MoS2 nanoflowers with expanded interlayer spacing of the (002) plane were synthesized and used as high-performance anode in Na-ion batteries. By controlling the cut-off voltage to the range of 0.4-3 V, an intercalation mechanism rather than a conversion reaction is taking place. The MoS2 nanoflower electrode shows high discharge capacities of 350 mAh g(-1) at 0.05 A g(-1) , 300 mAh g(-1) at 1 A g(-1) , and 195 mAh g(-1) at 10 A g(-1) . An initial capacity increase with cycling is caused by peeling off MoS2 layers, which produces more active sites for Na(+) storage. The stripping of MoS2 layers occurring in charge/discharge cycling contributes to the enhanced kinetics and low energy barrier for the intercalation of Na(+) ions. The electrochemical reaction is mainly controlled by the capacitive process, which facilitates the high-rate capability. Therefore, MoS2 nanoflowers with expanded interlayers hold promise for rechargeable Na-ion batteries.

MoS 2 nanoflowers with expanded interlayer spacing of the (002) plane were synthesized and used as highperformance anode in Na-ion batteries. By controlling the cut-off voltage to the range of 0.4-3 V, an intercalation mechanism rather than a conversion reaction is taking place.The MoS 2 nanoflower electrode shows high discharge capacities of 350 mAh g À1 at 0.05 A g À1 , 300 mAh g À1 at 1 A g À1 , and 195 mAh g À1 at 10 A g À1 . An initial capacity increase with cycling is caused by peeling off MoS 2 layers, which produces more active sites for Na + storage. The stripping of MoS 2 layers occurring in charge/discharge cycling contributes to the enhanced kinetics and low energy barrier for the intercalation of Na + ions. The electrochemical reaction is mainly controlled by the capacitive process, which facilitates the high-rate capability. Therefore, MoS 2 nanoflowers with expanded interlayers hold promise for rechargeable Na-ion batteries.

Background and Aims Despite the presence of neutrophil extracellular traps [NETs] in inflamed colon having been confirmed, the role of NETs, especially the circulating NETs, in the progression and thrombotic tendency of inflammatory bowel disease [IBD] remains elusive. We extended our previous study to prove that NETs constitute a central component in the progression and prothrombotic state of IBD. Methods In all 48 consecutive patients with IBD were studied. Acute colitis was induced by the treatment of C57BL/6 mice with 3.5% dextran sulphate sodium [DSS] in drinking water for 6 days. Peripheral blood neutrophils and sera were collected from IBD patients and murine colitis models. Exposed phosphatidylserine [PS] was analysed with flow cytometry and confocal microscopy. Procoagulant activity was evaluated using clotting time, purified coagulation complex, and fibrin formation assays. Results We observed higher plasma NET levels and presence of NETs in colon tissue in patients with active IBD. More importantly, NETs were induced in mice with DSS colitis, and inhibition of NET release attenuated colitis as well as colitis-associated tumorigenesis. NET degradation through DNase administration decreased cytokine levels during DSS-induced colitis. In addition, DNase treatment also significantly attenuated the accelerated thrombus formation and platelet activation observed in DSS-induced colitis. NETs triggered PS-positive microparticle release and PS exposure on platelets and endothelial cells partially through TLR2 and TLR4, converting them to a procoagulant phenotype. Conclusions NETs exacerbate colon tissue damage and drive thrombotic tendency during active IBD. Strategies directed against NET formation may offer a potential therapeutic approach for the treatment of IBD.

Because of the importance of bradykinin in improving heart function in some conditions or in enhancing glucose uptake by skeletal muscle, we investigated kininases in these tissues. In P3 fraction of the heart and skeletal muscles, angiotensin I-converting enzyme (ACE) and neutral endopeptidase 24.11 (NEP) are the major kininases, as determined first with specific substrates and second with bradykinin. ACE activity was highest in guinea pig heart (2.7 +/- 0.07 mumol.h-1.mg protein-1) but decreased in other species in this order: dog atrium, rat heart, dog ventricle, and human atrium. The specific activity of NEP was lower: 0.45 mumol.h-1.mg protein-1 in cultured neonatal cardiac myocytes and varying between 0.12 and 0.05 mumol.h-1.mg protein-1 in human, dog, rat, and guinea pig heart. In the skeletal muscle P3, ACE was most active in guinea pig and rat (1.2 and 1.1 mumol.h-1.mg protein-1, respectively) but less so in dog (0.09 mumol.h-1.mg protein-1). NEP activity was higher in dog P3 (0.28 mumol.h-1.mg protein-1) but lower in rat and guinea pig (0.19 and 0.1 mumol.h-1.mg protein-1, respectively). Continuous density gradient centrifugation enriched NEP activity in dog and rat (from 0.3 to 1.0 and 0.49 mumol.h-1.mg protein-1, respectively). Immunoprecipitation with antiserum to purified NEP proved the specificity of the rat enzyme. Bradykinin (0.1 mmol/l) was inactivated in the presence and absence of inhibitors by rat skeletal muscle NEP, as measured by high-performance liquid chromatography. Here, 36% of the activity was caused by NEP and 19% by ACE. In radioimmunoassay (bradykinin 10 nmol/l), 46 and 55% of kininase in rat and dog skeletal muscle P3, respectively, was due to ACE; 36 and 28%, respectively, was due to NEP. Aside from these enzymes, an aminopeptidase in rat P3 also inactivates bradykinin. Thus, in conclusion, heart and skeletal muscle membranes contain kininase II-type enzymes, but their activity depends on the species.

