Biocompatible hydrogels have many applications, ranging from contact lenses to tissue engineering scaffolds. In most cases, rigorous sterilization is essential. Herein we show that a biocompatible diblock copolymer forms wormlike micelles via polymerization-induced self-assembly in aqueous solution. At a copolymer concentration of 10.0 w/w %, interworm entanglements lead to the formation of a free-standing physical hydrogel at 21 °C. Gel dissolution occurs on cooling to 4 °C due to an unusual worm-to-sphere order-order transition, as confirmed by rheology, electron microscopy, variable temperature (1)H NMR spectroscopy, and scattering studies. Moreover, this thermo-reversible behavior allows the facile preparation of sterile gels, since ultrafiltration of the diblock copolymer nanoparticles in their low-viscosity spherical form at 4 °C efficiently removes micrometer-sized bacteria; regelation occurs at 21 °C as the copolymer chains regain their wormlike morphology. Biocompatibility tests indicate good cell viabilities for these worm gels, which suggest potential biomedical applications.

Summary. The oral streptococci have undergone considerable taxonomic revision in recent years but there is still little information concerning associations between the newly defined species and disease. This study examined the identities of 47 strains of oral streptococci collected from 42 confirmed cases of infective endocarditis. By means of recently described physiological schemes, the most common species identified were Streptococcus sanguis sensu stricto (3 1.9 %), S. oralis (29.8 %) and S. gordonii (12.7 %). Other related species including S. mitis and " S. parasanguis" were less common. This indicates that attention should be focused on S. sanguis sensu stricto and S. oralis when considering possible pathogenic mechanisms involved in viridans streptococcal endocarditis.

Numerous studies have implicated bacteria in cardiovascular disease, but there is a paucity of information on the mechanism involved. In this study we show how the common oral bacterium Streptococcus sanguis can directly interact with platelets, resulting in activation and aggregate formation. Platelet aggregation was dependent on glycoprotein IIb/IIIa (GPIIb/ IIIa) and thromboxane. Platelets could also directly bind to S sanguis, but this interaction was not inhibited by GPIIb/IIIa antagonists. Antibodies to GPIb could inhibit both platelet aggregation and platelet adhesion to bacteria. This suggested a direct interaction between GPIb and S sanguis; however, this interaction did not require von Willebrand factor, the normal ligand for GPIb. By use of a range of monoclonal antibodies to GPIb and the enzyme mocharagin, which cleaves GPIb at amino acid 282, the interaction was localized to a region within the N-terminal 1-225 portion of GPIb␣. Furthermore S sanguis failed to induce aggregation of platelets from a patient with BernardSoulier disease, the organism bound to Chinese hamster ovary cells transfected with the GPIb␣ gene but did not bind to mock-transfected cells and biotin-labeled S sanguis cells bound to purified GPIb in ligand blots. It is suggested that the interaction between S sanguis and GPIb is important in the pathogenesis of infective endocarditis and may also play a contributory role in some cases of myocardial infarction. ( IntroductionRecent reports suggest a role for infectious agents in cardiovascular disease. Much of this work is in the form of clinical evidence of infection [1][2][3][4][5][6] or the effect of antibiotics on the incidence of cardiovascular disease. 7,8 Although studies have found evidence of bacteria in atherosclerotic plaques, 1,2,4,5,9-13 their role in the etiology of cardiovascular disease is uncertain. In contrast, the role of bacteria in infective endocarditis is well established and the molecular mechanisms involved may also occur in other forms of cardiovascular disease.Infective endocarditis involves inflammation of the heart valves due to infection and if untreated can lead to valve failure and death. In most cases there is one or more predisposing factors, which results in damage to the endothelium on or adjacent to the valves. This area of damage becomes covered with a platelet-fibrin vegetation and these can become colonized by bacteria that gain access to the blood. The 2 species most commonly involved are Streptococcus sanguis 14 and Staphylococcus aureus. 15 Historically oral streptococci have been referred to as Streptococcus viridans, but this name was never accepted as a recognized taxon because of the biochemical and serologic heterogeneity among isolates. Subsequent detailed biochemical and genetic studies allowed the definition of at least 17 taxa within what was originally called S viridans. However, the term viridans has survived but is now used as viridans group of streptococci to recognize the existence of various taxa and S sanguis is one taxon w...

Summary.Previous work has shown that the type strain of Streptococcus sanguis, NCTC 7863, induces aggregation of normal platelets by a complement-dependent mechanism. We investigated the roles of IgG and fibrinogen in the aggregation process. Plasma depleted of IgG by passage through protein A-sepharose failed to support platelet aggregation, as did plasma absorbed at 0ЊC with whole bacteria. However, absorption of plasma with a non-aggregating strain of S. sanguis, SK96, did not remove aggregating activity for NCTC 7863. Supplementing 0ЊC-absorbed plasma with purified IgG restored the aggregation supporting activity. A monoclonal antibody to the FcgRII receptor inhibited platelet aggregation by the bacteria, indicating a requirement for bacteria-IgG complexes interacting with the Fc receptor in platelet aggregation. There was a lag time to the onset of platelet aggregation of 7-19 min depending upon the platelet donor, but the length of this lag did not correlate with either total IgG concentration recognizing NCTC 7863 in subjects' plasma, or the concentration any of the four IgG subclasses or with IgG avidity levels.Fibrinogen was shown to bind rapidly to the bacterial cell surface. Monclonal antibody to GPIIb/IIIa, RGDS peptide, and a specific antagonist for the platelet fibrinogen receptor, GPIIb/IIIa, FK633, inhibited platelet aggregation by NCTC 7863, indicating that platelet aggregation is fibrinogen dependent. These data suggest that platelet aggregation by some strains of S. sanguis requires multiple stimuli/agonists, including IgG-Fc receptor interaction, complement and fibrinogen.