Nanosheets‐Assembled CuSe Crystal Pillar as a Stable and High‐Power Anode for Sodium‐Ion and Potassium‐Ion Batteries

Thanks to low costs and the abundance of the resources, sodium‐ion (SIBs) and potassium‐ion batteries (PIBs) have emerged as leading candidates for next‐generation energy storage devices. So far, only few materials can serve as the host for both Na⁺ and K⁺ ions. Herein, a cubic phase CuSe with crystal‐pillar‐like morphology (CPL‐CuSe) assembled by the nanosheets are synthesized and its dual functionality in SIBs and PIBs is comprehensively studied. The electrochemical measurements demonstrate that CPL‐CuSe enables fast Na⁺ and K⁺ storage as well as the sufficiently long duration. Specifically, the anode delivers a specific capacity of 295 mA h g^?1 at current density of 10 A g^?1 in SIBs, while 280 mA h g^?1 at 5 A g^?1 in PIBs, as well as the high capacity retention of nearly 100% over 1200 cycles and 340 cycles, respectively. Remarkably, CPL‐CuSe exhibits a high initial coulombic efficiency of 91.0% (SIBs) and 92.4% (PIBs), superior to most existing selenide anodes. A combination of in situ X‐ray diffraction and ex situ transmission electron microscopy tests fundamentally reveal the structural transition and phase evolution of CuSe, which shows a reversible conversion reaction for both cells, while the intermediate products are different due to the sluggish K⁺ insertion reaction.     

Structural basis for differential receptor binding of cholera and Escherichia coli heat-labile toxins: influence of heterologous amino acid substitutions in the cholera B-subunit

The closely related B-subunits of cholera toxin (CTB) and Escherichia coli heat-labile enterotoxin (LTB) both bind strongly to GM1 ganglioside receptors but LTB can also bind to additional glycolipids and glycoproteins. A number of mutant CT B-subunits were generated by substituting CTB amino acids with those at the corresponding positions in LTB. These were used to investigate the influence of specific residues on receptor-binding specificity. A mutated CTB protein containing the first 25 residues of LTB in combination with LTB residues at positions 94 and 95, bound to the same extent as native LTB to both delipidized rabbit intestinal cell membranes, complex glycosphingolipids (polyglycosylceramides) and neolactotetraosylceramide, but not to non-GM1 intestinal glycosphingolipids. In contrast, when LTB amino acid substitutions in the 1–25 region were combined with those in the 75–83 region, a binding as strong as that of LTB to intestinal glycosphingolipids was observed. In addition, a mutant LTB with a single Gly-33→Asp substitution that completely lacked affinity for both GM1 and non-GM1 glycosphingolipids could still bind to receptors in the intestinal cell membranes and to polyglycosylceramides. We conclude that the extra, non-GM1 receptors for LTB consist of both sialylated and non-sialylated glycoconjugates, and that the binding to either class of receptors is influenced by different amino acid residues within the protein.     

Mechanisms governing the effects of vacuum-assisted closure in cardiac surgery

SUMMARY:: Vacuum-assisted closure has been adopted as the first-line treatment for poststernotomy mediastinitis as a result of the excellent clinical outcome achieved with its use. Scientific evidence regarding the mechanisms by which vacuum-assisted closure promotes wound healing has started to emerge, although knowledge regarding the effects on heart and lung function is still limited. The organs in the mediastinum are hemodynamically crucial, and in patients with poststernotomy mediastinitis, vulnerable bypass grafts and reduced cardiac function must be taken into consideration during vacuum-assisted closure therapy. This article provides an overview of the effects of vacuum-assisted closure on heart and lung function and summarizes the current knowledge on the mechanisms by which vacuum-assisted closure therapy promotes wound healing.     

Lambda interferon (IFN-lambda) in serum is decreased in hantavirus-infected patients, and in vitro-established infection is insensitive to treatment with all IFNs and inhibits IFN-gamma-induced nitric oxide production

Hantaviruses, causing hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), are known to be sensitive to nitric oxide (NO) and to pretreatment with type I and II interferons (alpha interferon [IFN-alpha]/IFN-beta and IFN-gamma, respectively). Elevated serum levels of NO and IFN-gamma have been observed in HFRS patients, but little is known regarding the systemic levels of other IFNs and the possible effects of hantaviruses on innate antiviral immune responses. In Puumala virus-infected HFRS patients (n = 18), we report that the levels of IFN-alpha and IFN-beta are similar, whereas the level of IFN-lambda (type III IFN) is significantly decreased, during acute (day of hospitalization) compared to the convalescent phase. The possible antiviral effects of IFN-lambda on the prototypic hantavirus Hantaan virus (HTNV) replication was then investigated. Pretreatment of A549 cells with IFN-lambda alone inhibited HTNV replication, and IFN-lambda combined with IFN-gamma induced additive antiviral effects. We then studied the effect of postinfection treatment with IFNs. Interestingly, an already-established HTNV infection was insensitive to subsequent IFN-alpha, -beta, -gamma, and -lambda stimulation, and HTNV-infected cells produced less NO compared to noninfected cells when stimulated with IFN-gamma and IL-1beta. Furthermore, less phosphorylated STAT1 after IFN treatment was observed in the nuclei of infected cells than in those of noninfected cells. The results suggest that hantavirus can interfere with the activation of antiviral innate immune responses in patients and inhibit the antiviral effects of all IFNs. We believe that future studies addressing the mechanisms by which hantaviruses interfere with the activation and shaping of immune responses may bring more knowledge regarding HFRS and HCPS pathogenesis.     

