Quantifying Degradation Parameters of Single-Crystalline Ni-Rich Cathodes in Lithium-Ion Batteries.

Single-crystal LiNix Coy Mnz O2 (SC-NCM, x+y+z=1) cathodes are renowned for their high structural stability and reduced accumulation of adverse side products during long-term cycling. While advances have been made using SC-NCM cathode materials, careful studies of cathode degradation mechanisms are scarce. Herein, we employed quasi single-crystalline LiNi0.65 Co0.15 Mn0.20 O2 (SC-NCM65) to test the relationship between cycling performance and material degradation for different charge cutoff potentials. The Li/SC-NCM65 cells showed >77 % capacity retention below 4.6 V vs. Li+ /Li after 400 cycles and revealed a significant decay to 56 % for 4.7 V cutoff. We demonstrate that the SC-NCM65 degradation is due to accumulation of rock-salt (NiO) species at the particle surface rather than intragranular cracking or side reactions with the electrolyte. The NiO-type layer formation is also responsible for the strongly increased impedance and transition-metal dissolution. Notably, the capacity loss is found to have a linear relationship with the thickness of the rock-salt surface layer. Density functional theory and COMSOL Multiphysics modeling analysis further indicate that the charge-transfer kinetics is decisive, as the lower lithium diffusivity of the NiO phase hinders charge transport from the surface to the bulk.

Engineering Na+-layer spacings to stabilize Mn-based layered cathodes for sodium-ion batteries.

Layered transition metal oxides are the most important cathode materials for Li/Na/K ion batteries. Suppressing undesirable phase transformations during charge-discharge processes is a critical and fundamental challenge towards the rational design of high-performance layered oxide cathodes. Here we report a shale-like NaxMnO2 (S-NMO) electrode that is derived from a simple but effective water-mediated strategy. This strategy expands the Na+ layer spacings of P2-type Na0.67MnO2 and transforms the particles into accordion-like morphology. Therefore, the S-NMO electrode exhibits improved Na+ mobility and near-zero-strain property during charge-discharge processes, which leads to outstanding rate capability (100 mAh g-1 at the operation time of 6 min) and cycling stability (>3000 cycles). In addition, the water-mediated strategy is feasible to other layered sodium oxides and the obtained S-NMO electrode has an excellent tolerance to humidity. This work demonstrates that engineering the spacings of alkali-metal layer is an effective strategy to stabilize the structure of layered transition metal oxides.

The stability of P2-layered sodium transition metal oxides in ambient atmospheres.

Air-stability is one of the most important considerations for the practical application of electrode materials in energy-harvesting/storage devices, ranging from solar cells to rechargeable batteries. The promising P2-layered sodium transition metal oxides (P2-NaxTmO2) often suffer from structural/chemical transformations when contacted with moist air. However, these elaborate transitions and the evaluation rules towards air-stable P2-NaxTmO2 have not yet been clearly elucidated. Herein, taking P2-Na0.67MnO2 and P2-Na0.67Ni0.33Mn0.67O2 as key examples, we unveil the comprehensive structural/chemical degradation mechanisms of P2-NaxTmO2 in different ambient atmospheres by using various microscopic/spectroscopic characterizations and first-principle calculations. The extent of bulk structural/chemical transformation of P2-NaxTmO2 is determined by the amount of extracted Na+, which is mainly compensated by Na+/H+ exchange. By expanding our study to a series of Mn-based oxides, we reveal that the air-stability of P2-NaxTmO2 is highly related to their oxidation features in the first charge process and further propose a practical evaluating rule associated with redox couples for air-stable NaxTmO2 cathodes.

High-Efficiency Lithium Metal Anode Enabled by a Concentrated/Fluorinated Ester Electrolyte.

Lithium (Li) metal anode (LMA) has received growing attention due to its highest theoretical capacity (3860 mA h g-1) and lowest redox potential (-3.04 V versus standard hydrogen electrode). However, practical application of LMA is obstructed by the detrimental side reactions between Li metal and organic electrolytes, especially when cycled in traditional carbonate ester electrolytes. Herein, we propose a novel fluorinated carbonate ester-based electrolyte by combining diethyl fluorocarbonate (ETFEC) solvent and 5 M LiFSI concentration (M = mol L-1). Using this electrolyte, an ultrahigh Li plating/stripping Coulombic efficiency (CE) of 99.1% can be obtained in Li||Cu cells and a stable cycle performance of Li||LiFePO4 is achieved under the conditions of limited Li metal (5 mA h cm-2), moderate loading LiFePO4 (7-8 mg cm-2), and lean electrolyte (40 uL). The fundamental functioning mechanism of this novel electrolyte has been carefully investigated by scanning electronic microscopy (SEM), operando optical microscopy (OM), electrochemical impedance spectroscopy (EIS), X-ray photoelectron spectroscopy (XPS), and solid state nuclear magnetic resonance (SS-NMR). The results demonstrate that this optimized electrolyte facilitates formation of a high Li+ conductive SEI layer enriched with LiF and inorganic sulfur-containing species, which can effectively suppress the side reactions between electrolyte and Li metal and prevent formation of dead Li.

