As a public health emergency of international concern, coronavirus disease 2019 (COVID-19) still lacks specific antiviral drugs, and symptomatic treatment is currently the mainstay. The overactivated inflammatory response in COVID-19 patients is associated with a high risk of critical illness or even death. Low-intensity pulsed ultrasound (LIPUS) can mitigate inflammation and inhibit edema formation. We aimed to investigate the efficacy of LIPUS therapy for COVID-19 pneumonia. 62 patients were randomly assigned to a treatment group (LIPUS treatment area - Group 1; self-control area - Group 2) and an external control group (Group 3). The primary outcomes were the volume absorption rate (VAR) and the area absorption rate (AAR) of lung inflammation in CT images. After an average duration of treatment 7.2 days, there were significant differences in AAR and VAR between Group 1 and Group 2 (AAR 0.25 vs 0.12, p=0.013; VAR 0.35 vs 0.11, p=0.005), and between Group 1 and Group 3 (AAR 0.25 vs 0.11, p=0.047; VAR 0.35 vs 0.19, p=0.042). Neither AAR nor VAR was statistically different between Group 2 and Group 3. After treatment, C-reactive protein, interleukin-6, leukocyte, and fingertip arterial oxygen saturation (SaO2) improved in Group 1, while in Group 3 only fingertip SaO2 increased. LIPUS therapy reduced lung inflammation and serum inflammatory factor levels in hospitalized COVID-19 patients, which might be a major advancement in COVID-19 pneumonia therapy.

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality in the world. However, identifying key genes that can be exploited for the effective diagnosis and management of HCC remains difficult. The study aims to examine the prognostic and diagnostic value of TRIM28-H2AX-CDK4 axis in HCC. Analysis in TCGA, GSEA and Gene expression profiling interactive analysis online tools were performed to explore the expression profiles of TRIM28, H2AX and CDK4. Data demonstrating the correlation between TRIM28 expression levels and immune infiltration states or the expression of genes associated with immune checkpoints genes were exacted from TCGA and TIMER. Genetic alteration and enrichment analysis were performed using the cBioPortal and GEPIA2 tools. Finally, the expression of these proteins in HCC was then examined and validated in an independent cohort using immunohistochemistry. TRIM28 alteration exhibited co-occurrence instead of mutual exclusivity with a large number of immune checkpoint components and tumor-infiltrating immune cells, especially B cells, were found to serve roles in patients with HCC with different TRIM28 expression levels. Higher expression levels of TRIM28, H2AX and CDK4 were associated with a poorer prognosis and recurrence in patients with HCC according to TCGA, which was validated further in an independent cohort of patients with HCC. Area under curve revealed the superior predictive power of applying this three-gene signatures in this validation cohort. The diagnostic model based on this TRIM28-H2AX-CDK4 signature is efficient and provides a novel strategy for the clinical management of HCC.

The traditional chimney software architecture design, which is based on the application object, scale and equipment, is difficult to meet the urgent need of multi-resolution, multi-viewpoint, two-dimensional and three-dimensional consistent battlefield situation comprehensive display. Referring to the idea of U.S. Army's general operational diagram, the architecture of the current battlefield situation integrated display system is upgraded and improved. Aiming at the problems of information splitting and real-time undifferentiated access of multi-domain heterogeneous data, technical means such as spatial analysis and multi-source data integration are put forward, and the problems of fast loading and visualization of 3D models of the large battlefield space are solved by designing force clustering and motion trajectory smoothing algorithms. This method improves the service ability and the level of the battlefield situation comprehensive display system, and has a broad arrange of application.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the data shown for the Transwell cell migration and invasion assays in Figs.2C and 4C were strikingly similar to data appearing in different form in another article by different authors at a different research institution. Owing to the fact that the contentious data in the above article were under consideration for publication elsewhere at a similar time to when it was submitted to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 2712‑2718, 2018; DOI: 10.3892/mmr.2017.8131].

