Three-dimensional bottom diffraction in the North Pacific.

A significant aspect of bottom-interaction in deep water acoustic propagation, from point sources to point receivers, is the diffraction (or scattering) of energy from discrete seafloor locations along repeatable, deterministic paths in three-dimensions. These bottom-diffracted surface-reflected (BDSR) paths were first identified on the North Pacific acoustic laboratory experiment in 2004 (NPAL04) for a diffractor located on the side of a small seamount. On the adjacent deep seafloor, ambient noise and propagation in the ocean sound channel were sufficiently quiet that the BDSRs were the dominant arrival.

Added benefit of raxibacumab to antibiotic treatment of inhalational anthrax.

Although antibiotics treat bacteremia in inhalational anthrax, pathogenesis is mainly driven by bacterial exotoxins. Raxibacumab, an IgG1 monoclonal antibody, binds the protective antigen (PA) of Bacillus anthracis, thus blocking toxin effects and leading to improved survival in the rabbit and monkey models of inhalational anthrax. To assess raxibacumab's added benefit over levofloxacin (LVX) alone, rabbits surviving to 84 h after a challenge with 200 times the median (50%) lethal dose of B.

Deep seafloor arrivals in long range ocean acoustic propagation.

Ocean bottom seismometer observations at 5000 m depth during the long-range ocean acoustic propagation experiment in the North Pacific in 2004 show robust, coherent, late arrivals that are not readily explained by ocean acoustic propagation models. These "deep seafloor" arrivals are the largest amplitude arrivals on the vertical particle velocity channel for ranges from 500 to 3200 km. The travel times for six (of 16 observed) deep seafloor arrivals correspond to the sea surface reflection of an out-of-plane diffraction from a seamount that protrudes to about 4100 m depth and is about 18 km from the receivers.

Bacillus anthracis protective antigen kinetics in inhalation spore-challenged untreated or levofloxacin/ raxibacumab-treated New Zealand white rabbits.

Inhaled Bacillus anthracis spores germinate and the subsequent vegetative growth results in bacteremia and toxin production. Anthrax toxin is tripartite: the lethal factor and edema factor are enzymatic moieties, while the protective antigen (PA) binds to cell receptors and the enzymatic moieties. Antibiotics can control B.

Bottom interacting sound at 50 km range in a deep ocean environment.

Data collected during the 2004 Long-range Ocean Acoustic Propagation Experiment provide absolute intensities and travel times of acoustic pulses at ranges varying from 50 to 3200 km. In this paper a subset of these data is analyzed, focusing on the effects of seafloor reflections at the shortest transmission range of approximately 50 km. At this range bottom-reflected (BR) and surface-reflected, bottom-reflected energy interferes with refracted arrivals.

Protective antigen antibody augments hemodynamic support in anthrax lethal toxin shock in canines.

Background: Anthrax-associated shock is closely linked to lethal toxin (LT) release and is highly lethal despite conventional hemodynamic support. We investigated whether protective antigen-directed monoclonal antibody (PA-mAb) treatment further augments titrated hemodynamic support.

Methods And Results: Forty sedated, mechanically ventilated, instrumented canines challenged with anthrax LT were assigned to no treatment (controls), hemodynamic support alone (protocol-titrated fluids and norepinephrine), PA-mAb alone (administered at start of LT infusion [0 hours] or 9 or 12 hours later), or both, and observed for 96 hours.

Deep seafloor arrivals: an unexplained set of arrivals in long-range ocean acoustic propagation.

Receptions, from a ship-suspended source (in the band 50-100 Hz) to an ocean bottom seismometer (about 5000 m depth) and the deepest element on a vertical hydrophone array (about 750 m above the seafloor) that were acquired on the 2004 Long-Range Ocean Acoustic Propagation Experiment in the North Pacific Ocean, are described. The ranges varied from 50 to 3200 km. In addition to predicted ocean acoustic arrivals and deep shadow zone arrivals (leaking below turning points), "deep seafloor arrivals," that are dominant on the seafloor geophone but are absent or very weak on the hydrophone array, are observed.

Raxibacumab for the treatment of inhalational anthrax.

