1,980 research outputs found
(1S*,5R*)-9-Phenyl-9-azaΒbicycloΒ[3.3.1]nonan-3-one
In the title compound, C14H17NO, the piperidinone and piperidine rings both adopt a chair conformation. The chiral crystals were obtained from a racemic reaction product via spontaneous resolution
One-step implementation of multi-qubit conditional phase gating with nitrogen-vacancy centers coupled to a high-Q silica microsphere cavity
The diamond nitrogen-vacancy (NV) center is an excellent candidate for
quantum information processing, whereas entangling separate NV centers is still
of great experimental challenge. We propose an one-step conditional phase flip
with three NV centers coupled to a whispering-gallery mode cavity by virtue of
the Raman transition and smart qubit encoding. As decoherence is much
suppressed, our scheme could work for more qubits. The experimental feasibility
is justified.Comment: 3 pages, 2 figures, Accepted by Appl. Phys. Let
Complete PHB mobilization in Escherichia coli enhances the stress tolerance: a potential biotechnological application
<p>Abstract</p> <p>Background</p> <p>Poly-<it>Ξ²</it>-hydroxybutyrate (PHB) mobilization in bacteria has been proposed as a mechanism that can benefit their host for survival under stress conditions. Here we reported for the first time that a stress-induced system enabled <it>E. coli</it>, a non-PHB producer, to mobilize PHB <it>in vivo </it>by mimicking natural PHB accumulation bacteria.</p> <p>Results</p> <p>The successful expression of PHB biosynthesis and PHB depolymerase genes in <it>E. coli </it>was confirmed by PHB production and 3-hydroxybutyrate secretion. Starvation experiment demonstrated that the complete PHB mobilization system in <it>E. coli </it>served as an intracellular energy and carbon storage system, which increased the survival rate of the host when carbon resources were limited. Stress tolerance experiment indicated that <it>E. coli </it>strains with PHB production and mobilization system exhibited an enhanced stress resistance capability.</p> <p>Conclusion</p> <p>This engineered <it>E. coli </it>with PHB mobilization has a potential biotechnological application as immobilized cell factories for biocatalysis and biotransformation.</p
Ryanodine receptors contribute to the induction of nociceptive input-evoked long-term potentiation in the rat spinal cord slice
<p>Abstract</p> <p>Background</p> <p>Our previous study demonstrated that nitric oxide (NO) contributes to long-term potentiation (LTP) of C-fiber-evoked field potentials by tetanic stimulation of the sciatic nerve in the spinal cord <it>in vivo</it>. Ryanodine receptor (RyR) is a downstream target for NO. The present study further explored the role of RyR in synaptic plasticity of the spinal pain pathway.</p> <p>Results</p> <p>By means of field potential recordings in the adult male rat <it>in vivo</it>, we showed that RyR antagonist reduced LTP of C-fiber-evoked responses in the spinal dorsal horn by tetanic stimulation of the sciatic nerve. Using spinal cord slice preparations and field potential recordings from superficial dorsal horn, high frequency stimulation of Lissauer's tract (LT) stably induced LTP of field excitatory postsynaptic potentials (fEPSPs). Perfusion of RyR antagonists blocked the induction of LT stimulation-evoked spinal LTP, while Ins(1,4,5)P3 receptor (IP<sub>3</sub>R) antagonist had no significant effect on LTP induction. Moreover, activation of RyRs by caffeine without high frequency stimulation induced a long-term potentiation in the presence of bicuculline methiodide and strychnine. Further, in patch-clamp recordings from superficial dorsal horn neurons, activation of RyRs resulted in a large increase in the frequency of miniature EPSCs (mEPSCs). Immunohistochemical study showed that RyRs were expressed in the dorsal root ganglion (DRG) neurons. Likewise, calcium imaging in small DRG neurons illustrated that activation of RyRs elevated [Ca<sup>2+</sup>]<sub>i </sub>in small DRG neurons.</p> <p>Conclusions</p> <p>These data indicate that activation of presynaptic RyRs play a crucial role in the induction of LTP in the spinal pain pathway, probably through enhancement of transmitter release.</p
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