Antibiotic therapies to eradicate medical device-associated infections often fail because of the ability of sessile bacteria, encased in their exopolysaccharide matrix, to be more drug resistant than planktonic organisms. In the last two decades, several strategies to prevent microbial adhesion and biofilm formation on the surfaces of medical devices, based mainly on the use of antiadhesive, antiseptic, and antibiotic coatings on polymer surfaces, have been developed. More recent alternative approaches are based on molecules able to interfere with quorum-sensing phenomena or to dissolve biofilms. Interestingly, a newly purified ␤-N-acetylglucosaminidase, dispersin B, produced by the gram-negative periodontal pathogen Actinobacillus actinomycetemcomitans, is able to dissolve mature biofilms produced by Staphylococcus epidermidis as well as some other bacterial species. Therefore, in this study, we developed new polymeric matrices able to bind dispersin B either alone or in combination with an antibiotic molecule, cefamandole nafate (CEF). We showed that our functionalized polyurethanes could adsorb a significant amount of dispersin B, which was able to exert its hydrolytic activity against the exopolysaccharide matrix produced by staphylococcal strains. When microbial biofilms were exposed to both dispersin B and CEF, a synergistic action became evident, thus characterizing these polymer-dispersin B-antibiotic systems as promising, highly effective tools for preventing bacterial colonization of medical devices.

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Summary. Twenty‐one patients with congenital factor VII deficiency belonging to 16 different kindreds were investigated. The existence of three immunochemical variants on the ground of factor VII activity (VII:C) and factor VII‐related antigen (VII:Ag) levels (VII−, VII+ and VIIR) was established. There was no correlation between the presence of factor VII:Ag and either the clinical picture or the specific function as studied with the Km calculations. Genetically the mode of inheritance is the same whatever the immunological variant, but the identification of carriers is simplified when the presence of factor VII‐related antigen is assayed throughout a kindred.

SummaryTwenty three patients belonging to 18 different pedigrees of Haemophilia B were studied with regard to ox-brain prothrombin time and its correlation to factor VII.Eleven among them were B-negative (no detectable factor IX antigen), five were B-reduced (factor IX antigen detectable but below the normal values) and seven were B-positive (normal levels of factor IX antigen).Ox-brain prothrombin time was found prolonged (≥ x̄ + 2.5 SD:99% confidence limits) in nine patients. Factor VII Activity (VII: C) was found reduced in 1/11 B-negative, in 2/5 B-reduced and in 4/7 B-positive patients. Factor VII Antigen (VII: Ag) was found normal in all but one patient.The ratio VII:C/VII:Ag was abnormal in eight patients independently from the variant of Haemophilia B. The underlying defect which causes the prolongation of Ox-brain prothrombin time due to factor VII: C mild deficiency is heterogeneous. Age, a mild Vitamin K deficiency, the presence of an inhibitor of Factor VII activation and other unknown causes, may be responsible for this pattern.

The factor VII related antigen (Pivka-VII) in 25 random patients under long term treatment with oral anticoagulants was studied. All the patients had Thrombotest levels well within the therapeutic range (3 to 11%) and had been receiving the drugs for at least 4 months. Factor VII activity (VII: C) mean levels were 8.7 u/dl(sem 0.78) and factor VII antigen (VII: Ag) mean levels were 30.7 u/dl(sem 1.99), (ratio Pivka/Activity 4.04). Barium chloride adsorbed the same mean amount of factor VII: C and factor VII: Ag (8.7 u/dl and 8.0 u/dl respectively). After exposure to cold in 4/25 subjects the “cold activation” phenomenon became evident, characterised by an increase of factor VII: C levels and immodified VII : Ag levels. In the remaining 21 patients, mean VII : C as well as VII: Ag levels did not show modifications (8.5 u/dl and 30.7 u/dl respectively). Moreover, three normal volunteers received three different oral anticoagulants ( Acenocoumarin, Coumarin and Ethyl-Biscomacetate). A sharp increase of factor VII:C levels was observed in all the three subjects (from 30 to 50%), a few hours after the beginning of the treatments, followed by consensual decrease of the two properties related to factor VII that reached the nadir after 48 hours. The vitamin K administration was followed by a rapid and consenual increase of the two parameters.