Filter and nested-lattice code design for fading MIMO channels with side-information

Linear-assignment Gel'fand-Pinsker coding (LA-GPC) is a coding technique for channels with interference known only at the transmitter, where the known interference is treated as side-information (SI). As a special case of LA-GPC, dirty paper coding has been shown to be able to achieve the optimal interference-free rate for interference channels with perfect channel state information at the transmitter (CSIT). In the cases where only the channel distribution information at the transmitter (CDIT) is available, LA-GPC also has good (sometimes optimal) performance in a variety of fast and slow fading SI channels. In this paper, we design the filters in nested-lattice based coding to make it achieve the same rate performance as LA-GPC in multiple-input multiple-output (MIMO) channels. Compared with the random Gaussian codebooks used in previous works, our resultant coding schemes have an algebraic structure and can be implemented in practical systems. A simulation in a slow-fading channel is also provided, and near interference-free error performance is obtained. The proposed coding schemes can serve as the fundamental building blocks to achieve the promised rate performance of MIMO Gaussian broadcast channels with CDIT or perfect CSITComment: submitted to IEEE Transactions on Communications, Feb, 200

Multi-user lattice coding for the multiple-access relay channel

This paper considers the multi-antenna multiple access relay channel (MARC), in which multiple users transmit messages to a common destination with the assistance of a relay. In a variety of MARC settings, the dynamic decode and forward (DDF) protocol is very useful due to its outstanding rate performance. However, the lack of good structured codebooks so far hinders practical applications of DDF for MARC. In this work, two classes of structured MARC codes are proposed: 1) one-to-one relay-mapper aided multiuser lattice coding (O-MLC), and 2) modulo-sum relay-mapper aided multiuser lattice coding (MS-MLC). The former enjoys better rate performance, while the latter provides more flexibility to tradeoff between the complexity of the relay mapper and the rate performance. It is shown that, in order to approach the rate performance achievable by an unstructured codebook with maximum-likelihood decoding, it is crucial to use a new K-stage coset decoder for structured O-MLC, instead of the one-stage decoder proposed in previous works. However, if O-MLC is decoded with the one-stage decoder only, it can still achieve the optimal DDF diversity-multiplexing gain tradeoff in the high signal-to-noise ratio regime. As for MS-MLC, its rate performance can approach that of the O-MLC by increasing the complexity of the modulo-sum relay-mapper. Finally, for practical implementations of both O-MLC and MS-MLC, practical short length lattice codes with linear mappers are designed, which facilitate efficient lattice decoding. Simulation results show that the proposed coding schemes outperform existing schemes in terms of outage probabilities in a variety of channel settings.Comment: 32 pages, 5 figure

Malignant phyllodes tumors display mesenchymal stem cell features and aldehyde dehydrogenase/disialoganglioside identify their tumor stem cells.

IntroductionAlthough breast phyllodes tumors are rare, there is no effective therapy other than surgery. Little is known about their tumor biology. A malignant phyllodes tumor contains heterologous stromal elements, and can transform into rhabdomyosarcoma, liposarcoma and osteosarcoma. These versatile properties prompted us to explore their possible relationship to mesenchymal stem cells (MSCs) and to search for the presence of cancer stem cells (CSCs) in phyllodes tumors.MethodsParaffin sections of malignant phyllodes tumors were examined for various markers by immunohistochemical staining. Xenografts of human primary phyllodes tumors were established by injecting freshly isolated tumor cells into the mammary fat pad of non-obese diabetic-severe combined immunodeficient (NOD-SCID) mice. To search for CSCs, xenografted tumor cells were sorted into various subpopulations by flow cytometry and examined for their in vitro mammosphere forming capacity, in vivo tumorigenicity in NOD-SCID mice and their ability to undergo differentiation.ResultsImmunohistochemical analysis revealed the expression of the following 10 markers: CD44, CD29, CD106, CD166, CD105, CD90, disialoganglioside (GD2), CD117, Aldehyde dehydrogenase 1 (ALDH), and Oct-4, and 7 clinically relevant markers (CD10, CD34, p53, p63, Ki-67, Bcl-2, vimentin, and Globo H) in all 51 malignant phyllodes tumors examined, albeit to different extents. Four xenografts were successfully established from human primary phyllodes tumors. In vitro, ALDH+ cells sorted from xenografts displayed approximately 10-fold greater mammosphere-forming capacity than ALDH- cells. GD2+ cells showed a 3.9-fold greater capacity than GD2- cells. ALDH+/GD2+cells displayed 12.8-fold greater mammosphere forming ability than ALDH-/GD2- cells. In vivo, the tumor-initiating frequency of ALDH+/GD2+ cells were up to 33-fold higher than that of ALDH+ cells, with as few as 50 ALDH+/GD2+ cells being sufficient for engraftment. Moreover, we provided the first evidence for the induction of ALDH+/GD2+ cells to differentiate into neural cells of various lineages, along with the observation of neural differentiation in clinical specimens and xenografts of malignant phyllodes tumors. ALDH+ or ALDH+/GD2+ cells could also be induced to differentiate into adipocytes, osteocytes or chondrocytes.ConclusionsOur findings revealed that malignant phyllodes tumors possessed many characteristics of MSC, and their CSCs were enriched in ALDH+ and ALDH+/GD2+ subpopulations

