bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intermittency and erraticity of charged particles produced in 28Si-Ag/Br interaction at 14.5 A GeV
Authors: Mali Provash , Mukhopadhyay Amitabha , Singh Gurmukh 
Published: September 2011

In this paper, we present the intermittency and the erraticity analyses of the distributions of charged particles produced in 28Si-Ag/Br interaction at incident energy 14.5 A GeV. The experimental results are compared with a Monte Carlo simulation using ultra-relativistic quantum molecular dynamics (UrQMD) model. The experimental data show the presence of a nonstatistical component in the produced charged-particle density. Neither the UrQMD simulation nor the purely statistical simulation was found to match the experimental data. The present set of results are compared to those obtained in similar measurements from earlier high-energy nucleus–nucleus experiments.
Self-compressed inhomogeneous stabilized jellium model and surface relaxation of simple metal thin films
Authors: Payami M. , Mahmoodi T. 
Published: September 2011

The interlayer spacing near the surface of a crystal is different from that of the bulk. As a result, the value of the ionic density in the normal direction and near to the surface shows some variation from the bulk value, which is oscillatory in shape. To describe this behavior simply, we have formulated the self-compressed inhomogeneous stabilized jellium model and have applied it to simple metal thin films. In this model, for a ν-layered slab, each ionic layer is replaced by a jellium slice of constant density. The equilibrium densities of the slices are determined by minimizing the total energy per electron of the slab with respect to the slice densities. However, to avoid the complications that arise because of the increasing number of independent slice-density parameters for large-ν slabs, we consider a simplified version of the model that consists of only three jellium slices: one inner bulk slice with density [Formula: see text] and two similar surface slices, each of density [Formula: see text]. In this simplified model, each slice may contain more than one ionic layer. Application of this model to ν-layered slabs (3 ≤ ν ≤ 10) of Al, Na, and Cs shows that, in the equilibrium state, [Formula: see text] differs from [Formula: see text]. The difference is significant in the Al case, and the slab is more stable than that predicted by the homogeneous model with only one density parameter for the whole jellium background. In addition, we have calculated the overall relaxations, the work functions, and the surface energies and compared them with the results of earlier works.
Thujone inhibits lung metastasis induced by B16F-10 melanoma cells in C57BL/6 mice
Authors: Siveen Kodappully S. , Kuttan Girija 
Published: September 2011

The antimetastatic potential of thujone, a naturally occurring monoterpene, was evaluated. Metastasis was induced in C57BL/6 mice by injecting highly metastatic B16F-10 melanoma cells through the lateral tail vein. Administration of thujone (1 mg·(kg body weight)–1), prophylactically and simultaneously with tumor induction, inhibited tumor nodule formation in the lungs by 59.45% and 57.54%, respectively, with an increase in the survival rate (33.67% and 32.16%) of the metastatic tumor bearing animals. These results correlated with biochemical parameters such as lung collagen hydroxyproline, hexosamine and uronic acid contents, serum sialic acid and γ-glutamyl transpeptidase levels, and histopathological analysis. Treatment with thujone downregulated the production of proinflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and granulocyte–monocyte colony-stimulating factor. Thujone administration downregulated the expression of matrix metalloproteinase (MMP)-2, MMP-9, extracellular signal-regulated kinase (ERK)-1, ERK-2, and vascular endothelial growth factor (VEGF) and also upregulated the expression of nm-23, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 in the lung tissue of metastasis-induced animals. Treatment with thujone inhibited the activity of MMP-2 and MMP-9 in gelatin zymographic analysis. Thujone treatment significantly inhibited the invasion of B16F-10 melanoma cells across the collagen matrix in a Boyden chamber. Thujone also inhibited the adhesion of tumor cells to collagen-coated microtire plate wells and the migration of B16F-10 melanoma cells across a polycarbonate filter in vitro. These results indicate that Thujone can inhibit the lung metastasis of B16F-10 cells through inhibition of tumor cell proliferation, adhesion, and invasion, as well as by regulating expression of MMPs, VEGF, ERK-1, ERK-2, TIMPs, nm23, and levels of proinflammatory cytokines and IL-2 in metastatic animals.
From idea to product
Authors: Reed Daniel , Guzdial Mark 
Published: September 2011

