S-wave Meson-Meson Scattering from Unitarized U(3) Chiral Lagrangians

An investigation of the s-wave channels in meson-meson scattering is performed within a U(3) chiral unitary approach. Our calculations are based on a chiral effective Lagrangian which includes the eta' as an explicit degree of freedom and incorporates important features of the underlying QCD Lagrangian such as the axial U(1) anomaly. We employ a coupled channel Bethe-Salpeter equation to generate poles from composed states of two pseudoscalar mesons. Our results are compared with experimental phase shifts up to 1.5 GeV and effects of the eta' within this scheme are discussed.Comment: 18 pages, 6 figure

Analyticity, Crossing Symmetry and the Limits of Chiral Perturbation Theory

The chiral Lagrangian for Goldstone boson scattering is a power series expansion in numbers of derivatives. Each successive term is suppressed by powers of a scale, $\Lambda_\chi$, which must be less than of order $4\pi f/\sqrt{N}$ where $f$ is the Goldstone boson decay constant and $N$ is the number of flavors. The chiral expansion therefore breaks down at or below $4 \pi f/\sqrt{N}$. We argue that the breakdown of the chiral expansion is associated with the appearance of physical states other than Goldstone bosons. Because of crossing symmetry, some ``isospin'' channels will deviate from their low energy behavior well before they approach the scale at which their low energy amplitudes would violate unitarity. We argue that the estimates of ``oblique'' corrections from technicolor obtained by scaling from QCD are untrustworthy.Comment: harvmac, 18 pages (3 figures), HUTP-92/A025, BUHEP-92-18, new version fixes a TeX problem in little mod

Another look at ππ\pi\pi scattering in the scalar channel

We set up a general framework to describe $\pi\pi$ scattering below 1 GeV based on chiral low-energy expansion with possible spin-0 and 1 resonances. Partial wave amplitudes are obtained with the $N/D$ method, which satisfy unitarity, analyticity and approximate crossing symmetry. Comparison with the phase shift data in the J=0 channel favors a scalar resonance near the $\rho$ mass.Comment: 17 pages, 5 figures, REVTe

Randomized, Double-Blind, Placebo-Controlled Phase III Study of Tasquinimod in Men With Metastatic Castration-Resistant Prostate Cancer

PURPOSE: Tasquinimod, a novel oral therapy targeting the tumor microenvironment, significantly improved progression-free survival (PFS) in a randomized, placebo-controlled phase II trial in men with metastatic castration-resistant prostate cancer (mCRPC). This phase III study was conducted to confirm the phase II results and to detect an overall survival (OS) benefit. PATIENTS AND METHODS: Men with chemotherapy-naïve mCRPC and evidence of bone metastases were assigned (2:1) to receive tasquinimod once per day or placebo until progression or toxicity. The primary end point was radiographic PFS (rPFS; time from random assignment to radiologic progression or death) per Prostate Cancer Working Group 2 criteria and RECIST 1.1. The study had 99.9% power to detect an rPFS hazard ratio (HR) of 0.6 with a two-sided alpha error of .05 and 80% power to detect a target HR of 0.8 for OS, the key secondary end point. RESULTS: In all, 1,245 patients were randomly assigned to either tasquinimod (n = 832) or placebo (n = 413) between March 2011 and December 2012 at 241 sites in 37 countries. Baseline characteristics were balanced between groups: median age, 71 years; Karnofsky performance status ≥ 90%, 77.3%; and visceral metastases, 21.1%. Estimated median rPFS by central review was 7.0 months (95% CI, 5.8 to 8.2 months) with tasquinimod and 4.4 months (95% CI, 3.5 to 5.5 months) with placebo (HR, 0.64; 95% CI, 0.54 to 0.75; P < .001). Median OS was 21.3 months (95% CI, 19.5 to 23.0 months) with tasquinimod and 24.0 months (95% CI, 21.4 to 26.9 months) with placebo (HR, 1.10; 95% CI, 0.94 to 1.28; P = .25). Grade ≥ 3 adverse events were more frequent with tasquinimod (42.8% v 33.6%), the most common being anemia, fatigue, and cancer pain. CONCLUSION: In chemotherapy-naïve men with mCRPC, tasquinimod significantly improved rPFS compared with placebo. However, no OS benefit was observed