Despite numerous studies, the impact of global warming on the tropical cyclone (TC) track and intensity by reasons of data inhomogeneity in remote sensing and large natural variability over a relatively short period of observation is still controversial. Three carbon-emission sensitivity experiments are conducted to investigate how TC track and intensity respond to changes in the oceanic and atmospheric environment under global warming. The results show a high sensitivity of the simulated TC track and intensity to global warming. On one hand, with increase in carbon emissions, the western Pacific subtropical high expands notably, increasing the poleward steering flow and eventually leading to a poleward shift of TC. On the other hand, the underlying sea-surface temperature and surface-entropy flux increase and, thus, favor the convections near the eyewall. Moreover, the TC structure becomes more upright, which is closely related to the larger pressure gradient near the eyewall. As a result, TC intensity increases with carbon emissions. However, this increase is notably smaller than the maximum potential intensity theory as the TC intensity can reach a threshold if carbon emission still increases in the future. The involved mechanisms on the changes of TC track and intensity are also revealed.

Both electromagnetic radiation (EMR) and low-frequency noise (LFN) are widespread and influential environmental factors, and operators are inevitably exposed to both EMR and LFN within a complex exposure environment. The potential adverse effects of such exposure on human health must be considered seriously. This study aimed to investigate the effects of EMR and LFN on cognitive function as well as their interaction effect, which remain unclear. Sixty young male college students were randomly grouped and experiments were conducted with a 2 × 2 factorial design in a shielded chamber. Mental workload (MWL) levels of the study subjects were measured and assessed using the NASA-task load index (TLX) subjective scale, an n-back task paradigm, and the functional near-infrared spectroscopy (fNIRS) imaging technique. For the 3-back task, the NASA-TLX subjective scale revealed a statistically significant main effect of LFN intensity, which enhanced the subjects' MWL level (F = 8.716, p < 0.01). Behavioral performance revealed that EMR intensity (430.1357 MHz, 10.75 W/m2) and LFN intensity (0-200 Hz, 72.9 dB) had a synergistic interaction effect, and the correct response time was statistically significantly prolonged by the combined exposure (F = 4.343, p < 0.05). The fNIRS imaging technique revealed a synergistic interaction effect between operational EMR intensity and operational LFN intensity, with statistically significant effects on the activation levels in the left and right dorsolateral prefrontal cortex (DLPFC). The mean β values of DLPFC were significantly increased (L-DLPFC F = 5.391, p < 0.05, R-DLPFC F = 4.222, p < 0.05), and the relative concentrations of oxyhemoglobin in the DLPFC were also significantly increased (L-DLPFC F = 4.925, p < 0.05, R-DLPFC F = 9.715, p < 0.01). We found a statistically significant interaction effect between EMR (430.1357 MHz, 10.75 W/m2) and LFN (0-200 Hz, 72.9 dB) when simultaneously exposing subjects to both for 30 min. We conclude that exposure to this complex environment can cause a statistically significant increase in the MWL level of operators, and even alterations in their cognitive function.

EMERGING-CTONG 1103 showed improved progression-free survival (PFS) with neoadjuvant erlotinib vs. chemotherapy for patients harbouring EGFR sensibility mutations and R0 resected stage IIIA-N2 non-small cell lung cancer (NSCLC) (NCT01407822). Herein, we report the final results. Recruited patients were randomly allocated 1:1 to the erlotinib group (150 mg/day orally; neoadjuvant phase for 42 days and adjuvant phase to 12 months) or to the GC group (gemcitabine 1250 mg/m2 plus cisplatin 75 mg/m2 intravenously; 2 cycles in neoadjuvant phase and 2 cycles in adjuvant phase). Objective response rate (ORR), complete pathologic response (pCR), PFS, and overall survival (OS) were assessed along with safety. Post hoc analysis was performed for subsequent treatments after disease recurrence. Among investigated 72 patients (erlotinib, n = 37; GC, n = 35), the median follow-up was 62.5 months. The median OS was 42.2 months (erlotinib) and 36.9 months (GC) (hazard ratio [HR], 0.83; 95% confidence interval [CI], 0.47–1.47; p = 0.513). The 3- and 5-year OS rates were 58.6% and 40.8% with erlotinib and 55.9% and 27.6% with GC (p3-y = 0.819, p5-y = 0.252). Subsequent treatment was administered in 71.9% and 81.8% of patients receiving erlotinib and GC, respectively; targeted therapy contributed mostly to OS (HR, 0.35; 95% CI, 0.18–0.70). After disease progression, the ORR was 53.3%, and the median PFS was 10.9 months during the EGFR-TKI rechallenge. During postoperative therapy, grade 3 or 4 adverse events (AEs) were 13.5% in the erlotinib group and 29.4% in the GC group. No serious adverse events were observed. Erlotinib exhibited clinical feasibility for resectable IIIA-N2 NSCLC over chemotherapy in the neoadjuvant setting.

