bluuebunny/crossref_metadata_2025_split huggingface dataset:
A mixture toxicity approach for environmental risk assessment of multiple insect resistance genes
Authors: Wolt Jeffrey D 
Published: December 2010

Abstract
Multiple substance considerations applied to chemical mixtures in ecological risk assessments can be logically extended to nontarget organism (NTO) risk assessment for pyramided trait crops expressing multiple insect resistance genes. A case instance is developed that considers a two-protein pyramid of Cry1F and Cry1Ac synthetic proteins expressed in cotton (Gossypium hirsutum L.). A mixture toxicity approach was used to arrive at the aggregated multisubstance potentially affected fraction (msPAF) of NTOs that may be at risk from exposure to Cry1F + Cry1Ac cotton in representative-use environments. Development of the msPAF for putative susceptible NTOs considered laboratory toxicity data for Lepidoptera expressed in terms of additive mixture toxicity as well as data on in planta expression of the Cry1F and Cry1Ac proteins and their translation into environmental loads and exposure concentrations. The msPAF based on tier 1 estimated environmental concentrations (EECs) and toxicity to Lepidoptera species—used as surrogate data for adverse effects to a putative susceptible species—provided a highly conservative estimate of effects on beneficial species and therefore is a ready means to conduct screening-level NTO risk assessments for pyramided crops. Environ. Toxicol. Chem. 2011; 30:763–772. © 2011 SETAC
AC pollution flashover circuit model for composite insulator based on multiple arcs series
Authors: Shu Lichun , Yuan Qianfei , Zhang Zhijing , Jiang Xingliang , Hu Qin , Sun Caixin 
Published: December 2010

AbstractWith the increasing application of composite insulator in the power system, pollution flashover often occurs. However, no model can exactly predict pollution flashover voltage of composite insulator at present. Based on high‐speed photography of AC pollution flashover process, a model, which is in view of pollution severity, air pressure, shed configuration, and hydrophobicity level and which is suitable for composite insulator with any shed configuration, is proposed. Influences of pollution severity and hydrophobicity on flashover voltage and pressure characteristic exponent are analyzed, from which derives a calculative formula of flashover voltage. Calculated results from the model, validated by experiments, demonstrate that there is a power function relationship between flashover voltage and hydrophobicity levelβ, and characteristic exponent of hydrophobicity levelβis the same as that of pollution severity. Meanwhile, the exponent characterizing the influence of air pressure increases with the fall of pollution severity and the rise of hydrophobicity. Copyright © 2010 John Wiley & Sons, Ltd.
Reliability analysis of voltage instability risk indicator based on a novel real‐time identification algorithm
Authors: Corsi Sandro , Taranto Glauco N. 
Published: December 2010

AbstractThis paper focuses the performance and robustness of an algorithm recently proposed in the literature for real‐time voltage instability risk indication. Based on local phasor measurements, the real‐time identification of the proximity of the equivalent Thevenin impedance seen from an EHV bus and its load impedance is the key to recognize the voltage instability risk at the time it is approaching. The paper highlights the impact of the dynamics of on‐load tap changing transformers and generators over‐excitation limiters on the Thevenin equivalent identification (and consequently on the timely voltage instability indication). The paper also shows the high reliability of the algorithm with respect to load characteristics and to critical load profiles corresponding to very large perturbations. The paper presents simulation results obtained from a detailed dynamic model of an equivalent single‐generator system, as well as from the actual Italian EHV network. Copyright © 2010 John Wiley & Sons, Ltd.
Depression in Alzheimer's disease: specificity of depressive symptoms using three different clinical criteria
Authors: Engedal Knut , Barca Maria Lage , Laks Jerson , Selbaek Geir 
Published: December 2010

