bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of a 3-year exercise intervention program on fracture risk, bone mass, and bone size in prepubertal children
Authors: Löfgren Bjarne , Detter Fredrik , Dencker Magnus , Stenevi-Lundgren Susanna , Nilsson Jan-Åke , Karlsson Magnus K 
Published: March 2011

Abstract
Published prospective pediatric exercise intervention studies are short term and use skeletal traits as surrogate endpoints for fractures, whereas other reports infer exercise to be associated with more trauma and fractures. This prospective, controlled exercise intervention study therefore followed both skeletal traits and fracture risk for 36 months. Fractures were registered in children aged 7 to 9 years; there were 446 boys and 362 girls in the intervention group (2129 person-years) and 807 boys and 780 girls in the control group (4430 person-years). The intervention included school physical education of 40 minutes per day for 3 years. The control children achieved the Swedish standard of 60 minutes per week. In a subsample of 76 boys and 48 girls in the intervention group and 55 boys and 44 girls in the control group, bone mineral content (BMC, g) and bone width (cm) were followed in the lumbar spine and hip by dual-energy X-ray absorptiometry (DXA). The rate ratio (RR) for fractures was 1.08 (0.71, 1.62) [mean (95% confidence interval)]. In the DXA-measured children, there were no group differences at baseline in age, anthropometrics, or bone traits. The mean annual gain in the intervention group in lumbar spine BMC was 0.9 SD higher in girls and 0.8 SD higher in boys (both p &lt; .001) and in third lumbar vertebra width 0.4 SD higher in girls and 0.3 SD higher in boys (both p &lt; .05) than in control children. It is concluded that a moderately intense 3-year exercise program in 7- to 9-year-old children increases bone mass and possibly also bone size without increasing fracture risk. © 2011 American Society for Bone and Mineral Research
HSP75 protects against cardiac hypertrophy and fibrosis
Authors: Zhang Yan , Jiang Ding‐Sheng , Yan Ling , Cheng Kuo‐Ju , Bian Zhou‐Yan , Lin Guo‐Sheng 
Published: March 2011

AbstractCardiac hypertrophy, a major determinant of heart failure, is associated with heat shock proteins (HSPs). HSP75 has been reported to protect against environmental stresses; however, its roles in cardiac hypertrophy remain unclear. Here, we generated cardiac‐specific inducible HSP75 transgenic mice (TG) and cardiac hypertrophy was developed at 4 weeks after aortic banding in TG mice and wild‐type littermates. The results revealed that overexpression of HSP75 prevented cardiac hypertrophy and fibrosis as assessed by heart weight/body weight ratio, heart weight/tibia length ratio, echocardiographic and hemodynamic parameters, cardiomyocyte width, left ventricular collagen volume, and gene expression of hypertrophic markers. Further studies showed that overexpression of HSP75 inhibited the activation of TAK/P38, JNK, and AKT signaling pathways. Thus, HSP75 likely reduces the hypertrophy and fibrosis induced by pressure overload through blocking TAK/P38, JNK, and AKT signaling pathways. J. Cell. Biochem. 112: 1787–1794, 2011. © 2011 Wiley‐Liss, Inc.
C/EBPβ regulates dexamethasone‐induced muscle cell atrophy and expression of atrogin‐1 and MuRF1
Authors: Gonnella Patricia , Alamdari Nima , Tizio Steven , Aversa Zaira , Petkova Victoria , Hasselgren Per‐Olof 
Published: March 2011

