bluuebunny/crossref_metadata_2025_split huggingface dataset:
Charles Lyell’s debt to North America: his lectures and travels from 1841 to 1853
Authors: Dott Robert H. 
Published: September 2007

AbstractCharles and Mary Lyell visited North America four times from 1841 to 1853. During the first three visits, Lyell lectured and they travelled widely. The lectures were great successes with the American public in spite of Lyell’s poor elocutionary skills. Comparisons of lecture topics covered over a decade provide insights into the rapid development of the young science of geology and of Lyell’s changing preoccupations. Included were crustal movements; uniformity of causes through time; coral reefs and oceanic subsidence; Carboniferous conditions; the early appearance of reptiles; palaeoclimate; the submergence of land and the origin of drift; biogeography; and a uniform organic plan with arguments against transmutation and historical progression.The Lyells saw more of the United States and Canada than had most citizens. Their conveyances included horseback, stagecoach, train, railroad handcar, and steamboat. Accommodation varied from elegant hostelries to dirt-floored shacks. Their travels took them from the Atlantic coast to the Ohio and Mississippi Rivers and from the St Lawrence valley to the Gulf Coast. America gained from Lyell the enhancement of the stature of geology, several original contributions to the understanding of its geology, and a positive impression of the New World conveyed back to Britain. Lyell’s reward was greater, however, thanks to the generosity of American guidance in his field work. He gained many fresh geological examples for his books, published two travel journals and more than 30 journal articles and presented at least eight lectures in Britain about American geology, making him the local British authority on America. He especially gained new evidence for his opposition to biological progression and for his submergence theory for the drift. Besides enhancing his geological reputation, Lyell also made an incisive comparison of British and American education, which drew him into public reforms at home sponsored by Prince Albert. Finally, his exposure to American Unitarianism, coupled with disenchantment with the Anglican Church, caused Lyell to shift his religious allegiance.
Charles Lyell and climatic change: speculation and certainty
Authors: Fleming James Rodger 
Published: September 2007

Abstract

In the first edition of the
Principles of Geology
, Charles Lyell announced his theory of the geographical determination of climate and speculated on possible climatic changes during the geological and historical past. In light of the subsequent discovery of ice ages, the proliferation of theories of climatic change, and the great climate debates of his time. Lyell’s theory remained remarkably stable. This paper examines Lyell’s appropriation, modification and rejection of the views of his contemporaries. It provides perspectives on elite and popular ideas of climate and climatic change from the late eighteenth century to 1875, examines Lyell’s position on climatic change in geological and historical times, and explores in some detail the mutual influences of Lyell and James Croll, the proponent of an astronomical theory of ice ages.
Sequence stratigraphy: a revolution without a cause?
Authors: Wilson R. C. L. 
Published: September 2007

Abstract
The paper presents personal reflections on the origins and utility of sequence stratigraphic models. These focus on two questions: (1) does sequence stratigraphy represent a revolution in our understanding of the stratigraphic record, and (2) does it provide a new means of global correlation? The first question is answered in the affirmative, at least insofar as sequence stratigraphy enables us to integrate a wide range of data and interpretations across a huge range of spatial and temporal scales. The recognition of the importance of stratal surfaces has led to a greater understanding of the response by sedimentary to climatic, tectonic and eustatic changes. But it has yet to be shown that eustatic signals can be detected unequivocally in the stratigraphic record. Therefore this ‘new global stratigraphy’, based on the premise that sequence boundaries are primarily controlled by eustatic changes, is not yet a reality. Testing this hypothesis is beyond the resolution of current biostratigraphic and chronostratigraphic techniques.
Earthquakes and Earth structure: a perspective since Hutton and Lyell
Authors: Bolt Bruce A. 
Published: September 2007

Abstract

Lyell’s interest in earthquakes as part of the
Principles of Geology
continues to be justified many fold. A quarter century after Lyell’s death, seismology began to open the window on the contemporary structure and tectonic deformation of the Earth. Detailed non-biased observations of the global distribution of earthquakes played a crucial role in the attack on preplate theories of Earth dynamics. There were three critical seismological assault tools: reliable hypocentre catalogues, uniform magnitude estimates, and fault source mechanisms. Previously used as evidence for plate tectonics, seismicity is now often taken as predicted by it. Nevertheless, earthquake occurrence remains unforecastable in definite temporal terms. Interplate and intraplate spatial patterns show complexity in macro-crustal and micro-crustal structures. In particular, the mechanism and dynamic implications of deep-focus earthquakes and subduction remain a challenge.