AbstractBackgroundPrevious studies report contradictory results on whether the symptoms of depression in Alzheimer's disease patients are the same as in cognitively normal persons. Thus, provisional criteria for depression in Alzheimer's disease (PDC‐dAD) have been developed.AimTo examine which symptoms in AD patients are significant in diagnosing depression according to PDC‐dAD compared to those for the DSM‐IV‐TR and ICD‐10 criteria.MethodsWe included 112 patients with Alzheimer's disease. They were interviewed by a psychiatrist who diagnosed depression according to PDC‐dAD, DSM‐IV‐TR and ICD‐10. Without knowledge of that diagnosis, trained nurses interviewed the caregivers of the patients using the Cornell scale for depression in dementia (CSDD).ResultsMean age of the patients was 83.0 (s.d. 7.9), 77 (69.6%) were female. The proportion with depression according to each set of criteria was: PDC‐dAD 53.5%, ICD‐10, 47.3% and DSM‐IV‐TR, 34.8%. Sadness, loss of interest and agitation/retardation were the most prevalent symptoms in depressed subjects as evaluated by the psychiatrists. According to CSDD sadness, anxiety, suicidal thoughts, poor self‐esteem, multiple physical complaints and pessimism best distinguished the depressed patients from the non‐depressed. In multiple logistic regression analyses poor self‐esteem, delusion and multiple physical complaints best predicted depression using PDC‐dAD criteria, whereas sadness, suicidal thoughts and poor self‐esteem best predicted depression using ICD‐10 and DSM‐IV‐TR.ConclusionThe most significant symptoms for a depressive disorder in AD are pretty much the same as for patients without dementia using the DSM‐IV‐TR and ICD‐10 criteria, whereas they differ using the PDC‐dAD criteria. Copyright © 2010 John Wiley & Sons, Ltd.
Enrichment of Nur77 Mediated by Retinoic Acid Receptor β Leads to Apoptosis of Human Hepatocellular Carcinoma Cells Induced by Fenretinide and Histone Deacetylase Inhibitors §Δ
Authors: Yang Hui , Zhan Qi , Wan Yu-Jui Yvonne 
Published: December 2010

Abstract

The synthetic retinoid fenretinide is one of the most promising clinically tested retinoids. Previously, we have shown that fenretinide induces apoptosis of Huh7 cells, but HepG2 cells are relatively resistant to fenretinide-induced apoptosis. This study examines the interactive role of fenretinide and histone deacetylase inhibitors (HDACi) in inducing apoptosis of human hepatocellular carcinoma (HCC) cells and the underlying mechanism. Trichostatin A and scriptaid can either enhance fenretinide-induced apoptosis in the fenretinide sensitive HCC cells (Huh7 and Hep3B) or sensitize the fenretinide resistant cells (HepG2) to become sensitive to the apoptotic effect of fenretinide in a cancer cell–specific manner. The sensitivity of cells to fenretinide-induced apoptosis was not associated with reactive oxygen species production nor with antioxidant gene expression. However, the level of retinoic acid receptor β (RARβ) and Nur77 (NR4A1) was important for inducing apoptosis. Upon fenretinide and HDACi treatment, the expression of RARβ and Nur77 were induced and colocalized in the cytosol. The induction of Nur77 protein level, but not the messenger RNA level, was RARβ-dependent. In addition, RARβ interacted with Nur77. Nur77 was essential for fenretinide-induced and HDACi-induced apoptosis of Huh7 cells. Induction of the expression, the interaction, and the nuclear export of RARβ and Nur77 mediate fenretinide-induced and HDACi-induced apoptosis.

Conclusion:

Our findings suggest that targeting Nur77 and RARβ simultaneously provides an effective way to induce HCC cell death. (Hepatology 2011)
Bile Proteomic Profiles Differentiate Cholangiocarcinoma From Primary Sclerosing Cholangitis and Choledocholithiasis §Δ
Authors: Lankisch Tim O. , Metzger Jochen , Negm Ahmed A. , Voβkuhl Katja , Schiffer Eric , Siwy Justyna , Weismüller Tobias J. , Schneider Andrea S. , Thedieck Kathrin , Baumeister Ralf , Zürbig Petra , Weissinger Eva M. , Manns Michael P. , Mischak Harald , Wedemeyer Jochen 
Published: December 2010

