bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complete Genome Sequence of Leuconostoc kimchii Strain C2, Isolated from Kimchi
Authors: Lee Seung Hyeon , Jung Ji Young , Lee Se Hee , Jeon Che Ok 
Published: September 2011

ABSTRACT

Leuconostoc kimchii
strain C2 was isolated from fermented kimchi in Korea. Here we announce the complete genome sequence of
Leuconostoc kimchii
strain C2, consisting of a 1,877,174-bp chromosome with a G+C content of 37.9% and no plasmid and describe major findings from its annotation.
Whole-Genome Shotgun Sequencing of the Sulfur-Oxidizing Chemoautotroph Tetrathiobacter kashmirensis
Authors: Ghosh Wriddhiman , George Ashish , Agarwal Atima , Raj Praveen , Alam Masrure , Pyne Prosenjit , Das Gupta Sujoy Kumar 
Published: September 2011

ABSTRACT

The chemolithoautotrophic betaproteobacterium
Tetrathiobacter kashmirensis
belongs to the family
Alcaligenaceae
and is phylogenetically closely related to pathogens such as
Taylorella
and
Bordetella
species. While a complete inorganic sulfur oxidation gene cluster,
soxCDYZAXWB
, is present in its genome, pathogenicity islands or genes associated with virulence, disease, cellular invasion, and/or intracellular resistance are completely absent.
Application of impulse oscillometry for within-breath analysis in patients with chronic obstructive pulmonary disease: pilot study
Authors: Ohishi Junichi , Kurosawa Hajime , Ogawa Hiromasa , Irokawa Toshiya , Hida Wataru , Kohzuki Masahiro 
Published: September 2011

BackgroundThe impulse oscillometry is increasingly used for assessing the oscillatory mechanics of the respiratory system. The within-breath behaviour of the oscillatory mechanics in chronic obstructive pulmonary disease (COPD) is a well-known physiological feature. The purpose of this study was to develop a new approach for assessing this feature using impulse oscillometry.MethodsThe oscillatory mechanics were assessed by a commercially available impulse oscillometry device. The respiratory system resistance (Rrs) and reactance (Xrs) were measured during tidal breathing in patients with COPD (n=39) and healthy subjects (n=5). Selected data, the Rrs at 5 Hz (R5), Rrs at 20 Hz (R20), Xrs at 5 Hz (X5), and resonant frequency of Xrs (Fres) every 0.2 s, were extracted from the device. These data were divided into eight time fractions during the respiratory cycle to form averaged respiratory phases.ResultsThe time courses of the R5 and X5 were notably dependent on the respiratory cycles in patients with COPD, while there was little such dependency in healthy subjects. Irrespective of respiratory phase, R5 and Fres increased, and X5 fell to a more negative level in patients with COPD in a severity-dependent fashion. The increase in the R5 and negative level in the X5 were more prominent in the middle of the expiratory phase. The severity dependence in the R20 was relatively small compared with that in the R5.ConclusionsThe results of this study suggest that impulse oscillometry can assess the within-breath behaviour of the oscillatory mechanics with high temporal resolution, which may be helpful for evaluating the severity of COPD. Further studies are needed to reveal which biomarkers obtained with this approach would be suitable for evaluating the airway obstruction.
Estimating the prevalence of gonococcal resistance to antimicrobials in England and Wales
Authors: Hughes Gwenda , Nichols Tom , Ison Catherine A 
Published: September 2011

BackgroundGonorrhoea can rapidly develop resistance to antimicrobials and treatment options are becoming depleted. Treatment guidelines require robust estimates of the prevalence of resistance but sentinel surveillance systems may not be representative nationally.ObjectiveTo investigate the effectiveness of the sentinel Gonococcal Resistance to Antimicrobials Surveillance System (GRASP) at estimating resistance prevalence in England and Wales.MethodsAnnual cross-sectional data on reported gonorrhoea diagnoses between 2000 and 2008 were compared between GRASP (26 clinics) and national mandatory (KC60) reporting (229 clinics). Resistance prevalence estimates in GRASP were weighted according to the national distribution of relevant patient characteristics: age group, gender, sexual orientation and geographical region. Trends in actual and weighted estimates were plotted.ResultsGonorrhoea cases reported through GRASP were more likely to be from London and to be men who have sex with men (MSM) and were less likely to be women and heterosexual men than those reported through KC60. Weighting for national distributions of demographic characteristics reduced estimates of resistance prevalence, particularly ciprofloxacin in 2006 (27% to 21%). Emerging resistance to cefixime in 2008 was reduced from 1.5% to 1.0%. Weighting did not adjust resistance prevalence above or below the 5% threshold for any antimicrobial.ConclusionsAlthough over-representing MSM and under-representing women and heterosexual men, GRASP has provided reliable estimates of resistance prevalence in England and Wales. However, weighting for the national distribution of patient characteristics should be considered in future. As resistance usually emerges in MSM, enhanced surveillance of high-risk populations could enable development of more tailored (and therefore optimal) treatment strategies.
FOXO3a-Dependent Mechanism of E1A-Induced Chemosensitization
Authors: Su Jen-Liang , Cheng Xiaoyun , Yamaguchi Hirohito , Chang Yi-Wen , Hou Chao-Feng , Lee Dung-Fang , Ko How-Wen , Hua Kuo-Tai , Wang Ying-Nai , Hsiao Michael , Chen PoShen B. , Hsu Jung-Mao , Bast Robert C. , Hortobagyi Gabriel N. , Hung Mien-Chie 
Published: September 2011

