A-LLTO Nanoparticles Embedded Composite Solid Polymer Electrolyte for Room Temperature Operational Li-metal Batteries.

Solid-state batteries (SSBs) have the potential to revolutionize the current energy storage sector. A significant portion of the current development of electric vehicles and the electrification of various appliances relies on Lithium (Li)-ion batteries. However, future energy demands will require the development of stronger and more reliable batteries. This report presents a novel solid state electrolyte (SSE) composed of a self-healing composite solid polymer electrolyte (CSPE) matrix and aluminum-doped (Li0.33La0.56)1.005Ti0.99Al0.01O3 (A-LLTO) nanofillers. The CSPE contains Jeffamine ED-2003 monomer, Benzene-1,3,5-tricarbaldehyde (BTC) crosslinker dissolved in a 1:1 ratio of Dimethylformamide (DMF) to LiPF6, and a certain amount (x) of A-LLTO nanofillers (x = 5, 7.5, 10, 12.5%). A CSPE containing x-amount of A-LLTO fillers (referred to as CAL-x%) demonstrates excellent ion-conducting properties and stable battery performance. The CAL-10% demonstrates 1.1 × 10-3 S cm-1 of ionic conductivity at room temperature (RT). A-LLTO nanofillers dispersed uniformly within the polymer matrix form a percolation network, which is believed to improve ionic conductivity and the diffusion of Li+ ions. The CR-2032 cell, consisting of LiFePO4 (LFP)║CAL-10%║Li, at RT offers an initial discharge capacity of ≈165 mAh g-1 at 0.1C rate for 120 cycles with 98.85% coulombic efficiency (C.E.).

Simulating Expansion of the Intracranial Space to Accommodate Brain Swelling after Decompressive Craniectomy: Volumetric Quantification in a 3D CAD Skull Model with Contour Elevation.

Background: Decompressive craniectomy (DC) can be used to augment intracranial space and halt brainstem compromise. However, a widely adopted recommendation for optimal surgical extent of the DC procedure is lacking. In the current study, we utilized three-dimensional (3D) computer-assisted design (CAD) skull models with defect contour elevation for quantitative assessment. Methods: DC was performed for 15 consecutive patients, and 3D CAD models of defective skulls with contour elevations (0-50 mm) were reconstructed using commercial software. Quantitative assessments were conducted in these CAD subjects to analyze the effects of volumetric augmentation when elevating the length of the contour and the skull defect size. The final positive results were mathematically verified using a computerized system for numerical integration with the rectangle method. Results: Defect areas of the skull CAD models ranged from 55.7-168.8 cm2, with a mean of 132.3 ± 29.7 cm2. As the contour was elevated outward for 6 mm or above, statistical significance was detected in the volume and the volume-increasing rate, when compared to the results obtained from the regular CAD model. The volume and the volume-increasing rate increased by 3.665 cm3, 0.285% (p < 0.001) per 1 mm of contour elevation), and 0.034% (p < 0.001) per 1 cm2 of increase of defect area, respectively. Moreover, a 1 mm elevation of the contour in Groups 2 (defect area 125-150 cm2) and 3 (defect area >150 cm2, as a proxy for an extremely large skull defect) was shown to augment the volume and the volume-increasing rate by 1.553 cm3, 0.101% (p < 0.001) and 1.126 cm3, 0.072% (p < 0.001), respectively, when compared to those in Group 1 (defect area <125 cm2). The volumetric augmentation achieved by contour elevation for an extremely large skull defect was smaller than that achieved for a large skull defect. Conclusions: The 3D CAD skull model contour elevation method can be effectively used to simulate the extent of a space-occupying swollen brain and to quantitatively assess the extent of brainstem protection in terms of volume augmentation and volume-increasing rate following DC. As the tangential diameter (representing the degree of DC) exceeded the plateau value, volumetric augmentation was attenuated. However, an increasing volumetric augmentation was detected before the plateau value was reached.

Induction of the early growth response 1 gene by Epstein-Barr virus lytic transactivator Zta.

Early growth response 1 (Egr-1) is a cellular transcription factor involved in diverse biologic functions. Egr-1 has been associated with Epstein-Barr virus (EBV) infection, but it is still unknown whether any EBV protein regulates Egr-1 expression. In this study, we first showed that EBV reactivation is involved in upregulation of Egr-1 and that Egr-1 can be induced by Zta, an EBV lytic transactivator. Zta not only binds to the Egr-1 promoter but also activates the ERK signaling pathway to trigger binding of Elk-1 to the Egr-1 promoter. In addition, knockdown of Egr-1 significantly reduces the spontaneous expression of Zta and Rta in EBV-infected 293 cells, suggesting that a positive-feedback network involving Egr-1 is required for EBV reactivation. This study also implies that Zta has the potential to affect expression of certain genes through Egr-1.