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With the rapid development of wireless communications, the occupation of time and frequency resources becomes more crowded. The exploitation of space resources is necessary and the diversity combining techniques have substantial applications. Diversity combining achieves great diversity gains and improves the ability to combat multipath fading, among which the maximum ratio combining (MRC) performs as the optimal linear combining approach. However, MRC suffers from detrimental factors such as channel fading and no Gaussian noise in practical scenarios. In this paper, we focus on a comprehensive investigation of MRC. Starting from the MRC principle and system model, we summarize typical scenarios and analyze the channel fading statistics. For the influential factors, we further review related literature on channel correlation, cochannel interference (CCI) and impulsive noise. Major performance criteria and performance bounds are derived and compared. MRC confronts new developing challenges and the major development directions are reviewed. The paper finally discusses recent works and open problems for MRC applications and development. Emerging techniques such as artificial intelligence provide novel solutions for MRC performance improvements. The paper aims to present a summarized insight to assist readers in clarifying the analyzed methodology of MRC, so as to motivate new technology integration and extensive applications of advanced communication systems. [ABSTRACT FROM AUTHOR]

Ship-radiated noise is the main basis for ship detection in underwater acoustic environments. Due to the increasing human activity in the ocean, the captured ship noise is usually mixed with or covered by other signals or noise. On the other hand, due to the softening effect of bubbles in the water generated by ships, ship noise undergoes non-negligible nonlinear distortion. To mitigate the nonlinear distortion and separate the target ship noise, blind source separation (BSS) becomes a promising solution. However, underwater acoustic nonlinear models are seldom used in research for nonlinear BSS. This paper is based on the hypothesis that the recovery and separation accuracy can be improved by considering this nonlinear effect in the underwater environment. The purpose of this research is to explore and discover a method with the above advantages. In this paper, a model is used in underwater BSS to describe the nonlinear impact of the softening effect of bubbles on ship noise. To separate the target ship-radiated noise from the nonlinear mixtures, an end-to-end network combining an attention mechanism and bidirectional long short-term memory (Bi-LSTM) recurrent neural network is proposed. Ship noise from the database ShipsEar and line spectrum signals are used in the simulation. The simulation results show that, compared with several recent neural networks used for linear and nonlinear BSS, the proposed scheme has an advantage in terms of the mean square error, correlation coefficient and signal-to-distortion ratio. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO), one of the products of heme oxygenase action on heme, prevents arteriosclerotic lesions that occur following aorta transplantation; pre-exposure to 250 parts per million of CO for 1 hour before injury suppresses stenosis after carotid balloon injury in rats as well as in mice. The protective effect of CO is associated with a profound inhibition of graft leukocyte infiltration/activation as well as with inhibition of smooth muscle cell proliferation. The anti-proliferative effect of CO in vitro requires the activation of guanylate cyclase, the generation of cGMP, the activation of p38 mitogen-activated protein kinases and the expression of the cell cycle inhibitor p21[sup.Cip1]. These findings demonstrate a protective role for CO in vascular injury and support its use as a therapeutic agent., Author(s): Leo E. Otterbein [1, 7]; Brian S. Zuckerbraun [2, 7]; Manabu Haga [3, 7]; Fang Liu [1]; Ruiping Song [1]; Anny Usheva [4]; Christina Stachulak [4]; Natalya Bodyak [4]; [...]

Asthma, a chronic inflammatory disease of the airways, involves the increased expression of inflammatory mediators, including granulocyte-monocyte colony-stimulating factor (GM-CSF). Heme oxygenase-1 (HO-1), a stress-response protein, confers protection against oxidative stress. We hypothesized that carbon monoxide (CO), a byproduct of HO-1-dependent heme catabolism, regulates GM-CSF synthesis in human airway smooth muscle cells (HASMC). IL-1[beta] treatment induced a time-dependent induction of GM-CSF in HASMC. Furthermore, IL-1[beta] stimulated the major MAPK pathways, including ERK1/ERK2, JNK, and p38 MAPK. Exposure of HASMC to CO at low concentration (250 ppm) markedly inhibited IL-1[beta]-induced GM-CSF synthesis (>90%) compared with air-treated controls. CO treatment inhibited IL-1[beta]-induced ERK1/2 activation but did not inhibit JNK and p38 MAPK. Furthermore, CO increased cGMP levels in HASMC. Inhibition of guanylate cyclase by IH-[1,2,4] oxadiazolo[4,3a]quinoxalin-1-1 (ODQ) abolished the inhibitory effects of CO on GM-CSF synthesis and ERK1/2 activation. Collectively, these data demonstrate that the inhibitory effect of CO on GM-CSF synthesis depends on ERK1/2 MAPK and guanylate cyclase/cGMP-dependent pathways. cyclic guanosine monophosphate; granulocyte-monocyte colony-stimulating factor; mitogen activated protein kinase; interleukin-1[beta]

