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Evidence is mounting that migration in ectotherms is more widespread than formerly believed. Thus, a number of insects living in temperate climates, including locusts, butterflies, moths and dragonflies, following seasonal migration strategies show high responsiveness to alterations in climatic processes, similar to a broad taxonomic range of birds. On global scales, migratory insects include iconic large butterflies, dragonflies and also a number of crop pests. However, insect migrations are ecologically distinct from those of vertebrates, often relying heavily on seasonal winds and multiple generations to complete a full annual cycle, due to short insect life spans.Here, we review publicly available online resources to identify key patterns of spatial, taxonomic scales and complexity of climatic responsiveness to environmental predictors in migratory insects.We found that migratory insects respond to various levels of complexity in climatic patterns, and these responses are predicted by life history and ecological traits: (i) responses to climatic effect type were predicted by climate zone(s) of the distribution area, whereas (ii) response to climatic complexity was predicted by body size. In conclusion, migratory insects respond to various levels of complexity in climatic processes, and this responsiveness is governed by a substantially wider array of environmental predictors than demonstrated in vertebrates. [ABSTRACT FROM AUTHOR]

Migratory birds employ a variety of mechanisms to ensure appropriate timing of migration based on integration of endogenous and exogenous information. The cues to fatten and depart from the non‐breeding area are often linked to exogenous cues such as temperature or precipitation and the endogenous program. Shorter distance migrants should rely heavily on environmental information when initiating migration given relatively close proximity to the breeding area. However, the ability to fatten and subsequently depart may be linked to individual circumstances, including current fuel load and body size. For early and late departing migrants, we investigate effects of temperature, precipitation, lean body mass, fuel load and day of year on the initiation of migration (i.e. fuel load and departure timing) from the non‐breeding region by analyzing 21 years of banding data for four species of short‐ and medium‐distance migrants. Temperatures at the non‐breeding area were related to temperatures at potential stopover areas. Despite local cues being predictive of conditions further north, the amount variation explained by local weather conditions in our models differed by species and temporal period but was low overall (< 33% variation explained). For each species, we also compared lean body mass and fuel load between early and late departing migrants, which showed mixed results. Our combined results suggest that most individuals migrating short or medium distances in our study did not time the initiation of migration with local predictive cues alone, but rather other factors such as lean body mass, fuel load, day of year, which may be a proxy for the endogenous program, and those beyond the scope of our study also influenced the initiation of migration. Our study contributes to understanding which factors influence departure decisions of short‐ and medium‐distance migrants as they transition from the non‐breeding to the migratory phase of the annual cycle. [ABSTRACT FROM AUTHOR]

The present work demonstrates the performance of a von Hámos high-energy-resolution X-ray spectrometer based on a non-conventional conical Si single-crystal analyzer. The analyzer is tested with different primary and secondary X-ray sources as well as a hard X-ray sensitive CCD camera. The spectrometer setup is also characterized with ray-tracing simulations. Both experimental and simulated results affirm that the conical spectrometer can efficiently detect and resolve the two pairs of two elements (Ni and Cu) Kα X-ray emission spectroscopy (XES) peaks simultaneously, requiring a less than 2 cm-wide array on a single position-sensitive detector. The possible applications of this simple yet broad-energy-spectrum crystal spectrometer range from quickly adapting it as another probe for complex experiments at synchrotron beamlines to analyzing X-ray emission from plasma generated by ultrashort laser pulses at modern laser facilities. [ABSTRACT FROM AUTHOR]

Summary: Filamentous fungi produce a wide variety of enzymes in order to efficiently degrade plant cell wall polysaccharides. The production of these enzymes is controlled by transcriptional regulators, which also control the catabolic pathways that convert the released monosaccharides. Two transcriptional regulators, GalX and GalR, control d‐galactose utilization in the model filamentous fungus Aspergillus nidulans, while the arabinanolytic regulator AraR regulates l‐arabinose catabolism. d‐Galactose and l‐arabinose are commonly found together in polysaccharides, such as arabinogalactan, xylan and rhamnogalacturonan I. Therefore, the catabolic pathways that convert d‐galactose and l‐arabinose are often also likely to be active simultaneously. In this study, we investigated the interaction between GalX, GalR and AraR in d‐galactose and l‐arabinose catabolism. For this, we generated single, double and triple mutants of the three regulators, and analysed their growth and enzyme and gene expression profiles. Our results clearly demonstrated that GalX, GalR and AraR co‐regulate d‐galactose catabolism in A. nidulans. GalX has a prominent role on the regulation of genes of d‐galactose oxido‐reductive pathway, while AraR can compensate for the absence of GalR and/or GalX. [ABSTRACT FROM AUTHOR]

