Liquid processing of interfacially grown iron-oxide flowers into 2D-platelets yields lithium-ion battery anodes with capacities of twice the theoretical value

Iron oxide (Fe2O3) is an abundant and potentially low-cost material for fabricating lithium-ion battery anodes. Here, the growth of α-Fe2O3 nano-flowers at an electrified liquid–liquid interface is demonstrated. Sonication is used to convert these flowers into quasi-2D platelets with lateral sizes in the range of hundreds of nanometers and thicknesses in the range of tens of nanometers. These nanoplatelets can be combined with carbon nanotubes to form porous, conductive composites which can be used as electrodes in lithium-ion batteries. Using a standard activation process, these anodes display good cycling stability, reasonable rate performance and low-rate capacities approaching 1500 mAh g−1, consistent with the current state-of-the-art for Fe2O3. However, by using an extended activation process, it is found that the morphology of these composites can be significantly changed, rendering the iron oxide amorphous and significantly increasing the porosity and internal surface area. These morphological changes yield anodes with very good cycling stability and low-rate capacity exceeding 2000 mAh g−1, which is competitive with the best anode materials in the literature. However, the data implies that, after activation, the iron oxide displays a reduced solid-state lithium-ion diffusion coefficient resulting in somewhat degraded rate performance.</p

Drastically Enhanced High-Rate Performance of Carbon-Coated LiFePO₄ Nanorods Using a Green Chemical Vapor Deposition (CVD) Method for Lithium Ion Battery: A Selective Carbon Coating Process

Application of LiFePO₄ (LFP) to large current power supplies is greatly hindered by its poor electrical conductivity (10^–9 S cm^–1) and sluggish Li⁺ transport. Carbon coating is considered to be necessary for improving its interparticle electronic conductivity and thus electrochemical performance. Here, we proposed a novel, green, low cost and controllable CVD approach using solid glucose as carbon source which can be extended to most cathode and anode materials in need of carbon coating. Hydrothermally synthesized LFP nanorods with optimized thickness of carbon coated by this recipe are shown to have superb high-rate performance, high energy, and power densities, as well as long high-rate cycle lifetime. For 200 C (18s) charge and discharge, the discharge capacity and voltage are 89.69 mAh g^–1 and 3.030 V, respectively, and the energy and power densities are 271.80 Wh kg^–1 and 54.36 kW kg^–1, respectively. The capacity retention of 93.0%, and the energy and power density retention of 93.6% after 500 cycles at 100 C were achieved. Compared to the conventional carbon coating through direct mixing with glucose (or other organic substances) followed by annealing (DMGA), the carbon phase coated using this CVD recipe is of higher quality and better uniformity. Undoubtedly, this approach enhances significantly the electrochemical performance of high power LFP and thus broadens greatly the prospect of its applications to large current power supplies such as electric and hybrid electric vehicles

Frequencies, Laboratory Features, and Granulocyte Activation in Chinese Patients with <i>CALR - Fig 1 </i>-Mutated Myeloproliferative Neoplasms

<p><b>(A) LAP scoring images of CALR and JAK2V617F mutant patients</b>. Peripheral blood smear of a representative CALR mutant patient displays a poor LAP expression (positive-cells:1%; score:1). In contrast, peripheral blood smear of a representative JAK2V617F mutant patient reveals a marked LAP expression (positive-cells:90%; score:194). Peripheral blood smear of a representative positive control (Puerperal) shows the highest intensity level of the stain (level: 3). <b>(B) Leukocyte alkaline phosphatase (LAP) scores in circulating granulocytes of peripheral blood from different categories of patients carrying <i>JAK2</i>V617F or <i>CALR</i> mutation</b>. LAP values are shown in a scatter plot; diamond indicates the median. (i) LAP score levels of 38 PV, 74 ET, and 24 PMF patients carrying <i>JAK2</i>V617F mutant alleles. LAP values of all patients are above normal (>80). The Kruskal–Wallis test showed significant differences between the three disorders (<i>P</i> < 0.001 for all comparisons). (ii) LAP score levels of 18 ET patients and 1 PMF patient carrying <i>CALR</i> mutant alleles. The entire data showed no significant differences between the ET and PMF groups. Both ET and PMF patients carrying the <i>CALR</i> mutation exhibited lower LAP scores than the normal value. (iii) LAP score levels of 74 ET patients with <i>JAK2</i>V617F mutant alleles and 18 ET patients carrying the <i>CALR</i> mutation. The Mann–Whitney U test showed significant differences between both groups (<i>P</i> < 0.001). (iv) LAP score levels of 24 PMF patients with <i>JAK2</i>V617F mutant alleles and 1 PMF patient carrying the <i>CALR</i> mutation. These data show that LAP score levels of PMF patients with <i>JAK2</i>V617F mutation are markedly higher than those with the <i>CALR</i> mutation.</p

Demographic and laboratory features at diagnosis of PMF patients with different types of <i>CALR</i> and <i>JAK2</i>V617F mutations.

<p>WBC: white blood cell; Hb: hemoglobin; PLT: platelet; “—” indicates no analysis performed.</p><p>Demographic and laboratory features at diagnosis of PMF patients with different types of <i>CALR</i> and <i>JAK2</i>V617F mutations.</p

Demographic and laboratory features at diagnosis of ET and PMF patients with <i>CALR</i> and <i>JAK2</i>V617F mutations.

<p>WBC: white blood cell; Hb: hemoglobin; PLT: platelet.</p><p>Demographic and laboratory features at diagnosis of ET and PMF patients with <i>CALR</i> and <i>JAK2</i>V617F mutations.</p

Demographic and laboratory features at diagnosis of ET patients with different types of <i>CALR</i> and <i>JAK2</i>V617F mutations.

<p>WBC: white blood cell; Hb: hemoglobin; PLT: platelet.</p><p>Demographic and laboratory features at diagnosis of ET patients with different types of <i>CALR</i> and <i>JAK2</i>V617F mutations.</p