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Acute lung injury (ALI) is a severe inflammatory lung disease associated with macrophages. Somatic nuclear autoantigenic sperm protein (sNASP) is a negative regulator of Toll-like receptor (TLR) signaling that targets tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) in macrophages, which is required to maintain homeostasis of the innate immune response. In the present study, we generated a cell permeable PEP-sNASP peptide using the sNASP protein N-terminal domain, and examined its potential therapeutic effect in a mouse model of ALI induced by the intranasal administration of lipopolysaccharide (LPS) and elucidated the underlying molecular mechanisms in RAW 264.7 cells.In vivo, PEP-sNASP peptide treatment markedly ameliorated pathological injury, reduced the wet/dry (W/D) weight ratio of the lungs and the production of proinflammatory cytokines (interleukin (IL)-1β, IL-6, and TNF-α).In vitro, we demonstrated that when the PEP-sNASP peptide was transduced into RAW 264.7 cells, it bound to TRAF6, which markedly decreased LPS-induced proinflammatory cytokines by inhibiting TRAF6 autoubiquitination, nuclear factor (NF)-κB activation, reactive oxygen species (ROS) and cellular nitric oxide (NO) levels. Furthermore, the PEP-sNASP peptide also inhibited NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. Our results therefore suggest that the PEP-sNASP may provide a potential protein therapy against oxidative stress and pulmonary inflammationviaselective TRAF6 signaling.

Recognition of invading pathogens by Toll-like receptors (TLRs) activates innate immunity through signaling pathways that involved multiple protein kinases and phosphatases. We previously demonstrated that somatic nuclear autoantigenic sperm protein (sNASP) binds to TNF receptor–associated factor 6 (TRAF6) in the resting state. Upon TLR4 activation, a signaling complex consisting of TRAF6, sNASP, interleukin (IL)-1 receptor–associated kinase 4, and casein kinase 2 (CK2) is formed. CK2 then phosphorylates sNASP to release phospho-sNASP (p-sNASP) from TRAF6, initiating downstream signaling pathways. Here, we showed that protein phosphatase 4 (PP4) is the specific sNASP phosphatase that negatively regulates TLR4-induced TRAF6 activation and its downstream signaling pathway. Mechanistically, PP4 is directly recruited by phosphorylated sNASP to dephosphorylate p-sNASP to terminate TRAF6 activation. Ectopic expression of PP4 specifically inhibited sNASP-dependent proinflammatory cytokine production and downstream signaling following bacterial lipopolysaccharide (LPS) treatment, whereas silencing PP4 had the opposite effect. Primary macrophages and mice infected with recombinant adenovirus carrying a gene encoding PP4 (Ad-PP4) showed significant reduction in IL-6 and TNF-α production. Survival of Ad-PP4–infected mice was markedly increased due to a better ability to clear bacteria in a sepsis model. These results indicate that the serine/threonine phosphatase PP4 functions as a negative regulator of innate immunity by regulating the binding of sNASP to TRAF6.

Streptococcus suis (S. suis) is an important zoonotic pathogen that can cause high morbidity and mortality in both humans and swine. As the most important life-threatening infection of the central nervous system (CNS), meningitis is an important syndrome of S. suis infection. The vancomycin resistance associated sensor/regulator (VraSR) is a critical two-component signal transduction system that affects the ability of S. suis to resist the host innate immune system and promotes its ability to adhere to brain microvascular endothelial cells (BMECs). Prior work also found mice infected with ΔvraSR had no obvious neurological symptoms, unlike mice infected with wild-type SC19. Whether and how VraSR participates in the development of S. suis meningitis remains unknown. Here, we found ΔvraSR-infected mice did not show obvious meningitis, compared with wild-type SC19-infected mice. Moreover, the proinflammatory cytokines and chemokines in serum and brains of ΔvraSR-infected mice, including IL-6, TNF-α, MCP-1 and IFN-γ, were significantly lower than wild-type infected group. Besides, blood-brain barrier (BBB) permeability also confirmed that the mutant had lower ability to disrupt BBB. Furthermore, in vivo and in vitro experiments showed that SC19 could increase BBB permeability by downregulating tight junction (TJ) proteins such as ZO-1, β-Catenin, Occludin, and Clauidn-5, compared with mutant ΔvraSR. These findings provide new insight into the influence of S. suis VraSR on BBB disruption during the pathogenic process of streptococcal meningitis, thereby offering potential targets for future preventative and therapeutic strategies against this disease.