Mycobacterium tuberculosis blocks crosslinking of annexin-1 and apoptotic envelope formation on infected macrophages to maintain virulence.

Macrophages infected with attenuated Mycobacterium tuberculosis strain H37Ra become apoptotic, which limits bacterial replication and facilitates antigen presentation. Here we demonstrate that cells infected with H37Ra became apoptotic after the formation of an apoptotic envelope on their surface was complete. This process required exposure of phosphatidylserine on the cell surface, followed by deposition of the phospholipid-binding protein annexin-1 and then transglutaminase-mediated crosslinking of annexin-1 through its amino-terminal domain. In macrophages infected with the virulent strain H37Rv, in contrast, the amino-terminal domain of annexin-1 was removed by proteolysis, thus preventing completion of the apoptotic envelope, which resulted in macrophage death by necrosis. Virulent M. tuberculosis therefore avoids the host defense system by blocking formation of the apoptotic envelope, which leads to macrophage necrosis and dissemination of infection in the lung.

Hypercholesterolemia impairs immunity to tuberculosis.

We demonstrate that apolipoprotein E -deficient (ApoE(-/-)) mice are highly susceptible to tuberculosis and that their susceptibility depends on the severity of hypercholesterolemia. Wild-type (WT) mice and ApoE(-/-) mice fed a low-cholesterol (LC) or high-cholesterol (HC) diet were infected with approximately 50 CFU Mycobacterium tuberculosis Erdman by aerosol. ApoE(-/-) LC mice were modestly more susceptible to tuberculosis than WT LC mice. In contrast, ApoE(-/-) HC mice were extremely susceptible, as evidenced by 100% mortality after 4 weeks with tuberculosis. The lung pathology of ApoE(-/-) HC mice was remarkable for giant abscess-like lesions, massive infiltration by granulocytes, elevated inflammatory cytokine production, and a mean bacterial load approximately 2 log units higher than that of WT HC mice. Compared to WT HC mice, the gamma interferon response of splenocytes restimulated ex vivo with M. tuberculosis culture filtrate protein was delayed in ApoE(-/-) HC mice, and they failed to control M. tuberculosis growth in the lung. OT-II cells adoptively transferred into uninfected ApoE(-/-) HC mice had a weak proliferative response to their antigen, indicating impaired priming of the adaptive immune response. Our studies show that ApoE(-/-) deficiency is associated with delayed expression of adaptive immunity to tuberculosis caused by defective priming of the adaptive immune response and that elevated serum cholesterol is responsible for this effect.

Tuberculosis susceptibility of diabetic mice.

Increased susceptibility to infections, including tuberculosis (TB), is a major cause of morbidity and mortality in patients with diabetes. Despite the clinical importance of this problem, little is known about how diabetes impairs protective immunity. We modeled this phenomenon by infecting acute (< or = 1 mo) or chronic (> or = 3 mo) diabetic mice with a low aerosol dose of Mycobacterium tuberculosis (Mtb) Erdman. Diabetes was induced by streptozotocin (STZ) treatment of C57BL/6 mice, while another mouse strain and diabetes model were used to confirm key observations. Lungs from acute diabetic and euglycemic mice had similar bacterial burdens, cytokine expression profiles, and histopathology. In contrast, chronic diabetic mice had > 1 log higher bacterial burden and more inflammation in the lung compared with euglycemic mice. The expression of adaptive immunity was delayed in chronic diabetic mice, shown by reduced early production of IFN-gamma in the lung and by the presence of fewer Mtb antigen (ESAT-6)-responsive T cells compared with euglycemic mice within the first month of infection. However, after 2 months of TB disease proinflammatory cytokines levels were higher in chronic diabetic than euglycemic mice. Here we show that Mtb infection of STZ-treated mice provides a useful model to study the effects of hyperglycemia on immunity. Our data indicate that the initiation of adaptive immunity is impaired by chronic hyperglycemia, resulting in a higher steady-state burden of Mtb in the lung.

Interleukin-16 inhibits interleukin-13 production by allergen-stimulated blood mononuclear cells.

