bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is Bruxism a Risk Factor for Dental Implants? A Systematic Review of the Literature
Authors: Manfredini Daniele , Poggio Carlo E. , Lobbezoo Frank 
Published: November 2012

AbstractPurposeTo systematically review the literature on the role of bruxism as a risk factor for the different complications on dental implant‐supported rehabilitations.Material and MethodsA systematic search in the National Library of Medicine's Medline Database was performed to identify all peer‐reviewed papers in the English literature assessing the role of bruxism, as diagnosed with any other diagnostic approach (i.e., clinical assessment, questionnaires, interviews, polysomnography, and electromyography), as a risk factor for biological (i.e., implant failure, implant mobility, and marginal bone loss) or mechanical (i.e., complications or failures of either prefabricated components or laboratory‐fabricated suprastructures) complications on dental implant‐supported rehabilitations. The selected articles were reviewed according to a structured summary of the articles in relation to four main issues, viz., “P” – patients/problem/population, “I” – intervention, “C” – comparison, and “O” – outcome.ResultsA total of 21 papers were included in the review and split into those assessing biological complications (n = 14) and those reporting mechanical complications (n = 7). In general, the specificity of the literature for bruxism diagnosis and for the study of the bruxism's effects on dental implants was low. From a biological viewpoint, bruxism was not related with implant failures in six papers, while results from the remaining eight studies did not allow drawing conclusions. As for mechanical complications, four of the seven studies yielded a positive relationship with bruxism.ConclusionsBruxism is unlikely to be a risk factor for biological complications around dental implants, while there are some suggestions that it may be a risk factor for mechanical complications.
Northward extrusion of the ultrahigh‐pressure units in the southern Dabie metamorphic belt, east‐central China
Authors: Yamamoto Hiroshi , Terabayashi Masaru , Okura Hyugo , Matsui Takashi , Kaneko Yoshiyuki , Ishikawa Masahiro , Maruyama Shigenori 
Published: November 2012

AbstractThe Dabie orogenic belt in central China extends along the Triassic suture between the Sino–Korean and Yangtze cratons. The structure of the metamorphic rocks have been investigated in the Shima–Wumiao area near the southeastern end of the Dabie orogenic belt. Detailed mapping revealed that the metamorphic sequence in this area can be subdivided into four subhorizontal lithotectonic units. These units are denoted by I, II, III, and IV in the order of structural bottom to top. Unit I is composed of felsic gneiss, eclogite, and minor pelitic gneiss. Unit II consists of felsic gneiss and eclogite with coesite pseudomorphs. Unit III consists of felsic gneiss, pelitic gneiss, metacarbonate, and eclogite with occasional coesite inclusion. Unit IV is composed of felsic gneiss, amphibolite, and minor pelitic gneiss. Those metamorphic rocks underwent penetrative ductile deformation which is denoted by gently south‐dipping or subhorizontal foliation and NNW‐trending mineral lineation. Deformation microstructures in oriented samples from Units I and II indicate consistent northward displacements of the hanging wall and those from Units III and IV indicate southward displacements. The subhorizontal structure and opposite shear directions between Units I–II and Units III–IV suggest northward extrusion of UHP metamophic units (II and III). The subduction polarity could be opposite to the extrusion trend. The UHP metamorphism in the Dabie orogenic belt is attributable to southward subduction of the Sino–Korean craton beneath the Yangtze craton.
Preincubation in the Prothrombinase‐induced Clotting Time test (PiCT) is necessary for in vitro evaluation of fondaparinux and to be avoided for the reversible, direct factor Xa inhibitor, rivaroxaban
Authors: Kluft C. , Meijer P. , Kret R. , Burggraaf J. 
Published: November 2012