House dust mites (HDMs) are a common source of respiratory allergens responsible for allergic asthma and innate immune responses in human diseases. Since HDMs are critical factors in the triggering of allergen-induced airway mucosa from allergic asthma, we aimed to investigate the mechanisms of Toll-like receptors (TLR) in the signaling of the HDM extract that is involved in mucus hypersecretion and airway inflammation through the engagement of innate immunity. Previously, we reported that the somatic nuclear autoantigenic sperm protein (sNASP)/tumor necrosis factor receptor-associated factor 6 (TRAF6) axis controls the initiation of TLRs to maintain the homeostasis of the innate immune response. The present study showed that the HDM extract stimulated the biogenesis of Mucin 5AC (MUC5AC) in bronchial epithelial cells via the TLR2/4 signaling pathway involving MyD88 and TRAF6. Specifically, sNASP binds to TRAF6 in unstimulated bronchial epithelial cells to prevent the activation of TRAF6-depenedent kinases. Upon on HDMs’ stimulation, sNASP is phosphorylated, leading to the activation of TRAF6 downstream of the p38 MAPK and NF-κB signaling pathways. Further, NASP-knockdown enhanced TRAF6 signaling and MUC5AC biogenesis. In the HDM-induced mouse asthma model, we found that the HDM extract promoted airway hyperresponsiveness (AHR), MUC5AC, and allergen-specific IgE production as well as IL-5 and IL-13 for recruiting inflammatory cells. Treatment with the PEP-NASP peptide, a selective TRAF6-blocking peptide, ameliorated HDM-induced asthma in mice. In conclusion, this study indicated that the sNASP/TRAF6 axis plays a regulatory role in asthma by modulating mucus overproduction, and the PEP-NASP peptide might be a potential target for asthma treatment.

Many Toll-like receptors (TLRs) signal through TNF receptor–associated factor 6 (TRAF6) to activate innate immune responses. Here, we show that somatic nuclear autoantigenic sperm protein (sNASP) binds to TRAF6 to prevent TRAF6 autoubiquitination in unstimulated macrophages. Following LPS stimulation, a complex consisting of sNASP, TRAF6, IRAK4, and casein kinase 2 (CK2) is formed. CK2 phosphorylates sNASP at serine 158, allowing sNASP to dissociate from TRAF6. Free TRAF6 is then autoubiquitinated, followed by activation of downstream signaling pathways. In sNasp S158A knockin (S158A-KI) mice, LPS-treated macrophages could not phosphorylate sNASP, which remained bound to TRAF6. S158A-KI mice were more susceptible to sepsis due to a marked reduction in IL-1β, TNF-α, and IFN-γ production accompanied by an inability to clear bacteria and recruit leukocytes. Furthermore, phosphorylation-regulated release of sNASP from TRAF6 is observed following activation of TLR-1, -2, -4, -5, and -6. Thus, sNASP is a negative regulator of TLR signaling to modulate the innate immune response.