Abstract

Early detection of malignant biliary tract diseases, especially cholangiocarcinoma (CC) in patients with primary sclerosing cholangitis (PSC), is very difficult and often comes too late to give the patient a therapeutic benefit. We hypothesize that bile proteomic analysis distinguishes CC from nonmalignant lesions. We used capillary electrophoresis mass spectrometry (CE-MS) to identify disease-specific peptide patterns in patients with choledocholithiasis (n = 16), PSC (n = 18), and CC (n = 16) in a training set. A model for differentiation of choledocholithiasis from PSC and CC (PSC/CC model) and another model distinguishing CC from PSC (CC model) were subsequently validated in independent cohorts (choledocholithiasis [n = 14], PSC [n = 18] and CC [n = 25]). Peptides were characterized by sequencing. Application of the PSC/CC model in the independent test cohort resulted in correct exclusion of 12/14 bile samples from patients with choledocholithiasis and identification of 40/43 patients with PSC or CC (86% specificity, 93% sensitivity). The corresponding receiver operating characteristic (ROC) analysis revealed an area under the curve (AUC) of 0.93 (95% confidence interval [CI]: 0.82-0.98,

P

= 0.0001). The CC model succeeded in an accurate detection of 14/18 bile samples from patients with PSC and 21/25 samples with CC (78% specificity, 84% sensitivity) in the independent cohort, resulting in an AUC value of 0.87 (95% CI: 0.73-0.95,

P

= 0.0001) in ROC analysis. Eight out of 10 samples of patients with CC complicating PSC were identified.

Conclusion:

Bile proteomic analysis discriminates benign conditions from CC accurately. This method may become a diagnostic tool in future as it offers a new possibility to diagnose malignant bile duct disease and thus enables efficient therapy particularly in patients with PSC. (Hepatology 2010;)
Concerted Action of Sulfiredoxin and Peroxiredoxin I Protects Against Alcohol-Induced Oxidative Injury in Mouse Liver σ
Authors: Bae Soo Han , Sung Su Haeng , Cho Eun Jung , Lee Se Kyoung , Lee Hye Eun , Woo Hyun Ae , Yu Dae-Yeul , Kil In Sup , Rhee Sue Goo 
Published: December 2010

Abstract

Peroxiredoxins (Prxs) are peroxidases that catalyze the reduction of reactive oxygen species (ROS). The active site cysteine residue of members of the 2-Cys Prx subgroup (Prx I to IV) of Prxs is hyperoxidized to cysteine sulfinic acid (Cys-SO2) during catalysis with concomitant loss of peroxidase activity. Reactivation of the hyperoxidized Prx is catalyzed by sulfiredoxin (Srx). Ethanol consumption induces the accumulation of cytochrome P450 2E1 (CYP2E1), a major contributor to ethanol-induced ROS production in the liver. We now show that chronic ethanol feeding markedly increased the expression of Srx in the liver of mice in a largely Nrf2-dependent manner. Among Prx I to IV, only Prx I was found to be hyperoxidized in the liver of ethanol-fed wildtype mice, and the level of Prx I-SO2 increased to ≈30% to 50% of total Prx I in the liver of ethanol-fed Srx−/− mice. This result suggests that Prx I is the most active 2-Cys Prx in elimination of ROS from the liver of ethanol-fed mice and that, despite the up-regulation of Srx expression by ethanol, the capacity of Srx is not sufficient to counteract the hyperoxidation of Prx I that occurs during ROS reduction. A protease protection assay revealed that a large fraction of Prx I is located together with CYP2E1 at the cytosolic side of the endoplasmic reticulum membrane. The selective role of Prx I in ROS removal is thus likely attributable to the proximity of Prx I and CYP2E1.

