505 research outputs found
Cavity QED with a Bose-Einstein condensate
Cavity quantum electrodynamics (cavity QED) describes the coherent
interaction between matter and an electromagnetic field confined within a
resonator structure, and is providing a useful platform for developing concepts
in quantum information processing. By using high-quality resonators, a strong
coupling regime can be reached experimentally in which atoms coherently
exchange a photon with a single light-field mode many times before dissipation
sets in. This has led to fundamental studies with both microwave and optical
resonators. To meet the challenges posed by quantum state engineering and
quantum information processing, recent experiments have focused on laser
cooling and trapping of atoms inside an optical cavity. However, the tremendous
degree of control over atomic gases achieved with Bose-Einstein condensation
has so far not been used for cavity QED. Here we achieve the strong coupling of
a Bose-Einstein condensate to the quantized field of an ultrahigh-finesse
optical cavity and present a measurement of its eigenenergy spectrum. This is a
conceptually new regime of cavity QED, in which all atoms occupy a single mode
of a matter-wave field and couple identically to the light field, sharing a
single excitation. This opens possibilities ranging from quantum communication
to a wealth of new phenomena that can be expected in the many-body physics of
quantum gases with cavity-mediated interactions.Comment: 6 pages, 4 figures; version accepted for publication in Nature;
updated Fig. 4; changed atom numbers due to new calibratio
Falkner-Skan Flow Over a Wedge with Slip Boundary Conditions
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76718/1/AIAA-2009-476-210.pd
Bacterial porin disrupts mitochondrial membrane potential and sensitizes host cells to apoptosis
The bacterial PorB porin, an ATP-binding beta-barrel protein of pathogenic Neisseria gonorrhoeae, triggers host cell apoptosis by an unknown mechanism. PorB is targeted to and imported by host cell mitochondria, causing the breakdown of the mitochondrial membrane potential (delta psi m). Here, we show that PorB induces the condensation of the mitochondrial matrix and the loss of cristae structures, sensitizing cells to the induction of apoptosis via signaling pathways activated by BH3-only proteins. PorB is imported into mitochondria through the general translocase TOM but, unexpectedly, is not recognized by the SAM sorting machinery, usually required for the assembly of beta-barrel proteins in the mitochondrial outer membrane. PorB integrates into the mitochondrial inner membrane, leading to the breakdown of delta psi m. The PorB channel is regulated by nucleotides and an isogenic PorB mutant defective in ATP-binding failed to induce delta psi m loss and apoptosis, demonstrating that dissipation of delta psi m is a requirement for cell death caused by neisserial infection
Intracellular Serotonin Modulates Insulin Secretion from Pancreatic β-Cells by Protein Serotonylation
Non-neuronal, peripheral serotonin deficiency causes diabetes mellitus and identifies an intracellular role for serotonin in the regulation of insulin secretion
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