// Tasneem Bawa-Khalfe 1 , Feng-Ming Yang 2 , Joan Ritho 2 , Hui-Kuan Lin 3,4 , Jinke Cheng 5,6 and Edward T.H. Yeh 2 1 Department of Biology & Biochemistry, Center for Nuclear Receptors & Cell Signaling, University of Houston, Houston, Texas, USA 2 Department of Internal Medicine, The University of Missouri, Columbia, MO, USA 3 Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA 4 Department of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA 5 Department of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China 6 State Key Laboratory of Oncogenes & Related Genes, Shanghai Cancer Institute, Shanghai Jiao Tong University School of Medicine, Shanghai, China Correspondence to: Tasneem Bawa-Khalfe, email: // Edward T.H. Yeh, email: // Keywords : SENP1, PTEN, WWP2, SUMO, prostate carcinogenesis Received : May 27, 2016 Accepted : November 07, 2016 Published : November 10, 2016 Abstract SUMO protease SENP1 is elevated in multiple carcinomas including prostate cancer (PCa). SENP1 exhibits carcinogenic properties; it promotes androgen receptor-dependent and -independent cell proliferation, stabilizes HIF1α, increases VEGF, and supports angiogenesis. However, mice expressing an androgen-responsive promoter driven SENP1-transgene (SENP1-Tg) develop high-grade prostatic intraepithelial neoplasia, but not carcinoma. We now show that tumor suppressive PTEN signaling is induced in SENP1-Tg to enhance prostate epithelial cell apoptosis. SENP1 blocks SUMO1-dependent ubiquitylation and degradation of PTEN. In the absence of SENP1, SUMO1-modified PTEN is sequestered in the cytosol, where binding to ubiquitin-E3 ligase WWP2 occurs. Concurrently, WWP2 is also SUMOylated, which potentiates its interaction with PTEN. Thus, SENP1 directs ubiquitin-E3-substrate association to control PTEN stability. PTEN serves as a barrier for SENP1-mediated prostate carcinogenesis as SENP1-Tg mice develop invasive carcinomas only after PTEN reduction. Hence, SENP1 modulates multiple facets of carcinogenesis and may serve as a target specifically for aggressive PTEN-deficient PCa.

Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3′-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis.

As an orphan member of the nuclear receptor family, liver receptor homologue-1 (LRH-1) controls a tremendous range of transcriptional programmes that are essential for metabolism and hormone synthesis. Our previous studies have shown that nuclear localization of the LRH-1 protein is mediated by two nuclear localization signals (NLSs) that are karyopherin/importin-dependent. It is unclear whether LRH-1 can be actively exported from the nucleus to the cytoplasm. In the present study, we describe a nuclear export domain containing two leucine-rich motifs [named nuclear export signal (NES)1 and NES2] within the ligand-binding domain (LBD). Mutation of leucine residues in NES1 or NES2 abolished nuclear export, indicating that both NES1 and NES2 motifs are essential for full nuclear export activity. This NES-mediated nuclear export was insensitive to the chromosomal region maintenance 1 (CRM1) inhibitor leptomycin B (LMB) or to CRM1 knockdown. However, knockdown of calreticulin (CRT) prevented NES-mediated nuclear export. Furthermore, our data show that CRT interacts with LRH-1 and is involved in the nuclear export of LRH-1. With full-length LRH-1, mutation of NES1 led to perinuclear accumulation of the mutant protein. Immunofluorescence analysis showed that these perinuclear aggregates were co-localized with the centrosome marker, microtubule-associated protein 1 light chain 3 (LC3), ubiquitin and heat shock protein 70 (Hsp70), indicating that the mutant was misfolded and sequestered into aggresome-like structures via the autophagic clearance pathway. Our study demonstrates for the first time that LRH-1 has a CRT-dependent NES which is not only required for cytoplasmic trafficking, but also essential for correct protein folding to avoid misfolding-induced aggregation.

