bluuebunny/crossref_metadata_2025_split huggingface dataset:
Time to get off the fence: The need for definitive international guidance on statistical analysis of ecotoxicity data
Authors: van Dam Rick A , Harford Andrew J , Warne Michael St J 
Published: February 2012

Abstract
The use of the no observed effect concentration (NOEC) and lowest observed effect concentration (LOEC) in ecotoxicology has been consistently criticized for over 30 years. A search of the literature from the past 30 years found 22 articles challenging the validity and/or appropriateness of NOEC/LOEC data compared to only one in defense of such data. Notwithstanding this compelling weight of evidence, the NOEC and LOEC remain commonly published measures of toxicity from ecotoxicological studies. In this article we argue that the major reason for the continued generation and publication of NOEC/LOEC data is that key government and intergovernmental organizations have been “sitting on the fence” on the issue for more than a decade. Although most key environmental quality guideline, toxicity testing, and associated guidance documents have now recognized the limitations of NOEC/LOEC data, to date no such document or standard toxicity test method has formally ceased recommending or providing guidance on the generation of such data. This is a problem because it is these very guidance documents and test methods that regulatory agencies demand be used by industry for regulatory activities, and on which commercial testing facilities attain and maintain their testing accreditation. Consequently, there will be little impetus for change to statistical analysis practices unless changes to the key guidance documents and test methods necessitate it. Although some progress on this has been made (e.g., in Canada, Australia and New Zealand), there needs to be stronger and universal action to ensure NOEC/LOEC data are no longer generated. Integr Environ Assess Manag 2012; 8: 242–245. © 2012 SETAC
Multipotent progenitors resident in the skeletal muscle interstitium exhibit robust BMP-dependent osteogenic activity and mediate heterotopic ossification
Authors: Wosczyna Michael N , Biswas Arpita A , Cogswell Catherine A , Goldhamer David J 
Published: February 2012

Abstract
Heterotopic ossification is a debilitating condition that can result from traumatic injury, surgery, or genetic disease. We investigated the cellular origins of heterotopic skeletogenesis in the mouse using lineage tracing and bioassays of heterotopic ossification based on intramuscular transplantation. We identified, characterized, and purified a tissue-resident stem/progenitor cell population that exhibits robust osteogenic potential and represents a major cell-of-origin for heterotopic ossification. These progenitors reside in the interstitium of skeletal muscle and other tissues, and are distinct from the endothelium, which does not exhibit osteogenic activity in response to bone morphogenetic protein 2 (BMP2) stimulation. Intramuscular transplantation, together with clonal analysis in culture, revealed that these progenitors are multipotent, exhibiting the capacity for both BMP-dependent skeletogenic differentiation and spontaneous adipogenic differentiation. Identifying the cells-of-origin responsible for heterotopic ossification provides a potential therapeutic target to treat, mitigate, or prevent this disabling condition. © 2012 American Society for Bone and Mineral Research.
Effect of vertebroplasty on pain relief, quality of life, and the incidence of new vertebral fractures: A 12-month randomized follow-up, controlled trial
Authors: Blasco Jordi , Martinez-Ferrer Angeles , Macho Juan , San Roman Luis , Pomés Jaume , Carrasco Josep , Monegal Ana , Guañabens Nuria , Peris Pilar 
Published: February 2012

Abstract
Uncertainty regarding the benefits of vertebroplasty (VP) for the treatment of acute osteoporotic vertebral fractures has recently arisen. A prospective, controlled, randomized single-center trial (ClinicalTrials.gov registration number NCT00994032) was designed to compare the effects of VP versus conservative treatment on the quality of life and pain in patients with painful osteoporotic vertebral fractures, new fractures and secondary adverse effects were also analyzed during a 12-month follow-up period. A total of 125 patients were randomly assigned to receive conservative treatment or VP. The primary end point was to compare the evolution of the quality of life (Quality of Life Questionnaire of the European Foundation for Osteoporosis [Qualeffo-41] and pain (Visual Analogue Scale [VAS]) during a 12 month follow-up. Secondary outcomes included comparison of analgesic consumption, clinical complications, and radiological vertebral fractures at the same time points. Both arms showed significant improvement in VAS scores at all time points, with greater improvement (p = 0.035) in the VP group at the 2-month follow-up. Significant improvement in Qualeffo total score was seen in the VP group throughout the study, whereas this was not seen in the conservative treatment arm until the 6-month follow-up. VP treatment was associated with a significantly increased incidence of vertebral fractures (odds ratio [OR], 2 · 78; 95% confidence interval [CI], 1.02–7.62, p = 0.0462). VP and conservative treatment are both associated with significant improvement in pain and quality of life in patients with painful osteoporotic vertebral fractures over a 1-year follow-up period. VP achieved faster pain relief with significant improvement in the pain score at the 2-month follow-up but was associated with a higher incidence in vertebral fractures. © 2012 American Society for Bone and Mineral Research.
Therapeutic plasma exchange in Streptococcus pneumoniae‐associated hemolytic uremic syndrome: A case report
Authors: Petras Melissa L. , Dunbar Nancy M. , Filiano James J. , Braga Matthew S. , Chobanian Michael C. , Szczepiorkowski Zbigniew M. 
Published: February 2012

