bluuebunny/crossref_metadata_2025_split huggingface dataset:
Competitive success of natural oak regeneration in clearcuts during the stem exclusion stage
Authors: Morrissey Robert C. , Jacobs Douglass F. , Seifert John R. , Fischer Burnell C. , Kershaw John A. 
Published: June 2008

We sampled dominant and codominant regeneration on 70 clearcuts, 21–35 years old, on the Hoosier National Forest in southern Indiana, USA, to evaluate influence of site variables on the competitive success of natural oak ( Quercus L.) over time. Collected data was compared with data collected on these same sites 20 years prior. Regression tree analysis indicated aspect, natural region, and oak abundance in preharvest stands had the greatest influence on competitive success (relative density, RD) of oak species in the latter sampling, which was then examined across sites as defined by these three variables. Oak RD increased across all mid- and some lower-slope positions, sites on which oaks are expected to be replaced by faster growing species. Drought events between sampling periods apparently contributed to a decline in RD and vigor of yellow-poplar ( Liriodendron tulipifera L.), a major competitor for growing space. Stump sprouts contributed 45% of dominant oak stems. Mean oak diameters were not significantly lower than those of other species groups, with the exception of yellow-poplar in younger stands and at mid-slope positions. Oak species drought tolerance, relative to more mesic species found on these sites, and the large proportion of oak stump sprouts likely contributed to oak competitive success.
THE EFFECTIVENESS OF THE COMPONENT IMPACT TEST METHOD FOR THE SIDE IMPACT INJURY ASSESSMENT OF THE DOOR TRIM
Authors: YOUN YOUNGHAN , KOO JEONG-SEO 
Published: June 2008

The complete evaluation of the side vehicle structure and the occupant protection is only possible by means of the full scale side impact crash test. But, auto part manufacturers such as door trim makers can not conduct the test especially when the vehicle is under the developing process. The main objective of this study is to obtain the design guidelines by a simple component level impact test. The relationship between the target absorption energy and impactor speed were examined using the energy absorbed by the door trim. Since each different vehicle type required different energy levels on the door trim. A simple impact test method was developed to estimate abdominal injury by measuring reaction force of the impactor. The reaction force will be converted to a certain level of the energy by the proposed formula. The target of absorption energy for door trim only and the impact speed of simple impactor are derived theoretically based on the conservation of energy. With calculated speed of dummy and the effective mass of abdomen, the energy allocated in the abdomen area of door trim was calculated. The impactor speed can be calculated based on the equivalent energy of door trim absorbed during the full crash test. With the proposed design procedure for the door trim by a simple impact test method was demonstrated to evaluate the abdominal injury. This paper describes a study that was conducted to determine sensitivity of several design factors for reducing abdominal injury values using the matrix of orthogonal array method. In conclusion, with theoretical considerations and empirical test data, the main objective, standardization of door trim design using the simple impact test method was established.
SURFACE SUBGROUPS OF RIGHT-ANGLED ARTIN GROUPS
Authors: CRISP JOHN , SAGEEV MICHAH , SAPIR MARK 
Published: June 2008

We consider the question of which right-angled Artin groups contain closed hyperbolic surface subgroups. It is known that a right-angled Artin group A(K) has such a subgroup if its defining graph K contains an n-hole (i.e. an induced cycle of length n) with n ≥ 5. We construct another eight "forbidden" graphs and show that every graph K on ≤ 8 vertices either contains one of our examples, or contains a hole of length ≥ 5, or has the property that A(K) does not contain hyperbolic closed surface subgroups. We also provide several sufficient conditions for a right-angled Artin group to contain no hyperbolic surface subgroups. We prove that for one of these "forbidden" subgraphs P2(6), the right-angled Artin group A(P2(6)) is a subgroup of a (right-angled Artin) diagram group. Thus we show that a diagram group can contain a non-free hyperbolic subgroup answering a question of Guba and Sapir. We also show that fundamental groups of non-orientable surfaces can be subgroups of diagram groups. Thus the first integral homology of a subgroup of a diagram group can have torsion (all homology groups of all diagram groups are free Abelian by a result of Guba and Sapir).
Osteoglossomorpha: phylogeny, biogeography, and fossil record and the significance of key African and Chinese fossil taxa
Authors: Wilson M. V. H. , Murray A. M. 
Published: June 2008