Previous studies have shown that local anesthetics may induce apoptosis in some cell types. In this study, we investigated the apoptotic effects of local anesthetics in human breast tumor cells.Human breast cancer (MCF-7) and mammary epithelial (MCF-10A) cell lines were treated with lidocaine and/or bupivacaine. Cell viability, DNA fragmentation, and annexin V immunofluorescence staining were assessed. The effects on apoptosis-related protein expression were investigated by Western blot analysis. The findings were extended to studies in an in vivo xenograft model.Treatment of breast tumor cells with lidocaine and bupivacaine resulted in inhibition of cell viability via induction of apoptosis. The effects were more prominent in MCF-7 cells than in MCF-10A cells. Treatment with local anesthetics induced caspase 7, 8, 9, and poly ADP-ribose polymerase cleavage. The cleavage of caspase 7 and poly ADP-ribose polymerase induced by local anesthetics were effectively blocked by caspase inhibitors. Furthermore, treatment of MCF-7 xenografts with local anesthetics resulted in higher expression of cleaved caspase 7 and an increase in terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining.Lidocaine and bupivacaine induce apoptosis of breast tumor cells at clinically relevant concentrations. Our results reveal previously unrecognized beneficial actions of local anesthetics and call for further studies to assess the oncologic advantages of their use during breast cancer surgery.

The board plays a central role in monitoring the management on behalf of shareholders, yet the efficacy of board monitoring is difficult to determine. This study proposes using board attendance as a proxy measure of board supervisory quality and investigates the factors influencing board attendance, as well as their impact on firms’ performance, by conducting a second-order regression analysis. The results show that board attendance decreases with multiple directorships, meeting frequency, and board size, indicating that busier directors and a more complex board combine to lower meeting attendance. The director shareholding rate and proportion of independent directors increase with board attendance, implying the convergence of interest among directors and companies and that strong external monitoring prompts higher board attendance. Finally, we find that higher board attendance enhances higher firm accounting performance, verifying that firms could view the attendance rate as an indication of the quality ...

This paper presents a dynamic rate selection (DRS) scheme to determine the transmission rate of video multicast services for ultra-wideband (UWB) systems. The DRS scheme utilizes the received signal quality of the beacon frame sent by each UWB device to estimate clients’ location distribution. It then determines the best data rate to transmit the enhancement layer portion of the multicast video stream. Considering the limited processing power of the USB device, a decision tree is further proposed to reduce the computational complexity of the DRS. The performance of the DRS scheme is verified via computer simulation. Simulation results demonstrate the effective of the proposed DRS scheme in various conditions.

The orphan nuclear receptor LRH-1 (liver receptor homologue-1; NR5A2) plays a critical role in development, bile acid synthesis and cholesterol metabolism. LRH-1 is also expressed in the ovary where it is implicated in the regulation of steroidogenic genes for steroid hormone synthesis. In the present study, we investigated the molecular mechanisms of the transcriptional regulation of CYP11A1 by LRH-1 and found that LRH-1-mediated transactivation was markedly repressed by PIASy [protein inhibitor of activated STAT (signal transducer and activator of transcription) y], the shortest member of the PIAS family. The suppression of LRH-1 activity requires the N-terminal repression domain. Although PIAS proteins also function as E3 SUMO (small ubiquitin-related modifier) ligases and enhance SUMO conjugation, PIASy-mediated repression was independent of LRH-1 SUMOylation status. In addition, histone deacetylase activity was not involved in the inhibition of LRH-1 by PIASy. Immunoprecipitation and mammalian two-hybrid analyses indicated that PIASy interacted with LRH-1 through the C-terminal region, including the AF-2 (activation function-2) motif, which was also involved in the interaction between LRH-1 and the co-activator SRC-1 (steroid receptor co-activator-1). PIASy inhibited the binding of SRC-1 to LRH-1, although overexpression of SRC-1 partially overcame the PIASy inhibition of LRH-1 induction of the CYP11A1 promoter. The results of the present study suggest that competition with co-activators may be an important mechanism underlying the PIASy repression of LRH-1-mediated transactivation.