Abstract
Gene therapy trials in human breast, ovarian, and head and neck tumors indicate that adenovirus E1A can sensitize cancer cells to the cytotoxic effects of paclitaxel in vitro and in vivo. Resistance to paclitaxel has been reported to occur in cells expressing low levels of the Forkhead transcription factor FOXO3a. In this article, we report that FOXO3a is critical for E1A-mediated chemosensitization to paclitaxel. RNA interference–mediated knockdown of FOXO3a abolished E1A-induced sensitivity to paclitaxel. Mechanistic investigations indicated that E1A indirectly stabilized FOXO3a by acting at an intermediate step to inhibit a ubiquitin-dependent proteolysis pathway involving the E3 ligase βTrCP and the FOXO3a inhibitory kinase IKKβ. E1A derepressed this inhibitory pathway by stimulating expression of the protein phosphatase 2A (PP2A)/C protein phosphatases, which by binding to the TGF-β–activated kinase TAK1, inhibited its ability to activate IKKβ and, thereby, to suppress βTrCP-mediated degradation of FOXO3a. Thus, by stimulating PP2A/C expression, E1A triggers a signaling cascade that stabilizes FOXO3a and mediates chemosensitization. Our findings provide a leap forward in understanding paclitaxel chemosensitization by E1A, and offer a mechanistic rational to apply E1A gene therapy as an adjuvant for improving therapeutic outcomes in patients receiving paclitaxel treatment. Cancer Res; 71(21); 6878–87. ©2011 AACR.
Acute Hypoglycemia Decreases Myocardial Blood Flow Reserve in Patients With Type 1 Diabetes Mellitus and in Healthy Humans
Authors: Rana Omar , Byrne Christopher D. , Kerr David , Coppini David V. , Zouwail Soha , Senior Roxy , Begley Joe , Walker Jeremy J. , Greaves Kim 
Published: September 2011

Background—
Hypoglycemia is associated with increased cardiovascular mortality, but the reason for this association is poorly understood. We tested the hypothesis that the myocardial blood flow reserve (MBFR) is decreased during hypoglycemia using myocardial contrast echocardiography in patients with type 1 diabetes mellitus (DM) and in healthy control subjects.

Methods and Results—

Twenty-eight volunteers with DM and 19 control subjects underwent hyperinsulinemic clamps with maintained sequential hyperinsulinemic euglycemia (plasma glucose, 90 mg/dL [5.0 mmol/L]) followed by hyperinsulinemic hypoglycemia (plasma glucose, 50 mg/dL [2.8 mmol/L]) for 60 minutes each. Low-power real-time myocardial contrast echocardiography was performed with flash impulse imaging using low-dose dipyridamole stress at baseline and during hyperinsulinemic euglycemia and hyperinsulinemic hypoglycemia. In control subjects, MBFR increased during hyperinsulinemic euglycemia by 0.57 U (22%) above baseline (B coefficient, 0.57; 95% confidence interval, 0.38 to 0.75;
P
<0.0001) and decreased during hyperinsulinemic hypoglycemia by 0.36 U (14%) below baseline values (B coefficient, −0.36; 95% confidence interval, −0.50 to −0.23;
P
<0.0001). Although MBFR was lower in patients with DM at baseline by 0.37 U (14%; B coefficient, −0.37; 95% confidence interval, −0.55 to −0.19;
P
=0.0002) compared with control subjects at baseline, the subsequent changes in MBFR during hyperinsulinemic euglycemia and hyperinsulinemic hypoglycemia in DM patients were similar to that observed in control subjects. Finally, the presence of microvascular complications in the patients with DM was associated with a reduction in MBFR of 0.52 U (24%; B coefficient, −0.52; 95% confidence interval, −0.70 to −0.34;
P
<0.0001).

