bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Tethyan Himalaya: palaeogeographical and tectonic constraints from Ordovician palaeomagnetic data
Authors: TORSVIK TROND H. , PAULSEN TIMOTHY S. , HUGHES NIGEL C. , MYROW PAUL M. , GANERØD MORGAN 
Published: June 2009

Abstract:To test whether the Tethyan Himalaya were part of the northern margin of India in the early Palaeozoic we have produced the first primary palaeomagnetic data (bedding-corrected declination 267.5°, inclination 63.0°, α95= 10°; pole latitude 20.2°N, longitude 28.6°E) from low metamorphic grade Ordovician red beds in the Tethyan Himalaya (Shian Formation). The palaeomagnetic data are of excellent quality, and a statistically positive fold test combined with a comparison with late Cambrian–Ordovician Gondwana poles suggests a primary hematite-bearing magnetization, acquired between 470 and 500 Ma. This is in excellent agreement with stratigraphic, faunal and provenance age estimates, and the palaeomagnetic data demonstrate that the Tethyan Himalaya must have been located in proximity to the Indian craton during early Ordovician times, and are therefore consistent with a continuous margin at that time. The Shian Formation pole overlaps with 470–500 Ma Gondwana poles, but an even better fit can be obtained by invoking a post-Ordovician clockwise rotation of 13° ± 4°. Such a rotation is similar in both sense and magnitude to clockwise rotations recorded in primary Triassic sequences as well as Palaeogene palaeomagnetic overprint data from the Tethyan Himalaya: rotations of the Tethyan Himalaya compared with cratonic India are thus probably all of post late Eocene age. Triassic and Early Ordovician data do not imply any crustal shortening between Tethyan Himalaya and cratonic India. However, in the Early Ordovician, India was rotated 90° compared with its present orientation, and any enlargement of India would not be detected by palaeomagnetic data.
Radiolarian age constraints on Mesotethyan ocean evolution, and their implications for development of the Bangong–Nujiang suture, Tibet
Authors: Baxter Alan T. , Aitchison Jonathan C. , Zyabrev Sergey V. 
Published: June 2009

Abstract:
Radiolarian discoveries indicate that deep-marine conditions prevailed in central Tibet from the early Middle Jurassic until well into the Early Cretaceous (late Hauterivian–early Aptian; 131–121 Ma) and help to constrain the temporal extent of oceanic conditions along the Bangong–Nujiang suture. These new fossils occur in chert or siliceous mudstone blocks associated with the Lagkor Tso ophiolitic mélange. Basin inversion associated with closure of Mesotethys between the Qiangtang and Lhasa terranes was accompanied by mélange formation and predated regionally widespread deposition of overlying shallow-marine late Aptian–Albian orbitolinid limestones.
Stress change over short geological time: the case of Scandinavia over 9000 years since the Ice Age
Authors: Gregersen Soren , Voss Peter 
Published: June 2009

Abstract
Palaeoseismological investigations are used in many regions of the world to extend back in time the earthquake statistics of historical written or oral records as well as instrumental information. This is very valuable for discussions of earthquake hazard, but it only applies to areas of stable stress regime. Although the intraplate areas of Scandinavia and Greenland have experienced only rather small earthquakes within the human timescale, they serve as a clear warning on the application of palaeoseismology for hazard studies in regions where the stresses have changed.
In a small part of Scandinavia, where recent earthquake activity is not significantly different from that of its surroundings, large faults have been discovered and several have been investigated via palaeoseismology. They are interpreted to show the occurrence of large earthquakes about 9000 years ago. Signs of this are coincident landslides as well as liquefaction in loose sediments, which are well dated through varve-counting.
In contrast to this the present-day stress release in earthquakes and in surface rock deformations is mainly caused by plate motion. Regional investigations in Scandinavia and Greenland/North America, as well as those included in the World Stress Map Project of the 1990s, have shown compression within the plate, mainly in the direction of absolute plate motion. The ice cap influence has disappeared. So stress reorganization is clearly indicated over the short geological timespan of 9000 years. Into this argument goes the observation from Greenland and Antarctica, that no earthquakes occur under the ice caps. For Scandinavia the argument is that no earthquakes occurred under the ice sheet during the Ice Age, and that the stored stresses were released when the ice sheet melted 9000 years ago. This does emphasize a warning. There are regions of the globe where palaeoseismological investigations can give a fantastic extension of the short-term historical earthquake records. But in some regions stress reorganization has changed this condition.
Late Holocene earthquake geology in Sweden
Authors: Mörner Nils-Axel 
Published: June 2009

