Synthesis and comparative study of the structural and optical properties of binary ZnO-based composites for environmental applications.

The development of photoactive systems to solve serious environmental problems is a key objective of researchers and remains a real challenge. Herein, n-p heterojunction ZnO-based composites were developed to achieve better photocatalytic performance in methylene blue (MB) degradation under natural solar irradiation. The hydrothermal technique was used to synthesize zinc oxide (ZnO)/metal oxide (MO) composites, with a molar ratio of 1 : 1 (MO = Mn3O4; Fe3O4; CuO; NiO). Various characterization techniques were used for the analysis of the structural, morphological and optical properties. X-ray diffraction (XRD), Scanning Electron Microscopy (SEM), Energy Dispersive X-ray Spectroscopy (EDX) Diffuse Reflectance Spectroscopy analysis (DRS), and Diffuse Reflectance Spectroscopy analysis (DRS) validated the presence of two phases for each sample, excluding any impurities. Indeed, the ZnO structure was not affected by the coupling with MO, confirming that MO was well dispersed on the surface of the ZnO crystalline lattice for each composite. Eventually, the photocatalytic performance evaluation test of the synthesized photocatalysts was carried out on aqueous MB solution. According to the results, the ZnO/Fe3O4 nano-catalyst showed the best photodegradation efficiency. This result suggests that the formation of Fe3O4/ZnO as a p/n heterojunction reduces the recombination of photo-generated electron/hole pairs and broadens the solar spectral response range, resulting in significant photocatalytic efficiency. Meanwhile, the possible mechanism for degradation of the MB was discussed.

Non-doped and transition metal-doped CuO nano-powders: structure-physical properties and anti-adhesion activity relationship.

Bacterial contamination and biofilm formation generate severe problems in many fields. Among these biofilm-forming bacteria, Staphylococcus epidermidis (S. epidermidis) has emerged as a major cause of nosocomial infection (NI). However, with the dramatic rise in resistance toward conventional antibiotics, there is a pressing need for developing effective anti-biofilms. So, fabrication of copper oxide nanoparticles (NPs) is one of the new strategies to combat biofilms. Notably, doped CuO NPs in anti-biofilm therapy have become a hot spot of attention in recent years due to their physicochemical properties. In this context, the present work deals with the investigation of undoped and transition metal (TM)-doped CuO NPs (TM = Zn, Ni, Mn, Fe and Co), synthesized via the co-precipitation method. The synthesized CuO NPs are characterized using X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, field-emission scanning electron microscopy (FE-SEM), energy dispersive spectroscopy (EDS) and X-ray photoelectron spectroscopy (XPS). Results consistently revealed the successful formation of CuO NPs using the co-precipitation method and confirmed that TM ions are successfully inserted into CuO crystal lattice. We found that doping changes the morphology of the CuO NPs and increases their crystallite size. The XPS results show a non-uniform distribution of the doping concentration, with a depletion or an enrichment of the NP surface depending on the element considered. Furthermore, the anti-adhesive potential of CuO NPs against S. epidermidis S61 biofilm formation is evaluated in this study by crystal violet and fluorescence microscopy assays. All synthesized NPs exhibit considerable anti-adhesive activity against S. epidermidis S61 biofilm. Interestingly, compared to undoped CuO, Fe and Ni-doped oxides show an improved activity when used at high concentrations, whereas Mn-doped CuO is the most efficient at low concentrations. This makes TM-doped CuO a promising candidate to be used in biomedical applications.

[Activated protein C resistance and factor V Leiden: clinical interest]. / Résistance à la protéine C activée et facteur V Leiden : intérêt clinique.

