bluuebunny/crossref_metadata_2025_split huggingface dataset:
Whole‐genome analyses of loss of heterozygosity and methylation analysis of four tumor‐suppressor genes in N‐methyl‐N′‐nitro‐N‐nitrosoguanidine‐induced rat stomach carcinomas
Authors: Niwa Tohru , Yamashita Satoshi , Tsukamoto Tetsuya , Kuramoto Takashi , Nomoto Tomoko , Wakazono Kuniko , Fujita Hirofumi , Matsushima Taijiro , Tatematsu Masae , Sugimura Takashi , Ushijima Toshikazu 
Published: July 2005

N‐Methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG)‐induced rat stomach carcinomas are considered to be a good model for differentiated‐type human stomach carcinomas. However, as for their molecular basis, only infrequent mutations of Catnb (β‐catenin) and Trp53 (p53) have been observed. Here, we carried out a whole‐genome analysis of loss of heterozygosity (LOH) using 21 stomach carcinomas induced by MNNG in F1 hybrids of ACI and BUF rats, and also analyzed promoter methylation of four tumor‐suppressor genes. LOH analysis was performed using 130 polymorphic markers covering rat chromosomes 1–20 with an average interval of 20 Mbp. Despite adapting conditions so that LOH could be detected with up to a 50% contamination of stromal cells, no LOH was detected at any loci. CpG islands in putative promoter regions of four tumor‐suppressor genes, Cdh1 (E‐cadherin), Cdkn2a (p16), Mlh1, and Rassf1a, were analyzed by methylation‐specific polymerase chain reaction (PCR). However, no methylation was detected. In contrast, the promoter region of Pgc (pepsinogen C), which lacks a CpG island, was methylated in all 21‐cancer samples. These results indicated that LOH spanning a chromosomal region larger than 30–40 Mbp or silencing of Cdh1, Cdkn2a, Mlh1, and Rassf1a, was not involved in MNNG‐induced rat stomach carcinomas. The search for other genes involved in these carcinomas needs to be continued. (Cancer Sci 2005; 96: 409  – 413)
Increased DNA methyltransferase 1 (DNMT1) protein expression in precancerous conditions and ductal carcinomas of the pancreas
Authors: Peng Dun‐Fa , Kanai Yae , Sawada Morio , Ushijima Saori , Hiraoka Nobuyoshi , Kosuge Tomoo , Hirohashi Setsuo 
Published: July 2005

Aberrant DNA methylation has been shown to play an important role during multistage carcinogenesis in various human organs. The aim of the present study was to evaluate the significance of DNA methyltransferase 1 (DNMT1) protein expression during pancreatic carcinogenesis. Immunohistochemical analysis of DNMT1 in 48 peripheral pancreatic duct epithelia showing no remarkable histological findings without an inflammatory background (DE), 54 peripheral pancreatic duct epithelia with an inflammatory background (DEI), 188 pancreatic intraepithelial neoplasias (PanIN), and 220 areas of invasive ductal carcinoma from surgical specimens resected from 100 patients, was carried out. The average incidence of DNMT1 immunoreactivity increased progressively from DE to DEI (P = 0.003), from DE and DEI to PanIN (P < 0.0001), among PanIN with different grades of dysplasia (from PanIN I to PanIN II, P = 0.0012), from PanIN to invasive ductal carcinomas (P < 0.0001) and among invasive ductal carcinomas with different grades of histological differentiation (from well or moderately to poorly differentiated adenocarcinomas, P < 0.0001). High‐level DNMT1 protein expression in invasive ductal carcinomas was correlated significantly with an advanced t category (P = 0.0224) and an advanced stage (P = 0.0294). Moreover, patients with invasive ductal carcinomas showing high‐level DNMT1 protein expression had a poorer outcome (P = 0.0469). These data suggest that increased DNMT1 protein expression participates in multistage pancreatic carcinogenesis from the precancerous stage to malignant progression of ductal carcinomas and may be a biological predictor of poor prognosis. (Cancer Sci 2005; 96: 403–408)
Trends in the prevalence of peptic ulcer disease and Helicobacter pylori infection in family physician‐referred uninvestigated dyspeptic patients in Hong Kong
Authors: XIA B. , XIA H. H. X. , MA C. W. , WONG K. W. , FUNG F. M. Y. , HUI C. K. , CHAN C. K. , CHAN A. O. O. , LAI K. C. , YUEN M. F. , WONG B. C. Y. 
Published: July 2005