Local and global seismographic networks are increasingly enhanced by broadband digital seismometry. This modern instrumentation provides high resolution of strong ground shaking and crustal and deeper interior structure. Second-order structural variations are now being mapped in the upper mantle and more detailed boundary conditions for convection models are being resolved in the lithosphere and in the D″ mantle-core layer. Recently, seismological evidence for scattering anomalies throughout the mantle has become persuasive.
Humanity and the modern environment
Authors: Knill John 
Published: September 2007

Abstract
The geological record is a chronicle of change in which long periods of apparent climatic stability were successively replaced by new environmental conditions. These broad cycles of change were punctuated by shorter-term events, some of which had catastrophic implications. Lyell recognized that this menu of environmental scenarios recorded in the past was well reflected by the range of environmental conditions which occur at the present day.
It is now recognized that human influence on climate and the environment is engendering a new event which has all the hallmarks of a phase which might, if preserved in the geological record, be interpreted as cataclysmic. However, the Earth system has proved remarkably effective in recovering from extremes of climate or devastating reductions in biodiversity.
Humankind has two alternatives. To accept the inevitable, adapting to such changes as can occur, whether of human or natural origin, and facing the possibility of ultimate extinction as a species, thereby leaving the Earth ultimately to recover. Or to attempt to control man-made change so effectively that eventually it will be possible to manage the Earth’s natural processes. Our understanding of the past is therefore central to our ability to survive in the future.
Spatiotemporal Differences in CXCL12 Expression and Cyclic AMP Underlie the Unique Pattern of Optic Glioma Growth in Neurofibromatosis Type 1
Authors: Warrington Nicole M. , Woerner B. Mark , Daginakatte Girish C. , Dasgupta Biplab , Perry Arie , Gutmann David H. , Rubin Joshua B. 
Published: September 2007

Abstract
Astrocytoma (glioma) formation in neurofibromatosis type 1 (NF1) occurs preferentially along the optic pathway during the first decade of life. The molecular basis for this unique pattern of gliomagenesis is unknown. Previous studies in mouse Nf1 optic glioma models suggest that this patterning results from cooperative effects of Nf1 loss in glial cells and the action of factors derived from the surrounding Nf1+/− brain. Because CXCL12 is a stroma-derived growth factor for malignant brain tumors, we tested the hypothesis that CXCL12 functions in concert with Nf1 loss to facilitate NF1-associated glioma growth. Whereas CXCL12 promoted cell death in wild-type astrocytes, it increased Nf1−/− astrocyte survival. This increase in Nf1−/− astrocyte survival in response to CXCL12 was due to sustained suppression of intracellular cyclic AMP (cAMP) levels. Moreover, the ability of CXCL12 to suppress cAMP and increase Nf1−/− astrocyte survival was a consequence of mitogen-activated protein/extracellular signal-regulated kinase kinase–dependent inhibition of CXCL12 receptor (CXCR4) desensitization. In support of an instructive role for CXCL12 in facilitating optic glioma growth, we also show that CXCL12 expression along the optic pathway is higher in infant children and young mice and is associated with low levels of cAMP. CXCL12 expression declines in multiple brain regions with increasing age, correlating with the age-dependent decline in glioma growth in children with NF1. Collectively, these studies provide a mechanism for the unique pattern of NF1-associated glioma growth. [Cancer Res 2007;67(18):8588–95]
Semaphorin SEMA3F Affects Multiple Signaling Pathways in Lung Cancer Cells
Authors: Potiron Vincent A. , Sharma Girish , Nasarre Patrick , Clarhaut Jonathan A. , Augustin Hellmut G. , Gemmill Robert M. , Roche Joëlle , Drabkin Harry A. 
Published: September 2007

