bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multigroup Construct Validity Evidence of the HOPE Scale: Instrumentation to Identify Low-Income Elementary Students for Gifted Programs
Authors: Peters Scott J. , Gentry Marcia 
Published: September 2010

Students with exceptional academic potential who come from low-income families are frequently not identified for and consequently are underrepresented in gifted and talented programs. Because of this, new means of identifying such children must be developed. This article presents the findings of exploratory and confirmatory factor analyses conducted on the HOPE Scale, a 13-item teacher-rating instrument designed to identify academic and social components of giftedness in elementary-aged students. Participants included 349 teachers who completed HOPE Scales on 5,995 ethnically and economically diverse students from three rural and two metropolitan school districts in the Midwest. Multigroup confirmatory factor analysis was also used to evaluate measurement invariance between income groups. Findings suggest a two-factor model represents good fit for the data while remaining loyal to the latent constructs of academic and social giftedness. Although showing some legitimate mean differences, invariance test results suggested equivalence of model form, factor loading, and factor variances across income groups. Putting the Research to Use This research has important implications for practice. Frequently, traditional measures of achievement or aptitude under-identify children from low-income families. Concerns exist about the usefulness of teacher-ratings forms or scales in gifted and talented student identification. However, when given specific items or descriptors, teachers can provide useful information concerning student performance. The HOPE Scale provides items that teachers can use to rate specific social and academic behaviors of their students. Findings from this study revealed that teaches can effectively nominate low-income students for gifted programs. Further, items on the HOPE Scale were not biased against low-income students as rated by their teachers, meaning that the social and academic scales provided similar information concerning students in either income group. However, mean scores for student from low-income families on both scales were lower than their non-low income peers, providing evidence that instruments need to be normed on the specific groups for which their use is intended. Practitioners, should not shy away from using teacher nomination instruments, but they should consider the psychometric information available concerning the use of these instruments or rating forms as used with students in demographic groups of intended use. The HOPE Scale, as developed with indicated revisions, will provide educators and researchers with a simple, psychometrically sound instrument to help with identification of underrepresented student for gifted education services.
Anti-amnesic and neuroprotective potentials of the mixed muscarinic receptor/sigma1(σ1) ligand ANAVEX2-73, a novel aminotetrahydrofuran derivative
Authors: Villard Vanessa , Espallergues Julie , Keller Emeline , Vamvakides Alexandre , Maurice Tangui 
Published: September 2010

Tetrahydro-N, N-dimethyl-2, 2-diphenyl-3-furanmethanamine hydrochloride (ANAVEX2-73) binds to muscarinic acetylcholine and sigma1(σ1) receptors with affinities in the low micromolar range. We characterized its anti-amnesic and neuroprotective potentials in pharmacological and pathological amnesia models. Spatial working memory was evaluated using spontaneous alternation in the Y-maze and non-spatial memory using passive avoidance procedures. ANAVEX2-73 (0.01–3.0 mg/kg i.p.) alleviated the scopolamine- and dizocilpine-induced learning impairments. ANAVEX2-73 (300 µg/kg) also reversed the learning deficits in mice injected with Aβ25-35peptide, a non-transgenic Alzheimer’s disease model. When the drug was injected simultaneously with Aβ25-35, 7 days before the tests, it blocked the appearance of learning impairments. This protective activity was confirmed since ANAVEX2-73 blocked the Aβ25-35-induced oxidative stress in the hippocampus. This effect was differentially sensitive to the muscarinic receptor antagonist scopolamine or the σ1protein antagonist BD1047, confirming the mixed muscarinic/σ1pharmacological action. Finally, its unique demethyl metabolite, ANAVEX19-144, was also effective and ANAVEX2-73 presented a longer duration of action, effective 12 h before Aβ25-35, than its related compound ANAVEX1-41. The neuroprotective activity of ANAVEX2-73, its mixed cholinergic/σ1activity, its low active dose range and its long duration of action together reinforce its therapeutic potential in Alzheimer’s disease.
In Vivo Visualization of Vascular Patterns of Rotator Cuff Tears Using Contrast-Enhanced Ultrasound
Authors: Funakoshi Tadanao , Iwasaki Norimasa , Kamishima Tamotsu , Nishida Mutsumi , Ito Yoichi , Kondo Makoto , Minami Akio 
Published: September 2010