AbstractMuscle wasting in catabolic patients is in part mediated by glucocorticoids and is associated with increased expression and activity of the transcription factor C/EBPβ. It is not known, however, if C/EBPβ is causally linked to glucocorticoid‐induced muscle atrophy. We used dexamethasone‐treated L6 myoblasts and myotubes to test the role of C/EBPβ in glucocorticoid‐induced expression of the muscle‐specific ubiquitin ligases atrogin‐1 and MuRF1, protein degradation, and muscle atrophy by transfecting cells with C/EBPβ siRNA. In myoblasts, silencing C/EBPβ expression with siRNA inhibited dexamethasone‐induced increase in protein degradation, atrogin‐1 and MuRF1 expression, and muscle cell atrophy. Similar effects of C/EBPβ siRNA were seen in myotubes except that the dexamethasone‐induced increase in MuRF1 expression was not affected by C/EBPβ siRNA in myotubes. In additional experiments, overexpressing C/EBPβ did not influence atrogin‐1 or MuRF1 expression in myoblasts or myotubes. Taken together, our observations suggest that glucocorticoid‐induced muscle wasting is at least in part regulated by C/EBPβ. Increased C/EBPβ expression alone, however, is not sufficient to upregulate atrogin‐1 and MuRF1 expression. J. Cell. Biochem. 112: 1737–1748, 2011. © 2011 Wiley‐Liss, Inc.
EGFR signaling suppresses osteoblast differentiation and inhibits expression of master osteoblastic transcription factors Runx2 and osterix
Authors: Zhu Ji , Shimizu Emi , Zhang Xianrong , Partridge Nicola C. , Qin Ling 
Published: March 2011

AbstractThe epidermal growth factor receptor (EGFR) and its ligands regulate key processes of cell biology, such as proliferation, survival, differentiation, migration, and tumorigenesis. We previously showed that, EGFR signaling pathway is an important bone regulator and it primarily plays an anabolic role in bone metabolism. In this study, we demonstrated that EGF‐like ligands strongly inhibited osteoblast differentiation and mineralization in several lines of osteoblastic cells. Real‐time RT‐PCR and promoter reporter assays revealed that EGF‐like ligands suppressed the expression of both early and late bone marker genes at the transcriptional level in the differentiating osteoblasts via an EGFR‐dependent manner. This inhibitory effect of EGFR signaling was not dependent on its mitogenic activity. Furthermore, we demonstrated that EGFR signaling reduced the expression of two major osteoblastic transcription factors Runx2 (type II) and Osterix in osteoblast differentiating cells. EGFR‐induced decrease in Runx2 transcriptional activity was confirmed by Runx2 reporter and chromatin immunoprecipitation assays. EGFR signaling increased the protein amounts of transcription co‐repressors HDAC4 and 6 and over‐expression of HDAC4 decreased Runx2 amount in differentiating osteoblasts, implying that HDACs contribute to the down‐regulation of Runx2 by EGFR. Moreover, activation of EGFR in undifferentiated osteoprogenitors attenuated the expression of early bone markers and Osterix and decreased Runx2 protein amounts. Together with our previous data, that EGFR stimulates osteoprogenitor proliferation and that blocking EGFR activity in osteoblast lineage cells results in fewer osteoprogenitors and an osteopenic phenotype, we conclude that EGFR signaling is important for maintaining osteoprogenitor population at an undifferentiated stage. J. Cell. Biochem. 112: 1749–1760, 2011. © 2011 Wiley‐Liss, Inc.
Transcriptional regulation of claudin‐18 via specific protein kinase C signaling pathways and modification of DNA methylation in human pancreatic cancer cells
Authors: Ito Tatsuya , Kojima Takashi , Yamaguchi Hiroshi , Kyuno Daisuke , Kimura Yasutoshi , Imamura Masafumi , Takasawa Akira , Murata Masaki , Tanaka Satoshi , Hirata Koichi , Sawada Norimasa 
Published: March 2011

