Fibrinogen Deposition on Silicone Oil-Infused Silver-Releasing Urinary Catheters Compromises Antibiofilm and Anti-Encrustation Properties.

Slippery silicone-oil-infused (SOI) surfaces have recently emerged as a promising alternative to conventional anti-infection coatings for urinary catheters to combat biofilm and encrustation formation. Benefiting from the ultralow low hysteresis and slippery behavior, the liquid-like SOI coatings have been found to effectively reduce bacterial adhesion under both static and flow conditions. However, in real clinical settings, the use of catheters may also trigger local inflammation, leading to release of host-secreted proteins, such as fibrinogen (Fgn) that deposits on the catheter surfaces, creating a niche that can be exploited by uropathogens to cause infections. In this work, we report on the fabrication of a silicone oil-infused silver-releasing catheter which exhibited superior durability and robust antibacterial activity in aqueous conditions, reducing biofilm formation of two key uropathogens Escherichia coli and Proteus mirabilis by ∼99%, when compared with commercial all-silicone catheters after 7 days while remaining noncytotoxic toward L929 mouse fibroblasts. After exposure to Fgn, the oil-infused surfaces induced conformational changes in the protein which accelerated adsorption onto the surfaces. The deposited Fgn blocked the interaction of silver with the bacteria and served as a scaffold, which promoted bacterial colonization, resulting in a compromised antibiofilm activity. Fgn binding also facilitated the migration of Proteus mirabilis over the catheter surfaces and accelerated the deposition and spread of crystalline biofilm. Our findings suggest that the use of silicone oil-infused silver-releasing urinary catheters may not be a feasible strategy to combat infections and associated complications arising from severe inflammation.

The transcription factors MS188 and AMS form a complex to activate the expression of CYP703A2 for sporopollenin biosynthesis in Arabidopsis thaliana.

The sexine layer of pollen grain is mainly composed of sporopollenins. The sporophytic secretory tapetum is required for the biosynthesis of sporopollenin. Although several enzymes involved in sporopollenin biosynthesis have been reported, the regulatory mechanism of these enzymes in tapetal layer remains elusive. ABORTED MICROSPORES (AMS) and MALE STERILE 188/MYB103/MYB80 (MS188/MYB103/MYB80) are two tapetal cell-specific transcription factors required for pollen wall formation. AMS functions upstream of MS188. Here we report that AMS and MS188 target the CYP703A2 gene, which is involved in sporopollenin biosynthesis. We found that AMS and MS188 were localized in tapetum while CYP703A2 was localized in both tapetum and locule. Chromatin immunoprecipitation (ChIP) showed that MS188 directly bound to the promoter of CYP703A2 and luciferase-inducible assay showed that MS188 activated the expression of CYP703A2. Yeast two-hybrid and electrophoretic mobility shift assays (EMSAs) further demonstrated that MS188 complexed with AMS. The expression of CYP703A2 could be partially restored by the elevated levels of MS188 in the ams mutant. Therefore, our data reveal that MS188 coordinates with AMS to activate CYP703A2 in sporopollenin biosynthesis of plant tapetum.

Partial splenic embolization using Bletilla striata particles for hypersplenism in cirrhosis: a prospective study.

The article evaluates the long-term follow-up results of PSE using Bletilla striata (BS) particles for hypersplenism in cirrhosis, as compared to PSE using gelfoam particles. Fifty-nine patients with cirrhosis-induced hypersplenism were treated with PSE. The patients were randomly assigned into two groups: gelfoam group, which includes 32 patients using gelfoam particles as the embolic material, and BS group, which includes 27 patients using BS particles. The peripheral blood cell counts and parameters for complications associated with PSE were measured during the follow-up. The mean values of leukocyte and thrombocyte, but not hemoglobin, were significantly increased after PSE (p < 0.01) in both groups. The values of leukocyte and thrombocyte during the long-term follow-up were significantly improved in BS group than that in gelfoam group (both p < 0.01). The frequency of bleeding episodes from esophageal varices in both groups was significantly reduced after PSE (both p < 0.01), but the post-PSE bleeding episodes showed no remarkable differences between the two groups (p = 0.084). Post-embolization syndrome consisted mainly of fever, nausea and vomiting, and abdominal pain in the two groups. The incidence of grade II to III abdominal pain in BS group (82.8%, 27/33) was significantly higher than in gelfoam group (57.9%, 33/57) (p = 0.020). The mean survival time was 61.5 ± 9.1 (median 60, 1-157) months in gelfoam group and 63.4 ± 9.9 (median 52, 0-161) months in BS group, which showed no significant difference (p = 0.930). In conclusion, BS particles could be used as the embolic material in PSE. Compared to gelfoam used in PSE, BS can achieve even better efficacy in alleviating hypersplenism. It provides a long-term effect on the hematological parameters, bleeding from esophageal varices and good palliation, and improved clinical status contributing to symptomatic control.