Use of fluorescent nanoparticles to investigate nutrient acquisition by developing Eimeria maxima macrogametocytes

The enteric disease coccidiosis, caused by the unicellular parasite Eimeria, is a major and reoccurring problem for the poultry industry. While the molecular machinery driving host cell invasion and oocyst wall formation has been well documented in Eimeria, relatively little is known about the host cell modifications which lead to acquisition of nutrients and parasite growth. In order to understand the mechanism(s) by which nutrients are acquired by developing intracellular gametocytes and oocysts, we have performed uptake experiments using polystyrene nanoparticles (NPs) of 40 nm and 100 nm in size, as model NPs typical of organic macromolecules. Cytochalasin D and nocodazole were used to inhibit, respectively, the polymerization of the actin and microtubules. The results indicated that NPs entered the parasite at all stages of macrogametocyte development and early oocyst maturation via an active energy dependent process. Interestingly, the smaller NPs were found throughout the parasite cytoplasm, while the larger NPs were mainly localised to the lumen of large type 1 wall forming body organelles. NP uptake was reduced after microfilament disruption and treatment with nocodazole. These observations suggest that E. maxima parasites utilize at least 2 or more uptake pathways to internalize exogenous material during the sexual stages of development

Proposal for reading out anyon qubits in non-abelian ν=12/5\nu = 12/5 quantum Hall state

To detect non-abelian statistics in the $\nu = 12/5$ quantum Hall state through interferometry, we apply an analysis similar to the ones proposed for the non-abelian $\nu = 5/2$ quantum Hall state. The result is that the amplitude of the Aharonov-Bohm oscillation of this interference is dependent on the internal states of quasiholes, but, in contrast to the $\nu = 5/2$ quantum Hall state, independent of the number of quasiholes. However, if the quasiholes are in a superposition state, it is necessary for the interferometer to have certain additional features to obtain the coefficients.Comment: 16 pages, 2 figures, Latex. Reference added, some errors corrected, some content changed, some changes in the abstrac

Spectroscopic characterization of highly doped ZnO films grown by atomic-layer deposition for three-dimensional infrared metamaterials

We systematically study the optical spectra of ZnO grown by atomic-layer deposition as a function of Al (and Ti) doping concentration. The spectra measured on films are well described by fits using a Drude free-electron model. The derived plasma frequencies are consistent with the expected amount of doping and can be continuously and controllably tuned from small values to about 400 THz. The losses (damping) are also quantified. In addition, we achieve smooth conformal coatings of three-dimensional polymer templates made by direct laser writing. Altogether, Al:ZnO appears as an attractive "tunable metal" for three-dimensional infrared metamaterials or transformation-optics architectures

Whole body and hepatic insulin action in normal, starved, and diabetic rats

In normal (N), 3-days starved (S), and streptozotocin-treated (65 mg/kg) 3-days diabetic (D) rats we examined the in vivo dose-response relationship between plasma insulin levels vs. whole body glucose uptake (BGU) and inhibition of hepatic glucose production (HGP) in conscious rats, as determined with the four-step sequential hyperinsulinemic euglycemic clamp technique, combined with [3-3H]glucose infusion. Twelve-hour fasting (basal) HGP was 3.0 +/- 0.2, 2.1 +/- 0.2, and 5.4 +/- 0.5 mg/min in N, S, and D rats, respectively. Next, all rats were clamped at matched glycemia (6 mM). Lowering plasma glucose in D rats from +/- 20 to 6.0 mM did not increase plasma norepinephrine, epinephrine, glucagon, and corticosterone levels. For BGU, insulin sensitivity was increased (70 +/- 11 microU/ml) in S and unchanged (113 +/- 21 microU/ml) in D compared with N rats (105 +/- 10 microU/ml). Insulin responsiveness was unchanged (12.4 +/- 0.8 mg/min) in S and decreased (8.5 +/- 0.8 mg/min) in D compared with N rats (12.3 +/- 0.7 mg/min). For HGP, insulin sensitivity was unchanged (68 +/- 10 microU/ml) in S and decreased (157 +/- 21 microU/ml) in D compared with N rats (71 +/- 5 microU/ml). Insulin responsiveness was identical among N, S, and D rats (complete suppression of HGP). In summary, 1) insulin resistance in D rats is caused by hepatic insensitivity and by a reduction in BGU responsiveness. 2) S rats show normal hepatic insulin action, but insulin sensitivity for BGU is increased. Therefore, S and D rats both suffering from a comparable catabolic state (10-15% body wt loss in 3 days) show opposite effects on in vivo insulin action. This indicates that in vivo insulin resistance in D rats is not caused by the catabolic state per se

