bluuebunny/crossref_metadata_2025_split huggingface dataset:
Difference in apolipoprotein E type 4 allele (APOE ɛ4) among dentate and edentulous subjects
Authors: Bergdahl Maud , Bergdahl Jan , Nyberg Lars , Nilsson Lars‐Göran 
Published: March 2008

Objectives:  To evaluate the frequency of apolipoprotein (APOE) alleles and determine whether APOE type 4 allele (ɛ4) was associated with edentulousness even when certain factors were controlled.Background:  The APOE are important in lipid homeostasis, and APOE ɛ4 has been found in many diseases and to have a negative impact on longevity. Tooth loss is more common in ill aged subjects with low income and education.Materials and methods:  In a population‐based study involving 1860 subjects between 35 and 85 years 1321 dentate (mean age = 54; 54% women, 46% men) and 539 edentulous (mean age = 72; 62% women, 38% men) subjects were studied. Logistic regression was performed with dentate/edentulous as dependent variables and years of education, socio‐economic status, social network, stress level, handicap from birth, 23 various diseases and APOE ɛ4 as covariates. Thereafter, APOE ɛ4 frequencies were studied in 342 dentate and 336 edentulous subjects 50–85 years of age. The subjects were matched with regard to age, gender, years of education, living condition, stress level, handicap from birth and 23 various diseases.Results:  APOE allele frequency in the total group was ɛ2 = 7.8%, ɛ3 = 76.4% and ɛ4 = 15.8%. Age, living condition, years of education and APOE ɛ4 were significant covariates in edentulous subjects (p ≤ 0.001). APOE ɛ4 in the matched groups revealed significant differences between the dentate group and the edentulous group (χ2 = 5.68; p = 0.017). There was no group effect (F(29,648) = 0.849; p < 0.696; Wilks’ lambda = 0.963). In the dentate group, the frequencies of APOE were: ɛ2 = 8.8%, ɛ3 = 77.9% and ɛ4 = 13.3%. Corresponding frequencies of APOE in the edentulous group were: ɛ2 = 6.6%, ɛ3 = 75.4% and ɛ4 = 18.0%.Conclusion:  Despite matching both groups with regard to different background factors, the edentulous group had a higher frequency of APOE ɛ4 than the dentate group. Thus, genetic factors might contribute to greater risk in developing complex oral diseases leading to tooth loss or just be an indication that the subjects in our study carrying APOE ɛ4 are more fragile.
Fast-ion-beam laser-induced-fluorescence measurements of branching fractions and oscillator strengths in Nd II
Authors: Li R , Rehse S J , Scholl T J , Sharikova A , Chatelain R , Holt R A , Rosner S D 
Published: March 2008

We measured the spontaneous-emission branching fractions of 46 levels in Nd II, selectively populated via single-frequency laser excitation of a 10 keV ion beam. The levels studied had term energies up to 29 955 cm–1, and decay branches with spontaneous emission in the range 372–850 nm were detected. The experimental accuracy for branching fractions over 0.1 was ~7%. We used these branching fractions along with our previously determined radiative lifetimes to infer transition probabilities and oscillator strengths for 430 transitions, which are useful for stellar abundance determinations. PACS Nos.: 32.70Cs, 95.30Ky
Non π/N scattering of CP1 solitons
Authors: Cova R J , Amundsen D , Zakrzewski W J 
Published: March 2008

Using numerical simulations we investigate topological charge N = 3, 4 soliton head-on collisions in the CP1 model on a flat torus T2. We observe dual-polygon scattering π/N except for configurations of three solitons starting far away from each other. PACS Nos.: 11.10.–z; 02.60.–x; 03.50.Kk
Effect of gap harvesting on epiphytes and bark-dwelling arthropods in the Acadian forest of central Maine
Authors: Miller Kathryn M. , Wagner Robert G. , Woods Stephen A. 
Published: March 2008

