bluuebunny/crossref_metadata_2025_split huggingface dataset:
Coating of carbon fiber‐reinforced polyetheretherketone implants with titanium to improve bone apposition
Authors: Devine Declan M. , Hahn Joachim , Richards R.Geoffery , Gruner Heiko , Wieling Ronald , Pearce Simon G. 
Published: December 2012

AbstractCarbon fiber‐reinforced polyetheretherketone (CF/PEEK) is a thermoplastic composite biomaterial exhibiting properties suitable for load‐bearing orthopedic implants. However, the hydrophobic surface of CF/PEEK implants induces the deposition of a peri‐implant fibrous tissue capsule preventing bone apposition. However, if bone apposition was improved, the use of CF/PEEK in orthopedics could be increased as it has many advantages compared with metallic implants. In this study, CF/PEEK screws were coated with titanium (Ti) using two different techniques, namely vacuum plasma spraying (VPS) and physical vapor deposition (PVD) with uncoated screws as controls. These coatings were characterized and implanted in a loaded sheep tibia model. In the characterization of the screw surfaces using microscopy techniques, the uncoated screws were seen to have an irregular surface. The PVD coating appeared smooth and consistent, whereas the VPS coating appeared to be a rough coating with some inhomogeneities, which did not cover the entire surface area. Nevertheless, in the ex vivo analysis the VPS‐coated screws had a screw removal torque which was statistically greater than uncoated and PVD‐coated screws (p ≤ 0.002 for both comparisons). Additionally, the VPS‐coated screws had a statistically higher bone contact area than the uncoated screws (p = 0.006), whereas no statistical difference was detected between VPS and PVD coating types (p = 0.11). Thereby illustrating that Ti coating of CF/PEEK screws significantly improve bone apposition and removal torque compared with uncoated CF/PEEK screws. © 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2013.
Novel dental adhesive containing antibacterial agents and calcium phosphate nanoparticles
Authors: Melo Mary Anne S. , Cheng Lei , Weir Michael D. , Hsia Ru‐Ching , Rodrigues Lidiany K. A. , Xu Hockin H.K. 
Published: December 2012

AbstractSecondary caries remains the main reason for dental restoration failure. Replacement of failed restorations accounts for 50%–70% of all restorations performed. Antibacterial adhesives could inhibit biofilm acids at tooth‐restoration margins, and calcium phosphate (CaP) ions could remineralize tooth lesions. The objectives of this study were to: (1) incorporate nanoparticles of silver (NAg), quaternary ammonium dimethacrylate (QADM), and nanoparticles of amorphous calcium phosphate (NACP) into bonding agent; and (2) investigate their effects on dentin bonding and microcosm biofilms. An experimental primer was made with pyromellitic glycerol dimethacrylate (PMGDM) and 2‐hydroxyethyl methacrylate (HEMA). An adhesive was made with bisphenol‐A‐glycerolate dimethacrylate (BisGMA) and triethylene glycol dimethacrylate (TEGDMA). NAg was incorporated into primer at 0.1 wt %. The adhesive contained 0.1% NAg and 10% QADM, and 0%–40% NACP. Incorporating NAg into primer and NAg‐QADM‐NACP into adhesive did not adversely affect dentin bond strength (p > 0.1). Scanning electron microscopy showed numerous resin tags, and transmission electron microscopy revealed NAg and NACP in dentinal tubules. Viability of human saliva microcosm biofilms on primer/adhesive/composite disks was substantially reduced via NAg and QADM. Metabolic activity, lactic acid, and colony‐forming units of biofilms were much lower on the new bonding agents than control (p < 0.05). In conclusion, novel dental bonding agents containing NAg, QADM, and NACP were developed with the potential to kill residual bacteria in the tooth cavity and inhibit the invading bacteria along tooth‐restoration margins, with NACP to remineralize tooth lesions. The novel method of combining antibacterial agents (NAg and QADM) with remineralizing agent (NACP) may have wide applicability to other adhesives for caries inhibition. © 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2013.
SNX10 mutations define a subgroup of human autosomal recessive osteopetrosis with variable clinical severity
Authors: Pangrazio Alessandra , Fasth Anders , Sbardellati Andrea , Orchard Paul J , Kasow Kimberly A , Raza Jamal , Albayrak Canan , Albayrak Davut , Vanakker Olivier M , De Moerloose Barbara , Vellodi Ashok , Notarangelo Luigi D , Schlack Claire , Strauss Gabriele , Kühl Jörn-Sven , Caldana Elena , Lo Iacono Nadia , Susani Lucia , Kornak Uwe , Schulz Ansgar , Vezzoni Paolo , Villa Anna , Sobacchi Cristina 
Published: December 2012

