bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induced volatiles in soybean and pigeon pea plants artificially infested with the neotropical brown stink bug, Euschistus heros, and their effect on the egg parasitoid, Telenomus podisi
Authors: Carolina Blassioli Moraes Maria , Laumann Raul , Sujii Edson R. , Pires Carmen , Borges Miguel 
Published: April 2005

AbstractHerbivory is known to increase the emission of volatiles, which attract natural enemies to herbivore‐damaged plants in laboratory and agricultural systems. We report on signalling through volatiles induced by Euschistus heros (F.) (Heteroptera: Pentatomidae) in two legumes that influence the attraction and retention of the egg parasitoid Telenomus podisi (Ashmead) (Hymenoptera: Scelionidae). Air‐borne extracts obtained from two host plants of E. heros, soybean, Glycine max, and pigeon pea, Cajanus cajan (Leguminosae), produce a different blend of emitted volatiles when attacked by adult males or females and nymphs of the pest species, compared with the undamaged plants. The same results were obtained when the plants were treated with extracted saliva of E. heros which had been mechanically introduced into the plants. This indicates that some substance in the saliva contributed to the release of the volatiles. Bioassays in a Y‐tube olfactometer with female T. podisi and treated plants confirmed the significant preference of the egg parasitoid for plants attacked by either males, females, or fourth instar nymphs of the pest species. On the other hand, volatile extracts obtained from soybean subjected to the velvetbean caterpillar, Anticarsia gemmatalis, a non‐host species for T. podisi, showed a different blend of volatiles compared to those obtained from plants subjected to E. heros. Additionally, the volatiles obtained from this plant–host complex were not attractive to T. podisi. These results indicate that E. heros causes an increase in the emission of specific plant volatiles, and that the induction is possibly caused by an elicitor present in the pest saliva. The possibility that these plant volatiles play an important role in the attraction and retention of the egg parasitoid T. podisi is discussed.
THE CAPITAL STRUCTURE PUZZLE: ANOTHER LOOK AT THE EVIDENCE
Authors: Barclay Michael J. , Smith Clifford W. 
Published: April 2005

Since the formulation of the M & M irrelevance propositions 40 years ago, financial economists have been debating whether there is such a thing as optimal capital structure—a proportion of debt to equity that maximizes current firm value. Some finance scholars have followed M & M by arguing that both capital structure and dividend policy are largely “irrelevant” in the sense that they have no significant, predictable effects on corporate market values. Another school of thought holds that corporate financing choices reflect an attempt by corporate managers to balance the tax shields and disciplinary benefits of greater debt against the increased probability and costs of financial distress. Yet another theory says that companies do not have capital structure targets, but instead follow a financial pecking order in which retained earnings are preferred to outside financing, and debt is preferred to equity when outside funding is required.In reviewing the evidence that has accumulated since M & M, the authors argue that taxes, bankruptcy (and other “contracting”) costs, and information costs (the main factor in the pecking order theory) all appear to play an important role in corporate financing decisions. While much if not most of the evidence is consistent with the argument that companies set target leverage ratios, there is also considerable support for the pecking order theory's contention that firms are willing to deviate widely from their targets for long periods of time.According to the authors, the key to reconciling the different theories—and thus to solving the capital structure puzzle—lies in achieving a better understanding of the relation between corporate financing stocks (leverage ratios) and flows (specific choices between debt and equity). Even if companies have target leverage ratios, there will be an optimal deviation from those targets—one that will depend on the transactions and information costs associated with adjusting back to the target relative to the costs of deviating from the target. As the authors argue in closing, a complete theory of capital structure must take account of these adjustment costs and how they affect expected deviations from the target.
INTERNET INVESTMENT BANKING: THE IMPACT OF INFORMATION TECHNOLOGY ON RELATIONSHIP BANKING
Authors: Wilhelm William J. 
Published: April 2005