Abstract
Loss of SEMA3F occurs frequently in lung cancer and correlates with advanced stage of disease. We previously reported that SEMA3F blocked tumor formation by H157 lung cancer cells in a rat orthotopic model. This was associated with loss of activated αVβ3 integrin, impaired cell adhesion to extracellular matrix components, and down-regulation of phospho-extracellular signal-regulated kinase 1/2 (ERK1/2). These results suggested that SEMA3F might interfere with integrin outside-in signaling. In the present report, we found that SEMA3F decreased adhesion to vitronectin, whereas integrin-linked kinase (ILK) kinase activity was down-regulated in SEMA3F-expressing H157 cells. Exposure to SEMA3F-conditioned medium led to diminution of phospho-ERK1/2 in four of eight lung cancer cell lines, and ILK silencing by small interfering RNA led to similar loss of phospho-ERK1/2 in H157 cells. Moreover, SEMA3F expression (with constitutive and inducible systems) also reduced AKT and signal transducer and activator of transcription 3 (STAT3) phosphorylation independently of ILK-ERK1/2. These signaling changes extended downstream to hypoxia-inducible factor-1α (HIF-1α) protein and vascular endothelial growth factor (VEGF) mRNA levels, which were both reduced in three of four SEMA3F-transfected cell lines. Mechanistically, the effects on HIF-1α were consistent with inhibition of its AKT-driven protein translation initiation, with no effect on HIF-1α mRNA level or protein degradation. Furthermore, when H157 cells were injected s.c. in nude mice, tumors derived from SEMA3F-expressing cells showed lower microvessel density and tumor growth. These results show that SEMA3F negatively affects ILK-ERK1/2 and AKT-STAT3 signaling, along with inhibition of HIF-1α and VEGF. These changes would be anticipated to contribute significantly to the observed antitumor activity of SEMA3F. [Cancer Res 2007;67(18):8708–15]
Degradation of HER2 by Cbl-Based Chimeric Ubiquitin Ligases
Authors: Li Xia , Shen Liangliang , Zhang Jing , Su Jin , Shen Lan , Liu Xinping , Han Hua , Han Wei , Yao Libo 
Published: September 2007

Abstract
Targeting disease-causing proteins for ubiquitination and degradation by chimeric molecules represents a promising alternative therapeutic strategy in cancer. Here, several Cbl-based chimeric ubiquitin ligases were recombined to achieve effective down-regulation of HER2. These chimeric molecules consisted of the Cbl NH2-terminal tyrosine kinase binding domain, linker, and RING domain, with the Src homology 2 domain replaced with that from growth factor receptor binding protein 2 (Grb2), Grb7, p85, or Src. The chimeric proteins not only interacted with HER2 but also enhanced the down-regulation of endogenous overexpressed HER2. After the chimeric proteins were introduced into HER2-overexpressing breast cancer SK-BR-3 cells or ovarian cancer SK-OV-3 cells, they effectively promoted HER2 ubiquitination and degradation in a RING finger domain–dependent manner. Consequently, expression of these chimeric molecules led to an inhibition of colony formation, increased the proportion of cells in the G1 cycle, and suppressed tumorigenicity. Collectively, our findings suggest that the Cbl-based chimeric ubiquitin ligases designed in the present study may represent a novel approach for the targeted therapy of HER2-overexpressing cancers. [Cancer Res 2007;67(18):8716–24]
Characterization of Viral Particles Isolated from Primary Cultures of Human Breast Cancer Cells
Authors: Melana Stella M. , Nepomnaschy Irene , Sakalian Michael , Abbott Andrea , Hasa Jennifer , Holland James F. , Pogo Beatriz G.T. 
Published: September 2007

Abstract
The association of human breast cancer with sequences similar to the mouse mammary tumor virus (MMTV) has been shown, but convincing evidence for the presence of viral particles in breast tumors has been lacking. We have described the complete proviral structure of a retrovirus in human breast cancer. This provirus, designated as human mammary tumor virus (HMTV), was 95% homologous to MMTV and revealed features of a replication-competent virus. We have therefore investigated the production of viral particles in primary cultures of human breast cancer (MSSM). Cells isolated from ascites or pleural effusions of patients with metastatic breast cancer contained viral sequences in their DNA, expressed Env protein, and showed retroviral particles by electron microscopy. Viral particles from culture media exhibited morphologic features of β-retroviruses sedimenting at buoyant densities of 1.12 to 1.18 g/mL in sucrose gradients and showed reverse transcriptase activity. cDNA sequences from virion RNA were synthesized, amplified, and sequenced and all the virion genes were detected and 70% of the virion RNA was sequenced. The sequence homologies were, respectively, 85% to 95% compared with the MMTV and HMTV proviruses we have previously described. These results clearly show that breast cancer cells in primary cultures produced HMTV viral particles that are similar to the mouse virus and which may play a role in human breast cancer pathogenesis. [Cancer Res 2007;67(18):8960–5]
PC-1/PrLZ Contributes to Malignant Progression in Prostate Cancer
Authors: Zhang Hui , Wang Jian , Pang Bo , Liang Rui-xia , Li Suping , Huang Pei-tang , Wang Ruoxiang , Chung Leland W.K. , Zhau Haiyen E. , Huang Cuifen , Zhou Jian-guang 
Published: September 2007

