bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinicopathologic Profile of Benign Breast Conditions in Indian Women: Prospective Study Based on Aberrations of Normal Development and Involution Classification
Authors: Kaur Navneet , Agarwal Nitin , Panwar Pankaj , Mishra Kiran 
Published: June 2012

AbstractBackgroundBenign conditions of the breast are common, but a great deal of confusion exists in their nomenclature, classification, and, treatment protocols. The Aberration of Normal Development and Involution (ANDI) classification provides a comprehensive framework within which to correlate clinical presentation with pathogenesis. Most clinical studies have not used this classification system. We studied the spectrum of benign breast conditions in Indian patients with reference to the ANDI system and performed a clinicopathologic correlation.MethodsThis prospective study was carried out on 262 consecutive patients attending the surgery department on an outpatient basis for benign breast conditions.ResultsA total of 199 (76 %) patients had a diagnosis of benign breast disorder, and 44 (17 %) had benign breast disease. There were 19 (7 %) women with non‐ANDI and other conditions. The spectrum of benign breast disorders included fibroadenoma 77, mastalgia with nodularity 98, galactocele 7, cysts 4, and nipple discharge (ND) 13. Benign breast diseases included giant/multiple fibroadenomas 18, incapacitating mastalgia and nodularity 13, subareolar abscess with mammary fistula 7, periductal mastitis with suppuration 4, and ND 2. Cytopathologic correlation performed in 115 patients showed nonproliferative disease in 82, proliferative disease without atypia in 19, proliferative disease with atypia in 3, and miscellaneous 11.ConclusionsThe ANDI classification is a comprehensive system that delineates the borderline between normal and abnormal, achieves correlation of clinical signs and symptoms with histologic changes, and provides risk stratification and pragmatic definition of management protocols.
Impact of Posttransplant Portosystemic Shunts on Liver Transplantation
Authors: Sanada Yukihiro , Mizuta Koichi , Urahashi Taizen , Wakiya Taiichi , Ihara Yoshiyuki , Okada Noriki , Yamada Naoya , Nakata Manabu , Yasuda Yoshikazu 
Published: June 2012

AbstractBackgroundPosttransplant portosystemic shunts may result in severe fatty changes, portal vein complications, or graft liver failure because they reduce the effectiveness of portal perfusion through a portal steal phenomenon. However, the indications and timing of surgical and interventional treatments for posttransplant portosystemic shunts are still a matter of debate. We performed a retrospective investigation of the present state of long‐term outpatients with posttransplant portosystemic shunts.MethodsThis study comprised 150 outpatients who underwent liver transplantation between October 1988 and August 2006 in our department and other facilities. The diagnosis was based on the presence of any portosystemic shunts with the diameter of more than 5 mm indicated by computed tomography.ResultsA total of 16 patients (16/150, 10.7 %) were diagnosed as having posttransplant portosystemic shunt. Among them, eight patients (8/16, 50.0 %) developed portal vein complications, and 1 (1/16, 6.3 %) developed graft liver failure.ConclusionsThe persistence of posttransplant portosystemic shunts results in portal vein complications or graft liver failure. Therefore, surgical and interventional treatment for patients with posttransplant portosystemic shunts should be performed based on the clinical and radiologic findings.
MicroRNA 17–92 expressed by a transposone‐based vector changes expression level of cell‐cycle‐related genes
Authors: Attar Marzieh , Arefian Ehsan , Nabiuni Mohammad , Adegani Fatemeh Jamshidi , Bakhtiari Seyed Hamid Aghaee , Karimi Zahra , Barzegar Mansoureh , Soleimani Masoud 
Published: June 2012

AbstractThe miR‐17‐92 cluster is composed of seven miRNAs (microRNAs; miR‐17‐5p, miR‐17‐3p, miR‐18a, miR‐19a, miR‐20a, miR‐19b‐1 and miR‐92a‐1). Previous studies have indicated that this cluster is involved in cell proliferation and their overexpression has been seen in several types of cancer. We have assessed the overexpression effects of miR‐17‐92 on the expression of several genes associated with cell‐cycle regulation. The human miR‐17‐92 gene was cloned into a transposone‐based vector, piggyBac and transfected into HEK‐293T [HEK‐293 cells (human embryonic kidney cells) expressing the large T‐antigen of SV40 (simian virus 40)] cell line. Gene expression analysis indicated that up‐regulation of this cluster causes significant changes in the expression of several cell‐cycle related genes, including CDK2 (cyclin‐dependent kinase 2), cyclin‐D2, c‐Myc and CREB (cAMP‐response‐element‐binding protein). Other methods of transcripts assessment confirmed miR‐17‐92 overexpression enhances cell proliferation.
PDGFRβ triggered by bFGF promotes the proliferation and migration of endothelial progenitor cells via p‐ERK signalling
Authors: Guo Sufen , Yu Libo , Cheng Yongxia , Li Caijuan , Zhang Jifei , An Jindan , Wang Hongwei , Yan Bin , Zhan Tao , Cao Yong , Zheng Huizhe , Li Zhiqiang 
Published: June 2012

