Eccentric-orbit extreme-mass-ratio-inspiral radiation. II. 1PN correction to leading-logarithm and subleading-logarithm flux sequences and the entire perturbative 4PN flux

In a recent paper we showed that for eccentric-orbit extreme-mass-ratio inspirals the analytic forms of the leading-logarithm energy and angular momentum post-Newtonian (PN) flux terms (radiated to infinity) can, to arbitrary PN order, be determined by sums over the Fourier spectrum of the Newtonian quadrupole moment. We further showed that an essential part of the eccentricity dependence of the related subleading-logarithm PN sequences, at lowest order in the symmetric mass ratio ?, stems as well from the Newtonian quadrupole moment. Once that part is factored out, the remaining eccentricity dependence is more easily determined by black hole perturbation theory. In this paper we show how the sequences that are the 1PN corrections to the entire leading-logarithm series, namely terms that appear at PN orders x3k+1logk(x) and x3k+5/2logk(x) (for PN compactness parameter x and integers k=0), at lowest order in ?, are determined by the Fourier spectra of the Newtonian mass octupole, Newtonian current quadrupole, and 1PN part of the mass quadrupole moments. We also develop a conjectured (but plausible) form for 1PN correction to the leading logs at second order in ?. Further, in analogy to the first paper, we show that these same source multipole moments also yield nontrivial parts of the 1PN correction to the subleading-logarithm series, and that the remaining eccentricity dependence (at lowest order in ?) can then more easily be determined using black hole perturbation theory. We use this method to determine the entire analytic eccentricity dependence of the perturbative (i.e., lowest order in ?) 4PN nonlog terms, R4(et) and Z4(et), for energy and angular momentum respectively

Eccentric-orbit extreme-mass-ratio-inspiral radiation: Analytic forms of leading-logarithm and subleading-logarithm flux terms at high PN orders

We present new results on the analytic eccentricity dependence of several sequences of gravitational wave flux terms at high post-Newtonian (PN) order for extreme-mass-ratio inspirals. These sequences are the leading logarithms, which appear at PN orders x3klogk(x) and x3k+3/2logk(x) for integers k≥0 (x is a PN compactness parameter), and the subleading logarithms, which appear at orders x3klogk-1(x) and x3k+3/2logk-1(x) (k≥1), in both the energy and angular momentum radiated to infinity. For the energy flux leading logarithms, we show that to arbitrarily high PN order, their eccentricity dependence is determined by particular sums over the function g(n,et), derived from the Newtonian mass quadrupole moment, that normally gives the spectral content of the Peters-Mathews flux as a function of radial harmonic n. An analogous power spectrum g(n,et) determines the leading logarithms of the angular momentum flux. For subleading logs, the quadrupole power spectra are again shown to play a role, providing a distinguishable part of the eccentricity dependence of these flux terms to high PN order. With the quadrupole contribution understood, the remaining analytic eccentricity dependence of the subleading logs can, in principle, be determined more easily using black hole perturbation theory. We show this procedure in action, deriving the complete analytic structure of the x6log(x) subleading-log term and an analytic expansion of the x9/2 subleading log to high order in a power series in eccentricity. We discuss how these methods might be extended to other sequences of terms in the PN expansion involving logarithms

Administration of Endotoxin, Tumor Necrosis Factor, or Interleukin 1 to Rats Activates Skeletal Muscle Branched-Chain α-Keto Acid Dehydrogenase

Protein catabolic states (i.e., sepsis and trauma) are thought to be associated with accelerated oxidation of branched-chain amino acids (BCAA). Branched-chain α-keto acid dehydrogenase (BCKAD), the rate-limiting enzyme for BCAA oxidation by muscle, is regulated by phosphorylation/dephosphorylation. Skeletal muscle BCKAD was only 2-4% active in control rats. Intravenous injection of Salmonella enteritidis endotoxin (0.25-10 mg/kg) did not change total BCKAI) activity, but increased the percent active enzyme in muscle three- to four-fold in 4-6 h. Identical results were observed in adrenalectomized rats pretreated with one dose of α-methylprednisolone (2.5 mg/kg i.p.) 30-60 min before saline or endotoxin injection, indicating that endotoxin\u27s effect was not mediated by hypersecretion of adrenal hormones. Cortisone pretreatment of normal rats (100 mg/kg per d) for 2 d prevented endotoxin-induced activation of muscle BCKAD, suggesting that endogenous secretion products mediated BCKAD activation by endotoxin. Human recombinant tumor necrosis factor-α and/or IL-1β or α (50 μg/kg) increased muscle BCKAD activation two- to fourfold in normal rats 4-6 h after intravenous injection. We conclude that cytokine-mediated activation of muscle BCKAD may contribute to accelerated BCAA oxidation in septicemia

