Rapid displacement of dengue virus type 1 by type 4, Pacific region, 2007-2009

Since 2000-2001, dengue virus type 1 has circulated in the Pacific region. However, in 2007, type 4 reemerged and has almost completely displaced the strains of type 1. If only 1 serotype circulates at any time and is replaced approximately every 5 years, DENV-3 may reappear in 2012.

ACE research vignette 024 : New firm formation and job creation by type of firm an type of region.

This series of research vignettes is aimed at sharing current and interesting research findings from our team of international Entrepreneurship researchers. This vignette, written by Mr. Darren Kavanagh and Professor Per Davidsson, takes a closer look at job creation by new firms.

Binding of two DNA molecules by type II topoisomerases for decatenation

Topoisomerases (topos) maintain DNA topology and influence DNA transaction processes by catalysing relaxation, supercoiling and decatenation reactions. In the cellular milieu, division of labour between different topos ensures topological homeostasis and control of central processes. In Escherichia coli, DNA gyrase is the principal enzyme that carries out negative supercoiling, while topo IV catalyses decatenation, relaxation and unknotting. DNA gyrase apparently has the daunting task of undertaking both the enzyme functions in mycobacteria, where topo IV is absent. We have shown previously that mycobacterial DNA gyrase is an efficient decatenase. Here, we demonstrate that the strong decatenation property of the enzyme is due to its ability to capture two DNA segments in trans. Topo IV, a strong dedicated decatenase of E. coli, also captures two distinct DNA molecules in a similar manner. In contrast, E. coli DNA gyrase, which is a poor decatenase, does not appear to be able to hold two different DNA molecules in a stable complex. The binding of a second DNA molecule to GyrB/ParE is inhibited by ATP and the non-hydrolysable analogue, AMPPNP, and by the substitution of a prominent positively charged residue in the GyrB N-terminal cavity, suggesting that this binding represents a potential T-segment positioned in the cavity. Thus, after the GyrA/ParC mediated initial DNA capture, GyrB/ParE would bind efficiently to a second DNA in trans to form a T-segment prior to nucleotide binding and closure of the gate during decatenation.

Critical Role for STAT4 Activation by Type 1 Interferons in the Interferon-Y Response to Viral Infection

Interferons (IFNs) are essential for host defense. Although the antiviral effects of the type 1 IFNs IFN- and IFN- (IFN-/) have been established, their immunoregulatory functions, especially their ability to regulate IFN- production, are poorly understood. Here we show that IFN-/ activate STAT4 directly (STAT, signal transducers and activators of transcription) and that this is required for IFN- production during viral infections of mice, in concert with T cell receptor-derived signals. In contrast, STAT1 appears to negatively regulate IFN-/ induction of IFN-. Thus, type 1 IFNs, in addition to interleukin-12, provide pathways for innate regulation of adaptive immunity, and their immunoregulatory functions are controlled by modulating the activity of individual STATs.

Summary of Criminal Records Disposition by Type For Period 7/1/2013 Thru 6/30/2014

This gives a summary of criminal records disposition by type.

Tightening of DNA knots by supercoiling facilitates their unknotting by type II DNA topoisomerases.

Using numerical simulations, we compare properties of knotted DNA molecules that are either torsionally relaxed or supercoiled. We observe that DNA supercoiling tightens knotted portions of DNA molecules and accentuates the difference in curvature between knotted and unknotted regions. The increased curvature of knotted regions is expected to make them preferential substrates of type IIA topoisomerases because various earlier experiments have concluded that type IIA DNA topoisomerases preferentially interact with highly curved DNA regions. The supercoiling-induced tightening of DNA knots observed here shows that torsional tension in DNA may serve to expose DNA knots to the unknotting action of type IIA topoisomerases, and thus explains how these topoisomerases could maintain a low knotting equilibrium in vivo, even for long DNA molecules.