Abstract
As a function of the rapid rate of glacial isostatic uplift, deglacial palaeoseismicity in Sweden was exceptionally high, in magnitude as well as frequency. Today, seismic activity is low to moderately low with occasional events reaching M 4–5. In the Late Holocene, 11 events in the order of M 6–7 are recorded. These palaeoseismic events seem also to be recorded in several old place names, as in the tale of the Fenris Wolf. Some of the events generated local to regional tsunamis. The palaeoseismic activity recorded in Late Holocene time implies that our short-term seismic hazard assessment must include the possibility of future events in the order of up to M 7. For long-term hazard assessment, repeating glacial/deglacial phases, we must work with magnitudes of M 8 to 9.
Testing a seismic scenario for the damage of the Neolithic wooden well of Erkelenz-Kückhoven, Germany
Authors: Hinzen Klaus-G. , Weiner Jürgen 
Published: June 2009

Abstract

A Neolithic wooden well was discovered and excavated between 1989 and 1992 near Erkelenz in the Lower Rhine Embayment. The construction, 3×3 m in size and 13 m deep, was exceptionally large for its time. The larger outer box-frame contained two smaller frames whose construction could be interpreted as an attempt to repair the damaged original well. The outer box was made from 160 oak elements of about 3 m length built in the blockhouse method. The large box is dated to 5090
bc
and the two smaller ones to 5057±5
bc
by dendrochronological analysis. At
c
. 8 m depth several elements of the large box are vertically sheared off and the broken parts moved inward and downward. The cause of this damage has not yet been determined. As the well is located only 3 km from one of the active tectonic faults in the Lower Rhine Embayment, a seismogenic origin of the damage is considered and tested in this paper. This question has relevance for determination of seismic hazard in an area with present-day moderate seismicity but documented occurrence of strong surface-rupturing earthquakes from the palaeoseismic record. First, a geotechnical model for the construction pit with a total volume of
c
. 540–550 m
3
is used to prove the stability of the open pit during well construction and to help explain how the well was built. The seismogenic hypothesis is tested in a deterministic approach using theoretically derived ground motion at the site of the well for two simulated earthquakes with magnitudes 6.2 and 6.8. Ground deformation and relative displacement calculated with a finite element model of the casing are found to be too small to account for the documented damage. Among other potential sources of damage, swelling, shrinking or rotting of the wood elements are possible explanations; however, a conclusive answer to this question remains to be found.
Earthquake intensity assessment based on environmental effects: principles and case studies
Authors: Tatevossian R. E. , Rogozhin E. A. , Arefiev S. S. , Ovsyuchenko A. N. 
Published: June 2009

Abstract

The comparison of intensity assessments based on macroseismic data and Earthquake Environmental Effects (EEE) is presented. Specific problems faced when assessing intensities using different types of scales are discussed. Two case studies of recent earthquakes with magnitudes M
S
=7.4 (Altai, 2003, and Neftegorsk, 1995) are used to illustrate the applicability of the INQUA EEE scale. The Altai earthquake was accompanied by surface faulting of
c.
70 km length and up to 2 m of horizontal and 70 cm of vertical offset; secondary EEE were observed over 3000 km
2
. The dominant type of surface faulting during the Neftegorsk earthquake was strike-slip. The length of surface faulting was up to 46 km, maximum horizontal offset was 8.1 m, and average offset coherent with seismic moment was 3.9 m; secondary EEE were observed occasionally at considerable distance from the epicentre on wet seashore sands. Application of the INQUA scale shows the epicentral intensity of the Altai earthquake to be X degrees. Most consistent with all types of data (rupture length, maximum and average offsets) intensity assessment for the Neftegorsk earthquake which is within the X–XI degree range. Taking into account environmental effects in intensity scales is an essential requirement: it follows from the complex nature of an earthquake impact, which spans a very broad frequency range, including static deformations. The case studies illustrate that the intensity assessment of an earthquake, based only on damage to buildings, will be essentially incomplete.
Ground effects of the 18 October 1992, Murindo earthquake (NW Colombia), using the Environmental Seismic Intensity Scale (ESI 2007) for the assessment of intensity
Authors: Mosquera-Machado S. , Lalinde-Pulido C. , Salcedo-Hurtado E. , Michetti A. M. 
Published: June 2009

