Development and Performance Assessment of the High-Performance Shrinkage Reducing Agent for Concrete

To develop a high-performance shrinkage reducing agent, this study investigated several shrinkage reducing materials and supplements for those materials. Fluidity and air content were satisfactory for the various shrinkage reducing materials. The decrease in viscosity was the lowest for glycol-based materials. The decrease in drying shrinkage was most prominent for mixtures containing glycol-based materials. In particular, mixtures containing G2 achieved a 40% decrease in the amount of drying shrinkage. Most shrinkage reducing materials had weaker level of compressive strength than that of the plain mixture. When 3% triethanolamine was used for early strength improvement, the strength was enhanced by 158% compared to that of the plain mixture on day 1; enhancement values were 135% on day 7 and 113% on day 28. To assess the performance of the developed high-performance shrinkage reducing agent and to determine the optimal amount, 2.0% shrinkage reducing agent was set as 40% of the value of the plain mixture. While the effect was more prominent at higher amounts, to prevent deterioration of the compressive strength and the other physical properties, the recommended amount is less than 2.0%

Concomitant Laparoendoscopic Single-Site Surgery for Vesicolithotomy and Finger-Assisted Single-Port Transvesical Enucleation of the Prostate

Transurethral resection of the prostate is the most common surgery for benign prostatic hyperplasia. However, it doesn't work best for men with very large prostate and bladder stones. Herein we report our initial experience with concomitant laparoendoscopic single-site surgery and finger-assisted single-port transvesical enucleation of the prostate for the treatment of the condition

Role of S5b/PSMD5 in Proteasome Inhibition Caused by TNF-α/NFκB in Higher Eukaryotes

SummaryThe ubiquitin-proteasome system is essential for maintaining protein homeostasis. However, proteasome dysregulation in chronic diseases is poorly understood. Through genome-wide cell-based screening using 5,500 cDNAs, a signaling pathway leading to NFκB activation was selected as an inhibitor of 26S proteasome. TNF-α increased S5b (HGNC symbol PSMD5; hereafter S5b/PSMD5) expression via NFκB, and the surplus S5b/PSMD5 directly inhibited 26S proteasome assembly and activity. Downregulation of S5b/PSMD5 abolished TNF-α-induced proteasome inhibition. TNF-α enhanced the interaction of S5b/PSMD5 with S7/PSMC2 in nonproteasome complexes, and interference of this interaction rescued TNF-α-induced proteasome inhibition. Transgenic mice expressing S5b/PSMD5 exhibited a reduced life span and premature onset of aging-related phenotypes, including reduced proteasome activity in their tissues. Conversely, S5b/PSMD5 deficiency in Drosophila melanogaster ameliorated the tau rough eye phenotype, enhanced proteasome activity, and extended the life span of tau flies. These results reveal the critical role of S5b/PSMD5 in negative regulation of proteasome by TNF-α/NFκB and provide insights into proteasome inhibition in human disease