bluuebunny/crossref_metadata_2025_split huggingface dataset:
Energy Transport by Nonlinear Internal Waves
Authors: Moum J. N. , Klymak J. M. , Nash J. D. , Perlin A. , Smyth W. D. 
Published: August 2007

Abstract
Winter stratification on Oregon’s continental shelf often produces a near-bottom layer of dense fluid that acts as an internal waveguide upon which nonlinear internal waves propagate. Shipboard profiling and bottom lander observations capture disturbances that exhibit properties of internal solitary waves, bores, and gravity currents. Wavelike pulses are highly turbulent (instantaneous bed stresses are 1 N m−2), resuspending bottom sediments into the water column and raising them 30+ m above the seafloor. The wave cross-shelf transport of fluid often counters the time-averaged Ekman transport in the bottom boundary layer. In the nonlinear internal waves that were observed, the kinetic energy is roughly equal to the available potential energy and is O(0.1) megajoules per meter of coastline. The energy transported by these waves includes a nonlinear advection term 〈uE〉 that is negligible in linear internal waves. Unlike linear internal waves, the pressure–velocity energy flux 〈up〉 includes important contributions from nonhydrostatic effects and surface displacement. It is found that, statistically, 〈uE〉 ≃ 2〈up〉. Vertical profiles through these waves of elevation indicate that up(z) is more important in transporting energy near the seafloor while uE(z) dominates farther from the bottom. With the wave speed c estimated from weakly nonlinear wave theory, it is verified experimentally that the total energy transported by the waves is 〈up〉 + 〈uE〉 ≃ c〈E〉. The high but intermittent energy flux by the waves is, in an averaged sense, O(100) watts per meter of coastline. This is similar to independent estimates of the shoreward energy flux in the semidiurnal internal tide at the shelf break.
Vertical Structure of Dissipation in the Nearshore
Authors: Feddersen Falk , Trowbridge J. H. , Williams A. J. 
Published: August 2007

Abstract
The vertical structure of the dissipation of turbulence kinetic energy was observed in the nearshore region (3.2-m mean water depth) with a tripod of three acoustic Doppler current meters off a sandy ocean beach. Surface and bottom boundary layer dissipation scaling concepts overlap in this region. No depth-limited wave breaking occurred at the tripod, but wind-induced whitecapping wave breaking did occur. Dissipation is maximum near the surface and minimum at middepth, with a secondary maximum near the bed. The observed dissipation does not follow a surfzone scaling, nor does it follow a “log layer” surface or bottom boundary layer scaling. At the upper two current meters, dissipation follows a modified deep-water breaking-wave scaling. Vertical shear in the mean currents is negligible and shear production magnitude is much less than dissipation, implying that the vertical diffusion of turbulence is important. The increased near-bed secondary dissipation maximum results from a decrease in the turbulent length scale.
Wave Breaking Dissipation in the Wave-Driven Ocean Circulation
Authors: Restrepo Juan M. 
Published: August 2007

Abstract
If wave breaking modifies the Lagrangian fluid paths by inducing an uncertainty in the orbit itself and this uncertainty on wave motion time scales is observable as additive noise, it is shown that within the context of a wave–current interaction model for basin- and shelf-scale motions it persists on long time scales. The model of McWilliams et al. provides the general framework for the dynamics of wave–current interactions. In addition to the deterministic part, the vortex force, which couples the total flow vorticity to the residual flow due to the waves, will have a part that is associated with the dissipative mechanism. At the same time the wave field will experience dissipation, and tracer advection is affected by the appearance of a dissipative term in the Stokes drift velocity. Consistency leads to other dynamic consequences: the boundary conditions are modified to take into account the diffusive process and proper mass/momentum balances at the surface of the ocean. In addition to formulating how a wave–current interaction model is modified by the presence of short-time events that induce dissipation, this study proposes a stochastic parameterization of dissipation. Its relation to other alternative parameterizations is given. Two focal reasons make stochastic parameterizations attractive: one can draw from extensive practical modeling experience in other fields, and it ties in a very natural way to a wealth of observational data via statistics.
CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer–binding protein alpha
Authors: Koschmieder Steffen , D'Alò Francesco , Radomska Hanna , Schöneich Christine , Chang Ji Suk , Konopleva Marina , Kobayashi Susumu , Levantini Elena , Suh Nanjoo , Di Ruscio Annalisa , Voso Maria Teresa , Watt Julie C. , Santhanam Ramasamy , Sargin Bülent , Kantarjian Hagop , Andreeff Michael , Sporn Michael B. , Perrotti Danilo , Berdel Wolfgang E. , Müller-Tidow Carsten , Serve Hubert , Tenen Daniel G. 
Published: August 2007