SummaryBackground:  Peptic ulcer disease is mainly caused by Helicobacter pylori infection and the use of non‐steroidal anti‐inflammatory drugs.Aim:  To investigate the trends in the prevalence of peptic ulcer disease, H. pylori infection and non‐steroidal anti‐inflammatory drug use in uninvestigated dyspeptic patients over recent years in Hong Kong.Methods:  Data from consecutive patients with uninvestigated dyspeptic symptoms referred by family physicians for open access upper endoscopy during 1997 and 2003 were analysed in relation to peptic ulcer disease, H. pylori infection and non‐steroidal anti‐inflammatory drug use.Results:  Among 2700 patients included, 405 (15%) had peptic ulcer disease and 14 (0.5%) had gastric cancer. There was a reduced trend from 1997 to 2003 in the prevalence of peptic ulcer disease (17, 20, 14, 16, 13, 14 and 14%, respectively, χ2 = 5.80, P = 0.016) (mainly because of decrease in duodenal ulcers), H. pylori infection (44, 50, 49, 44, 40, 40, 36 and 43%, respectively, χ2 = 13.55, P < 0.001) and non‐steroidal anti‐inflammatory drug use (13, 5, 5, 6, 3, 4, 4 and 5% respectively, χ2 = 13.61, P < 0.001). The prevalence of peptic ulcer disease, H. pylori infection and non‐steroidal anti‐inflammatory drug use between 2001 and 2003 were significantly lower than that between 1997 and 2000 (17% vs. 13%, OR = 0.78, 95% CI: 0.63–0.96, P = 0.020 for peptic ulcer disease; 47% vs. 39%, OR =0.72, 95% CI: 0.60–0.86, P < 0.001 for H. pylori infection; and 6% vs. 4%, OR = 0.56, 95% CI: 0.39–0.82, P = 0.002 for non‐steroidal anti‐inflammatory drug use). H. pylori infection was associated with both duodenal ulcer (OR = 15.87, 95% CI: 10.60–23.76, P < 0.001) and gastric ulcer (OR = 3.12, 95% CI: 2.15–4.53, P < 0.001) whereas non‐steroidal anti‐inflammatory drug use was only associated with gastric ulcer (OR = 2.97, 95% CI: 1.70–5.20, P < 0.001).Conclusions:  The prevalence of peptic ulcer disease, mainly duodenal ulcers, was reduced in association with a decreasing trend in the prevalence of H. pylori infection and non‐steroidal anti‐inflammatory drug use from 1997 to 2003.
Inhibition of infectious haematopoietic necrosis virus in cell cultures with peptide‐conjugated morpholino oligomers
Authors: Alonso M , Stein D A , Thomann E , Moulton H M , Leong J C , Iversen P , Mourich D V 
Published: July 2005

AbstractDelivery of phosphorodiamidate morpholino oligomers (PMO) into fish cells in vitro and tissues in vivo was examined. Uptake was evaluated by fluorescence microscopy and flow cytometry after treating cultured cells or live rainbow trout with 3′ fluorescein‐tagged PMO. Arginine‐rich peptide conjugated to the 5′ end of the PMO markedly enhanced cellular uptake in culture by 8‐ to 20‐fold compared with non‐peptide‐conjugated PMO as determined by flow cytometry. Enhanced uptake of PMO conjugated to peptide was also observed in tissues of fish treated by immersion. The efficacy of PMO as inhibitors of infectious haematopoietic necrosis virus (IHNV) replication was determined in vitro. Peptide‐conjugated PMOs targeting sequences within the IHNV genomic RNA (negative polarity) or antigenomic RNA (positive polarity) significantly inhibited replication in a dose‐dependent and sequence‐specific manner. A PMO complementary to sequence near the 5′ end of IHNV genomic RNA was the most effective, diminishing titre by 97%, as measured by plaque assay and Western blot. These data demonstrate that replication of a negative‐stranded non‐segmented RNA virus can be inhibited by antisense compounds that target positive polarity viral RNA, or by a compound that targets negative polarity viral RNA.
Facilitated diffusion in chromatin lattices: mechanistic diversity and regulatory potential
Authors: Kampmann Martin 
Published: July 2005

