PubMed Health⌕ Search

Biomedical subjects

C Amore

Publications and source records attributed to C Amore.

At least 19 recordsLinked to original sources
PubMed2004

Polymorphisms of the interleukin-1beta gene affect the risk of myocardial infarction and ischemic stroke at young age and the response of mononuclear cells to stimulation in vitro.

OBJECTIVE: To investigate the role of interleukin-1beta (IL-1beta) gene polymorphisms as a link between inflammation, coagulation, and risk of ischemic vascular disease at young age. METHODS AND RESULTS: A total of 406 patients with myocardial infarction (MI) at young age, frequency-matched for age, sex, and recruitment center, with 419 healthy population-based controls and 134 patients with ischemic stroke at young age, matched by age and sex, with 134 healthy population-based controls, were studied. Subjects carrying the TT genotype of the -511C/T IL-1beta polymorphism showed a decreased risk of MI (odds ratio [OR], 0.36; 95% CI, 0.20 to 0.64) and stroke (OR, 0.32; 95% CI, 0.13 to 0.81) after adjustment for conventional risk factors. In both studies, the T allele showed a codominant effect (P=0.0020 in MI; P=0.021 in stroke). Mononuclear cells from volunteers carrying the T allele showed a decreased release of IL-1beta and a decreased expression of tissue factor after stimulation with lipopolysaccharide compared with CC homozygotes. The presence of a monoclonal antibody against IL-1beta during cell stimulation resulted in a marked reduction of tissue factor activity expression. CONCLUSIONS: -511C/T IL-1beta gene polymorphism affects the risk of MI and ischemic stroke at young age and the response of mononuclear cells to inflammatory stimulation.

Adolescent↗
PubMed2004

Laterally moved, coronally advanced flap: a modified surgical approach for isolated recession-type defects.

BACKGROUND: Various modifications of the laterally sliding flap have been proposed to reduce the risk of gingival recession at the donor tooth site, but the reported root coverage predictability was quite low. The goal of the present study was to evaluate the effectiveness with respect to root coverage of a modified surgical approach of the laterally moved flap procedure for the treatment of an isolated type of recession defect. METHODS: One hundred and twenty (120) isolated gingival recessions (Miller Class I or II) with specific features of the keratinized tissue lateral to the defects were treated with a new approach to the laterally moved flap. The main surgical modifications consisted of the coronal advancement of the laterally moved flap and the different thickness during flap elevation. Clinical evaluation was made 1 year after the surgery. RESULTS: At the 1-year examination, 97% of the root surface was covered with soft tissue and 96 defects (80%) showed complete root coverage. A statistical and clinically significant increase of keratinized tissue was observed. These favorable results were accomplished with no change in the position of gingival margin or in the height of gingival tissue at the donor tooth/site. CONCLUSIONS: The laterally moved, coronally advanced surgical technique was very effective in treating isolated gingival recessions. It combined the esthetic and root coverage advantages of the coronally advanced flap with the increase in gingival thickness and keratinized tissue associated with the laterally moved flap. The ideal gingival conditions must be present lateral to an isolated recession defect in order to render the proposed surgical technique an highly effective and predictable root coverage surgical procedure.

Chlorhexidine↗
PubMed2003

Bilaminar techniques for the treatment of recession-type defects. A comparative clinical study.

OBJECTIVES: Complete root coverage is the primary objective to be accomplished when treating gingival recessions in patients with aesthetic demands. Furthermore, in order to satisfy patient demands fully, root coverage should be accomplished by soft tissue, the thickness and colour of which should not be distinguishable from those of adjacent soft tissue. The aim of the present split-mouth study was to compare the treatment outcome of two surgical approaches of the bilaminar procedure in terms of (i) root coverage and (ii) aesthetic appearance of the surgically treated sites. MATERIAL AND METHODS: Fifteen young systemically and periodontally healthy subjects with two recession-type defects of similar depth affecting contralateral teeth in the aesthetic zone of the maxilla were enrolled in the study. All recessions fall into Miller class I or II. Randomization for test and control treatment was performed by coin toss immediately prior to surgery. All defects were treated with a bilaminar surgical technique: differences between test and control sites resided in the size, thickness and positioning of the connective tissue graft. The clinical re-evaluation was made 1 year after surgery. RESULTS: The two bilaminar techniques resulted in a high percentage of root coverage (97.3% in the test and 94.7% in the control group) and complete root coverage (gingival margin at the cemento-enamel junction (CEJ)) (86.7% in the test and 80% in the control teeth), with no statistically significant difference between them. Conversely, better aesthetic outcome and post-operative course were indicated by the patients for test compared to control sites. CONCLUSIONS: The proposed modification of the bilaminar technique improved the aesthetic outcome. The reduced size and minimal thickness of connective tissue graft, together with its positioning apical to the CEJ, facilitated graft coverage by means of the coronally advanced flap.