AbstractStreptococcus pneumoniae‐associated hemolytic uremic syndrome (pHUS) is an atypical form of HUS associated with microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. Although less common than diarrhea‐associated HUS, incidence appears to be increasing. We report a case of a child with pHUS who underwent a course of therapeutic plasma exchange (TPE) and had complete recovery. This report adds to the existing literature supporting TPE in cases of pHUS. J. Clin. Apheresis, 2012. © 2012 Wiley Periodicals, Inc.
The relationships between snail1 and estrogen receptor signaling in breast cancer cells
Authors: Scherbakov Alexander M. , Andreeva Olga E. , Shatskaya Valentina A. , Krasil'nikov Mikhail A. 
Published: February 2012

AbstractThe loss of hormonal dependency of breast tumor cells is often accompanied with the appearance of epithelial‐mesenchymal transition (EMT) features and increase in cell metastasis and invasiveness. The central role in the EMT belongs to transcription factors Snail responded for the decrease in E‐cadherin expression and cell contacts, stimulation of cell mobility and invasiveness. Aim was to study the relationships between estrogen receptor machinery and Snail1 signaling, and mechanism of Snail1 regulation in hormone‐resistant breast cancer cells. The experiments were performed on the estrogen‐dependent MCF‐7 breast cancer cells, estrogen‐hyposensitive MCF‐7/LS subline generated through long‐term cultivation of the parental cells in steroid‐free medium, and ER‐negative estrogen‐resistant HBL‐100 cells. Snail1, estrogen receptor, p65 NF‐κB, E‐cadherin levels were analyzed by Western blot. We found that decrease in the estrogen dependency is correlated with increase in Snail1 expression and activity, we demonstrated the Snail1 involvement in the negative regulation of ER, and showed that Snail1 inhibition partially restores the sensitivity of the estrogen‐hyposensitive cells to antiestrogen tamoxifen. Furthermore, NF‐κB was found to serve as a positive regulator of Snail1 in breast cancer cells, and simultaneous inhibition of NF‐κB and Snail1 resulted in additional increase in cell response to tamoxifen. In general, the results obtained demonstrate the phenomenon of Snail1 activation in the hormone‐resistant breast cancer cells, and show that Snail1 and NF‐κB may serve as an important targets in the treatment of breast cancer, both estrogen‐dependent and estrogen‐independent tumors. J. Cell. Biochem. 113: 2147–2155, 2012. © 2012 Wiley Periodicals, Inc.
Phenotypic characterization of transgenic mice harboring Nf1+/− or Nf1−/− osteoclasts in otherwise Nf1+/+ background
Authors: Alanne Maria H. , Siljamäki Elina , Peltonen Sirkku , Väänänen Kalervo , Windle Jolene J. , Parada Luis F. , Määttä Jorma A. , Peltonen Juha 
Published: February 2012