Abstract2-Cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) induces differentiation and apoptosis of tumor cells in vitro and in vivo. Here we assessed the effects of CDDO on CCAAT enhancer–binding protein alpha (CEBPA), a transcription factor critical for granulocytic differentiation. In HL60 acute myeloid leukemia (AML) cells, CDDO (0.01 to 2 μM) induces apoptosis in a dose-dependent manner. Conversely, subapoptotic doses of CDDO promote phagocytic activity and granulocytic-monocytic differentiation of HL60 cells through increased de novo synthesis of p42 CEBPA protein. CEBPA translational up-regulation is required for CDDO-induced granulocytic differentiation and depends on the integrity of the CEBPA upstream open reading frame (uORF). Moreover, CDDO increases the ratio of transcriptionally active p42 and the inactive p30 CEBPA isoform, which, in turn, leads to transcriptional activation of CEBPA-regulated genes (eg, GSCFR) and is associated with dephosphorylation of eIF2α and phosphorylation of eIF4E. In concordance with these results, CDDO induces a CEBPA ratio change and differentiation of primary blasts from patients with acute myeloid leukemia (AML). Because AML is characterized by arrested differentiation, our data suggest the inclusion of CDDO in the therapy of AML characterized by dysfunctional CEBPA expression.
C/EBPα binds and activates the PU.1 distal enhancer to induce monocyte lineage commitment
Authors: Yeamans Christine , Wang Dehua , Paz-Priel Ido , Torbett Bruce E. , Tenen Daniel G. , Friedman Alan D. 
Published: August 2007

AbstractThe PU.1 gene contains a 237–base pair distal enhancer located 14 kilobases upstream of its promoter. We have identified 2 sites within the PU.1 enhancer that strongly bind C/EBPα in a gel shift assay, and interaction with endogenous C/EBPα was confirmed by chromatin immunoprecipitation. Mutation of these DNA elements reduced activity of a distal enhancer-promoter construct 2- or 5-fold in a myeloid cell line, while mutation of a weaker C/EBPα-binding site located in the promoter minimally reduced activity in this context. These findings strengthen the link between C/EBPα and PU.1 expression. Reduction of C/EBPα activity in cases of acute myeloid leukemia may therefore contribute to transformation by reducing PU.1 levels. In addition, induction of PU.1 by C/EBPα during normal hematopoiesis may contribute to stem cell commitment to the myeloid lineages and further commitment to monopoiesis. Consistent with a requirement for C/EBPα induction of PU.1 during myeloid development, we demonstrate that C/EBPα induces monocytic development when expressed in PU.1+/+, PU.1+/−, or PU.1+/kd marrow myeloid progenitors but induces granulocyte lineage commitment in PU.1kd/kd cells lacking the PU.1 distal enhancer and does not induce either lineage in PU.1−/− cells.
Time-dependent changes in pulmonary surfactant function and composition in acute respiratory distress syndrome due to pneumonia or aspiration
Authors: Schmidt Reinhold , Markart Philipp , Ruppert Clemens , Wygrecka Malgorzata , Kuchenbuch Tim , Walmrath Dieter , Seeger Werner , Guenther Andreas 
Published: August 2007