The paper demonstrates a tensor product (TP) model transformation‐based framework for an induction machine (IM). The state space model of an IM is highly nonlinear, thus the Takagi–Sugeno (TS) fuzzy model‐based quasi‐linear parameter‐varying (qLPV) representation can be a good alternative approach of machines modeling. The paper presents the basics of IM state space modeling, how the TP transformation can be applied in details. The control of IM is always a pivotal point; hence, options of feedback control are discussed. The main goal of this paper is to present the whole process of IM TP transformation‐based modeling including a control system. [ABSTRACT FROM AUTHOR]

1. Biparental care is stabilised if parents perform different tasks during care. Specialised parental roles may require different time and energy budgets that in turn are expected to influence the activity and space use of sexes. 2. Here we investigate movement patterns of the biparental Lethrus apterus beetle using a grid of pitfall traps in their natural habitat. 3. Sexes of the burrow building L. apterus perform different roles during caregiving, as females collect most of the leaves, which serve as food for the offspring while paired males stay mostly in the burrow. We hypothesised that sex differences in mate search and parental activities are reflected in movement patterns. 4. We found that females frequently travelled short distances, whereas males were detected less often but when detected, they travelled significantly longer distances than females. 5. Our results are consistent with the notion that efficient parental food provisioning requires more localised movement and activity patterns. Furthermore, the long distance movements of some males may indicate active mate searching behaviour. [ABSTRACT FROM AUTHOR]

Group 2 innate lymphoid cells (ILC2s) represent a rapid source of type 2 cytokines, such as IL-5 and IL-13, and play an important role in orchestrating type 2 immune response. Adenosine is an endogenous purine nucleoside, a catabolite of ATP that binds and activates ≥1 of 4 transmembrane G protein-coupled cell-surface adenosine receptors (ARs)--A1, A2A, A2B, and A3. Here, we studied the role of ARs in the regulation of cytokine production by ILC2s. We found that A2BARs suppress the production of both IL-5 and IL-13 by ILC2s, whereas A2AARs augment IL-5 production and fail to affect IL-13 release. Combined stimulation of all ARs led to the suppression of both IL-5 and IL-13 production, which indicated that A2BARs dominate A2AARs. Both pre- and post-transcriptional processes may be involved in the AR modulation of ILC2 IL-5 and IL-13 production. Thus, we identify adenosine as a novel negative regulator of ILC2 activation. [ABSTRACT FROM AUTHOR]

Interspecific comparisons of endocrine data are useful for drawing broad conclusions concerning the role of ecological variables in the evolution of physiological pathways. However, comparisons of endocrine data generated by different research groups are problematic, due to inter-laboratory variation in measured hormone values. To date, we know of no study which has quantified the extent of inter-laboratory variation in the measurement of hormone levels, outside of biomedical studies., To evaluate the extent to which laboratories differ in their measurement of hormones, we prepared seven samples of avian plasma with known concentrations of corticosterone and sent them for blind analyses to 19 laboratories and asked them to report the methods used and the values obtained., Both absolute hormone concentrations and the ratios between samples were equally variable, up to an order of magnitude different for some concentrations. Laboratory identity accounted for more than 80% of the variation in reported corticosterone, but we could not identify any methodological factors that consistently contributed to this inter-laboratory variation. In addition, laboratory measurement error was significantly correlated with the latitude of the primary study species for each laboratory, suggesting that inter-laboratory variation has the potential to drive trends in corticosterone datasets., Inter-laboratory variation in corticosterone measurement may have serious implications for quantitative comparisons of endocrine values across laboratories, although comparisons of qualitative patterns may be more robust because rank order of the samples was relatively consistent across laboratories. Ignoring laboratory effect and the non-independence of data may lead to an inflated rate of Type I error and spurious correlations. [ABSTRACT FROM AUTHOR]