Using a long-term silvicultural experiment, we (i) investigated how epiphyte and arthropod communities were affected by height on the stem, bark texture, and stem diameter of red maple ( Acer rubrum L.) trees, (ii) examined how harvest gaps influenced epiphyte and arthropod communities on red maple boles, and (iii) explored whether these effects influenced the relationship between the epiphyte and arthropod communities. Arthropod and epiphyte assemblages dwelling on the bark of red maple trees located in undisturbed forest and harvest gaps varied with height. Bryophytes, Cladonia spp., and cyanolichens were most abundant near the base of the tree, while noncyano, foliose lichens and fruticose lichens were most abundant 4–6 m above the ground. Acari, Araneae, and Collembola were most abundant near the base of the tree, while Diptera were most abundant above 2 m. A previously undocumented assemblage of dipterans (flies), primarily in the suborder Nematocera, was found. Gap harvesting reduced the abundance of bryophytes, Collembola (springtails), Araneae (spiders), and total arthropods on the bark of red maple. Canonical correlation analysis revealed a positive association between bryophytes, Collembola, and Araneae. A strong correlation between Collembola and Araneae suggested a possible trophic interaction that may be affected by gap harvesting through a reduction in bryophyte abundance.
Impacts of elevated ozone and nitrogen on growth and photosynthesis of European aspen (Populus tremula) and hybrid aspen (P. tremula × Populus tremuloides) clones
Authors: Häikiö Elina , Freiwald Vera , Silfver Tarja , Beuker Egbert , Holopainen Toini , Oksanen Elina 
Published: March 2008

Impacts of elevated tropospheric ozone and soil nitrogen amendment on two native European aspen ( Populus tremula L.) and eight hybrid aspen (P. tremula L. × Populus tremuloides Michx.) clones were studied in a free-air ozone exposure system. Potted saplings were exposed to ambient (ca. 20 ppb) or 1.5× ambient ozone and two levels of soil nitrogen (39 and 78 kg N·ha–1·year–1 in the first year, 60 and 140 kg N·ha–1·year–1 in the second year for low-nitrogen and high-nitrogen treatments, respectively) over two growing seasons. The plants were measured for photosynthesis, chlorophyll fluorescence, and biomass accumulation. Ozone decreased leaf-level net photosynthesis (Asat) in particular early in the growing season and maximum quantum yield of photosystem II (Fv/Fm) at the end of the growing season. Nitrogen amendment increased the growth of all plant parts and mitigated the adverse ozone effects. There were significant differences in ozone responses among the clones, and we were able to cluster the clones into sensitivity groups based on their growth responses. The most ozone-tolerant genotypes were hybrid aspen clones, indicating that populations that have already experienced selection for ozone-tolerant genotypes should be used to cross-breed with ozone-sensitive populations to achieve tolerance of a climate with increasing tropospheric ozone concentrations.
Impacts of postfire salvage logging on understory plant communities of the boreal mixedwood forest 2 and 34 years after disturbance
Authors: Kurulok Stephanie E. , Macdonald S. Ellen 
Published: March 2008

We compared understory vegetation composition and richness in aspen-dominated boreal mixedwood forest stands in Alberta, Canada, that had been burned by wildfire with those that burned and were subsequently salvage logged. Stands were examined at early and midsuccessional (2 and 34 years after disturbance(s), respectively) developmental stages. In comparison with wildfire stands, understory communities of early successional salvage-logged stands were characterized by greater species richness, weedy species presence, higher shrub abundance, and lower abundances of fire-specialist seed bank species. In constrained ordination, the understory community of early successional wildfire stands was related to greater canopy cover, sapling density, and moss depth, whereas that of salvage-logged stands was related to greater light, volume of downed deadwood, and litter and organic matter. Longer term effects of salvage logging on the understory community were minimal and, instead, reflected the influence of forest canopy redevelopment. In midsuccessional stands, understory composition was related to conifer density, litter cover, soil moisture, organic layer depth, tall shrub density, and bryophyte-covered microsite cover. Postfire salvage logging can have substantial short-term effects on the postfire understory plant community; in the longer term, effects will depend to a large extent on the influence of harvesting and subsequent management on canopy redevelopment.
Blocked Autophagy Sensitizes Resistant Carcinoma Cells to Radiation Therapy
Authors: Apel Anja , Herr Ingrid , Schwarz Heinz , Rodemann H. Peter , Mayer Andreas 
Published: March 2008