Abstract
PC-1/PrLZ gene overexpression has been identified to be associated with prostate cancer progression. Previous studies have revealed that PC-1 possesses transforming activity and confers malignant phenotypes to mouse NIH3T3 cells. However, the functional relevance of PC-1 expression changes during prostate cancer development and progression remains to be evaluated. In this study, gain-of-function and loss-of-function analyses in LNCaP and C4-2 cells, respectively, were implemented. Experimental data showed that PC-1 expression was in positive correlation with prostate cancer cell growth and anchor-independent colony formation in vitro, as well as tumorigenicity in athymic BALB/c mice. Moreover, PC-1 expression was also found to promote androgen-independent progression and androgen antagonist Casodex resistance in prostate cancer cells. These results indicate that PC-1 contributes to androgen-independent progression and malignant phenotypes in prostate cancer cells. Furthermore, molecular evidence revealed that PC-1 expression stimulated Akt/protein kinase B signaling pathway, which has been implicated to play important roles in promoting androgen refractory progression in prostate cancer. Increased PC-1 levels in C4-2 cells may represent an adaptive response in prostate cancer, mediating androgen-independent growth and malignant progression. Inhibiting PC-1 expression may represent a novel therapeutic strategy to delay prostate cancer progression. [Cancer Res 2007;67(18):8906–13]
The Requirement for DNAM-1, NKG2D, and NKp46 in the Natural Killer Cell-Mediated Killing of Myeloma Cells
Authors: El-Sherbiny Yasser M. , Meade Josephine L. , Holmes Tim D. , McGonagle Dennis , Mackie Sarah L. , Morgan Ann W. , Cook Gordon , Feyler Sylvia , Richards Stephen J. , Davies Faith E. , Morgan Gareth J. , Cook Graham P. 
Published: September 2007

Abstract
Recent evidence suggests a role for natural killer (NK) cells in the control of multiple myeloma. We show that expression of the NK cell receptor DNAM-1 (CD226) is reduced on CD56dim NK cells from myeloma patients with active disease compared with patients in remission and healthy controls. This suggested that this receptor might play a role in NK-myeloma interactions. The DNAM-1 ligands Nectin-2 (CD112) and the poliovirus receptor (PVR; CD155) were expressed by most patient myeloma samples analyzed. NK killing of patient-derived myelomas expressing PVR and/or Nectin-2 was DNAM-1 dependent, revealing a functional role for DNAM-1 in myeloma cell killing. In myeloma cell lines, cell surface expression of PVR was associated with low levels of NKG2D ligands, whereas cells expressing high levels of NKG2D ligands did not express PVR protein or mRNA. Furthermore, NK cell-mediated killing of myeloma cell lines was dependent on either DNAM-1 or NKG2D but not both molecules. In contrast, the natural cytotoxicity receptor NKp46 was required for the killing of all myeloma cell lines analyzed. Thus, DNAM-1 is important in the NK cell-mediated killing of myeloma cells expressing the cognate ligands. The importance of NKp46, NKG2D, and DNAM-1 in myeloma killing mirrors the differential expression of NK cell ligands by myeloma cells, reflecting immune selection during myeloma disease progression. [Cancer Res 2007;67(18):8444–9]
Nonclassic Functions of Human Topoisomerase I: Genome-Wide and Pharmacologic Analyses
Authors: Miao Ze-Hong , Player Audrey , Shankavaram Uma , Wang Yong-Hong , Zimonjic Drazen B. , Lorenzi Philip L. , Liao Zhi-Yong , Liu Hong , Shimura Tsutomu , Zhang Hong-Liang , Meng Ling-Hua , Zhang Yong-Wei , Kawasaki Ernest S. , Popescu Nicholas C. , Aladjem Mirit I. , Goldstein David J. , Weinstein John N. , Pommier Yves 
Published: September 2007