Conclusion:

The pivotal functions of Srx and Prx I in protection of the liver in ethanol-fed mice was evident from the severe oxidative damage observed in mice lacking either Srx or Prx I. (Hepatology 2011)
GC‐binding factor 2 interacts with dishevelled and regulates Wnt signaling pathways in human carcinoma cell lines
Authors: Ohtsuka Hideo , Oikawa Masaya , Ariake Kyohei , Rikiyama Toshiki , Motoi Fuyuhiko , Katayose Yu , Unno Michiaki , Johnson Alfred C. 
Published: December 2010

AbstractGC‐binding factor 2 (GCF2), a transcriptional repressor that decreases the activity of several genes is capable of binding directly to the GC‐rich sequence of the EGFR promoter and repressing the transcriptional activity of EGFR. In addition to its function as a transcriptional repressor, GCF2 can directly interact with other proteins such as flightless‐1 (Fli‐1). Many previous findings pertaining to the function of Fli‐1 have suggested a role for fli‐1 in providing a direct link between molecules involved in signal transduction pathways and the actin cytoskeleton. We hypothesized that GCF2, together with Fli‐1, plays a role in regulating cytoskeleton function, cell migration, and/or morphology. In our study, we observed that GCF2 is crucial for the activation of RhoA, a small GTPase that plays a key role in the regulation of the actin cytoskeleton. RhoA was markedly inactivated as a result of the decreased expression of GCF2. Co‐immunoprecipitations were subsequently performed to further investigate the mechanism for the repressive function. We identified dishevelled (Dvl), which is the key mediator for the Wnt pathway, as a binding partner with GCF2. These results strongly suggest that GCF2 plays a role in the Wnt‐noncanonical planar cell polarity (PCP) signaling pathway. Consequently, GCF2 may regulate the cytoskeleton or migration via Dvls and RhoA.
Serological AFP/Golgi protein 73 could be a new diagnostic parameter of hepatic diseases
Authors: Tian Liyuan , Wang Yu , Xu Dabin , Gui Junhao , Jia Xingwang , Tong Hongli , Wen Xinyu , Dong Zhennan , Tian Yaping 
Published: December 2010

AbstractWe have investigated the changing rule of serum form of GP73 (sGP73) in different hepato‐pathologic processes and identified the sGP73 role in inflammation, fibrosis and carcinogenesis since sGP73 has been regarded as a candidate tumor marker. Quantitative enzyme‐linked immunosorbent assay detected sGP73 in 535 subjects with hepatocellular carcinoma (HCC), liver cirrhosis (LC), hepatitis, focal nodular hyperplasia (FNH), angioma, intra‐hepatic cholangio‐carcinoma (ICC) and metastatic cancer from adenocarcinomas (MC). Median sGP73 in LC was higher than in HCC and hepatitis (p = 0.001), and sGP73 in all three groups were higher than those in healthy individuals (p < 0.001); sGP73 in LC patients with Child‐Pugh class A was lower than in class B and C (p = 0.001), no significant difference was found between early and advanced HCC groups (110.4 μg/L vs. 102.8 μg/L). AFP/GP73 had a sensitivity of 75.8% and specificity of 79.7% with an area under the receiver operating curve (AUROC) of 0.844 vs. 0.812 for AFP (p = 0.055) with a sensitivity of 95.2% and specificity of 47.1%; in detecting early HCC, AUROC of AFP/GP73 was 0. 804 vs. 0.766 for AFP (p = 0.086). sGP73 correlated with AST, AST/ALT, ALB, A/G and ALP in LC. The positive rate of sGP73 in angioma, FNH, ICC, and MC was 0, 50, 63.3, 53.3%, respectively; AFP/GP73 was 0.796 with the sensitivity of 81.4% and specificity of 70.0% when differentiating MC from AFP‐negative HCC. Increased sGP73 is related to hepatic impairment and chronic fibrosis, and when combined with AFP could improve the differential diagnosis of hepatic diseases.
PTH receptor signaling in osteocytes governs periosteal bone formation and intracortical remodeling
Authors: Rhee Yumie , Allen Matthew R , Condon Keith , Lezcano Virginia , Ronda Ana C , Galli Carlo , Olivos Naomi , Passeri Giovanni , O'Brien Charles A , Bivi Nicoletta , Plotkin Lilian I , Bellido Teresita 
Published: December 2010

