyses on the outcomes of these programs on three suites of subsets of protein‐ligand complexes indicate that these programs are less capable to handle really flexible ligands and relatively flat binding sites, and they have different preferences to hydrophilic/hydrophobic binding sites. Our evaluation can help other researchers to make reasonable choices among available molecular docking programs. It is also valuable for program developers to improve their methods further. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Cognitive‐behavioral treatment for chronic nightmares in trauma‐exposed persons: assessing physiological reactions to nightmare‐related fear
Authors: Rhudy Jamie L. , Davis Joanne L. , Williams Amy E. , McCabe Klanci M. , Bartley Emily J. , Byrd Patricia M. , Pruiksma Kristi E. 
Published: February 2010

AbstractCognitive‐behavioral treatments (CBTs) that target nightmares are efficacious for ameliorating self‐reported sleep problems and psychological distress. However, it is important to determine whether these treatments influence objective markers of nightmare‐related fear, because fear and concomitant physiological responses could promote nightmare chronicity and sleep disturbance. This randomized, controlled study (N=40) assessed physiological (skin conductance, heart rate, facial electromyogram) and subjective (displeasure, fear, anger, sadness, arousal) reactions to personally relevant nightmare imagery intended to evoke nightmare‐related fear. Physiological assessments were conducted at pretreatment as well as 1‐week, 3‐months, and 6‐months posttreatment. Results of mixed effects analysis of variance models suggested treatment reduced physiological and subjective reactions to nightmare imagery, gains that were generally maintained at the 6‐month follow‐up. Potential implications are discussed. © 2010 Wiley Periodicals, Inc. J Clin Psychol 66: 1–18, 2010.
Proteomic analysis of early‐response to mechanical stress in neonatal rat mandibular condylar chondrocytes
Authors: Li Huang , Yang Han‐Shuo , Wu Tuo‐Jiang , Zhang Xiang‐Yu , Jiang Wen‐Hui , Ma Qiao‐Lin , Chen Yang‐Xi , Xu Yun , Li Song , Hua Zi‐Chun 
Published: February 2010

AbstractThe objectives of this study were to investigate the early response to mechanical stress in neonatal rat mandibular chondrocytes by proteomic analysis. To evaluate its molecular mechanism, chondrocytes were isolated and cultured in vitro, then loaded mechanical stress by four‐point bending system on different patterns. Morphological observation, flow cytometric analysis, and MTT assays indicated that 4,000 µstrain loading for 60 min was an appropriate mechanical stimulus for the following proteome analysis, which produced a transient but obvious inhibitory effect on the cell cycle. Therefore, we took a proteomic approach to identify significantly differential expression proteins in chondrocytes under this mechanical stress. Using 2‐DE and MALDI‐TOF, we identified seven differentially expressed proteins including the MAPK pathway inhibitor RKIP, cytoskeleton proteins, actin and vimentin, and other selected proteins. Some differentially expressed proteins were validated by both Western blot analysis and fluorescent staining of cytoskeleton at different loading times. The vimentin and RKIP responsive expression were also proven in vivo in oral orthopedic treatment rats, which was in line with the result in vitro. The histological changes in cartilage also showed the inhibition effect. Furthermore, the expressional level of phosphorylated ERK was increased, which demonstrates the changes in MAPK activity. Taken together, these data indicate that mechanical stress resulted in vimentin expression changes first and then led to the subsequent changes in actin expression, MAPK pathway regulated by RKIP and heat shock protein GRP75. All those changes contributed to the cytoskeleton remolding and cell cycle inhibition, finally led to condylar remodeling. J. Cell. Physiol. 223:610–622, 2010. © 2010 Wiley‐Liss, Inc.