This paper considers the massive connectivity application in which a large number of potential devices communicate with a base-station (BS) in a sporadic fashion. The detection of device activity pattern together with the estimation of the channel are central problems in such a scenario. Due to the large number of potential devices in the network, the devices need to be assigned non-orthogonal signature sequences. The main objective of this paper is to show that by using random signature sequences and by exploiting sparsity in the user activity pattern, the joint user detection and channel estimation problem can be formulated as a compressed sensing single measurement vector (SMV) problem or multiple measurement vector (MMV) problem, depending on whether the BS has a single antenna or multiple antennas, and be efficiently solved using an approximate message passing (AMP) algorithm. This paper proposes an AMP algorithm design that exploits the statistics of the wireless channel and provides an analytical characterization of the probabilities of false alarm and missed detection by using the state evolution. We consider two cases depending on whether the large-scale component of the channel fading is known at the BS and design the minimum mean squared error (MMSE) denoiser for AMP according to the channel statistics. Simulation results demonstrate the substantial advantage of exploiting the statistical channel information in AMP design; however, knowing the large-scale fading component does not offer tangible benefits. For the multiple-antenna case, we employ two different AMP algorithms, namely the AMP with vector denoiser and the parallel AMP-MMV, and quantify the benefit of deploying multiple antennas at the BS.
Natural killer (NK) cells are found in lymphoid and non-lymphoid organs. In addition to important roles in immune surveillance, some NK cells contribute to angiogenesis and circulatory regulation. The uterus of early pregnancy is a non-lymphoid organ enriched in NK cells that are specifically recruited to placental attachment sites. In species with invasive hemochorial placentation, these uterine natural killer (uNK) cells, via secretion of cytokines, chemokines, mucins, enzymes and angiogenic growth factors, contribute to the physiological change of mesometrial endometrium into the unique stromal environment called decidua basalis. In humans, uNK cells have the phenotype CD56 bright CD16 dim and they appear in great abundance in the late secretory phase of the menstrual cycle and early pregnancy. Gene expression studies indicate that CD56 bright CD16 dim uterine and circulating cells are functionally distinct. In humans but not mice or other species with post-implantation decidualization, uNK cells may contribute to blastocyst implantation and are of interest as therapeutic targets in female infertility. Histological and genetic studies in mice first identified triggering of the process of gestation spiral arterial modification as a major uNK cell function, achieved via interferon (IFN)-c secretion. During spiral arterial modification, branches from the uterine artery that traverse the endometrium/decidua transiently lose their muscular coat and ability to vasoconstrict. The expression of vascular markers changes from arterial to venous as these vessels dilate and become low-resistance, high-volume channels. Full understanding of the vascular interactions of human uNK cells is difficult to obtain because endometrial time-course studies are not possible in pregnant women. Here we briefly review key information concerning uNK cell functions from studies in rodents, summarize highlights concerning human uNK cells and describe our preliminary studies on development of a humanized, pregnant mouse model for in vivo investigations of human uNK cell functions.
The biocide chlorhexidine (CHX) as well as additional membrane-active agents were shown to induce expression of the mexCD-oprJ multidrug efflux operon, dependent upon the AlgU stress response sigma factor. Hyperexpression of this efflux system in nfxB mutants was also substantially AlgU dependent. CHX resistance correlated with efflux gene expression in various mutants, consistent with MexCD-OprJ being a determinant of CHX resistance.Pseudomonas aeruginosa is an opportunistic human pathogen characterized by an innate resistance to multiple antimicrobials (13), resistance increasingly attributable to the operation of broadly specific, tripartite multidrug efflux systems of the resistance-nodulation-division (RND) family (35,36). One of these, MexCD-OprJ, was originally identified as a determinant of fluoroquinolone resistance (17) but is known to accommodate a variety of clinically relevant antimicrobials (35, 36) as well as biocides (5), dyes, detergents, and organic solvents (27,45,46). MexCD-OprJ is typically quiescent in wild-type cells (20,46), with expression following mutation of the nfxB gene (16,22,23,50) that is divergently transcribed from the mexCDoprJ operon and encodes a repressor of mexCD-oprJ expression (37). Little is known about the signal(s) to which this regulator responds in naturally promoting efflux gene expression, although mexCD-oprJ is inducible by the biocides benzalkonium chloride and chlorhexidine (CHX) (33). These biocides are known to interact with and disrupt bacterial membranes (8), with the possibility that mexCD-oprJ expression is a response to membrane damage/envelope stress. Envelope stress responses (ESRs) are well documented in bacteria (40, 41), with the extracytoplasmic sigma factor RpoE being a key regulator of ESRs in Escherichia coli and other gram-negative bacteria (1,40,41). The RpoE homologue in P. aeruginosa is AlgU, first identified as a regulator of alginate production in mucoid isolates recovered from the lungs of cystic fibrosis patients (15, 28) and shown to be functionally interchangeable with RpoE (51). This study was undertaken to assess the contribution of MexCD-OprJ to biocide resistance in P. aeruginosa and its possible regulation as part of an ESR.Bacterial strains and plasmids used in this study are listed in Table 1. Bacteria were cultivated at 37°C in Luria broth (LB) (34) supplemented with antibiotics to maintain plasmids as needed (for pEX18Tc and derivatives, tetracycline was used [10 g/ml for E. coli and 50 to 100 g/ml for P. aeruginosa]; for pMMB206 and derivatives, chloramphenicol was used [10 g/ml for E. coli and 150 g/ml for P. aeruginosa]; for pK18MobSacB and derivatives, kanamycin was used [50 g/ml for E. coli and 750 to 1,500 g/ml for P. aeruginosa as indicated]; for miniCTX-lacZ and derivatives, tetracycline was used [10 g/ml for E. coli and 25 g/ml for P. aeruginosa]; and for pUC19 and derivatives, ampicillin was used [100 g/ml for E. coli]). AlgU-encoding plasmid pSF02 was constructed by amplifying the algU gene from the chromosome (isol...
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