Open Access LMU

    The Optimal Regulation of Credit Rating Agencies

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    Credit rating agencies (CRAs) very often have been criticized for announcing inaccurate credit ratings and are suspected of being exposed to conflicts of interest. Despite these objections CRAs remained largely unregulated. Based on Pagano & Immordino (2007), we study the optimal regulation of CRAs in a model where rating quality is unobservable and enforcing regulation is costly. The model shows that minimum rating standards increase the social value of credit ratings. The model also analyzes implications for regulation in the presence of conflicts of interest between the CRA and the rated clients by direct bribes and by the joint provision of rating and consulting services

    The association between reported and calculated reservation wages

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    Do reported reservation wages correspond to the concept of reservation wages that economists have? Using panel data on British unemployed I calculate reservation wages from a search model and compare these with reported reservation wages. It is shown that men's reported reservation wages are greater than what the model predicts, and that for women there is hardly a relation between the two variables

    The properties of nerve cell precursors in hydra

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    Two signals, the head activator and an injury stimulus, control differentiation of nerve cells from uncommitted stem cells in hydra [Th. Holstein, H. C. Schaller, and C. N. David, (1986) Dev. Biol. 115, 9–17]. The time of action of these signals in the precursor cell cycle was determined. Methanol extracts of hydra containing 10−13 M head activator cause nerve cell commitment in S phase of the precursor cell cycle. Committed precursors complete the cell cycle, divide, and arrest in G1. Injury relieves the G1 block and precursors differentiate nerve cells. Under these conditions the time from commitment to nerve differentiation is 12 hr, the time from the end of S phase to nerve differentiation is 9 hr, and the time from the G1 block to nerve differentiation is 4 hr. Committed precursors blocked in G1 are unstable, decaying with a half-life of 12 hr if not stimulated to differentiate by an injury stimulus

    Coordination Chemistry of Perhalogenated Cyclopentadienes and Alkynes. 17. Reaction of Dichloroethyne With Platinum(0) Phosphine Complexes: Formation of a .pi.-Complex, Isomerization to .beta.-Chloroethynyl Complexes, and Syntheses of Diplatinioethyne Derivatives. Molecular Structures of (Ph3P)2Pt(.eta.2-ClC.tplbond.CCl) and Cl(Ph3P)2PtC.tplbond.CPt(PPh3)2Cl

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    Dichloroethyne ClCECCl reacts with Pt(PPh3)2(C2H4) or Pt(PPh& to give the a-complex Pt(PPh3)2(+21C=CC1) (l),w hich can be isomerized by prolonged refluxing in toluene to trans- (Ph3P)zC1Pt-C==CC1 (2). 2 easily undergoes exchange reactions with alkylphosphines and with halide anions to yield trans-(R3P)2ClPt-C=CCl (R = Et (3)) Bu (4)) and trans-(Ph3P)z- (X)Pt-C=CCl (X = F (5a), Br (5b), I (5c)), respectively. The alkylphosphine complexes 3 and 4 can also be obtained by reaction of Pt(PR3)4 (R = Et, “Bu) with ClCECCl or from 1 and the corresponding phosphine. When Pt(PPh&(CzH4) is added to a solution of 3, a dinuclear complex 6 is formed, in which the C=C-Cl group acts as a a,a-bridging ligand. Upon standing, oxidative addition of the remaining C-C1 bond occurs and the p-ethynediyl complex trans- C1(R3P)2Pt-C=C-Pt(PPh3)2C1-Cis (R = Et (7a)) can be obtained. The corresponding p-ethynediyl complex 7b (R = Ph) is formed directly from 2 and Pt(PPh&(CzH4). 7b isomerizes upon heating in toluene to the symmetrical all-trans isomer 8. The molecular structures of 1 and 8 were determined by X-ray diffraction (1: C ~ ~ H ~ ~ C ~ Z P ~ Pa ~=C 10H.3Z11C(3~) AZ,, b = 10.392(4) A, c = 33.675(16) A, P = 90.17(3)’, monoclinic, P21/n, 2 = 4. 8: C74H&1zP4Ptz9 a = 12.938(2) A, b = 19.964(3) A, c = 24.844(3) A, P = 96.14(1)’, monoclinic, C2/c, 2 = 4)