Adolescent↗
PubMed2003

Enamel matrix proteins and bovine porous bone mineral in the treatment of intrabony defects: a comparative controlled clinical trial.

BACKGROUND: Various clinical studies have demonstrated that applying commercially available enamel matrix proteins (EMP) on the instrumented root surface during access flap surgery promotes clinically significant gains of clinical attachment and bone in intrabony defects. The aim of the present controlled clinical trial was to evaluate the adjunctive effect of filling the intrabony lesion with bovine porous bone mineral (BPBM) to a simplified papilla preservation (SPP) flap and EMP surgical procedure. METHODS: Sixty deep interproximal intrabony lesions in 60 patients with chronic periodontitis were treated with the SPP flap and EMP. In the 30 test defects, the intrabony component was filled with BPBM particles previously reconstituted with the EMP gel. A stringent infection control program was adopted for 1 year. The clinical and radiographical reevaluation was made 1 year after surgery. RESULTS: Both techniques resulted in clinically and statistically significant improvements between baseline and 1 year, in terms of clinical attachment level (CAL) gain, probing depth (PD) reduction, and radiographic bone fill; however, the BPBM test treatment showed statistically significantly greater CAL (5.8 +/- 1.1 versus 4.9 +/- 1.0) and radiographic bone (DEPTH) level gains (5.3 +/- 1.1 versus 4.3 +/- 1.5), and less increase in gingival recession (0.4 +/- 0.6 versus 0.9 +/- 0.5) than the control surgical procedure. CONCLUSION: The present study data supported the hypothesis that the adjunctive use of BPBM in grafting intrabony defects has the ability to improve clinical and radiographical outcomes achievable with EMP alone.

Adult↗
PubMed2001

Experimental arterial thrombosis in genetically or diet induced hyperlipidemia in rats--role of vitamin K-dependent clotting factors and prevention by low-intensity oral anticoagulation.

To investigate the relationship among lipids, coagulation and thrombosis in the absence of atherosclerosis, spontaneous or dietary-induced hyperlipidemic (FHL) rats were studied. FHL showed higher levels of coagulation factors VII, IX, X, VIII and XII and a shortening of the occlusion time (OT) of an artificial arterial prosthesis as compared with normolipidemic (FNL) animals. Damage of abdominal aorta of FHL was followed by increased fibrin deposition in the vascular intima as compared to FNL. After 5 months of cholesterol-rich diet FNL showed increased cholesterol, triglycerides and factor II, VII, IX, X, XII levels. A significant shortening of the OT and increased fibrin deposition was also observed. Two-month diet withdrawal restored the initial condition. Warfarin treatment, at a dose decreasing vitamin K-dependent factor to levels found in FNL, prolonged the OT and reduced fibrin deposition, without modifying F XII or changing lipid profile. An increase in the activated form of F VII was observed. In contrast, no difference was found in F VII clearance. High lipid levels favour the process of thrombus formation by increasing the activation of vitamin K-dependent coagulation factors. Low-dose warfarin treatment reverts the prothrombotic effect of hyperlipidemia.

Administration, Oral↗
PubMed2000

The decanucleotide insertion/deletion polymorphism in the promoter region of the coagulation factor VII gene and the risk of familial myocardial infarction.