Abstract

The macroseismic intensity of the 18 October 1992 Murindo-Atrato earthquake that affected the northwestern states of Colombia (Chocó and Antioquia) is reassessed using the newly developed INQUA Environmental Seismic Intensity Scale (ESI 2007) which is based on the evaluation of earthquake environmental effects. To generate the ESI 2007 isoseismal map of northwestern Colombia, a geographical information system was used. Unifying the available information on the seismological and active tectonics framework including historical seismicity, hypocentral depths, foreshocks, aftershocks, focal mechanism, macroseismic data under the same GIS and the map of Quaternary faults allowed us to reinterpret the geological and environmental effects of the 1992 earthquakes sequence. A total of 24 sites from the areas of Quibdó, Bojayá, Rio Sucio, Murindo, Vigía del Fuerte and Turbo were evaluated. A systematic comparison among evaluated intensities (Modified Mercalli and ESI scale) revealed differences from one to two degrees. According to the ESI 2007 scale, the epicentral intensity I
o
is XI. This represents one degree higher than the epicentral intensity obtained using MM and Medveded Sponhauer Karnik (MSK) intensity scales, probably due to the lack of suitable observations on building damage in this poorly populated and developed region. This information is also useful in order to shed some light on the persistent question of the exact location and dimension of the main rupture zone associated with the earthquake. The isoseismal map derived from the integration of the whole set of environmental effects with other macroseismic data strongly suggests that the causative tectonic structure is the Murindo fault. However, the rupture length derived from the distribution of ground effects is greater than the Murindo fault length, implying that other nearby fault segments were activated during the 1992 event. The new isoseismal map resulting from this work is relevant for the assessment of future seismic risk in the northwestern region of Colombia. Overall, the application of the ESI 2007 scale to the 18 October 1992 earthquake, and to similar strong events in the region, can be useful for disaster management and planning, estimation of damage, and post-earthquake recovery efforts.
Smad2 and Smad3 Phosphorylated at Both Linker and COOH-Terminal Regions Transmit Malignant TGF-β Signal in Later Stages of Human Colorectal Cancer
Authors: Matsuzaki Koichi , Kitano Chiaki , Murata Miki , Sekimoto Go , Yoshida Katsunori , Uemura Yoshiko , Seki Toshihito , Taketani Shigeru , Fujisawa Jun-ichi , Okazaki Kazuichi 
Published: June 2009

AbstractTransforming growth factor (TGF)-β initially inhibits growth of mature epithelial cells. Later, however, autocrine TGF-β signaling acts in concert with the Ras pathway to induce a proliferative and invasive phenotype. TGF-β activates not only TGF-β type I receptor (TβRI) but also Ras-associated kinases, which differentially phosphorylate the mediators Smad2 and Smad3 to create distinct phosphorylated forms: COOH-terminally phosphorylated Smad2/3 (pSmad2C and pSmad3C) and both linker and COOH-terminally phosphorylated Smad2/3 (pSmad2L/C and pSmad3L/C). In this study, we investigated actions of pSmad2L/C and pSmad3L/C in cancer progression. TGF-β inhibited cell growth by down-regulating c-Myc oncoprotein through the pSmad2C and pSmad3C pathway; TGF-β signaling, in turn, enhanced cell growth by up-regulating c-Myc through the cyclin-dependent kinase (CDK) 4–dependent pSmad2L/C and pSmad3L/C pathways in cell nuclei. Alternatively, TβRI and c-Jun NH2-terminal kinase (JNK) together created cytoplasmic pSmad2L/C, which entered the nucleus and stimulated cell invasion, partly by up-regulating matrix metalloproteinase-9. In 20 clinical samples, pSmad2L/C and pSmad3L/C showed nuclear localization at invasion fronts of all TGF-β–producing human metastatic colorectal cancers. In vitro kinase assay confirmed that nuclear CDK4 and cytoplasmic JNK obtained from the tumor tissue could phosphorylate Smad2 or Smad3 at their linker regions. We suggest that CDK4, together with JNK, alters tumor-suppressive TGF-β signaling to malignant characteristics in later stages of human colorectal cancer. The linker phosphorylation of Smad2 and Smad3 may represent a target for intervention in human metastatic cancer. [Cancer Res 2009;69(13):5321–30]
Ferritin Heavy Chain–Mediated Iron Homeostasis and Subsequent Increased Reactive Oxygen Species Production Are Essential for Epithelial-Mesenchymal Transition
Authors: Zhang Ke-Hua , Tian Hong-Yu , Gao Xia , Lei Wei-Wei , Hu Ying , Wang Dong-Mei , Pan Xin-Chao , Yu Mei-Lan , Xu Gen-Jun , Zhao Fu-Kun , Song Jian-Guo 
Published: June 2009