The production “technology” of investment banking, particularly in the pricing and distribution of securities offerings, has long depended on the ability of bankers to build and maintain networks of relationships with institutional investors and client firms. Among other benefits, these relationships enabled banks to economize on communications with investors at a time when communicating with the investment community was quite costly. But recent advances in information technology are forcing banks to reevaluate this relationship‐based technology. For example, Goldman Sachs recently purchased a stake in Wit Capital's efforts to build a retail distribution channel via the Internet. And William Hambrecht, founder of Hambrect & Quist, has gone so far as to propose that IPOs be put up for auction over the Internet.This article offers both historical and economic perspective on these technological innovations in investment banking. In so doing, it provides a framework for thinking about how this segment of the industry is likely to evolve in the near future. It also discusses how advances in information technology coupled with the increasing codification of investment banking practices could reduce the central role of human capital and relationships elsewhere within investment banks, and how this might influence both the organization of individual banks and the industry in general.
A SURVEY OF U.S. CORPORATE FINANCING INNOVATIONS: 1970–1997
Authors: Carow Kenneth A. , Erwin Gayle R. , McConnell John J. 
Published: April 2005

In the past 30 years, major changes have occurred not only in the kinds of securities issued, but also in the way securities are issued and in the national markets where they are issued. Traditional registered offerings have been partly displaced by shelf registered offerings and Rule 144A private offerings. And once exclusively domestic U.S offerings are increasingly being supplemented by foreign market offerings by U.S. companies, and by simultaneously domestic and foreign offerings. In 1997, for example, 11% of all proceeds raised by U.S. corporations were issued in one or more foreign markets. Of the $105 billion raised in these offerings, $31 billion was denominated in currencies other than the U.S. dollar.While traditional securities still dominate the market, the authors' research indicates that the pace of innovation in the design of securities also increased markedly during the 1980s and has continued strong throughout the 1990s. In 1997, for example, innovative securities accounted for almost 30% of total domestic offerings. Three of the most common objectives of such securities have been (1) to manage the interest rate (and other financial price) risk faced by investors and issuers; (2) to reduce information costs faced by investors when buying securities from issuers with better information about their own prospects (a condition known as “information asymmetry”); and (3) to increase the tradability of financial assets.
ESTIMATING THE EQUITY RISK PREMIUM AND EQUITY COSTS: NEW WAYS OF LOOKING AT OLD DATA
Authors: Booth Laurence 
Published: April 2005

This article examines three alternative ways of estimating the expected return on the equity market in using the CAPM or some other risk premium model. The three techniques are (1) direct estimation of the average nominal equity return for use as a forecast nominal equity return; (2) estimation of the average real equity return, which can then be added to a forecast inflation rate; and (3) estimation of an average equity risk premium, which is then added to a current risk‐free rate. Ibbotson and Sinquefeld's data on annual holding period returns are used to test the validity of their assumption that the equity risk premium follows a random walk and that the third of these approaches is thus the best method.The paper reaches three major conclusions. First, each of these three techniques involves a “bias” of some kind. The use of average equity returns as a forecast is subject to “risk‐free rate” and “inflation rate” biases, while the use of an average equity risk premium is subject to a “term premium” bias. As a result, only the data can tell us which approach is best. Second, from analyzing equity and bond return data and the trend in interest rates, the author concludes that the term premium bias when using average historic equity risk premium is by far the largest of the three sources of bias. Indeed, the popular practice of adding an historic average equity risk premium to the 30‐year Treasury bond rate significantly overstates equity costs. Third, after examining equity rates of return back to 1871, the author concludes that the real equity return seems to follow a process that is close to a random walk and is thus the “best” of the three techniques to use as a “naive” forecast.
DOLLARIZATION FOR ARGENTINA
Authors: Hanke Steve H. 
Published: April 2005