Abstract
The biological functions of nuclear topoisomerase I (Top1) have been difficult to study because knocking out TOP1 is lethal in metazoans. To reveal the functions of human Top1, we have generated stable Top1 small interfering RNA (siRNA) cell lines from colon and breast carcinomas (HCT116-siTop1 and MCF-7-siTop1, respectively). In those clones, Top1 is reduced ∼5-fold and Top2α compensates for Top1 deficiency. A prominent feature of the siTop1 cells is genomic instability, with chromosomal aberrations and histone γ-H2AX foci associated with replication defects. siTop1 cells also show rDNA and nucleolar alterations and increased nuclear volume. Genome-wide transcription profiling revealed 55 genes with consistent changes in siTop1 cells. Among them, asparagine synthetase (ASNS) expression was reduced in siTop1 cells and in cells with transient Top1 down-regulation. Conversely, Top1 complementation increased ASNS, indicating a causal link between Top1 and ASNS expression. Correspondingly, pharmacologic profiling showed l-asparaginase hypersensitivity in the siTop1 cells. Resistance to camptothecin, indenoisoquinoline, aphidicolin, hydroxyurea, and staurosporine and hypersensitivity to etoposide and actinomycin D show that Top1, in addition to being the target of camptothecins, also regulates DNA replication, rDNA stability, and apoptosis. Overall, our studies show the pleiotropic nature of human Top1 activities. In addition to its classic DNA nicking-closing functions, Top1 plays critical nonclassic roles in genomic stability, gene-specific transcription, and response to various anticancer agents. The reported cell lines and approaches described in this article provide new tools to perform detailed functional analyses related to Top1 function. [Cancer Res 2007;67(18):8752–61]
Nuclear Factor of Activated T3 Is a Negative Regulator of Ras-JNK1/2-AP-1–Induced Cell Transformation
Authors: Yao Ke , Cho Yong-Yeon , Bergen H. Robert , Madden Benjamin J. , Choi Bu Young , Ma Wei-Ya , Bode Ann M. , Dong Zigang 
Published: September 2007

Abstract
The c-jun-NH2-kinases (JNK) play a critical role in tumor promoter–induced cell transformation and apoptosis. Here, we showed that the nuclear factor of activated T3 (NFAT3) is phosphorylated by JNK1 or JNK2 at Ser213 and Ser217, which are located in the conserved SP motif. The transactivation domain of NFAT3 is found between amino acids (aa) 113 and 260 and includes the phosphorylation targets of JNK1 and JNK2. NFAT3 transactivation activity was suppressed in JNK1−/− or JNK2−/− mouse embryonic fibroblast (MEF) cells compared with wild-type MEF cells. Moreover, a 3xNFAT-luc reporter gene assay indicated that NFAT3 transcriptional activity was increased in a dose-dependent manner by JNK1 or JNK2. Double mutations at Ser213 and Ser217 suppressed NFAT3 transactivation activity; and SP600125, a JNK inhibitor, suppressed NFAT3-induced 3xNFAT-luciferase activity. Knockdown of JNK1 or JNK2 suppressed foci formation in NIH3T3 cells. Importantly, ectopic expression of NFAT3 inhibited AP-1 activity and suppressed foci formation. Furthermore, knockdown of NFAT3 enhanced Ras-JNK1 or JNK2-induced foci formation in NIH3T3 cells. Taken together, these results provided direct evidence for the anti-oncogenic potential of the NFAT3 transcription factor. [Cancer Res 2007;67(18):8725–35]
17β-Estradiol Up-regulates the Insulin-like Growth Factor Receptor through a Nongenotropic Pathway in Prostate Cancer Cells
Authors: Pandini Giuseppe , Genua Marco , Frasca Francesco , Squatrito Sebastiano , Vigneri Riccardo , Belfiore Antonino 
Published: September 2007

Abstract
Prostate carcinomas frequently express estrogen receptors (ER), irrespective of androgen receptor (AR) expression; however, the role of ERs and estrogens in prostate cancer is controversial. We found that 17β-estradiol (E2) is able to markedly up-regulate insulin-like growth factor (IGF)-I receptor (IGF-IR) mRNA and protein expression in both AR-positive (LNCaP cells) and AR-negative (PC-3 cells) prostate cancer cells. This effect occurs not only via ERα but also via ERβ stimulation and is specific for IGF-IR because it does not involve the cognate insulin receptor. IGF-IR up-regulation is associated with increased IGF-IR phosphorylation and with increased mitogenic and motogenic activities in response to IGF-I. IGF-IR up-regulation by E2 does not require ER binding to DNA and is poorly sensitive to antiestrogen blockade, whereas it is associated with the activation of cytosolic kinase cascades involving Src, extracellular signal–regulated kinase (ERK)-1/2, and, to a lesser extent, phosphatidylinositol 3-kinase and is sensitive to the inhibition of these kinases. In conclusion, our data indicate that estrogens may contribute to IGF system deregulation in prostate cancer through the activation of a nongenotropic pathway. Estrogens may have a role, therefore, in tumor progression to androgen independence. Inhibition of the IGF-IR or the Src-ERK pathway should be considered, therefore, as an adjuvant therapy in prostate cancer. [Cancer Res 2007;67(18):8932–41]