Activated protein C resistance (APCR) is a coagulation abnormality often linked to FV Leiden mutation, a single nucleotide G1691A substitution resulting in arginine 506→glutamine missense factor V mutation. FV Leiden has a frequency of 20 to 30% in groups of patients with venous thrombosis while it is of 4 to 10% in normal subjects. FV Leiden is considered as a weak risk factor of thrombosis except in homozygote. FV Leiden is implicated in deep venous thrombosis occurrence. Duration of oral anticoagulant treatment is six months in patients developing a first venous thrombosis except in patients with combined defects or a clinical context suggesting a high risk of severe relapse. Detection of APCR by coagulation methods is often used in first intention with a high specificity if plasmas tested are diluted in factor V deficient plasma. Genotyping study is essential to establish the heterozygote or homozygote statute and certain teams perform it directly. Nevertheless, APCR not related to FV Leiden could be an independent thrombosis risk factor. APCR and FV Leiden are included in laboratory investigations of thrombophilic markers in patients less than 50 years with venous thrombosis. In arterial thrombosis, FV Leiden implication is weak or absent. FV Leiden increases the risk of thrombosis in other situations as in patients with cancer. An association with recurrent miscarriages and other vasculoplacental complications is also reported in many studies but the data concerning the efficacy of antithrombotic treatment to prevent recurrence are currently insufficient.

[Congenital protein S deficiencies; diagnostic difficulties]. / Les déficits congénitaux en protéineS ; difficultés diagnostiques.

Protein S is a physiologic inhibitor of coagulation acting as a cofactor of activated protein C (APC) that inhibits factor Va and VIII. Approximately 60% of PS is bound to C4bBP, a protein of the complement system and only the free PS has a cofactor PCa role. Congenital PS deficiencies are diagnosed by immunologic dosage of free and total PS and functional assay evaluating APC cofactor activity. However, it has been demonstrated a direct anticoagulant activity of free PS, non-dependant of APC on the cascade coagulation and even PS bound to C4bBP seems to have anticoagulant properties. So, it appears that functional assays available estimate only a part of PS anticoagulant activities and, in addition, many interferences are reported with these tests (lupus anticoagulant, factor V Leiden, factor VIII excess...). Immunologic dosages are more reliable in spite of rare qualitative PS deficiencies that could be non-diagnosed. PS deficiencies are often difficult to diagnose because of an overlapping between normal and pathological values. Familial studies are necessary to prove the hereditary origin because there are several causes of acquired and sometimes persistent PS deficiencies (liver insufficiency, vitamin K absence, hormonal therapy in women, PS auto immune deficiency). About 200 different mutations were retrieved and, therefore, molecular studies are not of current practice. It is recommended currently to measure in first intention the free PS, if possible in association with PCa cofactor activity.

[Resistance to curative treatment by unfractionned heparin]. / Les résistances aux traitements curatifs par l'héparine non fractionnée.

Unfractionated heparin has been used as antithrombotic therapy for many years. Its main effect is attributed to the activation of antithrombin (AT), the heparin/AT complex inactivating both factor IIa (thrombin) and factor Xa. Resistance to unfractionated heparin with clinical or biological expression is uncommon. The occurrence of venous or arterial thrombosis or the extension of thrombosis in a patient receiving unfractionated heparin, should always raise suspicion of either AT deficiency or type 2 heparin-induced thrombocytopenia (HIT type 2). HIT type 2 is not a true heparin resistance but an immune complication that requires heparin discontinuation and the use of alternative anticoagulants. Biological heparin resistance is suspected in the presence of a normal or not prolonged activated partial thromboplastin time despite the administration of increasing dose of heparin. Measurement of anti-Xa activity is useful to adjust heparin treatment. Isolated biological heparin resistance is encountered in several physiological and pathological situations including inflammatory and infectious disorders, pregnancy and thrombocytosis. It also occurs in acquired antithrombin deficiency of nephrotic syndrome, l-asparaginase treatment or cardiopulmonary bypass. Biological heparin resistance is relatively common, but clinically significant resistance to heparin is rare and should always raise suspicion of either AT deficiency or type 2 heparin-induced thrombocytopenia.

Enhanced photocatalytic activity against crystal violet dye of Co and In doped ZnO thin films grown on PEI flexible substrate under UV and sunlight irradiations.

