bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrametamorphism in Precambrian granulite terranes: Evidence from Mg‐AI granulites and calc‐silicate granulites of the Eastern Ghats, India
Authors: Dasgupta Somnath , Sengupta Pulak 
Published: February 2007

AbstractHigh Mg‐Al granulites and calc‐silicate granulites provide evidence for ultra‐high temperatures of metamorphism (ca. 1000°C) at moderate pressures (9–10 kbar) in the Eastern Ghats Belt, India. Lack of proper geochronological data prevents the dating of this extreme metamorphism. High Mg‐Al granulites contain different subsets of mineral assemblages involving spinel, quartz, sapphirine, cordierite, orthopyroxene, garnet and sillimanite coexisting with either rutile‐ilmenite or titanohaematite‐ferrianilmenite. These high Mg‐AI rocks are poor in Zn and Cr, as reflected primarily in the composition of spinel. Evidence of ultra‐high temperature metamorphism comes from (i) textural interpretation of the former coexistence of spinel‐cordierite‐quartz and sapphirine‐quartz and stabilization of the assemblages orthopyroxene‐sillimanite‐cordierite and spinel‐quartz‐sapphirine‐garnet and (ii) the high Al2O3 content of orthopyroxene coexisting with garnet and/or cordierite. Consideration of the sequence of deduced mineral reactions in petrogenetic grids in the system FMAS attests to an anticlockwise P‐T path of evolution for the granulites. In calc‐silicate granulites stabilization of nearly pure meionite and of the wollastonite‐plagioclase‐andradite‐rich garnet, wollastonite‐scapolite‐grandite garnet‐calcite association corroborate high temperatures of metamorphism. Conventional mineralogical geothermobarometry in all the rocks record lower temperatures (maximum 950°C) at 9–10 kbar pressures, attributed to resetting of the mineral compositions during cooling. Following peak metamorphism, the rocks firstly experienced near‐isobaric cooling followed by near‐isothermal decompression. On the basis of the available evidence it appears that non‐extensional lithospheric thinning and/or heat input from basic/enderbitic magma are the causes of such ultra‐high temperature metamorphism on an anticlockwise path in the Eastern Ghats Belt.
Pressure‐temperature‐time paths and the relationship between collision, deformation and metamorphism in the north‐west Himalaya
Authors: Treloar Peter J. 
Published: February 2007

AbstractTertiary collision in the NW Himalaya was between the Indian plate and the Kohistan island arc, the leading edge of the Indian plate being subducted beneath the arc along the Main Mantle Thrust (MMT). Porphyroblast‐matrix relationships show that metamorphism within Indian plate cover sediments exposed on the footwall of the MMT was synchronous with ductile shearing which marks the main deformation phase. The P‐T‐t paths, derived from inclusion assemblages and forward modelling of garnet zonation patterns, show that this metamorphism was along a path of increasing pressure. These data are consistent with Indian plate metamorphism occurring during active subduction beneath the Kohistan island arc. Geochronological data date the metamorphic peak as pre‐50 Ma. As initial collision cannot have pre‐dated 65 Ma, there was thus insufficient time for the long time‐scales of metamorphism generally predicted by conductive models of post‐thickening thermal relaxation. The cover sediments show a metamorphic inversion, argued previously as the result entirely of post‐metamorphic thrusting and imbrication. By contrast, basement gneisses exposed beneath the MMT have largely been unaffected by Tertiary metamorphism. The relationship between ductile shearing and metamorphism on the footwall of the MMT during active subduction, and the concentration of the highest metamorphic grades in the stratigraphically youngest rocks, suggests that early Tertiary metamorphism was controlled by dissipative shear heating distributed across the uppermost cover sediments of the subducting Indian plate. This generated a primary, inverted metamorphic sequence shortly after collision, an inversion reinforced by subsequent thrusting associated with accretion of the metamorphic pile onto the base of the over‐riding arc. This conclusion stresses the importance of dissipative shear heating in controlling metamorphism within thrust systems and provides a mechanism by which areas of apparently large regional extent can undergo regional metamorphism over short time‐scales, but in the absence of any magmatic heating.
Epidemiology of carcinogen metabolism genes and risk of squamous cell carcinoma of the head and neck
Authors: Ho Tang , Wei Qingyi , Sturgis Erich M. 
Published: February 2007

