bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracellular Interleukin-1α Mediates Interleukin-8 Production Induced byChlamydia trachomatisInfection via a Mechanism Independent of Type I Interleukin-1 Receptor
Authors: Cheng Wen , Shivshankar Pooja , Zhong Youmin , Chen Ding , Li Zhongyu , Zhong Guangming 
Published: December 2007

ABSTRACTChlamydia trachomatisinfection induces a wide array of inflammatory cytokines and chemokines, which may contribute to chlamydia-induced pathologies. However, the precise mechanisms by whichChlamydiainduces cytokines remain unclear. Here we demonstrate that the proinflammatory cytokine interleukin-1α (IL-1α) plays an essential role in chlamydial induction of the chemokine IL-8. Cells deficient in IL-1α expression or IL-1α-competent cells treated with IL-1α-specific small interfering RNA failed to produce IL-8 in response to chlamydial infection. However, neutralization of extracellular IL-1α or blockade of or deficiency in type I IL-1 receptor (IL-1RI) signaling did not affect chlamydial induction of IL-8 in cells capable of producing IL-1α. These results suggest that IL-1α can mediate the chlamydial induction of IL-8 via an intracellular mechanism independent of IL-1RI, especially during the early stage of the infection cycle. This conclusion is further supported by the observations that expression of a transgene-encoded full-length IL-1α fusion protein in the nuclei enhanced IL-8 production and that nuclear localization of chlamydia-induced precursor IL-1α correlated with chlamydial induction of IL-8. Thus, we have identified a novel mechanism for chlamydial induction of the chemokine IL-8.
Characterization of Two Putative Cytochrome
c
Peroxidases of
Campylobacter jejuni
Involved in Promoting Commensal Colonization of Poultry
Authors: Bingham-Ramos Lacey K. , Hendrixson David R. 
Published: December 2007

ABSTRACT

Campylobacter jejuni
is a leading cause of bacterial gastroenteritis in humans throughout the world, but infection of animals, especially poultry, results in a commensal colonization of the intestines. We previously found that a mutant lacking
docA
, which encodes a putative cytochrome
c
peroxidase (CCP), demonstrates up to a 10
5
-fold reduction in colonization of the chick cecum compared to wild-type
C. jejuni
strain 81-176. Predictions from genomic sequences identified CJJ0382 as a second locus in
C. jejuni
encoding a CCP, making the bacterium unusual in having two putative CCPs. To understand what advantages are imparted by having two putative CCPs, we compared the colonization requirements of
C. jejuni
mutants lacking DocA or Cjj0382. Unlike the Δ
docA
mutant, a ΔCJJ0382 mutant demonstrates a maximal 50-fold colonization defect that is dependent on the inoculum dose. The colonization differences of mutants lacking DocA or Cjj0382 suggest that the two predicted CCPs are unlikely to perform redundant functions during in vivo growth. In the characterizations of DocA and Cjj0382, we found that they are stable periplasmic proteins with an apparent heme-dependent peroxidase activity, which are characteristics of bacterial CCPs. However, the peroxidase activities of the proteins do not appear to contribute to resistance to hydrogen peroxide. Instead, we found that resistance to hydrogen peroxide in
C. jejuni
is mostly attributed to the cytoplasmic catalase KatA. Our data suggest that DocA and Cjj0382 have characteristics of CCPs but likely perform different physiological functions for the bacterium in colonization that are not related to resisting oxidative stress.
Job adjustment and absence from work in mid-pregnancy in the Norwegian Mother and Child Cohort Study (MoBa)
Authors: Kristensen P , Nordhagen R , Wergeland E , Bjerkedal T 
Published: December 2007

Background:Pregnant women at work have special needs, and sick leave is common. However, job adjustment in pregnancy is addressed in European legislation. Our main objective was to examine if job adjustment was associated with reduced absence.Methods:This study is based on the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health. 28 611 employed women filled in questionnaires in weeks 17 and 30 in pregnancy. The risk of absence for more than 2 weeks was studied among those who were not absent in week 17 (n = 22 932), and the probability of return to work in week 30 among those who were absent in week 17 (n = 5679). Data were based on self-report. The influence of job adjustment (three categories: not needed, needed but not obtained, needed and obtained) was analysed in additive models in multivariable binomial regression. Associations with other job characteristics and work environment factors were also analysed.Results:The risk of absence for more than 2 weeks was 0.308 and the probability of return to work was 0.137. Compared with women who needed but did not achieve job adjustment, obtained job adjustment was associated with a 0.107 decreased risk of absence (95% confidence interval 0.090 to 0.125) in a model including other job characteristics and work environment factors. Job adjustment was correspondingly associated with a 0.041 (0.023 to 0.059) increased probability of return to work. Absence was associated with adverse work environment, whereas the opposite pattern was found for return to work among those who started off being absent.Conclusions:Job adjustment was associated with reduced absence from work in pregnancy. Results should be interpreted cautiously because of low participation in MoBa and potential information bias from self-reported data.
ENCODING VIDEO SEQUENCES IN FRACTAL-BASED COMPRESSION
Authors: SANKARAGOMATHI B. , GANESAN L. , ARUMUGAM S. 
Published: December 2007

