bluuebunny/crossref_metadata_2025_split huggingface dataset:
Wildland fire effects on understory plant communities in two fire-prone forests
Authors: Laughlin Daniel C. , Fulé Peter Z. 
Published: March 2008

Our understanding of wildland fire effects on understory plant communities is limited because of a lack of repeated measurements before and after lightning-ignited fires. We examined vegetation responses to a surface fire in a ponderosa pine forest and a mixed-severity fire in a spruce–fir–aspen forest using before–after, control–impact (BACI) study designs. We hypothesized that the surface fire would stimulate plant species richness and minimally alter community composition, but that the mixed-severity fire would decrease richness and significantly alter composition. In ponderosa pine forests, total species richness and plant cover increased slightly because of annual and biennial forb and grass establishment in soils where duff layers were reduced by the surface fire. In spruce–fir–aspen forests, total species richness and plant cover were similar in burned and unburned forests after 2 years, although annual and biennial forbs and graminoids increased significantly in the burned area. Plant community composition was altered by both fires. Wildfires may indirectly influence the understory plant community through the mediating effects of overstory basal area and litter depth. Fire effects on plant species richness and cover were weaker than effects due to environmental factors. Managers should anticipate increases in both native and non-native ruderal species following landscape-scale fires.
Effects of time since stand-replacing fire and overstory composition on live-tree structural diversity in the boreal forest of central Canada
Authors: Brassard Brian W. , Chen Han Y.H. , Wang Jian R. , Duinker Peter N. 
Published: March 2008

Stand structure diversity is hypothesized (i) to increase with stand development and (ii) to be greater in mixedwood stands than in conifer and broadleaf stands. We examined the effects of time since stand-replacing fire (TSF) and overstory type on stand volume, stand density, and tree-size variability, which is measured using Shannon’s diversity index (H′) and coefficient of variation, in fire-origin boreal forest stands. We sampled 36 stands representing conifer, mixedwood, and broadleaf overstory types, ranging in ages from 72 to 201 years TSF on upland mesic sites in northwestern Ontario, Canada. Stand volume decreased in older mixedwood and broadleaf stands, but followed a U-shaped pattern in conifer stands with TSF. Diameter-at-breast-height-based H′ followed an inverse U-shaped pattern with TSF for all overstory types. Height-based H′ decreased with TSF in conifer and mixedwood stands but peaked at the intermediate age class in broadleaf stands. Diameter-at-breast-height- and height-based coefficient of variation indices followed an inverse U-shaped distribution with TSF. Our results partially supported the two hypotheses, as (i) the 124- to 139-year-old stands were most diverse and (ii) mixedwood stands were more than or as equally diverse as conifer and broadleaf stands, depending on stand development stage and the diversity indices used.
Effect of fertilization and genetic variation on susceptibility ofPinus radiataseedlings toHylobius abietisdamage
Authors: Zas Rafael , Sampedro Luis , Moreira Xoaquín , Martíns Patricia 
Published: March 2008

The effects of establishment fertilization and pine genotype on pine weevil ( Hylobius abietis L.) damage was studied in a radiata pine ( Pinus radiata D. Don) naturally infected family × fertilization genetic trial in Galicia (northwestern Spain). Fertilization strongly increased both growth and H. abietis damage, especially when calcium phosphate was included in the fertilization treatment. Fertilized plants showed higher degree of debarking, greater leader loss, and higher mortality than unfertilized controls. Because of the greater leader loss, fertilization did not significantly increase the actual height (height of live stem) 1 year after planting. In contrast, after the second growing season, fertilized plants overcompensated for the weevil damage and reached greater height than the unfertilized controls. However, considering the effects on survival and the stem deformities resulting from the leader losses, fertilization should be avoided (or delayed) in P. radiata plantations on clear-cut coniferous areas if the risk of H. abietis is high. Our results also indicate a strong genetic variation in H. abietis susceptibility within the Galician P. radiata breeding population. The high family-mean and the moderate individual-tree heritability estimates suggest that improving resistance to this pest by conventional breeding techniques is possible. The use of planting stock with improved resistance should be considered as another prophylactic measure to supplement the traditional methods employed against this pest.
Site index in agroforestry systems: age-dependent and age-independent dynamic diameter growth models forQuercus ilexin Iberian open oak woodlands
Authors: Gea-Izquierdo G. , Cañellas I. , Montero G. 
Published: March 2008

