bluuebunny/crossref_metadata_2025_split huggingface dataset:
Slope stability hazard assessment: Coalport Railway Bridge, Shropshire
Authors: Shilston D. T. 
Published: December 2007

Objectives

Escalating costs, disputes and delays can arise during construction as a result of inadequate research at the early stages of project development. The assessment of slope stability hazard described in this case history illustrates the relative ease, and therefore low cost, of rapidly accessing and evaluating a wide range of desk study and walkover survey data pertinent to a construction project.

The project

Coalport is a village on the north bank of the River Severn in the Ironbridge Gorge, near the new town of Telford, Shropshire. Coalport Railway Bridge (BC 17) is at the site of the former Coalport Railway Station. It is immediately adjacent to the much older Coalport (river) Bridge and carries the road from the river bridge across the former railway line (see Figs 1 and 2).
As part of a programme of bridge inspection and strengthening, the Commission for New Towns engaged WS Atkins to assess the condition of Railway Bridge BC 17 and make recommendations for remedial measures.
An initial inspection of the Railway Bridge concluded that it was in a poor state of repair and that it may be at risk from ground movements caused by landslipping, being in an area that is well known for the presence of landslips (Carson & Fisher 1991). A more detailed desk study, including a walk-over survey, was therefore carried out specifically to assess the landslide hazard at the railway bridge and to help design the ground investigation that was planned as part of the design of remedial works to the bridge’s abutments.
Evolution of deformation styles at a major restraining bend, constraints from cooling histories, Mae Ping fault zone, western Thailand
Authors: Morley C. K. , Smith M. , Carter A. , Charusiri P. , Chantraprasert S. 
Published: December 2007

Abstract

The
c.
500-km-long Mae Ping fault zone trends NW–SE across Thailand into eastern Myanmar and has probably undergone in excess of 150 km sinistral motion during the Cenozoic. A large,
c.
150-km-long, restraining bend in this fault zone lies on the western margin of the Chainat duplex. The duplex is a low-lying region dominated by north–south-trending ridges of Mesozoic and Palaeozoic sedimentary, metamorphic and igneous rocks, flanked by flat, post-rift basins of Pliocene–Recent age to the north and south. A review of published cooling-age data, plus new apatite and zircon fission-track results indicates that significant changes in patterns of exhumation occurred along the fault zone with time. Oldest uplift and erosion (Eocene) occurred in the Umphang Gneiss region, west of an inferred thrust-dominated restraining-bend setting. From 36 Ma to 30 Ma, exhumation was strongest north of the duplex, along the NW–SE-trending segment of the fault zone at the (northern) exiting bend of the Chainat duplex. This region of the fault zone is characterized by a mid-crustal level shear zone 5–6 km wide (Lan Sang Gneisses), that passes to the NW into an apparent strike-slip duplex geometry. The deformation is interpreted to have occurred during passage around the northern restraining bend, which resulted in vertical thickening, uplift, erosion and extensional collapse of the northern side of the shear zone. This concentration of deformation at the bends at the ends of the restraining bend is thought to be a characteristic of strike-slip-dominated restraining bends. Following Late Oligocene–Early Miocene extension, there is apatite fission-track evidence for 22–18 Ma exhumation in the Chainat duplex, that coincides with a phase of inversion in the Phitsanulok Basin to the north. The Miocene–Recent history of the Chainat duplex is one of minor sinistral and dextral displacements, related to a rapidly evolving stress field, influenced by the numerous tectonic reorganizations that affected SE Asia during that time.
Evolution of a poly-deformed relay zone between fault segments in the eastern Southern Alps, Italy
Authors: Zampieri D. , Massironi M. 
Published: December 2007