Abstract

The Osteoglossomorpha are a clade of primitive teleostean fishes with modern representatives in five biogeogeographic regions and fossil representatives on six continents. The centre of modern diversity is in Africa but the centre of fossil diversity is in E Asia. Key fossil taxa include: †
Phareodus
, †
Joffrichthys
, and †
Ostariostoma
in N America; †
Lycoptera
, †
Paralycoptera
, and †
Huashia
among others in E Asia; †
Brychaetus
and possibly †
Thaumaturus
in Europe; †
Palaeonotopterus
, †
Singida
, and †
Chauliopareion
in Africa; †
Tavernichthys
in India; and †
Musperia
in SE Asia.

Morphological phylogenies to date have disagreed on three main points: the relationships of †
Lycoptera
, of
Pantodon
, and of Notopterids and Mormyrids. Molecular phylogenies have similarly differed on the last two points. In this study a combined set of morphological data was generated from previous studies, including data from three recently described or redescribed taxa (the African †
Singida
and †
Chauliopareion
and the Chinese †
Xixiaichthys
) and maximum parsimony was used to generate a revised hypothesis of relationships. Our analysis recovered †
Lycoptera
, †
Paralycoptera
+ †
Tanolepis
, and †
Xixiaichthys
as stem-group osteoglossomorphs, †
Singida
as sister to
Pantodon
within Osteoglossidae, †
Chauliopareion
as a stem osteoglossid, †
Ostariostoma
as a stem osteoglossiform, and Notopteridae as sister to Mormyroidea and †
Palaeonotopterus
.

These results do not lend themselves to easy explanations of osteoglossomorph biogeography involving either dispersal from a centre of origin or vicariant division of a widely distributed ancestor. Recent suggestions of an ancient (Palaeozoic) origin for osteoglossomorphs are flawed. The evidence, instead, is consistent with an origin within the Mesozoic and the biogeographic explanation involves extensive extinction of clades from continents where they occurred in the past.
Fishes and the Break-up of Pangaea: an introduction
Authors: Cavin Lionel , Longbottom Alison , Richter Martha 
Published: June 2008

Abstract
There is general agreement that a tight relationship exists between evolutionary histories of living lineages and the shifting geography of the Earth during the Phanerozoic, but how to depict that link has been much disputed in recent decades. The issue is fundamental, as it involves two supposedly-irreconcilable paradigms for how we interpret past and present distributions: the Darwin–Wallace biogeographic paradigm that involves dispersal from centres of origin, and the vicariance paradigm. When dealing with extinct organisms, for which we have only sparse and fragmentary fossil remains, the limit between the two paradigms becomes blurred. Here, all available data about time (stratigraphy) and space (palaeogeography) need to be gathered in order to detect biogeographical signals.
Because of the incompleteness of the fossil record, the analyses may lead to storytelling style descriptions of biogeographic scenarios (phylogenies are often weakly supported, datings are frequently vague and occurrences are sparse). But these scenarios are always open to refutation if new fossils are found and, accordingly, are genuine scientific hypotheses. The Darwin–Wallace biogeographic paradigm and the vicariance paradigm have been described as the extreme points of a pendulum; in this book, examples of relationships between the evolutionary history of fish clades and the break-up of Pangaea are described using approaches that lie between these extreme points of the pendulum.
New eugeneodontid sharks from the Lower Triassic Sulphur Mountain Formation of Western Canada
Authors: Mutter Raoul J. , Neuman Andrew G. 
Published: June 2008