SummaryThe interaction between a protein and a specific DNA site is the molecular basis for vital processes in all organisms. Location of the DNA target site by the protein commonly involves facilitated diffusion. Mechanisms of facilitated diffusion vary among proteins; they include one‐ and two‐dimensional sliding along DNA, direct transfer between uncorrelated sites, as well as combinations of these mechanisms. Facilitated diffusion has almost exclusively been studied in vitro. This review discusses facilitated diffusion in the context of the living cell and proposes a theoretical model for facilitated diffusion in chromatin lattices. Chromatin structure differentially affects proteins in different modes of diffusion. The interplay of facilitated diffusion and chromatin structure can determine the rate of protein association with the target site, the frequency of association–dissociation events at the target site, and, under particular conditions, the occupancy of the target site. Facilitated diffusion is required in vivo for efficient DNA repair and bacteriophage restriction and has potential roles in fine‐tuning gene regulatory networks and kinetically compartmentalizing the eukaryotic nucleus.
Mutagenesis of PepA suggests a new model for the Xer/cer synaptic complex
Authors: Reijns Martin , Lu Yangjie , Leach Stephen , Colloms Sean D. 
Published: July 2005

SummaryPepA is an aminopeptidase and also functions as a DNA‐binding protein in two unrelated systems in Escherichia coli: Xer site‐specific recombination and transcriptional regulation of carAB. In these systems, PepA binds to and brings together distant segments of DNA to form interwrapped, nucleosome‐like structures. Here we report the selection of PepA mutants that were unable to support efficient Xer recombination. These mutants were defective in DNA‐binding and in transcriptional regulation of carAB, but had normal peptidase activity. The mutations define extended patches of basic residues on the surface of the N‐terminal domain of PepA that flank a previously proposed DNA‐binding groove in the C‐terminal domain of PepA. Our results suggest that DNA passes through this C‐terminal groove in the PepA hexamer, and is bound by N‐terminal DNA‐binding determinants at each end of the groove. Based on our data, we propose a new model for the Xer synaptic complex, in which two recombination sites are wrapped around a single hexamer of PepA, bringing the cross‐over sites together for strand exchange by the Xer recombinases. In this model, PepA stabilizes negative plectonemic interwrapping between two segments of DNA by passing one segment through the C‐terminal groove while the other is held in place in a loop over the groove.
Selection and characterization of Yersinia pestis YopN mutants that constitutively block Yop secretion
Authors: Ferracci Franco , Schubot Florian D. , Waugh David S. , Plano Gregory V. 
Published: July 2005

SummarySecretion of Yop effector proteins by the Yersinia pestis plasmid pCD1‐encoded type III secretion system (T3SS) is regulated in response to specific environmental signals. Yop secretion is activated by contact with a eukaryotic cell or by growth at 37°C in the absence of calcium. The secreted YopN protein, the SycN/YscB chaperone and TyeA form a cytosolic YopN/SycN/YscB/TyeA complex that is required to prevent Yop secretion in the presence of calcium and prior to contact with a eukaryotic cell. The mechanism by which these proteins prevent secretion and the subcellular location where the block in secretion occurs are not known. To further investigate both the mechanism and location of the YopN‐dependent block, we isolated and characterized several YopN mutants that constitutively block Yop secretion. All the identified amino‐acid substitutions that resulted in a constitutive block in Yop secretion mapped to a central domain of YopN that is not directly involved in the interaction with the SycN/YscB chaperone or TyeA. The YopN mutants required an intact TyeA‐binding domain and TyeA to block secretion, but did not require an N‐terminal secretion signal, an intact chaperone‐binding domain or the SycN/YscB chaperone. These results suggest that a C‐terminal domain of YopN complexed with TyeA blocks Yop secretion from a cytosolic, not an extracellular, location. A hypothetical model for how the YopN/SycN/YscB/TyeA complex regulates Yop secretion is presented.
Involvement of SRD2‐mediated activation of snRNA transcription in the control of cell proliferation competence in Arabidopsis
Authors: Ohtani Misato , Sugiyama Munetaka 
Published: July 2005

SummaryThe transcription machinery of small nuclear RNA (snRNA) genes has been investigated extensively in human cell‐free systems, but its physiological function in vivo has not been addressed. This paper demonstrates the physiological role of an activator of snRNA transcription using a temperature‐sensitive mutant of Arabidopsis thaliana, srd2. Phenotypic characteristics of the srd2 mutant suggest that the SRD2 gene participates in the control of competence in cell proliferation. The SRD2 gene encodes a nuclear protein that shares sequence similarity with the human SNAP50 protein, which is a subunit of SNAPc and is required for snRNA transcription in vitro. Our results, obtained from analysis of snRNA expression in the srd2 mutant, indicate that the SRD2 protein functions in the upregulation of transcription of snRNA genes, the promoters of which contain the upstream sequence element, to elevate cell proliferation competence.
Light and plastid signals regulate the expression of the pea plastocyanin gene through a common region at the 5′ end of the coding region
Authors: Brown Naomi J. , Sullivan James A. , Gray John C. 
Published: July 2005