AbstractWe have examined the effects of bFGF (basic fibroblast growth factor) on p‐ERK (phosphorylated extracellular signal‐regulated kinase) through PDGFRβ (platelet‐derived growth factor receptor β) in the proliferation and migration of EPCs (endothelial progenitor cells). EPC migration was detected using the Transwell system. The expression of PDGFRβ mRNA and protein, total ERK and p‐ERK proteins was respectively assessed by real‐time PCR and Western blottings. bFGF promote the proliferation and migration of EPCs, the effects of bFGF being implemented by activating ERK signalling through the expression of PDGFRβ, whereas an anti‐bFGF antibody and inhibitor of PDGF (platelet‐derived growth factor) receptor kinase (AG1296) could respectively decrease the expression of PDGFRβ mRNA and protein and p‐ERK protein. Total ERK protein did not change under the same experimental conditions, and an inhibitor of p‐ERK (PD98059) inhibited the proliferation and migration of EPCs. The findings strongly suggest that a PDGFRβ/p‐ERK signalling pathway triggered by bFGF plays an important role in the proliferation and migration of EPCs.
Surfactant effects of gallium on quality of AlN epilayers grown via metal-organic chemical-vapour deposition on SiC substrates
Authors: Al tahtamouni T M , Li J , Lin J Y , Jiang H X 
Published: June 2012

Abstract
Effects of gallium as a surfactant for the growth of AlN epilayers on SiC substrates by metal-organic chemical-vapour deposition have been studied. It was found that the use of gallium as a surfactant enables the growth of thick, crack-free AlN epilayers on SiC substrates. The photoluminescence and x-ray diffraction (XRD) analysis show that gallium surfactant can reduce some of the tensile strain in AlN epilayers and it improves the surface smoothness. XRD rocking curves yielded decreased full widths at half maximum for the (1 0 5) and (0 0 2) reflections, indicating a reduction in threading dislocation density in the AlN epilayers.
Study of dc micro-discharge arrays made in silicon using CMOS compatible technology
Authors: Kulsreshath M K , Schwaederle L , Overzet L J , Lefaucheux P , Ladroue J , Tillocher T , Aubry O , Woytasik M , Schelcher G , Dussart R 
Published: June 2012

Abstract
In this paper we present the fabrication technology used to make micro-discharge ‘reactors’ on a silicon (Si) substrate. For the fabrication of these reactors we have used Si wafers with 4 inch diameter and standard cleanroom facilities. The fabrication technology used is compatible with standard CMOS device fabrication and the fabricated micro-discharge reactors can be used to produce dc discharges. These micro-discharges operate at near atmospheric pressure. They were given ring-shaped anodes separated from the cathode by a SiO2 dielectric with a thickness of approximately 5–6 µm rather than the much more common ∼100 µm. The micro-discharge reactors can consist of either a single hole or multiple holes and we have built devices with holes from 25 to 150 µm in diameter. The micro-discharge measurements were obtained for helium and argon dc plasmas between 100 and 1000 Torr. We used a single ballast resistor to produce micro-discharges in multi-hole array. This resistor also acted to limit the discharge power. An average current density of 0.8 A cm−2 was calculated for the 1024 holes array with 100 µm diameter holes. In addition, we will report on stability of micro-discharges depending on the cavity configuration of the micro-reactors and the ignition trends for the micro-discharge arrays. Finally, we discuss the life time of micro-discharge arrays as well as the factors affecting them (cathode sputtering, thermally affected zones, etc).
The effect of metformin on insulin resistance and exercise parameters in patients with heart failure
Authors: Wong Aaron K.F. , Symon Ruth , AlZadjali Matlooba A. , Ang Donald S.C. , Ogston Simon , Choy AnnaMaria , Petrie John R. , Struthers Allan D. , Lang Chim C. 
Published: June 2012