Liver receptor homolog-1 (LRH-1; NR5A2) is an orphan member of the nuclear receptor superfamily, mainly expressed in endoderm-derived tissues and in the ovary. In ovarian granulosa and luteal cells, LRH-1 regulates the expression of genes associated with ovarian steroidogenesis. LRH-1 can be transported to transcriptionally inactive nuclear bodies after conjugation with small ubiquitin-related modifier (SUMO). In the present study, we investigated the effects of SUMO modification at five lysine residues of LRH-1 in rat granulosa cells. Lysine 289 could be conjugated with SUMO-1 in vitro, and the mutation K289R increased transcriptional activity of LRH-1, suggesting that SUMO conjugation is associated with transcription repression. Coexpression of SUMO-1 targets LRH-1 to the dot-like nuclear bodies, but the effect of lysine mutations on blocking subnuclear localization depended on the cell type. In COS-7 cells, mutation of either K173 or K289 prevented SUMO-1-mediated translocation of LRH-1 into nuclear bodies and also reduced the conjugation by SUMO-1, suggesting that K289 and K173 are two important sites involved in SUMO-1 modification. In granulosa cells, three or more altered lysine residues were required for nucleoplasm retention. This result suggests that multiple lysine residues are targets for SUMO conjugation in vivo and granulosa cells are more sensitive to SUMO-1-mediated LRH-1 localization to nuclear bodies. Nuclear body localization of LRH-1 was suppressed by forskolin and cholera toxin. Forskolin treatment obviously influences the expression of members involved in the SUMO pathway. The results obtained in the present study suggest that cAMP signaling could change the dynamic process of sumoylation and repress LRH-1 targeting to nuclear speckles in rat granulosa cells.

Dense heterogeneous networks (HetNets) that comprise a number of small cells and their overlay macro cells is viewed as the solution for supporting explosive-growth user traffic in the next decade. In order to reduce the number of handovers in HetNets, the high speed mobiles should attach to the macro cells as much as possible. This paper proposes a Doppler-based Speed Classification (DSC) method for the mobiles to classify its speed into the high-speed or the low-speed classes. The classification results could be further used for the mobiles to select an appropriate cell for attaching. The DSC method is low complexity and requires no mobility-related records. Simulation results show that the DSC method is effective in broad range of scenarios.

This paper proposes an AVS/H.264 dual mode video decoder targeted at high definition video applications. The proposed design is compatible to decode H.264-BP/MP/HP and AVS-JP bit-streams with optimization on both system and component levels. On system level, we simplify the control of H.264 MBAFF coding, and reduce buffer size for storing prediction data. On component level, we improve the throughput in bit-stream decoding and integrate AVS/H.264 processing units together to reduce hardware cost. Through the optimization techniques, the proposed design can achieve real-time HD1080 (1920×1088@30Hz) decoding at 150MHz.

Due to the limited bandwidth usage of wireless transmission, one of the major research topics is how to make a higher system throughput to support the multiple users based on limited bandwidth resources. This paper proposed a cross-layer subcarrier permutation mechanism (CLSP) and designed the service scheduling in the IEEE 802.16e system. The simulation results showed that when the throughput of system transmission become completely in use, the throughput of cross-layer proportional fair subcarrier permute mechanism is 28 percent more than the throughput of PUSC (Partial Usage of sub-channels) model formed by the IEEE 802.16e committee. In the user capacity, the number of users of cross-layer proportional fair subcarrier permute mechanism is 17 percent more than the number of users of PUSC. Moreover, cross-layer proportional fair subcarrier permute mechanism has a lower delay time as well as a long-term fairness among different users during the different service flows simulation.

Liver receptor homologue-1 (LRH-1) is a member of the nuclear receptor superfamily. We characterized two functional nuclear localization signals (NLSs) in LRH-1. NLS1 (residues 117–168) overlaps the second zinc finger in the DNA binding domain. Mutagenesis showed that the zinc finger structure and two basic clusters on either side of the zinc finger loop are critical for nuclear import of NLS1. NLS2 (residues 169–204) is located in the Ftz-F1 box that contains a bipartite signal. In full-length LRH-1, mutation of either NLS1 or NLS2 had no effect on nuclear localization, but disruption of both NLS1 and NLS2 resulted in the cytoplasmic accumulation of LRH-1. Either NLS1 or NLS2 alone was sufficient to target LRH-1 to the nucleus. Both NLS1 and NLS2 mediate nuclear transport by a mechanism involving importin α/β. Finally, we showed that three crucial basic clusters in the NLSs are involved in the DNA binding and transcriptional activities of LRH-1.

