bluuebunny/crossref_metadata_2025_split huggingface dataset:
MOISTURE REDISTRIBUTION AND TEXTURAL CHANGES IN STORED MODEL SANDWICHES
Authors: BARRETT ANN , CARDELLO ARMAND , MAGUIRE PAUL , PELEG MICHA 
Published: November 2005

ABSTRACT Moisture migration and instrumental and sensory texture changes were determined in model cheese sandwich structures in which bread water activity was varied by glycerol level. Sandwiches and components were evaluated both after assembly and 4‐week ambient storage by uniaxial compression and mathematical description of stress‐strain relationships, assessment of sensory characteristics by a trained panel, correspondence between predicted and actual stress‐strain relationships, and mass‐balance analysis of moisture migration between cheese, bread crumb and bread crust. Textural changes occurred as a result of both aging and moisture migration, and the accuracy of fitted “predicted” stress‐strain relationships of the composites varied according to the extent of moisture migration. Sensory assessments of key textural attributes of sandwich composites and components, before and after storage, were significantly correlated with measured mechanical parameters.
Characterization of the
Bacillus subtilis
Spore Morphogenetic Coat Protein CotO
Authors: McPherson D. C. , Kim H. , Hahn M. , Wang R. , Grabowski P. , Eichenberger P. , Driks A. 
Published: December 2005

ABSTRACT

Bacillus spores are protected by a structurally and biochemically complex protein shell composed of over 50 polypeptide species, called the coat. Coat assembly in
Bacillus subtilis
serves as a relatively tractable model for the study of the formation of more complex macromolecular structures and organelles. It is also a critical model for the discovery of strategies to decontaminate
B. anthracis
spores. In
B. subtilis
, a subset of coat proteins is known to have important roles in assembly. Here we show that the recently identified
B. subtilis
coat protein CotO (YjbX) has an especially important morphogenetic role. We used electron and atomic force microscopy to show that CotO controls assembly of the coat layers and coat surface topography as well as biochemical and cell-biological analyses to identify coat proteins whose assembly is CotO dependent.
cotO
spores are defective in germination and partially sensitive to lysozyme. As a whole, these phenotypes resemble those resulting from a mutation in the coat protein gene
cotH
. Nonetheless, the roles of CotH and CotO and the proteins whose assembly they direct are not identical. Based on fluorescence and electron microscopy, we suggest that CotO resides in the outer coat (although not on the coat surface). We propose that CotO and CotH participate in a late phase of coat assembly. We further speculate that an important role of these proteins is ensuring that polymerization of the outer coat layers occurs in such a manner that contiguous shells, and not unproductive aggregates, are formed.
Importance of Tetramer Formation by the Nitrogen Assimilation Control Protein for Strong Repression of Glutamate Dehydrogenase Formation in
Klebsiella pneumoniae
Authors: Rosario Christopher J. , Bender Robert A. 
Published: December 2005

ABSTRACT

The nitrogen assimilation control protein (NAC) from
Klebsiella pneumoniae
is a very versatile regulatory protein. NAC activates transcription of operons such as
hut
(histidine utilization) and
ure
(urea utilization), whose products generate ammonia. NAC also represses the transcription of genes such as
gdhA
, whose products use ammonia. NAC exerts a weak repression at
gdhA
by competing with the binding of a lysine-sensitive activator. NAC also strongly represses transcription of
gdhA
(about 20-fold) by binding to two separated sites, suggesting a model involving DNA looping. We have identified negative control mutants that are unable to exert this strong repression of
gdhA
expression but still activate
hut
and
ure
expression normally. Some of these negative control mutants (e.g., NAC
86ter
and NAC
132ter
) delete the C-terminal domain, thought to be required for tetramerization. Other negative control mutants (e.g., NAC
L111K
and NAC
L125R
) alter single amino acids involved in tetramerization. In this work we used gel filtration to show that NAC
86ter
and NAC
L111K
are dimers in solution, even at high concentration (NAC
WT
is a tetramer). Moreover, using a combination of DNase I footprints and gel mobility shifts assays, we showed that when NAC
WT
binds to two adjacent sites on a DNA fragment, NAC
WT
binds as a tetramer that bends the DNA fragment significantly. NAC
L111K
binds to such a fragment as two independent dimers without inducing the strong bend. Thus, NAC
L111K
is a dimer in solution or when bound to DNA. NAC
L111K
(typical of the negative control mutants) is wild type for every other property tested: (i) it activates transcription at
hut
and
ure
; (ii) it competes with the lysine-sensitive activator for binding at
gdhA
; (iii) it binds to the same sites at the
hut
,
ure
,
nac
, and
gdhA
promoters as NAC
WT
; (iv) the relative affinity of NAC
L111K
for these sites follows the same order as NAC
WT
(
ure
>
gdhA
>
nac
>
hut
); (v) it induces the same slight bend as dimers of NAC
WT
; and (vi) its DNase I footprints at these sites are indistinguishable from those of NAC
WT
(except for features ascribed to tetramer formation). The only two phenotypes we know for negative control mutants of NAC are their inability to tetramerize and their inability to cause the strong repression of
gdhA
. Thus, we propose that in order for NAC
WT
to exert the strong repression, it must form a tetramer that bridges the two sites at
gdhA
(similar to other DNA looping models) and that the negative control mutants of NAC, which fail to tetramerize, cannot form this loop and thus fail to exert the strong repression at
gdhA
.
Role of the
Pseudomonas fluorescens
Alginate Lyase (AlgL) in Clearing the Periplasm of Alginates Not Exported to the Extracellular Environment
Authors: Bakkevig Karianne , Sletta Håvard , Gimmestad Martin , Aune Randi , Ertesvåg Helga , Degnes Kristin , Christensen Bjørn Erik , Ellingsen Trond E. , Valla Svein 
Published: December 2005