Abstract
Human Autosomal Recessive Osteopetrosis (ARO) is a genetically heterogeneous disorder caused by reduced bone resorption by osteoclasts. In 2000, we found that mutations in the TCIRG1 gene encoding for a subunit of the proton pump (V-ATPase) are responsible for more than one-half of ARO cases. Since then, five additional genes have been demonstrated to be involved in the pathogenesis of the disease, leaving approximately 25% of cases that could not be associated with a genotype. Very recently, a mutation in the sorting nexin 10 (SNX10) gene, whose product is suggested to interact with the proton pump, has been found in 3 consanguineous families of Palestinian origin, thus adding a new candidate gene in patients not previously classified. Here we report the identification of 9 novel mutations in this gene in 14 ARO patients from 12 unrelated families of different geographic origin. Interestingly, we define the molecular defect in three cases of “Västerbottenian osteopetrosis,” named for the Swedish Province where a higher incidence of the disease has been reported. In our cohort of more than 310 patients from all over the world, SNX10-dependent ARO constitutes 4% of the cases, with a frequency comparable to the receptor activator of NF-κB ligand (RANKL), receptor activator of NF-κB (RANK) and osteopetrosis-associated transmembrane protein 1 (OSTM1)-dependent subsets. Although the clinical presentation is relatively variable in severity, bone seems to be the only affected tissue and the defect can be almost completely rescued by hematopoietic stem cell transplantation (HSCT). These results confirm the involvement of the SNX10 gene in human ARO and identify a new subset with a relatively favorable prognosis as compared to TCIRG1-dependent cases. Further analyses will help to better understand the role of SNX10 in osteoclast physiology and verify whether this protein might be considered a new target for selective antiresorptive therapies. © 2013 American Society for Bone and Mineral Research.
DNA damage drives accelerated bone aging via an NF-κB–dependent mechanism
Authors: Chen Qian , Liu Kai , Robinson Andria R , Clauson Cheryl L , Blair Harry C , Robbins Paul D , Niedernhofer Laura J , Ouyang Hongjiao 
Published: December 2012

Abstract
Advanced age is one of the most important risk factors for osteoporosis. Accumulation of oxidative DNA damage has been proposed to contribute to age-related deregulation of osteoblastic and osteoclastic cells. Excision repair cross complementary group 1–xeroderma pigmentosum group F (ERCC1-XPF) is an evolutionarily conserved structure-specific endonuclease that is required for multiple DNA repair pathways. Inherited mutations affecting expression of ERCC1-XPF cause a severe progeroid syndrome in humans, including early onset of osteopenia and osteoporosis, or anomalies in skeletal development. Herein, we used progeroid ERCC1-XPF–deficient mice, including Ercc1-null (Ercc1−/−) and hypomorphic (Ercc1−/Δ) mice, to investigate the mechanism by which DNA damage leads to accelerated bone aging. Compared to their wild-type littermates, both Ercc1−/− and Ercc1−/Δ mice display severe, progressive osteoporosis caused by reduced bone formation and enhanced osteoclastogenesis. ERCC1 deficiency leads to atrophy of osteoblastic progenitors in the bone marrow stromal cell (BMSC) population. There is increased cellular senescence of BMSCs and osteoblastic cells, as characterized by reduced proliferation, accumulation of DNA damage, and a senescence-associated secretory phenotype (SASP). This leads to enhanced secretion of inflammatory cytokines known to drive osteoclastogenesis, such as interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and receptor activator of NF-κB ligand (RANKL), and thereby induces an inflammatory bone microenvironment favoring osteoclastogenesis. Furthermore, we found that the transcription factor NF-κB is activated in osteoblastic and osteoclastic cells of the Ercc1 mutant mice. Importantly, we demonstrated that haploinsufficiency of the p65 NF-κB subunit partially rescued the osteoporosis phenotype of Ercc1−/Δ mice. Finally, pharmacological inhibition of the NF-κB signaling via an I-κB kinase (IKK) inhibitor reversed cellular senescence and SASP in Ercc1−/Δ BMSCs. These results demonstrate that DNA damage drives osteoporosis through an NF-κB–dependent mechanism. Therefore, the NF-κB pathway represents a novel therapeutic target to treat aging-related bone disease. © 2013 American Society for Bone and Mineral Research.
Hip and spine strength effects of adding versus switching to teriparatide in postmenopausal women with osteoporosis treated with prior alendronate or raloxifene
Authors: Cosman Felicia , Keaveny Tony M , Kopperdahl David , Wermers Robert A , Wan Xiaohai , Krohn Kelly D , Krege John H 
Published: December 2012