Abstract
The periosteal and endocortical surfaces of cortical bone dictate the geometry and overall mechanical properties of bone. Yet the cellular and molecular mechanisms that regulate activity on these surfaces are far from being understood. Parathyroid hormone (PTH) has profound effects in cortical bone, stimulating periosteal expansion and at the same time accelerating intracortical bone remodeling. We report herein that transgenic mice expressing a constitutive active PTH receptor in osteocytes (DMP1-caPTHR1 mice) exhibit increased cortical bone area and an elevated rate of periosteal and endocortical bone formation. In addition, DMP1-caPTHR1 mice display a marked increase in intracortical remodeling and cortical porosity. Crossing DMP1-caPTHR1 mice with mice lacking the Wnt coreceptor, LDL-related receptor 5 (LRP5), or with mice overexpressing the Wnt antagonist Sost in osteocytes (DMP1-Sost mice) reduced or abolished, respectively, the increased cortical bone area, periosteal bone formation rate, and expression of osteoblast markers and Wnt target genes exhibited by the DMP1-caPTHR1 mice. In addition, DMP1-caPTHR1 lacking LRP5 or double transgenic DMP1-caPTHR1;DMP1-Sost mice exhibit exacerbated intracortical remodeling and increased osteoclast numbers, and markedly decreased expression of the RANK decoy receptor osteoprotegerin. Thus, whereas Sost downregulation and the consequent Wnt activation is required for the stimulatory effect of PTH receptor signaling on periosteal bone formation, the Wnt-independent increase in osteoclastogenesis induced by PTH receptor activation in osteocytes overrides the effect on Sost. These findings demonstrate that PTH receptor signaling influences cortical bone through actions on osteocytes and defines the role of Wnt signaling in PTH receptor action. © 2011 American Society for Bone and Mineral Research.
An atypical subtrochanteric femoral fracture from pycnodysostosis: A lesson from nature
Authors: Yates Christopher J , Bartlett Miriam J , Ebeling Peter R 
Published: December 2010

Abstract
This case describes a man with an unusual cause of an atypical subtrochanteric fracture, pycnodysostosis. This condition results from mutations involving the cathepsin K gene. New antiresorptive treatments for osteoporosis inhibit the cathepsin K enzyme in osteoclasts. Therefore, there should be vigilant monitoring for the development of long-term complications noted to occur in diseases of reduced osteoclast function, including pycnodysostosis, in patients receiving these novel antiresorptive agents. © 2011 American Society for Bone and Mineral Research.
Ganoderma atrum polysaccharide induces anti‐tumor activity via the mitochondrial apoptotic pathway related to activation of host immune response
Authors: Li Wen‐Juan , Chen Yi , Nie Shao‐Ping , Xie Ming‐Yong , He Ming , Zhang Shen‐Shen , Zhu Ke‐Xue 
Published: December 2010

AbstractGanoderma atrum polysaccharide (PSG‐1), the major active ingredient isolated from Ganoderma atrum, has been suggested as a candidate for cancer therapy. The aim of this study was to investigate the anti‐tumor effect of PSG‐1 using sarcoma 180 (S‐180) transplanted mice and further to examine the molecular mechanisms of PSG‐1‐induced anti‐tumor effect. Results showed that PSG‐1 significantly inhibited tumor growth in S‐180‐bearing mice. PSG‐1‐induced tumor apoptosis was associated with the alteration of Bcl‐2 family proteins, increase of reactive oxygen species generation, loss of mitochondrial membrane potential (Δψm), release of cytochrome c from the mitochondria into cytosol, and activation of caspase‐3 and ‐9. Elevation of immune function was also shown during PSG‐1‐induced tumor apoptosis, as evidenced by increase of spleen and thymus indexes, lymphocyte proliferation, concentrations of tumor necrosis factor (TNF)‐α, and interleukin‐2 in serum. Furthermore, the combined treatment of PSG‐1 and cyclophosphamide (CTX) results in an enhancement of the anti‐tumor effect of CTX alone via increased host immune response. These results suggested that PSG‐1 had a potent anti‐tumor activity by induction of tumor apoptosis through mitochondrial pathways, and immunoenhancement effect of PSG‐1 was related to its anti‐tumor effect. In addition, PSG‐1 enhanced CTX‐induced anti‐tumor activity in S‐180‐bearing mice. J. Cell. Biochem. 112: 860–871, 2011. © 2010 Wiley‐Liss, Inc.
Polyamines, androgens, and skeletal muscle hypertrophy
Authors: Lee Nicole K. L. , MacLean Helen E. 
Published: December 2010