Extracellular ATP binds to and signals through P2X7 receptors (P2X7Rs) to modulate immune function in both inflammasome-dependent and -independent manners. In this study, P2X7-/- mice, the pharmacological agonists ATP-magnesium salt (Mg-ATP; 100 mg/kg, EC50 ≈ 1.32 µM) and benzoylbenzoyl-ATP (Bz-ATP; 10 mg/kg, EC50 ≈ 285 µM), and antagonist oxidized ATP (oxi-ATP; 40 mg/kg, IC50 ≈ 100 µM) were used to show that P2X7R activation is crucial for the control of mortality, bacterial dissemination, and inflammation in cecal ligation and puncture-induced polymicrobial sepsis in mice. Our results with P2X7-/- bone marrow chimeric mice, adoptive transfer of peritoneal macrophages, and myeloid-specific P2X7-/- mice indicate that P2X7R signaling on macrophages is essential for the protective effect of P2X7Rs. P2X7R signaling protects through enhancing bacterial killing by macrophages, which is independent of the inflammasome. By using the connexin (Cx) channel inhibitorGap27 (0.1mg/kg, IC50 ≈ 0.25 µM) and pannexin channel inhibitor probenecid (10 mg/kg, IC50 ≈ 11.7 µM), we showed that ATP release through Cx is important for inhibiting inflammation and bacterial burden. In summary, targeting P2X7Rs provides a new opportunity for harnessing an endogenous protective immune mechanism in the treatment of sepsis. [ABSTRACT FROM AUTHOR]

Gonadal steroid hormones enhance cognitive performance, particularly spatial and vocal learning, in mammals and birds. However, it is unknown whether problem-solving ability is similarly regulated. We propose that androgens, such as testosterone and 5α-dihydrotestosterone, play a role in mediating problem-solving behavior as well. As a test, male white-crowned sparrows ( Zonotrichia leucophrys gambelii) were either castrated and administered a blank (Blank-castrate) or testosterone-filled implant (T-castrate) or were sham operated and were exposed to a novel feeder, which they had to open to receive a food reward, in two trials. Testosterone treatment affected neither a neophobic response nor problem-solving performance. However, T-castrates were more persistent in manipulating the feeder than Blank-castrates or Shams. Furthermore, their persistence correlated positively with circulating levels of both testosterone and 5α-dihydrotestosterone. We suggest that a positive correlation between sex steroids and persistence in foraging and problem-solving contexts may lead to an adaptive increase in resource acquisition in the breeding season. Given the overall low success on the problem-solving test, we cannot confidently conclude that androgens do not play a role in mediating problem-solving behavior. However, unlike in mammals, it seems these hormones do not significantly influence neophobia in foraging contexts in birds. [ABSTRACT FROM AUTHOR]

Sepsis remains the leading cause of morbidity and mortality in critically ill patients. Excessive inflammation is a major cause of organ failure and mortality in sepsis. Ectonucleoside triphosphate diphosphohydrolase 1, ENTPDasel (CD39) is a cell surface nucleotide-metabolizing enzyme, which degrades the extracellular purines ATP and ADP, thereby regulating purinergic receptor signaling. Although the role of purinergic receptor signaling in regulating inflammation and sepsis has been addressed previously, the role of CD39 in regulating the host's response to sepsis is unknown. We found that the CD39 mimic apyrase (250 U/kg) decreased and knockout or pharmacologic blockade with sodium polyoxotungstate (5 mg/kg; IC50 ≈ 10 µM) of CD39 increased mortality of mice with polymicrobial sepsis induced by cecal ligation and puncture. CD39 decreased inflammation, organ damage, immune cell apoptosis, and bacterial load. Use of bone marrow chimeric mice revealed that CD39 expression on myeloid cells decreases inflammation in septic mice. CD39 expression is upregulated during sepsis in mice, as well as in both murine and human macrophages stimulated with Escherichia coli. Moreover, E. coli increases CD39 promoter activity in macrophages. Altogether, these data indicate CD39 as an evolutionarily conserved inducible protective pathway during sepsis. We propose CD39 as a novel therapeutic target in the management of sepsis. [ABSTRACT FROM AUTHOR]

Adenosine has been implicated in suppressing the proinflammatory responses of classically activated macrophages induced by Th1 cytokines. Alternative macrophage activation is induced by the Th2 cytokines interleukin (IL)-4 and IL-13; however, the role of adenosine in governing alternative macrophage activation is unknown. We show here that adenosine treatment of IL-4- or IL-13-activated macrophages augments the expression of alternative macrophage markers arginase-1, tissue inhibitor of matrix metalloproteinase- 1 (TIMP-1), and macrophage galactose-type C-type lectin- 1. The stimulatory effect of adenosine required primarily A2B receptors because the nonselective adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) increased both arginase activity (EC50 = 261.8 nM) and TIMP-1 production (EC50 - 80.67 nM), and both pharmacologic and genetic blockade of A2B receptors prevented the effect of NECA. A2A receptors also contributed to the adenosine augmentation of IL-4-induced TIMP-1 release, as both adenosine and NECA were less efficacious in augmenting TIMP-1 release by A2A receptor-deficient than control macrophages. Of the transcription factors known to drive alternative macrophage activation, CCAAT-enhancer-binding protein β was required, while cAMP response element-binding protein and signal transducer and activator of transcription 6 were dispensable in mediating the effect of adenosine. We propose that adenosine receptor activation suppresses inflammation and promotes tissue restitution, in part, by promoting alternative macrophage activation. [ABSTRACT FROM AUTHOR]