In January 1999, President Carlos Menem suggested replacing the Argentine peso with the U.S. dollar. President Menem's announcement has sparked a debate throughout Latin America and Eastern Europe about what has been termed “dollarization.” That debate prompted U.S. Treasury Secretary Robert Rubin to deliver a major policy speech on alternative exchange‐rate regimes on April 21, 1999 and the U.S. Senate Banking Committee to hold dollarization hearings the following day featuring Fed Chairman Alan Greenspan and Deputy Secretary of the Treasury Lawrence Summers.This article presents a case for officially dollarizing Argentina. Dollarization is not new. Unofficial dollarization is widespread in emerging market countries; in fact, as much as 70% of the stock of U.S. dollars now circulates abroad. Twenty‐eight countries and dependent territories are officially dollarized. Although official dollarization would result in Argentina losing seigniorage of about 0.22 percent of GDP, the author estimates that this cost would be more than offset by a reduction in interest rates that would increase Argentina's trend rate of GDP growth by about two percent.After debunking the most common criticisms of dollarization, the article closes by offering recommendations about the specific form of dollarization and presenting a detailed dollarization statute for Argentina. The author proposes a competitive currency regime for Argentina, one in which all foreign money would be legal tender.
Acanthamoeba castellanii
Induces Host Cell Death via a Phosphatidylinositol 3-Kinase-Dependent Mechanism
Authors: Sissons James , Kim Kwang Sik , Stins Monique , Jayasekera Samantha , Alsam Selwa , Khan Naveed Ahmed 
Published: April 2005

ABSTRACT

Granulomatous amoebic encephalitis due to
Acanthamoeba castellanii
is a serious human infection with fatal consequences, but it is not clear how the circulating amoebae interact with the blood-brain barrier and transmigrate into the central nervous system. We studied the effects of an
Acanthamoeba
encephalitis isolate belonging to the T1 genotype on human brain microvascular endothelial cells, which constitute the blood-brain barrier. Using an apoptosis-specific enzyme-linked immunosorbent assay, we showed that
Acanthamoeba
induces programmed cell death in brain microvascular endothelial cells. Next, we observed that
Acanthamoeba
specifically activates phosphatidylinositol 3-kinase.
Acanthamoeba
-mediated brain endothelial cell death was abolished using LY294002, a phosphatidylinositol 3-kinase inhibitor. These results were further confirmed using brain microvascular endothelial cells expressing dominant negative forms of phosphatidylinositol 3-kinase. This is the first demonstration that
Acanthamoeba
-mediated brain microvascular endothelial cell death is dependent on phosphatidylinositol 3-kinase.
Induction of Nitric Oxide Synthase inAnopheles stephensibyPlasmodium falciparum: Mechanism of Signaling and the Role of Parasite Glycosylphosphatidylinositols
Authors: Lim Junghwa , Gowda D. Channe , Krishnegowda Gowdahalli , Luckhart Shirley 
Published: April 2005

ABSTRACTMalaria parasite (Plasmodiumspp.) infection in the mosquitoAnopheles stephensiinduces significant expression ofA. stephensinitric oxide synthase (AsNOS) in the midgut epithelium as early as 6 h postinfection and intermittently thereafter. This induction results in the synthesis of inflammatory levels of nitric oxide (NO) in the blood-filled midgut that adversely impact parasite development. In mammals,P. falciparumglycosylphosphatidylinositols (PfGPIs) can induceNOSexpression in immune and endothelial cells and are sufficient to reproduce the major effects of parasite infection. These effects are mediated in part by mimicry of insulin signaling by PfGPIs. In this study, we demonstrate that PfGPIs can induceAsNOSexpression inA. stephensicells in vitro and in the midgut epithelium in vivo. Signaling byP. falciparummerozoites and PfGPIs is mediated throughA. stephensiAkt/protein kinase B and a pathway involving DSOR1, a mitogen-activated protein kinase kinase, and an extracellular signal-regulated kinase. However, despite the involvement of kinases that are also associated with insulin signaling inA. stephensicells, signaling byP. falciparumand by PfGPIs is distinctively different from signaling by insulin. Therefore, although mimicry of insulin by PfGPIs appears to be restricted to mammalian hosts ofP. falciparum, the conservation of PfGPIs as a prominent parasite-derived signal of innate immunity can now be extended to includeAnophelesmosquitoes, indicating that parasite signaling of innate immunity is conserved in mosquito and mammalian cells.
Immunological and Protective Effects of Diepitopic Subunit Dental Caries Vaccines
Authors: Smith Daniel J. , King William F. , Rivero Joy , Taubman Martin A. 
Published: April 2005

