Non-Perturbative Corrections and Modularity in N=1 Type IIB Compactifications

Non-perturbative corrections and modular properties of four-dimensional type IIB Calabi-Yau orientifolds are discussed. It is shown that certain non-perturbative alpha' corrections survive in the large volume limit of the orientifold and periodically correct the Kahler potential. These corrections depend on the NS-NS two form and have to be completed by D-instanton contributions to transform covariantely under symmetries of the type IIB orientifold background. It is shown that generically also the D-instanton superpotential depends on the two-form moduli as well as on the complex dilaton. These contributions can arise through theta-functions with the dilaton as modular parameter. An orientifold of the Enriques Calabi-Yau allows to illustrate these general considerations. It is shown that this compactification leads to a controlled four-dimensional N=1 effective theory due to the absence of various quantum corrections. Making contact to the underlying topological string theory the D-instanton superpotential is proposed to be related to a specific modular form counting D3, D1, D(-1) degeneracies on the Enriques Calabi-Yau.Comment: 35 page

Hadron Spectroscopy: Theory and Experiment

Many new results on hadron spectra have been appearing in the past few years thanks to improved experimental techniques and searches in new channels. New theoretical techniques including refined methods of lattice QCD have kept pace with these developments. Much has been learned about states made of both light (u, d, and s) and heavy (c, b) quarks. The present review treats light-quark mesons, glueballs, hybrids, particles with a single c or b quark, charmonium, and bottomonium states. Some prospects for further study are noted.Comment: 29 pages, 9 figures, to be published in Journal of Physics G. Further updating of reference

No Exit? Withdrawal Rights and the Law of Corporate Reorganizations

Bankruptcy scholarship is largely a debate about the comparative merits of a mandatory regime on one hand and bankruptcy by free design on the other. By the standard account, the current law of corporate reorganization is mandatory. Various rules that cannot be avoided ensure that investors’ actions are limited and they do not exercise their rights against specialized assets in a way that destroys the value of a business as a whole. These rules solve collective action problems and reduce the risk of bargaining failure. But there are costs to a mandatory regime. In particular, investors cannot design their rights to achieve optimal monitoring as they could in a system of bankruptcy by free design. This Article suggests that the academic debate has missed a fundamental feature of the law. Bankruptcy operates on legal entities, not on firms in the economic sense. For this reason, sophisticated investors do not face a mandatory regime at all. The ability of investors to place assets in separate entities gives them the ability to create specific withdrawal rights in the event the firm encounters financial distress. There is nothing mandatory about rules like the automatic stay when assets can be partitioned off into legal entities that are beyond the reach of the bankruptcy judge. Thus, by partitioning assets of one economic enterprise into different legal entities, investors can create a tailored bankruptcy regime. In this way, legal entities serve as building blocks that can be combined to create specific and varied but transparent investor withdrawal rights. This regime of tailored bankruptcy has been unrecognized and underappreciated and may be preferable to both mandatory and free design regimes. By allowing a limited number of investors to opt out of bankruptcy in a particular, discrete, and visible way, investors as a group may be able to both limit the risk of bargaining failure and at the same time enjoy the disciplining effect that a withdrawal right brings with it

Losartan Decreases p42/44 MAPK Signaling and Preserves LZ+ MYPT1 Expression

Heart failure is associated with impairment in nitric oxide (NO) mediated vasodilatation, which has been demonstrated to result from a reduction in the relative expression of the leucine zipper positive (LZ+) isoform of the myosin targeting subunit (MYPT1) of myosin light chain phosphatase. Further, captopril preserves normal LZ+ MYPT1 expression, the sensitivity to cGMP-mediated vasodilatation and modulates the expression of genes in the p42/44 MAPK and p38 MAPK signaling cascades. This study tests whether angiotensin receptor blockade (ARB) with losartan decreases p42/44 MAPK or p38 MAPK signaling and preserves LZ+ MYPT1 expression in a rat infarct model of heart failure. In aortic smooth muscle, p42/44 MAPK activation increases and LZ+ MYPT1 expression falls after LAD ligation. Losartan treatment decreases the activation of p42/44 MAPK to the uninfarcted control level and preserves normal LZ+ MYPT1 expression. The expression and activation of p38 MAPK, however, is low and does not change following LAD ligation or with losartan therapy. These data suggest that either reducing or blocking the effects of circulating angiotensin II, both decreases the activation of the p42/44 MAPK signaling cascade and preserves LZ+ MYPT1 expression. Thus, the ability of ACE-inhibitors and ARBs to modulate the vascular phenotype, to preserve normal flow mediated vasodilatation may explain the beneficial effects of these drugs compared to other forms of afterload reduction in the treatment of heart failure

Inferring Gene-Phenotype Associations via Global Protein Complex Network Propagation