Abstract

Eugeneodontid sharks, previously believed to have become virtually extinct during the great end-Permian extinction event, are here shown to be diverse in the Early Triassic of western Canada. Although the specimens are probably predominantly Olenekian in age, they show an abundance similar to that of the Late Permian of East Greenland. Similar in size and morphology to their Palaeozoic predecessors, this diverse assemblage is seen to have a short duration within the Early Triassic. A number of identifiable dentitions and postcranial skeletal remains suggest the presence of at least two caseodontid species (
Caseodus varidentis
sp. nov. and
Fadenia uroclasmato
sp. nov.) and an edestoid (
Paredestus bricircum
gen. et sp. nov.) Many other specimens recovered from the Lower Triassic Vega-Phroso Siltstone Member (Sulphur Mountain Formation) at Wapiti Lake are too poorly preserved for identification but help demonstrate the major taxonomic problems in eugeneodontid systematics. We discuss the survival of this highly specialized group of ‘sharks’ and comment on their biogeographical distribution across the Permo-Triassic boundary.
Mel-18 Negatively Regulates INK4a/ARF-Independent Cell Cycle Progression via Akt Inactivation in Breast Cancer
Authors: Lee Jeong-Yeon , Jang Ki-Seok , Shin Dong-Hui , Oh Mi-Yun , Kim Hyun-Jun , Kim Yongseok , Kong Gu 
Published: June 2008

Abstract
Mel-18, a polycomb group (PcG) protein, has been suggested as a tumor suppressor in human breast cancer. Previously, we reported that Mel-18 has antiproliferative activity in breast cancer cells. However, its functional mechanism has not been fully elucidated. Here, we investigated the role of Mel-18 in human breast cancer. We saw an inverse correlation between Mel-18 and phospho-Akt, which were expressed at low and high levels, respectively, in primary breast tumor tissues from 40 breast cancer patients. The effect of Mel-18 on cell growth was examined in two breast cancer cell lines, SK-BR-3 and T-47D, which express relatively low and high levels of endogenous Mel-18, respectively. On Mel-18 overexpression in SK-BR-3 cells, cell growth was attenuated and G1 arrest was observed. Likewise, suppression of Mel-18 by antisense expression in T-47D cells led to enhanced cell growth and accelerated G1-S phase transition. In these cells, cyclin-dependent kinase (Cdk)-4 and Cdk2 activities were affected by Mel-18, which were mediated by changes in cyclin D1 expression and p27Kip1 phosphorylation at Thr157, but not by INK4a/ARF genes. The changes were both dependent on the phosphatidylinositol 3-kinase/Akt signaling pathway. Akt phosphorylation at Ser473 was reduced by Mel-18 overexpression in SK-BR-3 cells and enhanced by Mel-18 suppression in T-47D cells. Akt-mediated cytoplasmic localization of p27Kip1 was inhibited by Mel-18 in SK-BR-3 cells. Moreover, Mel-18 overexpression showed reduced glycogen synthase kinase-3β phosphorylation, β-catenin nuclear localization, T-cell factor/lymphoid enhancer factor promoter activity, and cyclin D1 mRNA level. Taken together, we established a linear relationship between Mel-18→Akt→G1 phase regulators. [Cancer Res 2008;68(11):4201–9]
Functional and Clinical Evidence for NDRG2 as a Candidate Suppressor of Liver Cancer Metastasis
Authors: Lee Dong Chul , Kang Yun Kyung , Kim Woo Ho , Jang Ye Jin , Kim Dong Joon , Park In Young , Sohn Bo Hwa , Sohn Hyun Ahm , Lee Hee Gu , Lim Jong Seok , Kim Jae Wha , Song Eun Young , Kim Dong Min , Lee Mi-Ni , Oh Goo Taeg , Kim Soo Jung , Park Kyung Chan , Yoo Hyang Sook , Choi Jong Young , Yeom Young Il 
Published: June 2008