AbstractBackgroundAlterations to pulmonary surfactant composition have been encountered in the Acute Respiratory Distress Syndrome (ARDS). However, only few data are available regarding the time-course and duration of surfactant changes in ARDS patients, although this information may largely influence the optimum design of clinical trials addressing surfactant replacement therapy. We therefore examined the time-course of surfactant changes in 15 patients with direct ARDS (pneumonia, aspiration) over the first 8 days after onset of mechanical ventilation.MethodsThree consecutive bronchoalveolar lavages (BAL) were performed shortly after intubation (T0), and four days (T1) and eight days (T2) after intubation. Fifteen healthy volunteers served as controls. Phospholipid-to-protein ratio in BAL fluids, phospholipid class profiles, phosphatidylcholine (PC) molecular species, surfactant proteins (SP)-A, -B, -C, -D, and relative content and surface tension properties of large surfactant aggregates (LA) were assessed.ResultsAt T0, a severe and highly significant reduction in SP-A, SP-B and SP-C, the LA fraction, PC and phosphatidylglycerol (PG) percentages, and dipalmitoylation of PC (DPPC) was encountered. Surface activity of the LA fraction was greatly impaired. Over time, significant improvements were encountered especially in view of LA content, DPPC, PG and SP-A, but minimum surface tension of LA was not fully restored (15 mN/m at T2). A highly significant correlation was observed between PaO2/FiO2and minimum surface tension (r = -0.83; p < 0.001), SP-C (r = 0.64; p < 0.001), and DPPC (r = 0.59; p = 0.003). Outcome analysis revealed that non-survivors had even more unfavourable surfactant properties as compared to survivors.ConclusionWe concluded that a profound impairment of pulmonary surfactant composition and function occurs in the very early stage of the disease and only gradually resolves over time. These observations may explain why former surfactant replacement studies with a short treatment duration failed to improve outcome and may help to establish optimal composition and duration of surfactant administration in future surfactant replacement studies in acute lung injury.
Maternal allergic contact dermatitis causes increased asthma risk in offspring
Authors: Lim Robert H , Arredouani Mohamed S , Fedulov Alexey , Kobzik Lester , Hubeau Cedric 
Published: August 2007

Abstract

Background
Offspring of asthmatic mothers have increased risk of developing asthma, based on human epidemiologic data and experimental animal models. The objective of this study was to determine whether maternal allergy at non-pulmonary sites can increase asthma risk in offspring.

Methods
BALB/c female mice received 2 topical applications of vehicle, dinitrochlorobenzene, or toluene diisocyanate before mating with untreated males. Dinitrochlorobenzene is a skin-sensitizer only and known to induce a Th1 response, while toluene diisocyanate is both a skin and respiratory sensitizer that causes a Th2 response. Both cause allergic contact dermatitis. Offspring underwent an intentionally suboptimal protocol of allergen sensitization and aerosol challenge, followed by evaluation of airway hyperresponsiveness, allergic airway inflammation, and cytokine production. Mothers were tested for allergic airway disease, evidence of dermatitis, cellularity of the draining lymph nodes, and systemic cytokine levels. The role of interleukin-4 was also explored using interleukin-4 deficient mice.

Results
Offspring of toluene diisocyanate but not dinitrochlorobenzene-treated mothers developed an asthmatic phenotype following allergen sensitization and challenge, seen as increased Penh values, airway inflammation, bronchoalveolar lavage total cell counts and eosinophilia, and Th2 cytokine imbalance in the lung. Toluene diisocyanate treated interleukin-4 deficient mothers were able to transfer asthma risk to offspring. Mothers in both experimental groups developed allergic contact dermatitis, but not allergic airway disease.

Conclusion
Maternal non-respiratory allergy (Th2-skewed dermatitis caused by toluene diisocyanate) can result in the maternal transmission of asthma risk in mice.
Automating document classification for the Immune Epitope Database
Authors: Wang Peng , Morgan Alexander A , Zhang Qing , Sette Alessandro , Peters Bjoern 
Published: August 2007

Abstract

Background
The Immune Epitope Database contains information on immune epitopes curated manually from the scientific literature. Like similar projects in other knowledge domains, significant effort is spent on identifying which articles are relevant for this purpose.

Results
We here report our experience in automating this process using Naïve Bayes classifiers trained on 20,910 abstracts classified by domain experts. Improvements on the basic classifier performance were made by a) utilizing information stored in PubMed beyond the abstract itself b) applying standard feature selection criteria and c) extracting domain specific feature patterns that e.g. identify peptides sequences. We have implemented the classifier into the curation process determining if abstracts are clearly relevant, clearly irrelevant, or if no certain classification can be made, in which case the abstracts are manually classified. Testing this classification scheme on an independent dataset, we achieve 95% sensitivity and specificity in the 51.1% of abstracts that were automatically classified.