Background Hypoxia and decreased blood supply have been proposed as risks for tendon rupture. Visualization of the vascularity of intact and torn rotator cuffs would be useful for improving treatments for rotator cuff tear. Purpose To assess vascularity inside a tendon or an adjacent rotator cuff insertion point in patients differing in age and extent of damage to the tendon. Study Design Cross-sectional study; Level of evidence, 3. Methods Ten volunteers (all men) and 15 patients (10 men, 5 women) consented to participate in the study. Contrast agent for enhanced ultrasound was injected intravenously. Enhanced ultrasound images of the torn cuff and the contralateral shoulder were recorded for 1 minute. Four small regions of interest, the articular and bursal sides of the tendon and the medial and lateral sides of the bursa, were studied in all shoulders. Results There was a significant decrease in blood flow in the intratendinous region in elderly subjects compared with young subjects, but age had no effect on blood flow in bursal tissue. Blood flow in ruptured rotator cuffs did not differ from that in intact rotator cuffs. The intraclass correlation coefficient for intraobserver reproducibility was 0.82 (95% confidence interval: 0.77-0.86). Conclusions The findings of this investigation were the hypovascular pattern in intratendinous tissue compared with the subacromial bursa, the age-related decrease in intratendinous vascularity, and the hypovascular pattern in the tendon, regardless of rupture of the tendon. Clarification of vascular patterns inside or around the torn ends of a rotator cuff will assist in the development of successful treatments for torn rotator cuffs.
Autologous Chondrocyte Implantation for Treatment of Focal Cartilage Defects in Patients Age 40 Years and Older
Authors: Niemeyer Philipp , Köstler Wolfgang , Salzmann Gian M. , Lenz Philipp , Kreuz Peter C. , Südkamp Norbert P. 
Published: September 2010

Background Autologous chondrocyte implantation (ACI) is an accepted surgical treatment in patients with isolated cartilage defects of the knee. Age has been considered as a limiting factor and the technique has not been recommended in patients older than 40 to 50 years. Nevertheless, some more recent studies report satisfying clinical results in middle-aged patients. Hypothesis Analogous to the microfracture technique, age over 40 years is associated with inferior clinical outcome after ACI. Study Design Cohort study; Level of evidence, 2. Methods Thirty-seven patients with an average age of 47.8 years (group 1) were matched with 37 patients with an average age of 31 years (group 2). Both groups underwent ACI for treatment of isolated cartilage defects of the knee. All patients were enrolled prospectively and followed for a period of 24 months using International Knee Documentation Committee (IKDC), Lysholm scale, Cincinnati sports scale, and Tegner activity evaluation instruments. Results Statistical analysis revealed a significant increase in function after ACI in both groups as early as 6 months after surgery until the end of the study period. There was only a slight tendency for better clinical outcome in younger patients (IKDC at 24 months: group 1, 72.2 ± 15.8 [standard deviation]; group 2: 76.1 ± 14.1; P = .261; Lysholm at 24 months: group 1: 80.42 ± 15.37; group 2: 80.65 ± 12.01), no statistical significant differences were found between patients of group 1 and group 2 at any of the time points investigated. Conclusion In contrast to other cartilage repair techniques, patients 40 years and older do not have an inferior outcome up to 24 months after ACI for isolated cartilage defects when compared with younger patients.
Role of complement and Fcγ receptors in the protective activity of the long pentraxin PTX3 against Aspergillus fumigatus
Authors: Moalli Federica , Doni Andrea , Deban Livija , Zelante Teresa , Zagarella Silvia , Bottazzi Barbara , Romani Luigina , Mantovani Alberto , Garlanda Cecilia 
Published: September 2010