Bio-inspired artemether-loaded human serum albumin nanoparticles for effective control of malaria-infected erythrocytes

Aim: The intra-erythrocytic development of the malarial parasite is dependent on active uptake of nutrients, including human serum albumin (HSA), into parasitized red blood cells (pRBCs). We have designed HSA-based nanoparticles as a potential drug-delivery option for antimalarials. Methods: Artemether-loaded nanoparticles (AANs) were designed and antimalarial activity evaluated in vitro/in vivo using Plasmodium falciparum/Plasmodium berghei species, respectively. Results: Selective internalization of AAN into Plasmodium-infected RBCs in preference to healthy erythrocytes was observed using confocal imaging. In vitro studies showed 50% dose reduction for AAN as compared with drug-only controls to achieve IC50 levels of inhibition. The nanoparticles exhibited twofold higher peak drug concentrations in RBCs with antimalarial activity at 50% of therapeutic doses in P. bergei infected mice. Conclusion: Novel HSA-based nanoparticles offer safe and effective approach for selective targeting of antimalarial drugs

Familial Behçet‐like autoinflammatory disease‐3 (AIFBL3), caused by heterozygous mutation in the rela gene: a case report

Introduction: The autoinflammatory features of Behçet’s disease (BD) and the role of innate immunity dysregulation have been highlighted and BD can be considered as the crossroad of autoinflammatory and autoimmune diseases. Objectives: We describe the case of a 9-year-old caucasic male, who presented at age 6 y with recurrent episodes of fever, oral ulcers and pain at the limbs, hands, wrists. At the physical examination the child showed functional limitation of flexion and extension movements of the wrists (left > right) and a bilateral mild joint stiffness of the shoulders. He showed a mild delay in the stages of psychomotor development, and a mild hypotrophy of the muscles of the lower limbs. Methods: The metabolic disease expert excluded metabolic diseases, based on the metabolic diagnostic investigations. Ultrasound documented knees joint effusion in the lateral supra-patellar seat with synovial membrane’s thickening and evident right knee synovial phlogosis, minimal on the left. A Whole body MRI, reported intra joint fluid effusion in external lateral seat and in sub patellar seat of the left knee. Intraspongious edema of the cuboid of the right foot. The eye examination with slit lamp was normal; HLA-B27, Anti-streptolysin O titer, pharyngeal swab and specific serologies for infectious diseases were negative. Fecal calprotectin was normal. Antinuclear antibodies (ANA) were positive 1:320 with a granular pattern. Results: The genetic study in NGS for autoinflammatory diseases revealed a heterozygous mutation, defined as VUS, of the RELA gene: c.1537C>G (p.Pro513Ala). Mutations of the RELA gene are associated with a familiar autoinflammatory disease Behçet’s disease (BD)-like type 3, with an autosomal dominant transmission. The Familial Behçet-like autoinflammatory disease-3 (AIFBL3), caused by heterozygous mutation in the RELA gene on chromosome 11q13, is characterized predominantly by chronic mucocutaneous ulceration. Conclusion: The patient did not yet fulfil the paediatric BD (PEDBD) nor ICBD criteria for the diagnosis of paediatric BD, however it is well described that BD is an evolutionary disease, and clinical manifestations may appear over the years (1-3). Monogenic BD-like conditions are increasingly recognized and to date have been found to predominantly involve loss-of-function variants in TNFAIP3. This case describes a child carrying the RELA gene mutation, with clinical symptoms evoking BD. The RELA gene mutations are conditions related to dysregulated NF-κB activation and need a strict follow-up and a prompt start of treatment, also in patients who do not fulfil the diagnostic criteria for BD

Trace-Level Detection of Atrazine Using Immuno-Chemiluminescence: Dipstick and Automated Flow Injection Analyses Formats

A sensitive chemiluminescence (CL)-based immunoassay technique based on both dipstick and flow injection analytical formats is reported for the detection of atrazine. In the dipstick-based immunoassay technique, antibody (anti-atrazine) was first immobilized on the nitrocellulose membranes. The dipstick was then treated with atrazine and atrazine-horseradish peroxidase conjugate (atra-HRP) to facilitate the competitive binding. The dipstick was further treated with urea-hydrogen peroxide (U-H2O2) and luminol to generate photons. The number of photons generated was inversely proportional to the atrazine concentration. In the flow injection analysis (FIA) format, the antibody was immobilized on protein-A sepharose matrix and packed in a glass capillary column, which functioned as an immunoreactor. Competitive binding of antigen and antibody occurred. The CL signals generated during the biochemical reactions were correlated with atrazine concentrations in the analytical samples. By using dipstick technique, it was possible to detect atrazine concentration down to 0.1 ng/mL; with the FIA format, the detection of atrazine was down to 0.01 ng/mL