Low phosphorus (P) availability and salt stress are two major constraints for maize ( Zea mays L.) growth in north China. A combination of salinity and high P rather than low P is more detrimental to the growth of maize. However, little is known about the mechanisms by which P nutrition modifies the salt tolerance and P uptake of maize. The present study aimed to investigate the combined effects of salinity and P on maize growth and P uptake, and to address the physiological mechanisms of salt tolerance influenced by P availability in maize. Seedlings of a local maize cultivar XY335 were grown hydroponically for 35 days under low (5 μM) or sufficient P supply (200 μM) with or without 100 mM NaCl. Root morphological traits, tissue mass density, leaf osmolytes (sugars and proline) accumulation, and Na + /K + ratio were measured to allow evaluation of the combined effects of salinity and P on maize growth and P uptake. Both P deficiency and salinity markedly reduced the growth of maize. However, P deficiency had a more pronounced effect on shoot growth while salinity affected root growth more prominently. Combined effects of P deficiency and salinity on total root length, root surface area, and average root diameter were similar to that of plants grown under salt stress. The combination of P deficiency and salinity treatments had a more pronounced effect on tissue mass density, leaf proline and soluble sugars compared to individual treatment of either low P or NaCl. When exposed to salt stress, maize plants of sufficient P accumulated greater amount of Na + than those under P deficit, but similar amounts of K + were observed between the two P treatments. Salt stress significantly increased shoot P concentration of maize with sufficient P ( P < 0.01), but not for P-deficient plants. In sum, shoots and roots of maize exhibited different responses to P deficiency and salinity, with more marked effect of P deficiency on shoots and of salinity on roots. P deficiency improved salt tolerance of maize plants, which was associated with the increase of tissue mass density, accumulation of osmolytes, reduction of Na + accumulation, and selective absorption of K + over Na + .

Receptor for advanced glycation end-products (RAGE) and TLR4 play an important role in the inflammatory response against High-mobility group box 1 protein (HMGB1), a late proinflammatory cytokine and a damage-associated molecular pattern. As cell surface receptors, both RAGE and TLR4 are constantly trafficking between the cytoplasm and plasma membrane. However, whether TLR4 is related to the intracellular transport of RAGE in HMGB1-induced inflammation remains unknown. In this study, we demonstrated that HMGB1 not only increased RAGE expression in both the cytoplasm and plasma membrane but also upregulated the expression of TLR4 in the plasma membrane. Knocking out of RAGE led to decreased MAPK activation, TLR4 cellular membrane expression, and corresponding inflammatory cytokine generation. Meanwhile, inhibiting MAPK activation also decreased TLR4 surface expression. These results indicated that HMGB1 may bind to cell surface RAGE receptors on the cell surface, leading to MAPK activation, thus promoting TLR4 translocation on the cell surface, but does not regulate its transcription and translation. In contrast, TLR4 can increase the transcription and translation of RAGE, which translocates to the cell surface and is able to bind to more HMGB1. The cell surface receptors TLR4 and RAGE bind to HMGB1, leading to the transcription and secretion of inflammatory cytokines. Finally, we also observed these results in the mice pseudofracture model, which is closely related to HMGB1-induced inflammatory response. All these results demonstrated that the interplay between RAGE and TLR4 are critical for HMGB1-induced inflammatory response.

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Unmanned aerial vehicle (UAV) assisted communication is a promising technique for future wireless networks due to its characteristics of low cost and flexible deployment. However, the high possibility of line-of-sight (LoS) air-ground channels may result in a great risk of being attacked by malicious users. Especially compared to the encryption and physical layer security that prevent the eavesdropping, covert communication aims at hiding the existence of transmission, which is able to satisfy the more critical requirement of security. Thus, in this article, we focus on the covert communication issues of UAV-assisted wireless networks. First, the preliminaries of secure communications including encryption, physical layer security and covert communication are discussed. Then, current works and typical applications of UAV in covert communications are demonstrated. Furthermore, we propose two schemes to enhance the covertness of UAV-assisted networks for some typical scenarios. Specifically, to improve the covert rate in UAV-assisted data dissemination, an iterative algorithm is proposed to jointly optimize the time slot, transmit power and trajectory. For the covertness of ground-air communication, a friendly jammer is employed to confuse the wardens, where the location of jammer, the jamming power and the legitimate transmit power are jointly optimized. Numerical results are presented to validate the performance of these two proposed schemes. Finally, several challenges and promising directions are pointed out.

Gastric cancer (GC) is one of the most common cancers in the world. The cathepsin F (CTSF) gene has recently been found to participate in the progression of several types of cancer. However, the clinical characteristics and function of CTSF in GC as well as its molecular mechanisms are not clear. Six GC cell lines and 44 paired adjacent noncancerous and GC tissue samples were used to assess CTSF expression by quantitative polymerase chain reaction (qPCR). We used lentivirus-mediated small hairpin RNA (Lenti-shRNA) against CTSF to knock down the expression of CTSF in GC cells. Western blot and qPCR were used to analyze the mRNA and related protein expression. The biological phenotypes of gastric cells were examined by cell proliferation and apoptosis assays. Microarray-based mRNA expression profile screening was also performed to evaluate the potential molecular pathways in which CTSF may be involved. The CTSF mRNA level was associated with tumor differentiation, depth of tumor invasion, and lymph node metastasis. Downregulation of CTSF expression efficiently inhibited apoptosis and promoted the proliferation of GC cells. Moreover, a total of 1,117 upregulated mRNAs and 1,143 downregulated mRNAs were identified as differentially expressed genes (DEGs). Further analysis identified the involvement of these mRNAs in cancer-related pathways and various other biological processes. Nine DEGs in cancer-related pathways and three downstream genes in the apoptosis pathway were validated by Western blot, which was mainly in agreement with the microarray data. To our knowledge, this is the first report investigating the effect of CTSF on the growth and apoptosis in GC cells and its clinical significance. The CTSF gene may function as a tumor suppressor in GC and may be a potential therapeutic target in the treatment of GC.

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Calcineurin B-like protein-interacting protein kinases (CIPKs) play essential roles in plant abiotic stress response. In order to better understand salt tolerance, we cloned and analyzed the NtCIPK9 gene from the halophyte Nitraria tangutorum. Phylogenetic analysis shows that NtCIPK9 belongs to a sister clade with the Arabidopsis AtCIPK9 gene and is thought to localize to the plasma membrane. NtCIPK9 shows the highest expression level in the Nitraria tangutorum root under normal growth conditions, whereas after NaCl treatment, the highest expression was found in the blade. NtCIPK9-overexpressing Arabidopsis plants have a higher seed germination rate, longer root length, and displayed higher salt tolerance than wild type seedlings under salt stress conditions. Furthermore, NtCIPK9 overexpression might enhance the expression of genes related to K + transportation after NaCl treatment. Thus, we conclude that NtCIPK9 increases transgenic plant salt tolerance and reduces damage associated with salt stress by promoting the expression of genes controlling ion homeostasis. Our results suggest that NtCIPK9 could serve as an ideal candidate gene to genetically engineer salttolerant plants.