Polarization control of metal-enhanced fluorescence in hybrid assemblies of photosynthetic complexes and gold nanorods

Fluorescence imaging of hybrid nanostructures composed of a bacterial light-harvesting complex LH2 and Au nanorods with controlled coupling strength is employed to study the spectral dependence of the plasmon-induced fluorescence enhancement. Perfect matching of the plasmon resonances in the nanorods with the absorption bands of the LH2 complexes facilitates a direct comparison of the enhancement factors for longitudinal and transverse plasmon frequencies of the nanorods. We find that the fluorescence enhancement due to excitation of longitudinal resonance can be up to five-fold stronger than for the transverse one. We attribute this result, which is important for designing plasmonic functional systems, to a very different distribution of the enhancement of the electric field due to the excitation of the two characteristic plasmon modes in nanorods

Forward Neutron Production at the Fermilab Main Injector

We have measured cross sections for forward neutron production from a variety of targets using proton beams from the Fermilab Main Injector. Measurements were performed for proton beam momenta of 58 GeV/c, 84 GeV/c, and 120 GeV/c. The cross section dependence on the atomic weight (A) of the targets was found to vary as $A^(alpha)$ where $\alpha$ is $0.46\pm0.06$ for a beam momentum of 58 GeV/c and 0.54$\pm$0.05 for 120 GeV/c. The cross sections show reasonable agreement with FLUKA and DPMJET Monte Carlos. Comparisons have also been made with the LAQGSM Monte Carlo.Comment: Accepted for publication in Physical Review D. This version incorporates small changes suggested by referee and small corrections in the neutron production cross sections predicted by FLUK

The Cyst-Theca Relationship Of The Dinoflagellate Cyst Trinovantedinium Pallidifulvum, With Erection Of Protoperidinium Lousianensis Sp Nov And Their Phylogenetic Position Within The Conica Group

We establish the cyst-theca relationship of the dinoflagellate cyst species Trinovantedinium pallidifulvum Matsuoka 1987 based on germination experiments of specimens isolated from the Gulf of Mexico. We show that the motile stage is a new species, designated as Protoperidinium louisianensis. We also determine its phylogenetic position based on single-cell polymerase chain reaction (PCR) of a single cell germinated from the Gulf of Mexico cysts. To further refine the phylogeny, we determined the large subunit (LSU) sequence through single-cell PCR of the cyst Selenopemphix undulata isolated from Brentwood Bay (Saanich Inlet, BC, Canada). The phylogeny shows that P. louisianensis is closest to P. shanghaiense, the motile stage of T. applanatum, and is consistent with the monophyly of the genus Trinovantedinium. Selenopemphix undulata belongs to a different clade than Selenopemphix quanta (alleged cyst of P. conicum), suggesting that the genus Selenopemphix is polyphyletic. Trinovantedinium pallidifulvum is widely distributed with occurrences in the Gulf of Mexico, the North Atlantic, the northeast Pacific and southeast Asia. In addition, we illustrate the two other extant species, Trinovantedinium applanatum and Trinovantedinium variabile, and two morphotypes of Trinovantedinium. Geochemical analyses of the cyst wall of T. pallidifulvum indicate the presence of amide groups in agreement with other heterotrophic dinoflagellate species, although the cyst wall of T. pallidifulvum also includes some unique features

Alterations in the Interleukin-1/Interleukin-1 Receptor Antagonist Balance Modulate Cardiac Remodeling following Myocardial Infarction in the Mouse

Background Healing after acute myocardial infarction (AMI) is characterized by an intense inflammatory response and increased Interleukin-1 (IL-1) tissue activity. Genetically engineered mice lacking the IL-1 receptor (IL-1R1-/-, not responsive to IL-1) or the IL-1 receptor antagonist (IL-1Ra, enhanced response to IL-1) have an altered IL-1/IL-1Ra balance that we hypothesize modulates infarct healing and cardiac remodeling after AMI. Methods IL-1R1-/- and IL-1Ra-/- male mice and their correspondent wild-types (WT) were subjected to permanent coronary artery ligation or sham surgery. Infarct size (trichrome scar size), apoptotic cell death (TUNEL) and left ventricular (LV) dimensions and function (echocardiography) were measured prior to and 7 days after surgery. Results When compared with the corresponding WT, IL-1R1-/- mice had significantly smaller infarcts (−25%), less cardiomyocyte apoptosis (−50%), and reduced LV enlargement (LV end-diastolic diameter increase [LVEDD], −20%) and dysfunction (LV ejection fraction [LVEF] decrease, −50%), whereas IL-1Ra-/- mice had significantly larger infarcts (+75%), more apoptosis (5-fold increase), and more severe LV enlargement (LVEDD increase,+30%) and dysfunction (LVEF decrease, +70%)(all P values \u3c0.05). Conclusions An imbalance in IL-1/IL-1Ra signaling at the IL-1R1 level modulates the severity of cardiac remodeling after AMI in the mouse, with reduced IL-1R1 signaling providing protection and unopposed IL-1R1 signaling providing harm