Co-activation of JAK/STAT and p38 MAPK pathways by type I interferon enhances apoptosis in human basophils

It has previously been published that interferon-α (type I IFN) improves clinical symptoms of asthma patients. Since human basophils are major inflammatory cells in maintaining chronic allergic asthma we investigate whether type I IFN affect human blood basophils. Furthermore, previous studies have shown that spontaneous apoptosis of human basophils is slow due to constitutive expression of anti-apoptotic BCL-2 family members. In addition, IL-3 exceptionally promotes survival of basophils by enhancing constitutive expression of BCL-2 family members and by inducing de-novo expression of Pim-1 kinase. Thus, we also assessed whether type I IFN might overcome IL-3-induced survival of human basophils. Our data show that type I IFN enhances apoptosis in purified human blood basophils compared to spontaneous apoptosis of controls or type II IFN treated cells. Furthermore, we demonstrate that both type I IFN and FasL enhance apoptosis in human basophils with similar efficiency in a rather additive than synergistic way. Analyses of signaling pathways reveal that type I IFN promote prolonged phosphorylation of STAT1/STAT2. By using a pan-JAK inhibitor the phosphorylation of STAT1/STAT2 is inhibited and most importantly the pro-apoptotic effect of type I IFN is abolished. On the other hand, type I IFN do not reduce IL-3-induced de novo expression of Pim-1 and BCL-2. This is in line with our observation that IL-3-induced survival is dominant over type I IFN-enhanced apoptosis. In addition, phosphorylation of p38 MAPK in type I IFN treated cells is comparable to non-treated cells. Particularly however, inhibition of this p-p38 activity abrogates apoptosis as well. We conclude that type I IFN-enhanced apoptosis is tightly regulated by the cooperation of JAK/STAT and p38 MAPK pathways. Our study identifies a so far unknown effect of type I IFN and may explain the improved clinical symptoms of asthma patients treated with type I IFN.

Gini coefficient, dissimilarity index and Lorenz curve for the spanish port system by type of goods

This paper shows the Gini Coefficient, the dissimilarity Index and the Lorenz Curve for the Spanish Port System by type of goods from 1960 to the year 2010 for business units: Total traffic, Liquid bulk cargo, Solid bulk cargo, General Merchandise and Container (TEUs) with the aim of carcaterizar the Spanish port systems in these periods and propose future strategies.

Horizontal visibility graphs generated by type-I intermittency

The type-I intermittency route to (or out of) chaos is investigated within the horizontal visibility (HV) graph theory. For that purpose, we address the trajectories generated by unimodal maps close to an inverse tangent bifurcation and construct their associatedHVgraphs.We showhowthe alternation of laminar episodes and chaotic bursts imprints a fingerprint in the resulting graph structure. Accordingly, we derive a phenomenological theory that predicts quantitative values for several network parameters. In particular, we predict that the characteristic power-law scaling of the mean length of laminar trend sizes is fully inherited by the variance of the graph degree distribution, in good agreement with the numerics. We also report numerical evidence on how the characteristic power-law scaling of the Lyapunov exponent as a function of the distance to the tangent bifurcation is inherited in the graph by an analogous scaling of block entropy functionals defined on the graph. Furthermore, we are able to recast the full set of HV graphs generated by intermittent dynamics into a renormalization-group framework, where the fixed points of its graph-theoretical renormalization-group flow account for the different types of dynamics.We also establish that the nontrivial fixed point of this flow coincides with the tangency condition and that the corresponding invariant graph exhibits extremal entropic properties.