Abstract
In the eastern Southern Alps (NE Italy), Liassic north–south extensional structures are prominent. The southern Trento Platform also experienced extension during the Palaeogene, when reactivation of some pre-existing faults occurred, coupled with nucleation of new faults. During Neogene shortening, these structures were reactivated once again, but with strike-slip kinematics. In this framework, the Gamonda–Tormeno restraining stepover represents the final result of an overlap zone which evolved through time. In the first stage (Lias to Early Cretaceous) a prominent splay developed at the tip of the Gamonda Fault by lateral propagation and breaching of independent segments. At the same time, there was kinematic interaction between the antithetic Gamonda and Tormeno faults, followed by diachronous motion on crossing faults and the development of a narrow graben. During the second stage of extensional tectonics (Palaeocene to Early Oligocene), the reactivation and propagation of the overlapping faults along with the generation of new faults led to deepening of the graben. In the third stage (Miocene to present), the final structure of a strike-slip restraining stepover was accomplished. Due to the mechanical stratigraphy and complex inherited architecture of the relay zone where stratigraphic sequences with different rheological properties are juxtaposed, the style of shortening is different in the western and eastern sides of the stepover. The Gamonda–Tormeno structure represents a unique example of how a relay zone may change through time.
Transpressional structures on a Late Palaeozoic intracontinental transform fault, Canadian Appalachians
Authors: Waldron J. W. F. , Roselli C. , Johnston S. K. 
Published: December 2007

Abstract
The east–west Minas fault zone, separating the Early Palaeozoic Meguma and Avalon terranes of the Appalachians, experienced dextral strike-slip motion during the Carboniferous. Abundant oblique contractional structures indicate localized dextral transpression, immediately south of the zone, probably associated with a restraining bend. Subsurface data indicate that the deformed Horton Group clastic rocks are thrust above younger Windsor Group evaporites.

Excellent exposures on wave-cut platforms of the Bay of Fundy show structures developed in transpression, including NE-trending upright and inclined folds; south-verging thrust and reverse faults; and NW-striking normal faults. Northwest-trending boudins, which are perpendicular and slightly rotated in a clockwise sense relative to fold hinges, provide a field indicator for dextral transpression. The earliest folds (F
1
) are curvilinear and may have formed by deformation of wet sediment. F
2
tectonic folds show weak axial-planar cleavage. Locally, these have been rotated into reclined orientations; spectacular downward-facing folds are probably due to refolding by more east–west F
3
folds. The structures observed are consistent with pure-shear-dominated transpression, with the local angle of convergence α increasing over time. This strain history is compatible with progressive strain partitioning, probably associated with the spreading of topography developed at the restraining bend.
Relatively simple through-going fault planes at large-earthquake depth may be concealed by the surface complexity of strike-slip faults
Authors: Graymer R. W. , Langenheim V. E. , Simpson R. W. , Jachens R. C. , Ponce D. A. 
Published: December 2007

Abstract
At the surface, strike-slip fault stepovers, including abrupt fault bends, are typically regions of complex, often disconnected faults. This complexity has traditionally led geologists studying the hazard of active faults to consider such stepovers as important fault segment boundaries, and to give lower weight to earthquake scenarios that involve rupture through the stepover zone. However, recent geological and geophysical studies of several stepover zones along the San Andreas fault system in California have revealed that the complex nature of the fault zone at the surface masks a much simpler and direct connection at depths associated with large earthquakes (greater than 5 km). In turn, the simplicity of the connection suggests that a stepover zone would provide less of an impediment to through-going rupture in a large earthquake, so that the role of stepovers as segment boundaries has probably been overemphasized. However, counter-examples of fault complexity at depth associated with surface stepovers are known, so the role of stepovers in fault rupture behaviour must be carefully established in each case.
Kinematics of the Amanos Fault, southern Turkey, from Ar/Ar dating of offset Pleistocene basalt flows: transpression between the African and Arabian plates
Authors: Seyrek A. , Demi̇r T. , Pringle M. S. , Yurtmen S. , Westaway R. W. C. , Beck A. , Rowbotham G. 
Published: December 2007