Abstract
Autophagy or “self eating” is frequently activated in tumor cells treated with chemotherapy or irradiation. Whether autophagy represents a survival mechanism or rather contributes to cell death remains controversial. To address this issue, the role of autophagy in radiosensitive and radioresistant human cancer cell lines in response to γ-irradiation was examined. We found irradiation-induced accumulation of autophagosomes accompanied by strong mRNA induction of the autophagy-related genes beclin 1, atg3, atg4b, atg4c, atg5, and atg12 in each cell line. Transduction of specific target-siRNAs led to down-regulation of these genes for up to 8 days as shown by reverse transcription-PCR and Western blot analysis. Blockade of each autophagy-related gene was associated with strongly diminished accumulation of autophagosomes after irradiation. As shown by clonogenic survival, the majority of inhibited autophagy-related genes, each alone or combined, resulted in sensitization of resistant carcinoma cells to radiation, whereas untreated resistant cells but not sensitive cells survived better when autophagy was inhibited. Similarly, radiosensitization or the opposite was observed in different sensitive carcinoma cells and upon inhibition of different autophagy genes. Mutant p53 had no effect on accumulation of autophagosomes but slightly increased clonogenic survival, as expected, because mutated p53 protects cells by conferring resistance to apoptosis. In our system, short-time inhibition of autophagy along with radiotherapy lead to enhanced cytotoxicity of radiotherapy in resistant cancer cells. [Cancer Res 2008;68(5):1485–94]
A Human Breast Cell Model of Preinvasive to Invasive Transition
Authors: Rizki Aylin , Weaver Valerie M. , Lee Sun-Young , Rozenberg Gabriela I. , Chin Koei , Myers Connie A. , Bascom Jamie L. , Mott Joni D. , Semeiks Jeremy R. , Grate Leslie R. , Mian I. Saira , Borowsky Alexander D. , Jensen Roy A. , Idowu Michael O. , Chen Fanqing , Chen David J. , Petersen Ole W. , Gray Joe W. , Bissell Mina J. 
Published: March 2008

Abstract
A crucial step in human breast cancer progression is the acquisition of invasiveness. There is a distinct lack of human cell culture models to study the transition from preinvasive to invasive phenotype as it may occur “spontaneously” in vivo. To delineate molecular alterations important for this transition, we isolated human breast epithelial cell lines that showed partial loss of tissue polarity in three-dimensional reconstituted basement membrane cultures. These cells remained noninvasive; however, unlike their nonmalignant counterparts, they exhibited a high propensity to acquire invasiveness through basement membrane in culture. The genomic aberrations and gene expression profiles of the cells in this model showed a high degree of similarity to primary breast tumor profiles. The xenograft tumors formed by the cell lines in three different microenvironments in nude mice displayed metaplastic phenotypes, including squamous and basal characteristics, with invasive cells exhibiting features of higher-grade tumors. To find functionally significant changes in transition from preinvasive to invasive phenotype, we performed attribute profile clustering analysis on the list of genes differentially expressed between preinvasive and invasive cells. We found integral membrane proteins, transcription factors, kinases, transport molecules, and chemokines to be highly represented. In addition, expression of matrix metalloproteinases MMP9, MMP13, MMP15, and MMP17 was up-regulated in the invasive cells. Using small interfering RNA–based approaches, we found these MMPs to be required for the invasive phenotype. This model provides a new tool for dissection of mechanisms by which preinvasive breast cells could acquire invasiveness in a metaplastic context. [Cancer Res 2008;68(5):1378–87]
Chromosomal Breakpoints in Primary Colon Cancer Cluster at Sites of Structural Variants in the Genome
Authors: Camps Jordi , Grade Marian , Nguyen Quang Tri , Hörmann Patrick , Becker Sandra , Hummon Amanda B. , Rodriguez Virginia , Chandrasekharappa Settara , Chen Yidong , Difilippantonio Michael J. , Becker Heinz , Ghadimi B. Michael , Ried Thomas 
Published: March 2008

