bluuebunny/crossref_metadata_2025_split huggingface dataset:
Exploring the nature of myth and its role in science
Authors: Masse W. Bruce , Barber Elizabeth Wayland , Piccardi Luigi , Barber Paul T. 
Published: December 2007

AbstractThe scientific study of myth is dominated by a paradigm that recognizes myth as having been viewed as truthful narrative history by past traditional cultures and yet is considered false or otherwise suspect by the modern scholars who study myth. Although virtually all scholars recognize that myth was of critical importance for traditional cultures, the attempt to elicit scientific reasons for this importance has led to many competing theories, few of which place an emphasis on the validity of myths as representing the product of actual observed historical natural events. This paradox may hinder our understanding of the origins of myth and prevent us from fully appreciating a critical aspect of why myth was so highly valued by past cultures. To set the stage for our examination of the possible natural history core of myth, we discuss briefly the history of the western scientific study of myth, with an emphasis on geological sciences. We then explore the cognitive structure of myth and provide working principles about how the historical information contained in these myths can be transmitted faithfully through successive generations and can be elicited by scientific study. Although recognizing the extreme complexity of myth as a cultural product, our data indicate that a science-based natural history approach can lead to important insights regarding the nature of myth.
Environment and natural hazards in Roman and Medieval texts: presentation of the CLEMENS database project
Authors: Vittori Eutizio , Fulloni Sabina , Piccardi Luigi 
Published: December 2007

Abstract

CLEMENS, acronym for
Corpus Latinorum Et Mediaevalium Naturae Scriptorum
, is a new electronic archive of
excerpta
reporting environment-related data contained in the literary and epigraphic sources of classical Roman and Medieval age. The aim is to fill a gap in information about environmental disruptions or memorabilia that occurred in ancient times within the Mediterranean basin, and to verify whether any useful information has eluded our knowledge. One of the main purposes of the systematic gathering and cataloguing carried out by CLEMENS is to become an extensive easy-to-search tool, offering the scientific community complete annotated documentation of what is available inside ancient sources about the natural environment in the Mediterranean. This information, currently dispersed in a variety of publications that may be difficult to access, has often proven essential for hazard assessment in several areas of the former Roman empire. It also contributes significantly to the understanding of changes caused by environmental events over the centuries, and of their incidence on natural habitats and on cultural heritage. The analysis of such interconnections may lead to a much improved understanding of either natural environment, hazards and cultural setting, as shown by interdisciplinary investigations merging together science, archaeology and history or even myth.

Considering the vast amount of documentation, the work is still far from completion. However, the encouraging preliminary results will soon be available on the web.
Geological histories and geohazard potential of Pacific Islands illuminated by myths
Authors: Nunn Patrick D. , Pastorizo Ronna 
Published: December 2007

Abstract
Understanding of the geological history of the Pacific, especially its geohazard potential, can be improved using details in ancient and properly-authenticated Pacific Islander myths. To demonstrate this, a synthesis of Pacific Island origin myths involving islands having been either ‘fished up’ or ‘thrown down’ is presented, with an account of origin myths for the island Niue used as a case study. A discussion of geohazards and myths in the Pacific focuses on tsunami, coseismic uplift, and island flank collapse, the last being illustrated by the first analysis of myths recalling ‘vanished islands’ in the Pacific.
Giants and elephants of Sicily
Authors: Agnesi V. , Di Patti C. , Truden B. 
Published: December 2007

Abstract
In Sicily, the great abundance of fascinating and impressive natural phenomena, have fed the imagination of men, who have interpreted them as the manifestation of the existence of supernatural and fantastic beings giving rise to myth and legend. Amongst these many myths, that of the cyclops Polyphemus, is closely linked to the geopalaeontological history of Sicily. The discovery, often inside caves, of the fossil skulls of elephants, in which there is a great nasal hollow (in the frontal part) where there was a trunk in life, gave rise to the belief that one-eyed giants had existed, in the past. The nasal hollow was wrongly interpreted as the orbit of a single frontal eye that characterized these monstrous beings, and the gigantic size was inferred by the notable dimensions of the skulls and the bones that are frequently found. In 1830 Giorgio Cuvier, attested to the fossil nature of the bones and put an end to the different inferences formulated about their origin.
Sand and mud flux estimates using acoustic and optical backscatter sensors: measurements seaward of the Wash, southern North Sea
Authors: Bass Sarah J. , McCave I. N. , Rees J. M. , Vincent C. E. 
Published: December 2007

