33 research outputs found
Quantum optical coherence can survive photon losses: a continuous-variable quantum erasure correcting code
A fundamental requirement for enabling fault-tolerant quantum information
processing is an efficient quantum error-correcting code (QECC) that robustly
protects the involved fragile quantum states from their environment. Just as
classical error-correcting codes are indispensible in today's information
technologies, it is believed that QECC will play a similarly crucial role in
tomorrow's quantum information systems. Here, we report on the first
experimental demonstration of a quantum erasure-correcting code that overcomes
the devastating effect of photon losses. Whereas {\it errors} translate, in an
information theoretic language, the noise affecting a transmission line, {\it
erasures} correspond to the in-line probabilistic loss of photons. Our quantum
code protects a four-mode entangled mesoscopic state of light against erasures,
and its associated encoding and decoding operations only require linear optics
and Gaussian resources. Since in-line attenuation is generally the strongest
limitation to quantum communication, much more than noise, such an
erasure-correcting code provides a new tool for establishing quantum optical
coherence over longer distances. We investigate two approaches for
circumventing in-line losses using this code, and demonstrate that both
approaches exhibit transmission fidelities beyond what is possible by classical
means.Comment: 5 pages, 4 figure
SBF1 mutations associated with autosomal recessive axonal neuropathy with cranial nerve involvement
Biallelic mutations in the SBF1 gene have been identified in one family with demyelinating Charcot-Marie-Tooth disease (CMT4B3) and two families with axonal neuropathy and additional neurological and skeletal features. Here we describe novel sequence variants in SBF1 (c.1168C>G and c.2209_2210del) as the potential causative mutations in two siblings with severe axonal neuropathy, hearing loss, facial weakness and bulbar features. Pathogenicity of these variants is supported by co-segregation and in silico analyses and evolutionary conservation. Our findings suggest that SBF1 mutations may cause a syndromic form of autosomal recessive axonal neuropathy (AR-CMT2) in addition to CMT4B3
Isolation and Characterisation of a Human-Like Antibody Fragment (scFv) That Inactivates VEEV In Vitro and In Vivo
Venezuelan equine encephalitis virus (VEEV) belongs to the Alphavirus genus and several species of this family are pathogenic to humans. The viruses are classified as potential agents of biological warfare and terrorism and sensitive detection as well as effective prophylaxis and antiviral therapies are required