ABSTRACT

Many postmenopausal women treated with teriparatide for osteoporosis have previously received antiresorptive therapy. In women treated with alendronate (ALN) or raloxifene (RLX), adding versus switching to teriparatide produced different responses in areal bone mineral density (aBMD) and biochemistry; the effects of these approaches on volumetric BMD (vBMD) and bone strength are unknown. In this study, postmenopausal women with osteoporosis receiving ALN 70 mg/week (n = 91) or RLX 60 mg/day (n = 77) for ≥18 months were randomly assigned to add or switch to teriparatide 20 µg/day. Quantitative computed tomography scans were performed at baseline, 6 months, and 18 months to assess changes in vBMD; strength was estimated by nonlinear finite element analysis. A statistical plan specifying analyses was approved before assessments were completed. At the spine, median vBMD and strength increased from baseline in all groups (13.2% to 17.5%, p &lt; 0.01); there were no significant differences between the Add and Switch groups. In the RLX stratum, hip vBMD and strength increased at 6 and 18 months in the Add group but only at 18 months in the Switch group (Strength, Month 18: 2.7% Add group, p &lt; 0.01 and 3.4% Switch group, p &lt; 0.05). In the ALN stratum, hip vBMD increased in the Add but not in the Switch group (0.9% versus –0.5% at 6 months and 2.2% versus 0.0% at 18 months, both p ≤ 0.004 group difference). At 18 months, hip strength increased in the Add group (2.7%, p &lt; 0.01) but not in the Switch group (0%); however, the difference between groups was not significant (p = 0.076). Adding or switching to teriparatide conferred similar benefits on spine strength in postmenopausal women with osteoporosis pretreated with ALN or RLX. Increases in hip strength were more variable. In RLX-treated women, strength increased more quickly in the Add group; in ALN-treated women, a significant increase in strength compared with baseline was seen only in the Add group.
Augmentation of smad-dependent BMP signaling in neural crest cells causes craniosynostosis in mice
Authors: Komatsu Yoshihiro , Yu Paul B , Kamiya Nobuhiro , Pan Haichun , Fukuda Tomokazu , Scott Gregory J , Ray Manas K , Yamamura Ken-ichi , Mishina Yuji 
Published: December 2012

ABSTRACT

Craniosynostosis describes conditions in which one or more sutures of the infant skull are prematurely fused, resulting in facial deformity and delayed brain development. Approximately 20% of human craniosynostoses are thought to result from gene mutations altering growth factor signaling; however, the molecular mechanisms by which these mutations cause craniosynostosis are incompletely characterized, and the causative genes for diverse types of syndromic craniosynostosis have yet to be identified. Here, we show that enhanced bone morphogenetic protein (BMP) signaling through the BMP type IA receptor (BMPR1A) in cranial neural crest cells, but not in osteoblasts, causes premature suture fusion in mice. In support of a requirement for precisely regulated BMP signaling, this defect was rescued on a Bmpr1a haploinsufficient background, with corresponding normalization of Smad phosphorylation. Moreover, in vivo treatment with LDN-193189, a selective chemical inhibitor of BMP type I receptor kinases, resulted in partial rescue of craniosynostosis. Enhanced signaling of the fibroblast growth factor (FGF) pathway, which has been implicated in craniosynostosis, was observed in both mutant and rescued mice, suggesting that augmentation of FGF signaling is not the sole cause of premature fusion found in this model. The finding that relatively modest augmentation of Smad-dependent BMP signaling leads to premature cranial suture fusion suggests an important contribution of dysregulated BMP signaling to syndromic craniosynostoses and potential strategies for early intervention.
Particulate Matter Containing Environmentally Persistent Free Radicals and Adverse Infant Respiratory Health Effects: A Review
Authors: Saravia Jordy , Lee Greg I. , Lomnicki Slawo , Dellinger Barry , Cormier Stephania A. 
Published: December 2012