Despite Quercus ilex L. being one of the most widespread tree species in the Mediterranean basin, there are no growth models in the literature for this species. In this study, we compare age-dependent and age-independent dynamic diameter growth models and discuss the concept of dominance in open stands. A posteriori dominance was determined to fit potential age-dependent growth models and a site index based on diameter growth was defined. Formulations derived from power decline base models (Korf and Hossfeld) best described diameter growth. The best approach for age-dependent models was a polymorphic and with variable asymptotes generalized algebraic difference approach formulation. Residual errors in trees between 20 and 55 cm ranged from ~7.0% in potential growth models to ~15% in age-independent models expanded by density. Using a unique age-dependent dynamic equation for all trees, regardless of dominance, did not increase the error very much. In age-independent models, the inclusion of the defined site index reduced the prediction error but requires that the age of trees is estimated to determine the site index. The difficulty of estimating Q. ilex age makes age-independent models very attractive for system modelling. Age-independent models could be useful in other ecosystems where age estimation is problematic.
Using fuel and weather variables to predict the sustainability of surface fire spread in maritime pine stands
Authors: Fernandes Paulo M. , Botelho Hermínio , Rego Francisco , Loureiro Carlos 
Published: March 2008

Thresholds for surface fire spread were examined in maritime pine ( Pinus pinaster Ait.) stands in northern Portugal. Fire sustainability was assessed after ignition of 2 m fire lines or in larger burns conducted in 10–15 m wide plots. The experiments were carried out from November to June in three fuel types: litter, litter plus shrubs, and litter with a nonwoody understorey. Moisture content of fine dead fuels, on-site weather variables, and descriptors of the fuel complex all had a highly significant influence on the probability of self-sustaining fire spread. A logistic model based solely on fuel moisture content correctly classified the fire sustainability status of 88% of the observations. Nonetheless, the subjectivity of the moisture of extinction concept was apparent, and further accuracy was achieved by the consecutive addition of fire spread direction (forward or backward), fuel type, and ambient temperature. Fully sustained fire spread, in opposition to marginal burns with broken fire fronts, was similarly dependent on fuel moisture but was affected also by fire spread direction and time since rain. The models can benefit fire research and fire management operations but can be made more practical if integrated in a fire danger rating system.
Potential change in lodgepole pine site index and distribution under climatic change in Alberta
Authors: Monserud Robert A. , Yang Yuqing , Huang Shongming , Tchebakova Nadja 
Published: March 2008

We estimated the impact of global climate change on lodgepole pine ( Pinus contorta Dougl. ex Loud. var. latifolia Engelm.) site productivity in Alberta based on the Alberta Climate Model and the A2 SRES climate change scenario projections from three global circulation models (CGCM2, HADCM3, and ECHAM4). Considerable warming is apparent in all three models. On average, the increases in mean GDD5 (growing degree-days >5 °C) are 18%, 38%, and 65% by the 2020s, 2050s, and 2080s, respectively. Change in precipitation is essentially nil. This results in proportional increases in dryness index. We used the dryness index to predict the potential future range and GDD5 to predict its potential productivity. Generally, lodgepole pine site index is predicted to increase steadily by 3 m for each 30-year period. Offsetting this increase is a large reduction in suitable area as drying increases. At first, the warming increases the potential range up to 67% by the 2020s but then shrinks from 34% to 58% of its current area by 2080. Such major changes will need to be considered when setting long-term forest management plans. The increased risk of both wildfire and insect outbreaks further compounds this planning problem, especially because these disturbance events can interact and further increase risk.
Inhibition of Multiple Vascular Endothelial Growth Factor Receptors (VEGFR) Blocks Lymph Node Metastases but Inhibition of VEGFR-2 Is Sufficient to Sensitize Tumor Cells to Platinum-Based Chemotherapeutics
Authors: Sini Patrizia , Samarzija Ivana , Baffert Fabienne , Littlewood-Evans Amanda , Schnell Christian , Theuer Andreas , Christian Sven , Boos Anja , Hess-Stumpp Holger , Foekens John A. , Setyono-Han Buddy , Wood Jeanette , Hynes Nancy E. 
Published: March 2008