Caching and multicasting are two promising methods to alleviate redundant data transmissions and improve transmission capability in wireless networks. In this article, we focus on the joint resource optimization of cache placement, user association, and channel selection in cache-enabled multicasting small-cell networks. First, we present two weighted hypergraphs to analyze the complex transmission and interference relationships among mobile users (MUs) and small-cell base stations (SBSs) with different files multicasting in different channels. Then, we formulate the combinatorial problem as a nonlinear optimization problem. Considering the hierarchical actions of SBSs and MUs, we further divide the complicated combinatorial optimization problem into following two subproblems, i.e., i) the joint cache placement and channel selection, and ii) the user association. Simultaneously, we propose two potential games <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><tex-math notation="LaTeX">$G1$</tex-math></inline-formula> and <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><tex-math notation="LaTeX">$G2$</tex-math></inline-formula> to analyze the two subproblems, respectively. Thanks to the better response property of potential games, we propose a hierarchical resource allocation game <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><tex-math notation="LaTeX">$G_w$</tex-math></inline-formula> by combining <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><tex-math notation="LaTeX">$G1$</tex-math></inline-formula> and <inline-formula xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><tex-math notation="LaTeX">$G2$</tex-math></inline-formula> to optimize wireless resources iteratively. Lastly, we propose two hierarchical better response algorithms, which can converge to the hierarchical Nash equilibria. Simulation results show that our proposed distributed game method achieves good expectations of global accumulated downloading files.

Aiming at the problem that aviation products generally have multiple performance degradation indicators, which lead to difficulty in extracting degradation features and inaccurate prediction of remaining useful lifetime (RUL), a method for building health index and predicting RUL of aviation products based on multi-source degradation data fusion is proposed. This method is based on the accuracy of degradation modeling to construct the construction principle of health index and realizes the deep fusion of multi-source degradation data. On this basis, the distribution expression of the RUL is derived based on the distribution of the first hitting time of the Wiener process. The effectiveness of the method is verified through the example analysis.

Ozone pollution is a prominent public health issue, but there are few studies on the effect of ozone on the ultrastructure of respiratory system; we conducted this research. Exposed to 1.1 ppm O3 4 h per day, the mice lungs and bronchi were taken on the 15th or 30th day. The sections stained with HE and immunohistochemical streptavidin–peroxidase methods for NQO1, Nrf2, and Keap1 were observed and measured under the optical microscope. TEM was used for ultrastructure observation. The animals’ serums were detected for CRP and IL-6 levels. The HE-stained sections showed no obvious micromorphological changes in the O3 exposure, but the NQO1 average optical density was higher than the control on the 15th day (p &lt; 0.05). The ultrastructural changes were found in the O3 exposure group, such as bulges and vacuoles in type I alveolar cells, the increased evacuation of substance from lamellar bodies in the type II alveolar cells, the increased space around the goblet nucleus, binuclear goblet, and columnar cells. CRP and IL-6 levels increased compared with the control (p &lt; 0.05). Although inhaling 1.1 ppm O3 had no significant effect on the micromorphology of the mice lungs and bronchi, it did affect the ultrastructure with oxidative stress and inflammatory responses.