SummaryIntroductionThere is no clear consensus about tests in vitro that are suitable for evaluating various factor Xa inhibitors. The availability of reversible and irreversible inhibitors further complicates the application of available assays.MethodsWe evaluated the suitability of the prothrombinase‐induced clotting test (PiCT) for fondaparinux and rivaroxaban, as representatives for irreversible and reversible inhibition of factor Xa, with specific attention to preincubation times prior to re‐calcification, in the context of automate program limitations.ResultsWe demonstrate that the PiCT assay requires a preincubation step to allow inhibitory activity by fondaparinux. Without this step, inhibition in the test is minimal and lacking sufficient dynamic range. In contrast, to measure the reversible inhibition by rivaroxaban, we found any preincubation introduced an artifact in inhibition as exemplified by a biphasic pattern and only the test without a preincubation phase gave informative results.ConclusionIt is concluded that PiCT in its format with two steps is suitable for fondaparinux evaluation, while its format without preincubation (the one‐addition format) is suitable for reversible inhibitors such as rivaroxaban. Unfortunately, both types of inhibitors cannot be compared in vitro in a single assay format.
Systemic thromboembolism after anti‐cancer chemotherapy in a woman with ovarian germ cell tumor
Authors: Yanazume Shintaro , Tsuji Takahiro , Matsuo Takashi , Kamio Masaki , Terao Sayori , Douchi Tsutomu 
Published: November 2012

AbstractA high cure rate of ovarian germ cell tumors was achieved by establishment of a cisplatin‐containing regimen. We encountered a rare case of a 33‐year‐old, nulligravida Japanese woman with systemic thromboembolism following anti‐cancer chemotherapy with cisplatin, etoposide, and bleomycin in ovarian germ cell tumor. She suffered from brain infarction, multiple embolisms in the bilateral pulmonary artery and pelvic vein, and a broad range of deep vein thromboses in the right extremities vein. When thrombosis is detected during anti‐cancer chemotherapy, we must investigate whether the presence of thrombosis is systemic or local.
Burrow morphology of Uca uruguayensis and Uca leptodactylus (Decapoda: Ocypodidae) from a subtropical mangrove forest in the western Atlantic
Authors: MACHADO Glauco B. O. , GUSMÃO‐JUNIOR João B. L. , COSTA Tânia M. 
Published: November 2012

AbstractThe continuous excavation of burrows by fiddler crabs generates bioturbation in the sediment, which can be estimated from burrow morphology. The aim of the present study was to describe the burrow morphology of Uca uruguayensis and U. leptodactylus and its relationship with demography of resident individuals and to estimate the level of bioturbation in the sediment generated by each species. For all individuals from each of the 2 species, sex was determined and the carapace width (CW; mm) measured. Burrows were characterized according to burrow diameter (BD; mm), maximum burrow depth (MBD; mm) and burrow volume (BV; cm3). The density of each species in the study area was also evaluated. In both species, the males were larger and occupied burrows with higher BV compared to females. Differences between sexes in relation to the burrow characteristics might reflect sexual dimorphism within the group and are probably related to the fact that males use the burrows for mating. BD and BV showed significant positive relationships with the size of resident crabs. The amount of sediment removed per burrow was estimated from mean BV: 10.78 cm3 of sediment/burrow for U. uruguayensis and 12.38 cm3 of sediment/burrow for U. leptodactylus. Despite the density and depth differences between the 2 species, the similarity in burrow volume suggests that U. uruguayensis and U. leptodactylus present the same importance in terms of the bioturbation process. Burrow morphology is highly associated with characteristics of the occupant, although extrinsic factors should also be considered, and its description can provide estimates on the bioturbation generated by Uca species in mangrove forests.
Identification of Patients with Painful Diabetic Peripheral Neuropathy Who Have a Favorable Cost Profile with Pregabalin Treatment
Authors: Udall Margarita , Mardekian Jack , Cabrera Javier 
Published: November 2012

AbstractObjectiveTo characterize patient populations with favorable costs after the initiation of pregabalin for the treatment of painful diabetic peripheral neuropathy (pDPN) relative to duloxetine, gabapentin, and amitriptyline.MethodsPatients were identified from MarketScan having ≥ 1 claim for pDPN (ICD‐9‐CM codes 250.6 or 357.2) within 60 days of first prescription (index) for pregabalin, duloxetine, gabapentin, or amitriptyline in 2008 and continuous enrollment 12 months pre‐ and postindex. Pregabalin patients were propensity‐score‐matched to each comparator. Using cutoff values ≥ 80% proportion of days covered (PDC) and ≥ 65 years for age, pre‐ to postindex changes in healthcare costs were estimated for pregabalin vs. comparators.ResultsOf 987 patients initiated on pregabalin, 349 matched to duloxetine; 987 to gabapentin; 276 to amitriptyline. The pre‐ to postindex changes in total healthcare costs were similar between cohorts: $3272 with pregabalin vs. $2290 with duloxetine (P = 0.5280); $3687 with pregabalin vs. $5498 with amitriptyline (P = 0.5863); $3869 with pregabalin vs. $4106 with gabapentin (P = 0.8303). For the high‐age/high‐PDC population, the pre‐ to postindex differences in mean total costs were significantly lower with pregabalin (P < 0.001) relative to comparators ($3573 vs. $8288 for duloxetine; $1423 vs. $3167 for gabapentin; $2285 vs. $6160 for amitriptyline).ConclusionsThe association of lower total costs among older individuals with pDPN who maintain high adherence to pregabalin therapy relative to key comparators suggests a pharmacoeconomic advantage of pregabalin in this population combined with a need for strategies promoting adherence.
Integrated Bioinformatic and Targeted Deletion Analyses of the SRS Gene Superfamily Identify SRS29C as a Negative Regulator ofToxoplasmaVirulence
Authors: Wasmuth James D. , Pszenny Viviana , Haile Simon , Jansen Emily M. , Gast Alexandra T. , Sher Alan , Boyle Jon P. , Boulanger Martin J. , Parkinson John , Grigg Michael E. 
Published: November 2012