Single-shot divergence measurements of a laser-generated relativistic electron beam

Copyright 2010 American Institute of Physics. This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics. The following article appeared in Physics of Plasmas, 17(11), 113106_1-113106_7, 2010 and may be found at http://dx.doi.org/10.1063/1.351459

A microsporidian impairs Plasmodium falciparum transmission in Anopheles arabiensis mosquitoes

A possible malaria control approach involves the dissemination in mosquitoes of inherited symbiotic microbes to block Plasmodium transmission. However, in the Anopheles gambiae complex, the primary African vectors of malaria, there are limited reports of inherited symbionts that impair transmission. We show that a vertically transmitted microsporidian symbiont (Microsporidia MB) in the An. gambiae complex can impair Plasmodium transmission. Microsporidia MB is present at moderate prevalence in geographically dispersed populations of An. arabiensis in Kenya, localized to the mosquito midgut and ovaries, and is not associated with significant reductions in adult host fecundity or survival. Field-collected Microsporidia MB infected An. arabiensis tested negative for P. falciparum gametocytes and, on experimental infection with P. falciparum, sporozoites aren’t detected in Microsporidia MB infected mosquitoes. As a microbe that impairs Plasmodium transmission that is non-virulent and vertically transmitted, Microsporidia MB could be investigated as a strategy to limit malaria transmission

Chloroquine Mediated Modulation of Anopheles gambiae Gene Expression

Plasmodium development in the mosquito is crucial for malaria transmission and depends on the parasite's interaction with a variety of cell types and specific mosquito factors that have both positive and negative effects on infection. Whereas the defensive response of the mosquito contributes to a decrease in parasite numbers during these stages, some components of the blood meal are known to favor infection, potentiating the risk of increased transmission. The presence of the antimalarial drug chloroquine in the mosquito's blood meal has been associated with an increase in Plasmodium infectivity for the mosquito, which is possibly caused by chloroquine interfering with the capacity of the mosquito to defend against the infection.In this study, we report a detailed survey of the Anopheles gambiae genes that are differentially regulated by the presence of chloroquine in the blood meal, using an A. gambiae cDNA microarray. The effect of chloroquine on transcript abundance was evaluated separately for non-infected and Plasmodium berghei-infected mosquitoes. Chloroquine was found to affect the abundance of transcripts that encode proteins involved in a variety of processes, including immunity, apoptosis, cytoskeleton and the response to oxidative stress. This pattern of differential gene expression may explain the weakened mosquito defense response which accounts for the increased infectivity observed in chloroquine-treated mosquitoes.The results of the present study suggest that chloroquine can interfere with several putative mosquito mechanisms of defense against Plasmodium at the level of gene expression and highlight the need for a better understanding of the impacts of antimalarial agents on parasite transmission

Differential Plasmodium falciparum infection of Anopheles gambiae s.s. molecular and chromosomal forms in Mali

BACKGROUND: Anopheles gambiae sensu stricto (s.s.) is a primary vector of Plasmodium falciparum in sub-Saharan Africa. Although some physiological differences among molecular and chromosomal forms of this species have been demonstrated, the relative susceptibility to malaria parasite infection among them has not been unequivocally shown. The objective of this study was to investigate P. falciparum circumsporozoite protein infection (CSP) positivity among An. gambiae s.s. chromosomal and molecular forms. METHODS: Wild An. gambiae from two sites Kela (n = 464) and Sidarebougou (n = 266) in Mali were screened for the presence of P. falciparum CSP using an enzyme-linked immunosorbent assay (ELISA). Samples were then identified to molecular form using multiple PCR diagnostics (n = 713) and chromosomal form using chromosomal karyotyping (n = 419). RESULTS: Of 730 An. gambiae sensu lato (s.l.) mosquitoes, 89 (12.2%) were CSP ELISA positive. The percentage of positive mosquitoes varied by site: 52 (11.2%) in Kela and 37 (13.9%) in Sidarebougou. Eighty-seven of the positive mosquitoes were identified to molecular form and they consisted of nine Anopheles arabiensis (21.4%), 46 S (10.9%), 31 M (12.8%), and one MS hybrid (14.3%). Sixty of the positive mosquitoes were identified to chromosomal form and they consisted of five An. arabiensis (20.0%), 21 Savanna (15.1%), 21 Mopti (30.4%), 11 Bamako (9.2%), and two hybrids (20.0%). DISCUSSION: In this collection, the prevalence of P. falciparum infection in the M form was equivalent to infection in the S form (no molecular form differential infection). There was a significant differential infection by chromosomal form such that, P. falciparum infection was more prevalent in the Mopti chromosomal forms than in the Bamako or Savanna forms; the Mopti form was also the most underrepresented in the collection. Continued research on the differential P. falciparum infection of An. gambiae s.s. chromosomal and molecular forms may suggest that Plasmodium – An. gambiae interactions play a role in malaria transmission

