Presentation1.PDF

<p>Leptin is an adipose-derived hormone that plays an important role in the regulation of breathing. It has been demonstrated that obesity-related hypoventilation or apnea is closely associated with leptin signaling pathways. Perturbations of leptin signaling probably contribute to the reduced sensitivity of respiratory chemoreceptors to hypoxia/hypercapnia. However, the underlying mechanism remains incompletely understood. The present study is to test the hypothesis that leptin signaling contributes to modulating a hypoxic ventilatory response. The respiratory function was assessed in conscious obese Zucker rats or lean littermates treated with an injection of leptin. During exposure to hypoxia, the change in minute ventilation was lower in obese Zucker rats than chow-fed lean littermates or high fat diet-fed littermates. Such a change was abolished in all groups after carotid body denervation. In addition, the expression of phosphorylated signal transducers and activators of transcription 3 (pSTAT3), as well as putative O₂-sensitive K⁺ channels including TASK-1, TASK-3 and TASK-2 in the carotid body, was significantly reduced in obese Zucker rats compared with the other two phenotype littermates. Chronic administration of leptin in chow-fed lean Zucker rats failed to alter basal ventilation but vigorously increased tidal volume, respiratory frequency, and therefore minute volume during exposure to hypoxia. Likewise, carotid body denervation abolished such an effect. In addition, systemic leptin elicited enhanced expression of pSTAT3 and TASK channels. In conclusion, these data demonstrate that leptin signaling facilitates hypoxic ventilatory responses probably through upregulation of pSTAT3 and TASK channels in the carotid body. These findings may help to better understand the pathogenic mechanism of obesity-related hypoventilation or apnea.</p

Structural Transformation in a Sulfurized Polymer Cathode to Enable Long-Life Rechargeable Lithium–Sulfur Batteries

Sulfurized polyacrylonitrile (SPAN) represents a class of sulfur-bonded polymers, which have shown thousands of stable cycles as a cathode in lithium–sulfur batteries. However, the exact molecular structure and its electrochemical reaction mechanism remain unclear. Most significantly, SPAN shows an over 25% 1st cycle irreversible capacity loss before exhibiting perfect reversibility for subsequent cycles. Here, with a SPAN thin-film platform and an array of analytical tools, we show that the SPAN capacity loss is associated with intramolecular dehydrogenation along with the loss of sulfur. This results in an increase in the aromaticity of the structure, which is corroborated by a >100× increase in electronic conductivity. We also discovered that the conductive carbon additive in the cathode is instrumental in driving the reaction to completion. Based on the proposed mechanism, we have developed a synthesis procedure to eliminate more than 50% of the irreversible capacity loss. Our insights into the reaction mechanism provide a blueprint for the design of high-performance sulfurized polymer cathode materials