Alleviation of hand-skin roughness after use of alcohol-based hand rub with inhibitory effects on Staphylococcus aureus-producing δ-toxin.

INTRODUCTION: Staphylococcus aureus colonizes rough regions of the skin of the hand. Healing of S. aureus-mediated wounds is promoted by the application of RNA III inhibiting peptide, which inhibits the production of S. aureus virulence factors, including δ-toxin. Herein, we investigated the level of hand-skin roughness in healthcare professionals after they used an alcohol-based hand rub containing polyoxyethylene lauryl ether (formulation E), which inhibits S. aureus δ-toxin production. METHODS: The inhibition rate of S. aureus δ-toxin production by hand rubs, including formulation E, was calculated by quantifying S. aureus δ-toxin concentration in culture medium using high-performance liquid chromatography. Healthcare professionals used formulations E or S (reference alcohol-based hand rub) for 4 weeks. The surface evaluation of the scaliness (SEsc) value was used as an indicator of hand skin roughness. The ΔSEsc value was calculated by subtracting the SEsc value before using the alcohol-based hand rub from the SEsc value 4 weeks after use. RESULTS: The inhibition rates of S. aureus δ-toxin production by formulations E and S were 43% and 10%, respectively. Formulation E significantly reduced ΔSEsc. The difference in ΔSEsc values after using formulations E and S was significant. CONCLUSIONS: The inhibitory effect on S. aureus δ-toxin production was higher with formulation E than with formulation S. Compared to formulations S, formulation E was effective at reducing scaliness and alleviating hand-skin roughness. Furthermore, the inhibitory effect of formulation E on S. aureus δ-toxin production could be associated with a reduction in scaliness and alleviation of hand-skin roughness.

Nonfibrous beta-structured aggregation of an Abeta model peptide (Ad-2alpha) on GM1/DPPC mixed monolayer surfaces.

Adsorption and aggregation of transformed peptides and proteins onto the cell membrane surface is commonly associated with forms of amyloidosis such as Alzheimer's disease and prion disease. To address dynamic features of these pathological phenomena molecularly, the in situ Ad-2alpha model peptide deposition on glycolipid-containing monolayers was studied by using a 9 MHz quartz-crystal microbalance (QCM). The Ad-2alpha peptide has two amphiphilic alpha-helix segments, each modified with a 1-adamantanecarbonyl group at the N-terminal as a hydrophobic defect. The peptide folds in a 2alpha-helix structure in the bulk solution. In the presence of mixed monolayers of glycolipids (GM1, asialo-GM1, GM3, or LacCer) and/or dipalmitoyl phosphatidylcholine (DPPC) laminated on the QCM plate, the peptide deposition and the conformational change to beta-structure on the monolayers were accelerated. The adsorption kinetics and the amount of Ad-2alpha were dependent on the sort and contents of the glycolipid in the DPPC matrix. Although the Ad-2alpha peptide adsorbs onto most of the glycolipid membranes as monolayer coverage, it adsorbed largely onto the GM1/DPPC (30/70 mol%) mixed monolayer with characteristic kinetic behaviors. The accumulation of beta-structured nonfibrous aggregations was confirmed by AFM and fluorescence microscopy with Thioflavin T (ThT).

Hand hygiene using a new hand-cleansing formulation without sanitizers: Effect on Staphylococcus aureus removal and recovery of properties against skin damage.

BACKGROUND: Staphylococcus aureus is known to form a biofilm and colonize on damaged skin of the hands. We investigated changes in the quantity of S aureus on the hands and changes in skin damage when using a hand-cleansing formulation with potassium oleate but without a sanitizer (formulation A), which is highly effective in removing S aureus biofilm and causes minimal skin damage. MATERIAL AND METHODS: The participants (14 medical staff members) used 2 types of hand-cleansing formulations (formulations A and B), each for 4 weeks. S aureus of the hands was cultured from swab samples on agar plates. Surface of hands was measured using an ultraviolet light microscope. RESULTS AND DISCUSSION: The quantity of S aureus after using formulation A for 4 weeks was 10(1.08 ± 0.05) CFU/mL, a statistically significant decrease from the quantity of S aureus (10(1.59 ± 0.19) CFU/mL) just before use (P = .029). Also, dryness of hand surfaces decreased. With formulation B, the quantity of S aureus did not significantly change from before to after use (P > .05). This presumably occurs because formulation A gently removes S aureus biofilm. CONCLUSIONS: Formulation A removed S aureus from the hands of participants, and skin damage on the hands improved.

A retrovirus restriction factor TRIM5alpha is transcriptionally regulated by interferons.

TRIM5alpha is a member of tripartite motif protein family and recently identified as a restriction factor for retroviral infection in a species-specific manner. Human TRIM5alpha gene is located on chromosomal position 11p15 in a cluster with other TRIM genes including TRIM6, 21, 22, and 34. We show here that interferon (IFN) upregulates TRIM5alpha mRNA expression in HeLa and HepG2 cells by performing Northern blot analysis and quantitative real-time PCR. TRIM5alpha promoter activity was IFN inducible as confirmed by luciferase assay using a reporter plasmid that contained the 5'-flanking region of TRIM5alpha. Mutational analysis has revealed that IFNs activate TRIM5alpha promoter activity through a putative interferon-stimulated response element (ISRE). Intriguingly, another IFN-responsive protein signal transducer and activator of transcription factor 1 (STAT1) binds to the ISRE sequence as shown by electrophoretic mobility shift assay using HeLa cell extracts. We have raised a specific polyclonal antibody against TRIM5alpha and confirmed that TRIM5alpha protein expression is inducible by IFN-beta in HeLa cells. These results lead us to define that the transcription and protein synthesis of TRIM5alpha could be modulated by IFN, suggesting that TRIM5alpha may play a role in an IFN-induced antiviral state against retrovirus infection.

Ovarian hemangioma presenting as pseudo-Meigs' syndrome with elevated CA125.

We report the first case of ovarian hemangioma presenting as pseudo-Meigs' syndrome with elevated CA125. Abdominopelvic computed tomography (CT) assumed ovarian carcinoma. Chest CT revealed pleural effusion. Intraoperative frozen-section examination of the right ovary showed benign hemangioma. After operation, chest radiograph and ultrasonography showed no pleural effusion or ascites.