Energy and centrality dependences of charged multiplicity density in relativistic nuclear collisions

Using a hadron and string cascade model, JPCIAE, the energy and centrality dependences of charged particle pseudorapidity density in relativistic nuclear collisions were studied. Within the framework of this model, both the relativistic $p+\bar p$ experimental data and the PHOBOS and PHENIX $Au+Au$ data at $\sqrt s_{nn}$=130 GeV could be reproduced fairly well without retuning the model parameters. The predictions for full RHIC energy $Au+Au$ collisions and for $Pb+Pb$ collisions at the ALICE energy were given. Participant nucleon distributions were calculated based on different methods. It was found that the number of participant nucleons, $$, is not a well defined variable both experimentally and theoretically. Therefore, it is inappropriate to use charged particle pseudorapidity density per participant pair as a function of$$ for distinguishing various theoretical models.Comment: 10 pages, 4 figures, submitted to Phy. Lett.

Osteopontin mediates tumorigenic transformation of a preneoplastic murine cell line by suppressing anoikis: An Arg‐Gly‐Asp‐dependent‐focal adhesion kinase‐caspase‐8 axis

Osteopontin (OPN), an adhesive, matricellular glycoprotein, is a rate‐limiting factor in tumor promotion of skin carcinogenesis. With a tumor promotion model, the JB6 Cl41.5a cell line, we have shown that suppressing 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA)‐induced OPN expression markedly inhibits TPA‐induced colony formation in soft agar, an assay indicative of tumorigenic transformation. Further, the addition of exogenous OPN promotes colony formation of these cells. These findings support a function of OPN in mediating TPA‐induced neoplastic transformation of JB6 cells. In regard to the mechanism of action by OPN, we hypothesized that, for JB6 cells grown in soft‐agar, secreted OPN induced by TPA stimulates cell proliferation and/or prevents anoikis to facilitate TPA‐induced colony formation. Analyses of cell cycle and cyclin D1 expression, and direct cell counting of JB6 cells treated with OPN indicate that OPN does not stimulate cell proliferation relative to non‐treated controls. Instead, at 24 h, OPN decreases anoikis by 41%, as assessed by annexin V assays. Further, in suspended cells OPN suppresses caspase‐8 activation, which is mediated specifically through its RGD‐cell binding motif that transduces signals through integrin receptors. Transfection studies with wild‐type and mutant focal adhesion kinases (FAK) and Western blot analyses suggest that OPN suppression of caspase‐8 activation is mediated through phosphorylation of FAK at Tyr861. In summary, these studies indicate that induced OPN is a microenvironment modulator that facilitates tumorigenic transformation of JB6 cells by inhibiting anoikis through its RGD‐dependent suppression of caspase‐8 activity, which is mediated in part through the activation of FAK at Tyr861. © 2013 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111135/1/mc22108.pd

Inspiratory muscle warm-up does not improve cycling time-trial performance

Purpose: This study examined the effects of an active cycling warm-up, with and without the addition of an inspiratory muscle warm-up (IMW), on 10-km cycling time-trial performance