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

2,4-Dinitro-1-phenoxy­benzene

The title compound, C12H8N2O5, was obtained by the reaction of 1-chloro-2,4-dinitro­benzene and phenol in the presence of potassium carbonate. The nitro-substituted benzene ring lies on a mirror plane, with one NO2 group in the same plane and the other disordered across this plane. The phenoxy­benzene unit is placed perpendicular to this mirror, resulting in an exact orthogonal relationship between the phenyl and benzene rings in the mol­ecule. The crystal packing exhibits no significantly short inter­molecular contacts

Subtle mutations in the SMN1 gene in Chinese patients with SMA: p.Arg288Met mutation causing SMN1 transcript exclusion of exon7

BACKGROUND: Proximal spinal muscular atrophy (SMA) is a common neuromuscular disorder resulting in death during childhood. Around 81 ~ 95% of SMA cases are a result of homozygous deletions of survival motor neuron gene 1 (SMN1) gene or gene conversions from SMN1 to SMN2. Less than 5% of cases showed rare subtle mutations in SMN1. Our aim was to identify subtle mutations in Chinese SMA patients carrying a single SMN1 copy. METHODS: We examined 14 patients from 13 unrelated families. Multiplex ligation-dependent probe amplification analysis was carried out to determine the copy numbers of SMN1 and SMN2. Reverse transcription polymerase chain reaction (RT-PCR) and clone sequencing were used to detect subtle mutations in SMN1. SMN transcript levels were determined using quantitative RT-PCR. RESULTS: Six subtle mutations (p.Ser8LysfsX23, p.Glu134Lys, p.Leu228X, p.Ser230Leu, p.Tyr277Cys, and p.Arg288Met) were identified in 12 patients. The p.Tyr277Cys mutation has not been reported previously. The p.Ser8LysfsX23, p.Leu228X, and p.Tyr277Cys mutations have only been reported in Chinese SMA patients and the first two mutations seem to be the common ones. Levels of full length SMN1 (fl-SMN1) transcripts were very low in patients carrying p.Ser8LysfsX23, p.Leu228X or p.Arg288Met compared with healthy carriers. In patients carrying p.Glu134Lys or p.Ser230Leu, levels of fl-SMN1 transcripts were reduced but not significant. The SMN1 transcript almost skipped exon 7 entirely in patients with the p.Arg288Met mutation. CONCLUSIONS: Our study reveals a distinct spectrum of subtle mutations in SMN1 of Chinese SMA patients from that of other ethnicities. The p.Arg288Met missense mutation possibly influences the correct splicing of exon 7 in SMN1. Mutation analysis of the SMN1 gene in Chinese patients may contribute to the identification of potential ethnic differences and enrich the SMN1 subtle mutation database