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Four power stages for voltage regulator module (VRM) are adopted to provide high current driving capability and low output ripple in cloud computing. Thus, the time-shift current balance (TSCB) technique is proposed to achieve high performance power supply for servers. In addition, the power request, which includes the number of active phases and voltage identification, is acknowledged by servers for high driving capability during high throughput and high efficiency during standby mode. Furthermore, to equally distribute the current in each phase, the proposed TSCB technique in either voltage-mode or peak current-mode control improves the current balance performance and solves the stability problem. In the scale-down clouding computing prototype, the efficiency can be kept higher than 90% over a wide load current range of 2 A. In addition, the performance and operating frequency of the servers in stable operation are not limited by the VRM with the TSCB technique. [ABSTRACT FROM AUTHOR]

Background Matrix metalloproteinase-9 (MMP-9) has been shown to be induced by cytokines including TNF-α and may contribute to bone inflammatory diseases. However, the mechanisms underlying MMP-9 expression induced by TNF-α in MC3T3-E1 cells remain unclear. Results We applied gelatin zymography, Western blot, RT-PCR, real-time PCR, selective pharmacological inhibitors of transcription (actinomycin D, Act.D), translation (cycloheximide, CHI), c-Src (PP1), MEK1/2 (U0126), p38 MAPK (SB202190), JNK1/2 (SP600125), and NF-κB (Bay11-7082), respective siRNAs transfection, promoter assay, immunofluorescence staining, and ELISA to investigate the MMP-9 expression and soluble ICAM-1 (sICAM-1) release induced by TNF-α in MC3T3-E1 cells. Here we demonstrated that TNF-α-induced MMP-9 expression was attenuated by Act.D, CHI, PP1, U0126, SB202190, SP600125, and Bay11-7082, and by the transfection with siRNAs for ERK2, p38 MAPK, and JNK2. TNF-α-stimulated TNFR1, TRAF2, and c-Src complex formation was revealed by immunoprecipitation and Western blot. Furthermore, TNF-α-stimulated NF-κB phosphorylation and translocation were blocked by Bay11-7082, but not by PP1, U0126, SB202190, or SP600125. TNF-α time-dependently induced MMP-9 promoter activity which was also inhibited by PP1, U0126, SB202190, SP600125, or Bay11-7082. Up-regulation of MMP-9 was associated with the release of sICAM-1 into the cultured medium, which was attenuated by the pretreatment with MMP-2/9i, an MMP-9 inhibitor. Conclusions In this study, we demonstrated that TNF-α up-regulates MMP-9 expression via c-Src, MAPKs, and NF-κB pathways. In addition, TNF-α-induced MMP-9 expression may contribute to the production of sICAM-1 by MC3T3-E1 cells. The interplay between MMP-9 expression and sICAM-1 release may exert an important role in the regulation of bone inflammatory diseases. [ABSTRACT FROM AUTHOR]

The stability of conventional constant on-time control buck converter is constrained by the time constant, which is the product of the output capacitor and its equivalent series resistance (ESR). Specialty polymer capacitor which is mostly used as output capacitor for such a consideration although it limits the performance of converter. On the other hand, the multilayer ceramic capacitors are widely used in commercial power management ICs due to the advantages of low cost and ESR. However, the stability often confronts with the subharmonic problem caused by small time constant. A differential-zero compensator with the noise margin enhancement (DZC-NME) technique in constant on-time control buck dc-dc converter with output ceramic capacitor is proposed in this paper. Thus, the proposed DZC-NME technique not only eliminates the limit of large time constant but also tolerates the existence of equivalent series inductor (ESL) effect. Experiment results demonstrate small output ripple of 10 mV and high efficiency of 91% when ESR is smaller than 1 mΩ and large interference from ESL effect is 40 mV. [ABSTRACT FROM AUTHOR]