Conclusions—
Hypoglycemia decreases MBFR in both healthy humans and patients with DM. This finding may explain the association between hypoglycemia and increased cardiovascular mortality in susceptible individuals.
Impacts of Lapse Rates on Low-Level Rotation in Idealized Storms
Authors: Parker Matthew D. 
Published: September 2011

Abstract
Adiabatic lapse rates appear to be a common feature in the lower troposphere on tornado days. This article reviews physical reasons why lapse rates may influence surface vortex intensification and reports on numerical simulations designed to study the key processes. In the idealized numerical model, an initial mesocyclone-like vortex and nonvarying convection-like heat source are used in different environmental stability profiles. The scales of interest in these simulations typify those of a parent supercell, and the developing circulations constitute direct responses to the imposed heating.
Downward parcel displacements are needed for surface vortex development in environments with no preexisting surface vorticity. In the simulations, under neutral stratification there is strong heating-induced subsidence anchored near the storm edge, whereas under stable stratification there are instead gravity waves that propagate away to the far field. In addition, under weak or neutral low-level stratification there is very little resistance to downward parcel displacements. In the simulations, these two effects combine to bring high angular momentum air from aloft downward to the surface under neutral lapse rates; this in turn leads to surface vortex genesis, even without precipitation processes. When the lower troposphere is stable, surface vortex intensification is only simulated when there is already preexisting vertical vorticity at the ground. When the initial vortex is elevated (vertical vorticity falls off to zero above the ground), surface vortex intensification is only simulated under neutral low-level stability. The results are interpreted within the controlled experimental framework, after which the possible ramifications to processes in real storms are discussed.
Laminar flow around sharp and curved objects: the lattice Boltzmann method
Authors: Hayatdavoodi M 
Published: September 2011

The lattice Boltzmann method (LBM) is a relatively new computational method to model fluid flows by tracking collision, advection, and propagation of mesoscopic fluid particles. LBM originated from the cellular automata combined with kinetic theory and the Boltzmann equation. The method is used to solve the explicit finite-difference scheme lattice Boltzmann equations which are second order in space and first order in time. LBM does not attempt to solve the Navier–Stokes equations directly; however, it obeys the equations. The two-dimensional flows around square and circular cylinders are simulated with uniform and nonuniform grid structures using the LBM. The boundary layer growth and wake region physics are captured with small-scale details, and the results are validated by comparison with laboratory experiments for the Reynolds numbers between 50 and 350. Compatibility of the method in simulating flow around hydrofoil geometries and a combination of objects is also provided.
Etv2/ER71 induces vascular mesoderm from Flk1+PDGFRα+ primitive mesoderm
Authors: Kataoka Hiroshi , Hayashi Misato , Nakagawa Reiko , Tanaka Yosuke , Izumi Naoki , Nishikawa Satomi , Jakt Martin Lars , Tarui Hiroshi , Nishikawa Shin-Ichi 
Published: September 2011

AbstractEtv2 (Ets Variant 2) has been shown to be an indispensable gene for the development of hematopoietic cells (HPCs)/endothelial cells (ECs). However, how Etv2 specifies the mesoderm-generating HPCs/ECs remains incompletely understood. In embryonic stem cell (ESC) differentiation culture and Etv2-null embryos, we show that Etv2 is dispensable for generating primitive Flk-1+/PDGFRα+ mesoderm but is required for the progression of Flk-1+/PDGFRα+ cells into vascular/hematopoietic mesoderm. Etv2-null ESCs and embryonic cells were arrested as Flk-1+/PDGFRα+ and failed to generate Flk-1+/PDGFRα− mesoderm. Flk-1+/Etv2+ early embryonic cells showed significantly higher hemato-endothelial potential than the Flk-1+/Etv2− population, suggesting that Etv2 specifies a hemato-endothelial subset of Flk-1+ mesoderm. Critical hemato-endothelial genes were severely down-regulated in Etv2-null Flk-1+ cells. Among those genes Scl, Fli1, and GATA2 were expressed simultaneously with Etv2 in early embryos and seemed to be critical targets. Etv2 reexpression in Etv2-null cells restored the development of CD41+, CD45+, and VE-cadherin+ cells. Expression of Scl or Fli1 alone could also restore HPCs/ECs in the Etv2-null background, indicating that these 2 genes are critical downstream targets. Furthermore, VEGF induced Etv2 potently and rapidly in Flk-1+ mesoderm. We propose that Flk-1+/PDGFRα+ primitive mesoderm is committed into Flk-1+/PDGFRα− vascular mesoderm through Etv2 and that up-regulation of Etv2 by VEGF promotes this commitment.
Characterization of phenolic compounds from inner bark of Betula pendula
Authors: Liimatainen Jaana , Karonen Maarit , Sinkkonen Jari , Helander Marjo , Salminen Juha-Pekka 
Published: September 2011