AbstractPentraxin 3 (PTX3) is a soluble pattern recognition molecule playing a nonredundant role in resistance against Aspergillus fumigatus. The present study was designed to investigate the molecular pathways involved in the opsonic activity of PTX3. The PTX3 N-terminal domain was responsible for conidia recognition, but the full-length molecule was necessary for opsonic activity. The PTX3-dependent pathway of enhanced neutrophil phagocytic activity involved complement activation via the alternative pathway; Fcγ receptor (FcγR) IIA/CD32 recognition of PTX3-sensitized conidia and complement receptor 3 (CR3) activation; and CR3 and CD32 localization to the phagocytic cup. Gene targeted mice (ptx3, FcR common γ chain, C3, C1q) validated the in vivo relevance of the pathway. In particular, the protective activity of exogenous PTX3 against A fumigatus was abolished in FcR common γ chain-deficient mice. Thus, the opsonic and antifungal activity of PTX3 is at the crossroad between complement, complement receptor 3-, and FcγR-mediated recognition. Because short pentraxins (eg, C-reactive protein) interact with complement and FcγR, the present results may have general significance for the mode of action of these components of the humoral arm of innate immunity.
Steady-state generation of mucosal IgA+ plasmablasts is not abrogated by B-cell depletion therapy with rituximab
Authors: Mei Henrik E. , Frölich Daniela , Giesecke Claudia , Loddenkemper Christoph , Reiter Karin , Schmidt Stefanie , Feist Eugen , Daridon Capucine , Tony Hans-Peter , Radbruch Andreas , Dörner Thomas 
Published: September 2010

AbstractThe anti-CD20 antibody rituximab depletes human B cells from peripheral blood, but it remains controversial to what extent tissue-resident B cells are affected. In representative patients with rheumatoid arthritis, we here demonstrate that recently activated presumably short-lived plasmablasts expressing HLA-DRhigh and Ki-67 continuously circulate in peripheral blood after B-cell depletion by rituximab at 26%-119% of their initial numbers. They circulate independent of splenectomy, express immunoglobulin A (IgA), β7 integrin, and C-C motif receptor 10 (CCR10) and migrate along CCL28 gradients in vitro, suggesting their mucosal origin. These plasmablasts express somatically hypermutated VH gene rearrangements and spontaneously secrete IgA, exhibiting binding to microbial antigens. Notably, IgA+ plasmablasts and plasma cells were identified in the lamina propria of patients treated with rituximab during peripheral B-cell depletion. Although a relation of these “steady state”–like plasmablasts with rheumatoid arthritis activity could not be found, their persistence during B-cell depletion indicates that their precursors, that is, B cells resident in the mucosa are not deleted by this treatment. These data suggest that a population of mucosal B cells is self-sufficient in adult humans and not replenished by CD20+ B cells immigrating from blood, lymphoid tissue, or bone marrow, that is, B cells depleted by rituximab.
Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL
Authors: Jeannet Robin , Mastio Jérôme , Macias-Garcia Alejandra , Oravecz Attila , Ashworth Todd , Geimer Le Lay Anne-Solen , Jost Bernard , Le Gras Stéphanie , Ghysdael Jacques , Gridley Thomas , Honjo Tasuku , Radtke Freddy , Aster Jon C. , Chan Susan , Kastner Philippe 
Published: September 2010

Abstract
The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs). Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo. We investigated the role of Notch1 and Notch3 in T-ALL progression by a genetic approach, in mice bearing a knockdown mutation in the Ikaros gene that spontaneously develop Notch-dependent T-ALL. While deletion of Notch3 has little effect, T cell–specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis. Notch1-deleted tumors lack surface Notch1 but express γ-secretase–cleaved intracellular Notch1 proteins. In addition, these tumors accumulate high levels of truncated Notch1 transcripts that are caused by aberrant transcription from cryptic initiation sites in the 3′ part of the gene. Deletion of the floxed sequences directly reprograms the Notch1 locus to begin transcription from these 3′ promoters and is accompanied by an epigenetic reorganization of the Notch1 locus that is consistent with transcriptional activation. Further, spontaneous deletion of 5′ Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs. These results reveal a novel mechanism for the oncogenic activation of the Notch1 gene after deletion of its main promoter.
Multivariate Hawkes process models of the occurrence of regulatory elements
Authors: Carstensen Lisbeth , Sandelin Albin , Winther Ole , Hansen Niels R 
Published: September 2010

Abstract

Background
A central question in molecular biology is how transcriptional regulatory elements (TREs) act in combination. Recent high-throughput data provide us with the location of multiple regulatory regions for multiple regulators, and thus with the possibility of analyzing the multivariate distribution of the occurrences of these TREs along the genome.

