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With the development of intelligentizing of Urban Rail Transit (URT), the data that need to be transmitted between train and OCC (Operational Contral Center) has increased significantly, and the licensed spectrum range is gradually unable to satisfy the data transfer task of URT communication systems(URT-cs). Therefore, this article considers to use LTE-U (Long-Term-Evolution in unlicensed spectrum) technology to deploy this communication system in unlicensed spectrum. In view of the interference caused by the introduction to WLAN system which have already been deployed in unlicensed spectrum, a dynamic spectrum range duty cycle adjustment scheme based on Q-learning algorithm is proposed to achieve coexistence of the two system. The scheme takes spectrum range as state, modelling the spectrum range allocation as a Markov Decision Process, obtains the spectrum range allocation strategy through Q-learning algorithm. Simulation results show that, compared with fixed spectrum allocation, the proposed scheme has a higher throughput and user satisfaction. Realizing the transmission task of URT-cs while meeting the user satisfaction of the WLAN system, and the problem of spectrum resources insufficiency of URT-cs is well solved.

To carry out the experimental verification of the mechanical properties analysis of the radome considering the damage factors, the test matrix design is carried out according to the finite element analysis method of the equivalent elastic theory and the idea of building block test verification. Firstly, the necessity and basic principle of equivalent elasticity theory in the performance analysis of complex curvature products considering damage factors are explained. Then, combined with the theory, a modular test matrix design is carried out, which should be able to test the correctness of the equivalent elastic modulus. Finally, a case study is carried out, and the difference between the test results and the simulation results is analyzed with the damaged radome as the research object. The results show that the development of the equivalent elasticity theory and the design of the test matrix can make the analysis results meet the engineering requirements.

Biofilms are organised aggregates of bacteria that adhere to each other or surfaces. The matrix of extracellular polymeric substances that holds the cells together provides the mechanical stability of the biofilm. In this study, we have applied Brillouin microscopy, a technique that is capable of measuring mechanical properties of specimens on a micrometre scale based on the shift in frequency of light incident upon a sample due to thermal fluctuations, to investigate the micromechanical properties of an active, live Pseudomonas aeruginosa biofilm. Using this non-contact and label-free technique, we have extracted information about the internal stiffness of biofilms under continuous flow. No correlation with colony size was found when comparing the averages of Brillouin shifts of two-dimensional cross-sections of randomly selected colonies. However, when focusing on single colonies, we observed two distinct spatial patterns: in smaller colonies, stiffness increased towards their interior, indicating a more compact structure of the centre of the colony, whereas, larger (over 45 μm) colonies were found to have less stiff interiors. Biofilm structure: Shining a light on stiffness A specialized microscopy technique can monitor biofilm stiffness in a non-destructive manner, yielding insights into biofilm structure and development. The technique, called Brillouin imaging, uses changes in the frequency of light interacting with a substance to reveal fine detail about the material’s mechanical properties. Peter Török and colleagues at Imperial College London, with co-workers in Singapore, used Brillouin imaging to study biofilms of Pseudomonas aeruginosa bacteria at different stages in their life cycle. In young colonies, stiffness increased towards the interior of the biofilm, while mature colonies had less stiff interiors. The older biofilms may therefore have hollow interiors or may have been moving towards a phase of bacterial dispersal from the biofilm state. This non-disruptive method to study mechanical variations within and between living biofilms may help efforts to combat biofilms in clinical, environmental and industrial situations.

The transforming growth factor-β (TGF-β) family of cytokines and glucocorticoids regulate diverse biological processes through modulating the expression of target genes. Here we report that glucocorticoid receptor (GR) represses TGF-β transcriptional activation of the type-1 plasminogen activator inhibitor (PAI-1) gene in a ligand-dependent manner. Similarly, GR represses TGF-β activation of the TGF-β responsive sequencing containing Smad3/4-binding sites. Using mammalian two-hybrid assays, we demonstrate that GR inhibits transcriptional activation by both Smad3 and Smad4 C-terminal activation domains. Finally, we show that GR interacts with Smad3 both in vitro and in vivo. These results suggest a molecular basis for the cross-regulation between glucocorticoid and TGF-β signaling pathways.