Abstract

We report four new Ar/Ar dates and 18 new geochemical analyses of Pleistocene basalts from the Karasu Valley of southern Turkey. These rocks have become offset left-laterally by slip on the N20°E-striking Amanos Fault. The geochemical analyses help to correlate some of the less-obvious offset fragments of basalt flows, and thus to measure amounts of slip; the dates enable slip rates to be calculated. On the basis of four individual slip-rate determinations, obtained in this manner, we estimate a weighted mean slip rate for this fault of 2.89±0.05mm/a (±2σ). We have also obtained a slip rate of 2.68±0.54mm/a (±2σ) for the subparallel East Hatay Fault farther east. Summing these values gives 5.57±0.54mm/a (±2σ) as the overall left-lateral slip rate across the Dead Sea fault zone (DSFZ) in the Karasu Valley. These slip-rate estimates and other evidence from farther south on the DSFZ are consistent with a preferred Euler vector for the relative rotation of the Arabian and African plates of 0.434±0.012° Ma
−1
about 31.1°N, 26.7°E. The Amanos Fault is misaligned to the tangential direction to this pole by 52° in the transpressive sense. Its geometry thus requires significant fault-normal distributed crustal shortening, taken up by crustal thickening and folding, in the adjacent Amanos Mountains. The vertical component of slip on the Amanos Fault is estimated as
c.
0.15mm/a. This minor component contributes to the uplift of the Amanos Mountains, which reaches rates of
c.
0.2–0.4mm/a. These slip rate estimates are considered representative of time since. 3.73±0.05Ma, when the modern geometry of strike-slip faulting developed in this region; an estimated 11km of slip on the Amanos Fault and
c.
10km of slip on the East Hatay Fault have occurred since then. It is inferred that both these faults came into being, and the associated deformation in the Amanos Mountains began, at that time. Prior to that, the northern part of the Africa–Arabia plate boundary was located further east.
Targeting the Nuclear Factor-κB Rescue Pathway Has Promising Future in Human Renal Cell Carcinoma Therapy
Authors: Sourbier Carole , Danilin Sabrina , Lindner Véronique , Steger Jacques , Rothhut Sylvie , Meyer Nicolas , Jacqmin Didier , Helwig Jean-Jacques , Lang Hervé , Massfelder Thierry 
Published: December 2007

Abstract
Metastatic renal cell carcinoma (RCC) remains refractory to therapies. The nuclear factor-κB (NF-κB) transcription factor is involved in cell growth, cell motility, and vascularization. We evaluated whether targeting NF-κB could be of therapeutic and prognostic values in human RCC. The activation of the NF-κB pathway in human RCC cells and tumors was investigated by Western blot. In vitro, the effects of BAY 11-7085 and sulfasalazine, two NF-κB inhibitors, on tumor cell growth were investigated by cell counting, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis, terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling, and fluorescence-activated cell sorting. Their specificity toward NF-κB was analyzed by Western blot, confocal microscopy, NF-κB small interfering RNA, and NF-κB transcription assay. In vivo, the effects of BAY 11-7085 on the growth of human RCC tumors were investigated in nude mice. A tissue microarray (TMA) containing 241 cases of human RCC with 12 to 22 years of clinical follow-up and corresponding normal tissues was built up to assess prognostic significance of activated NF-κB. NF-κB is constitutively activated in cultured cells expressing or not the von Hippel-Lindau (VHL) tumor suppressor gene as a consequence of Akt kinase activation and in tumors. In vitro and in vivo NF-κB inhibition blocked tumor cell growth by inducing cell apoptosis. On the TMA, NF-κB activation was correlated with tumor dimension but was not found to be an independent prognostic factor for patient survival. This report provides strong evidence that the mechanisms responsible for the intrinsic resistance of RCC cells to apoptosis converge on NF-κB independently of VHL expression and that targeting this pathway has great anticancer potential. [Cancer Res 2007;67(24):11668–76]
Role of Tumor Necrosis Factor-α and TRAIL in High-Dose Radiation–Induced Bystander Signaling in Lung Adenocarcinoma
Authors: Shareef Mohammed M. , Cui Nuan , Burikhanov Ravshan , Gupta Seema , Satishkumar Sabapathi , Shajahan Shahin , Mohiuddin Mohammed , Rangnekar Vivek M. , Ahmed Mansoor M. 
Published: December 2007

