Serum Levels of LL-37 and Inflammatory Cytokines in Plaque and Guttate Psoriasis

Psoriasis is a chronic inflammatory skin disease. It is assumed that the plaque phenotype of psoriasis is associated with T helper (Th) 1 immune response activation, while the guttate phenotype is associated with the Th17 immune response. Previous investigations of differences in the serum levels of cytokines relative to the clinical psoriatic phenotype have yielded conflicting results. This study compared the levels of circulating inflammatory cytokines and LL-37 relative to the morphological phenotype in patients with psoriasis. Seventy-four age-matched patients with psoriasis (32 with guttate psoriasis and 42 with plaque psoriasis) and 12 healthy controls were included. A multiplex cytokine assay and enzyme-linked immunosorbent assay were used to measure levels of Th1- and Th17-derived cytokines and LL-37, respectively. Circulating levels of interferon- (IFN)-γ, interleukin- (IL)-1RA, IL-2, and IL-23, and LL-37 were significantly higher in patients with psoriasis than in healthy controls. However, the serum levels of inflammatory cytokines (IL-7, IL-22, and IL-23) and LL-37 did not differ significantly between the guttate and plaque phenotypes of psoriasis. There was a positive correlation between serum inflammatory cytokine levels and the Psoriasis Area and Severity Index score. The findings of this study suggest that the serum levels of inflammatory cytokines reflect the disease activity rather than determine the morphological phenotype

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