AbstractSince claudin‐18 (Cldn18) is overexpressed in precursor lesion PanIN and pancreatic duct carcinoma, it serves as a diagnostic marker and a target of immunotherapy. The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP‐1‐dependent pathway in PKC activator 12‐O‐tetradecanoylphorbol 13‐acetate (TPA)‐stimulated gastric cancer cells. However, little is known about how Cldn18 is regulated, not only in pancreatic duct carcinoma but also in normal human pancreatic duct epithelial cells (HPDE cells). In the present study, four pancreatic cancer cell lines, HPAF‐II, HPAC, PANC‐1 and BXPC3, and hTERT‐HPDE cells in which the hTERT gene was introduced into HPDE cells in primary culture, were treated with TPA. In all human pancreatic cancer cell lines and hTERT‐HPDE cells, Cldn18 mRNA indicated as Cldn18a2 was markedly induced by TPA and in well‐ or moderately differentiated human pancreatic cancer cells HPAF‐II and HPAC and hTERT‐HPDE cells, the protein was also strongly increased. The upregulation of Cldn18 by TPA in human pancreatic cancer cell lines was prevented by inhibitors of PKCδ, PKCε, and PKCα, whereas the upregulation of Cldn18 by TPA in hTERT‐HPDE cells was prevented by inhibitors of PKCδ, PKCθ, and PKCα. Furthermore, a CpG island was identified within the coding sequence of the Cldn18 gene and treatment with the demethylating agent 5‐azadeoxycytidine enhanced upregulation of Cldn18 by TPA in HPAF‐II and HPAC, but not hTERT‐HPDE cells. Our findings suggest that in human pancreatic cancer cells, Cldn18 is primarily regulated at the transcriptional level via specific PKC signaling pathways and modified by DNA methylation. J. Cell. Biochem. 112: 1761–1772, 2011. © 2011 Wiley‐Liss, Inc.
MicroRNA 21 regulates the proliferation of human adipose tissue‐derived mesenchymal stem cells and high‐fat diet‐induced obesity alters microRNA 21 expression in white adipose tissues
Authors: Kim Yeon Jeong , Hwang Soo Hyun , Cho Hyun Hwa , Shin Keun Koo , Bae Yong Chan , Jung Jin Sup 
Published: March 2011

AbstractA better understanding of the molecular mechanisms that govern human adipose tissue‐derived mesenchymal stem cells (hASCs) differentiation could provide new insights into a number of diseases including obesity. Our previous study demonstrated that microRNA‐21 (miR‐21) controls the adipogenic differentiation of hASCs. In this study, we determined the expression of miR‐21 in white adipose tissues in a high‐fat diet (HFD)‐induced obesity mouse model to examine the relationship between miR‐21 and obesity and the effect of miR‐21 on hASCs proliferation. Our study showed biphasic changes of miR‐21 expression and a correlation between miR‐21 level and adipocyte number in the epididymal fat of HFD mice. Over‐expression of miR‐21 decreased cell proliferation, whereas inhibiting miR‐21 with 2′‐O‐methyl‐antisense RNA increased it. Over‐expression of miR‐21 decreased both protein and mRNA levels of STAT3, whereas inhibiting miR‐21 with 2′‐O‐methyl‐antisense RNA increased these levels. The activity of a luciferase construct containing the miR‐21 target site from the STAT3 3′UTR was lower in LV‐miR21‐infected hASCs than in LV‐miLacZ infected cells. RNA interference‐mediated down‐regulation of STAT3 decreased cell proliferation without affecting adipogenic differentiation. These findings provide the evidence of the correlation between miR‐21 level and adipocyte number in the white adipose tissue of HFD‐induced obese mice, which provides new insights into the mechanisms of obesity. J. Cell. Physiol. 227: 183–193, 2012. © 2011 Wiley Periodicals, Inc.
β‐blockers as endocrine disruptors: the potential effects of human β‐blockers on aquatic organisms
Authors: Massarsky Andrey , Trudeau Vance L. , Moon Thomas W. 
Published: March 2011

