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.

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.

[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.

[Association of tow thrombotic risk factors: factor V Leiden and hyperhomocysteinemia. A case report]. / Association de deux facteurs de risque thrombotique: facteur V Leiden et hyperhomocystéinémie. A propos d'un cas.

The identification of constitutional and/or acquired risk factor is of major importance in the treatment of thromboembolic disease in young people; it contributes to evaluate the risk of recurrence and to define the period of oral prophylactic anticoagulant treatment. Several congenital or acquired abnormalities of haemostasis are actually defined. In this paper, we report the case of a 34-year-old man who developed a deep venous thrombosis, five months before the diagnosis of megaloblastic anemia, probably due to pernicious anemia. The thrombosis was partially explained by the acquired hyperhomocysteinemia induced by vitamin B12 deficiency. Moreover, activated protein C resistance due to factor V Leiden, was revealed in our patient. This latter improved under anticoagulant treatment combined with vitamin B12. Combination in one individual, of different risk factors predisposing to inherited and/or acquired thrombophilia, results in increased risk for thrombo-embolic disease, suggesting synergic interaction between these factors.

[Homozygous antithrombin type HBS deficiency; a family study]. / Déficit homozygote en antithrombine de type HBS; à propos d'une famille.

Congenital antithrombin (AT) deficiency is the most thrombotic genetic abnormality of haemostasis. Total quantitative deficits are lethal as early as life intra-uterine. Only homozygous mutations concerning the heparin-binding site are compatible with life. We report here the case of an 18 years old patient with recurrent deep venous thrombosis of the inferior members. Haemostasis exploration shows a decreased AT activity (11%) in the presence of heparin while AT progressive activity and AT antigen are normal. Two other homozygous sisters are identified in this family study. Molecular study of AT gene show Arg47-Cys substitution, already reported in the literature with patients of different geographic origins. Treatment of patients with homozygous AT type HBS deficiency is similar that for patients with heterozygous AT deficiency; a continuous prophylactic anticoagulant treatment is always necessary and AT concentrates infusions are required in all situations needing curative heparin treatment.

[Congenital factor XIII deficiency in the south of Tunisia]. / Déficit congénital en facteur XIII de la coagulation dans le sud tunisien.

Factor XIII deficiency is a rare autosomal recessive congenital disorder of haemostasis characterised by a plasmatic factor XIII level less than 1% in homozygote and bleeding as of the youth. We report a study about ten patients with congenital factor XIII deficiency from seven south-Tunisian families, there are seven females. Umbilical bleeding was common and only two patients had intracranial bleeding. The standard screening tests are normal. Factor XIII activity was less than 1% in all patients. A sub-unit A deficit was detected for the ten patients. Out hemorrhagic context, five patients receive regular prophylactic transfusion with fresh frozen plasma.

[Type 2B and pseudo type 2B Von Willebrand disease; a report of three cases]. / Maladie de Willebrand de type 2B et pseudomaladie de Willebrand de type 2B; à propos de trois observations.

Increased affinity of Von Willebrand factor (VWF) for its platelet receptor GPIb-GPIX complex is responsible of an hemorrhagic disease, which is the Von Willebrand disease (VWD) type 2B when the molecular abnormality is located on the VWF, and the platelet-type 2B VWD when the mutation concern the platelet receptor. Haemostatic abnormalities in these bleeding disorders are similar; prolonged bleeding time, fluctuating thrombocytopenia, decreased factor VIII-VWF complex, and an increased response to low dose of ristocetin in platelets rich plasma. High molecular weight VWF multimers are decreased. We report here 2 cases of type 2B VWD and 1 case of platelet type 2B VWD. The distinction between these 2 diseases was established by studying platelet aggregation with weak doses of ristocetin in mixtures of washed platelets (of normal control or patient)+poor platelets plasma (normal or patient). In one case, VWD 2B was discovered late in a 49 years old man, and the factor VIIIC-VWF complex was not diminished. The distinction between these two congenital diseases is important for the treatment of bleeding manifestations which need VWF concentrates infusions in type 2B VWD and administration of platelets concentrates in pseudo type 2B VWD.

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).

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.

[Atypical defibrination syndromes and acute leukemias with a t(9,22) translocation, apropos of 2 cases]. / Syndromes de défibrination atypiques et leucémies aiguës à translocation t(9,22); à propos de deux observations.