ABSTRACTTheToxoplasma gondiiSRSgene superfamily is structurally related toSRS29B(formerlySAG1), a surface adhesin that binds host cells and stimulates host immunity. Comparative genomic analyses of threeToxoplasmastrains identified 182SRSgenes distributed across 14 chromosomes at 57 genomic loci. Eight distinctSRSsubfamilies were resolved. A core 69 functional gene orthologs were identified, and strain-specific expansions and pseudogenization were common. Gene expression profiling demonstrated differential expression ofSRSgenes in a developmental-stage- and strain-specific fashion and identified nineSRSgenes as priority targets for gene deletion among the tissue-encysting coccidia. A Δsag1 ∆sag2Amutant was significantly attenuated in murine acute virulence and showed upregulated SRS29C (formerly SRS2) expression. Transgenic overexpression of SRS29C in the virulent RH parent was similarly attenuated. Together, these findings reveal SRS29C to be an important regulator of acute virulence in mice and demonstrate the power of integrated genomic analysis to guide experimental investigations.IMPORTANCEParasitic species employ large gene families to subvert host immunity to enable pathogen colonization and cause disease.Toxoplasma gondiicontains a large surface coat gene superfamily that encodes adhesins and virulence factors that facilitate infection in susceptible hosts. We generated an integrated bioinformatic resource to predict which genes from within this 182-gene superfamily of adhesin-encoding genes play an essential role in the host-pathogen interaction. Targeted gene deletion experiments with predicted candidate surface antigens identified SRS29C as an important negative regulator of acute virulence in murine models ofToxoplasmainfection. Our integrated computational and experimental approach provides a comprehensive framework, or road map, for the assembly and discovery of additional key pathogenesis genes contained within other large surface coat gene superfamilies from a broad array of eukaryotic pathogens.
Suboptimal access to primary healthcare among street-based sex workers in southwest Switzerland
Authors: Darling Katharine Elizabeth Anna , Gloor Elodie , Ansermet-Pagot Anne , Vaucher Paul , Durieux-Paillard Sophie , Bodenmann Patrick , Cavassini Matthias 
Published: November 2012

Abstract

Objectives
Street-based sex workers (SSWs) in Lausanne, Switzerland, are poorly characterised. We set out to quantify potential vulnerability factors in this population and to examine SSW healthcare use and unmet healthcare requirements.

Methods
We conducted a cross-sectional questionnaire-based survey among SSWs working in Lausanne's red light district between 1 February and 31 July 2010, examining SSW socio-demographic characteristics and factors related to their healthcare.

Results
We interviewed 50 SSWs (76% of those approached). A fifth conducted their interviews in French, the official language in Lausanne. 48 participants (96%) were migrants, of whom 33/48 (69%) held no residence permit. 22/50 (44%) had been educated beyond obligatory schooling. 28/50 (56%) had no health insurance. 18/50 (36%) had been victims of physical violence. While 36/50 (72%) had seen a doctor during the preceding 12 months, only 15/50 (30%) were aware of a free clinic for individuals without health insurance. Those unaware of free services consulted emergency departments or doctors outside Switzerland. Gynaecology, primary healthcare and dental services were most often listed as needed. Two individuals (of 50, 4%) disclosed positive HIV status; of the others, 24/48 (50%) had never had an HIV test.