Abstractβ‐Adrenergic blockers or β‐blockers have been used therapeutically to treat human hypertension since the late 1960s. The global market value and prescription rates of β‐blockers keep rising substantially each year, and over the past decade the number of prescriptions has doubled. The widespread use of β‐blockers has resulted in their appearance in the aquatic environment originating primarily from sewage effluents. The objective of this review is to analyze the literature as a means to determine the endocrine‐disrupting potential of β‐blockers in aquatic organisms. The mammalian adrenergic system is compared with the adrenergic system of fish and the homologous octopaminergic system in aquatic invertebrates, in particular mollusks. The structure and functions of these systems are linked to the molecular similarities between adrenoceptors and the octopaminergic/tyraminergic receptors, the various catecholamine molecules (epinephrine, norepinephrine, octopamine, and tyramine), and the processes controlled. Knowledge of these similarities as well as the effects of β‐blockers, mainly in humans, is then used to create a broad picture of the endocrine‐disrupting potential of β‐blockers, particularly during the stress response. The main conclusion is that β‐blockers have endocrine‐disrupting effects. J. Exp. Zool. 315:251–265, 2011. © 2011 Wiley‐Liss, Inc.
Maximal K3's and Hamiltonicity of 4‐connected claw‐free graphs
Authors: Fujisawa Jun , Ota Katsuhiro 
Published: March 2011

AbstractLet cl(G) denote Ryjáček's closure of a claw‐free graph G. In this article, we prove the following result. Let G be a 4‐connected claw‐free graph. Assume that G[NG(T)] is cyclically 3‐connected if T is a maximal K3 in G which is also maximal in cl(G). Then G is hamiltonian. This result is a common generalization of Kaiser et al.'s theorem [J Graph Theory 48(4) (2005), 267–276] and Pfender's theorem [J Graph Theory 49(4) (2005), 262–272]. © 2011 Wiley Periodicals, Inc. J Graph Theory
An intramolecular N‐arylation approach to 3‐functionalized 4,9‐dihydropyrrolo[2,1‐b]quinazolines
Authors: Suthiwangcharoen Nisaraporn , Pochini Steven M. , Sweat Daniel P. , Stephens Chad E. 
Published: March 2011

AbstractA series of 4,9‐dihydropyrrolo[2,1‐b]quinazolines containing electron withdrawing groups at the 3‐position have been prepared by the palladium‐catalyzed intramolecular N‐arylation of some 2‐aminopyrroles having a 2‐bromobenzyl group at the N‐1 position. Important for success of the reaction is the use of X‐phos, a biphenyl mono‐phosphine ligand, instead of xantphos, a more standard diphosphine ligand, and the use of t‐BuOH as reaction solvent. J. Heterocyclic Chem., (2011).
A solvent‐free protocol for one pot conversion of Baylis Hillman acetates to pyridopyrimidinones
Authors: Sreevani R. , Manjula A. , Rao B. Vittal 
Published: March 2011

AbstractA facile one pot transformation of Baylis Hillman acetates to pyrido[1,2‐a]pyrimidin‐2‐ones by reaction with 2‐amino pyridine in a total solvent‐free protocol is illustrated. The 3‐substituted‐2H‐pyrido[1,2‐a]pyrimidin‐2‐ones are obtained in pure form without involving any purification technique or solvent. J. Heterocyclic Chem., (2011).
Polycyclic N‐heterocyclic compounds. Part 66: Synthesis of N‐[2‐([1,2,4]oxadiazol‐5‐yl)cyclopenten‐1‐yl]formamide oximes and their evaluation as inhibitors of platelet aggregation
Authors: Okuda Kensuke , Zhang Ying‐Xue , Ohtomo Hiromi , Hirota Takashi , Sasaki Kenji 
Published: March 2011

AbstractN‐[2‐([1,2,4]Oxadiazol‐5‐yl)cyclopenten‐1‐yl]formamide oximes were synthesized by fusion of (6,7‐dihydro‐5H‐cyclopenta[1,2‐d]pyrimidin‐4‐yl)amidines and/or their amide oximes with hydroxylamine hydrochloride through a subsequent rearrangement reaction. Assay of the products for anti‐platelet aggregation activity revealed that certain of them showed promising inhibitory effect on arachidonic acid‐induced platelet aggregation. J. Heterocyclic Chem., (2011).
Long‐chain omega‐3 oils: Current and future supplies, food and feed applications, and stability
Authors: Wijesundera Chakra , Kitessa Soressa , Abeywardena Mahinda , Bignell Will , Nichols Peter D. 
Published: March 2011