Urocortin II: A member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by type 2 CRF receptors

Here we describe the cloning and initial characterization of a previously unidentified CRF-related neuropeptide, urocortin II (Ucn II). Searches of the public human genome database identified a region with significant sequence homology to the CRF neuropeptide family. By using homologous primers deduced from the human sequence, a mouse cDNA was isolated from whole brain poly(A)+ RNA that encodes a predicted 38-aa peptide, structurally related to the other known mammalian family members, CRF and Ucn. Ucn II binds selectively to the type 2 CRF receptor (CRF-R2), with no appreciable activity on CRF-R1. Transcripts encoding Ucn II are expressed in discrete regions of the rodent central nervous system, including stress-related cell groups in the hypothalamus (paraventricular and arcuate nuclei) and brainstem (locus coeruleus). Central administration of 1–10 μg of peptide elicits activational responses (Fos induction) preferentially within a core circuitry subserving autonomic and neuroendocrine regulation, but whose overall pattern does not broadly mimic the CRF-R2 distribution. Behaviorally, central Ucn II attenuates nighttime feeding, with a time course distinct from that seen in response to CRF. In contrast to CRF, however, central Ucn II failed to increase gross motor activity. These findings identify Ucn II as a new member of the CRF family of neuropeptides, which is expressed centrally and binds selectively to CRF-R2. Initial functional studies are consistent with Ucn II involvement in central autonomic and appetitive control, but not in generalized behavioral activation.

Mechanism of topology simplification by type II DNA topoisomerases

Type II DNA topoisomerases actively reduce the fractions of knotted and catenated circular DNA below thermodynamic equilibrium values. To explain this surprising finding, we designed a model in which topoisomerases introduce a sharp bend in DNA. Because the enzymes have a specific orientation relative to the bend, they act like Maxwell's demon, providing unidirectional strand passage. Quantitative analysis of the model by computer simulations proved that it can explain much of the experimental data. The required sharp DNA bend was demonstrated by a greatly increased cyclization of short DNA fragments from topoisomerase binding and by direct visualization with electron microscopy.

Novel Nuclear Signaling Pathway Mediates Activation of Fibroblast Growth Factor-2 Gene by Type 1 and Type 2 Angiotensin II Receptors

In bovine adrenal medullary cells synergistically acting type 1 and type 2 angiotensin II (AII) receptors activate the fibroblast growth factor-2 (FGF-2) gene through a unique AII-responsive promoter element. Both the type 1 and type 2 AII receptors and the downstream cyclic adenosine 1′,3′-monophosphate- and protein kinase C-dependent signaling pathways activate the FGF-2 promoter through a novel signal-transducing mechanism. This mechanism, which we have named integrative nuclear FGF receptor-1 signaling, involves the nuclear translocation of FGF receptor-1 and its subsequent transactivation of the AII-responsive element in the FGF-2 promoter.

Timing of metamorphosis and the onset of the negative feedback loop between the thyroid gland and the pituitary is controlled by type II iodothyronine deiodinase in Xenopus laevis

Two important features of amphibian metamorphosis are the sequential response of tissues to different concentrations of thyroid hormone (TH) and the development of the negative feedback loop between the pituitary and the thyroid gland that regulates TH synthesis by the thyroid gland. At the climax of metamorphosis in Xenopus laevis (when the TH level is highest), the ratio of the circulating precursor thyroxine (T4) to the active form 3,5,3′-triiodothyronine (T3) in the blood is many times higher than it is in tissues. This difference is because of the conversion of T4 to T3 in target cells of the tadpole catalyzed by the enzyme type II iodothyronine deiodinase (D2) and the local effect (cell autonomy) of this activity. Limb buds and tails express D2 early and late in metamorphosis, respectively, correlating with the time that these organs undergo TH-induced change. T3 is required to complete metamorphosis because the peak concentration of T4 that is reached at metamorphic climax cannot induce the final morphological changes. At the climax of metamorphosis, D2 expression is activated specifically in the anterior pituitary cells that express the genes for thyroid-stimulating hormone but not in the cells that express proopiomelanocortin. Physiological concentrations of T3 but not T4 can suppress thyrotropin subunit β gene expression. The timing and the remarkable specificity of D2 expression in the thyrotrophs of the anterior pituitary coupled with the requirement for locally synthesized T3 strongly support a role for D2 in the onset of the negative feedback loop at the climax of metamorphosis.

Using linked data to evaluate severity and outcome of injury by type of object struck (first object struck only) for motor vehicle crashes in Connecticut.

Federal Highway Administration, Washington, D.C.