Abstract
Optical and acoustic backscatter sensors, more sensitive to fine and sandy sediment respectively, were used to measure the mud and sand components of a mixed suspension at a site seaward of the Wash embayment, in the southern North Sea. Data were acquired from a free-standing instrument frame during a five-week deployment in 12 m water depth about 6 km offshore. Suspended mud at this site was characterized by tidal advection of fine sediment along the coast resulting in semi-diurnal peaks in concentration near slack water. Suspended sand concentrations correlated well with tidal current speeds indicating local resuspension behaviour. Predicted sand flux direction followed the residual current while mud fluxes at the site were different in direction to both the residual current and sand flux. Residual fluxes may be biased by cumulative errors resulting from instrument calibration and inferred vertical concentration profiles. These factors are assessed in relation to both predicted flux magnitudes and directions.
Modelling SPM on the NW European shelf seas
Authors: Souza Alejandro J. , Holt Jason T. , Proctor Roger 
Published: December 2007

Abstract
The Proudman Oceanographic Laboratory Coastal Ocean Modelling System (POLCOMS) has been developed to tackle multidisciplinary studies in coastal/shelf environments. The central core is a sophisticated three-dimensional hydrodynamic model that provides realistic flow fields to interact with, and transport environmental parameters. The model uses realistic forcing with ocean currents and hydrography at the boundary, atmospheric forcing and tides.
Suspended particulate matter (SPM) is transported within the water, like any other scalar in the model; it is advected using a high-order scheme and mixed vertically using diffusion coefficients from a second moment turbulence closure. In addition, the SPM transport is influenced by a number of processes unique to this problem, such as: the transfer between the lowest level of the model and the bed layer in which the resuspension and deposition takes place is dependent on the erosion rate, the particle settling velocity and the critical stresses for erosion and deposition. The particular application described in this paper is an annual simulation for the NW European shelf for a single sediment class.
The simulation shows the expected seasonal variation in spatial patterns and a clear tidal signal in the SPM resuspension. Also evident is a fortnightly/monthly variability due to the spring-neaps and the M2-N2 cycles. There are also quarter-diurnal and semi-diurnal cycles in SPM, due to tidal resuspension and advection respectively. The above tidal suspension behaviour, as well as, the net transport direction are in agreement with historical observations of SPM.
A late Atokan regional encrinite (early late Moscovian, Middle Pennsylvanian) in the Sierra Agua Verde, Sonora state, NW Mexico
Authors: Buitrón-Sánchez B. E. , Gómez-Espinosa C. , Almazán-Vázquez E. , Vachard D. 
Published: December 2007

Abstract

In the Sierra Agua Verde, central Sonora state, NW Mexico, the La Joya Formation exhibits an alternation (100 m thick) of calcareous siltstone and fossiliferous limestone with nodular cherts. This latter contains an abundant and diverse late Atokan (i.e. Podolskian = early late Moscovian, Middle Pennsylvanian) fossil assemblage composed of phylloid algae, fusulinids, chaetetids, tabulate corals, gastropods, fenestellid bryozoans, spiriferid and productid brachiopods, crinoids and conodonts. The crinoidal beds constitute a good example of a regional encrinite. They include several species of the parataxonomic stem form-genera
Cyclocaudex, Cyclocrista, Heterosteleschus, Mooreanteris, Pentagonopterix, Preptopremnum, Cycloscapus
and
Pentaridica
. Their preservation indicates the combination of preburial decay on the sea floor and post-burial decay within the sediment. The high degree of silicification of the crinoids indicates that they were possibly associated with siliceous organisms (Porifera?), not preserved in the assemblages. The studied thanatocoenosis is typical of tropical shallow seas, and reveals strong biogeographical affinities with the assemblages of the midcontinental and southern regions of the USA. Particularly, the Atokan crinoids of central Sonora are similar to those from Kansas and Texas, confirming the close palaeogeographic connection of southern USA and northern Mexico during the Middle Pennsylvanian.
c-myc Repression of TSC2 Contributes to Control of Translation Initiation and Myc-Induced Transformation
Authors: Ravitz Michael J. , Chen Li , Lynch Mary , Schmidt Emmett V. 
Published: December 2007