Abstract
A method has been developed for the characterization of biologically active silver birch (Betula pendula) inner bark phenolics based on high-performance liquid chromatography/diode array detector (HPLC-DAD)/electrospray ionization-mass spectrometry (ESI-MS). It was demonstrated that the inner bark contains high amounts of flavonoids, arylbutanoids, diarylheptanoids, simple phenolic compounds, phenolic acids, lignans, and procyanidins. Altogether, 30 individual compounds were characterized based on their ultraviolet (UV) and MS data. Structures of 22 compounds were confirmed by nuclear magnetic resonance (NMR) spectroscopy. In addition to previously reported phenolic compounds, 12 compounds were identified in silver birch inner bark for the first time; two of them are novel compounds: 3-β-glucopyranosyloxy-2-hydroxy-1-(4-hydroxy-3-methoxy-phenyl)-propan-1-one and 1,7-bis-(4-hydroxyphenyl)-3-heptanol 3-O-β-ap-iofuranosyl-(1→2)-β-glucopyranoside.
Loading Standardization of Postendodontic Restorations In Vitro: Impact of Restorative Stage, Static Loading, and Dynamic Loading
Authors: Sterzenbach G , Rosentritt M , Frankenberger R , Paris S , Naumann M 
Published: September 2011

SUMMARY

Objective
The load capability of post-restored endodontically treated teeth (ETT) can be determined at different restorative stages. It was the aim of this study to compare the load capability of ETT at these stages.

Materials and Methods
Maxillary central incisors were divided into 4 groups (n=10) and endodontically treated. Specimens were restored with: (I) only glass fiber posts (GFP); (II) GFP and composite build-up with 2 mm ferrule; (III and IV) with additional adhesively luted all-ceramic crowns. Group (I) to (III) were statically loaded, and group (IV) was exposed to thermomechanical loading (TML) and subsequent static loading.

Results
The lowest median load level of 73 N was determined for group (I). The maximum median load value of 331 N was found for group (III). The comparison of Fmax [N] of group (I), (II) and (III) revealed significant differences between the groups (p&lt;0.001). The specimens of group (IV) failed at significantly lower load values (p&lt;0.005) as similarly restored specimens of group (III) which were only statically loaded. The stage of restoration and TML loading prior to static loading had a significant impact on fracture patterns (p=0.006).

Conclusion
Every additional restorative step torwards a final crown-restored ETT significantly increased the load capability. TML prior to load-to-fracture testing of the complete restorative complex, ie. post, core and crown, significantly decreased maximum load capability.
T Cell Dynamics during Induction of Tolerance and Suppression of Experimental Allergic Encephalomyelitis
Authors: Divekar Rohit D. , Haymaker Cara L. , Cascio Jason A. , Guloglu Betul F. , Ellis Jason S. , Tartar Danielle M. , Hoeman Christine M. , Franklin Craig L. , Zinselmeyer Bernd H. , Lynch Jennifer N. , Miller Mark J. , Zaghouani Habib 
Published: September 2011

Abstract
The cell dynamics associated with induction of peripheral T cell tolerance remain largely undefined. In this study, an in vivo model was adapted to two-photon microscopy imaging, and T cell behavior was analyzed on tolerogen-induced modulation. FcγR-deficient (FcγR−/−) mice were unable to resist or alleviate experimental allergic encephalomyelitis when treated with Ig-myelin oligodendrocyte glycoprotein (MOG) tolerogen, an Ig carrying the MOG35–55 peptide. However, when FcγR+/+ dendritic cells (DCs) are adoptively transferred into FcγR−/− mice, uptake and presentation of Ig-MOG occurs and the animals were able to overcome experimental allergic encephalomyelitis. We then fluorescently labeled FcγR+/+ DCs and 2D2 MOG-specific TCR-transgenic T cells, transferred them into FcγR−/− mice, administered Ig-MOG, and analyzed both T cell–DC contact events and T cell motility. The results indicate that tolerance takes place in lymphoid organs, and surprisingly, the T cells do not become anergic but instead have a Th2 phenotype. The tolerant Th2 cells displayed reduced motility after tolerogen exposure similar to Th1 cells after immunization. However, the Th2 cells had higher migration speeds and took longer to exhibit changes in motility. Therefore, both Th1 immunity and Th2 tolerance alter T cell migration on Ag recognition, but the kinetics of this effect differ among the subsets.
Sensitization to Gliadin Induces Moderate Enteropathy and Insulitis in Nonobese Diabetic-DQ8 Mice
Authors: Galipeau Heather J. , Rulli Nestor E. , Jury Jennifer , Huang Xianxi , Araya Romina , Murray Joseph A. , David Chella S. , Chirdo Fernando G. , McCoy Kathy D. , Verdu Elena F. 
Published: September 2011