BACKGROUND: Phenotypically similar diseases have been found to be caused by functionally related genes, suggesting a modular organization of the genetic landscape of human diseases that mirrors the modularity observed in biological interaction networks. Protein complexes, as molecular machines that integrate multiple gene products to perform biological functions, express the underlying modular organization of protein-protein interaction networks. As such, protein complexes can be useful for interrogating the networks of phenome and interactome to elucidate gene-phenotype associations of diseases. METHODOLOGY/PRINCIPAL FINDINGS: We proposed a technique called RWPCN (Random Walker on Protein Complex Network) for predicting and prioritizing disease genes. The basis of RWPCN is a protein complex network constructed using existing human protein complexes and protein interaction network. To prioritize candidate disease genes for the query disease phenotypes, we compute the associations between the protein complexes and the query phenotypes in their respective protein complex and phenotype networks. We tested RWPCN on predicting gene-phenotype associations using leave-one-out cross-validation; our method was observed to outperform existing approaches. We also applied RWPCN to predict novel disease genes for two representative diseases, namely, Breast Cancer and Diabetes. CONCLUSIONS/SIGNIFICANCE: Guilt-by-association prediction and prioritization of disease genes can be enhanced by fully exploiting the underlying modular organizations of both the disease phenome and the protein interactome. Our RWPCN uses a novel protein complex network as a basis for interrogating the human phenome-interactome network. As the protein complex network can capture the underlying modularity in the biological interaction networks better than simple protein interaction networks, RWPCN was found to be able to detect and prioritize disease genes better than traditional approaches that used only protein-phenotype associations

Deep sequencing analysis of the developing mouse brain reveals a novel microRNA

Extent: 15p.Background: MicroRNAs (miRNAs) are small non-coding RNAs that can exert multilevel inhibition/repression at a post-transcriptional or protein synthesis level during disease or development. Characterisation of miRNAs in adult mammalian brains by deep sequencing has been reported previously. However, to date, no small RNA profiling of the developing brain has been undertaken using this method. We have performed deep sequencing and small RNA analysis of a developing (E15.5) mouse brain. Results: We identified the expression of 294 known miRNAs in the E15.5 developing mouse brain, which were mostly represented by let-7 family and other brain-specific miRNAs such as miR-9 and miR-124. We also discovered 4 putative 22-23 nt miRNAs: mm_br_e15_1181, mm_br_e15_279920, mm_br_e15_96719 and mm_br_e15_294354 each with a 70-76 nt predicted pre-miRNA. We validated the 4 putative miRNAs and further characterised one of them, mm_br_e15_1181, throughout embryogenesis. Mm_br_e15_1181 biogenesis was Dicer1-dependent and was expressed in E3.5 blastocysts and E7 whole embryos. Embryo-wide expression patterns were observed at E9.5 and E11.5 followed by a near complete loss of expression by E13.5, with expression restricted to a specialised layer of cells within the developing and early postnatal brain. Mm_br_e15_1181 was upregulated during neurodifferentiation of P19 teratocarcinoma cells. This novel miRNA has been identified as miR-3099. Conclusions: We have generated and analysed the first deep sequencing dataset of small RNA sequences of the developing mouse brain. The analysis revealed a novel miRNA, miR-3099, with potential regulatory effects on early embryogenesis, and involvement in neuronal cell differentiation/function in the brain during late embryonic and early neonatal development.King-Hwa Ling, Peter J Brautigan, Christopher N Hahn, Tasman Daish, John R Rayner, Pike-See Cheah, Joy M Raison, Sandra Piltz Jeffrey R Mann, Deidre M Mattiske, Paul Q Thomas, David L Adelson and Hamish S Scot

Minimal Flavour Violation Waiting for Precise Measurements of Delta M_s, S_{psi phi}, A^s_SL, |V_ub|, gamma and B^0_{s,d} -> mu+ mu-

We emphasize that the recent measurements of the B^0_s - bar B^0_s mass difference Delta M_s by the CDF and D0 collaborations offer an important model independent test of minimal flavour violation (MFV). The improved measurements of the angle gamma in the unitarity triangle and of |V_ub| from tree level decays, combined with future accurate measurements of Delta M_s, S_{psi K_S}, S_{psi phi}, Br(B_{d,s} -> mu+ mu-), Br(B -> X_{d,s} nu bar nu), Br(K+ -> pi+ nu bar nu) and Br(K_L -> pi^0 nu bar nu) and improved values of the relevant non-perturbative parameters, will allow to test the MFV hypothesis in a model independent manner to a high accuracy. In particular, the difference between the reference unitarity triangle obtained from tree level processes and the universal unitarity triangle (UUT) in MFV models would signal either new flavour violating interactions and/or new local operators that are suppressed in MFV models with low tan(beta), with the former best tested through S_{psi phi} and K_L -> pi^0 nu bar nu. A brief discussion of non-MFV scenarios is also given. In this context we identify in the recent literature a relative sign error between Standard Model and new physics contributions to S_{psi phi}, that has an impact on the correlation between S_{psi phi} and A^s_SL. We point out that the ratios S_{psi phi}/A^s_SL and (Delta M_s)/(Delta Gamma_s) will allow to determine (Delta M_s)/(Delta M_s)^SM. Similar proposals for the determination of (Delta M_d)/(Delta M_d)^SM are also given.Comment: 22 pages, 8 figures, 1 table. Extended discussion of the correlation between S_{psi phi} and A^s_SL and new proposals to determine Delta M_q/(Delta M_q)^SM from future measurements, with respect to the first version. Minor changes and few references adde

Prospects for e+e- physics at Frascati between the phi and the psi

We present a detailed study, done in the framework of the INFN 2006 Roadmap, of the prospects for e+e- physics at the Frascati National Laboratories. The physics case for an e+e- collider running at high luminosity at the phi resonance energy and also reaching a maximum center of mass energy of 2.5 GeV is discussed, together with the specific aspects of a very high luminosity tau-charm factory. Subjects connected to Kaon decay physics are not discussed here, being part of another INFN Roadmap working group. The significance of the project and the impact on INFN are also discussed. All the documentation related to the activities of the working group can be found in http://www.roma1.infn.it/people/bini/roadmap.html.Comment: INFN Roadmap Report: 86 pages, 25 figures, 9 table