bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quality of life, work ability, and self employment: a population survey of entrepreneurs, farmers, and salary earners
Authors: Saarni S I , Saarni E S , Saarni H 
Published: August 2007

Objectives:Self employment is increasing but it is not yet known how its different forms affect health, quality of life, and work ability. We compared the work ability, subjective quality of life (QoL), and health-related quality of life (HRQoL) of entrepreneurs both with and without personnel, farmers, and salaried workers. We investigated which domains of HRQoL are associated with work status.Methods:A nationally representative general population sample comprising 5834 Finns aged between 30 and 64. Work ability was measured using the work ability index (WAI), HRQoL using 15D and EQ-5D, and QoL with self reported global quality of life.Results:Entrepreneurs with personnel had better work ability than salary earners, but there were no differences in QoL or HRQoL between the entrepreneurs and salary earners. Farmers scored lowest on all measures; this finding remained even after adjusting for age, sex, marital status, education, and chronic conditions. The low WAI score of farmers was mainly explained by poor subjective work ability, while their low 15D score was mainly the result of poor functioning in the psychosocial domains of HRQoL. The low EQ-5D score of farmers was explained by problems with mobility, usual activities, and with pain or discomfort.Conclusions:Farmers have poorer work ability, QoL, and HRQoL than other working groups, but this does not appear to be caused by physical health problems. From a research point of view, farmers should be categorised separately from other forms of entrepreneurship. From a public health point of view, improving farmers’ wellbeing may require psychosocial interventions exceeding traditional health promotion.
SYMBOLIC IMPLEMENTATION OF ALTERNATING AUTOMATA
Authors: BLOEM RODERICK , CIMATTI ALESSANDRO , PILL INGO , ROVERI MARCO 
Published: July 2007

This paper addresses the challenges of symbolic model checking and language emptiness checking where the specification is given as an alternating Büchi automaton. We introduce a novel version of Miyano and Hayashi's construction that allows us to directly convert an alternating automaton to a polynomially-sized symbolic structure. We thus avoid building an exponentially-sized explicit representation of the corresponding nondeterministic automaton. For one-weak automata, Gastin and Oddoux' construction produces smaller automata than Miyano and Hayashi's construction. We present a (symbolic) hybrid approach that combines the benefits of both: while retaining full generality, it uses the cheaper construction for those parts of the automaton that are one-weak. We performed a thorough experimental comparison of the explicit and symbolic approaches and several variants of Miyano and Hayashi's construction, using both BDD-based and SAT-based model checking techniques. The symbolic approaches clearly outperform the explicit one.
BORDERS AND FINITE AUTOMATA
Authors: ŠIMŮNEK MARTIN , MELICHAR BOŘIVOJ 
Published: July 2007

A border of a string is a prefix of the string that is simultaneously its suffix. It is one of the basic stringology keystones used as a part of many algorithms in pattern matching, molecular biology, computer-assisted music analysis and others. The paper offers the automata-theoretical description of Iliopoulos's ALL_BORDERS algorithm. The algorithm finds all borders of a string with don't care symbols. We show that ALL_BORDERS algorithm is an implementation of a finite state transducer of specific form. We describe how such a transducer can be constructed and what should be the input string like. The described transducer finds a set of lengths of all borders. Last but not least, we define approximate borders and show how to find all approximate borders of a string when we concern Hamming distance definition. Our solution of this problem is based on transducers again. This allows us to use analogy with automata-based pattern matching methods. Finally we discuss conditions under which the same principle can be used for other distance measures.
Glaucony from the Eocene of the Isle of Wight (southern UK): implications for basin analysis and sequence-stratigraphic interpretation
Authors: AMOROSI ALESSANDRO , CENTINEO MARIA CARLA 
Published: July 2007