Abstract
Celiac disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit Abs against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to have a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but not insulitis. Administration of anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25+Foxp3+ T cells and led to severe insulitis, but did not exacerbate mucosal dysfunction. CD4+ T cells isolated from pancreatic lymph nodes of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubation with gliadin but not with BSA. CD4+ T cells isolated from nonsensitized controls did not response to gliadin or BSA. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice. However, insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T cells. This humanized murine model provides a mechanistic link to explain how the mucosal intolerance to a dietary protein can lead to insulitis in the presence of partial regulatory T cell deficiency.
IL-21–Dependent B Cell Death Driven by Prostaglandin E2, a Product Secreted from Follicular Dendritic Cells
Authors: Magari Masaki , Nishikawa Yumiko , Fujii Yasumasa , Nishio Yumi , Watanabe Koji , Fujiwara Michiya , Kanayama Naoki , Ohmori Hitoshi 
Published: September 2011

Abstract
In germinal centers (GCs), B cells are selected through interaction with follicular dendritic cells bearing immune complexes and follicular helper T (Tfh) cells secreting Tfh cytokines, including IL-21. To analyze these cellular interactions, we have explored culture conditions that can simulate GC B cell selection in vitro using a mouse follicular dendritic cell line, FL-YB. FL-YB cells efficiently enhanced viability of cocultured mouse B cells in a BAFF-dependent fashion. Interestingly, we found that addition of IL-21, a major Tfh cytokine, readily induced death of B cells that were cocultured with FL-YB cells, whereas IL-21 alone sustained viability of B cells in the absence of FL-YB cells. The IL-21–induced death was dependent on a low m.w. soluble factor that was released from FL-YB cells, which was finally identified as PGE2. Treatment of B cells with IL-21 plus PGE2, but not either alone, resulted in enhanced expression of a proapoptotic protein Bim and the upstream transcription factor Foxo1. A PGE2 receptor isoform, EP4, was responsible for IL-21/PGE2–induced B cell death. Thus, PGE2 is an endogenous chemical mediator that can switch pleiotropic actions of IL-21 on B cells. IL-21/PGE2–induced B cell death was rescued if B cells were costimulated via CD40. In immunized mice, deficiency of IL-21R in B cells led to a significant decrease in the frequency of activated caspase-3–positive GC B cells concomitant with impaired affinity maturation of Abs. Taken together, results implicate a physiological role of IL-21/PGE2–induced B cell death in GC B cell selection.
Hypoxia-Dependent Inhibition of Tumor Cell Susceptibility to CTL-Mediated Lysis Involves NANOG Induction in Target Cells
Authors: Hasmim Meriem , Noman Muhammad Zaeem , Lauriol Jessica , Benlalam Houssem , Mallavialle Aude , Rosselli Filippo , Mami-Chouaib Fathia , Alcaide-Loridan Catherine , Chouaib Salem 
Published: September 2011

Abstract
Hypoxia is a major feature of the solid tumor microenvironment and is known to be associated with tumor progression and poor clinical outcome. Recently, we reported that hypoxia protects human non-small cell lung tumor cells from specific lysis by stabilizing hypoxia-inducible factor-1α and inducing STAT3 phosphorylation. In this study, we show that NANOG, a transcription factor associated with stem cell self renewal, is a new mediator of hypoxia-induced resistance to specific lysis. Our data indicate that under hypoxic conditions, NANOG is induced at both transcriptional and translational levels. Knockdown of the NANOG gene in hypoxic tumor cells is able to significantly attenuate hypoxia-induced tumor resistance to CTL-dependent killing. Such knockdown correlates with an increase of target cell death and an inhibition of hypoxia-induced delay of DNA replication in these cells. Interestingly, NANOG depletion results in inhibition of STAT3 phosphorylation and nuclear translocation. To our knowledge, this study is the first to show that hypoxia-induced NANOG plays a critical role in tumor cell response to hypoxia and promotes tumor cell resistance to Ag-specific lysis.