Conclusions
This vulnerable population comprises SSWs who, whether through mobility, insufficient education or language barriers, are unaware of services they are entitled to. With half the participants reporting no HIV testing, there is a need to enhance awareness of available facilities as well as to increase provision and uptake of HIV testing.
Exposure to bisphenol A modulates hormone concentrations in Gammarus pseudolimnaeus
Authors: Lewis S.E. , Yokofich A. , Mohr M. , Kurth C. , Giuliani R. , Baldridge M.G. 
Published: November 2012

Bisphenol A (BPA) is an endocrine-disrupting compound that can enter aquatic systems through landfill leachate or wastewater effluent. Although impacts of BPA on vertebrates are well documented, its effects on invertebrates are less clear. Amphipods such as Gammarus pseudolimnaeus Bousfield, 1958 are often prevalent invertebrates in freshwater ecosystems and can provide a powerful invertebrate model system to investigate the endocrine-disruptive capabilities of BPA. However, techniques to assay hormone concentrations in amphipods, especially vertebrate-like steroid sex hormones, are not widespread. In this study, we (i) quantified estrogen concentrations in juveniles and in adult female amphipods; (ii) quantified testosterone concentrations in juveniles and in adult male amphipods; and (iii) delineated changes to estrogen and testosterone concentrations of adults and juveniles following a 9-day exposure to BPA at four levels: 0 (control), 10, 50, and 100 µg/L BPA. Tissue extracts from homogenized samples were analyzed for estrogen or testosterone concentrations via radioimmunoassay for each reproductive class of amphipod. Low concentrations of BPA significantly increased estrogen concentrations in adult females and in juveniles. Moderate and high concentrations of BPA significantly increased testosterone concentrations in adult males, and low and moderate concentrations of BPA significantly increased testosterone concentrations of juveniles.
mTOR Inhibitor RAD001 Promotes Metastasis in a Rat Model of Pancreatic Neuroendocrine Cancer
Authors: Pool Stefan E. , Bison Sander , Koelewijn Stuart J. , van der Graaf Linda M. , Melis Marleen , Krenning Eric P. , de Jong Marion 
Published: November 2012

Abstract
Inhibition of mTOR is commonly considered a valid target in cancer treatment, but this assertion does not address effects on the immune microenvironment that may be detrimental to cancer treatment. Here we show how administration of the mTOR inhibitor RAD001 (everolimus) results in the occurrence of distant metastasis in a rat model of pancreatic cancer. RAD001 was administered twice weekly for 4.5 weeks as a single treatment or combined with [177Lu-DOTA,Tyr3]octreotate (177Lu-DOTATATE), where the latter targets the somatostatin receptor-2. The hypothesized synergistic therapeutic effect of RAD001 combined with 177Lu-DOTATATE was, however, not observed in our experiments. The combination was shown to be less effective than 177Lu-DOTATATE alone. Unexpectedly, tumor metastasis was observed in 77% of the subjects treated with RAD001, either alone or as part of the combination treatment. This was a striking effect, because metastasis did not occur in control or 177Lu-DOTATATE-treated animals, including those where the primary tumor was surgically removed. These findings may be important clinically among noncompliant patients or patients that discontinue RAD001 therapy because of adverse effects. Cancer Res; 73(1); 12–18. ©2012 AACR.
Autophagy Control by the VEGF-C/NRP-2 Axis in Cancer and Its Implication for Treatment Resistance
Authors: Stanton Marissa J. , Dutta Samikshan , Zhang Heyu , Polavaram Navatha S. , Leontovich Alexey A. , Hönscheid Pia , Sinicrope Frank A. , Tindall Donald J. , Muders Michael H. , Datta Kaustubh 
Published: November 2012