Abstract
We searched for potential suppressors of tumor metastasis by identifying the genes that are frequently down-regulated in hepatocellular carcinomas (HCC) while being negatively correlated with clinical parameters relevant to tumor metastasis, and we report here on the identification of N-myc downstream regulated gene 2 (NDRG2) as a promising candidate. NDRG2 expression was significantly reduced in HCC compared with nontumor or normal liver tissues [87.5% (35 of 40) and 62% (62 of 100) at RNA and protein levels, respectively]. Reduction of NDRG2 expression was intimately associated with promoter hypermethylation because its promoter region was found to carry extensively methylated CpG sites in HCC cell lines and primary tumors. Immunohistochemical analysis of NDRG2 protein in 100 HCC patient tissues indicated that NDRG2 expression loss is significantly correlated with aggressive tumor behaviors such as late tumor-node-metastasis (TNM) stage (P = 0.012), differentiation grade (P = 0.024), portal vein thrombi (P = 0.011), infiltrative growth pattern (P = 0.015), nodal/distant metastasis (P = 0.027), and recurrent tumor (P = 0.021), as well as shorter patient survival rates. Ectopically expressed NDRG2 suppressed invasion and migration of a highly invasive cell line, SK-Hep-1, and experimental tumor metastasis in vivo, whereas small interfering RNA–mediated knockdown resulted in increased invasion and migration of a weakly invasive cell line, PLC/PRF/5. In addition, NDRG2 could antagonize transforming growth factor β1–mediated tumor cell invasion by specifically down-regulating the expression of matrix metalloproteinase 2 and laminin 332 pathway components, with concomitant suppression of Rho GTPase activity. These results suggest that NDRG2 can inhibit extracellular matrix–based, Rho-driven tumor cell invasion and migration and thereby play important roles in suppressing tumor metastasis in HCC. [Cancer Res 2008;68(11):4210–20]
ASAP1, a Gene at 8q24, Is Associated with Prostate Cancer Metastasis
Authors: Lin Dong , Watahiki Akira , Bayani Jane , Zhang Fang , Liu Lin , Ling Victor , Sadar Marianne D. , English John , Fazli Ladan , So Alan , Gout Peter W. , Gleave Martin , Squire Jeremy A. , Wang Yu-Zhuo 
Published: June 2008

Abstract
Metastatic prostate cancer is a terminal disease, and the development of reliable prognostic tools and more effective therapy is critically important for improved disease survival and management. This study was aimed at identifying genes that are differentially expressed in metastatic and nonmetastatic prostate cancer cells and, as such, could be critical in the development of metastasis. Long-SAGE analysis was used to compare a transplantable human metastatic prostate cancer subline, PCa1-met, with a nonmetastatic counterpart, PCa2. Both sublines were developed from a patient's prostate cancer specimen via subrenal capsule grafting and subsequent orthotopic implantation into SCID mice. Among various differentially expressed genes identified, ASAP1, an 8q24 gene encoding an ADP-ribosylation factor GTPase-activating protein not previously associated with prostate cancer, was up-regulated in the metastatic subline as confirmed by quantitative real-time PCR. Immunohistochemistry of xenograft sections showed that cytoplasmic ASAP1 protein staining was absent or weak in benign tissue, significantly stronger in nonmetastatic PCa2 tissue, and strongest in PCa1-met tissue. In clinical specimens, ASAP1 protein staining was elevated in 80% of primary prostate cancers and substantially higher in metastatic lesions compared with benign prostate tissue. Moreover, additional ASAP1 gene copies were detected in 58% of the primary prostate cancer specimens. Small interfering RNA–induced reduction of ASAP1 protein expression markedly suppressed in vitro PC-3 cell migration (∼50%) and Matrigel invasion (∼67%). This study suggests that the ASAP1 gene plays a role in prostate cancer metastasis and may represent a therapeutic target and/or biomarker for metastatic disease. [Cancer Res 2008;68(11):4352–9]
Interleukin-21 Augments the Efficacy of T-Cell Therapy by Eliciting Concurrent Cellular and Humoral Responses
Authors: Iuchi Takekazu , Teitz-Tennenbaum Seagal , Huang Jianhua , Redman Bruce G. , Hughes Steven D. , Li Mu , Jiang Guihua , Chang Alfred E. , Li Qiao 
Published: June 2008

