Instantaneous spectral analysis (ISA) is a continuous timefrequency analysis technique that provides a frequency spectrum for each time sample of a seismic trace. ISA achieves both excellent time and frequency localization utilizing wavelet transforms to avoid windowing problems that complicate conventional Fourier analysis. Applications of the method include enhanced resolution, improved visualization of stratigraphic features, thickness estimation for thin beds, noise suppression, improved spectral balancing, and direct hydrocarbon indication. We have seen four distinct ways in which ISA can help in the detection of hydrocarbons: (1) anomalously high attenuation in thick or very unconsolidated gas reservoirs, (2) low-frequency shadows in reservoirs where the thickness is not sufficient to result in significant attenuation, (3) preferential illumination at the "tuning" frequency which can be different for gas or brine-saturated rocks, and (4) frequency-dependent AVO. In this paper, we describe the ISA technique, compare it to other spectral decomposition methods, and show some examples of the use of ISA to detect lowfrequency shadows beneath gas reservoirs.The ISA method involves the following steps: (1) decompose the seismogram into constituent wavelets using wavelet transform methods such as Mallat's matching pursuit decomposition, (2) sum the Fourier spectra of the individual wavelets in the time-frequency domain to produce "frequency gathers," and (3) sort the frequency gathers to produce common (constant) frequency cubes, sections, time slices, and horizon slices. The results can be viewed using animation techniques available in commercial interpretation and visualization packages. Figure 1 shows a synthetic seismic trace and the corresponding ISAtime-frequency analysis. The time-frequency plot shows amplitude spectra for each time sample. We refer to this kind of plot as a "frequency gather." The first arrival on the synthetic seismogram results from an isolated reflector. The frequency spectrum is the spectrum of the wavelet. Note that the duration of the spectrum is identical to the duration of the arrival in the time domain as opposed to Fourier-based methods in which the time duration is equal to the window length. The second event is a composite of two events of differing center frequency arriving precisely at the same time. The frequency spectrum indicates a low-frequency arrival spread over time and a higher-frequency arrival that is more localized in time. The third event is caused by two interfering arrivals of the same frequency. Although the presence of two arrivals is not immediately apparent on the seismogram, the time-frequency decomposition clearly shows two distinct arrivals. The fourth event is a composite of four waveforms arriving at two distinct times evident on the time-frequency analysis. The final event consists of three arrivals of the same frequency that are very closely spaced in time. The three distinct arrivals cannot be resolved at low frequencies, but the separation is clearly...

The critical issue that hinders the translation of nanomaterials from basic research to clinical trials is their potential toxicity caused by long‐term body retention. It is still a huge challenge to integrate renal‐clearable and theranostic properties into one nanomedicine, especially exploring the nanomaterials with optical absorption in the second near‐infrared light (NIR II) biowindow with deep penetration and less tissue scattering. Here, ultrasmall polypyrrole (PPy, ≈2 nm)‐based theranostic agents via a facile and green one‐step method, which exhibit fluorescence (FL)/photoacoustic (PA)/NIR II multimodal imaging, superior photostability, as well as high photothermal conversion efficiency of 33.35% at 808 nm and 41.97% at 1064 nm is developed. Importantly, these ultrasmall PPy‐PEG nanoparticles (NPs) reveal abundant tumor accumulation and efficient renal clearance. Both in vitro and in vivo studies indicate that ultrasmall PPy‐PEG NPs have excellent photothermal effect under NIR II laser irradiation that can effectively eliminate the tumors with extremely low systemic toxicity.

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Abstract. The natural killer cell line NK-92 shows great cytotoxicity against various types of cancer. Several types of solid tumor cells, however, can effectively resist NK-mediated lysis by interaction of major histocompatibility complex (MHC) molecules with NK cell inhibitory receptors. To generate a eukaryotic expression vector encoding chimeric antigen receptor scFv anti-erbB2-CD28-ζ and to investigate the expression and action of this chimeric antigen receptor in cancer cells both in vitro and in vivo, NK-92 cells were genetically modified with an scFv anti-erbB2-CD28-ζ chimeric recep tor by optimized electro poration using the Amaxa Nucleofector system. The expression of the chimeric receptor was evaluated by RT-PCR and immunofluorescence. The ability of the genetically modified NK-92 cells to induce cell death in tumor targets was assessed in vitro and in vivo. The transduced NK-92-anti-erbB2 scFv-CD28-ζ cells expressing high levels of the fusion protein on the cell surface were analyzed by fluorescence-activated cell-sorting (FACS) analysis. These cells specifically enhanced the cell death of the erbB2-expressing human breast cancer cell lines MDA-MB-453 and SKBr3. Furthermore, adoptive transfer of genetically modified NK-92 cells specifically reduced tumor size and lung metastasis of nude mice bearing established MDA-MB-453 cells, and significantly enhanced the survival period of these mice. The genetically modified NK-92 cells significantly enhanced the killing of erbB2-expressing cancer and may be a novel therapeutic strategy for erbB2-expressing cancer cells.