ABSTRACT

As a prelude to development of broader-spectrum vaccines for dental caries, we explored the immune potential of constructs combining epitopes from mutans streptococcal glucosyltransferases (GTF) and glucan binding protein B (GbpB). Two diepitopic peptide constructs were synthesized in a multiple antigenic peptide (MAP) format. Both constructs contained SYI, a 20-mer GbpB peptide that included a sequence having major histocompatibility complex class II binding characteristics. One diepitopic construct (SYI-CAT) also contained a 22-mer sequence from the catalytic domain of GTF. Another diepitopic construct (SYI-GLU) contained a 22-mer sequence from the glucan binding domain of GTF. To assess the ability of each construct to induce antibody reactive with GbpB and GTF native proteins, rats were injected subcutaneously with SYI-CAT, SYI-GLU, or the constituent monoepitopic constructs. Only the SYI-CAT construct induced significant levels of serum immunoglobulin G (IgG) and IgA antibody to both pathogenesis-associated proteins. Also, immunization with SYI-CAT significantly (
P
< 0.001) enhanced the antibody response to the CAT peptide. Experiments then compared experimental dental caries after immunization with SYI-CAT, SYI, or CAT MAP constructs, followed by infection with
Streptococcus mutans
strain SJr. Dental caries were lower in each peptide-immunized group than in the sham-injected group. The level of protection after SYI-CAT immunization was similar to that after immunization with constituent MAP constructs. In another experiment, rats were infected with
Streptococcus sobrinus
strain 6715 under an identical protocol. Significant protection was observed on buccal surfaces in both SYI-CAT and CAT construct-immunized, but not in the SYI construct-immunized, groups. Thus, addition of the GbpB-derived SYI peptide to the GTF-derived CAT peptide construct not only enhanced the immunological response to CAT and GTF epitopes, but also extended the protective effect of the construct to include both
S. mutans
and
S. sobrinus
.
Identification and Characterization of Human Surfactant Protein A Binding Protein ofMycoplasma pneumoniae
Authors: Kannan T. R. , Provenzano D. , Wright J. R. , Baseman J. B. 
Published: April 2005

ABSTRACTMycoplasma pneumoniaeinfections represent a major primary cause of human respiratory diseases, exacerbate other respiratory disorders, and are associated with extrapulmonary pathologies. Cytadherence is a critical step in mycoplasma colonization, aided by a network of mycoplasma adhesins and cytadherence accessory proteins which mediate binding to host cell receptors. Furthermore, the respiratory mucosa is enriched with extracellular matrix components, including surfactant proteins, fibronectin, and mucin, which provide additional in vivo targets for mycoplasma parasitism. In this study we describe interactions betweenM. pneumoniaeand human surfactant protein-A (hSP-A). Initially, we found that viableM. pneumoniaecells bound to immobilized hSP-A in a dose- and calcium (Ca2+)-dependent manner. Mild trypsin treatment of intact mycoplasmas reduced binding markedly (80 to 90%) implicating a surface-associated mycoplasma protein(s). Using hSP-A-coupled Sepharose affinity chromatography and polyacrylamide gel electrophoresis, we identified a 65-kDa hSP-A binding protein ofM. pneumoniae. The presence of Ca2+enhanced binding of the 65-kDa protein to hSP-A, which was reduced by the divalent cation-chelating agent, EDTA. The 65-kDa hSP-A binding protein ofM. pneumoniaewas identified by sequence analysis as a novel protein (MPN372) possessing a putative S1-like subunit of pertussis toxin at the amino terminus (amino acids 1 to 226), with the remaining amino acids (227 to 591) exhibiting no homology with other subunits of pertussis toxin, other known toxins, or any reported proteins. Recombinant MPN372 (MPN372) bound to hSP-A in a dose-dependent manner, which was markedly reduced by preincubation with mouse recombinant MPN372 antisera. Also, adherence of viableM. pneumoniaecells to hSP-A was inhibited by recombinant MPN372 antisera, demonstrating that MPN372, a previously designated hypothetical protein, is surface exposed and mediates mycoplasma attachment to hSP-A.
TheBrucella abortusCu,Zn Superoxide Dismutase Is Required for Optimal Resistance to Oxidative Killing by Murine Macrophages and Wild-Type Virulence in Experimentally Infected Mice
Authors: Gee Jason M. , Valderas Michelle Wright , Kovach Michael E. , Grippe Vanessa K. , Robertson Gregory T. , Ng Wai-Leung , Richardson John M. , Winkler Malcolm E. , Roop R. Martin 
Published: April 2005

