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We present a wide range of testing results on an excellent moderate-energy-density lithium-ion pouch cell chemistry to serve as benchmarks for academics and companies developing advanced lithium-ion and other "beyond lithium-ion" cell chemistries to (hopefully) exceed. These results are far superior to those that have been used by researchers modelling cell failure mechanisms and as such, these results are more representative of modern Li-ion cells and should be adopted by modellers. Up to three years of testing has been completed for some of the tests. Tests include long-term charge-discharge cycling at 20, 40 and 55°C, long-term storage at 20, 40 and 55°C, and high precision coulometry at 40°C. Several different electrolytes are considered in this LiNi 0.5 Mn 0.3 Co 0.2 O 2 /graphite chemistry, including those that can promote fast charging. The reasons for cell performance degradation and impedance growth are examined using several methods. We conclude that cells of this type should be able to power an electric vehicle for over 1.6 million kilometers (1 million miles) and last at least two decades in grid energy storage. The authors acknowledge that other cell format-dependent loss, if any, (e.g. cylindrical vs. pouch) may not be captured in these experiments.

Single-crystal LiNi 0.5 Mn 0.3 Co 0.2 O 2 (NMC532) with a grain size of 2-3 μm was compared to conventional polycrystalline uncoated NMC532 and polycrystalline Al 2 O 3 -coated materials in this work. Studies were made to determine how single crystal NMC532 material with large grain size could be synthesized. Ultra high precision coulometry (UHPC), in-situ gas measurements and isothermal microcalorimetry were used to make comparative studies of the three materials in Li-ion pouch cells. All the diagnostic measurements suggested that the single crystal material should yield Li-ion cells with longer lifetime. Long-term cycling tests verified these predictions and showed that cells with single crystal NMC532 exhibited much better capacity retention than cells with the polycrystalline materials at both 40 • C and 55 • C when tested to an upper cutoff potential of 4.4 V. The reasons for the superior performance of the single crystal cells were explored using thermogravimetric analysis/mass spectrometry experiments on the charged electrode materials. The single crystal materials were extremely resistant to oxygen loss below 100 • C compared to the polycrystalline materials. The major drawback of the single crystal material is its slightly lower specific capacity compared to the polycrystalline materials. However, this may not be an issue for Li-ion cells designed for long lifetime applications. Lithium ion batteries with high energy density, long lifetime and low cost need to be developed for applications in electric vehicles and stationary energy storage. The family of Li(Ni x Mn y Co z )O 2 (x + y + z = 1) (NMC) materials with high nickel and low cobalt are used as positive electrode materials in lithium ion cells.1,2 One simple way to increase the energy density of NMC lithium ion cells is to increase their upper cutoff voltage which gives access to higher specific capacity from the positive electrode.3,4 However, increasing the upper cutoff voltage usually decreases the lifetime of cells due to an acceleration of 'unwanted' parasitic reactions between the electrolyte and the delithiated positive electrode surface at high voltages. Such reactions include oxidation of species found in the electrolyte, transition metal dissolution, etc. [5][6][7] In addition, structural reconstruction of the positive electrode surface can occur which can contribute to impedance growth and capacity loss. 3,4 The by-products of oxidation at the positive electrode can migrate to the negative electrode surface and be reduced there. 8,9 Such reactions can lead to the consumption of lithium ions from the electrolyte, (to maintain charge neutrality in the electrolyte), a reduction in lithium inventory, as well as a thickening of the negative electrode solid electrolyte interface (SEI) which together ultimately cause cell-failure.10,11 These processes are accelerated by higher charging potentials and higher temperatures.Methods such as modification of the positive electrode surface with coatings or dopants 12,13 and/or modification of electr...

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Severe spinal cord injuries above mid-thoracic levels can lead to a potentially life-threatening hypertensive condition termed autonomic dysreflexia, which is often triggered by painful distension of pelvic viscera (bladder or bowel) and consequent sensory fiber activation, including nociceptive C-fibers. Interruption of tonically active medullo-spinal pathways after injury causes disinhibition of thoracolumbar sympathetic preganglionic neurons, and intraspinal sprouting of nerve growth factor (NGF)-responsive primary afferent fibers is thought to contribute to their hyperactivity. We investigated spinal levels that are critical for eliciting autonomic dysreflexia using a model of noxious colorectal distension (CRD) after complete spinal transection at the fourth thoracic segment in rats. Post-traumatic sprouting of calcitonin gene-related peptide (CGRP)-immunoreactive primary afferent fibers was selectively altered at specific spinal levels caudal to the injury with bilateral microinjections of adenovirus encoding the growth-promoting NGF or growth-inhibitory semaphorin 3A (Sema3a) compared with control green fluorescent protein (GFP). Two weeks later, cardio-physiological responses to CRD were assessed among treatment groups before histological analysis of afferent fiber density at the injection sites. Dysreflexic hypertension was significantly higher with NGF overexpression in lumbosacral segments compared with GFP, whereas similar overexpression of Sema3a significantly reduced noxious CRD-evoked hypertension. Quantitative analysis of CGRP immunostaining in the spinal dorsal horns showed a significant correlation between the extent of fiber sprouting into the spinal segments injected and the severity of autonomic dysreflexia. These results demonstrate that site-directed genetic manipulation of axon guidance molecules after complete spinal cord injury can alter endogenous circuitry to modulate plasticity-induced autonomic pathophysiology.

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