Does Weak Governance Cause Weak Stock Returns? An Examination of Firm Operating Performance and Investors\u27 Expectations

We investigate Gompers, Ishii, and Metrick\u27s (2003) finding that firms with weak shareholder rights exhibit significant stock market underperformance. If the relation between poor governance and poor returns is causal, we expect that the market is negatively surprised by the poor operating performance of weak governance firms. We find that firms with weak shareholder rights exhibit significant operating underperformance. However, analysts\u27 forecast errors and earnings announcement returns show no evidence that this underperformance surprises the market. Our results are robust to controls for takeover activity. Overall, our results do not support the hypothesis that weak governance causes poor stock returns

Topological network alignment uncovers biological function and phylogeny

Sequence comparison and alignment has had an enormous impact on our understanding of evolution, biology, and disease. Comparison and alignment of biological networks will likely have a similar impact. Existing network alignments use information external to the networks, such as sequence, because no good algorithm for purely topological alignment has yet been devised. In this paper, we present a novel algorithm based solely on network topology, that can be used to align any two networks. We apply it to biological networks to produce by far the most complete topological alignments of biological networks to date. We demonstrate that both species phylogeny and detailed biological function of individual proteins can be extracted from our alignments. Topology-based alignments have the potential to provide a completely new, independent source of phylogenetic information. Our alignment of the protein-protein interaction networks of two very different species--yeast and human--indicate that even distant species share a surprising amount of network topology with each other, suggesting broad similarities in internal cellular wiring across all life on Earth.Comment: Algorithm explained in more details. Additional analysis adde

Gi- and Gs-coupled GPCRs show different modes of G-protein binding.

More than two decades ago, the activation mechanism for the membrane-bound photoreceptor and prototypical G protein-coupled receptor (GPCR) rhodopsin was uncovered. Upon light-induced changes in ligand-receptor interaction, movement of specific transmembrane helices within the receptor opens a crevice at the cytoplasmic surface, allowing for coupling of heterotrimeric guanine nucleotide-binding proteins (G proteins). The general features of this activation mechanism are conserved across the GPCR superfamily. Nevertheless, GPCRs have selectivity for distinct G-protein family members, but the mechanism of selectivity remains elusive. Structures of GPCRs in complex with the stimulatory G protein, Gs, and an accessory nanobody to stabilize the complex have been reported, providing information on the intermolecular interactions. However, to reveal the structural selectivity filters, it will be necessary to determine GPCR-G protein structures involving other G-protein subtypes. In addition, it is important to obtain structures in the absence of a nanobody that may influence the structure. Here, we present a model for a rhodopsin-G protein complex derived from intermolecular distance constraints between the activated receptor and the inhibitory G protein, Gi, using electron paramagnetic resonance spectroscopy and spin-labeling methodologies. Molecular dynamics simulations demonstrated the overall stability of the modeled complex. In the rhodopsin-Gi complex, Gi engages rhodopsin in a manner distinct from previous GPCR-Gs structures, providing insight into specificity determinants

Methods of quantifying change in multiple risk factor interventions

Objective: Risky behaviors such as smoking, alcohol abuse, physical inactivity, and poor diet are detrimental to health, costly, and often co-occur. Greater efforts are being targeted at changing multiple risk behaviors to more comprehensively address the health needs of individuals and populations. With increased interest in multiple risk factor interventions, the field will need ways to conceptualize the issue of overall behavior change. Method: Analyzing data from over 8000 participants in four multibehavioral interventions, we present five different methods for quantifying and reporting changes in multiple risk behaviors. Results: The methods are: (a) the traditional approach of reporting changes in individual risk behaviors; (b) creating a combined statistical index of overall behavior change, standardizing scores across behaviors on different metrics; (c) using a behavioral index; (d) calculating an overall impact factor; and (e) using overarching outcome measures such as quality of life, related biometrics, or cost outcomes. We discuss the methods\u27 interpretations, strengths, and limitations. Conclusion: Given the lack of consensus in the field on how to examine change in multiple risk behaviors, we recommend researchers employ and compare multiple methods in their publications. A dialogue is needed to work toward developing a consensus for optimal ways of conceptualizing and reporting changes in multibehavioral interventions