Results
We present a model of TRE occurrences known as the Hawkes process. We illustrate the use of this model by analyzing two different publically available data sets. We are able to model, in detail, how the occurrence of one TRE is affected by the occurrences of others, and we can test a range of natural hypotheses about the dependencies among the TRE occurrences. In contrast to earlier efforts, pre-processing steps such as clustering or binning are not needed, and we thus retain information about the dependencies among the TREs that is otherwise lost. For each of the two data sets we provide two results: first, a qualitative description of the dependencies among the occurrences of the TREs, and second, quantitative results on the favored or avoided distances between the different TREs.

Conclusions
The Hawkes process is a novel way of modeling the joint occurrences of multiple TREs along the genome that is capable of providing new insights into dependencies among elements involved in transcriptional regulation. The method is available as an R package from http://www.math.ku.dk/~richard/ppstat/.
Identification of response-modulated genetic interactions by sensitivity-based epistatic analysis
Authors: Batenchuk Cory , Tepliakova Lioudmila , Kærn Mads 
Published: September 2010

AbstractBackgroundHigh-throughput genomics has enabled the global mapping of genetic interactions based on the phenotypic impact of combinatorial genetic perturbations. An important next step is to understand how these networks are dynamically remodelled in response to environmental stimuli. Here, we report on the development and testing of a method to identify such interactions. The method was developed from first principles by treating the impact on cellular growth of environmental perturbations equivalently to that of gene deletions. This allowed us to establish a novel neutrality function marking the absence of epistasis in terms of sensitivity phenotypes rather than fitness. We tested the method by identifying fitness- and sensitivity-based interactions involved in the response to drug-induced DNA-damage of budding yeastSaccharomyces cerevisiaeusing two mutant libraries - one containing transcription factor deletions, and the other containing deletions of DNA repair genes.ResultsWithin the library of transcription factor deletion mutants, we observe significant differences in the sets of genetic interactions identified by the fitness- and sensitivity-based approaches. Notably, among the most likely interactions, only ~50% were identified by both methods. While interactions identified solely by the sensitivity-based approach are modulated in response to drug-induced DNA damage, those identified solely by the fitness-based method remained invariant to the treatment. Comparison of the identified interactions to transcriptional profiles and protein-DNA interaction data indicate that the sensitivity-based method improves the identification of interactions involved in the DNA damage response. Additionally, for the library containing DNA repair mutants, we observe that the sensitivity-based method improves the grouping of functionally related genes, as well as the identification of protein complexes, involved in DNA repair.ConclusionOur results show that the identification of response-modulated genetic interactions can be improved by incorporating the effect of a changing environment directly into the neutrality function marking the absence of epistasis. We expect that this extension of conventional epistatic analysis will facilitate the development of dynamic models of gene networks from quantitative measurements of genetic interactions. While the method was developed for growth phenotype, it should apply equally well for other phenotypes, including the expression of fluorescent reporters.
Indications and recommended approach for surgical intervention of metastatic disease to the gallbladder
Authors: Khan Zarrish S , Huth James , Kapur Payal , Huerta Sergio 
Published: September 2010