Abstract
The c-myc oncogene plays a key role in cellular growth control, and translation initiation factors are among the transcriptional targets of Myc. Here, we describe a defect in translation initiation control in myc-null cells due to alterations in the mammalian target of rapamycin (mTOR) pathway. Myc loss increased sensitivity to dominant inhibition of eukaryotic translation initiation factor 4E function. Polysomal profiles of myc−/− cells revealed decreased translation initiation rates, which were accompanied by decreased 40S/60S ribosomal subunit ratios. Because the 40S small ribosomal subunit contains the key regulatory ribosomal protein S6 (rpS6), we considered that myc loss might affect expression of components of the mTOR signaling pathway that regulate rpS6 function. Among mTOR signaling components, Myc directly affected transcription of tuberous sclerosis 2 (TSC2), as shown by quantitative mRNA analysis and by Myc binding to its promoter in chromatin immunoprecipitation assays. Importantly, Myc acted as a strong and direct repressor for TSC2 expression because its loss increased TSC2 mRNA in myc-null and in HL60 shRNA experiments, activation of a mycER construct in myc−/− cells suppressed TSC2 induction in a myc box II–dependent manner, and mycER activation recruited Myc to the TSC2 promoter. The biological significance of the effect of Myc on TSC2 expression was shown by markedly reduced TSC2 mRNA levels in myc-transformed cells, stimulation of S6 kinase activity in myc-null cells by TSC2 siRNA, and decreased Myc-induced soft agar colony formation following retroviral transduction of TSC2. Together, these findings show that regulation of TSC2 can contribute to the effects of Myc on cell proliferation and neoplastic growth. [Cancer Res 2007;67(23):11209–17]
Ribosomal Protein S27-like, a p53-Inducible Modulator of Cell Fate in Response to Genotoxic Stress
Authors: Li Jingsong , Tan Jing , Zhuang Li , Banerjee Birendranath , Yang Xiaojing , Chau Jenny Fung Ling , Lee Puay Leng , Hande Manoor Prakash , Li Baojie , Yu Qiang 
Published: December 2007

Abstract
Activation of the p53 tumor suppressor upon DNA damage elicits either cell cycle arrest or apoptosis, and the precise mechanism governing cell fate after p53 response has not been well defined. Through genomic analysis, we have identified the ribosomal protein S27-like (RPS27L) as a novel p53 transcriptional target gene. Although RPS27L mRNA levels were consistently induced after diverse p53 activating signals, its change in protein level was stimuli-dependent: it was up-regulated when cells were arrested in response to DNA-damaging agents Adriamycin or VP16 but was down-regulated when cells underwent apoptosis in response to antimetabolite agent 5-fluorouracil. RPS27L is a nuclear protein that forms nuclear foci upon DNA damage. Depletion of RPS27L resulted in deficiency in DNA damage checkpoints, leading to conversion of DNA damage–induced p53 response from cell cycle arrest to apoptosis. We further show that RPS27L positively regulates p21 protein expression. Through this mechanism, RPS27L induction by p53 facilitates p21-mediated cell cycle arrest and protects against DNA damage–induced apoptosis. Thus, RPS27L modulates DNA damage response and functions as a part of the control switch to determine cell fate to DNA damage–p53 response. [Cancer Res 2007;67(23):11317–26]
Histone Deacetylase Inhibitors Promote the Tumoricidal Effect of HAMLET
Authors: Brest Patrick , Gustafsson Mattias , Mossberg Ann-Kristin , Gustafsson Lotta , Duringer Caroline , Hamiche Ali , Svanborg Catharina 
Published: December 2007

Abstract
Histone deacetylase inhibitors (HDIs) and HAMLET (human α-lactalbumin made lethal to tumor cells) interact with histones, modify the structure of chromatin, and trigger tumor cell death. This study investigated how the combination of HDIs and HAMLET influences cell viability, histone acetylation, and DNA integrity. The pretreatment of tumor cells with HDIs was shown to enhance the lethal effect of HAMLET and the histone hyperacetylation response to HDIs increased even further after HAMLET treatment. HDIs and HAMLET were shown to target different histone domains as HAMLET bound tailless core histones, whereas HDIs modify the acetylation of the histone tail. DNA damage in response to HAMLET was increased by HDIs. The DNA repair response (p21WAFI expression) was induced by both agonists but abolished when the two agonists were combined. The results suggest that the synergy of HDIs and HAMLET is based on different but converging death pathways, both involving chromatin alterations. We speculate that HAMLET and HDIs might be combined to promote tumor cell death in vivo. [Cancer Res 2007;67(23):11327–34]
Role of CYP2E1 in Diethylnitrosamine-Induced Hepatocarcinogenesis In vivo
Authors: Kang Jin Seok , Wanibuchi Hideki , Morimura Keiichirou , Gonzalez Frank J. , Fukushima Shoji 
Published: December 2007