AbstractThe risk association between tobacco and alcohol use with squamous cell carcinoma of the head and neck (SCCHN) is well recognized. However, clearly not all individuals who smoke or drink develop SCCHN. Individual genetic susceptibility differences in carcinogen‐metabolizing enzyme function, mutagen sensitivity, apoptosis, and chromosomal aberrations either alone or in combination have been theorized to modify the risk of SCCHN. Nearly all carcinogens and procarcinogens require activation by metabolizing enzymes. Similarly, detoxifying enzymes exist and deactivate carcinogens as well as their intermediate by‐products. Together these enzymes are termed xenobiotic‐metabolizing enzymes; genetic polymorphisms of these enzymes can modify an individual's response to carcinogens and hence the carcinogenic potential of such exposures. In this review, we explore the available evidence in recent literature regarding the risk association between SCCHN and various xenobiotic‐metabolizing enzymes, including cytochrome P450s, glutathione S‐transferases, N‐acetyltransferases, NAD(P)H:quinone oxidoreductase 1, alcohol dehydrogenase, and aldehyde dehydrogenase. © 2007 Wiley Periodicals, Inc. Head Neck 2007
The increased expression of Y box‐binding protein 1 in melanoma stimulates proliferation and tumor invasion, antagonizes apoptosis and enhances chemoresistance
Authors: Schittek Birgit , Psenner Karin , Sauer Birgit , Meier Friedegund , Iftner Thomas , Garbe Claus 
Published: February 2007

AbstractIn previous studies we identified the transcription/translation factor Y‐box‐binding protein (YB‐1) as a gene that is upregulated in primary melanoma and melanoma metastases when compared to benign melanocytic nevi. To analyze whether YB‐1 expression correlates with melanoma progression in vitro and in vivo, we performed expression analysis on melanoma cell lines representing different stages of melanoma progression and on tissues of melanocytic nevi, primary melanoma and melanoma metastases. Our data indicate that compared to benign melanocytes YB‐1 expression is increased in melanoma cells in vitro and in vivo and that YB‐1 is translocated into the nucleus in invasive and metastatic melanoma cells. To reveal the functional role of YB‐1 in melanoma progression we achieved a stable downregulation of YB‐1 using shRNA in metastatic melanoma cells. Interestingly, YB‐1 downregulation resulted in a pronounced reduced rate of proliferation and an increased rate of apoptotic cell death. In addition, migration and invasion of melanoma cells in monolayer and in a three‐dimensional skin reconstruct in vitro was significantly reduced. These effects were accompanied by downregulation of genes involved in proliferation, survival and migration/invasion of melanoma cells such as MMP‐2, bcl‐2, Cyclin D1, p53 and p16INK4A. Furthermore, melanoma cells with a reduced YB‐1 expression showed a decreased resistance to the chemotherapeutic agents cisplatin and etoposide. These data suggest that YB‐1 is involved in malignant transformation of melanocytes and contributes to the stimulation of proliferation, tumor invasion, survival and chemoresistance. Thus, YB‐1 may be a promising molecular target in melanoma therapy. © 2007 Wiley‐Liss, Inc.
Genetic redundancy in human cervical carcinoma cells: Identification of cells with “normal” properties
Authors: Bachmann Anastasia , Zawatzky Rainer , Rösl Frank 
Published: February 2007

AbstractAlthough it is generally assumed that cancer arises from a singular cell, a tumor must be considered as a dynamic and emergent biological structure, whose organizing principle is determined by genetic and epigenetic modifications, occurring variably in response to microenvironmental selection conditions. As previously shown, HPV‐positive cervical carcinoma cells have lost their ability to induce IFN‐β upon TNF‐α treatment. However, regarding cancer as a non‐linear system, which may, even in the absence of an apparent selection pressure, fluctuate between different “metastable” phenotypes, we demonstrate that TNF‐α mediated IFN‐β induction is not irreversibly disturbed in all cells. Using the IFN‐β sensitive Encephalomyocarditis virus (EMCV) as a tool to monitor antiviral activity in long‐term established malignant HeLa cells, rare IFN‐β expressing clones were rescued from a population of non‐responsive and EMCV‐sensitive cells. Antiviral activity was mediated by the re‐expression of IRF‐1 and p48 (IRF‐9), both key regulatory molecules normally found to be suppressed in cervical carcinoma cells. Upon inoculating of selected clones into immunocompromised animals, a reduced or even an absence of tumorigenicity of initially highly malignant cells could be discerned. These data indicate that both the absence of interferon signaling and the ability to form tumors were reversed in a minority of cells. We provide a paradigm for the existence of innate genetic redundancy mechanisms, where a particular phenotype persists and can be isolated without application of drugs generally changing the epigenetic context. © 2007 Wiley‐Liss, Inc.
Body mass index and pancreatic cancer risk: A meta‐analysis of prospective studies
Authors: Larsson Susanna C. , Orsini Nicola , Wolk Alicja 
Published: February 2007