AbstractThe naturally occurring polyamines, spermidine, spermine, and their precursor putrescine, play indispensible roles in both prokaryotic and eukaryotic cells, from basic DNA synthesis to regulation of cell proliferation and differentiation. The rate‐limiting polyamine biosynthetic enzymes, ornithine decarboxylase (ODC) and S‐adenosylmethionine decarboxylase, are essential for mammalian development, with knockout of the genes encoding these enzymes, Odc1 and Amd1, causing early embryonic lethality in mice. In muscle, the involvement of polyamines in muscle hypertrophy is suggested by the concomitant increase in cardiac and skeletal muscle mass and polyamine levels in response to anabolic agents including β‐agonists. In addition to β‐agonists, androgens, which increase skeletal mass and strength, have also been shown to stimulate polyamine accumulation in a number of tissues. In muscle, androgens act via the androgen receptor to regulate expression of polyamine biosynthetic enzyme genes, including Odc1 and Amd1, which may be one mechanism via which androgens promote muscle growth. This review outlines the role of polyamines in proliferation and hypertrophy, and explores their possible actions in mediating the anabolic actions of androgens in muscle. J. Cell. Physiol. 226: 1453–1460, 2011. © 2010 Wiley‐Liss, Inc.
Polymethylmethacrylate and titanium alloy particles activate peripheral monocytes during periprosthetic inflammation and osteolysis
Authors: Yang Shang‐You , Zhang Kai , Bai Ling , Song Zheng , Yu Haiying , McQueen David A. , Wooley Paul H. 
Published: December 2010

AbstractWe investigated the interactions of particulate PMMA or titanium alloy, patient blood monocytes, and periprosthetic tissues using a SCID‐hu model of aseptic loosening. Periprosthetic tissues and bone chips obtained at revision surgery for loosening were transplanted into muscles of SCID mice. Peripheral blood monocytes (PBMCs) isolated from the same donors were fluorescently labeled and co‐cultured with PMMA or Ti‐6Al‐4V particles before intraperitoneal injection. Control mice with periprosthetic tissue or non‐inflammatory ligament xenografts received naive PBMCs transfusion. Mice were euthanized 2 weeks after PBMC transfusion. The human tissues were well accepted in SCID mice. Transfused fluorescent‐labeled PBMCs were markedly accumulated in transplanted periprosthetic tissues. Multinucleated osteoclast‐like cells were commonly seen within retrieved xenograft tissue, and focal bone erosions were ubiquitous. Total cell densities and CD68+ cells within the xenograft were significantly increased in mice transfused with PMMA and Ti‐provoked PBMCs compared to the naïve PBMC animals (p < 0.05). Immunohistochemical staining identified much stronger positive IL‐1 and TNF stains in xenografts from either PMMA or Ti‐stimulated monocytes transfusion groups (p < 0.05). TRAP+ cells were found around bone chips in both activated‐PBMCs groups, although markedly more aggregated TRAP+ cells in the PMMA‐challenged group than in the titanium group (p < 0.05). MicroCT assessment confirmed the significant decrease of bone mineral density in chips interacted with activated‐monocytes/osteoclasts. In conclusion, PMMA or titanium particles readily activate peripheral monocytes and promote the cell trafficking to the debris‐containing prosthetic tissues. Particles‐provoked PBMCs participated in and promoted the local inflammatory process, osteoclastogenesis, and bone resorption. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:781–786, 2011