Yoon-Soo Park

Effects of LiPON Thin-Film Coating on Thermal Behavior of Delithiated Li1 − x ( Ni0.53Co0.2Mn0.27 ) O2 Cathode

A lithium phosphorus oxynitride (LiPON) thin film, which is a solid ionic conductor, was deposited on a Li(Ni 0.53 Co 0.2 Mn 0.27 )O 2 electrode to improve the thermal stability of the delithiated cathode. The LiPON thin films were deposited by radio-frequency magnetron sputtering. The thermal stability of electrochemically delithiated Li 1-x (Ni 0.53 Co 0.2 Mn 0.27 )O 2 cathodes with electrolyte was investigated by differential scanning calorimetry (DSC), in which the cathode was charged to different upper cutoff voltages of 4.3, 4.5, and 4.7 V (vs Li/Li + ). The LiPON-coated Li(Ni 0.53 Co 0.2 Mn 0.27 )O 2 cathodes exhibited an enhanced cycle performance for a high upper cutoff voltage, i.e., 4.7 V. However, the LiPON film appears to be thermally unstable as compared to the delithiated Li 1-x (Ni 0.53 Co 0.2 Mn 0.27 )O 2 pristine electrodes, especially when charged to a higher upper cutoff voltage. As a result, the LiPON-coated electrodes exhibited a lower onset temperature and peak position of the exothermic peak in DSC scans than the pristine electrodes.

The relationship between low survival and acute increase of tumor necrosis factor α expression in the lung in a rat model of asphyxial cardiac arrest

Cardiac arrest (CA) is sudden loss of heart function and abrupt stop in effective blood flow to the body. The patients who initially achieve return of spontaneous circulation (RoSC) after CA have low survival rate. It has been known that multiorgan dysfunctions after RoSC are associated with high morbidity and mortality. Most previous studies have focused on the heart and brain in RoSC after CA. Therefore, the aim of this research was to perform serological, physiological, and histopathology study in the lung and to determine whether or how pulmonary dysfunction is associated with low survival rate after CA. Experimental animals were divided into sham-operated group (n=14 at each point in time), which was not subjected to CA operation, and CA-operated group (n=14 at each point in time), which was subjected to CA. The rats in each group were sacrificed at 6 hours, 12 hours, 24 hours, and 2 days, respectively, after RoSC. Then, pathological changes of the lungs were analyzed by hematoxylin and eosin staining, Western blot and immunohistochemistry for tumor necrosis factor α (TNF-α). The survival rate after CA was decreased with time past. We found that histopathological score and TNF-α immunoreactivity were significantly increased in the lung after CA. These results indicate that inflammation triggered by ischemia-reperfusion damage after CA leads to pulmonary injury/dysfunctions and contributes to low survival rate. In addition, the finding of increase in TNF-α via inflammation in the lung after CA would be able to utilize therapeutic or diagnostic measures in the future.