This work is focused on the photocatalytic activities of undoped ZnO, Co (1%) doped ZnO (CZO) and In (1%) doped ZnO (IZO) thin films grown on flexible PEI (Polyetherimide) substrate by spray pyrolysis. The photodegradation of crystal violet dye was investigated under UV and sunlight irradiations. Doping and excitation energy effects on photocatalytic efficiencies are discussed. All ZnO thin films show high photocatalytic efficiency up to 80% under either UV or sunlight irradiations for 210 min. However, CZO has the higher photocatalytic performance under UV irradiation. While, the photodegradation efficiency of IZO was enhanced under sunlight irradiation due to the narrowing of its optical gap. These results are discussed based on structural, morphological and optical investigations. The photocatalytic stability of ZnO films was studied as well. So, after three photocatalysis cycles, all ZnO thin films still effective. The obtained results are promising for the use of doped ZnO/PEI as talented photocatalysts for applications in large surfaces with various geometries for photodegradation of hazardous pollutants.

Amino acid structure and characterization of a heterodimeric disintegrin from Vipera lebetina venom.

A heterodimeric disintegrin designed as lebein was isolated from crude Vipera lebetina venom using gel filtration, anion and cation exchange chromatographies on FPLC. The amino acid sequence of each subunit determined by Edman degradation contains 64 residues with ten half-cystines and an RGD site at the C-terminal part of the molecule. The molecular mass of native lebein determined by mass spectrometry was found to be 14083.4 Da and those of alpha and beta subunits were 6992.05 and 7117.62, respectively. These value are in good agreement with those calculated from the sequences. This protein strongly inhibits ADP induced platelet aggregation on human platelet rich plasma with IC(50)=160 nM. Sequences of this protein subunits displayed significant sequence similarities with many other monomeric and dimeric disintegrins reported from snake venoms. We identified an amino acid residue (N) in the hairpin loop of both subunits (CNRARGDDMNDYC) which is different from all other reported motifs of disintegrins and this subtle difference may contribute to the distinct affinities and selectivities of this class of proteins.

Prevalence of inherited prothrombotic abnormalities and central venous catheter-related thrombosis in haematopoietic stem cell transplants recipients.

In this prospective study, we assessed the incidence of central venous catheter (CVC)-related thrombosis in haematopoietic stem cell transplant (HSCT) recipients. We determined the contribution of inherited prothrombotic abnormalities in blood coagulation to CVC-related thrombosis in these patients. The study was conducted between May 2002 and September 2004. CVCs were externalized, nontunneled, polyurethane double lumen catheters. Before catheter insertion, laboratory prothrombotic markers included factor V Leiden, the prothrombin gene Gly20210A mutation, plasma antithrombin levels, and protein C and S activity. All patients were systematically examined by ultrasonography just before, or <24 h after, catheter removal, and in case of clinical signs of thrombosis. A total of 171 patients were included during the 28-month study period. Five (2.9%) and three (1.7%) patients had evidence of protein C and protein S deficiency, respectively. Only one patient had an antithrombin deficiency (0.6%). In total, 10 patients (5.8%) were heterozygous for the factor V Leiden mutation, and one patient had heterozygous prothrombin G20210A mutation (0.6%). We observed a CVC-related thrombosis in 13 patients (7.6%). Thrombosis was diagnosed in four out of 20 patients (20%) with a inherited prothrombotic abnormality compared to nine of 151 patients (6%) who did not have a thrombophilic marker (relative risk 3.3 CI 95% 1.1-9.9). Our results suggest that inherited prothrombotic abnormalities contribute substantially to CVC-related thrombosis in HSCT recipients. In view of physicians' reluctance to prescribe prophylactic anticoagulant treatment in these patients, a priori determination of inherited prothrombotic abnormalities may form a basis to guide these treatment decisions.

Thrombophilia and venous thromboembolism. International consensus statement. Guidelines according to scientific evidence.

Thrombophilia is the term now used to describe predisposition to increased risk of venous and occasionally arterial thromboembolism due to hematological abnormalities. It can be a multifactorial disorder where congenital defects of anticoagulant or procoagulant factors may be combined with acquired hematological abnormalities. It should be considered in patients with a documented unexplained thrombotic episode or a positive family history. The aim of this document is to provide guidelines for investigation and management of patients with thrombophilia in the presence or absence of venous thromboembolism (VTE).

Protein S deficiency and antibodies to protein S in patients with Behçet's disease.