The benefits and challenges of multiple health behavior change in research and in practice

Objective: The major chronic diseases are caused by multiple risks, yet the science of multiple health behavior change (MHBC) is at an early stage, and factors that facilitate or impede scientists\u27 involvement in MHBC research are unknown. Benefits and challenges of MHBC interventions were investigated to strengthen researchers\u27 commitment and prepare them for challenges. Method: An online anonymous survey was e-mailed to listservs of the Society of Behavioral Medicine between May 2006 and 2007. Respondents (N = 69) were 83% female; 94% held a doctoral degree; 64% were psychologists, 24% were in public health; and 83% targeted MHBC in their work. Results: A sample majority rated 23 of the 24 benefits, but only 1 of 31 challenge items, as very to extremely important. Those engaged in MHBC rated the total benefits significantly higher than respondents focused on single behaviors, F(1,69) = 4.21, p \u3c .05, and rated the benefits significantly higher than the challenges: paired t(57) = 7.50, p \u3c .001. The two groups did not differ in ratings of challenges. Conclusion: It appears that individuals focused solely on single behaviors do not fully appreciate the benefits that impress MHBC researchers; it is not that substantial barriers are holding them back. Benefits of MHBC interventions need emphasizing more broadly to advance this research area

Metabolomic Profiling in LRRK2-Related Parkinson's Disease

Mutations in LRRK2 gene represent the most common known genetic cause of Parkinson's disease (PD).We used metabolomic profiling to identify biomarkers that are associated with idiopathic and LRRK2 PD. We compared plasma metabolomic profiles of patients with PD due to the G2019S LRRK2 mutation, to asymptomatic family members of these patients either with or without G2019S LRRK2 mutations, and to patients with idiopathic PD, as well as non-related control subjects. We found that metabolomic profiles of both idiopathic PD and LRRK2 PD subjects were clearly separated from controls. LRRK2 PD patients had metabolomic profiles distinguishable from those with idiopathic PD, and the profiles could predict whether the PD was secondary to LRRK2 mutations or idiopathic. Metabolomic profiles of LRRK2 PD patients were well separated from their family members, but there was a slight overlap between family members with and without LRRK2 mutations. Both LRRK2 and idiopathic PD patients showed significantly reduced uric acid levels. We also found a significant decrease in levels of hypoxanthine and in the ratios of major metabolites of the purine pathway in plasma of PD patients.These findings show that LRRK2 patients with the G2019S mutation have unique metabolomic profiles that distinguish them from patients with idiopathic PD. Furthermore, asymptomatic LRRK2 carriers can be separated from gene negative family members, which raises the possibility that metabolomic profiles could be useful in predicting which LRRK2 carriers will eventually develop PD. The results also suggest that there are aberrations in the purine pathway in PD which may occur upstream from uric acid

Production of neutral scalar Higgs bosons at eγe\gamma colliders

We study the production of neutral scalar (CP even) Higgs bosons in the process $e\gamma\to e h$ by including supersymmetric corrections to the dominant $t$-channel photon exchange amplitude. In addition to the standard model $W^{\pm}$ and fermion loops, there are substantial contributions from chargino loops. For some cases, these contributions can exceed those of the $W$'s and ordinary fermions. The cross sections in this channel are generally one or two orders of magnitude larger than those in the related channel $e\bar{e}\to\gamma h$.Comment: 12 pages RevTeX, 5 postscript figures included, uses epsf.st

Electron Spin Decoherence in Bulk and Quantum Well Zincblende Semiconductors

A theory for longitudinal (T1) and transverse (T2) electron spin coherence times in zincblende semiconductor quantum wells is developed based on a non-perturbative nanostructure model solved in a fourteen-band restricted basis set. Distinctly different dependences of coherence times on mobility, quantization energy, and temperature are found from previous calculations. Quantitative agreement between our calculations and measurements is found for GaAs/AlGaAs, InGaAs/InP, and GaSb/AlSb quantum wells.Comment: 11 pages, 3 figure