Abstract
In the present study, ionizing radiation (IR)–induced bystander effects were investigated in two lung cancer cell lines. A549 cells were found to be more resistant to radiation-conditioned medium (RCM) obtained from A549 cells when compared with the H460 exposed to RCM procured from H460 cells. Significant release of tumor necrosis factor-α (TNF-α) was observed in A549 cells after IR/RCM exposure, and the survival was reversed with neutralizing antibody against TNF-α. In H460 cells, significant release of TNF-related apoptosis-inducing ligand (TRAIL), but not TNF-α, was observed in response to IR, RCM exposure, or RCM + 2Gy, and neutralizing antibody against TRAIL diminished clonogenic inhibition. Mechanistically, TNF-α present in RCM of A549 was found to mediate nuclear factor-κB (NF-κB) translocation to nucleus, whereas the soluble TRAIL present in RCM of H460 cells mobilized the nuclear translocation of PAR-4 (a proapoptotic protein). Analysis of IR-inducible early growth response-1 (EGR-1) function showed that EGR-1 was functional in A549 cells but not in H460 cells. A significant decrease in RCM-mediated apoptosis was observed in both A549 cells stably expressing small interfering RNA EGR-1 and EGR-1−/− mouse embryonic fibroblast cells. Thus, the high-dose IR-induced bystander responses in A549 may be dependent on the EGR-1 function and its target gene TNF-α. These findings show that the reduced bystander response in A549 cells is due to activation of NF-κB signaling by TNF-α, whereas enhanced response to IR-induced bystander signaling in H460 cells was due to release of TRAIL associated with nuclear translocation of PAR-4. [Cancer Res 2007;67(24):11811–20]
Biological Role and Potential Therapeutic Targeting of the Chemokine Receptor CXCR4 in Undifferentiated Thyroid Cancer
Authors: De Falco Valentina , Guarino Valentina , Avilla Elvira , Castellone Maria Domenica , Salerno Paolo , Salvatore Giuliana , Faviana Pinuccia , Basolo Fulvio , Santoro Massimo , Melillo Rosa Marina 
Published: December 2007

Abstract
Anaplastic thyroid carcinoma (ATC) is a rare thyroid cancer type with an extremely poor prognosis. Despite appropriate treatment, which includes surgery, radiotherapy, and chemotherapy, this cancer is invariably fatal. CXCR4 is the receptor for the stromal cell–derived factor-1 (SDF-1)/CXCL12 chemokine and it is expressed in a variety of solid tumors, including papillary thyroid carcinoma. Here, we show that ATC cell lines overexpress CXCR4, both at the level of mRNA and protein. Furthermore, we found that CXCR4 was overexpressed in ATC clinical samples, with respect to normal thyroid tissues by real-time PCR and immunohistochemistry. Treatment of ATC cells with SDF-1 induced proliferation and increase in phosphorylation of extracellular signal–regulated kinases and protein kinase B/AKT. These effects were blocked by the specific CXCR4 antagonist AMD3100 and by CXCR4 RNA interference. Moreover, AMD3100 effectively reduced tumor growth in nude mice inoculated with different ATC cells. Thus, we suggest that CXCR4 targeting is a novel potential strategy in the treatment of human ATC. [Cancer Res 2007;67(24):11821–9]
Tumor Irradiation Increases the Recruitment of Circulating Mesenchymal Stem Cells into the Tumor Microenvironment
Authors: Klopp Ann H. , Spaeth Erika L. , Dembinski Jennifer L. , Woodward Wendy A. , Munshi Anupama , Meyn Raymond E. , Cox James D. , Andreeff Michael , Marini Frank C. 
Published: December 2007

Abstract
Mesenchymal stem cells (MSC) migrate to and proliferate within sites of inflammation and tumors as part of the tissue remodeling process. Radiation increases the expression of inflammatory mediators that could enhance the recruitment of MSC into the tumor microenvironment. To investigate this, bilateral murine 4T1 breast carcinomas (expressing renilla luciferase) were irradiated unilaterally (1 or 2 Gy). Twenty-four hours later, 2 × 105 MSC-expressing firefly luciferase were injected i.v. Mice were then monitored with bioluminescent imaging for expression of both renilla (tumor) and firefly (MSC) luciferase. Forty-eight hours postirradiation, levels of MSC engraftment were 34% higher in tumors receiving 2 Gy (P = 0.004) than in the contralateral unirradiated limb. Immunohistochemical staining of tumor sections from mice treated unilaterally with 2 Gy revealed higher levels of MSC in the parenchyma of radiated tumors, whereas a higher proportion of MSC remained vasculature-associated in unirradiated tumors. To discern the potential mediators involved in MSC attraction, in vitro migration assays showed a 50% to 80% increase in MSC migration towards conditioned media from 1 to 5 Gy–irradiated 4T1 cells compared with unirradiated 4T1 cells. Irradiated 4T1 cells had increased expression of the cytokines, transforming growth factor-β1, vascular endothelial growth factor, and platelet-derived growth factor-BB, and this up-regulation was confirmed by immunohistochemistry in tumors irradiated in vivo. Interestingly, the chemokine receptor CCR2 was found to be up-regulated in MSC exposed to irradiated tumor cells and inhibition of CCR2 led to a marked decrease of MSC migration in vitro. In conclusion, clinically relevant low doses of irradiation increase the tropism for and engraftment of MSC in the tumor microenvironment. [Cancer Res 2007;67(24):11687–95]
Endostatin Overexpression Inhibits Lymphangiogenesis and Lymph Node Metastasis in Mice
Authors: Brideau Gaëlle , Mäkinen Markus J. , Elamaa Harri , Tu Hongmin , Nilsson Gunnar , Alitalo Kari , Pihlajaniemi Taina , Heljasvaara Ritva 
Published: December 2007

