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We present a new approach to automatically recognize the pain expression from video sequences, which categorize pain as 4 levels: “no pain,” “slight pain,” “moderate pain,” and “ severe pain.” First of all, facial velocity information, which is used to characterize pain, is determined using optical flow technique. Then visual words based on facial velocity are used to represent pain expression using bag of words. Final pLSA model is used for pain expression recognition, in order to improve the recognition accuracy, the class label information was used for the learning of the pLSA model. Experiments were performed on a pain expression dataset built by ourselves to test and evaluate the proposed method, the experiment results show that the average recognition accuracy is over 92%, which validates its effectiveness.

Divergence gating, a novel method to generate far-field isolated attosecond pulses (IAPs) through controlling divergences of different pulses, is proposed and realized by relativistic chirped laser–plasma interactions. Utilizing various wavefronts for different cycles of incident chirped lasers, reflected harmonics with minimum divergences are obtained only at the peak cycle when plasma targets are adjusted to proper distances from foci of lasers. Therefore, the corresponding attosecond pulse is isolated in far field due to much slower decay during propagation than others. Confirmed by three-dimensional numerical simulations, millijoule-level sub-50 as IAPs with intensity approaching 10 16  W cm −2 (10 17 –10 18  W sr −1 ) are obtained by our scheme, where low-order harmonics can be preserved.

In our previous study, we have isolated cytochalasin H (CyH) from endophytic fungus derived from mangrove plant and found that CyH inhibited the proliferation of non-small cell lung cancer (NSCLC) cells. Recently, epidermal growth factor receptor (EGFR) activation and programmed cell death 1 ligand (PD-L1) expression have been demonstrated to mediate NSCLC resistance to gefitinib, first-generation EGFR tyrosine kinase inhibitor (EGFR-TKI). Here, we further investigated the effect of CyH on EGFR activation, PD-L1 expression, and gefitinib sensitivity in NSCLC cell lines, A549 (wild-type EGFR), HCC827 (EGFR mutation), and NCI-H1975 (dual EGFR mutations and acquired gefitinib resistance) and animal model. Our results showed that CyH significantly inhibited EGFR activation and PD-L1 expression in NSCLC cells. Additionally, CyH dramatically promoted the inhibitory effect of gefitinib on the proliferation of A549 and HCC827 cells, and enhanced the sensitivity to gefitinib in NCI-H1975 cells. Moreover, CyH increased the inhibitory effect of gefitinib on EGFR activation and PD-L1 expression in HCC827 and NCI-H1975 cells. Animal experiments further demonstrated that CyH significantly promoted the inhibitory effect of gefitinib on the growth of NSCLC and the expression of Ki-67, p-EGFR, and PD-L1 in NCI-H1975 NSCLC xenograft tumors of nude mice. Furthermore, CyH inhibited the activation of JAK3/STAT signaling pathway. Taken together, our findings suggest that CyH promotes the sensitivity to gefitinib in NSCLC cells through the inhibition of EGFR activation and PD-L1 expression.

Intense particle beams generated from the interaction of ultrahigh intensity lasers with sample foils provide options in radiography, high-yield neutron sources, high-energy-density-matter generation, and ion fast ignition. An accurate understanding of beam transportation behavior in dense matter is crucial for all these applications. Here we report the experimental evidence on one order of magnitude enhancement of intense laser-accelerated proton beam stopping in dense ionized matter, in comparison with the current-widely used models describing individual ion stopping in matter. Supported by particle-in-cell (PIC) simulations, we attribute the enhancement to the strong decelerating electric field approaching 1 GV/m that can be created by the beam-driven return current. This collective effect plays the dominant role in the stopping of laser-accelerated intense proton beams in dense ionized matter. This finding is essential for the optimum design of ion driven fast ignition and inertial confinement fusion. A detailed understanding of particle stopping in matter is essential for nuclear fusion and high energy density science. Here, the authors report one order of magnitude enhancement of intense laser-accelerated proton beam stopping in dense ionized matter in comparison with currently used models describing ion stopping in matter.

Background Understanding p53-independent regulatory mechanisms is crucial for predicting outcomes in lung adenocarcinoma (LUAD) and developing improved therapeutic strategies. Results We found that PDLIM4 is highly expressed in LUAD tumor tissues, where it induces G2/M phase cell cycle arrest and suppresses cell proliferation, suggesting its potential role in improving patient prognosis. Our study identified BRD4, a bromodomain and extraterminal (BET) family protein, as a key transcriptional regulator of PDLIM4, acting through its BD1 domain. Further analysis revealed that wild-type PDLIM4 stabilizes p21 by blocking its RNA degradation, leading to p21 protein accumulation and subsequent inhibition of cell proliferation. In contrast, the S116 mutation in PDLIM4 abrogates this regulatory effect. Notably, activation of the BRD4/PDLIM4/p21 pathway enhanced chemosensitivity to doxorubicin in both LUAD cells and xenograft tumor models. Conclusions Given the high mutation frequency of PDLIM4 recorded in the TCGA cancer database, our findings reveal a critical regulatory signaling pathway that suppresses LUAD progression and augments chemotherapy efficacy.

