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Non-blind invisibility cloaks allowing the concealed object to sense the outside world have great application potentials such as in high-precision sensing or underwater camouflage. However the existing designs based on coordinate transformation techniques need complicated spatially-varying negative index or intricate multi-layered configurations, substantially increasing the difficulty in practical realization. Here we report on the non-blind acoustic invisibility for a circular object in free space with simple distribution of cloak parameters. The mechanism is that, instead of utilizing the transformation acoustics technique, we develop the analytical formulae for fast prediction of the scattering from the object and then use an evolutionary optimization to retrieve the desired cloak parameters for minimizing the scattered field. In this way, it is proven possible to break through the fundamental limit of complementary condition that must be satisfied by the effective parameters of the components in transformation acoustics-based cloaks. Numerical results show that the resulting cloak produces a non-bflind invisibility as perfect as in previous designs, but only needs two layers with homogenous single-negative parameters. With full simplification in parameter distribution and broken symmetry in complementary relationship, our scheme opens new route to free-space non-blind invisibility, taking a significant step towards real-world application of cloaking devices. [ABSTRACT FROM AUTHOR]

Prognostic biomarkers for the pancreatic neuroendocrine tumors are needed. Proteomic study on insulinoma has been rarely reported. We identified the differential expression of proteins between insulinoma and their paired tissues by proteomic analysis, and evaluated the prognostic significance of specific proteins in pancreatic neuroendocrine tumors including insulinoma. The differential expression of select proteins was validated in more than 300 tumors using immunohistochemical staining and western blot. Methylation of UCH-L1 promoter in tumors was examined by methylation specific PCR and validated by sequencing. The concurrent expression of UCH-L1 and α-internexin was correlated with the prognosis in 2 independent collectives of patients with tumors. Sixty-two and 219 proteins were significantly down-regulated and up-regulated in insulinomas, respectively. Demethylation of UCH-L1 promoter was associated with UCH-L1 expression in tumors (p = 0.002). The concurrent expression of UCH-L1 and α-internexin in pancreatic neuroendocrine tumors was significantly associated with better overall survival and disease-free survival in the combination of both cohorts (log rank p = 3.90 × 10 -4 and p = 3.75 × 10 -5 , respectively) and in each of cohorts. The prognostic value of both proteins was also validated in patients with stage II and III tumors (p = 0.017 and p = 0.006, respectively). The proteins UCH-L1 and α-internexin could be independent prognostic biomarkers of pancreatic neuroendocrine tumors.

TfoX (Sxy) and CRP are two important competence activators. The link between tfoX and CRP has been shown in H. influenza but lacking evidence of direct interaction. Recently a Sxy-dependent CRP (CRP-S) site autoregulating Sxy was reported in E. coli. Here, we show that the cAMP-CRP complex transcriptionally regulates tfoX expression through multiple canonical CRP (CRP-N) sites in Vibrios. This conclusion is supported by an analysis of the tfoX mRNA levels and tfoX transcriptional reporter fusions. The reduced expression of tfoX(VC) was restored by trans-complementation of crp in ∆crp and by exogenous cAMP in ∆cya. A promoter deletion analysis and the site-directed mutagenesis of the putative CRP-N sites revealed the presence of two functional CRP-N sites. The direct binding of cAMP-CRP to the tfoX(VC)promoter was demonstrated by EMSA assays. Additionally, the transcriptional start site (TSS) of tfoX(VF) in V. fluvialis was determined, and -10/-35 regions were predicted. Further comparison of the tfoX promoter in Vibrios revealed the existence of similar -10 motifs and putative CRP-N sites, indicating the conserved mechanism of CRP regulation on tfoX. Our study demonstrates the direct binding of the cAMP-CRP complex to tfoX promoter, and broadens the understanding of the molecular mechanism regulating tfoX in Vibrios.