SummaryExpression of the pea plastocyanin gene (PetE) is regulated by light and plastid signals. Previous work indicated that light and plastid regulation of pea PetE operates post‐transcriptionally in transgenic tobacco, and requires the correct 5′ terminus of the PetE transcript and the PetE‐coding region. The post‐transcriptional light and plastid regulation of pea PetE has now been demonstrated to operate in transgenic Arabidopsis, where in contrast the endogenous PETE gene is regulated transcriptionally. Transgenic tobacco seedlings containing constructs with progressive 3′ deletions of the PetE‐coding region fused to the luciferase (Luc) reporter gene demonstrate that the first 60 nucleotides of the coding region are sufficient for regulated accumulation of Luc transcripts by light and plastid signalling pathways affected by treatment with norflurazon and lincomycin. PetE constructs containing premature stop codons were generated to investigate whether translation has a role in light or plastid regulation. Insertion of a stop codon in place of the second codon of the PetE‐coding region diminished both light and plastid regulation of PetE transcripts, whereas stop codons inserted later in the transcript had no effect on light or plastid regulation. These experiments indicate that the 5′ end of the plastocyanin‐coding region contains sequences important for regulation by light and plastid signals.
Validation of basophil histamine release against the autologous serum skin test and outcome of serum‐induced basophil histamine release studies in a large population of chronic urticaria patients
Authors: Platzer M. H. , Grattan C. E. H. , Poulsen L. K. , Skov P. S. 
Published: August 2005

Background:  Endogenous histamine‐releasing factors (HRFs) are involved in 30–60% of patients with chronic urticaria (CU). Evidence for their existence comes from in vivo studies of autoreactivity with the autologous serum skin test (ASST), in vitro immunoassays demonstrating autoantibodies against the immunoglobulin E (IgE) or the high affinity IgE receptor (FcɛRI) and serum‐induced histamine release (HR) from basophils and mast cells. We have examined the correlation between the ASST and a new basophil histamine‐releasing assay (the HR‐Urtikaria test) in a group of well‐characterized CU patients and subsequently determined the frequency of HR‐Urticaria‐positive sera from a larger population of CU patients.Subjects:  Group 1 consisted of 28 patients with CU (16 were ASST‐positive) 20 patients with atopic dermatitis, 24 patients with allergy to birch and nine healthy controls. Group 2 consisted of 873 unselected CU patients.Methods:  White blood cells containing 1–2% basophils from a healthy nonatopic donor were incubated with patients sera in the presence of interleukin (IL)‐3. Histamine was measured by the glass fibre method.Results:  Using the ASST as the true outcome, the HR‐Urticaria test showed a sensitivity and specificity of 75% in group 1 using a cut‐off value for HR of >16.5%. None of the controls was positive in the HR‐Urticaria test. In group 2, we found no difference in the frequency of positives between male (34.6%, n = 254) and female adults (35.1%, n = 576) but twice as many females as males were tested.Conclusions:  Our studies have shown that the HR‐Urticaria test has a good sensitivity and specificity for endogenous HRFs demonstrated by the ASST in patients with CU and that about one‐third of unselected patients with CU have a positive result.
Prevalence of food allergy and its relationship to asthma and allergic rhinitis in schoolchildren
Authors: Pénard‐Morand C. , Raherison C. , Kopferschmitt C. , Caillaud D. , Lavaud F. , Charpin D. , Bousquet J. , Annesi‐Maesano I. 
Published: August 2005

Background:  Food allergy (FA) is an important health problem. However, epidemiological studies at the population level are scarce. We assessed the prevalence of FA and its associations with respiratory manifestations among schoolchildren.Methods:  A total of 6672 schoolchildren aged 9–11 years recruited from 108 randomly chosen schools in six French cities underwent a clinical examination including skin prick test (SPT) to common food and aeroallergens and the standardized protocol of the run test to assess exercise‐induced bronchial hyper‐responsiveness (EIB). Asthma, allergic rhinitis (AR) and clinical symptoms of FA were determined using a standardized questionnaire completed by parents.Results:  About 2.1% of the children reported symptoms of FA, 1.9% were sensitized to food allergens, and 0.1% had SP‐tested FA. The AR was more prevalent than asthma (20.0% lifetime, 11.9% past year vs 9.8%, 8.7% respectively). Reported FA, food sensitization and SP‐tested FA were all positively associated with asthma and AR (P < 0.001). These associations persisted also for FA not manifesting as respiratory symptoms (P < 0.001). Asthma and AR remained significantly associated with reported symptoms of FA and allergic sensitization to food allergens after adjustment for confounders as well as for sensitization to aeroallergens. No relationship existed between EIB (9.0%) and FA.Conclusion:  The relationships between FA and asthma and AR could be totally explained neither by the existence of respiratory manifestations of FA nor by sensitization to aeroallergens. The FA might intervene differently in asthma and AR.
Identification and characterization of quantitative trait loci related to lodging resistance and associated traits in bread wheat
Authors: Verma V. , Worland A. J. , Savers E. J. , Fish L. , Caligari P. D. S. , Snape J. W. 
Published: July 2005