AbstractIncreasing recognition of the health benefits of omega‐3 long‐chain (⪈C20) polyunsaturated fatty acids (omega‐3 LC‐PUFA or LC omega‐3 oils) continues. But new sources are needed, with recent developments with novel land plants showing promise. The value of existing and future sources LC omega‐3 oils occurs through aquaculture, livestock and other feeding. There is also a need toenhance the stability of oils containing LC omega‐3 oils. Challenges include increasing DHA levels in land plants, increasing oxidative stability in food products and product labeling. Consumers have difficulty recognizing and differentiating long‐chain and shorter‐chain (SC, C18) omega‐3 PUFA, both of which are referred to as “omega‐3” fatty acids.
The Maillard reaction and lipid oxidation
Authors: Zamora Rosario , Hidalgo Francisco J. 
Published: March 2011

AbstractThe Maillard reaction and lipid oxidation are probably the two most important chemical reactions occurring in foods during processing and storage. However, these pathways are not independent and each of them influences the development of the other. Furthermore, the carbonyl compounds produced in the lipid oxidation pathway will compete with carbohydrate‐derived carbonyls for amino compounds to produce carbonyl‐amine reaction products with either beneficial or harmful properties. These reactions are the final step of the oxidation pathway when lipid oxidation occurs in the presence of amino compounds.
Models mecanique pour les fibres de polyethylene lineaire basse densite d'apres la variation du module d'elasticite avec l'etirage
Authors: Rossignol J. M. , Séguéla R. , Rietsch F. 
Published: March 2011

AbstractA mechanical model which accounts for the specific properties of linear low density polyethylene fibers is presented. This model is built on the classical High Modulus Takayanagy model which has been modified to interrupt the crystal continuity. It introduces two analogical parameters which are determined by thermal analysis and theoretical treatment of the stress strain curves of the fibers. The values of these parameters and their change with draw ratio are consistent with the increase of elastic modulus.
Etude de la reaction de condensation de systeme epoxyde‐amine par resonance magnetique nucleaire ‐ synthese de modeles epoxy‐amine
Authors: Francillette J. , Hoarau P. A. , Madec P. J. 
Published: March 2011

AbstractThis work is an approach to the analysis, by nuclear magnetic resonance of carbon 13, of epoxy‐aminated reticulates in the case of aliphatic aminated hardeners: butylamine, ethylene‐diamine, diethylenetriamine, triethylenetetramine. In order to characterize the various species formed at each stage of the reaction, and for various types of resin/hardener stoechiometry, the DGEBA (diglycidyl ether of bisphenol A)/polyamine couple has been modeled by characterizing the structures generated during the reactions of phenylglycidylether (PGE) with two aliphatic amines: n‐butylamine (BA) and ethylenediamine (EDA). This study deals with the characterization of non‐catalysed systems only (or at least systems without added catalyst).
Formulation d'un element fini adapte a la resolution des problemes de poutres stratifiees ou sandwiches
Authors: Sirot Bernard , Khelidj Abdelhafid 
Published: March 2011

AbstractAmong the numerical methods, there is the “finite element method” which is particularly adapted for the solution of the problems of the mechanics of continuous media.The presence of an interface in the case of anisotropic materials (stratified, sandwiches, etc .) is due to a disorder like delamination. Therefore, the modelling of this type of materials needs the formulation of an element susceptible to take into account this singularity.For solving this problem the formulation of a triangular element, having four degrees of freedom per node is needed, which permits at the interface the continuity of displacement, normal stress and shear stress. This element belongs to the Reissner element (assuring the continuity of stresses and displacements), but it is modified by an elimination method to keep only the degrees of freedom translating the continuity at the interface.The work of Aivaz‐Zadeh and Verchery is based on the developed element. A comparison of the results is presented.
Novel mutations in SPG11 cause hereditary spastic paraplegia associated with early‐onset levodopa‐responsive Parkinsonism
Authors: Guidubaldi Arianna , Piano Carla , Santorelli Filippo M. , Silvestri Gabriella , Petracca Martina , Tessa Alessandra , Bentivoglio Anna Rita 
Published: March 2011