ABSTRACT

Alginate is an industrially widely used polysaccharide produced by brown seaweeds and as an exopolysaccharide by bacteria belonging to the genera
Pseudomonas
and
Azotobacter
. The polymer is composed of the two sugar monomers mannuronic acid and guluronic acid (G), and in all these bacteria the genes encoding 12 of the proteins essential for synthesis of the polymer are clustered in the genome. Interestingly, 1 of the 12 proteins is an alginate lyase (AlgL), which is able to degrade the polymer down to short oligouronides. The reason why this lyase is associated with the biosynthetic complex is not clear, but in this paper we show that the complete lack of AlgL activity in
Pseudomonas fluorescens
in the presence of high levels of alginate synthesis is toxic to the cells. This toxicity increased with the level of alginate synthesis. Furthermore, alginate synthesis became reduced in the absence of AlgL, and the polymers contained much less G residues than in the wild-type polymer. To explain these results and other data previously reported in the literature, we propose that the main biological function of AlgL is to degrade alginates that fail to become exported out of the cell and thereby become stranded in the periplasmic space. At high levels of alginate synthesis in the absence of AlgL, such stranded polymers may accumulate in the periplasm to such an extent that the integrity of the cell is lost, leading to the observed toxic effects.
The ClgR Protein Regulates Transcription of theclpPOperon inBifidobacterium breveUCC 2003
Authors: Ventura Marco , Zhang Ziding , Cronin Michelle , Canchaya Carlos , Kenny John G. , Fitzgerald Gerald F. , van Sinderen Douwe 
Published: December 2005

ABSTRACTFiveclpgenes (clpC,clpB,clpP1,clpP2, andclpX), representing chaperone- and protease-encoding genes, were previously identified inBifidobacterium breveUCC 2003. In the present study, we characterize theB. breveUCC 2003clpPlocus, which consists of two paralogous genes, designatedclpP1andclpP2, whose deduced protein products display significant similarity to characterized ClpP peptidases. Transcriptional analyses showed that theclpP1andclpP2genes are transcribed in response to moderate heat shock as a bicistronic unit with a single promoter. The role of aclgRhomologue, known to control the regulation ofclpPgene expression inStreptomyces lividansandCorynebacterium glutamicum, was investigated by gel mobility shift assays and DNase I footprint experiments. We show that ClgR, which in its purified form appears to exist as a dimer, requires a proteinaceous cofactor to assist in specific binding to a 30-bp region of theclpPpromoter region. In pull-down experiments, a 56-kDa protein copurified with ClgR, providing evidence that the two proteins also interact in vivo and that the copurified protein represents the cofactor required for ClgR activity. The prediction of the ClgR three-dimensional structure provides further insights into the binding mode of this protein to theclpP1promoter region and highlights the key amino acid residues believed to be involved in the protein-DNA interaction.
Genetic Requirements for Potassium Ion-Dependent Colony Spreading inBacillus subtilis
Authors: Kinsinger Rebecca F. , Kearns Daniel B. , Hale Marina , Fall Ray 
Published: December 2005