We report two cases of atypical defibrination syndromes in patients with respectively acute monoblastic leukemia (chronic myeloid leukemia initially) and acute lymphoblastic leukemia. Hemostasis studies show low fibrinogen level, elevated D-dimers, decreased alpha 2 antiplasmin and factor V, normal antithrombin III values. Plasminogen is below the normal range in one patient. Soluble complexes, which are an important argument for diagnosis of intravascular coagulation disease, are not detected in both patients. Primary or secondary hyperfibrinolysis seems also excluded since euglobulin clot lysis time was normal. Enzymatic proteolysis of fibrinogen (or fibrin) by the blast cells has been reported by some authors; this mechanism could account for the hemostasis abnormalities observed in these two patients.

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.

[Activated protein C resistance in Behçet disease]. / Etude de la résistance à la protéine c activée au cours de la maladie de Behçet.

Behçet's disease is a systemic condition of unknown cause characterized in 20 to 40% of cases by venous and/or arterial thrombosis that is not fully explained by the hemostasis disorders reported in the literature. The present study investigated resistance to activated protein C in 65 Behçet's disease patients, 75 normal subjects, and 70 patients with a history of isolated thrombosis. The test used involved predilution in factor V-deficient plasma. Activated protein C resistance was found in six Behçet's disease patients (9.2%), eight normal subjects (10.6%), and 21 patients with isolated thrombosis (30%). Of the 26 Behçet's disease patients (40%) with a history of thrombosis, only one had activated protein C resistance. Activated protein C resistance does not explain the increased risk of thrombosis in Behçet's disease patients.

Cerastotin, a serine protease from Cerastes cerastes venom, with platelet-aggregating and agglutinating properties.

Cerastotin, a thrombin-like enzyme from the venom of the desert viper Cerastes cerastes, has been purified by gel filtration on Sephadex G-75 and two ion-exchange chromatographies on Mono S columns. It is a neutral glycoprotein (pI = 6.6), present as a single polypeptide chain of 40 kDa. Its N-terminal sequence shows strong similarity with those of other thrombin-like enzymes from snake venoms. Cerastotin possesses esterase and amidolytic activities measured with N(alpha)-tosyl-L-arginine methyl ester and the thrombin chromogenic substrate D-phenylalanyl-L-pipecolyl-L-arginine p-nitroanilide, respectively. The amidolytic activity is inhibited by phenylmethylsulfonyl fluoride, N(alpha)-tosyl-L-lysine chloromethane, N(alpha)-tosyl-L-phenylalanyl chloromethane, D-phenylalanyl-L-prolyl-L-arginyl chloromethane and benzamidine, suggesting that cerastotin is a serine protease. Cerastotin efficiently clots human plasma and cleaves preferentially the alpha chain of fibrinogen. Cerastotin did not induce aggregation of washed normal platelets, but did aggregate platelets in the presence of exogenous fibrinogen. A monoclonal antibody directed against glycoprotein (GPIb), which specifically inhibits induced agglutination by ristocetin also completely blocks platelet aggregation induced by cerastotin. However, another anti-GPIb monoclonal antibody, which specifically inhibits alpha-thrombin binding to GPIb, did not prevent this aggregation. Furthermore, platelets which were desensitised by alpha-thrombin still aggregate in the presence of cerastotin, but not alpha-thrombin. Similarly a monoclonal antibody, anti-GPIIb-IIIa, which blocks fibrinogen binding, did not inhibit cerastotin-induced platelet aggregation. This activity is abolished in the presence of 1 mM phenylmethylsulfonyl fluoride and/or 10 mM EDTA. Cerastotin also agglutinates formalin-fixed and washed platelets, only in the simultaneous presence of fibrinogen and of Von Willebrand factor.

[Hemorrhagic syndrome and isolated alpha 2-antiplasmin deficiency. Apropos of a case]. / Syndrome Hémorragique et déficit isolé en alpha 2 antiplasmine. A propos d'un cas.

An isolated alpha 2 plasmin inhibitor deficiency is reported in a 33 years old male, presenting repeated intramuscular hematomas since 5 years, spontaneously or after minor traumas. None of other family members were suffering from abnormal bleeding. Screening hemostatic examinations were normal except for a moderately shorted euglobulin lysis time (2 hours). Evaluation of fibrinolysis parameters (plasminogen, plasminogen activator inhibitor type 1, tissue plasminogen activator, fibrin and fibrinogen degradation products, alpha 2 plasmin inhibitor) showed normal values except for alpha 2 plasmin inhibitor which is markedly decreased (activity: 14%, antigen: < 5%). Familial hemostasis investigations have not been performed. This isolated alpha 2 plasmin inhibitor deficiency has been confirmed by two repeated control prelevments. Bleedings episodes were treated with antifibrinolytics agents (tranexamic acid). This case report shows the importance of the diagnostic approach in the laboratory to detect such rare hemostatic abnormalities associated with bleeding tendency.