Activation-induced cell death (AICD) is initiated by T-cell receptor (TCR) restimulation of already activated and expanded peripheral T cells and is mediated through Fas/Fas ligand (FasL) interactions. Adenosine is a purine nucleoside signaling molecule, and its immunomodulatory effects are mediated by 4 G-protein-coupled receptors: A1, A2A, A2B, and A3. In this study, we investigated the role of A2A receptors in regulating CD4+ T lymphocyte AICD. Our results showed that the selective A2A receptor agonist CGS21680 (EC50 = 15.2-32.6 nM) rescued mouse CD4+ hybridomas and human Jurkat cells from AICD and that this effect was reversed by the selective A2A receptor antagonist ZM241385 (EC50 = 2.3 nM). CGS21680 decreased phosphatidylserine exposure on the membrane, as well as the cleavage of caspase-3, caspase-8 and poly(ADPribose) polymerase indicating that A2A receptor stimulation blocks the extrinsic apoptotic pathway. In addition, CGS21680 attenuated both Fas and FasL mRNA expression. This decrease in FasL expression was associated with decreased activation of the transcription factor systems NF-ΚB, NF-ATp, early growth response (Egr)-1, and Egr-3. The antiapoptotic effect of A2A receptor stimulation was mediated by protein kinase A. Together, these results demonstrate that A2A receptor activation suppresses the AICD of peripheral T cells. [ABSTRACT FROM AUTHOR]

Each spring, millions of songbirds migrate across the Gulf of Mexico on their way to breeding sites in North America. Data from radar and migration monitoring stations have revealed broad patterns in the spatial and temporal course of trans-Gulf migration. Unfortunately, we have limited information on where these birds have previously spent the winter and where they are migrating to breed. Here we measure stable-hydrogen isotopes in feathers (δDf) to infer the breeding latitude of five species of songbirds – hooded warblers Wilsonia citrina, American redstarts Setophaga ruticilla, black-and-white warblers Mniotilta varia, ovenbirds Seiurus aurocapilla, and northern waterthrushes S. noveboracensis– that were captured at a stopover site along the coast of southwestern Louisiana in spring 2004. Values of δDf across all species ranged from −163 to −35‰ (n=212), and within most species the range was consistent with the latitudinal extent of known breeding sites in central and eastern North America. Individuals that arrived first along the northern Gulf coast had δDf values indicative of southerly breeding sites in hooded warblers, American redstarts, black-and-white warblers, and ovenbirds, but no relationship was found between passage timing and δDf for northern waterthrushes. Our findings suggest that spring passage is often timed to coincide with the emergence of suitable conditions on breeding areas, with southern breeding birds migrating first. [ABSTRACT FROM AUTHOR]

Adenosine is an immunosuppressive nucleoside, and adenosine A2A receptors inhibit T-cell activation. We investigated the role of A2A receptors in regulating T helper (Th) 1- and Th2-cell development and effector function. A2A-receptor stimulation suppressed the development of T-cell receptor (TCR) -stimulated naive T cells into both Th1 and Th2 cells, as indicated by decreased IFN-γ production by cells developed under Th1-skewing conditions and decreased interleukin (IL)-4, IL-5, and IL-10 production by cells developed under Th2-skewing conditions. Using A2A receptor-deficient mice, we demonstrate that A2A receptor activation inhibits Th1- and Th2-cell development by decreasing the proliferation and IL-2 production of naive T cells, irrespective of whether the cells are expanded under Th1- or Th2-skewing environment. Using in vivo established Th1 and Th2 cells, we further demonstrate the nonselective nature of A2A receptor-mediated immunosuppressive effects, because A2A receptor activation decreased IFN-γ and IL-4 secretion and mRNA level of TCR-stimulated effector Th1 and Th2 cells, respectively. A2A receptor mRNA expression in both Th1 and Th2 effector cells increased following TCR stimulation. In summary, these data demonstrate that A2A receptor activation has strong inhibitory actions during early developmental, as well as late effector, stages of Th1- and Th2-cell responses. [ABSTRACT FROM AUTHOR]