The compression of a double-notched specimen was used to determine the in-plane shear strength (IPSS) of a carbon/carbon composite in the paper. The effects of the notch distance ( L ), thickness ( T ), and notch width ( W ) and supporting jig on the IPSS of the double-notched specimens were investigated numerically and experimentally. The fracture surfaces were examined by a scanning electron microscope. It was found that the IPSS varied with L . Thin specimen yielded low strength. W has little effect on IPSS. The main failure modes include the matrix shear cracking, delamination, fracture and pullout of fibers or fiber bundles. Meanwhile, a supporting jig can provide lateral support and prevent buckling, therefore lead to the failure in a shear mode.

The Tat protein encoded by human immunodeficiency virus type 1 is a strong transcriptional activator of gene expression from the viral long terminal repeat and is essential for virus replication. We have investigated the molecular mechanism of Tat trans-activation by using a cell-free transcription system. We find that the trans-activation domain of Tat, amino acid residues 1-48 [Tat-(1-48)], can inhibit specifically-i.e., \"squelch,\" transcriptional activation by full-length Tat [Tat-(1-86)]. Squelching depends upon the functional integrity of the Tat trans-activation domain because the mutant [Ala41]Tat-(1-48), which is defective in Tat trans-activation in vivo and in vitro, does not squelch in vitro Tat trans-activation. Inhibition is selective because Tat-activated transcription, but not Tat-independent transcription, is squelched. Preincubation experiments with Tat or Tat-(1-48) and nuclear extracts show that the trans-activation region of Tat can interact with cellular coactivator(s) required for Tat trans-activation and that this interaction can occur in the absence of the human immunodeficiency virus long terminal repeat promoter. Furthermore, the putative coactivator(s) mediating trans-activation by Tat differ from those mediating trans-activation by the acidic activator VP16, as shown by reciprocal squelching experiments in vitro. Our results suggest that specific cellular coactivator(s) are required for mediating activated transcription by human immunodeficiency virus type 1 Tat.

The 243-amino acid adenovirus E1A oncoprotein both positively and negatively modulates the expression of cellular genes involved in the regulation of cell growth. The E1A transcription repression function appears to be linked with its ability to induce cellular DNA synthesis, cell proliferation, and cell transformation, as well as to inhibit cell differentiation. The mechanism by which E1A represses the transcription of various promoters has proven enigmatic. Here we provide several lines of evidence that the \"TATA-box\" binding protein (TBP) component of transcription factor TFIID is a cellular target of the E1A repression function encoded within the E1A N-terminal 80 amino acids. (i) The E1A N-terminal 80 amino acids [E1A-(1-80)protein] efficiently represses basal transcription from TATA-containing core promoters in vitro. (ii) TBP reverses completely E1A repression in vitro. (iii) TBP restores transcriptional activity to E1A-(1-80) protein affinity-depleted nuclear extracts. (iv) The N-terminal repression domain of E1A interacts directly and specifically with TBP in vitro. These results may help explain how E1A represses a set of genes that lack common upstream promoter elements.

This study employed probit regression analysis to determine the 90% effective dose (ED ) of oliceridine when combined with propofol for day-case hysteroscopy. 100 patients undergoing hysteroscopic surgery were randomized to receive intravenous oliceridine (0.01, 0.015, 0.02, 0.025, or 0.03 mg kg ) 3 minutes preoperatively. Propofol was administered intravenously at 2 mg kg induction and maintained at 6 mg kg h . Successful anesthesia was defined as absence of body movement during cervical dilation. Parameters recorded included the success rate, propofol consumption, total surgical duration, recovery time, postoperative pain, and adverse events. The ED of oliceridine for suppressing response to cervical dilation was 0.025 (95% confidence interval, CI, 0.020-0.050) mg kg . The incidence of propofol injection pain in the 0.01, 0.015, 0.02, 0.025, and 0.03 mg kg oliceridine groups (80%, 80%, 45%, 40%, and 30%, respectively) were significantly different (P = 0.001). There was no difference in the propofol requirements, time to anesthesia emergence, and visual analog scores(VAS) at 30 minutes postoperation among groups. No serious adverse events occurred in any patient. For healthy adult women undergoing day-case hysteroscopy, oliceridine 0.025 mg kg combined with propofol provides effective and safe anesthesia.