    Transplantation stimulates interstitial cell migration in hydra

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    Migration of interstitial cells and nerve cell precursors was analyzed in Hydra magnipapillata and Hydra vulgaris (formerly Hydra attenuata). Axial grafts were made between [3H]thymidine-labeled donor and unlabeled host tissue. Migration of labeled cells into the unlabeled half was followed for 4 days. The results indicate that the rate of migration was initially high and then slowed on Days 2–4. Regrafting fresh donor tissue on Days 2–4 maintained high levels of migration. Thus, migration appears to be stimulated by the grafting procedure itself

    Positional Effects on the Characterization of Ejectives in Waima’a

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    This paper presents results from an ongoing investigation into stop consonants in Waima’a, focusing on the issue of tense v. lax ejectives. Sources tend to describe ejectives in a given language as either tense or lax; however ejectives in Waima'a, do not fit squarely into either category [4]. Here we compare ejectives in word-initial and word-medial contexts, to specifically address the role of word-position in the tense/lax distinction. Results show that word-position affects the duration of all stop types analyzed, i.e. unaspirated, postaspirated, & ejective stops. Variability amongst the ejective tokens suggests that the notion of a tense/lax dichotomy should be replaced instead with that of a tense/lax continuum

    Tracking virus-specific CD4+ T cells during and after acute hepatitis C virus infection.

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    CD4+ T cell help is critical in maintaining antiviral immune responses and such help has been shown to be sustained in acute resolving hepatitis C. In contrast, in evolving chronic hepatitis C CD4+ T cell helper responses appear to be absent or short-lived, using functional assays. Here we used a novel HLA-DR1 tetramer containing a highly targeted CD4+ T cell epitope from the hepatitis C virus non-structural protein 4 to track number and phenotype of hepatitis C virus specific CD4+ T cells in a cohort of seven HLA-DR1 positive patients with acute hepatitis C in comparison to patients with chronic or resolved hepatitis C. We observed peptide-specific T cells in all seven patients with acute hepatitis C regardless of outcome at frequencies up to 0.65% of CD4+ T cells. Among patients who transiently controlled virus replication we observed loss of function, and/or physical deletion of tetramer+ CD4+ T cells before viral recrudescence. In some patients with chronic hepatitis C very low numbers of tetramer+ cells were detectable in peripheral blood, compared to robust responses detected in spontaneous resolvers. Importantly we did not observe escape mutations in this key CD4+ T cell epitope in patients with evolving chronic hepatitis C. During acute hepatitis C a CD4+ T cell response against this epitope is readily induced in most, if not all, HLA-DR1+ patients. This antiviral T cell population becomes functionally impaired or is deleted early in the course of disease in those where viremia persists

    Fusion of Sendai virus with the target cell membrane is required for T cell cytotoxicity

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    INFECTION of mice with viruses can generate cytotoxic T lymphocytes (CTL) which show restricted specificity for target cell lysis. Specific lysis requires that the virus used to prime the target cells must be of the same type as that used to sensitise the CTL, and that both target and CTL cells must express the same major histocompatability complex (MHC) gene product(s). The nature of the viral gene product(s) and their interaction with the MHC gene product(s) have been the subject of recent stud1−5. Previously we used Sendai virus to show that lysable target cells can be obtained using membrane vesicles which contain only the viral glycoproteins, indicating that these may be the specific viral gene products involved in target formation5. Sendai virus contains two glycoproteins—the haemagglutinin-neuraminidase (HANA) which promotes attachment of virus to cells and the fusion protein (F) which is involved in subsequent virus cell fusion7−9. Both activities are necessary for insertion of these viral glycoproteins into the plasma membrane of the cell10. In this letter we suggest that the insertion of the viral glycoproteins into the cell membrane is an essential step in target cell formation since we can show that virus containing an inactive fusion protein precursor (F0) cannot elicit T cell cytotoxicity unless the fusion activity is generated by proteolytic cleavage of the precursor. Sugamura et al. 6 have suggested that it is primarily the F glycoprotein of the Sendai virus envelope which is essential for the formation of the target antigen, as virus lacking the functional activities of F following trypsin digestion was inactive in priming target cells for T cell killing. However, we show that proteolytic inactivation of either of the two glycoproteins (F or HANA) of virus used to prime target cells will abolish the cytotoxic response
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