AbstractA number of studies have examined the association between body mass index (BMI) and risk of pancreatic cancer, but uncertainty about the relationship remains. We performed a meta‐analysis to summarize the evidence from prospective studies investigating this association. We searched MEDLINE for studies published in any language from 1966 to November 2006. Prospective studies were included if they reported relative risks (RRs) with 95% confidence intervals (CIs) for the association between BMI and pancreatic cancer incidence or mortality. Study‐specific RR estimates were combined by use of a random‐effects model. A total of 21 independent prospective studies, involving 3,495,981 individuals and 8,062 pancreatic cancer cases, met the inclusion criteria. The estimated summary RR of pancreatic cancer per 5 kg/m2 increase in BMI was 1.12 (95% CI, 1.06–1.17; p‐heterogeneity = 0.13) in men and women combined, 1.16 (95% CI, 1.05–1.28; p‐heterogeneity = 0.001) in men, and 1.10 (95% CI, 1.02–1.19; p‐heterogeneity = 0.12) in women. There was no evidence of publication bias (p = 0.58). Findings from this meta‐analysis of prospective studies support a positive association between BMI and risk of pancreatic cancer in men and women. © 2007 Wiley‐Liss, Inc.
Evidence for the role of aberrant DNA methylation in the pathogenesis of Lynch syndrome adenomas
Authors: Kaz Andrew , Kim Young‐Ho , Dzieciatkowski Slavomir , Lynch Henry , Watson Patrice , Kay Washington Mary , Lin Li , Grady William M. 
Published: February 2007

AbstractColorectal cancer (CRC) forms through a series of histologic steps that are accompanied by mutations and epigenetic alterations, which is called the polyp‐cancer sequence. The role of epigenetic alterations, such as aberrant DNA methylation, in the polyp‐cancer sequence in sporadic CRC and particularly in hereditary colon cancer is not well understood. Consequently, we assessed the methylation status of CDKN2A/p16, MGMT, MLH1 and p14ARF in adenomas arising in the Lynch syndrome, a familial colon cancer syndrome caused by MLH1 and MSH2 mutations, to determine if DNA methylation is a “second hit” mechanism in CRC and to characterize the role of DNA methylation in the polyp phase of the Lynch syndrome. We found MLH1 and p14ARF are methylated in 53 and 60% of the Lynch syndrome adenomas and in 4 and 20% of sporadic adenomas, whereas CDKN2A/p16 and MGMT are methylated in 6 and 14% of the Lynch syndrome adenomas versus 50 and 64% of sporadic adenomas. Therefore, the frequency and pattern of gene methylation varies between the Lynch syndrome and sporadic colon adenomas, implying differences in the molecular pathogenesis of the tumors. MLH1 methylation in the Lynch syndrome adenomas suggests gene methylation might have a role in the initiation of these neoplasms. © 2007 Wiley‐Liss, Inc.
Dynamic stromal‐epithelial interactions during progression of MCF10DCIS.com xenografts
Authors: Tait Larry R. , Pauley Robert J. , Santner Steven J. , Heppner Gloria H. , Heng Henry H. , Rak Janusz W. , Miller Fred R. 
Published: February 2007

AbstractMCF10DCIS.com cells form comedo type ductal carcinoma in situ in immune‐deficient mice before forming invasive ductal carcinoma. As the lesions mature, both stromal and epithelial cells undergo phenotypic changes detected by immunohistochemistry. Myofibroblasts are present before the formation of carcinoma in situ and after development of invasive carcinoma. MCF10DCIS. com lesions develop a myoepithelial layer prior to exhibiting a basement membrane surrounding the ductal mass. TGFβ1 is initially expressed by the epithelial cells but is expressed by stroma in invasive carcinoma. Stromal derived factor‐1 is detected in epithelial cells in early carcinoma in situ but is produced in stromal cells in invasive carcinoma. The receptor CXCR4 is expressed by epithelial cells in the xenografts at all times, as is the hepatocyte growth factor receptor c‐met. MCF10DCIS.com xenografts illustrate the dynamic interplay of epithelium and stroma in the development of carcinoma in situ and subsequent invasive carcinoma. Although the phenotype of the epithelial cells may be dependent upon the stroma, the malignant epithelium induces the development of the stroma necessary for progression to the invasive stage. © 2007 Wiley‐Liss, Inc.
Effects of combined exposure to pyridostigmine bromide and shaker stress on acoustic startle response, pre‐pulse inhibition and open field behavior in mice
Authors: Dubovicky M. , Paton S. , Morris M. , Mach M. , Lucot J. B. 
Published: February 2007

