A new mathematical model, described as hollow Gaussian beams (HGBs), is proposed to describe a dark hollow laser beam (DHB). The area of the dark region across the HGBs can easily be controlled by proper choice of the beam parameters. Based on the Collins integral, an analytical propagation formula for the HGBs through a paraxial optical system is derived. The HGBs also can be expressed as a superposition of a series of Lagurerre-Gaussian modes by use of a polynomial expansion. As a numerical example, the propagation properties of a DHB in free space are illustrated graphically. The HGBs provide a convenient and powerful way to describe and treat the propagation of DHBs and can be used conveniently to analyze atoms manipulated with a DHB.

An accurate description of a subcycle pulsed beam (SCPB) is presented based on the complex-source model. The fields are exact solutions of Maxwell's equations and applicable to a focused pulsed beam with a pulse duration down to and below one cycle of the carrier wave and with arbitrary polarization state. Depending on the pulse duration, the pulse is blueshifted, and its wings are chirped. This effect, which we refer to as "self-induced blueshift" goes beyond the carrier-envelope description. The corresponding phase is a temporal analog of the Gouy phase. The energy gain of a relativistic electron swept over by an SCPB is very sensitive to the proper form chosen to describe the pulse.

A 4 x 4 complex curvature tensor M>(-1) is introduced to describe partially coherent anisotropic Gaussian-Schell model (GSM) beams. An analytical propagation formula for the cross-spectral density of partially coherent anisotropic GSM beams is derived. The propagation law of M(-1) that is also derived may be called partially coherent tensor ABCD law. The analytical formulas presented here are useful in treating the propagation and transformation of partially coherent anisotropic GSM beams, which include previous results for completely coherent Gaussian beams as special cases.

FKBP3 is a member of FK506-binding proteins (FKBPs). Little is known about the expression and functional role(s) of FKBP3 in non-small cell lung cancer (NSCLC). In the present study, we demonstrated up-regulation of FKBP3 expression, both at mRNA and protein levels, in NSCLC samples which closely correlated with poor survival in NSCLC patients. In vitro and in vivo experiments revealed that FKBP3 could promote NSCLC cell proliferation. Furthermore, knockdown of FKBP3 significantly decreased histone deacetylase 2 (HDAC2) expression and increased p27 (a cell cycle inhibitor) expression. HDAC2 modulated the acetylation of histone H3K4 by directly binding to the p27 promoter. The proliferation-promoting effect of FKBP3 was dependent on HDAC2 and inhibited by p27. Also, FKBP3 induced HDAC2 promoter activity via inhibiting the ubiquitination of transcription factor Sp1. Additionally, we identified miR-145-5p as a regulator of FKBP3. miR-145-5p overexpression suppressed cell proliferation of NSCLC cells which was abrogated by FKBP3 overexpression. Taken together, our data clearly show that FKBP3/Sp1/HDAC2/p27 control cell proliferation during NSCLC development.

Non-small cell type lung cancer (NSCLC) is the most common malignancy and the leading cause of cancer related mortality. In this study, serine/threonine kinase 39 (STK39) was identified as an up-regulated gene in NSCLC tissues by next-generation RNA sequencing. Although STK39 gene polymorphisms may be prognostic of overall survival in patients with early stage NSCLC, the roles of STK39 in NSCLC cancer are poorly understood. In the current study, Genome Set Enrichment Analysis (GSEA) on the RNA-seq data of NSCLC specimens indicated that cancer-related process and pathways, including metastasis, cell cycle, apoptosis and p38 pathway, were significantly correlated with STK39 expression. STK39 expression was significantly increased in NSCLC cases and its protein expression was positively correlated with the poor tumor stage, large tumor size, advanced lymphnode metastasis and poor prognosis. Down-regulation of STK39 in NSCLC cells significantly decreased cell proliferation by blocking of cell cycle and inducing apoptosis. We also found that STK39 knockdown in NSCLC cells remarkably repressed cell migration and invasion. On the contrary, overexpression of STK39 in NSCLC cells had inverse effects on cell behaviors. Taken together, STK39 acts as a tumor oncogene in NSCLC and can be a potential biomarker of carcinogenesis.

Methylation analysis in tissue of RASSF1A, APC, ESR1, ABCB1 and HOXC9 genes confirmed 79.8% of the existing diagnosis for the stage I NSCLC at specificity: 73.1%. The insufficiency of predicting disease onset in China, using the previously recommended targets (MGMT, DAPK1 and PTEN) in the United States reflects a potential disease disparity between these two populations. Alternatively, methylated state of this set of genes may be more specific to the late rather than the early stage of NSCLC.

Analytical formulas are derived for the average irradiance and the degree of polarization of a radially or azimuthally polarized doughnut beam (PDB) propagating in a turbulent atmosphere by adopting a beam coherence-polarization matrix. It is found that the radial or azimuthal polarization structure of a radially or azimuthally PDB will be destroyed (i.e., a radially or azimuthally PDB is depolarized and becomes a partially polarized beam) and the doughnut beam spot becomes a circularly Gaussian beam spot during propagation in a turbulent atmosphere. The propagation properties are closely related to the parameters of the beam and the structure constant of the atmospheric turbulence.

Family with sequence similarity 83A (FAM83A) is a newly-found over-expressed oncogene in several types of cancers and associates with poor prognosis. However, the role that FAM83A may play in the carcinogenesis of non-small cell lung cancer (NSCLC) still needs to be defined. The present study aimed to investigate the function of FAM83A in NSCLC progression and to investigate the possible mechanism. Analysis of Gene Expression Omnibus (GEO) database and rt-PCR showed up-regulated expression of FAM83A in NSCLC. GEO and the Cancer Genome Atlas (TCGA) data analysis revealed that high expression level of FAM83A in NSCLC was associated with poor prognosis. In vitro experiments showed that depleting FAM83A by siRNA/shRNA significantly inhibited cell proliferation and induced cell apoptosis. Cell motility was also retarded after silencing FAM83A, as demonstrated by Transwell assay. FAM83A depletion in A549 cells also inhibited subcutaneous tumor growth and lung metastasis in vivo. Western blotting showed that silencing FAM83A decreased the phosphorylation of ERK and PI3K/Akt/mTOR. On the other hand, overexpressing FAM83A in vitro enhanced cell proliferation and invasiveness, which was repressed by PI3K inhibitor and ERK inhibitor separately. Taken together, our study suggests that FAM83A promotes tumorigenesis of NSCLC at least partly via ERK and PI3K/Akt/mTOR pathways, making it a promising therapeutic target.