AbstractMetastatic disease to the gallbladder is unusual. The most common malignancy metastatic to the gallbladder is melanoma, followed by renal cell carcinoma (RCC) and breast cancer. Due to the unusual nature of the disease, there are no trials available for review. Thus, the management for these patients has been based on institutional experience and review of case series. The indications for surgical intervention for melanoma are metastatic disease discrete to the gallbladder and biliary symptoms, which are uncommon for melanoma, but might occur due to cystic duct obstruction culminating in cholecystitis. Laparoscopic cholecystectomy without a lymphadenectomy is emerging as the preferred approach for this metastatic deposit. The vast majority of patients with metastases to the gallbladder from RCC carry a good prognosis and a laparoscopic cholecystectomy should be considered. Patients with metastases to the gallbladder from the breast classically present with biliary symptoms and commonly undergo a laparoscopic cholecystectomy, which invariably demonstrates a deposit in the gallbladder from lobular breast cancer. In the present report, we review the indications for surgical intervention from various malignancies metastatic to the gallbladder and the current consensus for the laparoscopic approach from the diverse metastatic deposits to the gallbladder.
The ketogenic diet reverses gene expression patterns and reduces reactive oxygen species levels when used as an adjuvant therapy for glioma
Authors: Stafford Phillip , Abdelwahab Mohammed G , Kim Do Young , Preul Mark C , Rho Jong M , Scheck Adrienne C 
Published: September 2010

Abstract

Background
Malignant brain tumors affect people of all ages and are the second leading cause of cancer deaths in children. While current treatments are effective and improve survival, there remains a substantial need for more efficacious therapeutic modalities. The ketogenic diet (KD) - a high-fat, low-carbohydrate treatment for medically refractory epilepsy - has been suggested as an alternative strategy to inhibit tumor growth by altering intrinsic metabolism, especially by inducing glycopenia.

Methods
Here, we examined the effects of an experimental KD on a mouse model of glioma, and compared patterns of gene expression in tumors vs. normal brain from animals fed either a KD or a standard diet.

Results
Animals received intracranial injections of bioluminescent GL261-luc cells and tumor growth was followed in vivo. KD treatment significantly reduced the rate of tumor growth and prolonged survival. Further, the KD reduced reactive oxygen species (ROS) production in tumor cells. Gene expression profiling demonstrated that the KD induces an overall reversion to expression patterns seen in non-tumor specimens. Notably, genes involved in modulating ROS levels and oxidative stress were altered, including those encoding cyclooxygenase 2, glutathione peroxidases 3 and 7, and periredoxin 4.

Conclusions
Our data demonstrate that the KD improves survivability in our mouse model of glioma, and suggests that the mechanisms accounting for this protective effect likely involve complex alterations in cellular metabolism beyond simply a reduction in glucose.
Paroxysmal autonomic instability with dystonia in a patient with tuberculous meningitis: a case report
Authors: Ramdhani Navin A , Sikma Maaike A , Witkamp Theo D , Slooter Arjen JC , de Lange Dylan W 
Published: September 2010

Abstract

Introduction
This case report describes an extremely rare combination of paroxysmal autonomic instability with dystonia and tuberculous meningitis. Paroxysmal autonomic instability with dystonia is normally associated with severe traumatic brain injury.

Case presentation
A 69-year-old man of Indonesian descent was initially suspected of having a community-acquired pneumonia, which was seen on chest X-ray and computed tomography of the chest. However, a bronchoscopy showed no abnormalities. He was treated with amoxicillin-clavulanic acid in combination with ciprofloxacin. However, nine days after admission he was disorientated and complained of headache. Neurological examination revealed no further abnormalities. A lumbar puncture revealed no evidence of meningitis. He was then transferred to our hospital. At that time, initial cultures of bronchial fluid for Mycobacterium tuberculosis turned positive, as well as polymerase chain reaction for Mycobacterium tuberculosis. Later, during his stay in our intensive care unit, he developed periods with hypertension, sinus tachycardia, excessive transpiration, decreased oxygen saturation with tachypnea, pink foamy sputum, and high fever. This constellation of symptoms was accompanied by dystonia in the first days. These episodes lasted approximately 30 minutes and improved after administration of morphine, benzodiazepines or clonidine. Magnetic resonance imaging showed an abnormal signal in the region of the hippocampus, thalamus and the anterior parts of the lentiform nucleus and caudate nucleus.

Conclusions
In patients with (tuberculous) meningitis and episodes of extreme hypertension and fever, paroxysmal autonomic instability with dystonia should be considered.