The Lower-Middle Eocene sequence of the Hampshire Basin, which includes an alternation of sands, silts and clays, interpreted as fluvial to open-marine deposits, is exposed at two locations on the western (Alum Bay) and eastern (Whitecliff Bay) margin of the Isle of Wight. Glaucony is encountered throughout the study units: sand-clay alternations of lagoonal origin and estuarine channel-fill sands include less than 10% of predominantly poorly evolved, allochthonous glaucony; shelf silts and sands generally comprise more than 20% of evolved, mostly autochthonous glaucony.
Vertical changes in maturity of glaucony confirm the trend predicted by recent models, indicating an overall upward increase in the transgressive systems tracts and decrease in the highstand systems tracts, with maximum values in coincidence with the condensed sections, where a remarkable peak in glaucony concentration is invariably recorded.
Comparison of glaucony characteristics at different sites of depositional sequences shows a slight increase in maturity and abundance from the proximal to the distal areas. This lateral tendency is interpreted to reflect more suitable conditions for glauconitization in open-marine environments than in shallow waters.
Despite documented intrasequential variability of glaucony characteristics, glaucony assemblages from distinct depositional sequences may be generally identified on the basis of more pronounced differences in maturity. Consequently, glaucony attributes can be used as an index for characterization of third-order sedimentary cycles.
The Hølonda Porphyrites, Norwegian Caledonides: geochemistry and tectonic setting of Early–Mid-Ordovician shoshonitic volcanism
Authors: GRENNE T.O.R. , ROBERTS DAVID 
Published: July 2007

Petrological and geochemical data denote that the Late Arenig–Early Llanvirn Hølonda Porphyrites belong to the subduction-related shoshonite association. Original compositions ranged from absarokite through shoshonite to latite, and their very evolved nature signifies a mature arc aYnity in an active continental margin setting. Much of the geochemical variation can be interpreted in terms of fractional crystallization followed by a varying admixture of cumulus phases to the ascending melt and accumulation of phenocrysts within the magmatic feeder system. Their eruptive products covered an area which was at least 20–25 km across, forming local islands with carbonate-rich shelves in a shallow to deeper marine environment.
The immediate substrate to the volcanosedimentary ‘Hølonda basin’ is the Løkken Ophiolite, which formed in a primitive oceanic arc/marginal basin setting some 10–20 Ma prior to the shoshonitic magmatic event. Arc–continent collision led to emplacement of the oceanic, arc and marginal basin crust onto the continental margin in pre-Late Arenig times. Strong uplift of the obducted oceanic plate occurred in response to the buoyancy effect of the underthrusting, less dense, continental margin. This is interpreted to have been followed by a reversal of subduction polarity and formation of a steeply dipping subduction zone against the continental margin lithosphere, and was succeeded by the very evolved Hølonda Porphyrite shoshonitic magmatism in volcanic islands along this submerged continental margin.
Human Tumor-Derived Exosomes Selectively Impair Lymphocyte Responses to Interleukin-2
Authors: Clayton Aled , Mitchell J. Paul , Court Jacquelyn , Mason Malcolm D. , Tabi Zsuzsanna 
Published: August 2007

Abstract
Exosomes are nanometer-sized vesicles, secreted by normal and neoplastic cells. The outcome following interaction between the cellular immune system and cancer-derived exosomes is not well understood. Interleukin-2 (IL-2) is a key factor supporting expansion and differentiation of CTL and natural killer (NK) cells but can also support regulatory T cells and their suppressive functions. Our study examined whether tumor-derived exosomes could modify lymphocyte IL-2 responses. Proliferation of healthy donor peripheral blood lymphocytes in response to IL-2 was inhibited by tumor exosomes. In unfractionated lymphocytes, this effect was seen in all cell subsets. Separating CD4+ T cells, CD8+ T cells, and NK cells revealed that CD8+ T-cell proliferation was not inhibited in the absence of CD4+ T cells and that NK cell proliferation was only slightly impaired. Other exosome effects included selective impairment of IL-2–mediated CD25 up-regulation, affecting all but the CD3+CD8− T-cell subset. IL-2–induced Foxp3 expression by CD4+CD25+ cells was not inhibited by tumor exosomes, and the suppressive function of CD4+CD25+ T cells was enhanced by exosomes. In contrast, exosomes directly inhibited NK cell killing function in a T-cell–independent manner. Analysis of tumor exosomes revealed membrane-associated transforming growth factor β1 (TGFβ1), which contributed to the antiproliferative effects, shown by using neutralizing TGFβ1-specific antibody. The data show an exosome-mediated mechanism of skewing IL-2 responsiveness in favor of regulatory T cells and away from cytotoxic cells. This coordinated “double hit” to cellular immunity strongly implicates the role of exosomes in tumor immune evasion. [Cancer Res 2007;67(15):7458–66]
Lysis of Dysplastic but not Normal Oral Keratinocytes and Tissue-Engineered Epithelia with Conditionally Replicating Adenoviruses
Authors: Gaballah Kamis , Hills Allison , Curiel David , Hallden Gunnel , Harrison Paul , Partridge Max 
Published: August 2007