AbstractSkeletal abnormalities in neurofibromatosis type 1 syndrome (NF1) are observed in ∼50% of patients. Here, we describe the phenotype of Nf1Ocl mouse model with Nf1‐deficient osteoclasts. Nf1Ocl mice with Nf1+/− or Nf1−/− osteoclasts in otherwise Nf1+/+ background were successfully generated by mating parental Nf1flox/flox and TRAP‐Cre mice. Contrary to our original hypothesis, osteoporotic or fragile bone phenotype was not observed. The µCT analysis revealed that tibial bone marrow cavity, trabecular tissue volume, and the perimeter of cortical bone were smaller in Nf1 mice compared to Nf1 control mice. Nf1 mice also a displayed narrowed growth plate in the proximal tibia. In vitro analysis showed increased bone resorption capacity and cytoskeletal changes including irregular cell shape and abnormal actin ring formation in Nf1−/− osteoclasts. Surprisingly, the size of spleen in Nf1 mice was two times larger than in controls and histomorphometric analysis showed splenic megakaryocytosis. In summary, Nf1Ocl mouse model presented with a mild but specific bone phenotype. This study shows that NF1‐deficiency in osteoclasts may have a role in the development of NF1‐related skeletal abnormalities, but Nf1‐deficiency in osteoclasts in Nf1+/+ background is not sufficient to induce skeletal abnormalities analogous to those observed in patients with NF1. J. Cell. Biochem. 113: 2136–2146, 2012. © 2012 Wiley Periodicals, Inc.
HDAC2 overexpression confers oncogenic potential to human lung cancer cells by deregulating expression of apoptosis and cell cycle proteins
Authors: Jung Kwang Hwa , Noh Ji Heon , Kim Jeong Kyu , Eun Jung Woo , Bae Hyun Jin , Xie Hong Jian , Chang Young Gyoon , Kim Min Gyu , Park Hanna , Lee Jung Young , Nam Suk Woo 
Published: February 2012

AbstractHistone deacetylase 2 (HDAC2) is crucial for embryonic development, affects cytokine signaling relevant for immune responses, and is often significantly overexpressed in solid tumors, but little is known of its role in human lung cancer. In this study, we demonstrated the aberrant expression of HDAC2 in lung cancer tissues and investigated oncogenic properties of HDAC2 in human lung cancer cell lines. HDAC2 inactivation resulted in regression of tumor cell growth and activation of cellular apoptosis via p53 and Bax activation and Bcl2 suppression. In cell cycle regulation, HDAC2 inactivation caused induction of p21WAF1/CIP1 expression, and simultaneously suppressed the expressions of cyclin E2, cyclin D1, and CDK2, respectively. Consequently, this led to the hypophosphorylation of pRb protein in G1/S transition and thereby inactivated E2F/DP1 target gene transcriptions of A549 cells. In addition, we demonstrated that HDAC2 directly regulated p21WAF1/CIP1 expression in a p53‐independent manner. However, HDAC1 was not related to p21WAF1/CIP1 expression and tumorigenesis of lung cancer. Lastly, we observed that sustained‐suppression of HDAC2 in A549 lung cancer cells attenuated in vitro tumorigenic properties and in vivo tumor growth of the mouse xenograft model. Taken together, we suggest that the aberrant regulation of HDAC2 and its epigenetic regulation of gene transcription in apoptosis and cell cycle components play an important role in the development of lung cancer. J. Cell. Biochem. 113: 2167–2177, 2012. © 2012 Wiley Periodicals, Inc.
Core–shell potential‐derived point charges
Authors: Tan Jeffrey S. , Boerrigter Stephan X. M. , Scaringe Raymond P. , Morris Kenneth R. 
Published: February 2012

AbstractThe present work details the development of a core‐shell model for the purposes of obtaining potential‐derived point charges from the ab initio molecular electrostatic potential. In contrast to atomic point charge models, the core‐shell model decomposes all atoms into a core with static charge located at a fixed atomic position and a shell with variable charge and position. The optimization of shell charges and positions is discussed. The core‐shell model was found to significantly improve description of the ab initio electrostatic potential when compared to potential‐derived net atomic point charge models as well as distributed multipoles with contributions up to atomic quadrupole moments. The core‐shell model was found to produce similar results as the Weller‐Williams lone‐pair model and differences in the implementation of the models are discussed. © 2012 Wiley Periodicals, Inc. J Comput Chem, 2012
Mental Health Implications of Human Attachment to Companion Animals
Authors: Peacock Jasmin , Chur‐Hansen Anna , Winefield Helen 
Published: February 2012

ObjectivesBecause of the contradictory nature of findings and methodological weaknesses identified within current human‐companion animal bond research, there is a need to further explore the connection between human‐animal bonds and mental health.DesignThe purpose of this survey questionnaire study was to explore the relationship of attachment to companion animal and human psychological distress after controlling for demographic variables, and to investigate whether the relationship between social supports and psychological distress would be moderated by attachment to a companion animal.ResultsResults highlight the psychological vulnerability of individuals reporting a strong bond with their companion animal.ConclusionsThese findings are discussed in terms of their implications for mental health services designed to anticipate and address client‐related companion animal needs.
The Factor Structure and Concurrent Validity of the Korean Version of the Metacognitions Questionnaire 30 (K‐MCQ‐30)
Authors: Cho Yongrae , Jahng Seungmin , Chai Sukhi 
Published: February 2012