Liver receptor homolog-1 (LRH-1; NR5A2) is an orphan member of the nuclear receptor superfamily, mainly expressed in endoderm-derived tissues and in the ovary. In ovarian granulosa and luteal cells, LRH-1 regulates the expression of genes associated with ovarian steroidogenesis. LRH-1 can be transported to transcriptionally inactive nuclear bodies after conjugation with small ubiquitin-related modifier (SUMO). In the present study, we investigated the effects of SUMO modification at five lysine residues of LRH-1 in rat granulosa cells. Lysine 289 could be conjugated with SUMO-1 in vitro, and the mutation K289R increased transcriptional activity of LRH-1, suggesting that SUMO conjugation is associated with transcription repression. Coexpression of SUMO-1 targets LRH-1 to the dot-like nuclear bodies, but the effect of lysine mutations on blocking subnuclear localization depended on the cell type. In COS-7 cells, mutation of either K173 or K289 prevented SUMO-1-mediated translocation of LRH-1 into nuclear bodies and also reduced the conjugation by SUMO-1, suggesting that K289 and K173 are two important sites involved in SUMO-1 modification. In granulosa cells, three or more altered lysine residues were required for nucleoplasm retention. This result suggests that multiple lysine residues are targets for SUMO conjugation in vivo and granulosa cells are more sensitive to SUMO-1-mediated LRH-1 localization to nuclear bodies. Nuclear body localization of LRH-1 was suppressed by forskolin and cholera toxin. Forskolin treatment obviously influences the expression of members involved in the SUMO pathway. The results obtained in the present study suggest that cAMP signaling could change the dynamic process of sumoylation and repress LRH-1 targeting to nuclear speckles in rat granulosa cells.

Adaptive modulation and coding (AMC), which is a technology used when channel condition changes, is adapted in mobile Worldwide Interoperability for Microwave Access (WiMAX). Scalable video coding (SVC) is a video coding scheme used for different users with bandwidth level. SVC encodes a video into a number of layers. Users receive different number of encoded layers based on their channel condition. In this paper, both AMC and SVC are employed to enhance the user perceived video quality in the system. Intermediate Control Server (ICS) is proposed to deal with the signaling between multimedia server and BS.

About two thirds of breast cancers in women are hormone-dependent and require estrogen for growth, its effects being mainly mediated through estrogen receptor alpha (ERalpha). Docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6) have opposite effects on carcinogenesis, with DHA suppressing and AA promoting tumor growth both in vitro and in vivo. However, the mechanism is not clear. Here, we examined whether the effect is mediated through changes in ERalpha distribution. MCF-7 cells, an ERalpha-positive human breast cancer cell line, was cultured in estrogen-free medium containing 0, 10 or 60 microM DHA or AA, then were stimulated with estradiol. DHA supplementation resulted in down-regulation of ERalpha expression (particularly in the extranuclear fraction), a reduction in phosphorylated MAPK, a decrease in cyclin D1 levels and an inhibition in cell viability. In contrast, AA had no such effects. The DHA-induced decrease in ERalpha expression resulted from proteasome-dependent degradation and not from decreased ERalpha mRNA expression. We propose that breast cancer cell proliferation is inhibited by DHA through proteasome-dependent degradation of ERalpha, reduced cyclin D1 expression and inhibition of MAPK signaling.

In this paper, we investigate how the quality of service (QoS) can be guaranteed and reliable transmission can be supported in the OBS-based Internet backbone. We propose the adjustable-time-counter-based (ATCB) burst assembly and the non-real time packet retransmission mechanisms, and apply them in the ingress router of the OBS Internet backbone to guarantee the quality of real time applications and lossless requirement of non-real time services. Simulation results show that the burst blocking probability using the ATCB burst assembly, compared with that using the time-counter-based (TCB) and burst-length-threshold-based (BLTB) mechanisms, acquires an improvement. The delay, loss and jitter of real time service conform to the QoS requirement. Meanwhile, the delay of non-real time service also falls in the acceptable range.