AbstractEndostatin, a proteolytic fragment of collagen XVIII, is a potent inhibitor of angiogenesis and tumor growth. We studied the development of carcinogen-induced skin tumors in transgenic J4 mice overexpressing endostatin in their keratinocytes. Unexpectedly, we did not observe any differences in tumor incidence and multiplicity between these and control mice, nor in the rate of conversion of benign papillomas to malignant squamous cell carcinomas (SCC). We did find, however, that endostatin regulates the terminal differentiation of keratinocytes because the SCCs in the J4 mice were less aggressive and more often well differentiated than those in the control mice. We observed an inhibition of tumor angiogenesis by endostatin at an early stage in skin tumor development, but more strikingly, there was a significant reduction in lymphatic vessels in the papillomas and SCCs in association with elevated endostatin levels and also a significant inhibition of lymph node metastasis in the J4 mice. We showed that tumor-infiltrating mast cells strongly expressed vascular endothelial growth factor-C (VEGF-C), and that the accumulation of these cells was markedly decreased in the tumors of the J4 mice. Moreover, endostatin inhibited the adhesion and migration of murine MC/9 mast cells on fibronectin in vitro. Our data suggest that endostatin can inhibit tumor lymphangiogenesis by decreasing the VEGF-C levels in the tumors, apparently via inhibition of mast cell migration and adhesion, and support the view that the biological effects of endostatin are not restricted to endothelial cells because endostatin also regulates tumor-associated inflammation and differentiation, and the phenotype of epithelial tumors. [Cancer Res 2007;67(24):11528–35]
Hepatocellular Carcinoma Associated with Liver-Gender Disruption in Male Mice
Authors: Rogers Arlin B. , Theve Elizabeth J. , Feng Yan , Fry Rebecca C. , Taghizadeh Koli , Clapp Kristen M. , Boussahmain Chakib , Cormier Kathleen S. , Fox James G. 
Published: December 2007

Abstract
Hepatocellular carcinoma (HCC) is a male-predominant cancer associated with chronic hepatitis. Like human viral hepatitis, murine Helicobacter hepaticus infection produces inflammation and HCC with a masculine bias. We used this model to identify potential mechanisms of male HCC predisposition. Male weanling A/JCr mice (n = 67) were gavaged with H. hepaticus or vehicle. At 1 year, mice were distributed into four groups: surgical castration, chemical castration, castration followed by dihydrotestosterone supplementation, or sexually intact controls. Responses to infection were compared with IFN-γ challenge alone. At 21 months, there was no significant difference in hepatitis between groups. Neither castration nor androgen receptor agonism altered tumor incidence. Infected mice with severe, but not mild, disease exhibited a mosaic of alterations to sexually dimorphic genes and microsomal long-chain fatty acids. By microarray, tumorigenic hepatitis was strongly associated with liver-gender disruption, defined as the loss of a gender-identifying hepatic molecular signature. IFN-γ alone produced similar changes, demonstrating a role for proinflammatory cytokines in this process. In conclusion, hepatocarcinogenesis in male mice with chronic hepatitis is maturationally imprinted and androgen-independent. Proinflammatory cytokines may promote HCC in a male-predominant fashion due to high sensitivity of the masculinized liver to loss of sex-specific transcriptional balance. Liver-gender disruption has pleiotropic implications for hepatic enzyme activity, lipid processing, nuclear receptor activation, apoptosis, and proliferation. We propose a multistep model linking chronic hepatitis to liver cancer through cytokine-mediated derangement of gender-specific cellular metabolism. This model introduces a novel mechanism of inflammation-associated carcinogenesis consistent with male-predominant HCC risk. [Cancer Res 2007;67(24):11536–46]