ObjectivesWe aimed to examine the factor structure of a Korean version of the Metacognitions Questionnaire 30 (K‐MCQ‐30) and to further evaluate its concurrent validity.MethodConfirmatory factor analyses were conducted on the data sets from two independent samples of Korean college students (n = 662; n = 664). Correlation and multiple regression analyses were conducted on the cross‐sectional data from another sample (n = 97).ResultsThe 5‐factor model of the K‐MCQ‐30 showed a good fit to the first sample after minor modification. The revised 5‐factor model was replicated with the second sample. Five factors of the K‐MCQ‐30 had positive correlations with measures of emotional disorder symptoms and predicted each of the symptoms in different ways.ConclusionsThese results provide general support for the 5‐factor structure of the K‐MCQ‐30 and its good concurrent validity in nonclinical samples.
Public Speaking in Social Phobia: A Pilot Study of Self‐Ratings and Observers' Ratings of Social Skills
Authors: Levitan Michelle Nigri , Falcone Eliane Mary , Placido Monique , Krieger Stephanie , Pinheiro Layse , Crippa Jose Alexandre , Bruno Leandro Marchetti , Pastore Daniele , Hallak Jaime , Nardi Antonio Egidio 
Published: February 2012

ObjectivesThe aim of this pilot study was to investigate whether patients with social anxiety disorder (SAD) differ from controls in the quality of skill‐related behaviors displayed during a speech and in overall behavioral adequacy as perceived by observers and by the patients themselves.DesignA total of 18 SAD patients and 18 controls were screened by a diagnostic interview and took part in a 3‐minute speech of their own choosing. For each videotaped speech, observers rated the adequacy of the skill‐related behaviors and overall performance adequacy. After the experiment, participants were asked to rate their own overall performance adequacy.ResultsThe results showed that SAD patients exhibited significantly worse voice intonation and fluency of the speech, however no differences were found in global self‐ratings. Moreover, the performance evaluations of the SAD group were consistent with the observers, while the controls evaluated their performance lower than the observers.ConclusionsThe results are inconsistent with the cognitive model, because patients with SAD did not underestimate their performance. Compared with spontaneous interactions, the clear rules established for such social situations as speeches may result in less cognitive distortion for SAD patients.
A Comparison of Three Theoretically Important Constructs: What Accounts For Symptoms of Borderline Personality Disorder?
Authors: Cheavens Jennifer S. , Strunk Daniel R. , Chriki Lyvia 
Published: February 2012

ObjectiveTheories point to different mechanisms through which borderline personality disorder (BPD) symptoms may be developed and maintained: (a) emotion regulation dysfunction, (b) problematic relations, and (c) nonintegrated self. However, researchers have not investigated the relative contribution of these mechanisms simultaneously in accounting for the variance observed in BPD symptoms.MethodDrawing from university students and Internet users, 462 adults (63% female, 77% Caucasian) completed self‐report measures of emotion regulation, interpersonal problems, sense of self, BPD symptoms, and depressive symptoms.ResultsAll predictors were independently associated with BPD symptoms, with emotion regulation difficulties having the strongest relation. For high BPD individuals (N = 94), emotional regulation difficulties was the only predictor uniquely associated with BPD symptoms and interpersonal problems was the sole unique predictor of depressive symptoms.ConclusionThese results suggest that emotion regulation difficulties and interpersonal problems may be particularly problematic for those with high BPD symptoms in different ways. Implications and future directions are discussed.
Estimating WAIS‐IV Indexes: Proration Versus Linear Scaling in a Clinical Sample
Authors: Umfleet Laura Glass , Ryan Joseph J. , Gontkovsky Sam T. , Morris Jeri 
Published: February 2012