The
Communications
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Daniel Reed discusses how researchers communicate their project ideas to companies and product groups and get them successfully adopted. Mark Guzdial considers whether schools of education could create more high school CS teachers.
Gene Regulation by Cohesin in Cancer: Is the Ring an Unexpected Party to Proliferation?
Authors: Rhodes Jenny M. , McEwan Miranda , Horsfield Julia A. 
Published: September 2011

Abstract
Cohesin is a multisubunit protein complex that plays an integral role in sister chromatid cohesion, DNA repair, and meiosis. Of significance, both over- and underexpression of cohesin are associated with cancer. It is generally believed that cohesin dysregulation contributes to cancer by leading to aneuploidy or chromosome instability. For cancers with loss of cohesin function, this idea seems plausible. However, overexpression of cohesin in cancer appears to be more significant for prognosis than its loss. Increased levels of cohesin subunits correlate with poor prognosis and resistance to drug, hormone, and radiation therapies. However, if there is sufficient cohesin for sister chromatid cohesion, overexpression of cohesin subunits should not obligatorily lead to aneuploidy. This raises the possibility that excess cohesin promotes cancer by alternative mechanisms. Over the last decade, it has emerged that cohesin regulates gene transcription. Recent studies have shown that gene regulation by cohesin contributes to stem cell pluripotency and cell differentiation. Of importance, cohesin positively regulates the transcription of genes known to be dysregulated in cancer, such as Runx1, Runx3, and Myc. Furthermore, cohesin binds with estrogen receptor α throughout the genome in breast cancer cells, suggesting that it may be involved in the transcription of estrogen-responsive genes. Here, we will review evidence supporting the idea that the gene regulation function of cohesin represents a previously unrecognized mechanism for the development of cancer. Mol Cancer Res; 9(12); 1587–607. ©2011 AACR.
Serum Response Factor Regulates Expression of Phosphatase and Tensin Homolog Through a MicroRNA Network in Vascular Smooth Muscle Cells
Authors: Horita Henrick N. , Simpson Peter A. , Ostriker Allison , Furgeson Seth , Van Putten Vicki , Weiser-Evans Mary C.M. , Nemenoff Raphael A. 
Published: September 2011

Objective—
Serum response factor (SRF) is a critical transcription factor in smooth muscle cells (SMCs) controlling differentiation and proliferation. Our previous work demonstrated that depleting SRF in cultured SMCs decreased expression of SMC markers but increased proliferation and inflammatory mediators. A similar phenotype has been observed in SMCs silenced for phosphatase and tensin homolog (PTEN), suggesting that SRF and PTEN may lie on a common pathway. Our goal was to determine the effect of SRF depletion on PTEN levels and define mechanisms mediating this effect.

Methods and Results—
In SRF-silenced SMCs, PTEN protein levels but not mRNA levels were decreased, suggesting posttranscriptional regulation. Reintroduction of PTEN into SRF-depleted SMCs reversed increases in proliferation and cytokine/chemokine production but had no effect on SMC marker expression. SRF-depleted cells showed decreased levels of microRNA (miR)-143 and increased miR-21, which was sufficient to suppress PTEN. Increased miR-21 expression was dependent on induction of Fos related antigen (FRA)-1, which is a direct target of miR-143. Introducing miR-143 into SRF-depleted SMCs reduced FRA-1 expression and miR-21 levels and restored PTEN expression.

Conclusion—
SRF regulates PTEN expression in SMCs through a miR network involving miR-143, targeting FRA-1, which regulates miR-21. Cross-talk between SRF and PTEN likely represents a critical axis in phenotypic remodeling of SMCs.
Positive Cross-Talk Between Hypoxia Inducible Factor-1α and Liver X Receptor α Induces Formation of Triglyceride-Loaded Foam Cells
Authors: Na Tae-Young , Lee Hyo-Jeong , Oh Hyeon-Jeong , Huh Seung , Lee In-Kyu , Lee Mi-Ock 
Published: September 2011

Objective—
Atherosclerosis is a chronic and progressive inflammatory disease of the arteries that is characterized by subendothelial accumulation of lipid-rich macrophages, called foam cells. We sought to identify the molecular details of cross-talk between liver X receptor α (LXRα) and hypoxia-inducible factor 1α (HIF-1α) for the formation of triglyceride-rich foam cells under hypoxic conditions.