ABSTRACTUndomesticated strains ofBacillus subtilisexhibit extensive colony spreading on certain soft agarose media: first the formation of dendritic clusters of cells, followed by spreading (pellicle-like) growth to cover the entire surface. These phases of colonization are dependent on the level of potassium ion (K+) but independent of flagella, as verified with a mutant with ahaggene replacement; this latter finding highlights the importance of sliding motility in colony spreading. Exploring the K+requirement, directed mutagenesis of the higher-affinity K+transporter KtrAB, but not the lower-affinity transporter KtrCD, was found to inhibit surface colonization unless sufficient KCl was added. To identify other genes involved in K+-dependent colony spreading, transposon insertion mutants in wild-type strain 3610 were screened. Disruption of genes for pyrimidine (pyrB) or purine (purD,purF,purH,purL,purM) biosynthetic pathways abolished the K+-dependent spreading phase. Consistent with a requirement for functional nucleic acid biosynthesis, disruption of purine synthesis with the folic acid antagonist sulfamethoxazole also inhibited spreading. Other transposon insertions disrupted acetoin biosynthesis (thealsSgene), acidifying the growth medium, glutamine synthetase (theglnAgene), and two surfactin biosynthetic genes (srfAA,srfAB). This work identified four classes of surface colonization mutants with defective (i) potassium transport, (ii) surfactin formation, (iii) growth rate or yield, or (iv) pH control. Overall, the ability ofB. subtilisto colonize surfaces by spreading is highly dependent on balanced nucleotide biosynthesis and nutrient assimilation, which require sufficient K+ions, as well as growth conditions that promote sliding motility.
Coexpression Patterns of σBRegulators inBacillus subtilisAffect σBInducibility
Authors: Zhang Shuyu , Reeves Adam , Woodbury Robyn L. , Haldenwang W. G. 
Published: December 2005

ABSTRACTRsbT is an essential component of the pathway that activates theBacillus subtilisσBtranscription factor in response to physical stress.rsbTis located within an operon that includes the genes for its principal negative regulator (RsbS) and the stress pathway component that it activates (RsbU), as immediate upstream and downstream neighbors. In the current work we demonstrate that RsbT's ability to function is strongly influenced by coexpression with these adjoining genes. WhenrsbTis expressed at a site displaced fromrsbSandrsbU, RsbT accumulates but it is unable to activate σBfollowing stress. RsbT activity is restored ifrsbTis cotranscribed at the alternative site with the genes that normally abut it. Additionally, anrsbSallele whose product allows constitutively high RsbT-dependent σBactivity displays this activity inrsbSmerodiploid strains only when cotranscribed withrsbTand is recessive to a wild-typersbSallele only if the wild-typersbSgene is not cotranscribed with anrsbTgene of its own. The data suggest that RsbS and RsbT are synthesized in equivalent amounts and interact coincidently with their synthesis to form stable regulatory complexes that maintain RsbT in a state from which it can be stress activated.
Inhibition of
Bacillus subtilis scoC
Expression by Multicopy
senS
Authors: Kawachi Eiji , Abe Sadanobu , Tanaka Teruo 
Published: December 2005

ABSTRACT

The
Bacillus subtilis aprE
gene, which encodes the extracellular alkaline protease, is regulated by many positive and negative transcriptional regulators. SenS is one such positive regulator consisting of 65 amino acids. We found that the
senS
gene on a multicopy plasmid, pSEN24, caused an increase in
aprE
expression in strains carrying the upstream region of
aprE
up to −340 with respect to the transcription initiation site but not in a strain carrying the region up to −299, which is within the binding site of the negative regulator ScoC (Hpr). Epistatic analysis showed that the pSEN24 effect was lost in a
scoC
-deleted mutant. In accordance with these results, the
scoC
transcription level as assayed by a
scoC-lacZ
fusion and Northern analysis was greatly reduced in the cells carrying pSEN24. From these results we conclude that multicopy
senS
enhances
aprE
expression by suppressing the transcription of
scoC
.
CLASSIFYING CREDIT CARD ACCOUNTS FOR BUSINESS INTELLIGENCE AND DECISION MAKING: A MULTIPLE-CRITERIA QUADRATIC PROGRAMMING APPROACH
Authors: SHI YONG , PENG YI , KOU GANG , CHEN ZHENGXIN 
Published: December 2005

