Low power wireless embedded systems

In this book, several advanced topics in the area of Power Management Analog and Mixed-Signal Circuits and Systems have been addressed. The fundamental aspects of these topics are discussed, and state-of-the-art developments are presented. The book covers subject areas like bio-sensors co-integration with nanotechnology, and for these CMOS circuits one popular application could be personalized medicine. Having seen the power assets for such technologies, and knowing what challenges these present for the circuits and systems designer, remote powering and sensors solutions are reviewed in the second chapter. The third chapter contains an industrial contribution on remote powering, presenting energy harvesting from the RF field to power a target wireless sensor network consumption. Having touched the idea of the low current consumption, µA or Nano-Amp range and their transient behaviours are also described. Digital and large-scale integrated circuits - seen from an academic point of view - is included in chapter five, and this same topic from an industrial point of view is given in the chapter thereafter. An additional topic on the hall sensor, applied in an automotive case study, is then also presented. Approaching the duty-cycling of active mode, oscillator for timers and system-level power management including the cloud are covered in the last chapters. Power Management for Internet of Everything targets post-graduate students and those persons active in industry, whom understand and can connect system design with system on chip (SoC) and mixed-signal design as broader set of circuits and systems. The topic of Internet of Things (IoT), ranging from data converters for sensor interfaces to radios and software application, is also addressed from the viewpoint of power and energy management. The contents ensures a good balance between academia and industry, combined with a judicious selection of distinguished international authors

TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance.

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. Trem1(-/-) mice are viable, fertile and show no altered hematopoietic compartment. In CD4(+) T cell- and dextran sodium sulfate-induced models of colitis, Trem1(-/-) mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1(-/-) mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected Trem1(-/-) mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1(-/-) mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as Trem1(+/+) controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control

Upon colitis induction, <i>Trem1^−/− x Rag2^−/−</i> mice exhibit substantially reduced inflammatory infiltrates and diminished expression of pro-inflammatory mediators.

<p>(A–C) Lamina propria cells were isolated from the colon of <i>Trem1^+/+ x Rag2^−/−</i> and <i>Trem1^−/− x Rag2^−/−</i> mice 12–13 days post adoptive transfer of colitogenic CD4 T cells or from untransferred mice (healthy colons) and analysed by FACS. (A) After exclusion of doublets and dead cells, CD11b⁺ cells were discriminated from CD4⁺ T cells and further subgated into MHCII^lo Gr1⁺ (gate 1) and MHCII^hi Gr1⁻ (gate 2) cells. In gate 1, monocytes and neutrophils were identified according to their Ly6C^hi Gr1^int and Ly6C^int Gr1^hi phenotype, respectively. In gate 2, MHCII⁺ cells were further subdivided into two populations of MHCII^int Ly6C^hi and MHCII^hi Ly6C^lo cells. (B, C) Absolute numbers of total cells recovered from individual mice (symbols; lines indicate mean values per group) and mean values ± SEM for CD45⁺ cells, CD4⁺ T cells, CD11b⁺ cells and subsets defined within the CD11b⁺ gate as illustrated in (A). Per group, n = 9 mice adoptively transferred with CD4 T cells (B) and n = 4 untransferred (C) mice were analysed. (D) TREM-1 surface expression by neutrophils (Ly6C^int Gr1^hi), monocytes (Ly6C^hi Gr1^int) and CD11b⁺ Gr1⁻ Ly6C⁺ versus Ly6C⁻ subsets identified in the lamina propria (according to the gating strategy depicted in D) of colitic (n = 9) versus healthy (n = 4) <i>Trem1^+/+ x Rag2^−/−</i> mice. (E) Colonic tissues were assessed for the expression of pro-inflammatory mediators by qRT-PCR. Bars show mean values ± SEM for n = 9 mice. ***, p<0.001; **, p<0.01; *, p<0.05. N.D. = not determined due to insufficient cell numbers.</p

<i>Trem1^−/− x Rag2^−/−</i> mice are protected from a CD4⁺ T cell-induced colitis.

<p>Colitis was induced in <i>Trem1^+/+ x Rag2^−/−</i> (filled circles) and <i>Trem1^−/− x Rag2^−/−</i> mice (white circles) by i.p. injection of 2×10⁵ CD4⁺ CD45RB^hi T cells. (A) Weight loss relative to the initial body weight. Mean values of n = 9 mice analysed per group are shown with error bars indicating the SEM. (B) Colon lengths were determined in individual mice (symbols). Lines show mean values for each group of mice. (C) Representative H&E-stained colonic tissue sections of a <i>Trem1^+/+ x Rag2^−/−</i> (histopathological score: 14) and <i>Trem1^−/− x Rag2^−/−</i> mouse (histopathological score: 2). (D) Total histopathological scores. Symbols show total scores for individual mice and lines indicate the mean value for each group of mice. Histopathological scores were determined for individual mice by a pathologist according to parameters defined in the <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003900#s4" target="_blank">Materials and Methods</a> section. (E) Individual parameters of histopathological scoring. Columns show mean values for n = 9 mice analysed per group and error bars indicate the SEM. ****, p<0.0001; ***, p<0.001; **, p<0.01. One representative experiment out of three independent experiments is shown.</p