ABSTRACTThe health impacts of airborne particulate matter (PM) are of global concern, and the direct implications to the development/exacerbation of lung disease are immediately obvious. Most studies to date have sought to understand mechanisms associated with PM exposure in adults/adult animal models; however, infants are also at significant risk for exposure. Infants are affected differently than adults due to drastic immaturities, both physiologically and immunologically, and it is becoming apparent that they represent a critically understudied population. Highlighting our work funded by the ONES award, in this review we argue the understated importance of utilizing infant models to truly understand the etiology of PM‐induced predisposition to severe, persistent lung disease. We also touch upon various mechanisms of PM‐mediated respiratory damage, with a focus on the emerging importance of environmentally persistent free radicals (EPFRs) ubiquitously present in combustion‐derived PM. In conclusion, we briefly comment on strengths/challenges facing current PM research, while giving perspective on how we may address these challenges in the future. © 2012 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:56‐68, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21465
Vitamin D Treatment Modulates Organic Dust–Induced Cellular and Airway Inflammatory Consequences
Authors: Golden Gregory A. , Wyatt Todd A. , Romberger Debra J. , Reiff Daniel , McCaskill Michael , Bauer Christopher , Gleason Angela M. , Poole Jill A. 
Published: December 2012

ABSTRACTExposure to organic dusts elicits airway inflammatory diseases. Vitamin D recently has been associated with various airway inflammatory diseases, but its role in agricultural organic dust exposures is unknown. This study investigated whether vitamin D reduces organic dust–induced inflammatory outcomes in cell culture and animal models. Organic dust extracts obtained from swine confinement facilities induced neutrophil chemokine production (human IL‐8, murine CXCL1/CXCL2). Neutrophil chemokine induction was reduced in human blood monocytes, human bronchial epithelial cells, and murine lung slices pretreated with 1,25‐(OH)2D3. Intranasal inhalation of organic dust extract induced neutrophil influx, and CXCL1/CXCL2 release was also decreased in mice fed a relatively high vitamin D diet as compared to mice fed a low vitamin D diet. These findings were associated with reduced tracheal epithelial cell PKCα and PKCε activity and whole lung TLR2 and TLR4 gene expression. Collectively, vitamin D plays a role in modulating organic dust–induced airway inflammatory outcomes. © 2012 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:77‐86, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21467
Synthesis and Characterization of β‐Co(OH)2, CuO and ZnO Nanostructures by Solvothermal Method without Any Additive
Authors: Mehdizadeh Robabeh , Saghatforoush Lotf Ali , Sanati Soheila 
Published: December 2012

Abstractβ‐Co(OH)2, CuO and ZnO nanostructures with plate‐like, particle‐like and flower‐like morphologies were prepared through the use of simple solvothermal method using of melt salt and 1,10‐phenanthroline as complexing agent and sodium hydroxide. β‐Co(OH)2 consisted of a plate‐like structure, and the nanoplates size was about 29 nm. The structure was comprised of regular sheets which were assembled together. Furthermore, the as‐obtained β‐Co(OH)2 nanoplates can be easily converted into Co3O4 nanoplates by calcining in air at 500 °C for 2 h. The results indicate that ZnO powder is of hexagonal wurtzite structure and well crystallized with high purity. CuO powder is pure monoclinic‐structured crystalline. The products were characterized by X‐ray diffraction (XRD), scanning electron microscopy (SEM), and Fourier transform infrared (FT‐IR) spectra. Possible formation mechanism of the nanostructures is proposed.
The Existence and Construction of (K5∖e)‐Designs of Orders 27, 135, 162, and 216
Authors: Kolotoğlu Emre 
Published: December 2012

AbstractThe problem of the existence of a decomposition of the complete graphinto disjoint copies ofhas been solved for all admissible ordersn, except for 27, 36, 54, 64, 72, 81, 90, 135, 144, 162, 216, and 234. In this paper, I eliminate 4 of these 12 unresolved orders. Let Γ be a‐design. I show thatdivides 2k3 for someand that. I construct‐designs by prescribingas an automorphism group, and show that up to isomorphism there are exactly 24‐designs withas an automorphism group. Moreover, I show that the full automorphism group of each of these designs is indeed. Finally, the existence of‐designs of orders 135, 162, and 216 follows immediately by the recursive constructions given by G. Ge and A. C. H. Ling, SIAM J Discrete Math 21(4) (2007), 851–864.
Interpersonal Motives in Anorexia Nervosa: The Fear of Losing One's Autonomy
Authors: Brockmeyer Timo , Holtforth Martin Grosse , Bents Hinrich , Kämmerer Annette , Herzog Wolfgang , Friederich Hans‐Christoph 
Published: December 2012