Abstract
The epithelial-mesenchymal transition (EMT) plays a critical role in tumor progression. To obtain a broad view of the molecules involved in EMT, we carried out a comparative proteomic analysis of transforming growth factor-β1 (TGF-β1)–induced EMT in AML-12 murine hepatocytes. A total of 36 proteins with significant alterations in abundance were identified. Among these proteins, ferritin heavy chain (FHC), a cellular iron storage protein, was characterized as a novel modulator in TGF-β1–induced EMT. In response to TGF-β1, there was a dramatic decrease in the FHC levels, which caused iron release from FHC and, therefore, increased the intracellular labile iron pool (LIP). Abolishing the increase in LIP blocked TGF-β1–induced EMT. In addition, increased LIP levels promoted the production of reactive oxygen species (ROS), which in turn activated p38 mitogen-activated protein kinase. The elimination of ROS inhibited EMT, whereas H2O2 treatment rescued TGF-β1–induced EMT in cells in which the LIP increase was abrogated. Overexpression of exogenous FHC attenuated the increases in LIP and ROS production, leading to a suppression of EMT. We also showed that TGF-β1–mediated down-regulation of FHC occurs via 3′ untranslated region–dependent repression of the translation of FHC mRNA. Moreover, we found that FHC down-regulation is an event that occurs between the early and highly invasive advanced stages in esophageal adenocarcinoma and that depletion of LIP or ROS suppresses the migration of tumor cells. Our data show that cellular iron homeostasis regulated by FHC plays a critical role in TGF-β1–induced EMT. [Cancer Res 2009;69(13):5340–8]
[6]-Gingerol Suppresses Colon Cancer Growth by Targeting Leukotriene A4 Hydrolase
Authors: Jeong Chul-Ho , Bode Ann M. , Pugliese Angelo , Cho Yong-Yeon , Kim Hong-Gyum , Shim Jung-Hyun , Jeon Young-Jin , Li Honglin , Jiang Hualiang , Dong Zigang 
Published: June 2009

Abstract
[6]-Gingerol, a natural component of ginger, exhibits anti-inflammatory and antitumorigenic activities. Despite its potential efficacy in cancer, the mechanism by which [6]-gingerol exerts its chemopreventive effects remains elusive. The leukotriene A4 hydrolase (LTA4H) protein is regarded as a relevant target for cancer therapy. Our in silico prediction using a reverse-docking approach revealed that LTA4H might be a potential target of [6]-gingerol. We supported our prediction by showing that [6]-gingerol suppresses anchorage-independent cancer cell growth by inhibiting LTA4H activity in HCT116 colorectal cancer cells. We showed that [6]-gingerol effectively suppressed tumor growth in vivo in nude mice, an effect that was mediated by inhibition of LTA4H activity. Collectively, these findings indicate a crucial role of LTA4H in cancer and also support the anticancer efficacy of [6]-gingerol targeting of LTA4H for the prevention of colorectal cancer. [Cancer Res 2009;69(13):5584–91]
Vaccination with Recombinant NY-ESO-1 Protein Elicits Immunodominant HLA-DR52b-restricted CD4+ T Cell Responses with a Conserved T Cell Receptor Repertoire
Authors: Bioley Gilles , Dousset Christelle , Yeh Alice , Dupont Bo , Bhardwaj Nina , Mears Gregory , Old Lloyd J. , Ayyoub Maha , Valmori Danila 
Published: June 2009

Abstract
Purpose: ESO is a tumor-specific antigen with wide expression in human tumors of different histologic types and remarkable spontaneous immunogenicity. We have previously shown that specific TH1 and antibody responses can be elicited in patients with no detectable preexisting immune responses by vaccination with rESO administered with Montanide ISA-51 and CpG ODN 7909. The purpose of the present study was to characterize vaccine-induced ESO-specific CD4+ T cell responses.
Experimental Design: We generated CD4+ T cell clones from patient C2, who had the highest CD4+ T cell response to the vaccine, and analyzed their fine specificity and HLA class II restriction to determine the recognized epitope. We then assessed the response to the identified epitope in all vaccinated patients expressing the corresponding HLA class II allele.
Results: We found that ESO-specific CD4+ T cell clones from patient C2 recognize peptide ESO119-143 (core region 123-137) presented by HLA-DR52b (HLA-DRB3*0202), a MHC class II allele expressed by about half of Caucasians. Importantly, following vaccination, all patients expressing DR52b developed significant responses to the identified epitope, accounting for, on average, half of the total CD4+ T cell responses to the 119-143 immunodominant region. In addition, analysis of ESO-specific DR52b-restricted CD4+ T cells at the clonal level revealed significant conservation of T cell receptor usage among different individuals.
Conclusions: The identification of a DR52b-restricted epitope from ESO that is immunodominant in the context of vaccine-elicited immune responses is instrumental for the immunologic monitoring of vaccination trials targeting this important tumor antigen.
Narciclasine, a plant growth modulator, activates Rho and stress fibers in glioblastoma cells
Authors: Lefranc Florence , Sauvage Sébastien , Van Goietsenoven Gwendoline , Mégalizzi Véronique , Lamoral-Theys Delphine , Debeir Olivier , Spiegl-Kreinecker Sabine , Berger Walter , Mathieu Véronique , Decaestecker Christine , Kiss Robert 
Published: June 2009