AbstractBackground: Autosomal recessive hereditary spastic paraplegia with thin corpus callosum is a neurodegenerative disorder characterized by spastic paraparesis, cognitive impairment, and peripheral neuropathy. The neuroradiologic hallmarks are thin corpus callosum and periventricular white matter changes. Mutations in the SPG11 gene have been identified to be a major cause of autosomal recessive hereditary spastic paraplegia with thin corpus callosum and recently also proven to be responsible for juvenile parkinsonism associated with spastic paraplegia.Methods: We describe one Italian autosomal recessive hereditary spastic paraplegia with thin corpus callosum patient who unusually presented at onset, 16 years, with parkinsonism‐like features, responsive to dopaminergic therapy. Then the clinical picture evolved and became more complex. A brain magnetic resonance imaging scan showed thin corpus callosum and hyperintense T2‐weighted lesions in periventricular regions, and the 123I‐ioflupane single‐photon emission coupled tomography was abnormal.Results: Genetic analysis detected two novel mutations, a c.3664insT variant in compound heterozygosity with a c.6331insG mutation, in SPG11.Discussion: This case confirms the high genetic and clinical heterogeneity associated with SPG11 mutations. It also offers further evidence that parkinsonism may initiate autosomal recessive hereditary spastic paraplegia with thin corpus callosum and that parkinsonian symptoms can have variable dopaminergic response in these patients. © 2011 Movement Disorder Society
Modulation of gait coordination by subthalamic stimulation improves freezing of gait
Authors: Fasano Alfonso , Herzog Jan , Seifert Elena , Stolze Henning , Falk Daniela , Reese René , Volkmann Jens , Deuschl Günther 
Published: March 2011

AbstractThe effect of subthalamic deep brain stimulation on gait coordination and freezing of gait in patients with Parkinson's disease is incompletely understood. The purpose of this study was to investigate the extent to which modulation of symmetry and coordination between legs by subthalamic deep brain stimulation alters the frequency and duration of freezing of gait in patients with Parkinson's disease. We recruited 13 post‐subthalamic deep brain stimulation patients with Parkinson's disease with off freezing of gait and evaluated them in the following 4 conditions: subthalamic deep brain stimulation on (ON) and stimulation off (OFF), 50% reduction of stimulation voltage for the leg with shorter step length (worse side reduction) and for the leg with longer step length (better side reduction). Gait analysis was performed on a treadmill and recorded by an optoelectronic analysis system. We measured frequency and duration of freezing of gait episodes. Bilateral coordination of gait was assessed by the Phase Coordination Index, quantifying the ability to generate antiphase stepping. From the OFF to the ON state, freezing of gait improved in frequency (2.0 ± 0.4 to 1.4 ± 0.5 episodes) and duration (12.2 ± 2.6 to 2.6 ± 0.8 seconds; P = .005). Compared with the ON state, only better side reduction further reduced freezing of gait frequency (0.2 ± 0.2) and duration of episodes (0.2 ± 0.2 seconds; P = .03); worse side reduction did not change frequency (1.3 ± 0.4) but increased freezing of gait duration (5.2 ± 2.1 seconds). The better side reduction–associated improvements were accompanied by normalization of gait coordination, as measured by phase coordination index (16.5% ± 6.0%), which was significantly lower than in the other 3 conditions. Reduction of stimulation voltage in the side contralateral to the leg with longer step length improves frequency and duration of freezing of gait through normalization of gait symmetry and coordination in subthalamic deep brain stimulation patients with Parkinson's disease. This identifies poor leg coordination as a risk factor for causing freezing of gait. © 2011 Movement Disorder Society