AbstractThe present study investigated the effect of combined exposure of pyridostigmine bromide (PB) and chronic shaker stress on acoustic startle responses (ASR), pre‐pulse inhibition (PPI) and open field behavior of adult C57BL/6J mice. PB (10 mg kg−1day−1for 7 days) or saline was administered subcutaneously using osmotic Alzet minipumps implanted under the skin on the back of the mice. At the same time, the mice were exposed to 7 days of intermittent shaker stress. They were tested for ASR (100 dB and 120 dB stimuli) and PPI (70 dB + 100 dB and 70 dB + 120 dB) in the acoustic startle monitor system. The mice were assessed during the shaker stress on days 2 and 7 and 7, 14, 21 and 28 days after discontinuation of treatment. Separate groups of mice were tested in the open field in 15 min sessions on days 1, 3 and 6 during shaker stress and PB treatment. Exposure of mice to PB resulted in an exaggerated ASR, reduced PPI and non‐significant decrease in locomotor activity. These behavioral changes were apparent only during exposure to PB. Repeated shaker stress did not have any effect on sensorimotor functions or open field behavior of mice. There was no prolonged or delayed effect of PB and/or stress on individual behavioral variables. The study found C57BL/6J mice to be behaviorally sensitive to PB treatment. Copyright © 2007 John Wiley & Sons, Ltd.
Adrenal toxicology: a strategy for assessment of functional toxicity to the adrenal cortex and steroidogenesis
Authors: Harvey Philip W. , Everett David J. , Springall Christopher J. 
Published: February 2007

AbstractThe adrenal is the most common toxicological target organ in the endocrine system in vivo and yet it is neglected in regulatory endocrine disruption screening and testing. There has been a recent marked increase in interest in adrenal toxicity, but there are no standardised approaches for assessment. Consequently, a strategy is proposed to evaluate adrenocortical toxicity. Human adrenal conditions are reviewed and adrenocortical suppression, known to have been iatrogenically induced leading to Addisonian crisis and death, is identified as the toxicological hazard of most concern. The consequences of inhibition of key steroidogenic enzymes and the possible toxicological modulation of other adrenal conditions are also highlighted. The proposed strategy involves an in vivo rodent adrenal competency test based on ACTH challenge to specifically examine adrenocortical suppression. The H295R human adrenocortical carcinoma cell line is also proposed to identify molecular targets, and is useful for measuring steroids, enzymes or gene expression. Hypothalamo‐pituitary‐adrenal endocrinology relevant to rodent and human toxicology is reviewed (with an emphasis on multi‐endocrine axis effects on the adrenal and also how the adrenal affects a variety of other hormones) and the endocrinology of the H295R cell line is also described. Chemicals known to induce adrenocortical toxicity are reviewed and over 60 examples of compounds and their confirmed steroidogenic targets are presented, with much of this work published very recently using H295R cell systems. In proposing a strategy for adrenocortical toxicity assessment, the outlined techniques will provide hazard assessment data but it will be regulatory agencies that must consider the significance of such data in risk extrapolation models. The cases of etomindate and aminoglutethimide induced adrenal suppression are clearly documented examples of iatrogenic adrenal toxicity in humans. Environmentally, sentinel species, such as fish, have also shown evidence of adrenal endocrine disruption attributed to exposure to chemicals. The extent of human sub‐clinical adrenal effects from environmental chemical exposures is unknown, and the extent to which environmental chemicals may act as a contributory factor to human adrenal conditions following chronic low‐level exposures will remain unknown unless purposefully studied. Copyright © 2007 John Wiley & Sons, Ltd.
Pre‐culture period of mesenchymal stem cells in osteogenic media influences their in vivo bone forming potential
Authors: Castano‐Izquierdo Harold , Álvarez‐Barreto José , Dolder Juliette van den , Jansen John A. , Mikos Antonios G. , Sikavitsas Vassilios I. 
Published: February 2007