A major challenge in credit card portfolio management is to classify and predict credit cardholders' behaviors in a reliable precision because cardholders' behaviors are rather dynamic in nature. This is crucial for creditors because it allows them to take proactive actions and minimize charge-off and bankruptcy losses. Although the methods used in the area of credit portfolio management have improved significantly, the demand for alternative and sophisticated analytical tools is still strong. The objective of this paper is to propose a multiple criteria quadratic programming (MCQP) to classify credit card accounts for business intelligence and decision making. MCQP is intended to predict credit cardholders' behaviors from a nonlinear perspective that is justifiable because both the objective functions and constraints in credit card accounts classification may be nonlinear. Using a real-life credit card dataset from a major US bank, the MCQP method is compared with popular and similar classification methods: linear discriminant analysis, decision tree, multiple criteria linear programming, support vector machine, and neural network. The results indicate that MCQP is a promising business intelligence method in credit card portfolio management.
Deciphering Protein Molecular Signatures in Cancer Tissues to Aid in Diagnosis, Prognosis, and Therapy
Authors: Caprioli Richard M. 
Published: December 2005

Abstract
Protein signatures in disease, a portion of the protein complement of cells that directly reflects disease related changes, provide a unique data set that may be correlated with or be an aid to more effective diagnosis, prognosis, and response to therapy. A recent article in this Journal from the author's laboratory described the protein analysis of glioma tissue and the discovery of protein signatures for assessing the stage of disease as well as their correlation with patient survival. This investigation used direct proteomic analysis of glioma biopsies, the discovery of molecular signatures for stage and outcome, and identification of specific proteins of this signature group. This minireview discusses the background and present state of the technology used in this work and the role that direct tissue analysis can play in the discovery of high-quality protein signatures.
Insulin-like Growth Factor-I Receptor/Human Epidermal Growth Factor Receptor 2 Heterodimerization Contributes to Trastuzumab Resistance of Breast Cancer Cells
Authors: Nahta Rita , Yuan Linda X.H. , Zhang Bing , Kobayashi Ryuji , Esteva Francisco J. 
Published: December 2005

AbstractThe majority of breast cancer patients who achieve an initial therapeutic response to the human epidermal growth factor receptor 2 (HER-2)–targeted antibody trastuzumab will show disease progression within 1 year. We previously reported the characterization of SKBR3-derived trastuzumab-resistant pools. In the current study, we show that HER-2 interacts with insulin-like growth factor-I receptor (IGF-IR) uniquely in these resistant cells and not in the parental trastuzumab-sensitive cells. The occurrence of cross talk between IGF-IR and HER-2 exclusively in resistant cells is evidenced by the IGF-I stimulation resulting in increased phosphorylation of HER-2 in resistant cells, but not in parental cells, and by the inhibition of IGF-IR tyrosine kinase activity leading to decreased HER-2 phosphorylation only in resistant cells. In addition, inhibition of IGF-IR tyrosine kinase activity by I-OMe-AG538 increased sensitivity of resistant cells to trastuzumab. HER-2/IGF-IR interaction was disrupted on exposure of resistant cells to the anti–IGF-IR antibody α-IR3 and, to a lesser extent, when exposed to the anti-HER-2 antibody pertuzumab. Heterodimer disruption by α-IR3 dramatically restored sensitivity to trastuzumab and resistant cells showed a slightly increased sensitivity to pertuzumab versus parental cells. Neither α-IR3 nor pertuzumab decreased HER-2 phosphorylation, suggesting that additional sources of phosphorylation other than IGF-IR exist when HER-2 and IGF-IR are not physically bound. Our data support a unique interaction between HER-2 and IGF-IR in trastuzumab-resistant cells such that cross talk occurs between IGF-IR and HER-2. These data suggest that the IGF-IR/HER-2 heterodimer contributes to trastuzumab resistance and justify the need for further studies examining this complex as a potential therapeutic target in breast cancers that have progressed while on trastuzumab.
Twist Overexpression Induces In vivo Angiogenesis and Correlates with Chromosomal Instability in Breast Cancer
Authors: Mironchik Yelena , Winnard Paul T. , Vesuna Farhad , Kato Yoshinori , Wildes Flonne , Pathak Arvind P. , Kominsky Scott , Artemov Dmitri , Bhujwalla Zaver , Van Diest Paul , Burger Horst , Glackin Carlotta , Raman Venu 
Published: December 2005