AbstractThere is no effective medical treatment for oral precancer, and surgery to remove these lesions is imprecise because abnormal mucosa extends beyond the visible lesion. Development of vectors for tumor-selective viral replication has been a significant advance, and viral lysis is well suited to destruction of oral precancerous mucosa. To facilitate evaluation of new treatments, we engineered dysplastic oral epithelium using keratinocytes isolated from dysplastic lesions. We show that these model systems recapitulate the key characteristics of the clinical lesions closely, and that topical delivery of the conditionally replicating adenovirus (CRAd) dl922-947 can lyse tissue-engineered epithelia that show mild, moderate, or severe dysplasia, but normal oral epithelia are very resistant to this treatment. The lytic effect is determined by various factors, including the grade and proliferation index of the dysplastic epithelia. The presence of suprabasal cycling cells, expression of the coxsackie adenovirus receptor (CAR), the transcription cofactor p300, and other aberrations that affect the regulation of the cell cycle or apoptosis and promote viral replication may also be important. The ability of dl922-947 to destroy engineered oral dysplasia was significantly greater than that observed using wild-type adenovirus, d/1520, or viruses modified to bypass cell entry dependent on the presence of CAR. Evidence of infection in clinical dysplastic lesions was also shown ex vivo using tissue explants. We conclude that dl922-947 may provide an efficient molecular cytotoxic to dissolve oral dysplastic lesions. [Cancer Res 2007;67(15):7284–94]
The Survival Kinase Mirk/Dyrk1B Is a Downstream Effector of Oncogenic K-ras in Pancreatic Cancer
Authors: Jin Kideok , Park Sunju , Ewton Daina Z. , Friedman Eileen 
Published: August 2007

Abstract
The kinase Mirk is overexpressed in many resected pancreatic adenocarcinomas and is amplified in a subset of pancreatic cancer cell lines. Depletion of Mirk has been shown to lead to apoptosis in pancreatic cancer cell lines, and thus to inhibit their clonogenic growth. Mirk is activated by signaling from activated Rac1 to MKK3 in MDCK cells, but the mechanism of activation of Mirk in pancreatic cancers is unknown. In this report, Mirk is shown to be a novel effector of K-ras, a gene mutated in ∼90% of pancreatic cancers. Activation of Mirk signaling from oncogenic K-ras through Rac1 was shown in transient expression systems and reporter assays. Mirk activation in pancreatic cancer cells was blocked by RNA interference using three different synthetic duplex RNAis to K-ras, or two RNAis to Rac1, by pharmacologic inhibition of Rac1, or by expression of dominant negative K-rasS17N. Rac1 was activated in four out of five pancreatic cancer cell lines, and was activated by signaling from oncogenic K-ras. Mirk knockout does not induce embryonic lethality, and depletion of Mirk had no effect on the survival of normal diploid fibroblasts. In contrast, the clonogenic ability of Panc1 and AsPc1 pancreatic cancer cell lines was reduced 8- to 12-fold by the depletion of Mirk, with a greater reduction seen following the depletion of K-ras or both genes. Mirk is a novel downstream effector of oncogenic K-ras and mediates some of the survival signals activated by ras signaling. [Cancer Res 2007;67(15):7247–55]
Therapeutic Relevance of Osteoprotegerin Gene Therapy in Osteosarcoma: Blockade of the Vicious Cycle between Tumor Cell Proliferation and Bone Resorption
Authors: Lamoureux François , Richard Peggy , Wittrant Yohann , Battaglia Séverine , Pilet Paul , Trichet Valérie , Blanchard Frédéric , Gouin François , Pitard Bruno , Heymann Dominique , Redini Françoise 
Published: August 2007