We have investigated the photocatalysis efficiency and electron transfer of the znic prophyrin/TiO2 composite photocatalyst, a sensitised hybrid porphyrin material, and prepared it successfully by sol-gel method. The UV-visible spectroscopy and electron paramagnetic resonance spectra are used to analyze and characterize the znic prophyrin/TiO2 composite photocatalyst. The proportions 0%, 0.2%, 0.5% and 0.9% (mass ratio) of zinc porphyrin, and the photocatalytic mechanism of TiO2 sensitized by zinc porphyrin are reasonably explained by ultraviolet visible spectroscopy and electron paramagnetic resonance spectroscopy (EPR). Different samples' UV-visible spectra show that the degradation efficiency of methyl orange solution by TiO2 may be improved via adding appropriate amount of zinc porphyrin sensitizer. Prohibitive incorporation of the sensitizer would cause excess of particles in the mixed catalyst, leading to the TiO2 surface covered by the sensitizer, thus affecting the absorption of photons, and the light degradation rate of TiO2 may be lowered, even lower than the pure TiO2. EPR spectra show the excited state of electrons in zinc prophyrin generated by irradiation of light can promote the generation of Ti3+ with strong oxidizing and superoxide radicals when using UV-visible light to irradiate the powder samples, thus effectively enhancing the separation of photogenerated electron-hole pairs, and improving the photocatalytic performance of TiO2.

In order to study how the ingredient, sintering temperature, oxygen, doping and other conditions affect magnetic properties of strontium ferrite powder, a strontium ferrite powder is prepared by sol-gel method, and a new method of studying magnetic properties of strontium ferrite powder based on an electron paramagnetic resonance (EPR) is established in this paper. The sintered samples are tested by electron paramagnetic resonance spectrometer. Results show that -Fe2O3, a paramagnetic intermediate, is most compared with other ratios under calcined at 400 ℃ and the strontium iron mole ratio of 1:9; while at the other temperatures it decreases and the ferromagnetic phase increases; the optimum calcination temperature is between 800 ℃ and 900 ℃. These facts are caused by both external magnetic field and other magnetic fields, thus resulting in some new stronger magnetic moment interactions. Results also show that a large quantity of paramagnetic -Fe2O3 is found under hypoxic annealing environment, which is not conducible to generating the ferrimagnetic phase; X-ray diffraction (XRD) analysis shows that the others are paramagnetic and ferrimagnetic phase except a bit of other phases; both EPR spectra and XRD spectra show that the paramagnetic phase is least, and ferrimagnetic phase is most in the sintering sample when strontium iron mole ratio is 1:9, so the sample owns the strongest magnetism. The sample remanence experiment by milli-tesla meter also confirms these results. It is also found that paramagnetic phase can effectively decrease and ferrimagnetism is enhanced when samples are doped by lanthanum ion accounting for 20%-30% of the total number of moles of strontium lanthanum.

A systolic array architecture based on an efficient data-flow management for implementing the full-search block-matching algorithm for HDTV motion estimation is described. It is capable of treating (16/spl times/16)-blocks, with a displacement of /spl minus/8/+7 pixels. Serial data inputs save the pin counts and all the input data in current frame are read only once to keep the requirements to external units to a minimum. A simplified PE design reduces the computation to 1/3 of that by directly implementing the original algorithm without any influence on the performance. Simulation results show that pixel rates at about 150 MHz can be reached with 0.8 /spl mu/m CMOS technology. Owing to the highly regular and modular properties, the proposed architecture is suitable for VLSI implementation. Transistor count is estimated about 320,000, which shows that the architecture can be realized in a single chip. >

This paper describes an architecture based on a new full search block-matching algorithm called vector-characterization algorithm (VCA). A single-chip realization in form of a 1.0 /spl mu/m CMOS standard cell design shows that the architecture is suitable for HDTV applications.