AimsChronic heart failure (CHF) is an insulin‐resistant state. The degree of insulin resistance (IR) correlates with disease severity and is associated with reduced exercise capacity. In this proof of concept study, we have examined the effect of metformin on IR and exercise capacity in non‐diabetic CHF patients identified to have IR.Methods and resultsIn a double‐blind, placebo‐controlled study, 62 non‐diabetic IR CHF patients (mean age, 65.2 ± 8.0 years; male, 90%; left ventricular ejection fraction, 32.6 ± 8.3%; New York Heart Association class I/II/III/IV, 11/45/6/0) were randomized to receive either 4 months of metformin (n = 39, 2 g/day) or matching placebo (n = 23). IR was defined by a fasting insulin resistance index (FIRI) ≥2.7. Cardiopulmonary exercise testing and FIRI were assessed at baseline and after 4 months of intervention. Compared with placebo, metformin decreased FIRI (from 5.8 ± 3.8 to 4.0 ± 2.5, P < 0.001) and resulted in a weight loss of 1.9 kg (P < 0.001). The primary endpoint of the study, peak oxygen uptake (VO2), did not differ between treatment groups. However, metformin improved the secondary endpoint of the slope of the ratio of minute ventilation to carbon dioxide production (VE/VCO2 slope), from 32.9 ± 15.9 to 28.1 ± 8.8 (P = 0.034). In the metformin‐treated group, FIRI was significantly related to the reduction of the VE/VCO2 slope (R = 0.41, P = 0.036).ConclusionMetformin treatment significantly improved IR but had no effect on peak VO2, the primary endpoint of our study. However, metformin treatment did result in a significant improvement in VE/VCO2 slope. Trial registration: NCT00473876.
Prognostic impact of Raf‐1 and p‐Raf‐1 expressions for poor survival rate in non‐small cell lung cancer
Authors: Qiu Zhi‐Xin , Wang Lei , Han Juan , Liu Dan , Huang Wei , Altaf Kiran , Qiu Xue‐Song , Javed Muhammad A. , Zheng Jing , Chen Bo‐Jiang , Li Wei‐Min 
Published: June 2012

Overexpression of Raf‐1 has commonly been observed in solid tumors including non‐small cell lung cancer (NSCLC). The objective of this study was to investigate whether overexpression of Raf‐1, phosphorylated‐Raf‐1 (p‐Raf‐1) or both correlates with poor survival rate in NSCLC patients and to explore associations between expression of these proteins and NSCLC cell fate both in vitro and in vivo. Expression of Raf‐1 and p‐Raf‐1 were detected by immunohistochemistry in tumor specimens from 152 NSCLC patients and associations between their expression and the clinicopathological characteristics were assessed. Five‐year median survival rate of patients were analyzed by Kaplan–Meier method, log‐rank test and Cox regression. Cell fate was compared between normal tumor cells and those with Raf‐1 silencing, in both the adenocarcinoma cell line A549 and xenografted mice that were infected with the A549 cell line. The incidence of overexpression of both Raf‐1 and p‐Raf‐1 in NSCLC was much higher than normal control (P < 0.05), and the survival rate of patients with positive expression of Raf‐1, p‐Raf‐1 or both was found to be significantly lower than the negative group (P < 0.05). Both univariate and multivariate analyses showed Raf‐1 (P = 0.000, P = 0.010), p‐Raf‐1 (P = 0.004, P = 0.046), or both (P = 0.001, P = 0.016) was good prognostic markers for poor survival rate in NSCLC patients. Suppression of Raf‐1 inhibited tumorigenesis by inducing apoptosis both in vitro and in vivo. These findings demonstrate that overexpression of Raf‐1, p‐Raf‐1 or both could be considered as a new independent prognostic biomarker for poor survival rates for NSCLC patients.
HrpM is involved in glucan biosynthesis, biofilm formation and pathogenicity in Xanthomonas citri ssp. citri
Authors: Malamud Florencia , Conforte Valeria P. , Rigano Luciano A. , Castagnaro Atilio P. , Marano María Rosa , Morais do Amaral Alexandre , Vojnov Adrian A. 
Published: June 2012