713-4 Inhibition of Vascular Superoxide Production in Hypercholesterolemic Rabbit Aorta by L-Arginine Contributes to Restored Endothelium-dependent Relaxation

Chronic oral administration of L-arginine (L-ARG) has been shown to enhance endothelial function in cholesterol (CHOL)-fed rabbits and to reduce atherogenesis. We investigated whether modulation of endogenous NO production (as assessed by urinary NO3-excretion) by L-ARG and the inhibitor of NO synthesis, L-NAME, affects vascular superoxide (O2-) production in hypercholesterolemic rabbits. Phorbol-myristate-acetate (PMA)-stimulated O2-production from isolated aortic rings was increased in rabbits given CHOL (+159±28%) or CHOL + L-NAME (+149±37%) as compared to controls (-22±7%), and endothelium-dependent relaxations by acetylcholine were diminished in both groups. In aortic rings from rabbits given CHOL + L-ARG, PMA-induced O2-production was restored to control levels (+14±17%; p<0.05), and endothelium-dependent cholinergic relaxations were also partly restored. Urinary NO3-excretion decreased in all animals fed a CHOL-enriched diet (p<0.01). As NO inactivated by O2-is also oxidized to NO3-, this indicates a decreased endothelial production of NO. NO3-excretion was further decreased by L-NAME (p<0.05 vs. CHOL), and partly restored by L-ARG (p<0.05). We conclude that both a decreased production of NO and an enhanced breakdown of NO by O2-contribute to the diminished biological activity of endothelial NO in hypercholesterolemia. L-ARG restores endothelial function by enhancing NO formation and by protecting NO from early breakdown by O2-

Flow equations for QED in the light front dynamics

The method of flow equations is applied to QED on the light front. Requiring that the partical number conserving terms in the Hamiltonian are considered to be diagonal and the other terms off-diagonal an effective Hamiltonian is obtained which reduces the positronium problem to a two-particle problem, since the particle number violating contributions are eliminated. No infrared divergencies appear. The ultraviolet renormalization can be performed simultaneously.Comment: 15 pages, Latex, 3 pictures, Submitted to Phys.Rev.

Restoring vascular nitric oxide formation by l-arginine improves the symptoms of intermittent claudication in patients with peripheral arterial occlusive disease

AbstractBackground. Administration of l-arginine improves nitric oxide (NO) formation and endothelium-dependent vasodilation in atherosclerotic patients.Objectives. We investigated in this double-blind, controlled study whether prolonged intermittent infusion therapy with l-arginine improves the clinical symptoms of patients with intermittent claudication, as compared with the endothelium-independent vasodilator prostaglandin E1, and control patients.Methods. Thirty-nine patients with intermittent claudication were randomly assigned to receive 2 × 8 g l-arginine/day, or 2 × 40 μg prostaglandin E1(PGE1)/day or no hemodynamically active treatment, for 3 weeks. The pain-free and absolute walking distances were assessed on a walking treadmill at 3 km/h, 12% slope, and NO-mediated, flow-induced vasodilation of the femoral artery was assessed by ultrasonography at baseline, at 1, 2 and 3 weeks of therapy and 6 weeks after the end of treatment. Urinary nitrate and cyclic guanosine-3′, 5′-monophosphate (GMP) were assessed as indices of endogenous NO production.Results. l-Arginine improved the pain-free walking distance by 230 ± 63% and the absolute walking distance by 155 ± 48% (each p < 0.05). Prostaglandin E1improved both parameters by 209 ± 63% and 144 ± 28%, respectively (each p < 0.05), whereas control patients experienced no significant change. l-Arginine therapy also improved endothelium-dependent vasodilation in the femoral artery, whereas PGE1had no such effect. There was a significant linear correlation between the l-arginine/asymmetric dimethylarginine (ADMA) ratio and the pain-free walking distance at baseline (r = 0.359, p < 0.03). l-Arginine treatment elevated the plasma l-arginine/ADMA ratio and increased urinary nitrate and cyclic GMP excretion rates, indicating normalized endogenous NO formation. Prostaglandin E1therapy had no significant effect on any of these parameters. Symptom scores assessed on a visual analog scale increased from 3.51 ± 0.18 to 8.3 ± 0.4 (l-arginine) and 7.0 ± 0.5 (PGE1; each p < 0.05), but did not significantly change in the control group (4.3 ± 0.4).Conclusions. Restoring NO formation and endothelium-dependent vasodilation by l-arginine improves the clinical symptoms of intermittent claudication in patients with peripheral arterial occlusive disease