Abstract
Osteosarcoma is the most frequent primary bone tumor that develops mainly in the young, the median age of diagnosis being 18 years. Despite improvement in osteosarcoma treatment, survival rate is only 30% at 5 years for patients with pulmonary metastases at diagnosis. This warrants exploration of new therapeutic options, and among them, osteoprotegerin (OPG), a naturally occurring protein that inhibits bone resorption, is very promising in blocking the vicious cycle between bone resorption and tumor proliferation that takes place during tumor development in bone site. As OPG binds and inhibits the activity of tumor necrosis factor–related apoptosis-inducing ligand, the truncated form of murine OPG 1-194 was used. The cDNA encoding OPG was administered by gene transfer using replication-defective adenoviral vector or was associated with an amphiphilic polymer in two models of rodent osteosarcoma. In both models, OPG gene transfer was effective in preventing the formation of osteolytic lesions associated with osteosarcoma development, in reducing the tumor incidence and the local tumor growth, leading to a 4-fold augmentation of mice survival 28 days postimplantation. On the contrary, OPG did not prevent the development of pulmonary metastasis alone, suggesting that bone environment is necessary for OPG therapeutic efficacy. Because OPG has no direct activity on osteosarcoma cells in vitro (cell binding, cell proliferation, apoptosis, or cell cycle distribution), we show that OPG exerts indirect inhibitory effect on tumor progression through the inhibition of RANKL whose production is enhanced in bone tumor environment, leading to osteolysis inhibition as reflected by osteoclast number decrease. [Cancer Res 2007;67(15):7308–18]
Estrogen Plus Progestin Use, Microsatellite Instability, and the Risk of Colorectal Cancer in Women
Authors: Newcomb Polly A. , Zheng Yingye , Chia Victoria M. , Morimoto Libby M. , Doria-Rose V. Paul , Templeton Allyson , Thibodeau Stephen N. , Potter John D. 
Published: August 2007

Abstract
Current users of postmenopausal hormones (PMH) have ∼30% to 40% lower risk of colorectal cancer (CRC), although associations with specific types of hormones have been inconsistent. Further, it is not clear whether some tumor types have a different risk. We conducted a case-control study to examine the relationship between PMH and CRC. Cases (n = 1,004), ages 50 to 74 years, were identified from the Surveillance Epidemiology and End Results registry in Washington from 1998 to 2002; controls (n = 1,062) were randomly selected from population lists. Case tissue samples were obtained for microsatellite instability (MSI) analyses. Interviews collected risk-factor data for CRC, including detailed information on PMH. Multivariable logistic regression models estimated odds ratios (OR) and 95% confidence intervals (95% CI). Current use of any PMH was associated with a 20% reduction in CRC risk (95% CI 0.6–0.9). This reduction in risk was limited to women who had taken estrogen plus progestin (EP) preparations only (OR = 0.6, 95% CI 0.5–0.9); there was no association with estrogen-only (E alone) use (OR = 0.9, 95% CI 0.7–1.1). For women with MSI-low or MSI-stable tumors, there was a statistically significant 40% reduction in CRC risk associated with EP use (95% CI 0.4–0.9); there was no clear association with MSI-high tumors. EP use was associated with a decreased risk of CRC; however, there seemed to be no association with E alone data that are consistent with the recent Women's Health Initiative findings. Progestin may enhance the estrogenic effect of conjugated estrogen so the combination may be more biologically active in the colon than E alone. [Cancer Res 2007;67(15):7534–9]
Identification of S664 TSC2 Phosphorylation as a Marker for Extracellular Signal-Regulated Kinase–Mediated mTOR Activation in Tuberous Sclerosis and Human Cancer
Authors: Ma Li , Teruya-Feldstein Julie , Bonner Pauline , Bernardi Rosa , Franz David Neal , Witte David , Cordon-Cardo Carlos , Pandolfi Pier Paolo 
Published: August 2007