With the rapid increase in the use of computers and the Internet, the demand for higher transmission and better storage is increasing as well. This paper describes the different techniques for data (image-video) compression in general and, in particular, the new compression technique called fractal image compression. Fractal image compression is based on self-similarity, where one part of an image is similar to the other part of the same image. Low bit rate color image sequence coding is very important for video transmission and storage applications. The most significant aspect of this work is the development of color images using fractal-based color image compression, since little work has been done previously in this area. The results obtained show that the fractal-based compression works for the color images works as well as for the gray-scale images. Nevertheless, the encoding of the color images takes more time than the gray-scale images. Color images are usually compressed in a luminance-chrominance coordinate space, with the compression performed independently for each coordinate by applying the monochrome image processing techniques. For image sequence compression, the design of an accurate and efficient algorithm for computing motion to exploit the temporal redundancy has been one of the most active research areas in computer vision and image compression. Pixel-based motion estimation algorithms address pixel correspondence directly by identifying a set of local features and computing a match between these features across the frames. These direct techniques share the common pitfall of high computation complexity resulting from the dense vector fields produced. For block matching motion estimation algorithms, the quad-tree data structure is frequently used in image coding to recursively decompose an image plane into four non-overlapping rectangular blocks.
Mapping for high pressure gas pipelines in South Wales
Authors: Birch G. P. 
Published: December 2007

Objectives

In order to mitigate against environmental impact, to satisfy the design criteria and to ensure the long-term integrity of the construction, the Transmission Department of Wales Gas sought geotechnical advice on the routing and design of a major gas transmission system. This system was being built to reinforce the gas supplies to the industrial valleys of South Wales. The opportunity was taken to apply geomorphological mapping at an early stage in route planning so as to avoid abortive design work on alignments which might subsequently prove unsuitable or too costly to engineer (Fig. 1). Pipeline engineers welcomed the approach, which commenced by obtaining an understanding of the client’s objectives and industry design guidance. Working as part of the project team, engineering geomorphologists provided guidance from initial routing studies through detailed design to construction, which was completed without contractual conflict arising out of unforeseen ground conditions.

The Project

Gas supplies to the industrial valleys of South Wales developed in piecemeal fashion outwards from the individual coking plants set up by collieries in the valley floors. The introduction of natural gas from the North Sea in the 1970s provided the opportunity to invest in a new transmission system emanating from the new high-pressure grid on the north edge of the Coal Field basin.
The ‘backbone’ of the project is a 30 km north-south, high-pressure, welded steel transmission/storage pipeline (oversized up to 1200 mm diameter to permit storage by pressure-packing) linking the North Sea feeder main at Dowlais, near Methyr Tydfil, with the Cardiff feeder main at Nantgarw, near Caerphilly (Fig. 2).
Functional Diversity of Human Protection of Telomeres 1 Isoforms in Telomere Protection and Cellular Senescence
Authors: Yang Qin , Zhang Ran , Horikawa Izumi , Fujita Kaori , Afshar Yalda , Kokko Antti , Laiho Päivi , Aaltonen Lauri A. , Harris Curtis C. 
Published: December 2007

