bluuebunny/crossref_metadata_2025_split huggingface dataset:
Historical Figuration: Poetics, Historiography, and New Genre Studies1
Authors: Howard W. Scott 
Published: July 2006

AbstractThis essay has four interconnected goals: 1) to reflect upon some of the major theoretical and methodological developments (since about 1950) in the fields of early modern literary studies and history vis‐à‐vis the question of historicism; 2) to address, within the context of seventeenth‐century England, inter‐relationships between poetics and historiography; 3) to examine that “interdisciplinarity” specifically in terms of the seventeenth‐century English poetic elegy; and 4) to trace (from Plato to Puttenham) and to argue for a specific theoretical aspect of that inter‐relationship, which I will callhistorical figuration. My argument will hinge upon these connecting points, especially the latter two. On the one hand, I will argue that an early modern paradigm shift from theocentric to increasingly secular narrative frameworks for personal and national histories contributes to a transformation in poetic genre. English poets began to formulate a new intra‐textual crisis of linguistic signification within the elegy's construction of loss and spiritual consolation as the experience of death and mourning became less theocentric and communal and more secular and individualized during the seventeenth century. This new intra‐textuality to elegiac resistance emerges gradually but consistently from approximately the 1620s onward, facilitating the genre's new articulations of consolation situated within and against historical contexts rather than projected toward a transcendental horizon. On the other hand, I will also argue that this distinctive inter‐relationship between poetics and historiography may be theorized as historical figuration, which may be linked directly to key contributions to the history of poetic theory from Plato to Puttenham. My two‐fold thesis thus attempts to engender and engage what some may see as a trans‐discursive poetics of culture. However, I would hesitate to place my argument within the new‐historicist camp, but would hope instead that this essay may contribute to the emerging, interdisciplinary sub‐field ofnew genre studies, which seeks to examine literary genres as manifestations of aesthetic forms and social discourses.
High Predation Pressure by an Introduced Flatworm on Land Snails on the Oceanic Ogasawara Islands1
Authors: Sugiura Shinji , Okochi Isamu , Tamada Hisashi 
Published: July 2006

ABSTRACTThe introduction of a predatory flatworm, Platydemus manokwari, has been considered a cause of the decline of endemic land snails on the tropical oceanic islands. To clarify the effect of P. manokwari on land snail survival in the field, we examined survival rates of snails experimentally placed in areas where snails are absent (i.e., P. manokwari is present) on Chichijima, Ogasawara (Bonin) Islands. We found that over 50 and 90 percent of the snails were dead after 3 and 11 d, respectively, and that the main cause of mortality was predation by P. manokwari.
TRAIL Induces Apoptosis in Human Colorectal Adenoma Cell Lines and Human Colorectal Adenomas
Authors: Jalving Mathilde , de Jong Steven , Koornstra Jan J. , Boersma-van Ek Wytske , Zwart Nynke , Wesseling Jelle , de Vries Elisabeth G.E. , Kleibeuker Jan H. 
Published: July 2006

AbstractPurpose: Recombinant human (rh) tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) is a potential new anticancer drug which can induce apoptosis in colorectal cancer cell lines. The aim of this study was to investigate whether it is possible to induce apoptosis in human adenoma cell lines and human adenomas using rhTRAIL.Experimental Design: Two human adenoma cell lines were exposed to 0.1 μg/mL of rhTRAIL for 5 hours. Apoptosis and caspase activation in cell lines were evaluated using immunocytochemistry, fluorimetric caspase assays, and Western blotting. Short-term explant cultures were established from freshly removed human adenomas (n = 38) and biopsies of normal colon epithelium (n = 15), and these were incubated for 5 hours in the presence or absence of 1 μg/mL of rhTRAIL. Apoptosis was determined in paraffin-embedded tissue using morphologic criteria and cleaved caspase-3 staining.Results: In the adenoma cell lines, rhTRAIL induced up to 55% apoptosis. This coincided with caspase-8 and caspase-3 activation and could be inhibited by a pan-caspase inhibitor. rhTRAIL induced caspase-dependent apoptosis in adenomas with high-grade dysplasia (n = 21) compared with the paired untreated counterparts (apoptotic index, 34 ± 5% versus 17 ± 2%, mean ± SE; P = 0.002), but not in adenomas with low-grade dysplasia (n = 17) or in normal colon epithelium (n = 15).Conclusions: Colorectal adenoma cell lines and adenomas with high-grade dysplasia are sensitive to rhTRAIL-induced apoptosis, whereas normal colon epithelium is not. This suggests the potential application of rhTRAIL in the treatment of adenomas with high-grade dysplasia.
ABCA3 as a Possible Cause of Drug Resistance in Childhood Acute Myeloid Leukemia
Authors: Steinbach Daniel , Gillet Jean-Pierre , Sauerbrey Axel , Gruhn Bernd , Dawczynski Kristin , Bertholet Vincent , de Longueville Françoise , Zintl Felix , Remacle Jose , Efferth Thomas 
Published: July 2006