Abstract
Cell motility and resistance to apoptosis characterize glioblastoma multiforme growth and malignancy. Narciclasine, a plant growth modulator, could represent a powerful new weapon targeting the Achilles' heel of glioblastoma multiforme and may offer the potential to better combat these devastating malignancies. The in vitro effects of narciclasine on cell proliferation, morphology, actin cytoskeleton organization, and the Rho/Rho kinase/LIM kinase/cofilin pathway and its antitumor activity in vivo have been determined in models of human glioblastoma multiforme. Narciclasine impairs glioblastoma multiforme growth by markedly decreasing mitotic rates without inducing apoptosis. The compound also modulates the Rho/Rho kinase/LIM kinase/cofilin signaling pathway, greatly increasing GTPase RhoA activity as well as inducing actin stress fiber formation in a RhoA-dependent manner. Lastly, the treatment of human glioblastoma multiforme orthotopic xenograft- bearing mice with nontoxic doses of narciclasine significantly increased their survival. Narciclasine antitumor effects were of the same magnitude as those of temozolomide, the drug associated with the highest therapeutic benefits in treating glioblastoma multiforme patients. Our results show for the first time that narciclasine, a plant growth modulator, activates Rho and stress fibers in glioblastoma multiforme cells and significantly increases the survival of human glioblastoma multiforme preclinical models. This statement is made despite the recognition that to date, irrespective of treatment, no single glioblastoma multiforme patient has been cured. [Mol Cancer Ther 2009;8(7):1739–50]
Ligand, receptor, and cell type–dependent regulation ofABCA1andABCG1mRNA in prostate cancer epithelial cells
Authors: Trasino Steven E. , Kim Young S. , Wang Thomas T.Y. 
Published: June 2009

AbstractRecent evidence suggests that the liver X receptor (LXR) is a potential anticancer target in prostate carcinoma. There is little characterization, however, of which of the two LXR isoforms, LXRα or LXRβ, regulates the LXR-responsive genes ATP-binding cassette subfamily members A1 (ABCA1) and G1 (ABCG1) in transformed prostatic epithelial cells. In this study, small interfering RNA (siRNA) was used to determine whether LXRα or LXRβ is involved in regulating ABCA1 and ABCG1 mRNA expression in LNCaP and PC-3 cells. Treatment of both cell lines with the synthetic LXR ligand T0901317 and oxysterols: 25-hydroxycholesterol (25HC) and 24(S), 25-epoxycholesterol (24,25EC), resulted in more than a 10-fold increase of ABCA1 and ABCG1 mRNA expression. Transfection of LNCaP cells with siRNA against either LXRβ or LXRα failed to inhibit T0901317 and 25HC-mediated increase of ABCA1 mRNA. siRNA silencing of LXRβ did, however, inhibit ABCA1 mRNA expression in 24,25EC-treated LNCaP cells. In contrast, LXRβ siRNA inhibited T0901317, 25HC, and 24,25EC induction of ABCA1 mRNA in PC-3 cells and ABCG1 mRNA in both LNCaP and PC-3 cells. Additional experiments revealed that T0901317 and 25HC induction of ABCA1 mRNA expression was significantly inhibited by the p38 stress kinase antagonist SB202190 and PKA inhibitor H89. Our study is the first to show that LXRβ, but not LXRα, is the major regulatory isoform of ABCG1 mRNA expression in LNCaP and PC-3 cells. Our study also reveals that ABCA1 gene expression is differentially regulated by synthetic and natural LXR ligands, possibly involving kinase mediated signal transduction. [Mol Cancer Ther 2009;8(7):1934–45]