Thrombosis occurs in 20 to 30% of patients with Behçet's disease (BD). Most of the reported hemostatic abnormalities are related to the inflammatory syndrome. We have assessed the activity of antithrombin III, protein C and protein S (PS), in 30 patients with BD and in 30 healthy controls. Thrombosis antecedents were found in 16 patients. Antithrombin III and protein C were within the normal range, however free PS and PSactivity were significantly decreased in patients as compared to control group. PS deficiency detected in eight patients, was associated to thrombosis in 6 of them. No correlation was found between free PS/total PS ratio and C4bBP levels. Antibodies to PS were screened by ELISA and were present in 6 patients, associated to PS deficiency in 4, and to thrombosis antecedents in 5 cases. PS deficiency was transient in two patients, associated to a persistent antiPS in one of them. These findings suggest that auto-immune acquired PS deficiency may be involved in the pathogenesis of thrombotic events in BD.

Further characterization and thrombolytic activity in a rat model of a fibrinogenase from Vipera lebetina venom.

Vipera lebetina fibrinogenase (VlF) was shown to render fibrinogen incoagulable and to solubilize fibrin. The fibrinogenolytic activity of this enzyme was found to be 33 mg fibrinogen/min/mg protein. The study of the specificity of this enzyme revealed that it has no effect on purified factor X, prothrombin and protein C and on the specific chromogenic substrates of their active form. Plasminogen was not activated by VlF but slightly degraded. We have also compared the effect of VlF and plasmin on fibrinogen and shown that these two enzymes have a different sites of cleavage. This enzyme inhibited human platelet aggregation on PRP initiated by ADP and collagen but was without effect on the aggregation of washed rabbit platelets using thrombin as agonist. Administration of VlF in rat did not show any necrosis or hemorrhage in treated rats organ's. We therefore, examined the thrombolytic activity of VlF in a rat model of venous thrombosis. Thrombus was produced in the posterior vena cava by injection of human fibrinogen and thrombin. Injection of 5 mg/Kg body weight showed an evident flow restoration after one hour and measurement of the fibrinogen level a decrease of about 30% after 3 hrs. VlF's action is not dependent on plasminogen activators and may act synergistically with them, thereby providing an intriguing potential clinical application for dissolution of blood clots.

Procoagulant and platelet-aggregating properties of cerastocytin from Cerastes cerastes venom.

Cerastocytin is a thrombin-like serine protease with potent platelet-proaggregating properties. It is able to activate factor XIII but is less active than thrombin on plasma coagulation. The aggregation induced by cerastocytin resembles that induced by thrombin, since rabbit washed platelets desensitized by a pretreatment with thrombin do not aggregate in the presence of cerastocytin. Furthermore, preincubation of platelets with monoclonal antibodies specific for glycoproteins GPIb or GPIIbIIIa blocks receptor sites for thrombin and fibrinogen, respectively, and prevents their aggregation induced by thrombin or cerastocytin. A monoclonal antibody, inhibitor of von Willebrand factor (VWF)-dependent agglutination, blocks the aggregation induced by cerastocytin. After activation with cerastocytin, washed rabbit platelets degranulate and secrete ATP and phospholipase A2. However, cerastocytin is less potent in inducing the release of phospholipase A2 than in inducing ATP secretion.

Further evidence for the presence of anti-protein S autoantibodies in patients with systemic lupus erythematosus.

Acquired protein S (PS) deficiency in systemic lupus erythematosus (SLE) has been previously reported, but its mechanism and its possible thrombotic role have not been established. The aim of our study was to provide further evidence for auto-immune PS deficiency in 27 Tunisian SLE patients, using PS-specific enzyme-linked immunosorbent assay (ELISA) and surface plasmon resonance technology (SPR). PS deficiencies for PS activity, free PS or total PS, respectively, were found in 19, 18 and 12 patients. A significant correlation (r= -0.475, P< 0.016) was found between free/total PS ratio and C4bBP levels, suggesting a role of inflammation in free PS deficiency. Immunoglobulin IgG antibodies to PS were detected in four patients by both ELISA and SPR, in six patients only by ELISA, and in two patients only by SPR. Signals for anti-PS IgG by ELISA and SPR were, however, significantly correlated (r = 0.549, P = 0.003). These results suggest that an auto-immune mechanism could account for low PS activity in patients with SLE. Auto-antibodies to PS may form immune complexes, inducing increased clearance of PS or interfering with the protein C-protein S system.