bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does antenatal identification of small‐for‐gestational age fetuses significantly improve their outcome?
Authors: Lindqvist P. G. , Molin J. 
Published: February 2005

AbstractObjectivesMost obstetric clinics have a program for the identification of small‐for‐gestational age (SGA) fetuses because of the increased risk of fetal complications that they present. We have a structured model for the identification and follow‐up of SGA pregnancies. We aimed to determine whether the recognition of SGA antepartum improves fetal outcome.MethodsAll pregnancies at Malmö University Hospital from 1990 to 1998 (n = 26 968) were reviewed. SGA fetuses identified prior to delivery (n = 681) were compared with those not identified (n = 573). Also, all pregnancies with SGA fetuses were compared with those appropriate‐for‐gestational age (AGA) (n = 24 585). The risk of serious fetal complications (hypoxic encephalopathy grade 2 or 3, intracranial hemorrhage, Apgar score <4 at 5 min, neonatal convulsions, umbilical pH <7.0, cerebral palsy, mental retardation, stillbirth, intrapartum or infant death) was assessed with cross‐tabulation and logistic regression analysis, adjusted for gestational age and degree of SGA.ResultsWhen compared with SGA fetuses identified before delivery (54%), SGA fetuses not identified before delivery were characterized by a four‐fold increased risk of adverse fetal outcome (odds ratio, 4.1; 95% CI, 2.5–6.8). Similarly, compared with AGA fetuses, SGA fetuses were associated with a four‐fold increased risk of serious fetal complications.ConclusionsA structured antenatal surveillance program for fetuses identified as SGA results in a lower risk of adverse fetal outcome, compared with cases of SGA fetuses not identified antepartum. Copyright © 2005 ISUOG. Published by John Wiley & Sons, Ltd.
Adjunctive use of reboxetine in schizophrenia
Authors: Raedler Thomas J. , Jahn Holger , Arlt Josef , Kiefer Falk , Schick Mildred , Naber Dieter , Wiedemann Klaus 
Published: February 2005

AbstractBackgroundSchizophrenia is frequently complicated by depressive or negative symptoms that respond only moderately to treatment with antipsychotic drugs. Reboxetine is a novel antidepressant, which inhibits the reuptake of norepinephrine. We sought to study the efficacy and tolerability of the adjunctive use of reboxetine in a cohort of schizophrenic patients with prominent depressive or negative symptoms.MethodsSixteen schizophrenic inpatients were recruited for this study. All subjects received 4–8 mg of reboxetine/day while the antipsychotic medication (typical antipsychotics = 4; atypical antipsychotics = 12) was continued. All subjects underwent a standardized assessment including PANSS, CGI, HAMD, and CDSS before and after treatment with reboxetine (mean 26 ± 17 d).ResultsAll subjects tolerated treatment with reboxetine. Adverse effects were mild and did not require discontinuation of reboxetine. All clinical scores (PANSS 93.1 vs. 63.1; CGI 5.4 vs. 4.1; HAMD 20.4 vs. 8.1; CDSS 12.5 vs. 4.6) improved significantly under adjunctive treatment with reboxetine (allP< 0.01).ConclusionThe adjunctive use of reboxetine in schizophrenic patients was safe and well-tolerated. Our results suggest that the adjunctive use of reboxetine may be an effective treatment for depressive and negative symptoms in schizophrenia.
The planning flexibility bottleneck in food processing industries
Authors: Van Wezel Wout , Van Donk Dirk Pieter , Gaalman Gerard 
Published: February 2005

AbstractProduction planners in food processing industries must continuously balance efficient production with flexible performance. On the basis of case studies, we state that flexibility is not only restrained by hard‐wired production process characteristics, but also by organizational procedures in the planning process. Planning practice in food processing industries is often not able to make the most of the available flexibility in the production processes, and our analysis shows that existing production planning approaches, ERP systems, and advanced planning systems can only partly resolve this. We propose a planning framework that can help to analyze the flexibility of the planning. The planning framework relates planning events to the way in which planning decisions are structured in the planning organization.
Replicative MCM7 protein as a proliferation marker in endometrial carcinoma: a tissue microarray and clinicopathological analysis
Authors: Li S S , Xue W C , Khoo U S , Ngan H Y S , Chan K Y K , Tam I Y S , Chiu P M , Ip P P C , Tam K F , Cheung A N Y 
Published: February 2005