Methods and Results—
We first observed that expression of LXRα and its target lipogenic genes was time-dependently induced in human primary macrophages and RAW 264.7 cells under hypoxia. Similarly, TO901317, an activator of LXRα, enhanced the expression level and the transcriptional activity of HIF-1α. Second, we demonstrated that LXRα increased HIF-1α protein stability through a physical interaction between the ligand binding domain of LXRα and the oxygen-dependent degradation domain of HIF-1α. Third, we found that the activation of HIF-1α or LXRα synergistically induced triglyceride accumulation in macrophages. Finally, we showed that LXRα and HIF-1α were codistributed in the macrophages of atherosclerotic lesions of patients.

Conclusion—
These results suggest that the positive feed-forward regulation of transcriptional activity and protein stability of LXRα and HIF-1α has an important impact in foam cell formation.
Novel In Vivo Method for Measuring Cholesterol Mass Flux in Peripheral Macrophages
Authors: Weibel Ginny L. , Hayes Sara , Wilson Aisha , Phillips Michael C. , Billheimer Jeffrey , Rader Daniel J. , Rothblat George H. 
Published: September 2011

Objective—
Reverse cholesterol transport is the process by which excess cholesterol is removed from peripheral tissue by HDL and delivered to the liver for excretion. Presently, methods of measuring in vivo reverse cholesterol transport do so by monitoring the appearance in the feces of labeled cholesterol that originated from peripheral macrophage foam cells. These methods do not account for changes in macrophage cholesterol mass. We have developed an in vivo assay to measure cholesterol mass changes in atherosclerotic foam cells.

Methods and Results—
Macrophages are entrapped in semipermeable (pore size 0.2 μm) hollow fibers and surgically implanted into the peritoneum of recipient mice. The fibers are removed from the peritoneum 24 hours after implantation. This method allows the complete recovery of the macrophages for quantification of changes in cholesterol mass and cellular protein. In wild-type mice we measured a significant reduction in total cell cholesterol (TC) when hollow fibers containing cholesterol-enriched macrophage cells were implanted (TC before implantation=105±18 μg/mg cell protein, TC 24 hours after implantation=60±16 μg/mg protein). Additionally, there was an increase in cholesterol content when hollow fibers containing cholesterol-normal macrophages were implanted in an atherogenic mouse model (LDLr/apobec dko) compared to a wild-type mouse (initial TC content=57±24 μg/mg protein, TC 24 hours after implantation: wild-type mice=52±10 μg/mg protein; LDLr/apobec dko mice=118±27 μg/mg protein).

Conclusion—
This assay can quantify in vivo both cholesterol mass accumulation, and reduction, in macrophages. This method permits quantitative analysis of the progression and regression of foam cells.
AMP-Activated Protein Kinase Suppresses Endothelial Cell Inflammation Through Phosphorylation of Transcriptional Coactivator p300
Authors: Zhang Yuan , Qiu Jian , Wang Xiaoming , Zhang Yuhua , Xia Min 
Published: September 2011

Objective—
Considerable evidence supports the early involvement of monocyte/macrophage recruitment to activated endothelial cells by leukocyte adhesion molecules during atherogenesis. AMP-activated protein kinase (AMPK) is highly expressed in vascular endothelial cells, but its impact on monocyte adhesion and the related mechanisms are not fully understood. The present study was designed to evaluate the impact of and gain mechanistic insight into the signaling coupling AMPK function to the antiinflammatory response.

Methods and Results—

5-Aminoimidazole-4-carboxamide-1-β-
d
-ribonucleotide (AICAR) treatment or overexpression of constitutively active AMPK markedly reduced human monocytic human acute monocytic leukemia cell line-1 cell adhesion and the expression of vascular cell adhesion molecule-1 in tumor necrosis factor-α–activated human aortic endothelial cells. Furthermore, AICAR or constitutively active AMPK overexpression strongly inhibited the histone acetyltransferase activity of the transcriptional coactivator p300 by phosphorylation of Ser89, which in turn decreased tumor necrosis factor-α-activated p300-mediated acetylation of nuclear factor-κB p65 on Lys221 and reduced the DNA binding activity of nuclear factor-κB by inhibiting its recruitment to its target gene promoters. AMPK phosphorylates the transcriptional coactivator p300 via the atypical protein kinase Cι/λ.