Abstract
CYP2E1 metabolizes many low–molecular weight toxins and carcinogens. Some in vitro experiments suggest that CYP2E1 may be involved in the metabolic activation of diethylnitrosamine. However, there has been no direct evidence demonstrating a role for CYP2E1 in diethylnitrosamine-mediated carcinogenesis in vivo. To clarify this, we carried out a diethylnitrosamine-induced hepatocarcinogenesis experiment using Cyp2e1-null mice. Male 14-day-old wild-type and Cyp2e1-null mice were treated with diethylnitrosamine (10 mg/kg of body weight) and killed at weeks 24 and 36 after diethylnitrosamine treatment for investigation of tumors and at 6, 24, and 48 h for examination of apoptosis and gene expression. Liver weights of Cyp2e1-null mice were significantly different at weeks 24 and 36 compared with wild-type mice (P &lt; 0.01). Liver tumor incidences of Cyp2e1-null mice were significantly decreased at weeks 24 and 36 compared with wild-type mice (P &lt; 0.01). Cyp2e1-null mice showed significant decrease in the multiplicities of hepatocellular adenoma at weeks 24 and 36 (P &lt; 0.05 and P &lt; 0.01, respectively), and of hepatocellular carcinoma at week 36 (P &lt; 0.01) compared with wild-type mice. Apoptotic index and caspase-3 and/or Bax mRNA expression of Cyp2e1-null mice were significantly different at 6, 24, and 48 h after diethylnitrosamine treatment compared with wild-type mice (P &lt; 0.05). We conclude that Cyp2e1-null mice show lower tumor incidence and multiplicity compared with wild-type mice in diethylnitrosamine-induced hepatocarcinogenesis. It is suggested that CYP2E1 completely participates in diethylnitrosamine-induced hepatocarcinogenesis, and high frequency of tumors in wild-type mice could be associated with the increased apoptosis. [Cancer Res 2007;67(23):11141–6]
Suppression of Proximal T Cell Receptor Signaling and Lytic Function in CD8+ Tumor-Infiltrating T Cells
Authors: Monu Ngozi , Frey Alan B. 
Published: December 2007

AbstractCD8+ tumor-infiltrating lymphocytes (TIL) lack in vivo and in vitro lytic function due to a signaling deficit characterized by failure to flux calcium or activate tyrosine kinase activity upon contact with cognate tumor cells. Although CD3ζ is phosphorylated by conjugation in vitro with cognate tumor cells, showing that TIL are triggered, PLCγ-1, LAT, and ZAP70 are not activated and LFA-1 is not affinity-matured, and because p56lck is required for LFA-1 activation, this implies that the signaling blockade is very proximal. Here, we show that TIL signaling defects are transient, being reversed upon purification and brief culture in vitro, implying a fast-acting “switch”. Biochemical analysis of purified nonlytic TIL shows that contact with tumor cells causes transient activation of p56lck (∼10 s) which is rapidly inactivated. In contrast, tumor-induced activation of p56lck in lytic TIL is sustained coincident with downstream TCR signaling and lytic function. Shp-1 is robustly active in nonlytic TIL compared with lytic TIL, colocalizes with p56lck in nonlytic TIL, and inhibition of Shp-1 activity in lytic TIL in vitro blocks tumor-induced defective TIL cytolysis. Collectively, our data support the notion that contact of nonlytic TIL with tumor cells, and not with tumor-infiltrating myeloid-derived suppressor cells, causes activation of Shp-1 that rapidly dephosphorylates the p56lck activation motif (Y394), thus inhibiting effector phase functions. [Cancer Res 2007;67(23):11447–54]
Identification and Characterization of a Membrane Receptor for Proteolysis-Inducing Factor on Skeletal Muscle
Authors: Todorov Penio T. , Wyke Stacey M. , Tisdale Michael J. 
Published: December 2007