AbstractInterleukin (IL)-21 modulates T-cell–associated, B-cell–associated, and natural killer cell–associated immunity. However, the potential of IL-21 to simultaneously stimulate cellular and humoral antitumor responses and the mechanisms involved have not yet been adequately explored. In this report, we examined the immune-modulating effect of IL-21 when used in vitro and its adjuvant effects when administrated concomitantly with T-cell transfer for cancer therapy. Use of IL-21 in concert with IL-2 in culture up-regulated both type 1 and type 2 cytokine production of activated tumor-draining lymph node cells and enhanced their therapeutic efficacy. Administration of IL-21 and IL-2 as an adjuvant to T-cell transfer resulted in simultaneously elicited cellular and humoral responses. This concurrent response has led to effective regression of established pulmonary metastatic tumors and s.c. tumors. T-cell transfer plus IL-21/IL-2 administration conferred systemic immunity to the treated hosts. This was evident by the induction of protective immunity against tumor rechallenge, expansion of memory T cells, and significantly elevated serum levels of IFNγ and IL-10. Furthermore, we observed significantly enhanced tumor-associated antibody response after T-cell + IL-2 + IL-21 therapy. Cytotoxic antibody subclass IgG2b increased strikingly in the sera of treated animals; they bound specifically to MCA205 tumor cells, and such immune sera mediated tumor cell lysis in the presence of complement. Use of B-cell–deficient mice provided direct evidence that humoral responses contribute to T-cell + IL-2 + IL-21–elicited antitumor immunity. Collectively, these findings provide a rationale to evaluate the use of IL-21 in T-cell therapy of human cancers. [Cancer Res 2008;68(11):4431–41]
Pediatric Malignant Germ Cell Tumors Show Characteristic Transcriptome Profiles
Authors: Palmer Roger D. , Barbosa-Morais Nuno L. , Gooding Emma L. , Muralidhar Balaji , Thornton Claire M. , Pett Mark R. , Roberts Ian , Schneider Dominik T. , Thorne Natalie , Tavaré Simon , Nicholson James C. , Coleman Nicholas ,   on behalf of Children's Cancer and Leukaemia Group
Published: June 2008

AbstractMalignant germ cell tumors (GCT) of childhood are rare and heterogeneous neoplasms thought to arise from primordial germ cells. They vary substantially in their natural history and show important clinical differences from their adult counterparts. To address the biological basis for these observations, we have undertaken a comprehensive analysis of global gene expression patterns in pediatric malignant GCTs and compared these findings with published data on adult testicular GCTs (TGCT). Our study included 27 primary tumors and assessed the principal malignant histologic types of pediatric GCT, yolk sac tumor (YST; n = 18), and seminoma (n = 9). Analysis of Affymetrix U133A GeneChip data was performed using the statistical software environment R, including gene set enrichment analysis, with cross-validation at the RNA and protein level. Unsupervised analysis showed complete separation of YSTs and seminomas by global gene expression profiles and identified a robust set of 657 discriminatory transcripts. There was no segregation of tumors of the same histology arising at different sites or at different ages within the pediatric range. In contrast, there was segregation of pediatric malignant GCTs and adult malignant TGCTs, most notably for the YSTs. The pediatric seminomas were significantly enriched for genes associated with the self-renewing pluripotent phenotype, whereas the pediatric YSTs were significantly enriched for genes associated with a differentiation and proliferation phenotype. We conclude that histologic type is the key discriminator in pediatric malignant GCTs and that the observed clinical differences between malignant GCTs of children and adults are mirrored by significant differences in global gene expression. [Cancer Res 2008;68(11):4239–47]
Immunoglobulin Allotypes Influence Antibody Responses to Mucin 1 in Patients with Gastric Cancer
Authors: Pandey Janardan P. , Nietert Paul J. , von Mensdorff-Pouilly Silvia , Klaamas Kersti , Kurtenkov Oleg 
Published: June 2008