Abstract
Vascular endothelial growth factor receptors (VEGFR) have important roles in cancer, affecting blood and lymphatic vessel functionality as well as tumor cells themselves. We compared the efficacy of a VEGFR tyrosine kinase inhibitor, PTK787/ZK222584 (PTK/ZK), which targets the three VEGFRs, with blocking antibodies directed against VEGFR-2 (DC101) or VEGF-A (Pab85618) in a metastatic melanoma model. Although all inhibitors exerted comparable effects on primary tumor growth, only PTK/ZK significantly reduced lymph node metastasis formation. A comparable decrease in lymphatic vessel density following blockade of VEGFR-2 (DC101) or the three VEGFRs (PTK/ZK) was observed in the metastases. However, the functionality of lymphatics surrounding the primary tumor was more significantly disrupted by PTK/ZK, indicating the importance of multiple VEGFRs in the metastatic process. The antimetastatic properties of PTK/ZK were confirmed in a breast carcinoma model. B16/BL6 tumor cells express VEGF ligands and their receptors. Blockade of a VEGFR-1 autocrine loop with PTK/ZK inhibited tumor cell migration. Furthermore, the tumor cells also showed enhanced sensitivity to platinum-based chemotherapy in combination with PTK/ZK, indicating that autocrine VEGFRs are promoting tumor cell migration and survival. In summary, our results suggest that, in addition to blocking angiogenesis, combined inhibition of the three VEGFRs may more efficiently target other aspects of tumor pathophysiology, including lymphatic vessel functionality, tumor cell dissemination, survival pathways, and response to chemotherapeutic compounds. [Cancer Res 2008;68(5):1581–92]
Vascular Endothelial Cadherin Promotes Breast Cancer Progression via Transforming Growth Factor β Signaling
Authors: Labelle Myriam , Schnittler Hans J. , Aust Daniela E. , Friedrich Katrin , Baretton Gustavo , Vestweber Dietmar , Breier Georg 
Published: March 2008

Abstract
Epithelial-to-mesenchymal transition (EMT) is an important event during carcinoma progression and leads to increased tumor cell malignancy. Here, we show that vascular endothelial (VE)-cadherin is induced during EMT in mammary tumor cells and is aberrantly expressed in invasive human breast carcinomas. VE-cadherin enhanced the capacity of fibroblastoid tumor cells to proliferate, form cord-like invasive structures, and adhere to endothelial cells, characteristics that are key contributors to their increased malignancy and metastatic potential. Consistently, VE-cadherin expression in malignant fibroblastoid tumor cells promoted the growth of experimental mammary carcinomas in vivo. Analysis of the signaling mechanisms involved revealed that VE-cadherin expression influences the levels of Smad2 phosphorylation and expression of target genes of transforming growth factor-β (TGF-β), a major mediator of advanced tumor progression and malignant tumor cell proliferation. VE-cadherin might thus promote tumor progression not only by contributing to tumor angiogenesis but also by enhancing tumor cell proliferation via the TGF-β signaling pathway. This article provides evidence for a novel function of VE-cadherin in tumor progression and reveals a previously unknown molecular link between VE-cadherin expression and TGF-β signaling. Our findings may have important implications for the clinical application of anti–VE-cadherin strategies. [Cancer Res 2008;68(5):1388–97]
DNA Damage–Dependent Translocation of B23 and p19ARF Is Regulated by the Jun N-Terminal Kinase Pathway
Authors: Yogev Orli , Saadon Keren , Anzi Shira , Inoue Kazushi , Shaulian Eitan 
Published: March 2008

Abstract
The dynamic behavior of the nucleolus plays a role in the detection of and response to DNA damage of cells. Two nucleolar proteins, p14ARF/p19ARF and B23, were shown to translocate out of the nucleolus after exposure of cells to DNA-damaging agents. This translocation affects multiple cellular functions, such as DNA repair, proliferation, and survival. In this study, we identify a pathway and scrutinize the mechanisms leading to the translocation of these proteins after exposure of cells to DNA-damaging agents. We show that redistribution of B23 and p19ARF after the exposure to genotoxic stress occurs preferentially when the c-Jun-NH2-kinase (JNK) pathway is activated and is inhibited when the JNK pathway is impaired. The stress-induced translocation of alternative reading frame (ARF) is JNK dependent and mediated by two activator proteins, c-Jun and JunB. Thr91 and Thr93 of c-Jun are required for the translocation, but the transcriptional activity of c-Jun is dispensable. Instead, c-Jun interacts with B23 in a dose-dependent manner. c-Jun itself is excluded from the nucleolus in a JNK-dependent manner. Hence, we suggest that c-Jun translocates B23 and ARF from the nucleolus after JNK activation by means of protein interactions. In senescent cells, JNK activity and c-Jun levels are reduced concomitantly with ARF nucleolar accumulation, and UV radiation does not cause the translocation of ARF. [Cancer Res 2008;68(5):1398–406]
Clonal Selection in Malignant Transformation of Human Fibroblasts Transduced with Defined Cellular Oncogenes
Authors: Mahale Alka M. , Khan Zahid A.T. , Igarashi Makoto , Nanjangud Gouri J. , Qiao Rui Fang , Yao Shen , Lee Sam W. , Aaronson Stuart A. 
Published: March 2008