Abstract
Aggressive cancer phenotypes are a manifestation of many different genetic alterations that promote rapid proliferation and metastasis. In this study, we show that stable overexpression of Twist in a breast cancer cell line, MCF-7, altered its morphology to a fibroblastic-like phenotype, which exhibited protein markers representative of a mesenchymal transformation. In addition, it was observed that MCF-7/Twist cells had increased vascular endothelial growth factor (VEGF) synthesis when compared with empty vector control cells. The functional changes induced by VEGF in vivo were analyzed by functional magnetic resonance imaging (MRI) of MCF-7/Twist-xenografted tumors. MRI showed that MCF-7/Twist tumors exhibited higher vascular volume and vascular permeability in vivo than the MCF-7/vector control xenografts. Moreover, elevated expression of Twist in breast tumor samples obtained from patients correlated strongly with high-grade invasive carcinomas and with chromosome instability, particularly gains of chromosomes 1 and 7. Taken together, these results show that Twist overexpression in breast cancer cells can induce angiogenesis, correlates with chromosomal instability, and promotes an epithelial-mesenchymal-like transition that is pivotal for the transformation into an aggressive breast cancer phenotype.
Hepatitis C Virus Core Protein Inhibits Tumor Suppressor Protein Promyelocytic Leukemia Function in Human Hepatoma Cells
Authors: Herzer Kerstin , Weyer Sandra , Krammer Peter H. , Galle Peter R. , Hofmann Thomas G. 
Published: December 2005

Abstract
Tumor suppressor protein promyelocytic leukemia (PML) is implicated in apoptosis regulation and antiviral response. PML localizes predominantly to PML-nuclear bodies (PML-NB), nuclear macromolecular complexes regulating tumor suppressor protein p53 activity. Consistent with the function of PML in the cellular antiviral response, PML-NBs represent preferential targets in viral infections. In the case of hepatitis C virus (HCV) infection, important characteristics are nonresponsiveness to IFN therapy and development of hepatocellular carcinoma. However, the mechanisms which lead to the development of hepatocellular carcinoma are largely unknown. Here, we show that HCV core protein localizes to the cell nucleus in PML-NBs, where it colocalizes with p53. The HCV core interacts with endogenously expressed PML isoform IV (PML-IV), a key regulator of p53 activity. Importantly, we show that HCV core protein inhibits PML-IV–induced apoptosis and interferes with the coactivator function of PML-IV for proapoptotic p53 target genes including CD95 (Fas/APO-1). In particular, we found that the HCV core inhibits p53-mediated target gene expression by predominantly targeting the coactivator function of PML-IV because HCV core–mediated p53 target gene repression was absent in PML-ablated cells. HCV core expression abrogated both p53 serine 15 phosphorylation and lysine 382 acetylation, two p53-activating posttranslational modifications which were previously linked to an increased PML-NB formation. Taken together, our results suggest a potential mechanism for HCV-associated development of hepatocellular carcinoma through HCV core–mediated inactivation of the PML tumor suppressor pathway.
Dihydroartemisinin Is Cytotoxic to Papillomavirus-Expressing Epithelial Cells In vitro and In vivo
Authors: Disbrow Gary L. , Baege Astrid C. , Kierpiec Katie A. , Yuan Hang , Centeno Jose A. , Thibodeaux Clare A. , Hartmann Dan , Schlegel Richard 
Published: December 2005

Abstract
Nearly all cervical cancers are etiologically attributable to human papillomavirus (HPV) infection and pharmaceutical treatments targeting HPV-infected cells would be of great medical benefit. Because many neoplastic cells (including cervical cancer cells) overexpress the transferrin receptor to increase their iron uptake, we hypothesized that iron-dependent, antimalarial drugs such as artemisinin might prove useful in treating HPV-infected or transformed cells. We tested three different artemisinin compounds and found that dihydroartemisinin (DHA) and artesunate displayed strong cytotoxic effects on HPV-immortalized and transformed cervical cells in vitro with little effect on normal cervical epithelial cells. DHA-induced cell death involved activation of the mitochondrial caspase pathway with resultant apoptosis. Apoptosis was p53 independent and was not the consequence of drug-induced reductions in viral oncogene expression. Due to its selective cytotoxicity, hydrophobicity, and known ability to penetrate epithelial surfaces, we postulated that DHA might be useful for the topical treatment of mucosal papillomavirus lesions. To test this hypothesis, we applied DHA to the oral mucosa of dogs that had been challenged with the canine oral papillomavirus. Although applied only intermittently, DHA strongly inhibited viral-induced tumor formation. Interestingly, the DHA-treated, tumor-negative dogs developed antibodies against the viral L1 capsid protein, suggesting that DHA had inhibited tumor growth but not early rounds of papillomavirus replication. These findings indicate that DHA and other artemisinin derivatives may be useful for the topical treatment of epithelial papillomavirus lesions, including those that have progressed to the neoplastic state.