Photovoltaic–thermoelectric temperature control using a closed-loop integrated cooler

The Closed-Loop Integrated Cooler (CLIC) is a novel technique deployed on experimental apparatus to accurately measure, monitor and control the temperature of optoelectronic devices. Demonstrated here within a Concentrator Photovoltaic-Thermoelectric (CPV-TE) hybrid device, the thermoelectric module was used as a solid state sensor and heat pump in order to control the operational temperature for a triple-junction solar cell. The technique was used to achieve stable, reproducible and repeatable Standard Test Conditions (STC) of 25oC cell temperature, with 1000W/m2 irradiance and AM1.5G spectrum. During testing with Secondary Optical Element (SOE) optics in a solar simulator, the CLIC enabled accurate temperature control of the CPV cell. This would otherwise be unfeasible due to the spectral, reflective and diffusive effects of the SOE optics. The CLIC was used to obtain temporal and spatial constant temperature of the CPV-TE hybrid receiver during Current-Voltage measurement. This method highlights the future potential of the CLIC for accurate temperature control of optoelectronic devices both during testing and in future semiconductor device applications where temperature control is essential to performance or lifetime

The stellar mass - size relation for cluster galaxies at z=1 with high angular resolution from the Gemini/GeMS multi-conjugate adaptive optics system

We present the stellar mass - size relation for 49 galaxies within the $z$ = 1.067 cluster SPT-CL J0546$-$5345, with FWHM $\sim$80-120 mas $K_{\mathrm s}$-band data from the Gemini multi-conjugate adaptive optics system (GeMS/GSAOI). This is the first such measurement in a cluster environment, performed at sub-kpc resolution at rest-frame wavelengths dominated by the light of the underlying old stellar populations. The observed stellar mass - size relation is offset from the local relation by 0.21 dex, corresponding to a size evolution proportional to $(1+z)^{-1.25}$, consistent with the literature. The slope of the stellar mass - size relation $\beta$ = 0.74 $\pm$ 0.06, consistent with the local relation. The absence of slope evolution indicates that the amount of size growth is constant with stellar mass. This suggests that galaxies in massive clusters such as SPT-CL J0546$-$5345 grow via processes that increase the size without significant morphological interference, such as minor mergers and/or adiabatic expansion. The slope of the cluster stellar mass - size relation is significantly shallower if measured in $HST$/ACS imaging at wavelengths blueward of the Balmer break, similar to rest-frame UV relations at $z$ = 1 in the literature. The stellar mass - size relation must be measured at redder wavelengths, which are more sensitive to the old stellar population that dominates the stellar mass of the galaxies. The slope is unchanged when GeMS $K_s$-band imaging is degraded to the resolution of $K$-band HST/NICMOS resolution but dramatically affected when degraded to $K_s$-band Magellan/FourStar resolution. Such measurements must be made with AO in order to accurately characterise the sizes of compact, $z$ = 1 galaxies.Comment: 24 pages, 13 figures, 3 tables. Accepted for publication in MNRAS. Typos corrected, DOI adde

Effects of the tat and nef gene products of human immunodeficiency virus type 1 (HIV-1) on transcription controlled by the HIV-1 long terminal repeat and on cell growth in macrophages

The RAW264 murine macrophage cell line was used as a model to examine the role of the tat and nef gene products in the transcription regulation of the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) in macrophages. Contrary to claims that the activity of the HIV-1 LTR responds poorly in rodent cells to trans activation by the viral tat gene product, cotransfection of RAW264 cells with a tat expression plasmid in transient transfection assays caused a > 20-fold increase in reporter gene expression that was inhibited by mutations in the TAR region. RAW264 cells stably transfected with the tat plasmid displayed similarly elevated HIV-1 LTR-driven reporter gene activity. By contrast to previous reports indicating a negative role for nef in HIV transcription, cotransfection of RAW264 cells with a nef expression plasmid trans activated the HIV-1 LTR driving either a chloramphenicol acetyltransferase or a luciferase reporter gene. The action of nef was specific to the LTR, as expression of nef had no effect on the activity of the simian virus 40, c-fms, urokinase plasminogen activator, or type 5 acid phosphatase promoter. trans-activating activity was also manifested by a frameshift mutant expressing only the first 35 amino acids of the protein. The effects of nef were multiplicative with those of tat gene product and occurred even in the presence of bacterial lipopolysaccharide, which itself activated LTR-directed transcription. Examination of the effects of selected mutations in the LTR revealed that neither the kappa B sites in the direct repeat enhancer nor the TAR region was required as a cis-acting element in nef action. The action of nef was not species restricted; it was able to trans activate in the human monocyte-like cell line Mono Mac 6. The presence of a nef expression cassette in a neomycin phosphotransferase gene expression plasmid greatly reduced the number of G418-resistant colonies generated in stable transfection of RAW264 cells, and many of the colonies that were formed exhibited very slow growth. The frameshift mutant was also active in reducing colony generation. Given the absence of any effect of the frameshift mutation on nef function, its actions on macrophage growth and HIV transcription are discussed in terms of the role of the N-terminal 30 amino acids and of stable secondary structures in the mRNA

