Rejection Sensitivity, Perceived Power, and HIV Risk in the Relationships of Low-Income Urban Women

The psychological processes associated with HIV infection in long-term relationships differ from those operative in casual sexual encounters, and relatively little research has considered the aspects of personality applicable in the ongoing heterosexual relationships in which women are at greatest risk. Sensitivity to rejection has been linked with efforts to prevent rejection at a cost to the self and, therefore, may be relevant to the health risks that many women incur in relationships. We examined the association of rejection sensitivity with women\u27s sexual risk behavior in a sample of women at heightened risk for HIV exposure. Women in long-term heterosexual relationships (N = 159) were recruited for study participation in the hospital emergency room serving a low-income neighborhood in New York City, in 2001-2003. Rejection sensitivity and known HIV risk factors were assessed using verbally administered questionnaires. Rejection sensitivity was associated with lower perceived relationship power and, in turn, more frequent unprotected sex with a partner perceived to be at risk for HIV. These results held when controlling for other HIV risk factors including partner violence, economic dependence, and substance use. Understanding the association of rejection concerns with lower perceived personal power in relationships may be important for HIV prevention

Computable randomness is about more than probabilities

We introduce a notion of computable randomness for infinite sequences that generalises the classical version in two important ways. First, our definition of computable randomness is associated with imprecise probability models, in the sense that we consider lower expectations (or sets of probabilities) instead of classical 'precise' probabilities. Secondly, instead of binary sequences, we consider sequences whose elements take values in some finite sample space. Interestingly, we find that every sequence is computably random with respect to at least one lower expectation, and that lower expectations that are more informative have fewer computably random sequences. This leads to the intriguing question whether every sequence is computably random with respect to a unique most informative lower expectation. We study this question in some detail and provide a partial answer

On the (non-)existence of polynomial kernels for Pl-free edge modification problems

Given a graph G = (V,E) and an integer k, an edge modification problem for a graph property P consists in deciding whether there exists a set of edges F of size at most k such that the graph H = (V,E \vartriangle F) satisfies the property P. In the P edge-completion problem, the set F of edges is constrained to be disjoint from E; in the P edge-deletion problem, F is a subset of E; no constraint is imposed on F in the P edge-edition problem. A number of optimization problems can be expressed in terms of graph modification problems which have been extensively studied in the context of parameterized complexity. When parameterized by the size k of the edge set F, it has been proved that if P is an hereditary property characterized by a finite set of forbidden induced subgraphs, then the three P edge-modification problems are FPT. It was then natural to ask whether these problems also admit a polynomial size kernel. Using recent lower bound techniques, Kratsch and Wahlstrom answered this question negatively. However, the problem remains open on many natural graph classes characterized by forbidden induced subgraphs. Kratsch and Wahlstrom asked whether the result holds when the forbidden subgraphs are paths or cycles and pointed out that the problem is already open in the case of P4-free graphs (i.e. cographs). This paper provides positive and negative results in that line of research. We prove that parameterized cograph edge modification problems have cubic vertex kernels whereas polynomial kernels are unlikely to exist for the Pl-free and Cl-free edge-deletion problems for large enough l

On The Power of Tree Projections: Structural Tractability of Enumerating CSP Solutions

The problem of deciding whether CSP instances admit solutions has been deeply studied in the literature, and several structural tractability results have been derived so far. However, constraint satisfaction comes in practice as a computation problem where the focus is either on finding one solution, or on enumerating all solutions, possibly projected to some given set of output variables. The paper investigates the structural tractability of the problem of enumerating (possibly projected) solutions, where tractability means here computable with polynomial delay (WPD), since in general exponentially many solutions may be computed. A general framework based on the notion of tree projection of hypergraphs is considered, which generalizes all known decomposition methods. Tractability results have been obtained both for classes of structures where output variables are part of their specification, and for classes of structures where computability WPD must be ensured for any possible set of output variables. These results are shown to be tight, by exhibiting dichotomies for classes of structures having bounded arity and where the tree decomposition method is considered

Subtype-Selective Positive Modulation of K\u3csub\u3eCa\u3c/sub\u3e2.3 Channels Increases Cilia Length