Abstract
Background: A major issue in the treatment of acute myeloid leukemia (AML) is resistance to chemotherapeutic drugs. Multidrug resistance can be caused by ATP-binding cassette (ABC) transporters that function as drug efflux pumps. The majority of these proteins have not yet been examined in malignant diseases.
Experimental Design: A newly developed microarray for the simultaneous quantification of 38 ABC transporter genes and Taqman real-time PCR was used to analyze the expression of ABC transporters in pediatric AML and healthy bone marrow. Small interfering RNA was used to verify the role of ABCA3 in drug resistance.
Results: Using the microarray, we identified four new ABC transporters, which were overexpressed in many AML samples compared with healthy bone marrow: ABCA2, ABCA3, ABCB2, and ABCC10. The overexpression of these four genes was verified by real-time PCR in 42 samples from children with AML and 18 samples of healthy bone marrow. The median expression of ABCA3 was three times higher in 21 patients who had failed to achieve remission after the first course of chemotherapy than in a well-matched group of 21 patients who had achieved remission at this stage (P = 0.023). Incubation of cell lines with a number of different cytostatic drugs induced an up-regulation of ABCA3. Down-regulation of ABCA3 by small interfering RNA sensitized cells to doxorubicin.
Conclusion: Our results show that ABCA2, ABCA3, ABCB2, and ABCC10 are overexpressed in childhood AML compared with healthy bone marrow. ABCA3 is the most likely transporter to cause drug resistance.
Overcoming Drug-Resistant Cancer by a Newly Developed Copper Chelate through Host-Protective Cytokine-Mediated Apoptosis
Authors: Mookerjee Ananda , Mookerjee Basu Jayati , Dutta Pranabananda , Majumder Surajit , Bhattacharyya Sankar , Biswas Jaydip , Pal Smarajit , Mukherjee Pratima , Raha Sanghamitra , Baral Rathindra N. , Das Tania , Efferth Thomas , Sa Gourisankar , Roy Shyamal , Choudhuri Soumitra K. 
Published: July 2006

AbstractPurpose: Previously, we have synthesized and characterized a novel Cu(II) complex, copper N-(2-hydroxy acetophenone) glycinate (CuNG). Herein, we have determined the efficacy of CuNG in overcoming multidrug-resistant cancer using drug-resistant murine and human cancer cell lines.Experimental Design: Action of CuNG following single i.m. administration (5 mg/kg body weight) was tested in vivo on doxorubicin-resistant Ehrlich ascites carcinoma (EAC/Dox)–bearing mice and doxorubicin-resistant sarcoma 180–bearing mice. Tumor size, ascitic load, and survival rates were monitored at regular intervals. Apoptosis of cancer cells was determined by cell cycle analysis, confocal microscopy, Annexin V binding, and terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling assay ex vivo. IFN-γ and tumor necrosis factor-α were assayed in the culture supernatants of in vivo and in vitro CuNG-treated splenic mononuclear cells from EAC/Dox-bearing mice and their apoptogenic effect was determined. Source of IFN-γ and changes in number of T regulatory marker-bearing cells in the tumor site following CuNG treatment were investigated by flow cytometry. Supernatants of in vitro CuNG-treated cultures of peripheral blood mononuclear cells from different drug-insensitive cancer patients were tested for presence of the apoptogenic cytokine IFN-γ and its involvement in induction of apoptosis of doxorubicin-resistant CEM/ADR5000 cells.Results: CuNG treatment could resolve drug-resistant cancers through induction of apoptogenic cytokines, such as IFN-γ and/or tumor necrosis factor-α, from splenic mononuclear cells or patient peripheral blood mononuclear cells and reduce the number of T regulatory marker-bearing cells while increase infiltration of IFN-γ-producing T cells in the ascetic tumor site.Conclusion: Our results show the potential usefulness of CuNG in immunotherapy of drug-resistant cancers irrespective of multidrug resistance phenotype.
Strategies to Enhance Epidermal Growth Factor Inhibition: Targeting the Mevalonate Pathway
Authors: Dimitroulakos Jim , Lorimer Ian A. , Goss Glenwood 
Published: July 2006