Conclusion—
Our findings demonstrate that transcriptional coactivator p300 phosphorylation at Ser89 by AMPK is critical for the therapeutic effect of AMPK and may be a potential target for pharmaceutical intervention in inflammatory diseases such as atherosclerosis.
Evaluating the Applicability of a Biodegradable Osteosynthesis Plating System in the Management of Zygomatico‐Maxillary Complex Fractures
Authors: Singh Virendra , Sharma Bindu , Bhagol Amrish 
Published: September 2011

ObjectiveThe present study was undertaken to evaluate and analyze the efficacy of bioresorbable plates and screws in internal fixation of zygomatico‐maxillary complex (ZMC) fractures and to evaluate the incidence of complications associated with the procedure.Study DesignCase series with planned data collection.SettingPt BD Sharma University of Health Sciences.Subject and MethodsA total of 14 patients with isolated ZMC fractures were included, and exclusion of grossly comminuted, pathological, and infected fractures was done. Open reduction internal fixation was done with biodegradable plates and screws. All patients were reviewed clinically and radiographically at regular follow‐up. Occlusion, stability of fracture segments, anesthesia or paresthesia of the infraorbital nerve region, and various complications were assessed periodically.ResultsFourteen patients with 34 fracture sites were included in the study. Intraoperatively, there were 2 incidences of screw head fracture. As observed clinically, there was complete stability of fracture segments, and no maxillomandibular fixation was required postoperatively. Paresthesia of the infraorbital nerve was present in 5 patients, but the sensation recovered completely in the first 3 months after surgery. The mean pain score was 3 on a visual analogue scale. In 1 case, ectropion developed, and dehiscence occurred in another patient in the early postoperative period. Postoperative radiographs were evaluated for the accuracy of fracture reduction and stability of fixation.ConclusionThe biodegradable osteosynthesis system exhibits adequate strength and has negligible complications. This system is technique sensitive with satisfactory results in the management of mild to moderately displaced ZMC fractures.
Tonsillectomy
Authors: Wilson Janet A. , Steen I. Nick , Lock Catherine A. , Eccles Martin P. , Carrie Sean , Clarke Ray , Kubba Haytham , Raine Chris H. , Zarod Andrew , Bond John 
Published: September 2011

ObjectiveTo compare the estimated cost‐effectiveness of childhood (adeno)tonsillectomy vs medical therapy for recurrent sore throats from the intention‐to‐treat (ITT) analysis of a randomized controlled trial (RCT) with that modeled on the recorded timing of surgical interventions as observed in all participants irrespective of their original group allocation.Study DesignA pragmatic RCT (trial) with a parallel nonrandomized patient preference group (cohort) of (adeno)tonsillectomy vs medical therapy.SettingFive secondary care UK otolaryngology departments.Subjects and MethodsEligible children, aged 4 to 15 years, were enrolled to the trial (268) or cohort (461) groups. Outcomes included sore throat diaries, quality of life, and general practice consultations. The RCT protocol ITT analysis was compared with an as‐treated analysis incorporating the cohort group, modeled to reflect the timing of tonsillectomy and the differential switch rates among the original groups.Results>In the RCT ITT analysis, tonsillectomy saved 3.5 sore throats, whereas the as‐treated model suggested an average reduction of more than 8 sore throats in 2 years for surgery within 10 weeks of consultation, falling to only 3.5 twelve months later due to the spontaneous improvement in the medical therapy group.ConclusionIn eligible UK school‐age children, tonsillectomy can save up to 8 sore throats at a reasonable cost, if performed promptly. Further prospective data collection, accounting for baseline and per‐trial preferences and choice, is urgently needed.
Donor-specific anti-HLA antibodies predict outcome in double umbilical cord blood transplantation
Authors: Cutler Corey , Kim Haesook T. , Sun Lixian , Sese Doreen , Glotzbecker Brett , Armand Philippe , Koreth John , Ho Vincent , Alyea Edwin , Ballen Karen , Ritz Jerome , Soiffer Robert J. , Milford Edgar , Antin Joseph H. 
Published: September 2011

