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We previously reported that low protein Z plasma levels are associated with acute coronary syndromes (ACS). Aim of the present study was to evaluate protein Z levels in different phases of activity of coronary atherosclerosis. Protein Z plasma levels were measured in 166 (131 male and 35 female) patients consecutively admitted to the University of Florence with a diagnosis of ACS (group A), 166 (131 male and 35 female) patients selected by age and gender in relation to group A from those with a clinical history of ACS who remained symptom- and/or event-free over the last year before the investigation (group B); and 332 (262 male and 70 female) controls comparable for age and gender with the other two groups. None had liver or renal dysfunction nor showed a positivity for antiphospholipid antibodies or for factor V Leiden mutation. Patients under warfarin therapy were excluded. Mean protein Z plasma levels were found to be significantly (P < 0.0001) lower in group A (1475 ± 684.1 ng mL−1) and group B (1327.6 ± 690.7 ng mL−1) as compared with control group (1650.1 ± 634.5 ng mL−1), while no significant differences existed between the two groups of patients (P = 0.06). A logistic regression analysis, performed after the division of the study population into quartiles of protein Z levels and adjusted for all possible confounders, showed a significant increased risk of ACS for the lowest (<1213 ng mL−1) as compared with the highest quartile of protein Z in both groups of patients [group A odds ratio (OR): 2.7, 95% CI 1.3–5.5, P = 0.007; group B OR: 3.2, 95% CI 1.1–8.9, P = 0.02). In conclusion, these results strengthen our previous data on low protein Z plasma levels in ACS and indicate a possible dose–response effect of decreasing protein Z plasma levels on the coronary atherosclerotic disease.

Carotid stenosis and atrial fibrillation are the strongest risk factors for ischemic stroke. Ongoing prevention efforts include the identification of novel factors that increase the risk for carotid atherosclerosis. The aim of this study was to determine the thrombophilic risk profile of patients with severe carotid stenosis by evaluating a number of genetic and metabolic risk factors [factor (F)II G20210A, factor V Leiden, MTHFR C677T polymorphisms, anticardiolipin antibodies (aCL), lipoprotein(a) (Lp(a)), and homocysteine (Hcy)]. The study population consisted of 615 patients [(410 M/205 F; median age 73 (26–94) years] with severe (> 70%) carotid stenosis, and 615 apparently healthy subjects [(410 M/205 F; age 73 (31–92) years]. On multivariate analysis, independent risk factors were elevated Hcy [odds ratio (OR) 7.6, 95% confidence interval (CI) 4.8, 11.8] and Lp(a) levels (OR 2.9, 95% CI 2.1, 3.9), the presence of aCL (OR 5.7, 95% CI 3.1, 10.4) and heterozygosity for FII G20210A polymorphism (OR 2.8, 95% CI 1.3, 5.9). In the subgroup of women, independent risk factors for severe carotid atherosclerosis were: high levels of Hcy and Lp(a) and the presence of aCL, whereas hyperhomocysteinemia, elevated Lp(a) levels, aCL, FII G20210A and MTHFR 677TT polymorphisms remained independent risk factors in the subgroup of men. The results of the present study demonstrate that the prevalence of the thrombophilic risk factors is increased in patients with severe carotid atherosclerosis.

Summary.:  Anaerobically light-grown cells of Rhodobacter capsulatus B100 are highly resistant to the toxic oxyanion tellurite (TeO32−; minimal inhibitory concentration, 250 μg/ml). This study examines, for the first time, some structural and biochemical features of cells and plasma membrane fragments of this facultative phototroph grown in the presence of 50μg of K2TeO3 per ml. Through the use of transmission microscopy and X-ray microanalysis we show that several “needlelike” shaped granules of elemental tellurium are accumulated into the cytosol near the intracytoplasmic membrane system. Flash-spectroscopy, oxygen consumption measurements, and difference spectra analysis indicated that membrane vesicles (chromatophores) isolated from tellurite-grown cells are able to catalyze both photosynthetic and respiratory electron transport activities, although they are characterized by a low c-type cytochrome content (mostly soluble cytochrome c 2). This feature is paralleled by a low cytochrome c oxidase activity and with an NADH-dependent respiration which is catalyzed by a pathway leading to a quinol oxidase (Qox) inhibited by high (millimolar) concentrations of cyanide (CN−). Conversely, membranes from R. capsulatus B100 cells grown in the absence of tellurite are characterized by a branched respiratory chain in which the cytochrome c oxidase pathway (blocked by CN− in the micromolar range) accounts for 35–40% of the total NADH-dependent oxygen consumption, while the remaining activity is catalyzed by the quinol oxidase pathway. These data have been interpreted to show that tellurite resistance of R. capsulatus B100 is characterized by the presence of a modified plasma-membrane-associated electron transport system.