Bactericidal activity of human eosinophilic granulocytes against Escherichia coli

Eosinophils participate in allergic inflammation and may have roles in the bodys defense against helminthic infestation. Even under noninflammatory conditions, eosinophils are present in the mucosa of the large intestine, where large numbers of gram-negative bacteria reside. Therefore, roles for eosinophils in host defenses against bacterial invasion are possible. In a system for bacterial viable counts, the bactericidal activity of eosinophils and the contribution of different cellular antibacterial systems against Escherichia coli were investigated. Eosinophils showed a rapid and efficient killing of E. coli under aerobic conditions, whereas under anaerobic conditions bacterial killing decreased dramatically. In addition, diphenylene iodonium chloride (DPI), an inhibitor of the NADPH oxidase and thereby of superoxide production, also significantly inhibited bacterial killing. The inhibitor of nitric oxide (NO) production L-N5-(1-iminoethyl)-ornithine dihydrochloride did not affect the killing efficiency, suggesting that NO or derivatives thereof are of minor importance under the experimental conditions used. To investigate the involvement of superoxide and eosinophil peroxidase (EPO) in bacterial killing, EPO was blocked by azide. The rate of E. coli killing decreased significantly in the presence of azide, whereas addition of DPI did not further decrease the killing, suggesting that superoxide acts in conjunction with EPO. Bactericidal activity was seen in eosinophil extracts containing granule proteins, indicating that oxygen-independent killing may be of importance as well. The findings suggest that eosinophils can participate in host defense against gram-negative bacterial invasion and that oxygen-dependent killing, i.e., superoxide acting in conjunction with EPO, may be the most important bactericidal effector function of these cells

Chymase-Dependent Generation of Angiotensin II from Angiotensin-(1-12) in Human Atrial Tissue

Since angiotensin-(1-12) [Ang-(1-12)] is a non-renin dependent alternate precursor for the generation of cardiac Ang peptides in rat tissue, we investigated the metabolism of Ang-(1-12) by plasma membranes (PM) isolated from human atrial appendage tissue from nine patients undergoing cardiac surgery for primary control of atrial fibrillation (MAZE surgical procedure). PM was incubated with highly purified 125I-Ang-(1-12) at 37°C for 1 h with or without renin-angiotensin system (RAS) inhibitors [lisinopril for angiotensin converting enzyme (ACE), SCH39370 for neprilysin (NEP), MLN-4760 for ACE2 and chymostatin for chymase; 50 µM each]. 125I-Ang peptide fractions were identified by HPLC coupled to an inline γ-detector. In the absence of all RAS inhibitor, 125I-Ang-(1-12) was converted into Ang I (2±2%), Ang II (69±21%), Ang-(1-7) (5±2%), and Ang-(1-4) (2±1%). In the absence of all RAS inhibitor, only 22±10% of 125I-Ang-(1-12) was unmetabolized, whereas, in the presence of the all RAS inhibitors, 98±7% of 125I-Ang-(1-12) remained intact. The relative contribution of selective inhibition of ACE and chymase enzyme showed that 125I-Ang-(1-12) was primarily converted into Ang II (65±18%) by chymase while its hydrolysis into Ang II by ACE was significantly lower or undetectable. The activity of individual enzyme was calculated based on the amount of Ang II formation. These results showed very high chymase-mediated Ang II formation (28±3.1 fmol×min−1×mg−1, n = 9) from 125I-Ang-(1-12) and very low or undetectable Ang II formation by ACE (1.1±0.2 fmol×min−1×mg−1). Paralleling these findings, these tissues showed significant content of chymase protein that by immunocytochemistry were primarily localized in atrial cardiac myocytes. In conclusion, we demonstrate for the first time in human cardiac tissue a dominant role of cardiac chymase in the formation of Ang II from Ang-(1-12)