ABSTRACTTwo-dimensional gel electrophoretic analysis of cell lysates fromBrucella abortus2308 and the isogenichfqmutant Hfq3 revealed that the RNA binding protein Hfq (also known as host factor I or HF-I) is required for the optimal stationary phase production of the periplasmic Cu,Zn superoxide dismutase SodC. An isogenicsodCmutant, designated MEK2, was constructed fromB. abortus2308 by gene replacement, and thesodCmutant exhibited much greater susceptibility to killing by O2−generated by pyrogallol and the xanthine oxidase reaction than the parental 2308 strain supporting a role for SodC in protecting this bacterium from O2−of exogenous origin. TheB. abortus sodCmutant was also found to be much more sensitive to killing by cultured resident peritoneal macrophages from C57BL6J mice than 2308, and the attenuation displayed by MEK2 in cultured murine macrophages was enhanced when these phagocytes were treated with gamma interferon (IFN-γ). The attenuation displayed by theB. abortus sodCmutant in both resting and IFN-γ-activated macrophages was alleviated, however, when these host cells were treated with the NADPH oxidase inhibitor apocynin. Consistent with its increased susceptibility to killing by cultured murine macrophages, theB. abortus sodCmutant also displayed significant attenuation in experimentally infected C57BL6J mice compared to the parental strain. These experimental findings indicate that SodC protectsB. abortus2308 from the respiratory burst of host macrophages. They also suggest that reduced SodC levels may contribute to the attenuation displayed by theB. abortus hfqmutant Hfq3 in the mouse model.
Differential Induction of the Toll-Like Receptor 4-MyD88-Dependent and -Independent Signaling Pathways by Endotoxins
Authors: Zughaier Susu M. , Zimmer Shanta M. , Datta Anup , Carlson Russell W. , Stephens David S. 
Published: April 2005

ABSTRACTThe biological response to endotoxin mediated through the Toll-like receptor 4 (TLR4)-MD-2 receptor complex is directly related to lipid A structure or configuration. Endotoxin structure may also influence activation of the MyD88-dependent and -independent signaling pathways of TLR4. To address this possibility, human macrophage-like cell lines (THP-1, U937, and MM6) or murine macrophage RAW 264.7 cells were stimulated with picomolar concentrations of highly purified endotoxins. Harvested supernatants from previously stimulated cells were also used to stimulate RAW 264.7 or 23ScCr (TLR4-deficient) macrophages (i.e., indirect induction).Neisseria meningitidislipooligosaccharide (LOS) was a potent direct inducer of the MyD88-dependent pathway molecules tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 3α (MIP-3α), and the MyD88-independent molecules beta interferon (IFN-β), nitric oxide, and IFN-γ-inducible protein 10 (IP-10).Escherichia coli55:B5 andVibrio choleraelipopolysaccharides (LPSs) at the same pmole/ml lipid A concentrations induced comparable levels of TNF-α, IL-1β, and MIP-3α, but significantly less IFN-β, nitric oxide, and IP-10. In contrast, LPS fromSalmonella entericaserovars Minnesota and Typhimurium induced amounts of IFN-β, nitric oxide, and IP-10 similar to meningococcal LOS but much less TNF-α and MIP-3α in time course and dose-response experiments. No MyD88-dependent or -independent response to endotoxin was seen in TLR4-deficient cell lines (C3H/HeJ and 23ScCr) and response was restored in TLR4-MD-2-transfected human embryonic kidney 293 cells. Blocking the MyD88-dependent pathway by DNMyD88 resulted in significant reduction of TNF-α release but did not influence nitric oxide release. IFN-β polyclonal antibody and IFN-α/β receptor 1 antibody significantly reduced nitric oxide release.N. meningitidisendotoxin was a potent agonist of both the MyD88-dependent and -independent signaling pathways of the TLR4 receptor complex of human macrophages.E. coli55:B5 andVibrio choleraeLPS, at the same picomolar lipid A concentrations, selectively induced the MyD88-dependent pathway, whileSalmonellaLPS activated the MyD88-independent pathway.