Aims : To assess, in tissue microarray (TMA), the proliferative activity of endometrial carcinoma using one of the minichromosome maintenance (MCM) proteins (MCM7), and to explore its potential value for prognosis. MCM proteins are essential for eukaryotic DNA replication and have recently been used to define the proliferative compartments in human tissues.Methods and results : Immunohistochemistry for MCM7 and Ki67 was performed on TMAs constructed from 212 cases of endometrial carcinoma. MCM7 and Ki67 expression was quantified according to the extent of nuclear staining. An analysis was carried out of the association between MCM7 expression and that of Ki67 and the clinicopathological characteristics of endometrial carcinoma. MCM7 and Ki67 immunoreactivity was clearly evident in the nuclei of tumour cells. MCM7 and Ki67 labelling indices in endometrial carcinomas correlated with each other (P < 0.001). A significant correlation existed between the MCM7 labelling index and histological grade (P = 0.008) and patients' age at diagnosis (P < 0.001). Well‐differentiated carcinomas and younger patients had a lower MCM7 index. Poor survival was observed in patients with endometrial carcinoma with a high MCM7 index (P = 0.03) and MCM7 was found to be an independent prognostic factor by multivariate analysis (P = 0.04). The Ki67 labelling index correlated with histological grade (P = 0.01) but had no significant prognostic impact (P = 0.50).Conclusions : In this TMA study on endometrial carcinoma, MCM7 was found to be a more reliable and useful marker than Ki67 in assessing tumour proliferation and in the prognosis of patients.
The expression of p53 and bcl‐2 in gastrointestinal stromal tumours is associated with anatomical site, and p53 expression is associated with grade and clinical outcome
Authors: Feakins R M 
Published: February 2005

Aims : To compare the expression of p53 and bcl‐2 in gastrointestinal stromal tumours (GISTs) with anatomical site, National Institutes of Health (NIH) risk category (grade), pathological features, and clinical outcome.Methods and results : The immunohistochemical expression of p53 and bcl‐2 in 105 GISTs (71 gastric, 20 small intestinal, four colonic, 10 rectal) was recorded. When all GISTs were assessed, there was p53 positivity in 28% and bcl‐2 positivity in 77%. Gastric tumours had a lower prevalence of p53 positivity (20%) than intestinal (40–50%). Rectal GISTs had the lowest prevalence of bcl‐2 positivity (20%) and gastric and small intestinal the highest (80% and 90%, respectively). In GISTs from all sites, p53 positivity was associated with size > 50 mm, epithelioid cell shape, nuclear atypia, mucosal invasion, and mitotic count > 5/50 high‐power fields. In gastric GISTs the associations were the same, apart from size and mitotic count. In GISTs from all sites and in gastric GISTs, p53 expression correlated with NIH risk category. When GISTs from all sites were subjected to univariate survival analysis, an adverse outcome was associated with p53 positivity, NIH risk category, and several established prognostic factors. When gastric GISTs were assessed, the associations were similar although size was not prognostic. In multivariate survival analysis, p53 expression was independently prognostic for gastric GISTs in some models, while it was never independently prognostic for GISTs from all sites. Whether all GISTs or gastric GISTs were assessed, bcl‐2 showed no association with clinical outcome or risk category.Conclusions : Anatomical site influences p53 and bcl‐2 expression in GISTs. p53 expression is associated with NIH risk category, various pathological features, and clinical outcome, and may be independently prognostic for gastric GISTs. Bcl‐2 expression has no prognostic value.
Expression of S100 proteins in normal human tissues and common cancers using tissue microarrays: S100A6, S100A8, S100A9 and S100A11 are all overexpressed in common cancers
Authors: Cross S S , Hamdy F C , Deloulme J C , Rehman I 
Published: February 2005