Abstract
Genomic aberrations on chromosome 8 are common in colon cancer, and are associated with lymph node and distant metastases as well as with disease susceptibility. This prompted us to generate a high-resolution map of genomic imbalances of chromosome 8 in 51 primary colon carcinomas using a custom-designed genomic array consisting of a tiling path of BAC clones. This analysis confirmed the dominant role of this chromosome. Unexpectedly, the position of the breakpoints suggested colocalization with structural variants in the human genome. In order to map these sites with increased resolution and to extend the analysis to the entire genome, we analyzed a subset of these tumors (n = 32) by comparative genomic hybridization on a 185K oligonucleotide array platform. Our comprehensive map of the colon cancer genome confirmed recurrent and specific low-level copy number changes of chromosomes 7, 8, 13, 18, and 20, and unveiled additional, novel sites of genomic imbalances including amplification of a histone gene cluster on chromosome 6p21.1-21.33 and deletions on chromosome 4q34-35. The systematic comparison of segments of copy number change with gene expression profiles showed that genomic imbalances directly affect average expression levels. Strikingly, we observed a significant association of chromosomal breakpoints with structural variants in the human genome: 41% of all copy number changes occurred at sites of such copy number variants (P &lt; 2.2e−16). Such an association has not been previously described and reveals a yet underappreciated plasticity of the colon cancer genome; it also points to potential mechanisms for the induction of chromosomal breakage in cancer cells. [Cancer Res 2008;68(5):1284–95]
A Novel RET Kinase–β-Catenin Signaling Pathway Contributes to Tumorigenesis in Thyroid Carcinoma
Authors: Gujral Taranjit S. , van Veelen Wendy , Richardson Douglas S. , Myers Shirley M. , Meens Jalna A. , Acton Dennis S. , Duñach Mireia , Elliott Bruce E. , Höppener Jo W.M. , Mulligan Lois M. 
Published: March 2008

Abstract
The RET receptor tyrosine kinase has essential roles in cell survival, differentiation, and proliferation. Oncogenic activation of RET causes the cancer syndrome multiple endocrine neoplasia type 2 (MEN 2) and is a frequent event in sporadic thyroid carcinomas. However, the molecular mechanisms underlying RET's potent transforming and mitogenic signals are still not clear. Here, we show that nuclear localization of β-catenin is frequent in both thyroid tumors and their metastases from MEN 2 patients, suggesting a novel mechanism of RET-mediated function through the β-catenin signaling pathway. We show that RET binds to, and tyrosine phosphorylates, β-catenin and show that the interaction between RET and β-catenin can be direct and independent of cytoplasmic kinases, such as SRC. As a result of RET-mediated tyrosine phosphorylation, β-catenin escapes cytosolic down-regulation by the adenomatous polyposis coli/Axin/glycogen synthase kinase-3 complex and accumulates in the nucleus, where it can stimulate β-catenin–specific transcriptional programs in a RET-dependent fashion. We show that down-regulation of β-catenin activity decreases RET-mediated cell proliferation, colony formation, and tumor growth in nude mice. Together, our data show that a β-catenin–RET kinase pathway is a critical contributor to the development and metastasis of human thyroid carcinoma. [Cancer Res 2008;68(5):1338–46]
Linking Antibody Fc Domain to Endostatin Significantly Improves Endostatin Half-life and Efficacy
Authors: Lee Tong-Young , Tjin Tham Sjin Robert M. , Movahedi Shahla , Ahmed Bissan , Pravda Elke A. , Lo Kin-Ming , Gillies Stephen D. , Folkman Judah , Javaherian Kashi 
Published: March 2008

Abstract
Purpose: The half-life of the antiangiogenic molecule endostatin that has been used in clinical trial is short (∼2 h). In addition, ∼50% of the clinical grade endostatin molecules lack four amino acids at their NH2 termini. Lack of these amino acids gives rise to a molecule that is devoid of zinc, resulting in no antitumor activity. Our goal was to develop a new version of endostatin that does not show such deficiency.
Experimental Design: A recombinant human endostatin conjugated to the Fc domain of IgG was constructed and expressed in mammalian cell culture. The presence of Fc has been shown by previous investigators to play a major role in increasing the half-life of the molecule. Fc-endostatin was tested in tumor-bearing mice, and its half-life was compared with the clinical grade endostatin.
Results: The antitumor dose of Fc-endostatin was found to be ∼100 times less than the clinical grade endostatin. The half-life of Fc-endostatin in the circulation was found to be weeks rather than hours, as observed for endostatin alone. In addition, a U-shaped curve was observed for antitumor activity of endostatin as a function of endostatin concentration delivered to the animals.
Conclusion: Fc-endostatin is a superior molecule to the original clinical endostatin. Due to its long half-life, the amount of protein required is substantially reduced compared with the clinically tested endostatin. Furthermore, in view of the U-shaped curve of efficacy observed for endostatin, we estimate that the requirement for Fc-endostatin is ∼700-fold less than endostatin alone. The half-life of endostatin is similar to that of vascular endothelial growth factor–Trap and Avastin, two other antiangiogenic reagents. We conclude that a new clinical trial of endostatin, incorporating Fc, may benefit cancer patients.
Immunohistochemical Analysis of Phosphotyrosine Signal Transducer and Activator of Transcription 3 and Epidermal Growth Factor Receptor Autocrine Signaling Pathways in Head and Neck Cancers and Metastatic Lymph Nodes
Authors: Seethala Raja R. , Gooding William E. , Handler Phoebe N. , Collins Bobby , Zhang Qing , Siegfried Jill M. , Grandis Jennifer R. 
Published: March 2008