MicroRNAs (miRNAs) have essential roles in carcinogenesis and tumor progression. Here, we investigated the roles and mechanisms of miR-143 in non-small cell lung cancer (NSCLC). miR-143 was significantly decreased in NSCLC tissues and cell lines. Overexpression of miR-143 suppressed NSCLC cell proliferation, induced apoptosis, and inhibited migration and invasion in vitro. Integrated analysis identified LIM domain kinase 1 (Limk1) as a direct and functional target of miR-143. Overexpression of Limk1 attenuated the tumor suppressive effects of miR-143 in NSCLC cells. Moreover, miR-143 was inversely correlated with Limk1 expression in NSCLC tissues. Together, our results highlight the significance of miR-143 and Limk1 in the development and progression of NSCLC.

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Colorectal cancer is one of the commonest of solid malignancy in the world. Activating transcription factor 3 (ATF3), a homolog of the mouse TI-241 and rat LFR-1, is a stress responsive gene that has been widely indicated in different malignancies. However, the role of ATF3 in colon cancer is paradoxical with both a suggested pro- and anti-tumorigenic role. The objective of the current study was to investigate the role of ATF3 in colon cancer metastasis using HT29 and CaCO2 colon cancer cell lines. Expression of ATF3 was initially evaluated in five pairs of colon cancer and matched noncancerous colon tissues. The role of ATF3 in promoting in vitro migration and invasion were evaluated by siRNA-mediated knockdown and adenovirus-mediated overexpression of ATF3. In addition, the role of ATF3 in promoting in vivo tumor growth and hepatic metastasis was investigated by shRNA-mediated knockdown of ATF3. Expression of ATF3 was more in the colon cancer tissues as compared with the pooled noncancerous control colon tissue. Our results showed that in both HT29 and CaCO2 cells, ATF3 promoted in vitro motility and invasion. Furthermore, knockdown of ATF3 attenuated subcutaneous tumor growth and CD31(+) neovasculature in xenograft assays with HT29 and CaCO2 cells and inhibited hepatic metastasis. Cumulatively, our results unequivocally show that ATF3 promotes colon cancer metastasis.

Current choices of second-line chemotherapy regimens for patients with advanced non-small-cell lung cancer (NSCLC) are extremely limited. We applied a new strategy of using nab-paclitaxel as single chemotherapy regimen in second-line setting for patients with unsuccessful first-line chemotherapy. The efficacy and safety were compared with patients who received standard second-line regimen pemetrexed. Patients with stage IIIB/IV NSCLC and unsuccessful first-line platinum-based chemotherapy were randomly divided into two arms. Arm I received pemetrexed 500 mg/m(2) intravenously (i.v.) on day 1 of 3-week cycle. Arm II received nab-paclitaxel 150 mg/m(2) i.v. on days 1 and 8 of 3-week cycle. The primary endpoint was overall survival (OS). One hundred and eleven patients were randomly assigned to receive pemetrexed (n = 56) and nab-paclitaxel (n = 55). Median OSs were 9.4 months (95% CI 7.1-12.5 months) for pemetrexed and 9.9 months (95% CI 8.2-11.9 months) for nab-paclitaxel. Median PFS was 4.6 months (95% CI 2.7-6.1 months) for pemetrexed and 5.1 months (95% CI 3.9-7.4 months) for nab-paclitaxel. While no CR was reported for either treatment, PRs + SDs were seen in 32/56 (57.1%) patients in pemetrexed arm and 36/55 (65.5%) patients in nab-paclitaxel arm. Grade 3 and grade 4 adverse events were comparable between two treatment arms. New second-line chemotherapy single-regimen nab-paclitaxel showed equivalent efficacy and toxicity profiles as pemetrexed in treating patients with NSCLC.