Aims : To survey the expression of members of the S100 family of calcium‐binding proteins in normal human tissues and common cancers using tissue microarrays. S100A6, S100A8, S100A9 and S100A11 have all been suggested to have potential roles in carcinogenesis and tumour progression but their expression has not been described in a wide range of human tissues and tumours.Methods and results : A custom‐made tissue array, containing 291 tissue cores representing 28 tissue types and 21 tumour types, was used to produce sections that were immunostained for S100A2, S100A6, S100A8, S100A9, S100A11, calbindin 1, calbindin 2, S100B and parvalbumin. S100A6, S100A8 and S100A9 were expressed in 32%, 12% and 28% of breast cancers, respectively. There was a translocation of S100A11 expression from exclusively nuclear in normal tissues to cytoplasmic and nuclear in all common cancers.Conclusions : S100A6, S100A8, S100A9 and S100A11 are all expressed in common cancers, especially breast cancer. In addition, S100A11 undergoes a nucleocytoplasmic translocation which may have a direct influence on the proliferation of the cancer cells.
LAG‐3 (CD223) reduces macrophage and dendritic cell differentiation from monocyte precursors
Authors: Buisson Sandrine , Triebel Frédéric 
Published: February 2005

SummaryMajor histocompatibility complex (MHC) class II molecules expressed on monocytes may play a role in the control of differentiation of antigen‐presenting cells. A soluble LAG‐3 (CD223) molecule (sLAG‐3) is a natural, high‐affinity ligand for MHC class II. It is known to induce maturation of monocyte‐derived dendritic cells in vitro and is used as a vaccine adjuvant to induce CD4 T helper type 1 responses and CD8 T‐cell responses in vivo. Here, we demonstrate that sLAG‐3 (but not an MHC class II‐specific monoclonal antibody) reduces the differentiation of monocytes into macrophages in the presence of granulocyte–macrophage colony‐stimulating factor (GM‐CSF) as well as their differentiation into dendritic cells in the presence of GM‐CSF and interleukin‐4, as shown by a decrease in CD14 and CD1a expression, respectively. Dendritic cells derived from monocytes in the presence of sLAG‐3 showed impaired antigen‐presentation function, as assessed by the reduced capability to induce proliferation of T cells. Our results suggest that activated LAG‐3+ lymphocytes present at sites of inflammation may reduce the differentiation of monocytes into macrophages or fully competent antigen‐presenting dendritic cells, thus limiting the magnitude of the ongoing T‐cell immune responses.
Iron‐regulated transcription and capsule formation in the fungal pathogen Cryptococcus neoformans
Authors: Lian Tianshun , Simmer Megan I. , D’Souza Cletus A. , Steen Barbara R. , Zuyderduyn Scott D. , Jones Steven J. M. , Marra Marco A. , Kronstad James W. 
Published: February 2005

Summary Cryptococcus neoformans is the leading cause of fungal meningitis in humans. Production of a polysaccharide capsule is a key virulence property for the fungus and capsule synthesis is regulated by iron levels. Given that iron acquisition is an important aspect of virulence for many pathogens, we employed serial analysis of gene expression (SAGE) to examine the transcriptome under iron‐limiting and iron‐replete conditions. Initially, we demonstrated by SAGE and Northern analysis that iron limitation results in an elevated transcript level for the CAP60 gene that is required for capsule production. We also identified genes encoding putative components for iron transport and homeostasis, including the FTR1 (iron permease) gene, with higher transcript levels in the low‐iron condition. An FTR1 disruption mutant grows more slowly than wild‐type cells in low‐iron medium, and shows delayed growth and altered capsule regulation in iron‐replete medium. Iron deprivation also resulted in elevated SAGE tags for putative extracellular mannoproteins and the GPI8 gene encoding a glycosylphosphatidylinositol (GPI) transamidase. The GPI8 gene appears to be essential while disruption of the CIG1 gene encoding a mannoprotein resulted in impaired growth in low‐iron medium and altered capsule response to the iron‐replete condition. Additionally, we found that iron‐replete conditions led to elevated transcripts for genes for iron storage, nitrogen metabolism, glycolysis, mitochondrial function, lipid metabolism and calmodulin‐calcineurin signalling. Overall, these studies provide the first view of the C. neoformans transcriptional response to different iron levels.
Bacterial transcription elongation factors: new insights into molecular mechanism of action
Authors: Borukhov Sergei , Lee Jookyung , Laptenko Oleg 
Published: February 2005