U(2)_{L}\times U(2)_{R} Chiral Theory of Mesons

A $U(2)_{L}\times U(2)_{R}$ chiral theory of pseudoscalar, vector, and axial-vector mesons has been proposed. VMD has been revealed from this theory. The physical processes of normal parity and abnormal parity have been studied by using the same lagrangian and the universality of coupling has been revealed. Two new mass relations between vector and axial-vector mesons have been found. Weinberg's first sum rule and new relations about the amplitude of $a_{1}$ decay are satisfied. KSFR sum rule is satisfied pretty well. The $\rho$ pole in pion form factor has been achieved. The theoretical results of $\rho\rightarrow\pi\pi$, $\omega\rightarrow \pi\pi$, $a_{1}\rightarrow\rho\pi$ and $\pi\gamma$, $\tau\rightarrow \rho\nu$, $\tau\rightarrow a_{1}\nu$, $\pi^{0}\rightarrow \gamma\gamma$, $\omega \rightarrow\pi\gamma$, $\rho\rightarrow\pi\gamma$, $f_{1} \rightarrow\rho\pi\pi$, $f_{1}\rightarrow\eta\pi\pi$, $\rho\rightarrow\eta\gamma$, $\omega \rightarrow\eta\gamma$ are in good agreement with data. Weinberg's $\pi\pi$ scattering lengths and slopes and $a^{0}_{2}$, $a^{2}_{2}$, and $b^{1}_{1}$ have been obtained. Especially, the $\rho$ resonance in the amplitude $T^{1}_{1}$ of $\pi\pi$ scattering has been revealed from this theory. Two coefficients of chiral perturbation theory have been determined and they are close to the values used by chiral perturbation theory.Comment: 55 pages, send e-mail to [email protected] to get the figur

Conserved Mosquito/Parasite Interactions Affect Development of Plasmodium falciparum in Africa

In much of sub-Saharan Africa, the mosquito Anopheles gambiae is the main vector of the major human malaria parasite, Plasmodium falciparum. Convenient laboratory studies have identified mosquito genes that affect positively or negatively the developmental cycle of the model rodent parasite, P. berghei. Here, we use transcription profiling and reverse genetics to explore whether five disparate mosquito gene regulators of P. berghei development are also pertinent to A. gambiae/P. falciparum interactions in semi-natural conditions, using field isolates of this parasite and geographically related mosquitoes. We detected broadly similar albeit not identical transcriptional responses of these genes to the two parasite species. Gene silencing established that two genes affect similarly both parasites: infections are hindered by the intracellular local activator of actin cytoskeleton dynamics, WASP, but promoted by the hemolymph lipid transporter, ApoII/I. Since P. berghei is not a natural parasite of A. gambiae, these data suggest that the effects of these genes have not been drastically altered by constant interaction and co-evolution of A. gambiae and P. falciparum; this conclusion allowed us to investigate further the mode of action of these two genes in the laboratory model system using a suite of genetic tools and infection assays. We showed that both genes act at the level of midgut invasion during the parasite's developmental transition from ookinete to oocyst. ApoII/I also affects the early stages of oocyst development. These are the first mosquito genes whose significant effects on P. falciparum field isolates have been established by direct experimentation. Importantly, they validate for semi-field human malaria transmission the concept of parasite antagonists and agonists