Background: Inhalational anthrax caused by Bacillus anthracis is associated with high mortality primarily due to toxin-mediated injury. Raxibacumab is a human IgG1lambda monoclonal antibody directed against protective antigen, a component of the anthrax toxin.

Methods: We evaluated the efficacy of raxibacumab as a prophylactic agent and after disease onset in a total of four randomized, placebo-controlled studies conducted in rabbits and monkeys.

Initial evaluation of a human immunoglobulin M monoclonal antibody (HA-1A) in humans.

A human monoclonal antibody (HA-1A) directed against bacterial endotoxin was administered to 15 patients with incurable malignant disease. No adverse effects were noted following single intravenous infusions of 0.05 to 100 mg.

Galactosamine-induced alpha 1-antitrypsin deficiency in rats. Alterations in plasma glycoproteins and alpha 1-antitrypsin carbohydrate composition.

Administration of D-galactosamine (GalNH2) is known to produce alterations in plasma glycoprotein levels, including alpha 1-antitrypsin. The authors have studied the effects of GalNH2 on circulating protein bound carbohydrates and on the plasma concentrations of two alpha 1-antiproteases, transferrin, IgG, and albumin in rats. The alpha 1-antiproteases from GalNH2-treated rats were isolated and their molecular weight, isoelectric point, and carbohydrate composition compared with those of control rat alpha 1-antiproteases.

Isolation and characterization of alpha 1-antitrypsin in PAS-positive hepatic granules from rats with experimental alpha 1-antitrypsin deficiency.

Chronic galactosamine (GalNH2) administration in rats decreases plasma alpha 1-antitrypsin (AAT) levels to 10-50% of control levels and induces the formation of diastase-resistant, PAS-positive granules, which contain AAT in hepatocytes. This report describes the isolation and purification of hepatic granule AAT by three different methods: solubilization with guanidine hydrochloride followed by gel filtration on Bio-gel A5M, extraction with methylamine and 2-chloroethanol, and solubilization with sodium dodecyl sulfate (SDS) followed by preparative SDS-polyacrylamide gel electrophoresis. All three methods yield a single protein which precipitates with anti-rat plasma AAT antibody, and which has an apparent molecular weight of 45,000 daltons, in contrast to the molecular weight of plasma AAT, 50,000 daltons.

Altered glycosidase activity in the liver of rats with galactosamine-induced alpha 1-antiprotease deficiency.

Previous studies have shown that chronic administration of D-galactosamine (GalNH2) in rats produces alpha 1-antiprotease (AAP) deficiency and causes accumulation of aberrantly glycosylated AAP in hepatic granules. In order to examine the disordered mechanism which produces this altered glycosylation, the activities of 6 glycosidases in liver homogenates of control and AAP-deficient rats were determined. GalNH2 treatment increases acid pH glycosidase activity, while it decreases intermediate pH alpha-mannosidase and alpha-glucosidase activities.

Vitamin A deficiency and serum or plasma fibronectin in the rat and in human subjects.

Fibronectin, a high-molecular-weight glycoprotein occurring in plasma and on the surface of many cells, is involved in cell adhesion and other cell-surface phenomena. Vitamin A deficiency in rats resulted in a threefold increase in the concentration of fibronectin in serum, as measured immunochemically. In vitamin A-depleted human subjects, on the other hand, no correlation could be found between plasma retinol and fibronectin levels.

Radioimmunoassay of a glycoprotein associated with malignancy.

A glycoprotein associated with malignancy was purified from the 0.6M perchloric acid-soluble fraction of serum obtained from cancer patients. The purified glycoprotein contained sialic acid, which was responsible for binding to wheat-germ agglutinin-Sepharose.

Retinoids and phorbol esters alter release of fibronectin from enucleated cells.

Addition of 12-tetradecanoylphorbol 13-acetate (TPA) to cultures of intact Swiss mouse 3T3 fibroblasts induced a dose-dependent increase in ornithine decarboxylase (OrnDCase) activity. Over the same concentration range, 10(-9) to 10(-6) M, TPA induced the release of radioactively labeled fibronectin (FN) from the cells into the culture medium. Retinoic acid, a derivative of vitamin A, inhibited in a dose-dependent manner both the increase in OrnDCase activity and the release of FN induced by TPA.