AbstractThere are significant interindividual differences in naturally occurring antibody responses to the tumor-associated antigen mucin 1 (MUC1), but the host genetic factors that might contribute to these differences have not been identified. The aim of the present investigation was to determine whether the variation in naturally occurring antibody levels to MUC1 in patients with gastric cancer is associated with GM and KM allotypes, genetic markers of IgG heavy chains and κ-type light chains, respectively. A total of 169 Caucasian subjects with gastric cancer were allotyped for several GM and KM markers. These subjects were also characterized for IgG and IgM antibodies to MUC1. GM 3 23 5,13 phenotype was highly significantly associated with MUC1 IgG levels; subjects with this phenotype had lower antibody levels compared with those lacking this phenotype (median IgG level 65.5 relative units versus 91.0 relative units, P = 0.0058). In addition, this phenotype had an interactive effect with KM phenotypes on the levels of IgG antibodies to this antigen (P = 0.0081). Levels of MUC1 IgM antibodies were not associated with these genetic markers. These results show, for the first time, that GM and KM allotypes contribute to the interindividual differences in humoral immunity to MUC1. [Cancer Res 2008;68(11):4442–6]
Defective Claudin-7 Regulation by Tcf-4 and Sox-9 Disrupts the Polarity and Increases the Tumorigenicity of Colorectal Cancer Cells
Authors: Darido Charbel , Buchert Michael , Pannequin Julie , Bastide Pauline , Zalzali Hassan , Mantamadiotis Theo , Bourgaux Jean-François , Garambois Véronique , Jay Philippe , Blache Philippe , Joubert Dominique , Hollande Frédéric 
Published: June 2008

Abstract
Tight junctions have recently emerged as essential signaling regulators of proliferation and differentiation in epithelial tissues. Here, we aimed to identify the factors regulating claudin-7 expression in the colon, and analyzed the consequences of claudin-7 overexpression in colorectal carcinoma (CRC). In healthy human colonic crypts, claudin-7 expression was found to be low in the stem/progenitor cell compartment, where Tcf-4 activity is high, but strong in differentiated and postmitotic cells, where Tcf-4 is inactive. In contrast, claudin-7 was overexpressed in areas with high Tcf-4 target gene levels in CRC samples. In vitro, Tcf-4 was able to repress claudin-7 expression, and the high mobility group–box transcription factor Sox-9 was identified as an essential mediator of this effect. Claudin-7 was strongly expressed in the intestine of Sox-9–deficient mice and in CRC cells with low Sox transcriptional activity. Sox-9 overexpression in these cells reinstated claudin-7 repression, and residual claudin-7 was no longer localized along the basolateral membrane, but was instead restricted to tight junctions. Using HT-29Cl.16E CRC cell spheroids, we found that Sox-9–induced polarization was completely reversed after virus-mediated claudin-7 overexpression. Claudin-7 overexpression in this context increased Tcf-4 target gene expression, proliferation, and tumorigenicity after injection in nude mice. Our results indicate that Tcf-4 maintains low levels of claudin-7 at the bottom of colonic crypts, acting via Sox-9. This negative regulation seems to be defective in CRC, possibly due to decreased Sox-9 activity, and the resulting claudin-7 overexpression promotes a loss of tumor cell polarization and contributes to tumorigenesis. [Cancer Res 2008;68(11):4258–68]