AbstractLodging is a major constraint to increasing yield in many crops, but is of particular importance in the small‐grained cereals. This study investigated the genetic control of lodging and component traits in wheat through the detection of underlying quantitative trait loci (QTL), The analysis was based on the identification of genomic regions which affect various traits related to lodging resistance in a population of 96‐doubled haploid lines of the cross ‘Milan’×‘Catbird’, mapped using 126‐microsatellite markers. Although major genes related to plant height (Rht genes) were responsible for increasing lodging resistance in this cross, several other traits independent of plant height were shown to be important such as fool and shoot traits, and various components of plant yield. Yield components such as grain number and weight were shown to be an indicator of plant susceptibility to lodging. QTL for lodging and associated traits were found on chromosomes IB, ID. 2B. 2D. 4B, 4D. 6D and 7D. QTL for yield and associated traits were identified on chromosomes IB, ID. 2A. 2B. 2D. 4D and 6A,
Backcross breeding for improved resistance to common bacterial blight in pinto bean (Phaseolus vulgaris L.)
Authors: Mutlu N. , Miklas P. , Reiser J. , Coyne D. 
Published: July 2005

AbstractCommon bacterial blight (CBB) caused by Xanthomonas campestris pv. phaseoli reduces common bean (Phaseolus vulgaris L.) yield and quality worldwide. Genetic resistance provides effective disease control; however. a high level of resistance is difficult to attain and does not exist in pinto bean, the most important dry bean market class in North America. Our objective was to determine if a backcross breeding approach with the aid of molecular markers linked to quantitative trait loci (QTL) for resistance to CBB in a donor parent could be used to attain higher levels of resistance to CBB in pinto bean. QTL conditioning CBB resistance from the donor parent XAN 159 were introgressed into the recurrent parent‘Chase’using classical backcross breeding and intermittent marker‐assisted selection.‘Chase’pinto bean is moderately resistant and the breeding line XAN 159 is highly resistant to Xanthomonas campestris. Marker assays confirmed the presence of independent QTL from GN no. 1 Sel 27 and XAN 159 in advanced backcross‐derived pinto bean lines with improved CBB resistance. Agronomic characteristics of‘Chase’were fully recovered in the backcross‐derived lines. An important QTL for CBB resistance from XAN 159 on linkage group B6 was not introgressed because tight linkage between this QTL and the dominant V allele that causes an unacceptable black‐mottled seed coat colour pattern in pinto bean could not be broken.
Mapping antixenosis genes on chromosome 6A of wheat to greenbug and to a new biotype of Russian wheat aphid
Authors: Castro A. M. , Vasicek A. , Manifiesto M. , Giménez D. O. , Tacaliti M. S. , Dobrovolskaya O. , Röder M. S. , Snape J. W. , Börner A. 
Published: July 2005

AbstractGreenbug and Russian wheat aphid (RWA) are two devastating pests of wheat. The first has a long history of new biotype emergence and recently. RWA resistance has just started to break down. Thus, it is necessary to find new sources of resistance that will broaden the genetic base against these pests in wheat. Seventy‐five doubled haploid recombinant (DHR) lines for chromosome 6A from the F1 of the cross between “Chinese Spring’ and the “Chinese Spring (Synthetic 6A) (Triticum dicoccoides × Aegilops tauschii)” substitution line were used as a mapping population for testing resistance to greenbug biotype C and to a new strain of RWA that appeared in Argentina in 2003. A quantitative trait locus (QTL) (br antixenosis to greenbug was significantly associated with the marker loci Xgwm1009 and Xgwm1185 located in the centromere region of chromosome 6A. Another QTL which accounted for most of the antixenosis against RWA was associated with the marker loci Xgwm1291 and Xiinni1150. both located on the long arm of chromosome 6A. This is the first report of greenbug and RWA resistance genes located on chromosome 6A. It is also the first report of antixenosis against the new strain of RWA. As most of the RWA resistance genes present in released cultivars have been located in [he D‐genome, it is highly desirable to find new sources in other genomes to combine the existing resistance genes with new sources.