SummaryXanthomonas citri ssp. citri (Xcc) is the causal agent of citrus canker. This bacterium develops a characteristic biofilm on both biotic and abiotic surfaces. A biofilm‐deficient mutant was identified in a screening of a transposon mutagenesis library of the Xcc 306 strain constructed using the commercial Tn5 transposon EZ‐Tn5 <KAN‐2> Tnp Transposome (Epicentre). Sequence analysis of a mutant obtained in the screening revealed that a single copy of the EZ‐Tn5 was inserted at position 446 of hrpM, a gene encoding a putative enzyme involved in glucan synthesis. We demonstrate for the first time that the product encoded by the hrpM gene is involved in β‐1,2‐glucan synthesis in Xcc. A mutation in hrpM resulted in no disease symptoms after 4 weeks of inoculation in lemon and grapefruit plants. The mutant also showed reduced ability to swim in soft agar and decreased resistance to H
2
O
2 in comparison with the wild‐type strain. All defective phenotypes were restored to wild‐type levels by complementation with the plasmid pBBR1‐MCS containing an intact copy of the hrpM gene and its promoter. These results indicate that the hrpM gene contributes to Xcc growth and adaptation in its host plant.
Some ways to improve QTL mapping accuracy
Authors: Korol Abraham , Frenkel Zeev , Orion Ori , Ronin Yefim 
Published: June 2012

SummaryIn this paper, we review some approaches for QTL mapping developed by our research group in collaboration with, following the recommendation of, or under inspiration of Moshe Soller. Specifically, we explain at a simple intuitive level the main principles and ideas of: (a) QTL mapping by fractioned DNA pooling, (b) increasing the detection power of QTL mapping (in the case of individual genotyping) by multiple‐trait analysis, and (c) the role of variance–covariance effects in QTL mapping. On each of these themes we had long and deep discussions with Soller on the statistical aspects of the proposed procedures. We hope that together we made important contributions towards making QTL mapping procedures easier and more effective.
Genetic parameters for paratuberculosis infection and effect of infection on production traits inIsraeliHolsteins
Authors: Shook G. E. , Chaffer M. , Wu X.‐L. , Ezra E. 
Published: June 2012

SummaryParatuberculosis (Johne's disease) is an infectious enteric disease in dairy cattle and other species that causes substantial economic loss worldwide. In this study, two recursiveGaussian‐threshold models were employed in order to infer the effects ofJohne's disease on milk yield, fat yield, and protein yield while simultaneously estimating genetic parameters (i.e. heritability and genetic correlation) in anIsraeliHolstein population. Disease diagnosis was based onELISAserum antibody tests. Data were available for 4694 daughters of 361 sires; 3.5% were positive; and 1.6% were suspect for the disease test. Disease status was coded either as a binary character (negative vs. positive) or as an ordered categorical trait (negative, suspect, and positive) in the two recursive models and as a binary trait in a linear model. Among sires with ≥50 daughters, predicted probability ofMycobacterium aviumssp.paratuberculosis(MAP) infection in future daughters ranged from <1% to 16.5%. Heritability estimates forJohne's disease were near 0.15, confirming a genetic contribution to disease susceptibility. Genetic correlation estimates forJohne's disease with the three yield traits were 0.15–0.22. Residual correlations forJohne's disease with the yield traits were between −0.01 and −0.10. For the linear regression model, yield losses associated with a positive disease diagnosis during 305 days of lactation were 300 kg milk and around 10 kg for fat and protein. Yield loss estimates from the recursive models were 25–50% less than linear model estimates. Recursive modeling has theoretical advantages over linear models for these phenotypes, but the estimated genetic parameters in this study did not differ significantly between the two types of models.
QTL mapping of complex binary traits in an advanced intercross line
Authors: Moradi Marjaneh M. , Martin I. C. A. , Kirk E. P. , Harvey R. P. , Moran C. , Thomson P. C. 
Published: June 2012

SummaryAn advanced intercross line (AIL) is an easier and more cost‐effective approach compared to recombinant inbred lines for fine mapping of quantitative trait loci (QTL) identified by F2designs. In an AIL, a complex binary trait can be mapped through analysis of either continuously distributed proxy traits for the liability of the binary trait or the liability itself, the latter presenting the greater statistical challenge. In another work, we successfully applied both approaches in an AIL to fine map previously identified QTL underlying anatomical parameters of the cardiac inter‐atrial septum including patent foramen ovale. Here, we describe the statistical methods that we used to analyse complex binary traits in our AIL design. This is achieved using a likelihood‐based method, with the expectation–maximisation algorithm allowing use of standard logistic regression methods for model fitting.
Variation in the ovocalyxin‐32 gene in commercial egg‐laying chickens and its relationship with egg production and egg quality traits
Authors: Fulton J. E. , Soller M. , Lund A. R. , Arango J. , Lipkin E. 
Published: June 2012