Abstract: It has been reported that the increase of plasminogen activator inhibitor-1 activity immediately after elective coronary angioplasty is related to subsequent clinical recurrence in patients with chronic coronary artery disease. The aims of our study were to evaluate the behaviour of plasminogen activator inhibitor-1 and d-Dimer after revascularization in acute myocardial infarction patients treated with angioplasty and stenting and if this behavior is predictive of subsequent clinical recurrence. d-Dimer and plasminogen activator inhibitor-1 activity were evaluated in two groups of patients. Group 1 consisted of 54 consecutive patients undergoing primary angioplasty for acute myocardial infarction and Group 2 consisted of 48 patients undergoing elective angioplasty. Patients underwent control coronary angiography only in the case of clinical recurrence and/or positivity of provocative tests. d-Dimer and plasminogen activator inhibitor-1 baseline levels were significantly higher in group 1 than in group 2 (P<0.0005 and P<0.05, respectively). The percentage of group 1 patients with a post-procedural increase in d-Dimer was significantly higher among those with subsequent clinical recurrence with restenosis (61%) than among those with no recurrence (25%, P<0.05). No difference was observed in group 2. The percentage of group 2 patients in whom no decrease of plasminogen activator inhibitor-1 was observed after angioplasty was significantly higher (83%) among those with subsequent recurrence than among those with no recurrence (38%, P<0.05). This pattern was not observed in group 1. In conclusion, the role of early changes in plasminogen activator inhibitor-1 in predicting clinical recurrence after primary angioplasty in acute myocardial infarction patients is less clear than that observed after elective angioplasty. A significant role seems to be played by a more-marked clotting activation with increased fibrin formation.

Hyperhomocysteinemia is a risk factor for arterial and venous thrombosis, whereas few data are available on the total cysteine (tCy) levels in thrombophilic patients. We studied 82 patients with a previous myocardial infarction (MI; group 1), 68 patients with a previous deep venous thrombosis (group 2), and 100 control subjects (group 3). We assayed total homocysteine (tHcy) and tCy levels by high-performance liquid chromatography with fluorimetric detection. The odds ratios (ORs) for high levels of tCy and tHcy in venous thrombosis and MI were markedly increased in group 1 (fasting tCy: OR, 3.6; 95% confidence interval [CI], 1.6-11.2; postmethionine tCy: OR, 0.97; CI, 0.3-4.0; fasting tHcy: OR, 8.3; CI, 3.9-18.6; postmethionine tHcy: OR, 12.5; CI, 6.8-27.2) and in group 2 (fasting tCy: OR, 2.9; CI, 1.1-7.8; postmethionine tCy: OR, 0.86; CI 0.2-2.6; fasting tHcy: OR, 8.0; CI 3.6-18.0; postmethionine tHcy: OR, 11.0; CI, 6.0-22.1). Our data suggest that plasma tCy levels are a risk factor for venous thrombosis and MI independently of tHcy levels and that it may be appropriate to study both variables simultaneously to thoroughly study the methionine metabolism.