Abstract
Protection of telomeres 1 (POT1) proteins in various organisms bind telomeres and regulate their structure and function. In contrast to mice carrying two distinct POT1 genes encoding two POT1 proteins (POT1a and POT1b), humans have the single POT1 gene. In addition to full-length POT1 protein (variant v1), the human POT1 gene encodes four other variants due to alternative RNA splicing (variants v2, v3, v4, and v5), whose functions are poorly understood. The functional analyses of the NH2-terminally and COOH-terminally truncated POT1 variants in this study showed that neither the single-stranded telomere-binding ability of the NH2-terminal oligonucleotide-binding (OB) folds nor the telomerase-dependent telomere elongation activity mediated by the COOH-terminal TPP1-interacting domain was telomere protective by itself. Importantly, a COOH-terminally truncated variant (v5), which consists of the NH2-terminal OB folds and the central region of unknown function, was found to protect telomeres and prevent cellular senescence as efficiently as v1. Our data revealed mechanistic and functional differences between v1 and v5: (a) v1, but not v5, functions through the maintenance of telomeric 3′ overhangs; (b) p53 is indispensable to v5 knockdown-induced senescence; and (c) v5 functions at only a fraction of telomeres to prevent DNA damage signaling. Furthermore, v5 was preferentially expressed in mismatch repair (MMR)-deficient cells and tumor tissues, suggesting its role in chromosome stability associated with MMR deficiency. This study highlights a human-specific complexity in telomere protection and damage signaling conferred by functionally distinct isoforms from the single POT1 gene. [Cancer Res 2007;67(24):11677–86]
Betulinic Acid, a Catalytic Inhibitor of Topoisomerase I, Inhibits Reactive Oxygen Species–Mediated Apoptotic Topoisomerase I–DNA Cleavable Complex Formation in Prostate Cancer Cells but Does Not Affect the Process of Cell Death
Authors: Ganguly Agneyo , Das Benubrata , Roy Amit , Sen Nilkantha , Dasgupta Somdeb Bose , Mukhopadhayay Sibabrata , Majumder Hemanta K. 
Published: December 2007

Abstract
The ubiquitious enzyme topoisomerase I can be targeted by drugs which turn these enzymes into cellular poisons and subsequently induce cell death. Drugs like staurosporine, which do not target topoisomerase I directly, can also lead to stabilization of topoisomerase I–DNA cleavable complexes by an indirect process of reactive oxygen species (ROS) generation and subsequent oxidative DNA damage. In this study, we show that betulinic acid, a catalytic inhibitor of topoisomerases, inhibits the formation of apoptotic topoisomerase I–DNA cleavable complexes in prostate cancer cells induced by drugs like camptothecin, staurosporine, and etoposide. Although events like ROS generation, oxidative DNA damage, and DNA fragmentation were observed after betulinic acid treatment, there is no topoisomerase I–DNA cleavable complex formation, which is a key step in ROS-induced apoptotic processes. We have shown that betulinic acid interacts with cellular topoisomerase I and prohibits its interaction with the oxidatively damaged DNA. Using oligonucleotide containing 8-oxoguanosine modification, we have shown that betulinic acid inhibits its cleavage by topoisomerase I in vitro. Whereas silencing of topoisomerase I gene by small interfering RNA reduces cell death in the case of staurosporine and camptothecin, it cannot substantially reduce betulinic acid–induced cell death. Thus, our study provides evidence that betulinic acid inhibits formation of apoptotic topoisomerase I–DNA complexes and prevents the cellular topoisomerase I from directly participating in the apoptotic process. [Cancer Res 2007;67(24):11848–58]
Proapoptotic BH3-Only BCL-2 Family Protein BIM Connects Death Signaling from Epidermal Growth Factor Receptor Inhibition to the Mitochondrion
Authors: Deng Jing , Shimamura Takeshi , Perera Samanthi , Carlson Nicole E. , Cai Dongpo , Shapiro Geoffrey I. , Wong Kwok-Kin , Letai Anthony 
Published: December 2007

Abstract
A subset of lung cancers expresses mutant forms of epidermal growth factor receptor (EGFR) that are constitutively activated. Cancers bearing activated EGFR can be effectively targeted with EGFR inhibitors such as erlotinib. However, the death-signaling pathways engaged after EGFR inhibition are poorly understood. Here, we show that death after inhibition of EGFR uses the mitochondrial, or intrinsic, pathway of cell death controlled by the BCL-2 family of proteins. BCL-2 inhibits cell death induced by erlotinib, but BCL-2–protected cells are thus rendered BCL-2–dependent and sensitive to the BCL-2 antagonist ABT-737. BH3 profiling reveals that mitochondrial BCL-2 is primed by death signals after EGFR inhibition in these cells. As this result implies, key death-signaling proteins of the BCL-2 family, including BIM, were found to be up-regulated after erlotinib treatment and intercepted by overexpressed BCL-2. BIM is induced by lung cancer cell lines that are sensitive to erlotinib but not by those resistant. Reduction of BIM by siRNA induces resistance to erlotinib. We show that EGFR activity is inhibited by erlotinib in H1650, a lung cancer cell line that bears a sensitizing EGFR mutation, but that H1650 is not killed. We identify the block in apoptosis in this cell line, and show that a novel form of erlotinib resistance is present, a block in BIM up-regulation downstream of EGFR inhibition. This finding has clear implications for overcoming resistance to erlotinib. Resistance to EGFR inhibition can be modulated by alterations in the intrinsic apoptotic pathway controlled by the BCL-2 family of proteins. [Cancer Res 2007;67(24):11867–75]
SNAI1 Is Required for Tumor Growth and Lymph Node Metastasis of Human Breast Carcinoma MDA-MB-231 Cells
Authors: Olmeda David , Moreno-Bueno Gema , Flores Juana M. , Fabra Angels , Portillo Francisco , Cano Amparo 
Published: December 2007