SummaryLike transcription initiation, the elongation and termination stages of transcription cycle serve as important targets for regulatory factors in prokaryotic cells. In this review, we discuss the recent progress in structural and biochemical studies of three evolutionarily conserved elongation factors, GreA, NusA and Mfd. These factors affect RNA polymerase (RNAP) processivity by modulating transcription pausing, arrest, termination or anti‐termination. With structural information now available for RNAP and models of ternary elongation complexes, the interaction between these factors and RNAP can be modelled, and possible molecular mechanisms of their action can be inferred. The models suggest that these factors interact with RNAP at or near its three major, nucleic acid‐binding channels: Mfd near the upstream opening of the primary (DNA‐binding) channel, NusA in the vicinity of both the primary channel and the RNA exit channel, and GreA within the secondary (backtracked RNA‐binding) channel, and support the view that these channels are involved in the maintenance of RNAP processivity.
Identification of amino acid residues of the Agrobacterium tumefaciens quorum‐sensing regulator TraR that are critical for positive control of transcription
Authors: White Catharine E. , Winans Stephen C. 
Published: February 2005

SummaryThe LuxR‐type quorum‐sensing transcription factor TraR regulates replication and conjugal transfer of the tumour‐inducing (Ti) plasmid in the plant pathogen Agrobacterium tumefaciens. TraR is a two‐domain protein with an N‐terminal domain that binds to the quorum‐sensing signal N‐3‐oxooctanoyl‐ l‐homoserine lactone (OOHL) and a C‐terminal domain that binds to specific DNA sequences called tra boxes. TraR–OOHL complexes form homodimers that activate transcription of at least seven promoters on the Ti plasmid. At five promoters, a tra box overlaps the binding site of core RNA polymerase (class II promoters), while in the other two promoters, this site is located farther upstream (class I promoters). In this study, we performed saturating point mutagenesis of the surface residues of the TraR C‐terminal domain. Each mutant was tested for proteolytic stability and transcription activity in vivo, and for DNA binding activity in vitro. Mutants of TraR with single substitutions at positions W184, V187, K189, E193Q, V197 and D217 have wild‐type levels of accumulation and DNA binding, but are defective in transcription of both types of promoters. These residues constitute a patch on the surface of the DNA‐binding domain. We propose that this patch is an activating region that recruits RNA polymerase to TraR‐dependent promoters through direct contact. As residues of this patch are critical for activation at both a class I and a class II promoter, we predict that these residues may contact the C‐terminal domain of the RNA polymerase α‐subunit.
CcpN (YqzB), a novel regulator for CcpA‐independent catabolite repression of Bacillus subtilis gluconeogenic genes
Authors: Servant Pascale , Le Coq Dominique , Aymerich Stéphane 
Published: February 2005

SummaryIn Bacillus subtilis, the NADPH‐dependent glyceraldehyde‐3‐phosphate dehydrogenase (GapB) and the phosphoenolpyruvate carboxykinase (PckA) enzymes are necessary for efficient gluconeogenesis from Krebs cycle intermediates. gapB and pckA transcription is repressed in the presence of glucose but not via CcpA, the major transcriptional regulator for catabolite repression in B. subtilis. A B. subtilis mini‐Tn10 transposant library was screened for clones affected in catabolite repression of gapB. Inactivation of a previously unknown gene, yqzB (renamed ccpN for control catabolite protein of gluconeogenic genes), was found to relieve not only gapB but also pckA transcription from catabolite repression. Purified CcpN specifically bound to the gapB and pckA promoters. ccpN is co‐transcribed constitutively with another unknown gene, yqfL. A yqfL deletion lowers the level of gapB and pckA transcription threefold under both glycolytic and gluconeogenic conditions and a ccpN deletion is epistatic over a yqfL deletion. YqfL is thus a positive regulator of the expression of gapB and pckA, the effect of which is not influenced by the metabolic regime of the cell but appears to be mediated by CcpN. ccpN has homologues in many Firmicutes, but not all, while yqfL homologues are widely distributed in Eubacteria and also present in some plants. In all analysed bacterial genomes, ccpN and yqfL are physically linked together or to putative gluconeogenic genes. CcpN thus orchestrates a novel CcpA‐independent mechanism for catabolite repression of gluconeogenic genes highly conserved in Firmicutes and appears as a functional analogue of FruR in Enterobacteria. The physiological significance of the regulation mediated via the three B. subtilis global transcription regulators, CcpA, CggR and CcpN, is discussed.
Pseudomonas aeruginosa fimL regulates multiple virulence functions by intersecting with Vfr‐modulated pathways
Authors: Whitchurch Cynthia B. , Beatson Scott A. , Comolli James C. , Jakobsen Thania , Sargent Jennifer L. , Bertrand Jacob J. , West Joyce , Klausen Mikkel , Waite Leslie L. , Kang Pil Jung , Tolker‐Nielsen Tim , Mattick John S. , Engel Joanne N. 
Published: February 2005

