Prestack depth migration produces blurred images resulting from limited acquisition apertures, complexities in the velocity model, and band-limited characteristics of seismic waves. This distortion can be partially corrected using the model-space least-squares migration/inversion approach, where a target-oriented wave-equation Hessian operator is computed explicitly and then inverse filtering is applied iteratively to deblur or invert for the reflectivity. However, one difficulty is the cost of computing the explicit Hessian operator, which requires storing a large number of Green's functions, making it challenging for large-scale applications. A new method to compute the Hessian operator for the waveequation-based least-squares migration/inversion problem modifies the original explicit Hessian formula, enabling efficient computation of this operator. An advantage is that the method eliminates disk storage of Green's functions. The modifications, however, also introduce undesired crosstalk artifacts. Two different phase-encoding schemes, planewave-phase encoding and random-phase encoding, suppress the crosstalk. When the randomly phase-encoded Hessian operator is applied to the Sigsbee2A synthetic data set, an improved subsalt image with more balanced amplitudes is obtained.

Homeostatic synaptic plasticity is a form of non-Hebbian plasticity that maintains stability of the network and fidelity for information processing in response to prolonged perturbation of network and synaptic activity. Prolonged blockade of synaptic activity decreases resting Ca2+ levels in neurons, thereby inducing retinoic acid (RA) synthesis and RA-dependent homeostatic synaptic plasticity; however, the signal transduction pathway that links reduced Ca2+-levels to RA synthesis remains unknown. Here we identify the Ca2+-dependent protein phosphatase calcineurin (CaN) as a key regulator for RA synthesis and homeostatic synaptic plasticity. Prolonged inhibition of CaN activity promotes RA synthesis in neurons, and leads to increased excitatory and decreased inhibitory synaptic transmission. These effects of CaN inhibitors on synaptic transmission are blocked by pharmacological inhibitors of RA synthesis or acute genetic deletion of the RA receptor RARα. Thus, CaN, acting upstream of RA, plays a critical role in gating RA signaling pathway in response to synaptic activity. Moreover, activity blockade-induced homeostatic synaptic plasticity is absent in CaN knockout neurons, demonstrating the essential role of CaN in RA-dependent homeostatic synaptic plasticity. Interestingly, in GluA1 S831A and S845A knockin mice, CaN inhibitor- and RA-induced regulation of synaptic transmission is intact, suggesting that phosphorylation of GluA1 C-terminal serine residues S831 and S845 is not required for CaN inhibitor- or RA-induced homeostatic synaptic plasticity. Thus, our study uncovers an unforeseen role of CaN in postsynaptic signaling, and defines CaN as the Ca2+-sensing signaling molecule that mediates RA-dependent homeostatic synaptic plasticity.

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An interesting but largely unanswered biological question is how eukaryotic organisms regulate the size of multicellular tissues. During development, a lawn of Dictyostelium cells breaks up into territories, and within the territories the cells aggregate in dendritic streams to form groups of ϳ20,000 cells. Using random insertional mutagenesis to search for genes involved in group size regulation, we found that an insertion in the cnrN gene affects group size. Cells lacking CnrN (cnrN ؊ ) form abnormally small groups, which can be rescued by the expression of exogenous CnrN. Relayed pulses of extracellular cyclic AMP (cAMP) direct cells to aggregate by chemotaxis to form aggregation territories and streams. cnrN ؊ cells overaccumulate cAMP during development and form small territories. Decreasing the cAMP pulse size by treating cnrN ؊ cells with cAMP phosphodiesterase or starving cnrN ؊ cells at a low density rescues the small-territory phenotype. The predicted CnrN sequence has similarity to phosphatase and tensin homolog (PTEN), which in Dictyostelium inhibits cAMP-stimulated phosphatidylinositol 3-kinase signaling pathways. CnrN inhibits cAMP-stimulated phosphatidylinositol 3,4,5-trisphosphate accumulation, Akt activation, actin polymerization, and cAMP production. Our results suggest that CnrN is a protein with some similarities to PTEN and that it regulates cAMP signal transduction to regulate territory size.

Esophageal squamous cell carcinoma (ESCC) is one of the most common types of cancer worldwide. However, operative diagnostic and prognostic systems for ESCC remain to be established. To improve assessment of the prognosis for patients with ESCC, the present study developed an online consensus survival tool for ESCC, termed OSescc. OSescc was built using 264 ESCC cases with gene expression data and relevant clinical information obtained from the Gene Expression Omnibus and The Cancer Genome Atlas databases. Kaplan-Meier survival plots with hazard ratios and P-values were generated by OSescc to predict the association between potential biomarkers and relapse free survival and overall survival. In addition, the current study integrated a function by which one could assess the prognosis based on an individual probe or the mean value of multiple probes for each gene, which helped improve the evaluation of the validity and reliability of the potential prognosis biomarkers. OSescc can be accessed at .