168 research outputs found
A high-precision polarimeter
We have built a polarimeter in order to measure the electron beam
polarization in hall C at JLAB. Using a superconducting solenoid to drive the
pure-iron target foil into saturation, and a symmetrical setup to detect the
Moller electrons in coincidence, we achieve an accuracy of <1%. This sets a new
standard for Moller polarimeters.Comment: 17 pages, 9 figures, submitted to N.I.
Final State Interaction Effects in pol 3He(pol e,e'p)
Asymmetries in quasi-elastic pol 3He(pol e,e'p) have been measured at a
momentum transfer of 0.67 (GeV/c)^2 and are compared to a calculation which
takes into account relativistic kinematics in the final state and a
relativistic one-body current operator. With an exact solution of the Faddeev
equation for the 3He-ground state and an approximate treatment of final state
interactions in the continuum good agreement is found with the experimental
data.Comment: 11 pages, 6 figures, submitted to Phys. Lett. B, revised version,
sensitivity study to relativity and NN-potential adde
Systematic Evaluation of Nanomaterial Toxicity: Utility of Standardized Materials and Rapid Assays
Measurement of the Electric Form Factor of the Neutron at Q^2=0.5 and 1.0 (GeV/c)^2
The electric form factor of the neutron was determined from measurements of
the \vec{d}(\vec{e},e' n)p reaction for quasielastic kinematics. Polarized
electrons were scattered off a polarized deuterated ammonia target in which the
deuteron polarization was perpendicular to the momentum transfer. The scattered
electrons were detected in a magnetic spectrometer in coincidence with neutrons
in a large solid angle detector. We find G_E^n = 0.0526 +/- 0.0033 (stat) +/-
0.0026 (sys) and 0.0454 +/- 0.0054 +/- 0.0037 at Q^2 = 0.5 and 1.0 (GeV/c)^2,
respectively.Comment: 5 pages, 2 figures, as publishe
The neutron charge form factor and target analyzing powers from 3He(e, e\u27n) scattering
The charge form factor of the neutron has been determined from asymmetries measured in quasi-elastic 3He(e, e\u27n) at a momentum transfer of 0.67 (GeV/c)2. In addition, the target analyzing power, Ayo, has been measured to study effects of final state interactions and meson exchange currents
Phagocytosis and digestion of pH-sensitive fluorescent dye (Eos-FP) transfected E. coli in whole blood assays from patients with severe sepsis and septic shock
The function of phagocytic and antigen presenting cells is of crucial importance to sustain immune competence against infectious agents as well as malignancies. We here describe a reproducible procedure for the quantification of phagocytosis by leukocytes in whole blood. For this, a pH-sensitive green-fluorescent protein- (GFP) like dye (Eos-FP) is transfected into infectious microroganisms. After UV-irradiation, the transfected bacteria emit green (≈5160 nm) and red (≈581 nm) fluorescent light at 490 nm excitation. Since the red fluorescent light is sensitive to acidic pH, the phagocytosed bacteria stop emitting red fluorescent light as soon as the phagosomes fuse with lysosomes. The green fluorescence is maintained in the phagolysosome until pathogen degradation is completed. Fluorescence emission can be followed by flow cytometry with filter settings documenting fluorescence 1 (FL 1, FITC) and fluorescence 2 (FL 2, phycoerythrin, PE). Eos-FP transfected bacteria can also be traced within phagocytes using microscopical techniques. A standardized assay has been developed which is suitable for clinical studies by providing clinicians with syringes pre-filled with fixed and appropriately UV-irradiated Eos-FP E. coli (TruCulture™). After adding blood or body fluids to these containers and starting the incubation at 37°C, phagocytosis by granulocytes proceeds over time. Cultures can be terminated at a given time by lysing red blood cells followed by flow cytometry. A pilot study demonstrated that Eos-FP E. coli phagocytosis and digestion was up-regulated in the majority of patients with either severe sepsis or septic shock as compared to healthy donors (p < 0.0001 after o/n incubation). Following treatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) in selected patients with sepsis, phagolysosome fusion appeared to be accelerated
Two distinct fluorescent quantum clusters of gold starting from metallic nanoparticles by pH-dependent ligand etching
Nasopharyngeal Bacterial Colonization and Gene Polymorphisms of Mannose-Binding Lectin and Toll-Like Receptors 2 and 4 in Infants
BACKGROUND: Human nasopharynx is often colonized by potentially pathogenic bacteria. Gene polymorphisms in mannose-binding lectin (MBL), toll-like receptor (TLR) 2 and TLR4 have been reported. The present study aimed to investigate possible association between nasopharyngeal bacterial colonization and gene polymorphisms of MBL, TLR2 and TLR4 in healthy infants. METHODOLOGY/PRINCIPAL FINDINGS: From August 2008 to June 2010, 489 nasopharyngeal swabs and 412 blood samples were taken from 3-month-old healthy Finnish infants. Semi-quantitative culture was performed and pyrosequencing was used for detection of polymorphisms in MBL structural gene at codons 52, 54, and 57, TLR2 Arg753Gln and TLR4 Asp299Gly. Fifty-nine percent of subjects were culture positive for at least one of the four species: 11% for Streptococcus pneumoniae, 23% for Moraxella catarrhalis, 1% for Haemophilus influenzae and 25% for Staphylococcus aureus. Thirty-two percent of subjects had variant types in MBL, 5% had polymorphism of TLR2, and 18% had polymorphism of TLR4. Colonization rates of S. pneumoniae and S. aureus were significantly higher in infants with variant types of MBL than those with wild type (p = .011 and p = .024). Colonization rates of S. aureus and M. catarrhalis were significantly higher in infants with polymorphisms of TLR2 and of TLR4 than those without (p = .027 and p = .002). CONCLUSIONS: Our study suggests that there is an association between nasopharyngeal bacterial colonization and genetic variation of MBL, TLR2 and TLR4 in young infants. This finding supports a role for these genetic variations in susceptibility of children to respiratory infections
Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury
Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis
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