ObjectiveThis study examined the widely held but insufficiently studied hypothesis of autonomy disturbances in anorexia nervosa.MethodA total sample of 112 participants comprising patients with acute anorexia nervosa (AN), women recovered from anorexia nervosa (REC), clinical controls (CC), and healthy controls (HC) completed measures of dependency and intimacy strivings, as well as measures of frustrations of these same strivings.ResultsIn comparison to HC and CC, AN showed a stronger motivation to avoid dependency and lower strivings for intimacy. Compared with HC, but not with CC, AN also showed stronger frustrations of the same motives. Whereas REC did not differ from AN regarding avoidance of dependency, they reported lower frustration of dependency avoidance (i.e., less actual experiences of dependency). Finally, REC reported higher intimacy motivation as well as better satisfaction of intimacy motivation as compared with AN.ConclusionsThe present findings suggest that a pronounced motive of avoiding dependency may be a vulnerability factor for anorexia nervosa that is disorder‐specific and trait‐like. Frustrations of this motive seem to be associated with psychopathology.
Trait Mindfulness, Repression, Suppression, and Self‐Reported Mood and Stress Symptoms Among Women With Breast Cancer
Authors: Tamagawa Rie , Giese‐Davis Janine , Speca Michael , Doll Richard , Stephen Joanne , Carlson Linda E. 
Published: December 2012

ObjectiveThis study sought to identify relationships between trait mindfulness, repressive, and suppressive emotional styles, and the relative importance of these traits in their association with self‐reported psychological health among women with breast cancer.MethodOf the 277 women with breast cancer accrued in the study, 227 (81.9%) completed a set of questionnaires assessing personality traits, stress symptoms, and mood.ResultsHigh levels of mindfulness were associated with fewer stress‐related symptoms and less mood disturbance, while high levels of suppression were associated with poorer self‐reported health.ConclusionIndividuals’ dispositional ways to manage negative emotions were associated with the experience of symptoms and aversive moods. Helping patients cultivate mindful insights and reduce deliberate emotional inhibition may be a useful focus for psycho‐oncological interventions.
Relationship of Self‐Reported and Acute Stress to Smoking in Emerging Adult Smokers
Authors: Conrad Megan , Wardle Margaret , King Andrea , de Wit Harriet 
Published: December 2012

ObjectiveIn the current study, we examined subjective and objective measures of stress and their relationship to baseline and future cigarette smoking behaviors over a 1‐year follow‐up in young adult experimental smokers.MethodParticipants (N = 56) completed two laboratory sessions to determine subjective and objective responses to a controlled laboratory stressor versus a control task. Baseline measures included drug use and smoking histories and a self‐report measure of habitual stress (i.e., daily hassles). They were re‐contacted 1 year after the laboratory sessions to determine smoking status.ResultsThere was wide variability in smoking trajectories, with 34% of participants increasing their smoking over the course of the year. Contrary to predictions, neither daily hassles nor stress reactivity was related to smoking at baseline or change over the year.ConclusionsThese preliminary findings suggest that daily stress or responses to acute social stress are not strong predictors of progression in emerging adult smokers.
The zebrafish myotome contains tonic muscle fibers: Morphological characterization and time course of formation
Authors: Marschallinger Julia , Obermayer Astrid , Steinbacher Peter , Stoiber Walter 
Published: December 2012

AbstractIt is long known that the skeletal muscle of teleost fish contains muscle fibers which are in all probability of a tonic type according to morphological criteria. However, the evidence for the existence of teleost tonic fibers is still confined to a very small number of species, and knowledge concerning their ontogeny and possible functions is even more restricted. A remarkable deficit in this context is that it is not even exactly known whether the zebrafish, which is widely used to study vertebrate developmental biology, has such fibers, or how they arise. The present study demonstrates the existence of tonic fibers in the zebrafish myotome. They are identical with a fiber population previously termed “red muscle rim” fibers. A combined histochemical, immunocytochemical, and ultrastructural approach is used to characterize the morphology and development of these fibers. This study provides a basis for using the zebrafish model system in the future research on the developmental regulation and the functions of tonic fibers. J. Morphol., 2013. © 2012 Wiley Periodicals, Inc.