In lung injury and progressive lung diseases, the multifunctional cytokine transforming growth factor-[[beta].sub.1] (TGF-[[beta].sub.1]) modulates inflammatory responses and wound repair. Heme oxygenase-1 (HO-1) is a stress-inducible protein that has been demonstrated to confer cytoprotection against oxidative injury and provide a vital function in maintaining tissue homeostasis. Here we report that TGF-[[beta].sub.1] is a potent inducer of HO-1 and examined the signaling pathway by which TGF-[[beta].sub.1] regulates HO-1 expression in human lung epithelial cells (A549). TGF-[[beta].sub.1] (1-5 ng/ml) treatment resulted in a marked time-dependent induction of HO-1 mRNA in A549 cells, followed by corresponding increases in HO-1 protein and HO enzymatic activity. Actinomycin D and cycloheximide inhibited TGF-[[beta].sub.1]-responsive HO-1 mRNA expression, indicating a requirement for transcription and de novo protein synthesis. Furthermore, TGF-[[beta].sub.1] rapidly activated the p38 mitogen-activated protein kinase (p38 MAPK) pathway in A549 cells. A chemical inhibitor of p38 MAPK (SB-203580) abolished TGF-[[beta].sub.1]-inducible HO-1 mRNA expression. Both SB-203580 and expression of a dominant-negative mutant of p38 MAPK inhibited TGF-[[beta].sub.1]-induced ho-1 gene activation, as assayed by luciferase activity of an ho-1 enhancer/luciferase fusion construct (pMHO1luc-33+SX2). These studies demonstrate the critical intermediacy of the p38 MAPK pathway in the regulation of HO-1 expression by TGF-[[beta].sub.1]. heme oxygenase; inflammation; mitogen-activated protein kinase; oxidant stress; transforming growth factor-[[beta].sub.1]

To better understand the molecular basis of chronic obstructive pulmonary disease (COPD), we used serial analysis of gene expression (SAGE) and microarray analysis to compare the gene expression patterns of lung tissues from COPD and control smokers. A total of 59,343 tags corresponding to 26,502 transcripts were sequenced in SAGE analyses. A total of 327 genes were differentially expressed (1.5-fold up- or down-regulated). Microarray analysis using the same RNA source detected 261 transcripts that were differentially ex- pressed to a significant degree between GOLD-2 and GOLD-O smokers. We confirmed the altered expression of a select number of genes by using real-time quantitative RT-PCR. These genes encode for transcription factors (EGRI and FOS), growth factors or related proteins (CTGF, CYR61, CX3CL1, TGFB1, and PDGFRA)S and extracellular matrix protein (COLIA1). Immunofluorescence studies on the same lung specimens localized the expression of Egr-1, CTGF, and Cyr61 to alveolar epithelial cells, airway epithelial cells, and stromal and inflammatory cells of GOLD-2 smokers. Cigarette smoke extract induced Egr-1 protein expression and increased Egr-1 DNA-binding activity in human lung fibroblast cells. Cytomix (tumor necrosis factor a, IL-I fi, and IFN-y) treatment showed that the activity of matrix metalloproteinase-2 (MMP-2) was increased in lung fibroblasts from EGRI control (+ 1+) mice but not detected in that of EGRI null (-I-) mice, whereas MMP-9 was regulated by EGR1 in a reverse manner. Our study represents the first comprehensive analysis of gene expression on GOLD-2 versus GOLD-0 smokers and reveals previously unreported candidate genes that may serve as potential molecular targets in COPD. [ABSTRACT FROM AUTHOR]

Hypoxial reoxygenation causes cellular injury and death associated with a number of pathophysiological conditions, including myocardial ischemia]reperfusion injury and stroke. The cell death pathways induced by hypoxia]reoxygenation and their underlying regulatory mechanisms remain poorly understood. Recent studies have shown that hypoxia/reoxygenation can induce Bax translocation and cytochrome c release. Using murine lung endothelial cells as a model, we found that the induction of apoptosis by hypoxia/reoxygenation involved the activation of both Bax-dependent and death receptor-mediated pathways. We demonstrated the activation of the death-inducing signal complex and Bid pathway after hypoxia/reoxygenation. Hepatocyte growth factor markedly inhibited hypoxia/reoxygenation-induced endothelial cell apoptosis. The cytoprotection afforded by hepatocyte growth factor was mediated in part by the stimulation of FLICE-like inhibiting protein expression, the attenuation of death-inducing signal complex formation, and the inhibition of Bid and Bax activation. Hepatocyte growth factor also prevented cell injury and death by increasing the expression of the antiapoptotic Bcl-XL protein. The inhibition of Bid/Bax-induced cell death by hepatocyte growth factor primarily involved p38 MAPK and in part Akt-dependent pathways but not ERK1/ERK2. [ABSTRACT FROM AUTHOR]