Abstract
Recent evidence has implied that disruption of a limited number of defined cellular pathways is necessary and sufficient for neoplastic conversion of a variety of normal human cell types in tissue culture. We show instead that malignancy in such models results from an iterative process of clonal selection in vitro and/or in vivo. Normal human fibroblasts underwent malignant transformation after transduction with telomerase, cyclin-dependent kinase 4, dominant-negative p53, and activated Ras or MEK. Furthermore, culture conditions favoring overgrowth resulted in clonal selection, which with added Ras or MEK oncogenes led to the emergence of tumorigenic clones. Such tumors showed variable degrees of malignancy with some even exhibiting metastasis. SV40 small t antigen (ST) has been reported to be necessary and sufficient to convert human fibroblasts with these pathway aberrations to a polyclonal tumor. However, we observed that clonal tumors emerged even with ST addition. Genomic instability was markedly increased by p53 and Rb pathway abrogation. Under the same conditions, fibroblasts with these alterations failed to induce tumors, implying that genomic instability may be necessary but not sufficient for malignant transformation. These findings indicate that the minimum number of events required for malignant transformation of human fibroblasts is greater than has been enumerated by such oncogene addition strategies and support a stochastic cancer progression model initiated by four defined cellular alterations. [Cancer Res 2008;68(5):1417–26]
Survival Advantage of EBV-Associated Gastric Carcinoma: Survivin Up-regulation by Viral Latent Membrane Protein 2A
Authors: Hino Rumi , Uozaki Hiroshi , Inoue Yoko , Shintani Yukako , Ushiku Tetsuo , Sakatani Takashi , Takada Kenzo , Fukayama Masashi 
Published: March 2008

Abstract
EBV-associated gastric carcinoma is a distinct subset of gastric carcinoma infected with EBV, which shows latency I type expression of EBV latent genes (EBNA1, EBER, BARF0, and LMP2A). To clarify the role of EBV in this type of gastric carcinoma, the cell biological characteristics (growth, apoptosis, and migration) were evaluated in gastric carcinoma cell lines (MKN-1, TMK1, MKN-74 and MKN-7) with and without infection of recombinant EBV harboring the neomycin resistance gene. The infection reiterated the latency I type infection, and the only difference observed in EBV-infected gastric carcinoma cell lines was the resistance to serum deprivation–induced apoptosis. Comparative analyses of transcripts of apoptosis-associated genes in MKN-1 and EBV–MKN-1 and subsequent quantitative reverse transcription-PCR analysis showed up-regulation of the cellular survivin gene in EBV-infected gastric carcinoma cell lines. Small interfering RNA–mediated knockdown of survivin increased apoptosis in EBV–MKN-1 to the level of the original MKN-1 cells. Transfection of EBV-latent genes into MKN-1 showed that LMP2A, but not EBNA1, EBER, or BARF0, up-regulated survivin gene expression. LMP2A-mediated survivin up-regulation in gastric carcinoma cells was inhibited with a nuclear factor-κB (NF-κB) inhibitor, Bay 11-7082. In parallel with these findings in vitro, survivin expression was frequent in carcinoma tissues of gastric carcinoma by immunohistochemistry, and significantly more in EBV-associated gastric carcinoma (12 of 13) than in EBV-negative gastric carcinoma in the advanced stage (P = 0.0307). Thus, EBV uses its latent protein, LMP2A, to activate the NF-κB–survivin pathway to rescue EBV-infected epithelial cells from serum deprivation, and up-regulation of survivin may play a role in the progression of this specific type of gastric carcinoma infected with EBV. [Cancer Res 2008;68(5):1427–35]
Altered TAB1:IκB Kinase Interaction Promotes Transforming Growth Factor β–Mediated Nuclear Factor-κB Activation during Breast Cancer Progression
Authors: Neil Jason R. , Schiemann William P. 
Published: March 2008