AbstractThe objective of this study was to investigate if the in vitro pre‐culture period in osteogenic media of rat mesenchymal stem cells (MSCs), influences their ability to regenerate bone when implanted in a critical size cranial defect. MSCs were harvested from the bone marrow of 6–8 weeks old male Fisher rats and expanded in vitro in osteogenic media for different time periods (4, 10, and 16 days) in tissue culture plates (TCP), seeded on sintered titanium fiber meshes without the extracellular matrix (ECM) generated in vitro, and implanted in the rat cranium after 12 h. Thirty two adult Fisher rats received the implants, divided in four groups. Three groups were implanted with cells cultured for 4, 10, or 16 days in osteogenic media and at that time their alkaline phosphatase activity and mineral deposition denoted that they were at different stages of their osteoblastic maturation (undifferentiated MSC, committed, and mature Osteoblasts, respectively). MSCs cultured without osteogenic media for 6 days were used as controls. The constructs were retrieved 4 weeks later and processed for histomorphometric analysis. Implants seeded with cells that have been cultured with osteogenic media for only 4 days revealed the highest bone formation. The lowest bone formation was obtained with the implants seeded with MSCs cultured for 16 days in the presence of osteogenic media. The results of this study suggested that the in vitro pre‐culture period of MSCs is a critical factor for their ability to regenerate bone when implanted to an orthotopic site. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Design of a biomimetic polymer‐composite hip prosthesis
Authors: Bougherara Habiba , Bureau Martin , Campbell Melissa , Vadean Aurelian , Yahia L'Hocine 
Published: February 2007

AbstractA new biomimetic composite hip prosthesis (stem) was designed to obtain properties similar to those of the contiguous bone, in particular stiffness, to allow normal loading of the surrounding femoral bone. This normal loading would reduce excessive stress shielding, known to result in bone loss, and micromotions at the bone‐implant interface, leading to aseptic prosthetic loosening. The design proposed is based on a hollow substructure made of hydroxyapatite‐coated, continuous carbon fiber (CF) reinforced polyamide 12 (PA12) composite with an internal soft polymer‐based core. Different composite configurations were studied to match the properties of host tissue. Nonlinear three‐dimensional analysis of the hip prosthesis was carried out using a three‐dimensional finite element bone model based on the composite femur. The performance of composite‐based hip and titanium alloy‐based (Ti‐6Al‐4V) stems embedded into femoral bone was compared. The effect of core stiffness and ply configuration was also analyzed. Results show that stresses in composite stem are lower than those in Ti stem, and that the femoral bone implanted with composite structure sustains more load than the one implanted with Ti stem. Micromotions in the composite stem are significantly smaller than those in Ti stem over the entire bone‐implant surface because of the favorable interfacial stress distribution. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
RUNX regulates stem cell proliferation and differentiation: Insights from studies of C. elegans
Authors: Kagoshima Hiroshi , Shigesada Katsuya , Kohara Yuji 
Published: February 2007

AbstractThe RUNX genes encode conserved transcription factors that play vital roles in the development of various animals and human diseases. Recent studies by a few groups including ours have demonstrated that this gene family, as represented by a single ortholog designeated rnt‐1, also occurs and plays intriguing roles in the simple model organism, Caenorhabditis elegans. Our genetic and molecular analyses revealed that rnt‐1 is allelic to mab‐2, which had previously been known to cause an abnormal development of the male tail. rnt‐1 was further shown to be predominantly expressed in the stem cell‐like lateral seam hypodermal cells. These cells are characterized by their abilities to undergo stem cell‐like asymmetric divisions giving rise to self‐renewing seam cells and various differentiated descendants of hypodermal and neuronal fates. We found that rnt‐1 mutants exhibit an impaired asymmetry in the division of T cells, the posterior‐most member of the seam cells. Mutant analysis indicated that rnt‐1 is involved in regulating T blast cell polarity in cooperation with the Wnt signaling pathway. On the other hand, Nimmo et al. independently discovered that rnt‐1 acts as a rate limiting regulator of cell proliferation in the seam cells, V1‐6. In this review, we will outline these new findings and discuss their general implications in the mechanism of coordination between proliferation and differentiation of stem cells. J. Cell. Biochem. 100: 1119–1130, 2007. © 2007 Wiley‐Liss, Inc.