AbstractLong‐term survival of renal transplant recipients appears to be influenced by the occurrence of thromboembolic complications and cardiovascular disease. In order to investigate the prevalence of new hemostasis‐related risk factors for venous and arterial thrombosis, we investigated 63 renal transplant recipients and 66 age‐ and sex‐matched control subjects. We assayed antiphospholipid antibodies [lupus anticoagulant (LA) and anticardiolipin antibodies (aCL)], lipoprotein (a) [Lp(a)], plasminogen activator inhibitor‐1 (PAI‐1), and total homocysteine (tHcy) levels. We found a significantly higher prevalence of positivity for LA (P< 0.001); no difference was detected in the prevalence of aCL between patients and controls. PAI‐1 levels were significantly higher in renal transplant recipients than in controls [12.3 IU/ml (2‐45.5) vs 7.9 IU/ml (4‐18.0); P< 0.0001] with an odd ratio (OR) of 11.8 (4.9‐28.5) in univariate analysis and of 5.8 (2.1‐15.4) in multivariate analysis. Lp(a) levels were higher in patients then in controls [159 mg/l (1‐992) vs 100.5 mg/l (10‐412); P< 0.005] with an OR of 5.9 (1.9‐18.4) in univariate analysis and of 3.5 (0.9‐13.4) in multivariate analysis. Fasting levels of tHcy were significantly higher in renal transplant recipients [7.0 μmol/l (4.0‐68) vs 8.1 μmol/l (2.0‐24.0); P< 0.00001] with an OR of 40.4 (14.7‐111) in univariate analysis and of 33.1 (11.1‐115.5) in multivariate analysis. After methionine loading test, we documented levels of tHcy above the 90th percentile of controls in 60/63 patients (95 %). Finally, we found a significant correlation between tHcy and PAI‐1 plasma levels (r= 0.76; P< 0.000001). Our results show a high prevalence of hemostasis‐related risk factors for arterial and venous thrombosis in renal transplant recipients, suggesting the need for the investigation of these patients for the presence of these risk factors in order to improve their long‐term survival and to tailor therapy.

Abstract Long-term survival of renal transplant recipients appears to be influenced by the occurrence of thromboembolic complications and cardiovascular disease. In order to investigate the prevalence of new hemostasis-related risk factors for venous and arterial thrombosis, we investigated 63 renal transplant recipients and 66 age- and sex-matched control subjects. We assayed antiphospholipid antibodies [lupus anticoagulant (LA) and anticardiolipin antibodies (aCL)], lipoprotein (a) [Lp(a)], plasminogen activator inhibitor-1 (PAI-1), and total homocysteine (tHcy) levels. We found a significantly higher prevalence of positivity for LA (P &lt; 0.001); no difference was detected in the prevalence of aCL between patients and controls. PAI-1 levels were significantly higher in renal transplant recipients than in controls [12.3 IU/ml (2–45.5) vs 7.9 IU/ml (4–18.0); P &lt; 0.0001] with an odd ratio (OR) of 11.8 (4.9–28.5) in univariate analysis and of 5.8 (2.1–15.4) in multivariate analysis. Lp(a) levels were higher in patients then in controls [159 mg/l (1–992) vs 100.5 mg/l (10–412); P &lt; 0.005] with an OR of 5.9 (1.9–18.4) in univariate analysis and of 3.5 (0.9–13.4) in multivariate analysis. Fasting levels of tHcy were significantly higher in renal transplant recipients [7.0 μmol/l (4.0–68) vs 8.1 μmol/l (2.0–24.0); P &lt; 0.00001] with an OR of 40.4 (14.7–111) in univariate analysis and of 33.1 (11.1–115.5) in multivariate analysis. After methionine loading test, we documented levels of tHcy above the 90th percentile of controls in 60/63 patients (95 %). Finally, we found a significant correlation between tHcy and PAI-1 plasma levels (r = 0.76; P &lt; 0.000 001). Our results show a high prevalence of hemostasis-related risk factors for arterial and venous thrombosis in renal transplant recipients, suggesting the need for the investigation of these patients for the presence of these risk factors in order to improve their long-term survival and to tailor therapy.