Small-conductance Ca2+-activated potassium (KCa2.x) channels are gated exclusively by intracellular Ca2+. The activation of KCa2.3 channels induces hyperpolarization, which augments Ca2+ signaling in endothelial cells. Cilia are specialized Ca2+ signaling compartments. Here, we identified compound 4 that potentiates human KCa2.3 channels selectively. The subtype selectivity of compound 4 for human KCa2.3 over rat KCa2.2a channels relies on an isoleucine residue in the HA/HB helices. Positive modulation of KCa2.3 channels by compound 4 increased flow-induced Ca2+ signaling and cilia length, while negative modulation by AP14145 reduced flow-induced Ca2+ signaling and cilia length. These findings were corroborated by the increased cilia length due to the expression of Ca2+-hypersensitive KCa2.3_G351D mutant channels and the reduced cilia length resulting from the expression of Ca2+-hyposensitive KCa2.3_I438N channels. Collectively, we were able to associate functions of KCa2.3 channels and cilia, two crucial components in the flow-induced Ca2+ signaling of endothelial cells, with potential implications in vasodilation and ciliopathic hypertension

Gcn4 misregulation reveals a direct role for the evolutionary conserved EKC/KEOPS in the t6A modification of tRNAs

The EKC/KEOPS complex is universally conserved in Archaea and Eukarya and has been implicated in several cellular processes, including transcription, telomere homeostasis and genomic instability. However, the molecular function of the complex has remained elusive so far. We analyzed the transcriptome of EKC/KEOPS mutants and observed a specific profile that is highly enriched in targets of the Gcn4p transcriptional activator. GCN4 expression was found to be activated at the translational level in mutants via the defective recognition of the inhibitory upstream ORFs (uORFs) present in its leader. We show that EKC/KEOPS mutants are defective for the N6-threonylcarbamoyl adenosine modification at position 37 (t6A37) of tRNAs decoding ANN codons, which affects initiation at the inhibitory uORFs and provokes Gcn4 de-repression. Structural modeling reveals similarities between Kae1 and bacterial enzymes involved in carbamoylation reactions analogous to t6A37 formation, supporting a direct role for the EKC in tRNA modification. These findings are further supported by strong genetic interactions of EKC mutants with a translation initiation factor and with threonine biosynthesis genes. Overall, our data provide a novel twist to understanding the primary function of the EKC/KEOPS and its impact on several essential cellular functions like transcription and telomere homeostasis

Equilibrium configurations of two charged masses in General Relativity

An asymptotically flat static solution of Einstein-Maxwell equations which describes the field of two non-extreme Reissner - Nordstr\"om sources in equilibrium is presented. It is expressed in terms of physical parameters of the sources (their masses, charges and separating distance). Very simple analytical forms were found for the solution as well as for the equilibrium condition which guarantees the absence of any struts on the symmetry axis. This condition shows that the equilibrium is not possible for two black holes or for two naked singularities. However, in the case when one of the sources is a black hole and another one is a naked singularity, the equilibrium is possible at some distance separating the sources. It is interesting that for appropriately chosen parameters even a Schwarzschild black hole together with a naked singularity can be "suspended" freely in the superposition of their fields.Comment: 4 pages; accepted for publication in Phys. Rev.

Mutations in CNNM4 Cause Jalili Syndrome, Consisting of Autosomal-Recessive Cone-Rod Dystrophy and Amelogenesis Imperfecta

The combination of recessively inherited cone-rod dystrophy (CRD) and amelogenesis imperfecta (AI) was first reported by Jalili and Smith in 1988 in a family subsequently linked to a locus on chromosome 2q11, and it has since been reported in a second small family. We have identified five further ethnically diverse families cosegregating CRD and AI. Phenotypic characterization of teeth and visual function in the published and new families reveals a consistent syndrome in all seven families, and all link or are consistent with linkage to 2q11, confirming the existence of a genetically homogenous condition that we now propose to call Jalili syndrome. Using a positional-candidate approach, we have identified mutations in the CNNM4 gene, encoding a putative metal transporter, accounting for the condition in all seven families. Nine mutations are described in all, three missense, three terminations, two large deletions, and a single base insertion. We confirmed expression of Cnnm4 in the neural retina and in ameloblasts in the developing tooth, suggesting a hitherto unknown connection between tooth biomineralization and retinal function. The identification of CNNM4 as the causative gene for Jalili syndrome, characterized by syndromic CRD with AI, has the potential to provide new insights into the roles of metal transport in visual function and biomineralization