ObjectivesWe compared the accuracy of proration and linear scaling for estimating Wechsler Adult Intelligence Scale–Fourth Edition (WAIS‐IV), Verbal Comprehension Index (VCI), and Perceptual Reasoning Index (PRI) composites from all possible two subtest combinations. The purpose was to provide practice relevant psychometric results in a clinical sample.DesignThe present investigation was an archival study that used mostly within‐group comparisons. We analyzed WAIS‐IV data of a clinical sample comprising 104 patients with brain damage and 37 with no known neurological impairment.ResultsIn both clinical samples, actual VCI and PRI scores were highly correlated with estimated index scores based on proration and linear scaling (all rs ≥.95). In the brain‐impaired sample, significant mean score differences between the actual and estimated composites were found in two comparisons, but these differences were less than three points; no other significant differences emerged.ConclusionsOverall, findings demonstrate that proration and linear scaling methods are feasible procedures when estimating actual Indexes. There was no advantage of one computational method over the other.
Myeloid Elf‐1‐like factor stimulates adipogenic differentiation through the induction of peroxisome proliferator‐activated receptor γ expression in bone marrow
Authors: Baek Kyunghwa , Cho Je‐Yoel , Hwang Hyo Rin , Kwon Arang , Lee Hye‐Lim , Park Hyun‐Jung , Qadir Abdul S. , Ryoo Hyun‐Mo , Woo Kyung Mi , Baek Jeong‐Hwa 
Published: February 2012

AbstractMyeloid Elf‐1 like factor (MEF) is one of the Ets transcription factors known to regulate cell proliferation and differentiation. A previous report has shown that osteoblast‐specific MEF transgenic mice (Col1a1‐MEF TG mice) have low bone mass but high bone marrow adiposity. In the present study, we explored a previously unappreciated mechanism whereby MEF promotes adipogenesis in bone marrow. An adipogenic colony‐forming unit assay showed that bone marrow cells derived from Col1a1‐MEF TG mice had a higher adipogenic differentiation potential compared to those from wild‐type. The levels of adipogenic marker genes expression in 3T3L1 cells were higher when co‐cultured with Col1a1‐MEF TG bone marrow cells than with wild‐type cells. MC3T3‐E1 preosteoblasts transfected with MEF secreted higher levels of 15‐deoxy‐delta (12, 14)‐prostaglandin J2, a potent endogenous ligand of peroxisome proliferator‐activated receptor γ (PPARγ), under adipogenic conditions. MEF overexpression increased the adipogenic marker genes expression including PPARγ and lipid droplet accumulation in MC3T3‐E1 preosteoblasts and 3T3L1 preadipocytes. Endogenous MEF expression levels increased as adipocyte differentiation proceeded. Knockdown of MEF by siRNA suppressed expression levels of adipogenic marker genes including PPARγ. MEF directly bound to the MEF binding element on the mouse PPARγ promoter, transactivating promoter activity. Immunohistochemical staining of tibia sections demonstrated that bone lining cells and bone marrow cells express higher levels of PPARγ protein in Col1a1‐MEF TG mice than in wild‐type mice. These results suggest that MEF transactivates PPARγ expression, which, in turn, enhances adipogenic differentiation. Furthermore, MEF overexpressing osteoblasts secrete higher levels of adipogenic factors, creating a marrow microenvironment that favors adipogenesis. J. Cell. Physiol. 227: 3603–3612, 2012. © 2012 Wiley Periodicals, Inc.
Ischemic tolerance in the brain: Endogenous adaptive machinery against ischemic stress
Authors: Kitagawa Kazuo 
Published: February 2012

AbstractAlthough more than 100 drugs have been examined clinically, tissue plasminogen activator remains the only drug approved for the treatment of acute ischemic stroke. Since the discovery of ischemic tolerance, it has been widely recognized that the brain possesses an endogenous protective machinery to protect against ischemic stress. Recent studies have clarified that both the upregulation of neuroprotective signaling and the downregulation of inflammatory or apoptotic pathways are involved equally in the acquisition of ischemic tolerance. The triggering stimuli for ischemic stresses are divided into hypoxic, oxidant/inflammatory, and glutamate stress. Glutamate stress, particularly the synaptic stimulation of the N‐methyl‐D‐aspartate receptor, leads to activation of the cAMP response element‐binding protein, which could subsequently induce gene expression of several neuroprotective molecules. Gene reprogramming and metabolic downregulation are intimately involved in ischemic tolerance as well as in hibernation and hypothermia. Micro‐RNAs may be a key player for tuning the level of gene expression in ischemic tolerance. Future research should be performed to investigate the most effective combination for brain protection, enhancement of cell survival signaling, and inhibition of the inflammatory or apoptotic pathways. © 2012 Wiley Periodicals, Inc.