Alcoholic liver disease (ALD) encompasses hepatic steatosis, which may progress to alcoholic hepatitis, fibrosis, and cirrhosis. It remains a leading cause of morbidity and mortality in the US and worldwide. The severity of liver disease correlates with plasma levels of bacterial products in patients, and experimental ALD depends on the level of gut derived bacterial products in rodents. Since intestinal decontamination and deficiency of bacterial product receptors or their downstream signaling molecules protect from alcohol-induced liver disease, bacterial translocation (BT), qualitative, and quantitative changes of the enteric microbiome are considered as being of fundamental importance in the pathogenesis of ALD. Recent enhancements in diagnostic technologies provide a better insight into these shifts. This review highlights vital events in ALD such as BT, the importance of Toll-like receptor (TLR) signaling, intestinal bacterial overgrowth (IBO), and changes in the intestinal microbiome. Furthermore, a treatment trial section of patients reviews possible future options of therapy for ALD modifying the enteric microbiome. [ABSTRACT FROM AUTHOR]

An abstract of the article "Biomakers in heart failure," by Wei-Chung Chen, Kimberly D. Tran, and Alan S. Maisel is presented.

Background: To understand the evolution of animals it is essential to have taxon sampling across a representative spread of the animal kingdom. With the recent rearrangement of most of the Bilateria into three major clades (Ecdysozoa, Lophotrochozoa and Deuterostomia) it has become clear that the Lophotrochozoa are relatively poorly represented in our knowledge of animal development, compared to the Ecdysozoa and Deuterostomia. We aim to contribute towards redressing this balance with data on the development of the muscular, nervous and ciliary systems of the annelid Pomatoceros lamarckii (Serpulidae). We compare our data with other lophotrochozoans. Results: P. lamarckii develops locomotory and feeding structures that enable it to become a swimming, planktotrophic larva within 24 hours. Formation of the trochophore includes development of a prototroch, metatroch and neurotroch, development of apical and posterior nervous elements at similar times, and development of musculature around the ciliary bands and digestive tract prior to development of any body wall muscles. The adult nervous and muscular systems are essentially preformed in the late larva. Interestingly, the muscular systems of the larvae and juvenile worms do not include the circular muscles of the body wall, which are considered to be plesiomorphic for annelids, although the possibility that circular muscles develop after these stages cannot be ruled out at this point. Conclusion: A comparison between polychaetes shows variability in the timing (heterochrony) of development of body wall muscles and elements of the nervous system. These heterochronies are one route for evolution of different life history strategies, such as adaptations to feeding requirements. [ABSTRACT FROM AUTHOR]

In Madin-Darby canine kidney (MDCK) cells, the effect of maprotiline, an antidepressant, on intracellular Ca2+ concentration ([Ca2+]i) was measured using fura-2. Maprotiline (>2.5 µM) caused a rapid rise of [Ca2+]i in a concentration-dependent manner (EC50 200 µM). Maprotiline-induced [Ca2+]i rise was reduced by removal of extracellular Ca2+ or by addition of La3+, but was not altered by voltage-gated Ca2+-channel blockers. Maprotiline-induced Mn2+ influx-associated fura-2 fluorescence quench directly suggests that maprotiline caused Ca2+ influx. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic [Ca2+]i rise, after which the increasing effect of maprotiline on [Ca2+]i was nearly abolished; also, pretreatment with maprotiline reduced a portion of thapsigargin-induced [Ca2+]i rise. U73122, an inhibitor of phospholipase C, abolished [Ca2+]i rise induced by ATP (but not by maprotiline). Overnight incubation with 1–10 µM maprotiline enhanced cell viability, but 20–50 µM maprotiline decreased it. These findings suggest that maprotiline rapidly increases [Ca2+]i in renal tubular cells by stimulating both extracellular Ca2+ influx and intracellular Ca2+ release, and may modulate cell proliferation in a concentration-dependent manner. [ABSTRACT FROM AUTHOR]