A novel conotoxin, -conotoxin (-BtX), has been purified and characterized from the venom of a wormhunting cone snail, Conus betulinus. The toxin, with four disulfide bonds, shares no sequence homology with any other conotoxins. Based on a partial amino acid sequence, its cDNA was cloned and sequenced. The deduced sequence consists of a 26-residue putative signal peptide, a 31-residue mature toxin, and a 13-residue extra peptide at the C terminus. The extra peptide is cleaved off by proteinase post-processing. All three Glu residues are ␥-carboxylated, one of the two Pro residues is hydroxylated at position 27, and its C-terminal residue is Pro-amidated. The monoisotopic mass of the toxin is 3569.0 Da. Electrophysiological experiments show that: 1) among voltage-gated channels, -BtX is a specific modulator of K ؉ channels; 2) among the K channels, -BtX specifically up-modulates the Ca 2؉ -and voltage-sensitive BK channels (252 ؎ 47%); 3) its EC 50 is 0.7 nM with a single binding site (Hill ‫؍‬ 0.88); 4) the time constant of wash-out is 8.3 s; and 5) -BtX has no effect on single channel conductance, but increases the open probability of BK channels. It is concluded that -BtX is a novel specific biotoxin against BK channels.

Current lung cancer diagnosis methods encounter delayed visual confirmation of tumor foci and low-resolution metrics in imaging findings, which delays the early treatment of tumors. Here, we developed a potent lung cancer imaging and treatment strategy centered around a nanotransformational concept of tumor iron mineralization in situ, which employs Prussian blue/calcium peroxide nanocomposites as a precursor. The resultant iron mineralization in tumor cells greatly facilitates the early and differential diagnosis of lung carcinoma from benign nodules via medical imaging, meanwhile introducing oxidative stress to activate the cellular apoptosis and ferroptosis pathways, resulting in inhibition of the malignant behavior of tumor cells. Tumor-microenvironment-triggered iron mineralization enables integration of the detection and prevention of tumor metastasis at its early stages with no assistance of toxic drugs, which offers a potential solution for the precise management of lung cancer with ideal outcomes.

Despite routine treatment of unselected acute promyelocytic leukemia (APL) with all--retinoic acid (ATRA), early death because of hemorrhage remains unacceptably common, and the mechanism underlying this complication remains elusive. We have recently demonstrated that APL cells undergo a novel cell death program, termed ETosis, which involves release of extracellular chromatin. However, the role of promyelocytic extracellular chromatin in APL-associated coagulation remains unclear. Our objectives were to identify the novel role of ATRA-promoted extracellular chromatin in inducing a hypercoagulable and hyperfibrinolytic state in APL and to evaluate its interaction with fibrin and endothelial cells (ECs). Results from a series of coagulation assays have shown that promyelocytic extracellular chromatin increases thrombin and plasmin generation, causes a shortening of plasma clotting time of APL cells, and increases fibrin formation. DNase I but not anti-tissue factor antibody could inhibit these effects. Immunofluorescence staining showed that promyelocytic extracellular chromatin and phosphatidylserine on APL cells provide platforms for fibrin deposition and render clots more resistant to fibrinolysis. Additionally, coincubation assays revealed that promyelocytic extracellular chromatin is cytotoxic to ECs, converting them to a procoagulant phenotype. This cytotoxity was blocked by DNase I by 20% or activated protein C by 31%. Our current results thus delineate the pathogenic role of promyelocytic extracellular chromatin in APL coagulopathy. Furthermore, the remaining coagulation disturbance in high-risk APL patients after ATRA administration may be treatable by intrinsic pathway inhibition via accelerating extracellular chromatin degradation.

In this paper, we first construct the H 2 (curl)-conforming finite elements both on a rectangle and a triangle. They possess some fascinating properties which have been proven by a rigorous theoretical analysis. Then we apply the elements to construct a finite element space for discretizing quad-curl problems. Convergence orders O(h k ) in the H(curl) norm and O(h k−1 ) in the H 2 (curl) norm are established. Numerical experiments are provided to confirm our theoretical results. 2000 Mathematics Subject Classification. 65N30 and 35Q60 and 65N15 and 35B45.