Abstract
Constitutive activation of extracellular signal-regulated kinases (Erk1/2) is frequently implicated in human cancers. Recently, aberrantly activated Erk was also found in brain lesions associated with tuberous sclerosis (TSC). We reported previously that Erk might contribute to tumorigenesis by phosphorylating TSC2 at specific residues, particularly S664. In our present study, 25 TSC-related cortical tubers or subependymal giant cell astrocytomas, as well as tissue microarrays of six types of human cancers, were analyzed for the expression of phospho-Erk (pErk) 1/2, S664-phospho-TSC2 (pTSC2), and phospho-S6 (pS6) by immunohistochemistry. We found that Erk-mediated TSC2 phosphorylation occurred at a high incidence and positively correlated with mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) activation in TSC-associated brain lesions as well as in various cancers. Interestingly, in certain types of cancers (e.g., breast carcinoma and colon carcinoma), S664-pTSC2 seemed to be a more sensitive marker than pErk. Furthermore, most of the pTSC2-positive samples (∼75%) were positive for pS6, but only 40% to 55% of the pS6-positive tumors exhibited TSC2 phosphorylation. Our results show that S664 TSC2 phosphorylation is a marker for Erk-mediated (as opposed to Akt-mediated) mTOR activation in TSC and human cancer. On the basis of these findings, TSC2 phosphorylation at S664 can be used to identify patients that may benefit from antitumor therapy with MAPK and mTOR inhibitors. Importantly, our results indicate that Erk-mediated phosphorylation and inactivation of TSC2 can be critical in development of hamartomatous lesions in TSC and cancer pathogenesis. [Cancer Res 2007;67(15):7106–12]
Clinical Validity of the Lung Cancer Biomarkers Identified by Bioinformatics Analysis of Public Expression Data
Authors: Kim Bumjin , Lee Hyun Joo , Choi Hye Young , Shin Youngah , Nam Seungyoon , Seo Gilju , Son Dae-Soon , Jo Jisuk , Kim Jaesang , Lee Jinseon , Kim Jhingook , Kim Kwhanmien , Lee Sanghyuk 
Published: August 2007

Abstract
Identification of molecular markers often leads to important clinical applications such as early diagnosis, prognosis, and drug targeting. Lung cancer, the leading cause of cancer-related deaths, still lacks reliable molecular markers. We have combined the bioinformatics analysis of the public gene expression data and clinical validation to identify biomarker genes for non–small-cell lung cancer. The serial analysis of gene expression and the expressed sequence tag data were meta-analyzed to produce a list of the differentially expressed genes in lung cancer. Through careful inspection of the predicted genes, we selected 20 genes for experimental validation using semiquantitative reverse transcriptase-PCR. The microdissected clinical specimens used in the study consisted of three groups: lung tissues from benign diseases and the paired (cancer and pathologic normal) tissues from non–small-cell lung cancer patients. After extensive statistical analyses, seven genes (CBLC, CYP24A1, ALDH3A1, AKR1B10, S100P, PLUNC, and LOC147166) were identified as potential diagnostic markers. Quantitative real-time PCR was carried out to additionally assess the value of the seven identified genes leading to the confirmation of at least two genes (CBLC and CYP24A1) as highly probable novel biomarkers. The gene properties of the identified markers, especially their relationship to lung cancer and cell signaling pathway regulation, further suggest their potential value as drug targets as well. [Cancer Res 2007;67(15):7431–8]
Environmental Tobacco Smoke and Bladder Cancer Risk in Never Smokers of Los Angeles County
Authors: Jiang Xuejuan , Yuan Jian-Min , Skipper Paul L. , Tannenbaum Steven R. , Yu Mimi C. 
Published: August 2007

Abstract
Cigarette smoking is a major risk factor for bladder cancer and a prominent point source of 4-aminobiphenyl (4-ABP), a recognized human bladder carcinogen. 4-ABP-hemoglobin (Hb) adducts are established biomarkers of 4-ABP exposure in humans. The role of environmental tobacco smoke (ETS) in the etiology of bladder cancer is largely unknown. As part of a large population-based bladder cancer study in Los Angeles County, California, lifetime exposure to ETS was ascertained for 148 cases and 292 control subjects who had never used any tobacco products over their lifetime. 4-ABP-Hb adducts were quantitatively measured on 230 control subjects. Female lifelong nonsmokers living with two or more smokers during childhood were significantly related to risk of bladder cancer [odds ratio (OR), 3.08; 95% confidence interval (95% CI), 1.16–8.22]. During adulthood, ∼2-fold risks were seen among women living with a spouse/domestic partner who smoked for ≥10 years or having a coworker who smoked in an indoor environment for ≥10 years. When all sources of ETS exposure were combined, a statistically significant, dose-dependent association (P for trend = 0.03) was noted in women, with the OR for the highest category of ETS exposure being 5.48 (95% CI, 1.06–28.36). Levels of 4-ABP-Hb adducts varied by ETS exposure status among female control subjects. Mean level was lowest in women never exposed to ETS (16.4 pg/g Hb) and highest in those with current ETS exposure (23.6 pg/g Hb). ETS exposure was associated with neither bladder cancer risk nor 4-ABP-Hb adduct levels in male lifelong nonsmokers. In conclusion, ETS is a risk factor for bladder cancer in women who were lifelong nonusers of any tobacco products. [Cancer Res 2007;67(15):7540–5]