Abstract
The transcription factor, SNAI1 (Snail), has recently been proposed as an important mediator of tumor invasion because of its role in E-cadherin down-regulation and induction of epithelial-mesenchymal transition. In human breast cancer, the expression of SNAI1 and/or the homologous SNAI2 (Slug) has been associated with E-cadherin repression, local or distant metastasis, tumor recurrence, or poor prognosis in different tumor series. However, the specific contribution of either factor to breast tumor progression is still unclear. We have analyzed the role of SNAI1 in human breast cancer by loss of function studies and provide evidence of a major role for SNAI1 in both primary tumor growth and metastasis of human breast carcinoma MDA-MB-231 cells. Specific silencing of SNAI1 by short hairpin RNA induces a decrease in mesenchymal and proinvasive markers (MMP9, ID1, SPARC) in MDA-MB-231 cells, concomitant with reduced in vitro invasive behavior. More importantly, stable SNAI1 silencing in MDA-MB-231 cells leads to a dramatic reduction of in vivo tumor incidence and growth rate. Tumors induced by MDA-MB-231-SNAI1–silenced cells show extensive necrotic regions and a significant decrease in invasive and angiogenic markers. Moreover, SNAI1 silencing increases the sensitivity of MDA-MB-231 cells to chemotherapeutics relevant in breast cancer treatments, gemcitabine and docetaxel. Remarkably, analysis of cell lines derived from lymph node metastasis indicates that SNAI1 expression is required for metastatic dissemination. [Cancer Res 2007;67(24):11721–31]
Identification of 14-3-3𝛉 as an Antigen that Induces a Humoral Response in Lung Cancer
Authors: Pereira-Faca Sandra R. , Kuick Rork , Puravs Eric , Zhang Qing , Krasnoselsky Alexei L. , Phanstiel Douglas , Qiu Ji , Misek David E. , Hinderer Robert , Tammemagi Martin , Landi Maria Teresa , Caporaso Neil , Pfeiffer Ruth , Edelstein Cim , Goodman Gary , Barnett Matt , Thornquist Mark , Brenner Dean , Hanash Samir M. 
Published: December 2007

Abstract
We have implemented a strategy to identify tumor antigens that induce a humoral immune response in lung cancer based on the analysis of tumor cell proteins. Chromatographically fractionated protein extracts from three lung cancer cell lines were subjected to Western blotting and hybridization with individual sera to determine serum antibody binding. Two sets of sera were initially investigated. One set consisted of sera from 19 newly diagnosed subjects with lung adenocarcinoma and 19 matched controls. A second independent set consisted of sera from 26 newly diagnosed subjects with lung adenocarcinoma and 24 controls matched for age, gender, and smoking history. One protein that exhibited significant reactivity with both sets of cancer sera (P = 0.0008) was confidently identified by mass spectrometry as 14-3-3𝛉. Remarkably, significant autoantibody reactivity against 14-3-3𝛉 was also observed in an analysis of a third set consisting of 18 prediagnostic lung cancer sera collected as part of the Beta-Carotene and Retinol Efficacy Trial cohort study, relative to 19 matched controls (P = 0.0042). A receiver operating characteristic curve constructed with a panel of three proteins consisting of 14-3-3𝛉 identified in this study, plus annexin 1 and protein gene product 9.5 proteins previously identified as associated with autoantibodies in lung cancer, gave a sensitivity of 55% at 95% specificity (area under the curve, 0.838) in discriminating lung cancer at the preclinical stage from matched controls. [Cancer Res 2007;67(24):12000–6]
Role of Rb-Dependent and Rb-Independent Functions of Papillomavirus E7 Oncogene in Head and Neck Cancer
Authors: Strati Katerina , Lambert Paul F. 
Published: December 2007