Her-2/neu (ErbB2) oncogene, the second member of the epidermal growth factor receptor (EGFR) family, encodes a transmembrane tyrosine kinase receptor in Her-2-positive tumors. Accumulating evidences demonstrate that signaling networks activated by EGFR and transcription factor NF-?B are associated with cell response to ionizing radiation (IR). The present study shows that overexpression of ErbB2 enhanced NF-?B activation induced by IR in human breast carcinoma MCF-7 cells transfected with ErbB2 genes (MCF-7/ErbB2). Stable transfection of dominant-negative mutant I?B (MCF-7/ErbB2/mI?B) or treatment with anti-ErbB2 antibody, Herceptin, inhibited NF-?B activation and radiosensitized MCF-7/ErbB2 cells. Consistent with NF-?B regulation, basal and IR-induced Akt, a kinase downstream of ErbB2, was activated in MCF-7/ErbB2 cells and inhibited by Herceptin. To identify specific genes affected by ErbB2-mediated NF-?B activation, a group of IR-responsive elements Cyclin B1, Cyclin D1, Bcl-2, Bcl/XL, BAD and BAX were evaluated. Basal levels of prosurvival elements Cyclin B1, Cyclin D1, Bcl-2 and Bcl/XL but not apoptotic BAD and BAX were upregulated in MCF-7/ErbB2 cells with striking enhancements in Bcl-2 and Bcl/XL. IR further induced Cyclin B1 and Cyclin D1 expression that was reduced by Herceptin. Bcl-2 kept a high steady level after Herceptin+IR treatment and, in contrast to control MCF-7/Vector cells, Bcl/XL was inhibited in MCF-7/ErbB2 cells by Herceptin+IR treatment. However, all four prosurvival proteins were downregulated by inhibition of NF-?B in MCF-7/ErbB2/mI?B cells. These results thus provide evidence suggesting that overexpression of ErbB2 is able to enhance NF-?B response to IR, and that a specific prosurvival network downstream of NF-?B is triggered by treatments using anti-ErbB2 antibody combined with radiation.Oncogene (2004) 23, 535-545. doi:10.1038/sj.onc.1207149 [ABSTRACT FROM AUTHOR]

Is the extreme derivation of the echinoderm body plan reflected in a derived echinoderm Hox genotype? Building on previous work, we exploited the sequence conservation of the homeobox to isolate putative orthologues of several Hox genes from two asteroid echinoderms. The 5-peptide motif (LPNTK) diagnostic of PG4 Hox genes was identified immediately downstream of one of the partial homeodomains from Patiriella exigua. This constitutes the first unequivocal report of a PG4 Hox gene orthologue from an echinoderm. Subsequent screenings identified genes of both PG4 and PG4/5 in Asterias rubens. Although in echinoids only a single gene (PG4/5) occupies these two contiguous cluster positions, we conclude that the ancestral echinoderm must have had the complete deuterostome suite of medial Hox genes, including orthologues of both PG4 and PG4/5 (= PG5). The reported absence of PG4 in the HOX cluster of echinoids is therefore a derived state, and the ancestral echinoderm probably had a HOX cluster not dissimilar to that of other deuterostomes. Modification of the ancestral deuterostome Hox genotype may not have been required for evolution of the highly derived echinoderm body plan. [ABSTRACT FROM AUTHOR]

The effects of five lignans (epi-aschantin, epi-magnolin, epi-yangambin, deoxypodophyllotoxin, yatein) isolated from Hernandia nymphaeifolia (Presl.) Kubitzki (Hernandiaceae) on intracellular Ca2+ levels ([Ca2+]i) in human neutrophils were investigated by using fura-2 as a fluorescent probe. In both Ca2+-containing and Ca2+-free media, the lignans (50–100 µM) did not alter basal [Ca2+]i but inhibited the [Ca2+]i increase induced by platelet activating factor (PAF, 10 µM), leukotriene B4 (LTB4, 0.2 µM), and thapsigargin (1 µM) to different extents. In Ca2+-free medium, after depleting stores of Ca2+ with PAF, LTB4 or thapsigargin, addition of 3 mM Ca2+ induced Ca2+ influx. Each of the lignans (50–100 µM) caused 39–89% inhibition of PAF-induced Ca2+ influx; whereas only epi-aschantin was able to inhibit LTB4- and thapsigargin-induced Ca2+ influx by 54–79%. Together, the results suggest that in human neutrophils, these lignans did not alter basal [Ca2+]i but inhibited Ca2+ movement induced by Ca2+ mobilizing agents. [ABSTRACT FROM AUTHOR]

The article discusses the use of probiotics in treating small intestinal bacterial overgrowth (SIBO), where bacteria are present in greater numbers that are mostly found in the colon. Topics discussed include recommended treatment for SIBO that is mostly concentrated on detection and elimination of underlying cause and the effectiveness of probiotics as SIBO treatment, as well as its limitations.

A correction to the article "TNF-a Induces MMP-9 Expression and Soluble ICAM-1 Release Via TRAF2, c-Src, MAPKs and NF-?B in Osteoblast-Like MC3T3-E1 Cells" that was published in the previous issue is presented.