2,250 research outputs found
Summary of recent investigations of inlet flow distortion effect on engine stability
A review is presented of recent experimental results, analytical procedures and test techniques employed to evaluate the effects of inlet flow distortion on the stability characteristics of representative afterburning turbofan and turbojet compression systems. Circumferential distortions of pressure and temperature, separately and in combination are considered. Resulting engine sensitivity measurements are compared with predictions based on simplified parallel compressor models and with several distortion descriptor parameters
Birational cobordism invariance of uniruled symplectic manifolds
A symplectic manifold is called {\em (symplectically) uniruled}
if there is a nonzero genus zero GW invariant involving a point constraint. We
prove that symplectic uniruledness is invariant under symplectic blow-up and
blow-down. This theorem follows from a general Relative/Absolute correspondence
for a symplectic manifold together with a symplectic submanifold. A direct
consequence is that symplectic uniruledness is a symplectic birational
invariant. Here we use Guillemin and Sternberg's notion of cobordism as the
symplectic analogue of the birational equivalence.Comment: To appear in Invent. Mat
Strengthening the Cohomological Crepant Resolution Conjecture for Hilbert-Chow morphisms
Given any smooth toric surface S, we prove a SYM-HILB correspondence which
relates the 3-point, degree zero, extended Gromov-Witten invariants of the
n-fold symmetric product stack [Sym^n(S)] of S to the 3-point extremal
Gromov-Witten invariants of the Hilbert scheme Hilb^n(S) of n points on S. As
we do not specialize the values of the quantum parameters involved, this result
proves a strengthening of Ruan's Cohomological Crepant Resolution Conjecture
for the Hilbert-Chow morphism from Hilb^n(S) to Sym^n(S) and yields a method of
reconstructing the cup product for Hilb^n(S) from the orbifold invariants of
[Sym^n(S)].Comment: Revised versio
Orientifolds, Unoriented Instantons and Localization
We consider world-sheet instanton effects in N=1 string orientifolds of
noncompact toric Calabi-Yau threefolds. We show that unoriented closed string
topological amplitudes can be exactly computed using localization techniques
for holomorphic maps with involution. Our results are in precise agreement with
mirror symmetry and large N duality predictions.Comment: 25 pages, 10 figures, published version; v4: typos correcte
Anomalous layering at the liquid Sn surface
X-ray reflectivity measurements on the free surface of liquid Sn are
presented. They exhibit the high-angle peak, indicative of surface-induced
layering, also found for other pure liquid metals (Hg, Ga and In). However, a
low-angle peak, not hitherto observed for any pure liquid metal, is also found,
indicating the presence of a high-density surface layer. Fluorescence and
resonant reflectivity measurements rule out the assignment of this layer to
surface-segregation of impurities. The reflectivity is modelled well by a 10%
contraction of the spacing between the first and second atomic surface layers,
relative to that of subsequent layers. Possible reasons for this are discussed.Comment: 8 pages, 9 figures; to be submitted to Phys. Rev. B; updated
references, expanded discussio
High Gradients In Linear Collider Superconducting Accelerator cavities By high Pulsed Power To Suppress Field Emission
Gate-defined graphene double quantum dot and excited state spectroscopy
A double quantum dot is formed in a graphene nanoribbon device using three
top gates. These gates independently change the number of electrons on each dot
and tune the inter-dot coupling. Transport through excited states is observed
in the weakly coupled double dot regime. We extract from the measurements all
relevant capacitances of the double dot system, as well as the quantized level
spacing
The Effects of Malignant Transformation on Susceptibility of Human Urothelial Cells to CD40-Mediated Apoptosis
Background: The tumor necrosis factor (TNF) superfamily of ligands and receptors mediates immune cell survival. Some members possess a death domain, a protein motif that functions to transmit apoptotic signals, whereas others, such as CD40, do not. CD40 is expressed by both normal and malignant epithelial cells. To investigate the functional significance of this expression, we studied the effects of ligation of CD40, Fas, and TNF receptors (TNFRs) on the proliferation and survival of normal and malignant human urothelial cells and urothelial cells with disabled p53 function. Methods: Normal and malignant human urothelial cells were cultured with soluble TNF family agonists (CD40 ligand [CD40L], TNF-α, anti-Fas antibody, or cocultured with mouse fibroblasts stably transfected with plasmids that caused the cells to constitutively express CD40L or CD32; cell proliferation was estimated by an [3H]thymidine incorporation assay, and apoptosis was determined by Annexin V staining and by a DNA fragmentation assay. Messenger RNA levels for CD40 and potential downstream effector molecules were quantified by polymerase chain reaction-based and ribonuclease protection assays, respectively, and nuclear factor (NF) κB nuclear translocation was detected by immunofluorescence. All statistical tests were two-sided. Results: Soluble trimeric CD40L inhibited the growth of normal and malignant urothelial cells but did not induce apoptosis. Cell surface-presented CD40L induced massive apoptosis in CD40-positive transitional cell carcinoma cells but not in normal urothelial cells. Normal cells underwent CD40L-mediated apoptosis only in the presence of other TNFR agonists. An agonistic anti-CD40 antibody presented on the surface of CD32-transfected fibroblasts also induced apoptosis in transitional cell carcinoma cells and in normal urothelial cells. Apoptotic responses of tumor (but not normal) cells to soluble agonists were enhanced by blocking protein synthesis. Karyotypically normal urothelial cells with disabled p53 function underwent apoptosis during coculture with CD40L-expressing fibroblasts alone but were not additionally sensitive to additional TNFR agonists. Conclusions: Susceptibility to CD40 ligation-induced apoptosis may be a novel mechanism for eliminating neoplastically transformed urothelial cells. Loss of CD40 expression may be an important adaptive mechanism for transitional cell carcinoma development and progressio
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