Abstract
Infection with high-risk human papillomaviruses (HPV) and in particular the expression of the viral proteins E6 and E7 have been associated with the etiology of a subset of head and neck squamous cell cancer (HNSCC). However, the individual consequences of E6 and E7 expression in an in vivo model have not been examined in these tissues. We have used transgenes that direct expression of the HPV16 E6 and E7 proteins to the head and neck tissues of mice to dissect the contribution of these proteins to head and neck carcinogenesis. We report here that E7 is the major transforming oncogene in HPV-associated HNSCC, whereas E6 is more likely to play a secondary role in contributing to later stages of carcinogenesis. Furthermore, a conditional deletion of Rb, a prominent target for E7, in the same tissues did not recapitulate all E7-mediated phenotypes. Although our results do not preclude an important role for the E7-pRb interaction, they highlight the importance of pRb-independent functions of E7 in head and neck carcinogenesis. [Cancer Res 2007;67(24):11585–93]
Different S/M Checkpoint Responses of Tumor and Non–Tumor Cell Lines to DNA Replication Inhibition
Authors: Rodríguez-Bravo Verónica , Guaita-Esteruelas Sandra , Salvador Noelia , Bachs Oriol , Agell Neus 
Published: December 2007

Abstract
Cell cycle checkpoint abrogation, especially the inhibition of Chk1 in combination with DNA-damaging treatments, has been proposed as a promising way of sensitizing cancer cells. However, less is known about the possibility to selectively affect tumor cells when they are treated with agents that block DNA synthesis in combination with replication checkpoint inhibitors. Here, we present clear insights in the different responses of tumor and non-transformed cells to the inhibition of DNA replication with hydroxyurea in combination with checkpoint abrogation via inhibition of Ataxia telangiectasia–mutated– (ATM) and Rad3-related/ATM (ATR/ATM) and Chk1 kinases. Interestingly, we find that non-transformed cell lines activate ATR/ATM- and Chk1-independent pathways in response to replication inhibition to prevent mitotic entry with unreplicated DNA. In contrast, tumor cell lines such as HCT116 and HeLa cells rely entirely on Chk1 activity for a proper response to replication inhibitors. Our results show that p38 is activated in response to hydroxyurea treatment and collaborates with Chk1 to prevent mitotic entry in non-transformed cell lines by maintaining cyclin B1/Cdk1 complexes inactive. Furthermore, DNA replication arrest down-regulates cyclin B1 promoter activity in non-transformed cells, but not in tumor cells in a Chk1- and p38-independent way. Thus, our data show that non-transformed cells present a more robust DNA replication checkpoint response compared with tumor cells that involves activation of the p38 pathway. We show that some of these responses to replication block can be lost in tumor cells, causing a defective checkpoint and providing a rationale for tumor-selective effects of combined therapies. [Cancer Res 2007;67(24):11648–56]
ERK-Dependent MKP-1–Mediated Cisplatin Resistance in Human Ovarian Cancer Cells
Authors: Wang Juan , Zhou Jun-Ying , Wu Gen Sheng 
Published: December 2007

Abstract
Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) is the MAPK phosphatase family member that negatively regulates MAPK signaling. Our previous study showed that MKP-1 is involved in cisplatin resistance, but the mechanism underlying its resistance is not understood. Here, we show that ERK2-mediated MKP-1 expression is critical for cisplatin resistance. Specifically, we showed that in the human ovarian cancer cell lines, cisplatin induces MKP-1 through phosphorylation. We also showed that inhibition of ERK2 activity by the MEK1/2 inhibitor U0126 or by small interfering RNA silencing decreases MKP-1 induction, leading to an increase in cisplatin-induced cell death, which mimicked the results obtained with cells in which MKP-1 is down-regulated. Importantly, down-regulation of ERK2 decreased cisplatin-induced MKP-1 phosphorylation, suggesting that MKP-1 phosphorylation depends on ERK2 activity. Furthermore, down-regulation of ERK2 or MKP-1 enhanced cisplatin-induced apoptosis. In addition, we showed that down-regulation of ERK2 or MKP-1 decreases the basal level of Bcl-2 protein and that inhibition of Bcl-2 activity sensitizes ovarian cancer cells to cisplatin. Collectively, our results indicate that induction of MKP-1 by cisplatin is through phosphorylation involving ERK signaling and that MKP-1 plays a critical role in ERK-mediated cisplatin resistance. Thus, our results suggest that targeting ERK-MKP-1 signaling could overcome cisplatin resistance in human ovarian cancer. [Cancer Res 2007;67(24):11933–41]