SummaryVirulence of Pseudomonas aeruginosa involves the co‐ordinate expression of a range of factors including type IV pili (tfp), the type III secretion system (TTSS) and quorum sensing. Tfp are required for twitching motility, efficient biofilm formation, and for adhesion and type III secretion (TTS)‐mediated damage to mammalian cells. We describe a novel gene (fimL) that is required for tfp biogenesis and function, for TTS and for normal biofilm development in P. aeruginosa. The predicted product of fimL is homologous to the N‐terminal domain of ChpA, except that its putative histidine and threonine phosphotransfer sites have been replaced with glutamine. fimL mutants resemble vfr mutants in many aspects including increased autolysis, reduced levels of surface‐assembled tfp and diminished production of type III secreted effectors. Expression of vfr in trans can complement fimL mutants. vfr transcription and production is reduced in fimL mutants whereas cAMP levels are unaffected. Deletion and insertion mutants of fimL frequently revert to wild‐type phenotypes suggesting that an extragenic suppressor mutation is able to overcome the loss of fimL. vfr transcription and production, as well as cAMP levels, are elevated in these revertants, while Pseudomonas quinolone signal (PQS) production is reduced. These results suggest that the site(s) of spontaneous mutation is in a gene(s) which lies upstream of vfr transcription, cAMP, production, and PQS synthesis. Our studies indicate that Vfr and FimL are components of intersecting pathways that control twitching motility, TTSS and autolysis in P. aeruginosa.
Mapping binding residues in the Plasmodium vivax domain that binds Duffy antigen during red cell invasion
Authors: Hans Dhiraj , Pattnaik Priyabrata , Bhattacharyya Arindam , Shakri Ahmad Rushdi , Yazdani Syed Shams , Sharma Monal , Choe Hyeryun , Farzan Michael , Chitnis Chetan E. 
Published: February 2005

Summary Plasmodium vivax depends on interaction with the Duffy antigen/receptor for chemokines (DARC) for invasion of human erythrocytes. The 140 kDa P. vivax Duffy‐binding protein (PvDBP) mediates interaction with DARC. The receptor‐binding domain of PvDBP maps to its N‐terminal, cysteine‐rich region, region II (PvRII), which contains approximately 300 amino acid residues including 12 conserved cysteines. Using surface plasmon resonance, we show that binding of PvRII to DARC is a high‐affinity interaction with a binding constant (KD) of 8.7 nM. The minimal binding domain of PvRII has been previously mapped to a central 170‐amino‐acid stretch that includes cysteines 5–8. Here, we have used site‐directed mutagenesis and quantitative binding assays to map amino acid residues within PvRII that make contact with DARC. Of the seven alanine replacement mutations that had an effect on binding, five were mutations in hydrophobic residues suggesting that hydrophobic interactions play a major role in the interaction of PvDBP with DARC. Genetic diversity studies have shown that six of the seven binding residues identified in PvRII are conserved in P. vivax field isolates, which provides support for their role in interaction with DARC.
Carcinoembryonic antigen‐related cell adhesion molecule (CEACAM)‐binding recombinant polypeptide confers protection against infection by respiratory and urogenital pathogens
Authors: Hill Darryl J. , Edwards Andrew M. , Rowe Helen A. , Virji Mumtaz 
Published: February 2005

SummaryThe human‐specific pathogens Neisseria meningitidis, N. gonorrhoea, Haemophilus influenzae and Moraxella catarrhalis share the property of targeting the carcinoembryonic antigen (CEA)‐related cell adhesion molecules (CEACAMs) expressed on human epithelia. CEACAMs are signalling receptors implicated in cell adhesion and regulation of several physiological functions. Their targeting by pathogens can lead to tissue invasion. Although the CEACAM‐binding ligands of the bacteria are structurally diverse, they target a common site on the receptor. We have generated a recombinant polypeptide that blocks the interactions of the mucosal pathogens with human epithelial cells and antibodies against it inhibit M. catarrhalis interactions with the receptor. As such, it is a potential antimicrobial agent to prevent infection via a strategy unlikely to promote bacterial resistance and a vaccine candidate against M. catarrhalis. In addition, it could serve more widely as a novel research tool and as a potential therapeutic agent in CEACAM‐based physiological disorders.