Growing evidence indicates that adenosine receptors could be promising therapeutic targets in autoimmune diseases. Here we studied the role of adenosine receptors in controlling the course of type 1 diabetes. Diabetes in CD-1 mice was induced by multiple- low-dose-streptozotocin (MLDS) treatment and in nonobese diabetic (NOD) mice by cyclophosphamide injection. The nonselective adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) prevented diabetes development in both MLDS-challenged mice and in cyclophosphamide-treated NOD mice. The effect of NECA was reversed by the selective A2B receptor antagonist N-(4-cyanophenyl)-2-[4-( 2,3,6,7-tetrahydro-2,6- dioxo-l,3-dipropyl-lH-purin-8-yl)phenoxy]acetamide (MRS 1754). The selective A1 receptor agonist 2-chloro- N6-cyclopentyladenosine (CCPA) and As receptor agonist N6- ( 3-iodobenzyl)-adenosine-5'-N-methyluronamide (IB-MECA) were less efficacious in ameliorating the course of diabetes. NECA inhibited diabetes in A2A receptor KO mice and the selective A2A receptor agonist 2-p-(2-carboxyethyl)phenethyl-amino- 5'-N-ethyl-carboxamidoadenosine (CGS21680) had no effect in normal mice, indicating a lack of role of A2A receptors. NECA failed to prevent cytokine-induced β-cell death in vitro, but NECA strongly suppressed expression of the proinflammatory cytokines TNF-α, MIP-1α, IL-12, and IFN-γ in pancreata, endotoxin, or anti-CD3-stimulated splenic cells, and T helper 1 lymphocytes, indicating that the beneficial effect of NECA was due to immunomodulation. These results demonstrate that adenosine receptor ligands are potential candidates for the treatment of type 1 diabetes. [ABSTRACT FROM AUTHOR]

Summary The anti-inflammatory agent sulphasalazine is an important component of several treatment regimens in the therapy of ulcerative colitis, Crohn's disease and rheumatoid arthritis. Sulphasalazine has many immunomodulatory actions, including modulation of the function of a variety of cell types, such as lymphocytes, natural killer cells, epithelial cells and mast cells. However, the effect of this agent on macrophage (Mφ) function has not been characterized in detail. In the present study, we investigated the effect of sulphasalazine and two related compounds – sulphapyridine and 5-aminosalicylic acid – on Mφ activation induced by bacterial lipopolysaccharide (LPS) and interferon-γ (IFN-γ). In J774 Mφ stimulated with LPS (10 µg/ml) and IFN-γ (100 U/ml), sulphasalazine (50–500 µm) suppressed nitric oxide (NO) production in a concentration-dependent manner. The expression of the inducible NO synthase (iNOS) was suppressed by sulphasalazine at 500 µm. Sulphasalazine inhibited the LPS/IFN-γ-induced production of both interleukin-12 (IL-12) p40 and p70. The suppression of both NO and IL-12 production by sulphasalazine was superior to that by either sulphapyridine or 5-aminosalicylic acid. Although the combination of LPS and IFN-γ induced a rapid expression of the active forms of p38 and p42/44 mitogen-activated protein kinases and c-Jun terminal kinase, sulphasalazine failed to interfere with the activation of any of these kinases. Finally, sulphasalazine suppressed the IFN-γ-induced expression of major histocompatibility complex class II. These results demonstrate that the Mφ is an important target of the immunosuppressive effect of sulphasalazine. [ABSTRACT FROM AUTHOR]

Inosine monophosphate (IMP) is the intracellular precursor for both adenosine monophosphate and guanosine monophosphate and thus plays a central role in intracellular purine metabolism. IMP can also serve as an extracellular signaling molecule, and can regulate diverse processes such as taste sensation, neutrophil function, and ischemia-reperfusion injury. How IMP regulates inflammation induced by bacterial products or bacteria is unknown. In this study, we demonstrate that IMP suppressed tumor necrosis factor (TNF)-α production and augmented IL-10 production in endotoxemic mice. IMP exerted its effects through metabolism to inosine, as IMP only suppressed TNF-α following its CD73-mediated degradation to inosine in lipopolysaccharide-activated macrophages. Studies with gene targeted mice and pharmacological antagonism indicated that A2A, A2B, and A3 adenosine receptors are not required for the inosine suppression of TNF-α production. The inosine suppression of TNF-α production did not require its metabolism to hypoxanthine through purine nucleoside phosphorylase or its uptake into cells through concentrative nucleoside transporters indicating a role for alternative metabolic/uptake pathways. Inosine augmented IL-β production by macrophages in which inflammasome was activated by lipopolysaccharide and ATP. In contrast to its effects in endotoxemia, IMP failed to affect the inflammatory response to abdominal sepsis and pneumonia. We conclude that extracellular IMP and inosine differentially regulate the inflammatory response. [ABSTRACT FROM AUTHOR]