Conclusion
By implementing text classification, we have sped up the reference selection process without sacrificing sensitivity or specificity of the human expert classification. This study provides both practical recommendations for users of text classification tools, as well as a large dataset which can serve as a benchmark for tool developers.
The utility of MAS5 expression summary and detection call algorithms
Authors: Pepper Stuart D , Saunders Emma K , Edwards Laura E , Wilson Claire L , Miller Crispin J 
Published: August 2007

Abstract

Background
Used alone, the MAS5.0 algorithm for generating expression summaries has been criticized for high False Positive rates resulting from exaggerated variance at low intensities.

Results
Here we show, with replicated cell line data, that, when used alongside detection calls, MAS5 can be both selective and sensitive. A set of differentially expressed transcripts were identified that were found to be changing by MAS5, but unchanging by RMA and GCRMA. Subsequent analysis by real time PCR confirmed these changes. In addition, with the Latin square datasets often used to assess expression summary algorithms, filtered MAS5.0 was found to have performance approaching that of its peers.

Conclusion
When used alongside detection calls, MAS5 is a sensitive and selective algorithm for identifying differentially expressed genes.
Specification of germ layer identity in the chick gastrula
Authors: Chapman Susan C , Matsumoto Kiyoshi , Cai Qin , Schoenwolf Gary C 
Published: August 2007

Abstract
Background
Chick definitive endoderm is an important source of signals that pattern the early embryo forming a central structure around which the body plan is constructed. Although the origin of definitive endoderm has been mapped in the chick, arising principally from rostral streak at elongating streak stages, it is not known when this layer first becomes fully committed to its germ layer fate, an important issue to resolve in light of its critical role in subsequent patterning of the early embryo.

Results
Through gene expression screening of chick gastrula, we identified molecular markers of definitive endoderm restricted to rostral (Sox17) and caudal (Gata5/6) regions, suggesting that at least two subpopulations of definitive endodermal cells exist during ingression. We show (1) that presumptive mesoderm cells migrate to the middle layer and remain mesenchymal when transplanted to rostral primitive streak, and prospective endoderm cells enter the lower layer and become epithelial when transplanted to caudal primitive streak; and (2) that presumptive endoderm cells and mesoderm cells lose normal gene expression (Sox17 and Wnt8c, respectively) when transplanted outside of their normal position of origin. Moreover, when rostral or caudal primitive streak segments are transplanted into rostral blastoderm isolates (RBIs), both types of transplants express Sox17 4–6 hours later–consistent with their new position, regardless of their presumptive germ layer origin–and prospective mesoderm transplants, which normally express Wnt8c, turn off expression, suggesting that signals within the rostral blastoderm induce endoderm gene expression, and repress mesoderm gene expression, during gastrulation.

Conclusion
Our results demonstrate that germ layer identity is fixed at the time populations of endoderm and mesoderm cells ingress through the primitive streak, whereas their gene expression patterns remain labile. In addition, our results show that inductive and repressive signals are present, and that these signals regulate gene expression of both ingressed endoderm and mesoderm cells. Thus, gastrula cells display elements of both pre-patterning and plasticity, with endoderm the first germ layer becoming committed to its fate during early gastrulation stages.
EGFR associated expression profiles vary with breast tumor subtype
Authors: Hoadley Katherine A , Weigman Victor J , Fan Cheng , Sawyer Lynda R , He Xiaping , Troester Melissa A , Sartor Carolyn I , Rieger-House Thais , Bernard Philip S , Carey Lisa A , Perou Charles M 
Published: August 2007

Abstract

Background
The epidermal growth factor receptor (EGFR/HER1) and its downstream signaling events are important for regulating cell growth and behavior in many epithelial tumors types. In breast cancer, the role of EGFR is complex and appears to vary relative to important clinical features including estrogen receptor (ER) status. To investigate EGFR-signaling using a genomics approach, several breast basal-like and luminal epithelial cell lines were examined for sensitivity to EGFR inhibitors. An EGFR-associated gene expression signature was identified in the basal-like SUM102 cell line and was used to classify a diverse set of sporadic breast tumors.

Results

In vitro, breast basal-like cell lines were more sensitive to EGFR inhibitors compared to luminal cell lines. The basal-like tumor derived lines were also the most sensitive to carboplatin, which acted synergistically with cetuximab. An EGFR-associated signature was developed in vitro, evaluated on 241 primary breast tumors; three distinct clusters of genes were evident in vivo, two of which were predictive of poor patient outcomes. These EGFR-associated poor prognostic signatures were highly expressed in almost all basal-like tumors and many of the HER2+/ER- and Luminal B tumors.