AbstractPurpose: To determine the effect of tyrosine-phosphorylated signal transducer and activator of transcription 3 (pSTAT3) immunoexpression on survival in two independent cohorts of patients with squamous cell carcinoma of the head and neck (SCCHN) and to evaluate pSTAT3, transforming growth factor-α (TGF-α), epidermal growth factor receptor (EGFR), and gastrin-releasing peptide receptor (GRPR) expression in matched tumor and lymph node metastases in one of these cohorts.Experimental Technique: Immunostaining for pSTAT3, TGF-α, EGFR, and GRPR was done in two SCCHN cohorts (cohort 1, 61 tumors; cohort 2, 69 paired primary tumors and lymph node metastases). Semiquantitative scores derived from the product of staining intensity (scale 0-3) score and percentage of positive tumor cells were correlated with clinical outcome.Results: Immunoexpression of pSTAT3 did not correlate with clinical outcome in either cohort (cohort 1, P = 0.914; cohort 2, P = 0.312). In cohort 2, TGF-α and EGFR expression in the primary tumors showed some association with decreased disease-free survival (P = 0.0306 and P = 0.0985, respectively). Both pSTAT3 and EGFR showed a correlation of expression between tumor and matched lymph node metastasis (P &lt; 0.0001 and P = 0.0046, respectively). In addition, the expression of EGFR and GRPR in the primary tumors correlated with TGF-α expression in paired nodal metastases (P = 0.0043 and P = 0.0268, respectively). In the nodal metastases, TGF-α expression correlated with EGFR expression (P = 0.0069). In primary tumors, GRPR expression correlated with TGF-α and EGFR expression (P = 0.0378 and P = 0.0026, respectively).Conclusions: These findings support an autocrine signaling pathway involving TGF-α, EGFR, and pSTAT3 in metastatic SCCHN as well as transactivation of EGFR by GRPR via TGF-α, but fails to identify an independent prognostic role for pSTAT3 immunoexpression.
Quantitative Monitoring of Adenocarcinoma Development in Rodents by Magnetic Resonance Imaging
Authors: Garbow Joel R. , Wang Min , Wang Yian , Lubet Ronald A. , You Ming 
Published: March 2008

Abstract
Purpose: Accurately following the time course of tumor progression and response to therapy in animal models of cancer is key to the development of better chemopreventive and chemotherapeutic agents. The goal of this work was to monitor quantitatively the development and progression of adenocarcinoma in a time course study of mice treated with the carcinogen urethane using in vivo small-animal magnetic resonance imaging (MRI).
Experimental Design: Mice treated with a single dose of urethane were imaged at four time points beginning 8 months after treatment. High-resolution images of mouse lung were obtained in vivo using respiratory-gated MRI methods. Individual tumors were manually segmented and their volumes calculated. At the end of the study, mice were euthanized and MRI tumor quantification was validated by histology and histopathology.
Results: Tumors as small as 0.4 mm in diameter can be detected and quantitatively measured in mice by in vivo MRI. Total tumor burden increased consistently in all mice studied, whereas the growth rate of individual tumors varied widely. The positions and diameters of individual tumors as measured by MRI correlated well with histology results. Histologic study of large, rapidly growing tumors showed that these were adenocarcinomas, whereas small, slowly growing lesions were predominantly adenomas.
Conclusions: Longitudinal in vivo MRI is a powerful modality that can be of great aid in elucidating the factors that control the onset of lung tumors and can serve as a platform for the development and preclinical testing of novel therapies having a high likelihood of efficacy in human clinical trials.