Search

X-ray photoemission electron microscopy (XPEEM), with its excellent spatial resolution, is a well-suited technique for elucidating the complex electrode-electrolyte interface reactions in Li-ion batteries. It provides element-specific contrast images that allows the study of the surface morphology and the identification of the various components of the composite electrode. It also enables the acquisition of local X-ray absorption spectra (XAS) on single particles of the electrode, such as the C and O K-edges to track the stability of carbonate-based electrolytes, F K-edge to study the electrolyte salt and binder stability, and the transition metal L-edges to gain insights into the oxidation/reduction processes of positive and negative active materials. Here we discuss the optimal measurement conditions for XPEEM studies of Li-ion battery systems, including (i) electrode preparation through mechanical pressing to reduce surface roughness for improved spatial resolution; (ii) corrections of the XAS spectra at the C K-edge to remove the carbon signal contribution originating from the X-ray optics; and (iii) procedures for minimizing the effect of beam damage. Examples from our recent work are provided to demonstrate the strength of XPEEM to solve challenging interface reaction mechanisms via post mortem measurements. Finally, we present a first XPEEM cell dedicated to operando/in situ experiments in all-solid-state batteries. Representative measurements were carried out on a graphite electrode cycled with LiI-incorporated sulfide-based electrolyte. This measurement demonstrates the strong competitive reactions between the lithiated graphite surface and the Li 2 O formation caused by the reaction of the intercalated lithium with the residual oxygen in the vacuum chamber. Moreover, we show the versatility of the operando XPEEM cell to investigate other active materials, for example, Li 4 Ti 5 O 12 .

The understanding of surface reactions at the electrode-electrolyte interfaces has been a longstanding challenge in Li-ion batteries. X-ray photoemission electron microscopy is used to throw light on the disputed aspects of the surface reactivity of high-energy Li-rich Li 1+ x (Ni a Co b Mn 1- a-b ) 1- x O 2 (HE-NCM) cycled in an aprotic electrolyte against Li 4 Ti 5 O 12 (LTO). Despite the highly oxidative potential of 5.1 V vs Li + /Li, there is no formation of a layer of oxidized electrolyte byproducts on any of the cathode particles; instead, a homogeneous organic-inorganic layer builds up across the particles of the LTO anode due to the electrolyte and poly(vinylidene fluoride) binder decomposition on HE-NCM. In addition, such a layer incorporates, already from the first charge, micrometer-sized agglomerates of transition metals (TMs). The presence of TMs on the anode is explained by the instability of the reduced Mn, Co, and Ni formed at the surface of HE-NCM mainly during delithiation. The reduced TMs are unstable and prone to be transported to the LTO, where they get further reduced to metallic-like clusters. These results demonstrate that a dual reaction takes place at the HE-NCM-electrolyte interface if subject to high potential, namely, degradation of the surface structure and decomposition of the electrolyte, affecting directly the anode surface through the migration-diffusion processes.

The hemodynamic effect of L-propionylcarnitine (LPC) administered intravenously was evaluated in a double-blind, randomized, three-period crossover study in 12 men (aged sixty to seventy-five years) with Leriche-Fontaine stage II peripheral arterial disease of lower limbs. At baseline, maximum working capacity of each patient was determined by a standardized ergometric test. This test was repeated at 80% of each patient's maximum working capacity before and after intravenous administration of LPC. Each patient received three single doses of 300 mg, 600 mg, and 1200 mg of LPC with a two-day rest period between them. Hemodynamic variables measured by strain-gauge plethysmography were: peak blood flow, peak flow time, and halftime and total time of hyperemia both after exercise and after induction of ischemia (with an occlusion cuff). LPC administration significantly shortened the halftime as well as the total time of hyperemia after exercise and after ischemia. With the two highest doses, LPC shortened the peak flow time after exercise. The peak blood flow after exercise and after ischemia increased, but this increase did not reach statistical significance. The results obtained indicate that LPC improves circulatory reserve of the ischemic limb and has no effect on heart rate and arterial blood pressure. No adverse events were reported. The effect of LPC on the hyperemic response to stress, mainly on halftime of hyperemia, is possibly due to a drug-induced increase of adenosine triphosphate utilization by the ischemic tissues.

In a random double-blind study versus placebo, 60 ambulatory patients with peripheral occlusive disease of the lower limbs and claudicatio intermittens (Leriche's stage 2), were treated for 60 days with defibrotide (400 mg b.i.d., oral, n = 30) or placebo (n = 30). Patients in the defibrotide group received additional treatment with the same drug at the reduced rate of 400 mg once daily for another 120 days for maintenance (total treatment duration 180 days). All patients were assessed at intake and 60 days for relative and absolute walking distance (RWD and AWD) in a standard treadmill test and for the Winsor Index (WI) at rest and after exercise; patients of the defibrotide treatment group were retested in the same way at 90-180 days. In a subgroup of patients (defibrotide = 11, placebo = 12), blood samples were obtained for the assessment of whole blood and plasma viscosity at intake and after 60 days of treatment. These samples could not be collected properly in the remaining cases, for technical reasons. At day 60, we compared the effects of the two treatments on physical performance: mean (SE) values of RWD were for defibrotide 148 (9.7) and 179 (12.4) m in basal and post-treatment conditions, respectively, and 209 (16.2) and 212 (17.1) m for placebo. Similar changes were observed for AWD: for defibrotide 206 (13.4) and 241 (15.2) m and for placebo 270 (22.9) and 272 (23.1) m. The mean changes were significantly larger with defibrotide: for RWD + 33 (7.1) vs. + 0.3 (3.8) m (p < 0.01) and for AWD + 34 (9.2) and -2 (6.6) m (p < 0.01). The overall gain of walking distance after maintenance therapy with the reduced defibrotide dosage amounted to approximately + 50% over basal (after 180 days). Blood and plasma viscosity improved in patients on defibrotide but the change fell short of statistical significance versus placebo. All findings confirm the potential usefulness of defibrotide in the treatment of peripheral arterial disease, at the same time encouraging further studies of the involved mechanisms of action.