Abstract
Proteolysis-inducing factor (PIF) is a sulfated glycoprotein produced by cachexia-inducing tumors, which induces atrophy of skeletal muscle. PIF has been shown to bind specifically with high affinity (Kd, in nanomolar) to sarcolemma membranes from skeletal muscle of both the mouse and the pig, as well as murine myoblasts and a human muscle cell line. Ligand binding was abolished after enzymatic deglycosylation, suggesting that binding was mediated through the oligosaccharide chains in PIF. Chondroitin sulfate, but not heparan or dermatan sulfate, showed competitive inhibition (Kd, 1.1 × 10−7 mol/L) of binding of PIF to the receptor, suggesting an interaction with the sulfated oligosaccharide chains. Ligand blotting of [35S]PIF to triton solublized membranes from C2C12 cells provided evidence for a binding protein of apparent Mr of ∼40,000. Amino acid sequence analysis showed the PIF receptor to be a DING protein. Antisera reactive to a 19mer from the N-terminal amino acid residues of the binding protein attenuated protein degradation and activation of the ubiquitin-proteasome pathway induced by PIF in murine myotubes. In addition, the antisera was highly effective in attenuating the decrease in body weight in mice bearing the MAC16 tumor, with a significant increase in muscle wet weight due to an increase in the rate of protein synthesis, together with a reduction in protein degradation through attenuation of the increased proteasome expression and activity. These results confirm that the PIF binding protein has a functional role in muscle protein atrophy in cachexia and that it represents a potential new therapeutic target. [Cancer Res 2007;67(23):11419–27]
MicroRNAs as Potential Agents to Alter Resistance to Cytotoxic Anticancer Therapy
Authors: Weidhaas Joanne B. , Babar Imran , Nallur Sunitha M. , Trang Phong , Roush Sarah , Boehm Michelle , Gillespie Erin , Slack Frank J. 
Published: December 2007

Abstract
Tumor cells use preexisting prosurvival signaling pathways to evade the damaging and cytotoxic effects of anticancer agents. Radiation therapy is a primary form of cytotoxic anticancer treatment, but agents that successfully modify the radiation response in vivo are lacking. MicroRNAs (miRNA) are global gene regulators that play critical roles in oncogenesis and have been found to regulate prosurvival pathways. However, there is little understanding of how cellular miRNA expression affects the response of a cancer to cytotoxic therapy and ultimately outcome. The let-7 family of miRNAs regulates expression of oncogenes, such as RAS, and is specifically down-regulated in many cancer subtypes. In fact, low levels of let-7 predict a poor outcome in lung cancer. Here, we report that the let-7 family of miRNAs is overrepresented in a class of miRNAs exhibiting altered expression in response to radiation. More strikingly, we also can create a radiosensitive state when the select let-7 family of miRNAs is overexpressed in vitro in lung cancer cells and in vivo in a Caenorhabditis elegans model of radiation-induced cell death, whereas decreasing their levels causes radioresistance. In C. elegans, we show that this is partly through control of the proto-oncogene homologue let-60/RAS and genes in the DNA damage response pathway. These findings are the first direct evidence that miRNAs can suppress resistance to anticancer cytotoxic therapy, a common feature of cancer cells, and suggest that miRNAs may be a viable tool to augment current cancer therapies. [Cancer Res 2007;67(23):11111–6]
Runx2 Disruption Promotes Immortalization and Confers Resistance to Oncogene-Induced Senescence in Primary Murine Fibroblasts
Authors: Kilbey Anna , Blyth Karen , Wotton Sandy , Terry Anne , Jenkins Alma , Bell Margaret , Hanlon Linda , Cameron Ewan R. , Neil James C. 
Published: December 2007

Abstract
The Runx genes play paradoxical roles in cancer where they can function either as dominant oncogenes or tumor suppressors according to context. We now show that the ability to induce premature senescence in primary murine embryonic fibroblasts (MEF) is a common feature of all three Runx genes. However, ectopic Runx–induced senescence contrasts with Ras oncogene–induced senescence, as it occurs directly and lacks the hallmarks of proliferative stress. Moreover, a fundamental role for Runx function in the senescence program is indicated by the effects of Runx2 disruption, which renders MEFs prone to spontaneous immortalization and confers an early growth advantage that is resistant to stress-induced growth arrest. Runx2−/− cells are refractory to H-RasV12–induced premature senescence, despite the activation of a cascade of growth inhibitors and senescence markers, and are permissive for oncogenic transformation. The aberrant behavior of Runx2−/− cells is associated with signaling defects and elevated expression of S-G2-M cyclins and their associated cyclin dependent kinase activities that may override the effects of growth inhibitory signals. Coupling of stress responses to the cell cycle represents a novel facet of Runx tumor suppressor function and provides a rationale for the lineage-specific effects of loss of Runx function in cancer. [Cancer Res 2007;67(23):11263–71]