Expression of interleukin (IL)-16 is increased in bronchial mucosal biopsies of atopic asthmatics compared to normal controls. The functional significance of increased expression of IL-16 at sites of allergic inflammation is not yet clear. We have previously shown that IL-16 inhibits IL-5 secretion by allergen-stimulated peripheral blood mononuclear cells (PBMC). We investigated whether IL-16 inhibits the production of other T helper 2 cytokines, namely IL-13 and IL-4, by allergen-specific T cells. PBMC from ragweed-sensitive atopic subjects were stimulated with allergen extract for cytokine production in the presence or absence of rhIL-16. Production of cytokines was assessed by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction. To evaluate whether the modulatory effect of IL-16 on cytokine synthesis was mediated by interferon-gamma (IFN-gamma), IL-10, IL-12 or IL-18, allergen-stimulated PBMC were cultured in presence of IL-16 and neutralizing concentrations of relevant antibodies. Allergen-stimulated PBMC produced significantly elevated levels of IL-13 (90-740 pg/ml) as compared to unstimulated PBMC (0-375 pg/ml, P < 0.01). Addition of rhIL-16 resulted in down-regulation of IL-13 mRNA expression as well as significantly reduced amounts of IL-13 released by allergen-stimulated PBMC (0-457 pg/ml, P < 0.001), as observed for IL-5. No effect of IL-16 was observed on IL-4 mRNA expression. Treatment with IL-16 resulted in increased levels of IL-10 and IL-18 in allergen-stimulated cell culture. Neutralization of IFN-gamma, IL-12, IL-10 or IL-18 did not alter the inhibitory effects of IL-16 on IL-13 and IL-5 secretion by allergen-stimulated PBMC. IL-16 did not modify IL-13 synthesis by anti-CD3-stimulated CD4(+) T cells, but it significantly reduced the production of IL-5. These data suggest that IL-16 may play an important immunoregulatory role in allergic states in response to allergen.

Regulation of nuclear Prointerleukin-16 and p27(Kip1) in primary human T lymphocytes.

Prointerleukin-16 (Pro-IL-16) is an abundant, PDZ domain-containing protein expressed in the nucleus and cytoplasm of resting human T lymphocytes. We have previously shown that ectopic expression of Pro-IL-16 in Pro-IL-16-negative human Jurkat cells represses transcription of the F-box protein, Skp2, resulting in accumulation of the cyclin-dependent kinase inhibitor, p27(Kip1), and G0/G1 cell cycle arrest. The current studies demonstrate the kinetics of Pro-IL-16 and p27(Kip1) expression in activated normal human T lymphocytes. We correlate nuclear Pro-IL-16 loss with decreased p27(Kip1) expression, increased cell cycle progression, and proliferation. Conversely, we show that constitutive expression of Pro-IL-16 by retroviral infection of activated human T lymphocytes induces G0/G1 cell cycle arrest, inhibits proliferation, and is associated with increased levels of p27(Kip1). These findings implicate nuclear Pro-IL-16 as a cell cycle regulatory protein for human T lymphocytes.

Pro-IL-16 regulation in activated murine CD4+ lymphocytes.

Prior DNA microarray studies suggested that IL-16 mRNA levels decrease following T cell activation, a property unique among cytokines. We examined pro-IL-16 mRNA and protein expression in resting and anti-CD3 mAb-activated primary murine CD4(+) T cells. Consistent with the microarray reports, pro-IL-16 mRNA levels fell within 4 h of activation, and this response is inhibited by cyclosporin A. Total cellular pro-IL-16 protein also fell, reaching a nadir at 48 h. Pro-IL-16 comprises a C-terminal cytokine domain and an N-terminal prodomain that are cleaved by caspase-3. Pro-IL-16 expressed in transfected tumor cells was previously shown to translocate to the nucleus and to promote G(0)/G(1) arrest by stabilizing the cyclin-dependent kinase inhibitor p27(Kip1). In the present study, we observed increased S-phase kinase-associated protein 2 mRNA expression in IL-16 null mice, but basal expression and activation-dependent regulation of p27(Kip1) were no different from wild-type mice. Stimulation with anti-CD3 mAb induced transiently greater thymidine incorporation in IL-16-deficient CD4(+) T cells than wild-type controls, but there was no difference in cell survival or in the CFSE dilution profiles. Analysis of CD4(+) T cell proliferation in vivo using BrdU labeling similarly failed to identify a hyperproliferative phenotype in T cells lacking IL-16. These data demonstrate that pro-IL-16 mRNA and protein expression are dynamically regulated during CD4(+) T cell activation by a calcineurin-dependent mechanism, and that pro-IL-16 might influence T cell cycle regulation, although not in a dominant manner.