Circular RNAs (circRNAs) have been identified play a vital role in various different types of cancer via sponging miRNAs (microRNAs). However, their role in lung adenocarcinoma (LUAD) remains largely unclear. In this study, we systematically characterized the circRNA expression profiles in the LUAD cancer tissues and paired adjacent noncancerous tissues. Three circRNAs were found to be significantly upregulated. Among them, has-circRNA-002178 was further confirmed to be upregulated in the LUAD tissues, and LUAD cancer cells. Subsequently, we also found has-circRNA-002178 could enhance PDL1 expression via sponging miR-34 in cancer cells to induce T-cell exhaustion. More importantly, circRNA-002178 could be detected in exosomes of plasma from LUAD patients and could serve as biomarkers for LUAD early diagnosis. Finally, we found circRNA-002178 could be delivered into CD8 + T cells to induce PD1 expression via exosomes. Taken together, our study revealed that circRNA-002178 could act as a ceRNA to promote PDL1/PD1 expression in lung adenocarcinoma.

An O(N) algorithm is proposed for calculating linear response functions of non-interacting electrons. This algorithm is simple and suitable to parallel-and vector-computation. Since it avoids O(N 3 ) computational effort of matrix diagonalization, it requires only O(N ) computational efforts where N is the dimension of the statevector. The use of this O(N ) algorithm is very effective since otherwise we have to calculate large number of eigenstates, i.e., the occupied one-electron states up to the Fermi energy and the unoccupied states with higher energy. The advantage of this method compared to the Chebyshev polynomial method recently developed by Wang (L.W. Wang, Phys. Rev. B 49, 10154 (1994);L.W. Wang, Phys. Rev. Lett. 73, 1039Lett. 73, (1994 ) is that our method can calculate linear response functions without any storage of huge statevectors on external storage.

A cold electron emitter has been fabricated based on nanocrystalline silicon (nc-Si) quantum dots formed in the gas phase by very-high-frequency plasma decomposition of SiH4. A small size of less than 10 nm and the spherical shape of the nc-Si dots facilitated the generation of hot electrons. Electrons with kinetic energies higher than the work function of the top electrode were extracted into vacuum through the electrode. A planarization process of the nc-Si layer by annealing enhanced the electron emission efficiency to 5%. Efficiency was optimized by varying the thicknesses of the nc-Si layer, the SiO2 layer, and the top electrode film.

BackgroundLong non-coding RNAs (lncRNAs) are tumor-associated biological molecules and have been found to be implicated in the progression of colorectal cancer (CRC). This study aims to examine the effects of lncRNA RP11-468E2.5 and its target genes (STAT5 and STAT6) on the biological activities of CRC cells via the Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway.MethodsWe initially screened the GEO database for differentially expressed lncRNAs related to CRC and then made a prediction of the implicated target genes. Then we collected CRC tissues and adjacent normal tissues from 169 CRC patients. Human CRC HCT116 and SW480 cells were treated with small interference RNA (siRNA) against RP11-468E2.5, AG490 (an inhibitor of the JAK/STAT signaling pathway), or both in combination. Next, we measured the effects of RP11-468E2.5 treatment on cellular activities such as cell viability, cycle distribution and cell apoptosis, and studied interactions among RP11-468E2.5, STAT5/STAT6, and the JAK/STAT signaling pathway. Finally, an in vivo tumor formation assay was performed to observe the effect of RP11-468E2.5 on tumor growth.ResultsThe CRC-related gene microarray data showed low expression of RP11-468E2.5 in CRC surgical specimens. However, RP11-468E2.5 was confirmed to target STAT5 and STAT6, which participate in the JAK/STAT signaling pathway. CRC tissues showed lower expression of RP11-468E2.5, higher expression of STAT5, STAT6 and of the cell cycle marker Cyclin D1 (CCND1), compared to the findings in adjacent normal tissues. The treatment of siRNA against RP11-468E2.5 increased expression of JAK2, STAT3, STAT5, STAT6, CCND1 and Bcl-2 along with the extent of STAT3, STAT5 and STAT6 phosphorylation, while lowering expression of P21 and P27. Treatment with AG490 exhibited approximately opposite effects, whereas siRNA against RP11-468E2.5 treatment stimulated CRC cell proliferation and reduced cell apoptosis, while promoting cell cycle entry; AG490 treatment reversed these results.ConclusionsAltogether, we conclude that up-regulation of RP11-468E2.5 inhibits the JAK/STAT signaling pathway by targeting STAT5 and STAT6, thereby suppressing cell proliferation and promoting cell apoptosis in CRC.

Erbium-related 1.54 μm emission dynamics of Er-doped ZnO thin films has been investigated for the different excitation conditions. The excitation was achieved either by exciting indirectly Er3+ ions due to an electron–hole-mediated process or exciting directly discrete energy levels of Er3+ ions. There is no change in the 1.54 μm emission spectrum feature in spite of the different excitation conditions, whereas dramatic change can be seen in the rise time of 1.54 μm emission. The shorter rise time of 1.54 μm emission observed for indirect excitation implies an excitation efficiency superior to direct excitation of Er3+ ions.