SHα\alphaDE: Survey description and mass-kinematics scaling relations for dwarf galaxies

The Study of H$\alpha$ from Dwarf Emissions (SH$\alpha$DE) is a high spectral resolution (R=13500) H$\alpha$ integral field survey of 69 dwarf galaxies with stellar masses $10^6<M_\star<10^9 \,\rm{M_\odot}$. The survey used FLAMES on the ESO Very Large Telescope. SH$\alpha$DE is designed to study the kinematics and stellar populations of dwarf galaxies using consistent methods applied to massive galaxies and at matching level of detail, connecting these mass ranges in an unbiased way. In this paper we set out the science goals of SH$\alpha$DE, describe the sample properties, outline the data reduction and analysis processes. We investigate the $\log{M_{\star}}-\log{S_{0.5}}$ mass-kinematics scaling relation, which have previously shown potential for combining galaxies of all morphologies in a single scaling relation. We extend the scaling relation from massive galaxies to dwarf galaxies, demonstrating this relation is linear down to a stellar mass of $M_{\star}\sim10^{8.6}\,\rm{M_\odot}$. Below this limit, the kinematics of galaxies inside one effective radius appear to be dominated by the internal velocity dispersion limit of the H$\alpha$-emitting gas, giving a bend in the $\log{M_{\star}}-\log{S_{0.5}}$ relation. Replacing stellar mass with total baryonic mass using gas mass estimate reduces the severity but does not remove the linearity limit of the scaling relation. An extrapolation to estimate the galaxies' dark matter halo masses, yields a $\log{M_{h}}-\log{S_{0.5}}$ scaling relation that is free of any bend, has reduced curvature over the whole mass range, and brings galaxies of all masses and morphologies onto the virial relation.Comment: 19 pages, 13 figures, 5 tables; published in MNRA

Responsiveness of serum C‐reactive protein, interleukin‐17A, and interleukin‐17F levels to ustekinumab in psoriatic arthritis: lessons from two phase III, multicenter, double‐blind, placebo‐controlled trials

Objective: To evaluate the associations of C‐reactive protein (CRP) and circulating Th17‐associated cytokine levels with psoriatic arthritis (PsA) disease activity and therapeutic response to ustekinumab. Methods: Interleukin‐17A (IL‐17A), IL‐17F, IL‐23, and CRP concentrations were measured in serum samples collected as part of the 2 PSUMMIT phase III studies of ustekinumab in PsA (n = 927). In post hoc analyses, relationships of IL‐17A, IL‐17F, and CRP levels at baseline, week 4, and week 24 with baseline skin and joint disease activity and response to therapy were evaluated using generalized linear models and Pearson's product‐moment correlation tests. Results: Baseline serum levels of IL‐17A and IL‐17F were positively correlated with baseline skin disease scores (r = 0.39–0.62). IL‐23 levels were correlated with skin disease scores to a lesser extent (r = 0.26–0.31). No significant correlations were observed between these cytokine or CRP levels and baseline joint disease activity. There was no significant association of baseline levels of IL‐17A, IL‐17F, IL‐23, or CRP with therapeutic response to ustekinumab in either the skin or joints. Significant reductions from baseline in levels of IL‐17A, IL‐17F, and CRP were seen in patients treated with ustekinumab compared to those treated with placebo. Ustekinumab‐treated patients in whom 75% improvement in the Psoriasis Area and Severity Index score or 20% improvement according to the American College of Rheumatology criteria was achieved after 24 weeks of treatment had greater reductions in CRP level (geometric mean decreases of 51–58% versus 32–33%; P &lt; 0.05), but not IL‐17A or IL‐17F levels, than nonresponders. Conclusion: Baseline serum IL‐23/IL‐17 levels correlated with skin, but not joint, disease activity, suggesting tissue‐specific variation. However, neither baseline Th17‐associated cytokine levels nor CRP level were predictive of therapeutic response to ustekinumab in the skin or joints, despite rapid reductions in their levels following ustekinumab therapy