SummaryAvian eggshell quality is an important trait for commercial egg production, as the eggshell is the primary packaging material and antimicrobial barrier for the internal food resource. Strong eggshells are essential to ensure that eggs can reach their final destination without damage. Ovocalyxin‐32 (OCX32) is a matrix protein found within the outer layers of the eggshell and in the cuticle. Numerous reports in the literature have identified association between variants in the gene encoding this protein, OCX32, and various eggshell quality traits. Thus, OCX32 is a candidate gene for selection for eggshell traits in commercial poultry populations. Sequencing of exons 2–6 of the OCX32 gene in eight elite brown and white eggshell commercial egg‐laying lines revealed 28 SNPs and one SNP/indel. Eighteen of these SNPs were predicted to alter the amino acid sequence of the protein. Clusters of SNPs in complete linkage disequilibrium were found in both exons 2 and 6. A total of 19 different versions or protein‐sequence haplotypes of the OCX32 protein were inferred, revealing considerable variation within commercial lines. Genotypes for 13 of the SNPs were determined for 330–1819 individuals per line. Trait association studies revealed a significant effect of OCX32 on shell color in white egg lines and line‐specific significant effects on albumen height, early egg weight, puncture score, and yolk weight. Three of the lines showed a significant change in OCX32 frequency over time, indicating selection pressure for certain variants of this gene during the breeding program.
Critical thinking in the chemical ecology of mammalian communication: roadmap for future studies
Authors: Charpentier Marie J. E. , Barthes Nicolas , Proffit Magali , Bessière Jean‐Marie , Grison Claude 
Published: June 2012

Summary1. Sophisticated and sensitive technologies now allow separation, quantification and chemical characterization of numerous compounds that play roles in chemical communication, chemical defence and aggression, in interactions between conspecific or heterospecific individuals. In the particular subfield of mammalian chemical communication, these rapid technological advances, combined with a frequent lack of technical background, have led to important errors in both chemical characterization of molecules and interpretation of their roles as chemical mediators of communication.2. The aim of this article is to highlight some of these methodological and analytical pitfalls and to provide a basis for better understanding of chemical mediation of communication in mammals. We compiled the recent literature treating molecules found in mammalian secretions and having putative roles in communication. A selection of 41 published studies dealing with 33 mammal species revealed reports of 857 different molecules. Based on the five main metabolic pathways responsible for the biosynthesis of most known secondary metabolites, we propose nine general biochemical rules that will help researchers to avoid errors of chemical characterization and to aid in interpreting the possible functional role of identified molecules as chemical mediators of mammal communication.3. Following these nine rules, we show that published studies include reports of molecules that are incorrectly or ambiguously named, molecules of exclusively non‐natural origin, molecules produced by other organisms but not directly by mammals, and molecules of biological origin and possibly produced by mammals. Only the last two of these classes could conceivably play roles as mediators of mammalian communication. We discuss the potential roles of these compounds as reported in the publications we reviewed.4. Our recommendations concerning technical, analytical and statistical aspects of the identification of compounds and interpretation of their roles should help chemical ecologists ask the appropriate questions about the accuracy of their identifications of molecules, the biological relevance of molecules they do identify and the possible functional roles of these molecules in mammalian communication.
Fine root dynamics with stand development in the boreal forest
Authors: Yuan Z. Y. , Chen Han Y. H. 
Published: June 2012

Summary1. Despite greater importance of below ground in influencing terrestrial carbon and nutrient cycling than above ground, how below‐ground biomass, production, turnover and mortality change with stand development remains poorly understood.2. Here, we used a postfire boreal forest chronosequence that spanned over 200 years (3, 11, 29, 94, 142 and 205 years since fire) to study how the dynamics of fine roots (≤2 mm in diameter) vary with stand age. We collected 756 sequential cores and 270 ingrowth cores, each separated to layers and live/dead, resulting in a total of 5076 fine root samples to quantify fine root biomass, production, mortality and turnover rates.3. With stand development, fine root biomass increased from 3 to 94‐year‐old, and declined thereafter, whereas necromass increased to 142‐year‐old and levelled off at 205‐year‐old. Fine root production and turnover increased from 3 to 11‐year‐old stands, and declined thereafter. Fine root mortality increased from 3 to 142‐year‐old stands.4. Our study, the first to show four simultaneous stand age–dependent below‐ground attributes, indicated that fine roots in young stands turn over faster than in old stands based on the estimates from both sequential and ingrowth cores. Despite some similarities among the studied attributes, the peaks they reached were not the same. Our results suggest that fine root dynamics are influenced by changes in species composition and soil properties associated with stand development in the boreal forest, especially the increase in forest floor nitrogen: phosphorus ratios as stand age increases.