Recently, an association has been found between factor VII polymorphisms and the risk of familial myocardial infarction. To obtain a thorough evaluation of the influence of factor VII gene on the risk of myocardial infarction, we extended our analysis to the role of a decanucleotide insertion/deletion functional polymorphism (-323 0/10-bp) in the promoter region of factor VII and to possible interactions with the HVR4 intron polymorphism. We performed a case-control study of 176 patients with myocardial infarction, over 45 years, who had a familial history of arterial thrombosis and 227 control subjects without a personal or family history of cardiovascular disease. The frequency of the rare allele of 10 bp was lower in cases (0.14 95% CI, 0.10-0.17) than in controls (0.19 95% CI, 0.16-0.23; chi(2)=4.7, p=0.03). Allowing for Hardy-Weinberg equilibrium in controls and testing for association under restricted maximisation, there was a significant difference in genotype frequency between cases and controls (p=0.02). Carriers of the 10-bp allele had an odds ratio for myocardial infarction of 0.65 (95% CI, 0.37-1.12), in multivariate logistic regression analysis. Combination analysis of -323 0/10-bp and HVR4 polymorphisms shows half reduction in the risk of myocardial infarction in comparison with the reference group for all the other groups, suggesting that there was no additivity between the effect of the 10-bp and the H7 alleles. Our findings suggest that the promoter polymorphism of factor VII gene may influence the risk of familial myocardial infarction.

Aged↗
PubMed2000

Effect of lipid-lowering treatment on factor VII profile in hyperlipidemic patients.

A link has been suggested between blood lipids and hemostatic activation. Factor VII (FVII) is a coagulation factor which plays a pivotal role in fibrin generation and thrombus formation. Clinical trials have demonstrated that inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase greatly reduce cardiovascular events in patients with and without coronary artery disease but few data, at this time, are available on the effects of lipid-lowering treatment on factor VII levels. We studied thirty-six IIA and IIB type hyperlipidemic patients who, after a preliminary period of lipid-lowering diet, added atorvastatin (20 mg/daily) or continued dietary treatment alone until they achieved LDL-C recommended levels (<4 mmol/L). Four to six weeks of lipid lowering treatment with diet plus atorvastatin, produced a significant reduction in FVII coagulant activity (FVIIc) and antigen (FVIIAg). No significant changes were observed in activated FVII (FVIIa). The lipid-lowering treatment with diet alone induced an improved lipid pattern, but no significant changes in FVII profile. Our study suggests a significant effect of lipid-lowering treatment on FVII levels. A possibile nonlipid mechanism that modifies FVII pathway may be suggested.

Adult↗
PubMed1998

Polymorphisms in the coagulation factor VII gene and the risk of myocardial infarction.

BACKGROUND: High blood levels of coagulation factor VII are associated with a risk of ischemic vascular disease. Although factor VII levels may be genetically determined, the relation between genetic polymorphisms of factor VII, factor VII blood levels, and the risk of myocardial infarction has not been established. METHODS: We performed a case-control study of 165 patients with familial myocardial infarction (mean [+/-SD] age, 55+/-9 years) and 225 controls without a personal or family history of cardiovascular disease (mean age, 56+/-8 years). The polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene were studied. Factor VII clotting activity and antigen levels were also measured. RESULTS: Patients with the QQ or H7H7 genotype had a decreased risk of myocardial infarction (odds ratios, 0.08 [95 percent confidence interval, 0.01 to 0.9] and 0.22 [95 percent confidence interval, 0.08 to 0.63], respectively). For the R353Q polymorphism, the RR genotype was associated with the highest risk, followed by the RQ genotype and then by the QQ genotype (P<0.001). For the polymorphism involving hypervariable region 4, the combined H7H5 and H6H5 genotypes were associated with the highest risk, followed in descending order by the H6H6, H6H7, and H7H7 genotypes (P<0.001). Patients with the QQ or H7H7 genotype had lower levels of both factor VII antigen and factor VII clotting activity than those with the RR or H6H6 genotype. Patients with the lowest level of factor VII clotting activity had a lower risk of myocardial infarction than those with the highest level (odds ratio, 0.13; 95 percent confidence interval, 0.05 to 0.34). CONCLUSIONS: Our findings suggest that certain polymorphisms of the factor VII gene may influence the risk of myocardial infarction. It is possible that this effect may be mediated by alterations in factor VII levels.