Abstract
The conversion of transforming growth factor β (TGF-β) from a tumor suppressor to a tumor promoter occurs frequently during mammary tumorigenesis, yet the molecular mechanisms underlying this phenomenon remain undefined. We show herein that TGF-β repressed nuclear factor-κB (NF-κB) activity in normal NMuMG cells, but activated this transcription factor in their malignant counterparts, 4T1 cells, by inducing assembly of TGF-β–activated kinase 1 (TAK1)–binding protein 1 (TAB1):IκB kinase β (IKKβ) complexes, which led to the stimulation of a TAK1:IKKβ:p65 pathway. TAB1:IKKβ complexes could only be detected in NMuMG cells following their induction of epithelial-mesenchymal transition (EMT), which, on TGF-β treatment, activated NF-κB. Expression of a truncated TAB1 mutant [i.e., TAB1(411)] reduced basal and TGF-β–mediated NF-κB activation in NMuMG cells driven to undergo EMT by TGF-β and in 4T1 cells stimulated by TGF-β. TAB1(411) expression also inhibited TGF-β–stimulated tumor necrosis factor-α and cyclooxygenase-2 expression in 4T1 cells. Additionally, the ability of human MCF10A-CA1a breast cancer cells to undergo invasion in response to TGF-β absolutely required the activities of TAK1 and NF-κB. Moreover, small interfering RNA–mediated TAK1 deficiency restored the cytostatic activity of TGF-β in MCF10A-CA1a cells. Finally, expression of truncated TAB1(411) dramatically reduced the growth of 4T1 breast cancers in syngeneic BALB/c, as well as in nude mice, suggesting a potentially important role of NF-κB in regulating innate immunity by TGF-β. Collectively, our findings have defined a novel TAB1:TAK1:IKKβ:NF-κB signaling axis that forms aberrantly in breast cancer cells and, consequently, enables oncogenic signaling by TGF-β. [Cancer Res 2008;68(5):1462–70]
A Novel Recurrent Chromosomal Inversion Implicates the Homeobox GeneDlx5in T-Cell Lymphomas from Lck-Akt2 Transgenic Mice
Authors: Tan Yinfei , Timakhov Roman A. , Rao Mamta , Altomare Deborah A. , Xu Jinfei , Liu Zemin , Gao Qingshen , Jhanwar Suresh C. , Di Cristofano Antonio , Wiest David L. , Knepper Janice E. , Testa Joseph R. 
Published: March 2008

AbstractThe oncogene v-akt was isolated from a retrovirus that induced murine thymic lymphomas. Transgenic mice expressing a constitutively activated form of the cellular homologue Akt2 specifically in immature T cells develop spontaneous thymic lymphomas. We hypothesized that tumors from these mice might exhibit oncogenic chromosomal rearrangements that cooperate with activated Akt2 in lymphomagenesis. Cytogenetic analysis revealed a recurrent clonal inversion of chromosome 6, inv(6), in thymic lymphomas from multiple transgenic founder lines, including one line in which 15 of 15 primary tumors exhibited this same rearrangement. Combined fluorescence in situ hybridization, PCR, and DNA sequence analyses showed that the distal inv(6) breakpoint resides at the T-cell receptor β chain locus, Tcrb. The proximal breakpoint maps to a region near a locus comprising the linked homeobox/transcription factor genes Dlx5 and Dlx6. Expression analysis of genes translocated to the vicinity of the Tcrb enhancer revealed that Dlx5 and Dlx6 are overexpressed in tumors exhibiting the inv(6). Experimental overexpression of Dlx5 in mammalian cells resulted in enhanced cell proliferation and increased colony formation, and clonogenic assays revealed cooperativity when both Dlx5 and activated Akt2 were coexpressed. In addition, DLX5, but not DLX6, was found to be abundantly expressed in three of seven human T-cell lymphomas tested. These findings suggest that the Dlx5 can act as an oncogene by cooperating with Akt2 to promote lymphomagenesis. [Cancer Res 2008;68(5):1296–302]