Abstract
Mevalonate metabolites play an essential role in transducing epidermal growth factor (EGF) receptor (EGFR)–mediated signaling, as several of these metabolites are required for the function of this receptor and the components of its signaling cascades. Thus, the depletion of mevalonate metabolites may have a significant effect on EGFR function. Lovastatin is a specific and potent inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Targeting 3-hydroxy-3-methylglutaryl CoA reductase using lovastatin induces a potent tumor-specific apoptotic response in a variety of tumor types at therapeutically achievable levels of this drug. The effects of lovastatin on EGFR function and the potential combination effects with EGFR tyrosine kinase inhibitors, such as gefitinib, were evaluated. Lovastatin treatment inhibited EGF-induced EGFR autophosphorylation and its downstream signaling cascades by 24 hours. Combining lovastatin and gefitinib showed enhanced inhibition and cooperative cytotoxicity in a variety of cell lines that included all eight squamous cell carcinomas, four non–small cell lung carcinoma, and four colon carcinoma cell lines tested. Isobologram analyses confirmed that this combination was synergistic, inducing a potent apoptotic response. A phase I study has shown the safety and potential clinical benefit of high-dose lovastatin in patients with recurrent squamous cell carcinoma. The use of lovastatin, which is metabolized by CYP3A4, is contraindicated with drugs, such as gefitinib and erlotinib, which are also metabolized by CYP3A4 due to greatly enhanced toxicity. Rosuvastatin, a relatively novel potent mevalonate pathway inhibitor that is not metabolized significantly by CYP3A4, is a more appropriate statin to combine with either erlotinib or gefitinib. The combination of erlotinib and rosuvastatin has been proposed for a phase I/II study in advanced non–small cell lung carcinoma.
“Oncogenic Shock”: Explaining Oncogene Addiction through Differential Signal Attenuation
Authors: Sharma Sreenath V. , Fischbach Michael A. , Haber Daniel A. , Settleman Jeffrey 
Published: July 2006

Abstract
“Oncogene addiction” describes the curious acquired dependence of tumor cells on an activated oncogene for their survival and/or proliferation, a phenomenon that has important implications for the success of targeted cancer therapies. However, the mechanisms explaining oncogene addiction remain elusive. We propose that “addiction” may be an illusion generated as a consequence of differential attenuation rates of prosurvival and proapoptotic signals emanating from an oncoprotein acutely following its inactivation. According to this model, which we call “oncogenic shock,” prosurvival signals dissipate quickly on oncoprotein inactivation whereas proapoptotic signals linger sufficiently long to commit the cell to an apoptotic death. This mechanism may contribute to the rapid and dramatic clinical responses observed in some cancer patients treated with selective tyrosine kinase inhibitors and could yield additional drug targets that determine the balance of signaling outputs from activated oncoproteins.
Inhibition of Growth and Metastasis of Mouse Mammary Carcinoma by Selective Inhibitor of Transforming Growth Factor-β Type I Receptor KinaseIn vivo
Authors: Ge Rongrong , Rajeev Vaishali , Ray Partha , Lattime Edmund , Rittling Susan , Medicherla Satya , Protter Andy , Murphy Alison , Chakravarty Jit , Dugar Sundeep , Schreiner George , Barnard Nicola , Reiss Michael 
Published: July 2006