Abstract
A major contributor to cancer mortality is recurrence and subsequent metastatic transformation following therapeutic intervention. Therefore, in order to develop new treatment modalities and improve the efficacy of current ones, it is important to understand the molecular mechanisms that promote resistance to therapy in cancer cells. One pathway contributing to therapy resistance is autophagy, a self-digestive process that can eliminate unnecessary or damaged organelles to protect cancer cells from death. We have found that the VEGF-C/NRP-2 axis is involved in the activation of autophagy, which helps cancer cell survival following treatment. Inhibition of mTOR complex 1 activity by this axis is the underlying mechanism for the activation of autophagy. Furthermore, we identified two VEGF-C/NRP-2-regulated genes, LAMP-2 and WDFY-1, that have previously been suggested to participate in autophagy and vesicular trafficking. Upregulation of WDFY-1 following VEGF-C or NRP-2 depletion contributes to cytotoxic drug-mediated cell death. Together, these data suggest a link between the VEGF-C/NRP-2 axis and cancer cell survival despite the presence of chemotherapy-induced stress. Effective targeting of this pathway may lead to the development of new cancer therapies. Cancer Res; 73(1); 160–71. ©2012 AACR.
STAT5 Is Crucial to Maintain Leukemic Stem Cells in Acute Myelogenous Leukemias Induced by MOZ-TIF2
Authors: Tam Winnie F. , Hähnel Patricia S. , Schüler Andrea , Lee Benjamin H. , Okabe Rachel , Zhu Nan , Pante Saskia V. , Raffel Glen , Mercher Thomas , Wernig Gerlinde , Bockamp Ernesto , Sasca Daniel , Kreft Andreas , Robinson Gertraud W. , Hennighausen Lothar , Gilliland D. Gary , Kindler Thomas 
Published: November 2012

Abstract
MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewal capability to hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays. Here, we report that FLT3-ITD transforms hematopoietic cells in cooperation with MOZ-TIF2 in vitro and in vivo. Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC). We show that STAT5, a major effector of aberrant FLT3-ITD signal transduction, is both necessary and sufficient for this cooperative effect. In addition, STAT5 signaling is essential for MOZ-TIF2–induced leukemic transformation itself. Lack of STAT5 in fetal liver cells caused rapid differentiation and loss of replating capacity of MOZ-TIF2–transduced cells enriched for LSCs. Furthermore, mice serially transplanted with Stat5−/− MOZ-TIF2 leukemic cells develop AML with longer disease latency and finally incomplete penetrance when compared with mice transplanted with Stat5+/+ MOZ-TIF2 leukemic cells. These data suggest that STAT5AB is required for the self-renewal of LSCs and represents a combined signaling node of FLT3-ITD and MOZ-TIF2 driven leukemogenesis. Therefore, targeting aberrantly activated STAT5 or rewired downstream signaling pathways may be a promising therapeutic option. Cancer Res; 73(1); 373–84. ©2012 AACR.
Common Single-Nucleotide Polymorphisms in the Estrogen Receptor β Promoter Are Associated with Colorectal Cancer Survival in Postmenopausal Women
Authors: Passarelli Michael N. , Phipps Amanda I. , Potter John D. , Makar Karen W. , Coghill Anna E. , Wernli Karen J. , White Emily , Chan Andrew T. , Hutter Carolyn M. , Peters Ulrike , Newcomb Polly A. 
Published: November 2012

AbstractLoss of estrogen receptor β (ERβ) expression in the gut is associated with colorectal cancer (CRC) initiation and progression. Germline single-nucleotide polymorphisms (SNP) in genes for the sex-steroid hormone receptors are not strongly associated with CRC risk; however, these SNPs have not previously been evaluated in relation to survival after diagnosis. We enrolled 729 women, ages 50 to 74, diagnosed with invasive CRC between 1997 and 2002 in 13 counties covered by the Seattle-Puget Sound Surveillance Epidemiology and End Results cancer registry. Participants provided germline DNA. We selected 99 tag-SNPs for the androgen receptor (AR), ERα (ESR1), ERβ (ESR2), and progesterone receptor (PGR) genes. Mortality outcomes were ascertained from the National Death Index. During a median of 6.6 years of follow-up, 244 deaths occurred (161 from CRC). We identified 20 SNPs (12 of ESR2 and 8 of PGR) for replication in 1,729 women diagnosed with incident invasive CRC (555 deaths; 405 from CRC) from three prospective cohort studies that participate in the Genetics and Epidemiology of Colorectal Cancer Consortium. Three correlated SNPs in the promoter of ESR2 (rs2987983, rs3020443, and rs2978381) were statistically significant predictors of CRC-specific and overall survival. Minor alleles of each were associated with improved survival [for rs2987983, CRC-specific HR, 0.77; 95% confidence interval (CI), 0.60–0.99 in the initial study, and HR, 0.79; CI, 0.64–0.98 in replication]. No associations were noted for SNPs of AR, ESR1, or PGR. SNPs in the promoter of ESR2 may be important to pathways related to the association between ERβ and tumor progression and metastasis. Cancer Res; 73(2); 767–75. ©2012 AACR.