Estrogen regulates T helper 17 phenotype and localization in experimental autoimmune arthritis

IntroductionThe incidence and progression of many autoimmune diseases are sex-biased, which might be explained by the immunomodulating properties of endocrine hormones. Treatment with estradiol potently inhibits experimental autoimmune arthritis. Interleukin-17-producing T helper cells (Th17) are key players in several autoimmune diseases, particularly in rheumatoid arthritis. The aim of this study was to investigate the effects of estrogen on Th17 cells in experimental arthritis.MethodsOvariectomized DBA/1 mice treated with 17β-estradiol (E2) or placebo were subjected to collagen-induced arthritis (CIA), and arthritis development was assessed. Th17 cells in joints and lymph nodes were studied by flow cytometry. Lymph node Th17 cells were also examined in ovariectomized estrogen receptor α–knockout mice (ERα^−/−) and wild-type littermates, treated with E2 or placebo and subjected to antigen-induced arthritis.ResultsE2-treated mice with established CIA showed reduced severity of arthritis and fewer Th17 cells in joints compared with controls. Interestingly, E2-treated mice displayed increased Th17 cells in lymph nodes during the early phase of the disease, dependent on ERα. E2 increased the expression of C-C chemokine receptor 6 (CCR6) on lymph node Th17 cells as well as the expression of the corresponding C-C chemokine ligand 20 (CCL20) within lymph nodes.ConclusionsThis is the first study in which the effects of E2 on Th17 cells have been characterized in experimental autoimmune arthritis. We report that E2 treatment results in an increase of Th17 cells in lymph nodes during the early phase of arthritis development, but leads to a decrease of Th17 in joints during established arthritis. Our data suggest that this may be caused by interference with the CCR6-CCL20 pathway, which is important for Th17 cell migration. This study contributes to the understanding of the role of estrogen in the development of autoimmune arthritis and opens up new fields for research concerning the sex bias in autoimmune disease.

Electronic supplementary material

The online version of this article (doi:10.1186/s13075-015-0548-y) contains supplementary material, which is available to authorized users.     

Selenium homeostasis and induction of thioredoxin reductase during long term selenite supplementation in the rat

Selenium is a candidate treatment for liver tumour prevention in chronic liver disease. In this study, we have studied selenium uptake, distribution and accumulation in rats provided with water containing tumour-preventive doses of sodium selenite for 10 weeks. Male Fischer 344 rats were given drinking water containing 1 μg/mL or 5 μg/mL sodium selenite. Selenium levels were monitored in serum and liver tissue over the 10-week period, and the kinetics of induction of the redox-active cytosolic selenoenzyme thioredoxin reductase were followed. Selenite exposure via drinking water caused a dose-dependent increase in blood and liver selenium levels, with plateaus at 6 and 8 weeks, respectively. These plateaus were reached at the same level of selenium regardless of dose, and no further accumulation was observed. A selenium-dependent increase in the activity of TrxR1 in parallel with the increase in liver selenium levels was also seen, and the induction of TrxR1 mRNA was seen only during the first three days of treatment, when the levels of selenium in the liver were increasing. Sodium selenite at 1 and 5 μg/mL did not affect body weight or relative liver mass. We concluded that long-term treatment with selenite did not cause accumulation of selenium and that the activity of TrxR1 in the liver rose with the selenium levels. We therefore suggest that sodium selenite at doses up to 5 μg/mL could be used for long-term tumour prevention.     

Genetic variation in <Emphasis Type="Italic">Delonix s.l.</Emphasis> (Leguminosae) in Madagascar revealed by AFLPs: fragmentation,conservation status and taxonomy

The distribution of genetic diversity has potential to inform conservation efforts but is rarely incorporated when conservation status is assigned to a species. These data can be beneficial to the conservation assessment process by providing information on subpopulations, gene flow and effective population sizes, thus achieving more successful assessments. In order to obtain a better understanding of the patterns of genetic variation and their relationship to conservation in the fragmented flora of Madagascar, this study assessed genetic diversity among and within Delonix s.l. (Leguminosae) using AFLP markers. The genetic diversity of eight species of Delonix s.l. (covering 79 sample sites and 254 individuals) showed a range of values (25–61% for polymorphic loci, and 0.076–0.192 Shannon’s Index). Results from an analysis of molecular variance (AMOVA) suggest that a majority of the genetic variance is attributed to variation within species (87%), which is also supported by a principle coordinate analysis of genetic distances between sites. The results were used to compare the genetic difference between species of different threat status and show that even closely related species with the same IUCN threat status differ in their genetic structure, probably arising from differences in life history traits, pollen and seed dispersal, and fragmentation. Species that are recently affected by habitat destruction and fragmentation are likely to be at high potential risk of genetic erosion contributing to their ongoing decline. Thus, genetic variation should be taken into consideration in conservation assessments, whenever possible, to provide accurate and targeted conservation recommendations in order to achieve more successful conservation outcomes.