AbstractPurpose: Transforming growth factor-β (TGF-β) suppresses tumor development by inhibiting cellular proliferation, inducing differentiation and apoptosis, and maintaining genomic integrity. However, once tumor cells escape from the tumor-suppressive effects of TGF-β, they often constitutively overexpress and activate TGF-β, which may promote tumor progression by enhancing invasion, metastasis, and angiogenesis and by suppressing antitumor immunity. The purpose of this study was to test this hypothesis using TGF-β pathway antagonists.Experimental Design: We examined the effects of selective TGF-β type I receptor kinase inhibitors, SD-093 and SD-208, on two murine mammary carcinoma cell lines (R3T and 4T1) in vitro and in vivo.Results: Both agents blocked TGF-β-induced phosphorylation of the receptor-associated Smads, Smad2 and Smad3, in a dose-dependent manner, with IC50 between 20 and 80 nmol/L. TGF-β failed to inhibit growth of these cell lines but stimulated epithelial-to-mesenchymal transdifferentiation, migration, and invasiveness into Matrigel in vitro. These effects were inhibited by SD-093, indicating that these processes are partly driven by TGF-β. Treatment of syngeneic R3T or 4T1 tumor-bearing mice with orally given SD-208 inhibited primary tumor growth as well as the number and size of metastases. In contrast, SD-208 failed to inhibit R3T tumor growth or metastasis in athymic nude mice. Moreover, in vitro anti-4T1 cell cytotoxic T-cell responses of splenocytes from drug-treated animals were enhanced compared with cells from control animals. In addition, SD-208 treatment resulted in a decrease in tumor angiogenesis.Conclusion: TGF-β type I receptor kinase inhibitors hold promise as novel therapeutic agents for metastatic breast cancer.
Effect of Epidermal Growth Factor Receptor Tyrosine Kinase Domain Mutations on the Outcome of Patients with Non–Small Cell Lung Cancer Treated with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors
Authors: Jänne Pasi A. , Johnson Bruce E. 
Published: July 2006

Abstract
Somatic mutations in the epidermal growth factor receptor (EGFR) have been identified in patients with advanced non–small cell lung cancer who achieve dramatic clinical and radiographic response to the EGFR tyrosine kinase inhibitors (TKI) gefitinib and erlotinib. These mutations in EGFR are found more frequently in patients with adenocarcinomas, nonsmokers, patients of Asian ethnicity, and in females: the same populations that are the most likely to have a clinical response when treated with EGFR TKIs. Retrospective studies comparing the outcomes of patients with and without EGFR mutations treated with EGFR TKIs show a significant clinical benefit of EGFR TKIs in patients with EGFR mutations. These findings suggest that for patients with advanced non–small cell lung cancer bearing EGFR mutations, treatment with an EGFR TKI should be incorporated as at least part of their initial therapy. These approaches are being studied in ongoing clinical trials and will spur the development of additional technology for EGFR mutation detection.
Evaluation of a self-management programme for congestive heart failure patients: design of a randomised controlled trial
Authors: Smeulders Esther STF , van Haastregt Jolanda CM , van Hoef Elisabeth FM , van Eijk Jacques ThM , Kempen Gertrudis IJM 
Published: July 2006

AbstractBackgroundCongestive heart failure (CHF) has a substantial impact on care utilisation and quality of life. It is crucial for patients to cope with CHF adequately, if they are to live an acceptable life. Self-management may play an important role in this regard. Previous studies have shown the effectiveness of the 'Chronic Disease Self-Management Program' (CDSMP), a group-based cognitive behavioural programme for patients with various chronic conditions. However, the programme's effectiveness has not yet been studied specifically among CHF patients. This paper presents the design of a randomised controlled trial to evaluate the effects of the CDSMP on psychosocial attributes, health behaviour, quality of life, and health care utilisation of CHF patients.Methods/DesignThe programme is being evaluated in a two-group randomised controlled trial. Patients were eligible if they had been diagnosed with CHF and experienced slight to marked limitation of physical activity. They were selected from the Heart Failure and/or Cardiology Outpatient Clinics of six hospitals. Eligible patients underwent a baseline assessment and were subsequently allocated to the intervention or control group. Patients allocated to the intervention group were invited to attend the self-management programme consisting of six weekly sessions, led by a CHF nurse specialist and a CHF patient. Those allocated to the control group received care as usual. Follow-up measurements are being carried out immediately after the intervention period, and six and twelve months after the start of the intervention.An effect evaluation and a process evaluation are being conducted. The primary outcomes of the effect evaluation are self-efficacy expectancies, perceived control, and cognitive symptom management. The secondary outcome measures are smoking and drinking behaviour, Body Mass Index (BMI), physical activity level, self-care behaviour, health-related quality of life, perceived autonomy, symptoms of anxiety and depression, and health care utilisation. The programme's feasibility is assessed by measuring compliance with the protocol, patients' attendance and adherence, and the opinions about the programme.DiscussionA total number of 318 patients were included in the trial. At present, follow-up data are being collected. The results of the trial become clear after completion of the data collection in January 2007.Trial RegistrationTrialregister (http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=467) ISRCTN88363287.
Having the nerve to home: trigeminal magnetoreceptor versusolfactory mediation of homing in pigeons
Authors: Gagliardo A. , Ioalè P. , Savini M. , Wild J. M. 
Published: July 2006