Conclusion
These results suggest that breast basal-like cell lines are sensitive to EGFR inhibitors and carboplatin, and this combination may also be synergistic. In vivo, the EGFR-signatures were of prognostic value, were associated with tumor subtype, and were uniquely associated with the high expression of distinct EGFR-RAS-MEK pathway genes.
New pleiotropic effects of eliminating a rare tRNA from Streptomyces coelicolor, revealed by combined proteomic and transcriptomic analysis of liquid cultures
Authors: Hesketh Andy , Bucca Giselda , Laing Emma , Flett Fiona , Hotchkiss Graham , Smith Colin P , Chater Keith F 
Published: August 2007

AbstractBackgroundInStreptomyces coelicolor,bldAencodes the only tRNA for a rare leucine codon, UUA. This tRNA is unnecessary for growth, but is required for some aspects of secondary metabolism and morphological development. We describe a transcriptomic and proteomic analysis of the effects of deletingbldAon cellular processes during submerged culture: conditions relevant to the industrial production of antibiotics.ResultsAt the end of rapid growth, a co-ordinated transient up-regulation of about 100 genes, including many for ribosomal proteins, was seen in the parent strain but not the ΔbldAmutant. Increased basal levels of the signal molecule ppGpp in the mutant strain may be responsible for this difference. Transcripts or proteins from a further 147 genes classified asbldA-influenced were mostly expressed late in culture in the wild-type, though others were significantly transcribed during exponential growth. Some were involved in the biosynthesis of seven secondary metabolites; and some have probable roles in reorganising metabolism after rapid growth. Many of the 147 genes were "function unknown", and may represent unknown aspects ofStreptomycesbiology. Only two of the 147 genes contain a TTA codon, but some effects ofbldAcould be traced to TTA codons in regulatory genes or polycistronic operons. Several proteins were affected post-translationally by thebldAdeletion. There was a statistically significant but weak positive global correlation between transcript and corresponding protein levels. Different technical limitations of the two approaches were a major cause of discrepancies in the results obtained with them.ConclusionAlthough deletion ofbldAhas very conspicuous effects on the gross phenotype, thebldAmolecular phenotype revealed by the "dualomic" approach has shown that only about 2% of the genome is affected; but this includes many previously unknown effects at a variety of different levels, including post-translational changes in proteins and global cellular physiology.
CD8α is expressed by human monocytes and enhances FcγR-dependent responses
Authors: Gibbings Derrick J , Marcet-Palacios Marcelo , Sekar Yokananth , Ng Marcus CY , Befus A Dean 
Published: August 2007

AbstractBackgroundCD8α enhances the responses of antigen-specific CTL activated through TCR through binding MHC class I, favoring lipid raft partitioning of TCR, and inducing intracellular signaling. CD8α is also found on dendritic cells and rat macrophages, but whether CD8α enhances responses of a partner receptor, like TCR, to activate these cells is not known. TCR and FcR, use analogous or occasionally interchangeable signaling mechanisms suggesting the possibility that CD8α co-activates FcR responses. Interestingly, CD8α+ monocytes are often associated with rat models of disease involving immune-complex deposition and FcR-mediated pathology, such as arthritis, glomerulonephritis, ischaemia, and tumors. While rat macrophages have been shown to express CD8α evidence for CD8α expression by mouse or human monocytes or macrophages was incomplete.ResultsWe detected CD8α, but not CD8β on human monocytes and the monocytic cell line THP-1 by flow cytometry. Reactivity of anti-CD8α mAb with monocytes is at least partly independent of FcR as anti-CD8α mAb detect CD8α by western blot and inhibit binding of MHC class I tetramers. CD8α mRNA is also found in monocytes and THP-1 suggesting CD8α is synthesized by monocytes and not acquired from other CD8α+ cell types. Interestingly, CD8α from monocytes and blood T cells presented distinguishable patterns by 2-D electrophoresis. Anti-CD8α mAb alone did not activate monocyte TNF release. In comparison, TNF release by human monocytes stimulated in a FcR-dependent manner with immune-complexes was enhanced by inclusion of anti-CD8α mAb in immune-complexes.ConclusionHuman monocytes express CD8α. Co-engagement of CD8α and FcR enhances monocyte TNF release, suggesting FcR may be a novel partner receptor for CD8α on innate immune cells.