In this paper, we propose a partially-parallel irregular LDPC decoder for IEEE 802.11n standard. The design is based on a novel sum-delta message passing schedule to achieve high throughput and low area cost design. We further improve the design with pipeline structure and parallel computation. The synthesis result in TSMC 0.18 CMOS technology demonstrates that for (648,324) irregular LDPC code, our decoder achieves 7.5X improvement in throughput, which reaches 402 Mbps at the frequency of 200 MHz, with 11% area reduction.

BACKGROUND:Donor-specific blood transfusion (DST) prior to solid organ transplantation has been shown to induce long-term allograft survival in the absence of immunosuppressive therapy. Although the mechanisms underlying DST-induced allograft tolerance are not well defined, there is evidence to suggest DST induces one or more populations of antigen-specific regulatory cells that suppress allograft rejection. However, neither the identity nor the regulatory properties of these tolerogenic lymphocytes have been reported. Therefore, the objective of this study was to define the kinetics, phenotype and suppressive function of the regulatory cells induced by DST alone or in combination with liver allograft transplantation (LTx).METHODOLOGY/PRINCIPAL FINDINGS:Tolerance to Dark Agouti (DA; RT1(a)) rat liver allografts was induced by injection (iv) of 1 ml of heparinized DA blood to naïve Lewis (LEW; RT1(l)) rats once per week for 4 weeks prior to LTx. We found that preoperative DST alone generates CD4(+) T-cells that when transferred into naïve LEW recipients are capable of suppressing DA liver allograft rejection and promoting long-term survival of the graft and recipient. However, these DST-generated T-cells did not express the regulatory T-cell (Treg) transcription factor Foxp3 nor did they suppress alloantigen (DA)-induced activation of LEW T-cells in vitro suggesting that these lymphocytes are not fully functional regulatory Tregs. We did observe that DST+LTx (but not DST alone) induced the time-dependent formation of CD4(+)Foxp3(+) Tregs that potently suppressed alloantigen-induced activation of naïve LEW T-cells in vitro and liver allograft rejection in vivo. Finally, we present data demonstrating that virtually all of the Foxp3-expressing Tregs reside within the CD4(+)CD45RC(-) population whereas in which approximately 50% of these Tregs express CD25.CONCLUSIONS/SIGNIFICANCE:We conclude that preoperative DST, in the absence of liver allograft transplantation, induces the formation of CD4(+) T-cells that are not themselves Tregs but give rise directly or indirectly to fully functional CD4(+)CD45RC(-)Foxp3(+)Tregs when transferred into MHC mismatched recipients prior to LTx. These Tregs possess potent suppressive activity and are capable of suppressing acute liver allograft rejection. Understanding the mechanisms by which preoperative DST induces the generation of tolerogenic Tregs in the presence of alloantigens may lead to the development of novel antigen-specific immunological therapies for the treatment of solid organ rejection.

This paper presents a high-throughput and highly-reliable baseband processor LSI based on LDPC coding OFDM UWB. This LSI targets for wireless LAN systems inside a car which enable to translate a high-resolution video under noisy environment. A chip capable of operating at 147 MHz was fabricated using UMC 0.13 mum 1P8M CMOS technology. By adopting the OFDM modulation with 1024 sub-carriers, it achieves a throughput of 820 Mb/s and 10-4 BER performance under 30 dB CNR with 5/6 coding rate. Power dissipation is 189 mW/391 mW (TX/RX).

The mouse model of liver ischemia and reperfusion injury has proven to be valuable for our understanding of the role that reactive oxygen and nitrogen metabolites play in postischemic tissue injury. This methods paper provides a detailed protocol for inducing partial liver ischemia followed by reperfusion. Liver ischemia is induced in anesthetized mice by cross-clamping the hepatic artery and portal vein for varying lengths of time, resulting in deprivation of blood flow to approximately 70% of the liver. Restoration of blood flow to the ischemic lobes enhances superoxide production concomitant with a rapid and marked decrease in the bioavailability of nitric oxide, resulting in alterations in the redox state of the liver in favor of a more oxidative environment. This hepatocellular oxidative stress induces the activation of oxidant-sensitive transcription factors followed by the upregulation of proinflammatory cytokines and mediators that ultimately lead to liver injury. This model can be induced in any strain or sex of mouse and requires 1–2 months of practice to become proficient in the surgery and animal manipulation. The roles of various reactive metabolites of oxygen and nitrogen may be evaluated using genetically engineered mice as well as selective molecular, cellular, and/or pharmacological agents.