Uropathogenic Escherichia coli virulence and innate immune responses during urinary tract infection

Urinary tract infections (UTI) are among the most common infectious diseases of humans and are the most common nosocomial infections in the developed world. It is estimated that 40-50% of women and 5% of men will develop a UTI in their lifetime, and UTI accounts for more than 1 million hospitalizations and $1.6 billion in medical expenses each year in the USA. Uropathogenic Escherichia coli (UPEC) is the primary cause of UTI. This review presents an overview of recent discoveries related to the primary virulence factors of UPEC and major innate immune responses to infection of the lower urinary tract. New and emerging themes in UPEC research are discussed in the context of the interface between host and pathogen

Innate immune perturbations, accumulating DAMPs and inflammasome dysregulation: a ticking time bomb in ageing

Ageing has pronounced effects on the immune system, including on innate immune cells. Whilst most studies suggest that total numbers of different innate immune cell populations do not change dramatically during ageing, many of their functions such as phagocytosis, antigen presentation and inflammatory molecule secretion decline. In contrast, many endogenous damage-associated molecular patterns (DAMPs) accumulate during ageing. These include reactive oxygen species (ROS) released from damaged mitochondria, extracellular nucleotides like ATP, high mobility group box (HMGB) 1 protein, oxidized low density lipoprotein, amyloid-beta (Aβ), islet amyloid polypeptide and particulates like monosodium urate (MSU) crystals and cholesterol crystals. Some of these DAMPs trigger the activation of inflammasomes, cytosolic danger sensing signalling platforms that drive both the maturation of specific pro-inflammatory mediators such as IL-1β, as well as the initiation of pro-inflammatory pyroptotic cell death. Herein, we review the evidence that dysregulated inflammasome activation, via altered innate immune cell functions and elevated levels of DAMPs, contributes to the establishment of chronic, low-grade inflammation (characterized by elevated levels of IL-6 and C-reactive protein) and the development of age-related pathological processes

Macrophages exposed continuously to lipopolysaccharide and other agonists that act via toll-like receptors exhibit a sustained and additive activation state

BACKGROUND: Macrophages sense microorganisms through activation of members of the Toll-like receptor family, which initiate signals linked to transcription of many inflammation associated genes. In this paper we examine whether the signal from Toll-like receptors [TLRs] is sustained for as long as the ligand is present, and whether responses to different TLR agonists are additive. RESULTS: RAW264 macrophage cells were doubly-transfected with reporter genes in which the IL-12p40, ELAM or IL-6 promoter controls firefly luciferase, and the human IL-1β promoter drives renilla luciferase. The resultant stable lines provide robust assays of macrophage activation by TLR stimuli including LPS [TLR4], lipopeptide [TLR2], and bacterial DNA [TLR9], with each promoter demonstrating its own intrinsic characteristics. With each of the promoters, luciferase activity was induced over an 8 hr period, and thereafter reached a new steady state. Elevated expression required the continued presence of agonist. Sustained responses to different classes of agonist were perfectly additive. This pattern was confirmed by measuring inducible cytokine production in the same cells. While homodimerization of TLR4 mediates responses to LPS, TLR2 appears to require heterodimerization with another receptor such as TLR6. Transient expression of constitutively active forms of TLR4 or TLR2 plus TLR6 stimulated IL-12 promoter activity. The effect of LPS, a TLR4 agonist, was additive with that of TLR2/6 but not TLR4, whilst that of lipopeptide, a TLR2 agonist, was additive with TLR4 but not TLR2/6. Actions of bacterial DNA were additive with either TLR4 or TLR2/6. CONCLUSIONS: These findings indicate that maximal activation by any one TLR pathway does not preclude further activation by another, suggesting that common downstream regulatory components are not limiting. Upon exposure to a TLR agonist, macrophages enter a state of sustained activation in which they continuously sense the presence of a microbial challenge