A high-performance Si/carbon/graphite composite in which Si nanoparticles are attached onto the surface of natural graphite by carbonization of coal-tar pitch is proposed for use in lithium-ion batteries. This multicomponent structure is favorable for improving Li(+) storage capability because the amorphous carbon layer encapsulating Si nanoparticles offers sufficient electric conductivity and strong elasticity to facilitate relaxation of strain caused by electrochemical reaction of Si during cycles. The Si/carbon/graphite composite exhibits a specific capacity of 712 mAh g(-1) at a constant current density of 130 mA g(-1), and maintains more than 80% of its initial capacity after 100 cycles. Moreover, it shows a high capacity retention of approximately 88% even at a high current density of 5 C (3250 mA g(-1)). On the basis of electrochemical and structural analyses, we suggest that a rational design of the Si/carbon/graphite composite is mainly responsible for delivering a high reversible capacity and stable cycle performance. Furthermore, the proposed synthetic route for the Si/carbon/graphite composite is simple and cost-effective for mass production.

Rationale: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation, alveolar destruction, and airway and vascular remodeling. However, the mechanisms that lead to these diverse alterations have not been defined. Objectives: We hypothesized that IL-18 plays a central role in the pathogenesis of these lesions. Methods: We generated and characterized lung-specific, inducible IL-18 transgenic mice. Measurements and Main Results: Here we demonstrate that the expression of IL-18 in the mature murine lung induces inflammation that is associated with the accumulation of CD4 1 , CD8 1 , CD19 1 , and NK1.1 1 cells; emphysema; mucus metaplasia; airway fibrosis; vascular remodeling; and right ventricle cardiac hypertrophy. We also demonstrate that IL-18 induces type 1, type 2, and type 17 cytokines with IFN-g-inhibiting macrophage, lymphocyte, and eosinophil accumulation while stimulating alveolar destruction and genes associated with cell cytotoxicity and IL-13 and IL-17A inducing mucus metaplasia, airway fibrosis, and vascular remodeling. We also highlight interactions between these responses with IL-18 inducing IL-13 via an IL-17A-dependent mechanism and the type 1 and type17/ type 2 responses counterregulating each another. Conclusions: These studies define the spectrum of inflammatory, parenchymal, airway, and vascular alterations that are induced by pulmonary IL-18; highlight the similarities between these responses and the lesions in COPD; and define the selective roles that type 1, type 2, and type 17 responses play in the generation of IL-18-induced pathologies.Keywords: IL-18; chronic obstructive pulmonary disease; airway fibrosis; mucus metaplasia; vascular remodeling Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis (1, 2). It is a major unmet medical need in the United States and worldwide where it is the fourth and fifth leading cause of morbidity and mortality, respectively (3, 4). This is caused partly by our limited ability to treat people with COPD and a distinct lack of disease-modifying therapies (4, 5). Tissues from patients with COPD are characterized pathologically by chronic inflammation and varying degrees of emphysematous alveolar destruction, airway remodeling with tissue fibrosis and mucus metaplasia (6, 7), vascular remodeling with intimal hyperplasia, smooth muscle proliferation, and collagen deposition (8, 9). Importantly, a mechanistic construct that adequately accounts for the simultaneous existence of these varied tissue pathologic responses has not been put forth and animal models that simultaneously elicit these varied responses have not been commonly used. In particular, a mechanism that allows tissue destruction (emphysema) to coexist millimeters away from airway and vascular fibrotic responses has not been described (7).Inflammation with infiltrating macrophages, neutrophils, lymphocytes, and occasionally eosinophils is seen throughout the bronchial tree and parenchyma of lung...

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RuO2 nanorods on electrospun carbon nanofibers were simply grown by precipitation and recrystallization methods for studying their capacitive behaviors for supercapacitor applications. Recrystallization by heat treatment is carefully performed at various temperatures: 180, 220, and 300 °C. Under optimal growth conditions, application of RuO2-carbon nanofibers annealed at 220 °C with a very low loading concentration of Ru as the electrode material in a KOH aqueous electrolyte leads to a good capacitance capability of 188 F g–1 at a current density of 1 mA cm–2 and a high energy density of 22–15 W h kg–1 in the power density range of 400–4000 W kg–1 for supercapacitor applications. The capacitance of RuO2-carbon nanofibers after 3000 cycles also maintains approximately 93% of its initial value at a discharge current density of 1 mA cm–2. The excellent electrochemical performance of RuO2-carbon nanofibers is mainly attributed to their large surface area with many mesopores as well as their electroactive functional sites, which have the appropriate degree of crystallinity. Therefore, a larger mesopore volume and low-dimensional RuO2 nanorods on carbon nanofibers are beneficial for low internal resistance, leading to ion charge diffusion and charge storage in the bulk of amorphous material.