Donor-specific blood transfusion (DST) has been shown to be effective at inducing tolerance and long-term survival in animals transplanted with MHC-mismatched tissue. The objective of this study was to ascertain how DST alone or in combination with liver allograft transplantation (LTx) affects the generation and function of regulatory T-cells in vitro and in vivo. We found that DST alone generates CD4+ T-cells that when transferred into naïve recipients suppress liver allograft rejection despite expressing little or no Foxp3 at the time of adoptive transfer. In addition, we present the novel finding that DST plus LTx (but not DST alone) increases the formation of Foxp3-expressing regulatory T-cells (Tregs) that suppress alloantigen-induced activation in vitro as well as induce long term tolerance to liver allografts when adoptively transferred into naïve recipients prior to LTx. Finally we demonstrate that virtually all Foxp3-expressing Tregs reside within the CD4+CD45RC- population whereas these Tregs are equally distributed between the CD4+CD25+ and CD4+CD25- populations. Taken together, our data suggest that DST administration, in the absence of allograft transplantation, induces the formation of CD4+ T-cells that are not Tregs themselves but develop into fully functional Foxp3+ Tregs or help to induce the formation of Foxp3+ Tregs following allograft transplantation.

Ischemia and reperfusion (I/R)-induced liver injury occurs in several pathophysiological disorders including hemorrhagic shock and burn as well as resectional and transplantation surgery. One of the earliest events associated with reperfusion of ischemic liver is endothelial dysfunction characterized by the decreased production of endothelial cell-derived nitric oxide (NO). This rapid post-ischemic decrease in NO bioavailability appears to be due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide or both. This review presents the most current evidence supporting the concept that decreased bioavailability of NO concomitant with enhanced production of reactive oxygen species initiates hepatocellular injury and that endogenous NO or exogenous NO produced from nitrite play important roles in limiting post-ischemic tissue injury.

A partially-parallel decoder architecture for irregular LDPC code targeting high throughput and low cost applications is proposed. The design is based on a novel sum-delta message passing algorithm that facilitates the decoding throughput by removing redundant computations and decreases the hardware cost by optimizing the storage. Techniques such as binary sorting, parallel column operation, high performance pipelining are used to further speed up the message passing procedure. The synthesis result in TSMC 0.18 CMOS technology demonstrates that for (648,324) irregular LDPC code, our decoder achieves 7.5X improvement in throughput, which reaches 402 Mbps at the frequency of 200MHz, with 11% area reduction.

In this paper, we propose a partially-parallel irregular LDPC decoder based on IEEE 802.1 In standard targeting high throughput and small area applications. The design is based on a novel sum-delta message passing algorithm characterized as follows: (i) Decoding throughput is greatly improved by utilizing the difference value between the updated and the original value to remove redundant computations. (H) Registers and memory are optimized to store only the frequently used messages to decrease the hardware cost. (iii) Techniques such as binary sorting, parallel column operation, high performance pipelining are used to further speed lip the message passing procedure. The synthesis result in TSMC 0.18 CMOS technology demonstrates that for (648,324) irregular LDPC code, our decoder achieves 7.5X improvement in throughput, which reaches 402 Mbps at the frequency of 200 MHz, with 11% area reduction. The synthesis result also demonstrates the competitiveness to the fully-parallel regular LDPC decoders in terms of the tradeoff between throughput, area and power.

SUMMARYHepatic resection with concomitant periods of ischaemia and reperfusion (I/R) is required to perform reduced‐size liver (RSL) transplantation procedures, such as living donor or split liver transplantation. Although a great deal of progress has been made using these types of surgical procedures, a significant number of patients develop tissue injury from these procedures, ultimately resulting in graft failure.Because of this, there is a real need to understand the different mechanisms responsible for the tissue injury induced by I/R of RSL transplantation (RSL + I/R), with the ultimate goal to develop new and improved therapeutic agents that may limit the tissue damage incurred during RSL transplantation.The present paper reviews the recent studies that have been performed examining the role of reactive metabolites of oxygen and nitrogen in a mouse model of RSL + I/R. In addition, we present data demonstrating how the pathophysiological mechanisms identified in this model compare with those observed in a model of RSL transplantation in rats.

This paper proposes an improved message passing schedule for irregular LDPC decoder. Redundant memory accesses and column operations are removed by utilizing the characteristics of partial-parallel irregular LDPC decoding algorithm. As a result, the memory access frequency and hardware cost are efficiently reduced. According to the experimental results and comparison with existing work, proposed decoder provides a 30% hardware area reduction and a 36% power consumption saving with the same error correcting performance.