Backscattering due to laser plasma instabilities (LPIs) presents a risk in the laser-driven inertial confinement fusion. Generally, it is assumed that the backscattering of laser beams in the same cone is identical in hohlraum physics studies. In the experiments performed at SG-100kJ laser facility, we find that the backscattering of laser beams in the same cone are quite different. Our investigation reveals the main reason for this phenomenon is that the laser beams in the same cone obtain different power from their neighbor beams via crossed-beam energy transfer (CBET) depending on their polarizations. The dependence of multi-beam CBET on laser polarization arrangement is confirmed in a specially designed experiment. These findings are crucial for understanding the backscattering, CBET, energy deficit and the azimuthal drive asymmetry in cylindrical hohlraums. Laser plasma instabilities are the main factors contributing to degradation of hohlraum performance in inertial confinement fusion experiments. Here, the authors show asymmetric backscattering within the same laser cone at the SG-100kJ laser facility, unveiling the role of crossed-beam energy transfer and laser polarization.

We demonstrate theoretically and numerically that intense isolated circularly polarized (CP) attosecond pulses can be generated from ultrathin foil targets irradiated by two relativistic lasers from opposite sides, where their polarizations are orthogonal to each other. With a proper matching condition, the compressed oscillating plasma mirrors on both sides of the foil are pushed inside by laser radiation pressures, eventually merging together to form a dense electron nanobunch under the effect of orthogonal laser fields. This nanobunch reaches both high density and high energy in only half a laser cycle and smears out in others, resulting in coherent synchrotron emission of a single attosecond pulse with circular polarization. Two-dimensional particle-in-cell simulations show that an intense isolated CP attosecond XUV pulse with an intensity of 1.2 × 10 19 W cm −2 and a duration of ∼75 as can be obtained by two lasers with the same intensity of 2.1 × 10 20 W cm −2 .

In laser-driven inertial confinement fusion, driving pressure boosting and smoothing are major challenges. A proposed hybrid-drive (HD) scheme can offer such ideal HD pressure performing stable implosion and nonstagnation ignition. Here we report that in the hemispherical and planar ablator targets installed in the semicylindrical hohlraum scaled down from the spherical hohlraum of the designed ignition target, under indirect-drive (ID) laser energies of ~43–50 kJ, the peak radiation temperature of 200 ± 6 eV is achieved. And using only direct-drive (DD) laser energies of 3.6–4.0 kJ at an intensity of 1.8 × 10 15 W/cm 2 , in the hemispherical and planar targets the boosted HD pressures reach 3.8–4.0 and 3.5–3.6 times the radiation ablation pressure respectively. In all the above experiments, significant HD pressure smoothing and the important phenomenon of how a symmetric strong HD shock suppresses the asymmetric ID shock pre-compressed fuel are demonstrated. The backscattering and hot-electron energy fractions both of which are about one-third of that in the DD scheme are also measured. In laser-driven inertial fusion, finding optimal driving pressure is a major challenge. Here, the authors use a 100 kJ SG laser and a hybrid-drive scheme to demonstrate such driving pressure with the help of the direct-drive laser such that the indirect-drive radiation ablation pressure is turned into a well-smoothed hybrid-drive pressure much greater than the radiation ablation pressure.

Heart transplantation is the gold standard for treating patients with advanced heart failure. Although improvements in immunosuppressive therapies have significantly reduced the frequency of cardiac graft rejection, the incidences of T cell-mediated rejection (TCMR) and antibody-mediated rejection remain almost unchanged. A four-archetype analysis (4AA) model, developed by Philip F. Halloran, illustrated this problem well. It provided a new dimension to improve the accuracy of diagnoses and an independent system for recalibrating the histology guidelines. However, this model was based on the invasive method of endocardial biopsy, which undoubtedly increased the postoperative risk of heart transplant patients. Currently, little is known regarding the associated genes and specific functions of the different phenotypes. We performed bioinformatics analysis (using machine-learning methods and the WGCNA algorithm) to screen for hub-specific genes related to different phenotypes, based Gene Expression Omnibus accession number GSE124897. More immune cell infiltration was observed with the ABMR, TCMR, and injury phenotypes than with the stable phenotype. Hub-specific genes for each of the four archetypes were verified successfully using an external test set (accession number GSE2596). Logistic-regression models based on TCMR-specific hub genes and common hub genes were constructed with accurate diagnostic utility (area under the curve > 0.95). RELA, NFKB1, and SOX14 were identified as transcription factors important for TCMR/injury phenotypes and common genes, respectively. Additionally, 11 Food and Drug Administration-approved drugs were chosen from the DrugBank Database for each four-archetype model. Tyrosine kinase inhibitors may be a promising new option for transplant rejection treatment. KRAS signaling in cardiac transplant rejection is worth further investigation. Our results showed that heart transplant rejection subtypes can be accurately diagnosed by detecting expression of the corresponding specific genes, thereby enabling precise treatment or medication.

To explore the effects and mechanisms of tetraspanin TSPAN7 on the progression of non-small-cell lung cancer (NSCLC) cells. All 125 lung cancer specimens and 60 metastatic tissues were obtained from patients diagnosed with NSCLC, and we used immunohistochemistry to detect the expression of TSPAN7 in NSCLC tissues and adjacent normal tissues. Cell proliferation and invasion ability were determined by MTT, colony formation, and cell migration. The relative protein expression level was analyzed by Western blot analysis. Our clinical data showed that among 125 patients with lung cancer, TSPAN7 was associated with lymph node status, differentiation, tumor size, and poor prognosis. TSPAN7 knockout inhibited cell proliferation and migration. In addition, TSPAN7 increased the expression of N-cadherin in NSCLC cells by reducing the expression of E-cadherin and vimentin and promoting the cell epithelial-mesenchymal transition (EMT) process. Xenograft transplantation model confirmed the role of TSPAN7 in NSCLC metastasis. TSPAN7-mediated EMT is the key to NSCLC migration. TSPAN7 is a potential target for NSCLC therapy.