Background Thromboembolism occurs in 0.4% to 2% of the subjects undergoing radiofrequency ablation (RFA), but its mechanisms remain unclear. Our aim was to evaluate several parameters of the hemostatic system in relation to the electrophysiologic procedure. Methods Thirty consecutive patients were enrolled in the study. Fifteen underwent electrophysiologic study and 15 underwent radiofrequency ablation. Before the ablation procedure, all subjects were given an intravenous heparin bolus (2500 IU). Blood samples were drawn immediately before, at the end of, and 24 hours after the procedures. Spontaneous platelet aggregation in whole blood and in platelet-rich plasma, markers of clotting activation (prothrombin fragment 1+2 and the thrombin-antithrombin complex) and the fibrinolytic system (plasminogen activator inhibitor and D -dimer) levels were evaluated. Results At the end of the procedure, spontaneous platelet aggregation in whole blood, prothrombin fragment 1+2, thrombin-antithrombin complex, and D -dimer levels increased significantly in all patients. The hemostatic changes were more marked after RFA than after electrophysiology. Spontaneous aggregation in whole blood, prothrombin fragment 1+2, and thrombin-antithrombin complex levels at 24 hours after the procedure were similar to those observed before the procedure in both groups; D -dimer levels were still elevated with respect to preprocedure levels, with a trend toward higher levels in patients undergoing RFA rather than electrophysiology. A significantly more marked activation of coagulation (prothrombin fragment 1+2, P < .005) was found in patients in whom the mean duration of energy application was higher than 23.5 seconds. Conclusions Our data suggest that antithrombotic prevention with a prolonged administration of heparin and/or the association of antiplatelet agents should be considered in patients undergoing RFA. (Am Heart J 1999;138:128-32.)

Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) are frequently detected in sera from patients affected by systemic lupus erythematosus (SLE). However, the role of antiphospholipid antibodies (aPL) in thrombus formation has not been defined as yet.Twenty-two patients affected by SLE, all fulfilling the 1982 ARA revised criteria, and twenty healthy subjects were investigated for the presence of LA, aCL and other aPLs. Monocyte procoagulant activity-PCA (Tissue Factor production) was evaluated by one stage plasma recalcification time. In all patients the plasma levels of F1 + 2 and of plasmin ogen activator inhibitor (PAI) were also determined. Monocyte PCA was significantly higher in SLE patients with LA and/or aCL in comparison to SLE patients without LA and/or aCL (p< 0.01) and to controls (p< 0.05). However, no connection was observed between PCA expression by mononuclear cells and LA or aCL levels. No differences in F1 + 2 and PAI plasma levels were found between SLE patients with or without aPL and controls. In our SLE patients LA and/or aCL positivity appears strictly related to an increased monocyte activation that could play an important role in the occurrence of thrombotic events.

Alginate polymer was evaluated as a carrier for seed inoculation with a genetically modified strain Pseudomonas fluorescens F113LacZY, which protects sugar-beet against Pythium-mediated damping-off. F113LacZY survived in alginate beads at 5 log₁₀ CFU/ bead or higher counts for 8 weeks of storage, regardless of the conditions of incubation. In plant inoculation experiments, colonisation of the growing area of the root by F113LacZY, derived from alginate beads placed in the soil next to the seed or from an alginate coating around the seeds, was improved compared with application of just free cells of the strain. F113LacZY trapped in alginate beads was an effective producer of antifungal phloroglucinols as indicated by direct HPLC quantification of phloroglucinols and in vitro inhibition of both the indicator bacterium Bacillus subtilis A1 and the pathogenic fungus Pythium ultimum. Alginate polymer represents a promising carrier for the delivery of biocontrol inoculants for root colonisation and production of antifungal metabolites.

Physiological saline with or without substance P (50 ng/ml) was infused into the humeral artery in 6 healthy males. Indices of fibrinolytic activity (whole blood diluted lysis time, euglobulin lysis time, lysis areas in non-heated fibrin plates produced by plasma or euglobulin precipitate, plasminogen plasma levels, α2-macroglobulin, Cl-inhibitor, and α2-antiplasmin) were evaluated in the homolateral antecubital vein before and after 5 min of substance P or saline infusion. After substance P the fibrinolytic activity increased, as can be seen from the shortening of lysis times (p<0.01) and enlargement of the lysis areas (p<0.01). A reduction of plasminogen plasma levels (p<0.01), associated with a decrease in α2-anitplasmin (p<0.01), was also found. Alpha2-macroglobulin and Cl-inhibitor were instead unaltered by the peptide. The saline infusion, on the other hand, was unable to modify any of the examined indices. We concluded that exogenous substance P given intra-arterially increases fibrinolytic activity in locally-sampled venous blood through a mechanism which remains to be elucidated.