Abstract
Using a uniform detection method for donor-specific anti-HLA antibodies (DSAs), we sought to determine the effect of preformed DSAs on outcomes in double umbilical cord blood transplantation. DSAs were associated with an increased incidence of graft failure (5.5% vs 18.2% vs 57.1% for none, single, or dual DSA positivity; P = .0001), prolongation of the time to neutrophil engraftment (21 vs 29 days for none vs any DSA; P = .04), and excess 100-day mortality or relapse (23.6% vs 36.4% vs 71.4% for none, single, or dual DSA positivity; P = .01). The intensity of DSA reactivity was correlated with graft failure (median of mean fluorescent intensity 17 650 vs 1 850; P = .039). There was inferior long-term progression-free and overall survival when comparing patients with DSAs against both umbilical cord blood units to those without DSAs (3-year progression-free survival, 0% vs 33.5%, P = .004; 3-year overall survival 0% vs 45.0%, P = .04). We conclude that identification of preformed DSAs in umbilical cord blood recipients should be performed and that the use of umbilical cord blood units where preformed host DSAs exist should be avoided.
The phylogenomic analysis of the anaphase promoting complex and its targets points to complex and modern-like control of the cell cycle in the last common ancestor of eukaryotes
Authors: Eme Laura , Trilles Aurélie , Moreira David , Brochier-Armanet Céline 
Published: September 2011

Abstract

Background
The Anaphase Promoting Complex or Cyclosome (APC/C) is the largest member of the ubiquitin ligase [E3] family. It plays a crucial role in the control of the cell cycle and cell proliferation by mediating the proteolysis of key components by the proteasome. APC/C is made of a dozen subunits that assemble into a large complex of ~1.5 MDa, which interacts with various cofactors and targets.

Results
Using comparative genomic and phylogenetic approaches, we showed that 24 out of 37 known APC/C subunits, adaptors/co-activators and main targets, were already present in the Last Eukaryotic Common Ancestor (LECA) and were well conserved to a few exceptions in all present-day eukaryotic lineages. The phylogenetic analysis of the 24 components inferred to be present in LECA showed that they contain a reliable phylogenetic signal to reconstruct the phylogeny of the domain Eucarya.

Conclusions
Taken together our analyses indicated that LECA had a complex and highly controlled modern-like cell cycle. Moreover, we showed that, despite what is generally assumed, proteins involved in housekeeping cellular functions may be a good complement to informational genes to study the phylogeny of eukaryotes.
A deletion of FGFR2 creating a chimeric IIIb/IIIc exon in a child with Apert syndrome
Authors: Fenwick Aimee L , Bowdin Sarah C , Klatt Regan EM , Wilkie Andrew OM 
Published: September 2011

AbstractBackgroundSignalling by fibroblast growth factor receptor type 2 (FGFR2) normally involves a tissue-specific alternative splice choice between two exons (IIIb and IIIc), which generates two receptor isoforms (FGFR2b and FGFR2c respectively) with differing repertoires of FGF-binding specificity. Here we describe a unique chimeric IIIb/c exon in a patient with Apert syndrome, generated by a non-allelic homologous recombination event.Case PresentationWe present a child with Apert syndrome in whom routine genetic testing had excluded theFGFR2missense mutations commonly associated with this disorder. The patient was found to harbour a heterozygous 1372 bp deletion betweenFGFR2exons IIIb and IIIc, apparently originating from recombination between 13 bp of identical DNA sequence present in both exons. The rearrangement was not present in the unaffected parents.ConclusionsBased on the known pathogenesis of Apert syndrome, the chimeric FGFR2 protein is predicted to act in a dominant gain-of-function manner. This is likely to result from its expression in mesenchymal tissues, where retention of most of the residues essential for FGFR2b binding activity would result in autocrine activation. This report adds to the repertoire of rare cases of Apert syndrome for which a pathogenesis based on atypicalFGFR2rearrangements can be demonstrated.