SUMMARY
The ability of pigeons to find their way home from unfamiliar sites located up to hundreds of kilometers away is well known, but the mechanisms underlying this ability remain controversial. One proposed mechanism is based on the suggestion that pigeons are equipped with magnetoreceptors that can enable the detection of either the earth's magnetic field and/or magnetic field anomalies in the local terrain over which the pigeons fly. Recent reports have suggested that these magnetoreceptors are located in the upper beak where they are innervated by the ophthalmic branch of the trigeminal nerve. Moreover, this nerve has been shown to mediate pigeons' ability to discriminate the presence versus the absence of a magnetic field anomaly in a conditioning situation. In the present study, however, we show that an intact ophthalmic branch of the trigeminal nerve is neither necessary nor sufficient for good homing performance from unfamiliar locations, but that an intact olfactory nerve is necessary.
Diversification of gut morphology in caterpillars is associated with defensive behavior
Authors: Grant Jacqualine Bonnie 
Published: July 2006

SUMMARYThe relationship between insect gut structure and foraging strategy has been studied for several hundred years; however, we know little about how, or even if, other common insect behaviors are linked to gut morphology. For example, many insects defend themselves by regurgitation, a behavior which is expected to be closely connected to gut structure. Caterpillars belong to an insect taxon, the Lepidoptera, with a particularly well-studied digestive tract and a known predilection for defensive regurgitation. I have explored whether defensive regurgitation is associated with specific gut structure by examining the relationship between defensive behavior and gut morphology in the larvae of 36 butterfly and moth species. My analysis shows that predilection to defensively regurgitate is closely associated with fore- and midgut morphology. Species that primarily regurgitate in defense have enlarged foreguts and shortened midguts, whereas the opposite relationship is seen among those that do not readily regurgitate. These results reveal that: (i)defensive regurgitation is not the primary defense of all caterpillars, and(ii) gut morphology can be associated with other factors than the chemical and mechanical properties of ingested foods. These findings challenge long held beliefs concerning the ubiquity of defensive regurgitation in caterpillars and the causes of diversification of gut morphology, and further reinforce the gut's standing as a complex and sophisticated organ.
Neuromodulation of the locust frontal ganglion during the moult: a novel role for insect ecdysis peptides
Authors: Zilberstein Y. , Ewer J. , Ayali A. 
Published: July 2006

SUMMARYIn insects, continuous growth requires the periodic replacement of the exoskeleton during the moult. A moulting insect displays a stereotypical set of behaviours that culminate in the shedding of the old cuticle at ecdysis. Moulting is an intricate process requiring tightly regulated physiological changes and behaviours to allow integration of environmental cues and to ensure the proper timing and sequence of its components. This is under complex hormonal regulation, and is an important point of interaction between endocrine and neural control.Here, we focus on the locust frontal ganglion (FG), an important player in moulting behaviour, as a previously unexplored target for ecdysis peptides. We show that application of 10-7 mol l-1 ecdysis-triggering hormone (ETH) or 10-7 mol l-1 and 10-6 mol l-1 Pre-ecdysis-triggering hormone (PETH) to an isolated FG preparation caused an increase in bursting frequency in the FG, whereas application of 10-6 mol l-1 eclosion hormone (EH) caused an instantaneous, though temporary, total inhibition of all FG rhythmic activity. Crustacean cardioactive peptide (CCAP), an important peptide believed to turn on ecdysis behaviour, caused a dose-dependent increase of FG burst frequency. Our results imply a novel role for this peptide in generating air-swallowing behaviour during the early stages of ecdysis. Furthermore, we show that the modulatory effects of CCAP on the FG motor circuits are dependent on behavioural state and physiological context. Thus, we report that pre-treatment with ETH caused CCAP-induced effects similar to those induced by CCAP alone during pre-ecdysis. Thus, the action of CCAP seems to depend on pre-exposure to ETH, which is thought to be released before CCAP in vivo.
Delayed Thermal Excimer Fluorescence of Acriflavine in a Stretched PVA Sheet
Authors: Sato Masao , Azumi Tohru , Azumi Hiroshi 
Published: July 2006

Abstract
A long-lived emission of acriflavine absorbed into a polyvinylalcohol sheet has been investigated. At higher concentrations, a new, previously-unobserved emission band has been observed. It has been shown that the newly-observed band can be interpreted by a mechanism in which the thermal excitation of the triplet state to the excimer state takes place, followed by an emission. The term “delayed thermal excimer fluorescence” has been given to specify the emission of this type.