Analysis of Variance↗
PubMed1998

4G/5G promoter PAI-1 gene polymorphism is associated with plasmatic PAI-1 activity in Italians: a model of gene-environment interaction.

The PAI-1 gene promoter 4G/5G polymorphism was found to be associated with plasma PAI-1 activity in Northern and Central Europe populations, but no data are available on the association between this polymorphism and PAI-1 levels in Southern Europe countries (such as Italy) where the incidence of ischemic disorders is lower. This study shows that among populations with different incidence of atherothrombotic disorders the 4G/5G PAI-1 gene promoter polymorphism has the same importance in the regulation of plasma PAI-1 activity. Moreover, we have analysed some gene-environmental interactions: the correlation between PAI-1 and cholesterol in non dyslipidemic subjects and the correlation between PAI-1 activity and tryglicerides in dyslipidemic subjects differed according to the 4G/5G genotype class. Thus, our findings suggest that, among subjects with or without metabolic disorders such as dyslipidemia, completely different gene-environment interactions may occur.

Adult↗
PubMed1998

[The role of 4G/5G polymorphism in the regulation of plasma levels of PAI-1: a model of interaction between genetic and environmental factors].

Previous studies have suggested that a decreased fibrinolytic potential can play a role as risk factor for thrombotic events. Blood levels of factors of the fibrinolytic system are highly heritable, supporting the importance of the genetic background. To better understand the impact of two common polymorphisms of the tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) genes on the in vivo regulation of fibrinolysis, we have studied this genetic variables together with other clinical and metabolic factors in a sample of the Italian population. Two hundred-eighteen subjects without history of atherothrombosis or mayor diseases entered the study. A detailed clinical history was collected and evaluations of blood levels of cholesterol, triglycerides, PAI-1 activity, PAI-1 antigen, t-PA activity, t-PA antigen were performed on standard conditions. Genotypes at the locus of the 4G/5G polymorphism of PAI-1 gene promoter and at locus of the insertion/deletion Alu-repeat polymorphism of t-PA gene intron h were studied. No detectable effect was found for the t-PA gene polymorphism in our population. On the other hand, the 4G/5G polymorphism was found to modulate plasma PAI-1 activity levels and the interaction between PAI-1 plasma activity levels and blood lipids. Moreover, such regulation by genotype was found to be affected by the presence or absence of dyslipidemia. In conclusion, our findings suggest that, among subjects with or without metabolic disorders such as dyslipidemia, completely different gene-environment interactions may occur, and could affect the individual risk of thrombosis.

Adult↗
PubMed1998

Genetic modulation of coagulation factor VII plasma levels: contribution of different polymorphisms and gender-related effects.

We studied the relationships among different polymorphisms of FVII gene in determining FVII levels, in a sample of 335 male and female Italian volunteers. The hypervariable region 4 (HVR4), the promoter decanucleotide insertion (-323 0/10 bp) and the R353Q polymorphisms of FVII gene were evaluated. The association of HVR4 or -323 0/10 bp polymorphism with plasma FVII levels differed between gender (Interaction term: p = 0.02 and p = 0.03, respectively), showing stronger effect in males than in females. In males, the R353Q and the HVR4 polymorphisms showed an incremental influence on FVII variance (F = 8.9, p <0.001 and F = 4.4, p = 0.01, respectively). Moreover, the effects of Q and 10 bp alleles on the reduction of FVII activity levels were significantly potentiated by the presence of H7 allele of HVR4 (Interaction term p = 0.03 for R353Q*HVR4 and p = 0.03 for -323 0/10 bp*HVR4). In conclusion, the effect of FVII polymorphisms on FVII levels was gender dependent and derived from a complex interaction among them. The HVR4 polymorphism seems to add an independent, albeit small, contribution to the regulation of FVII plasma levels.

Adult↗
PubMed1997

Bcl I polymorphism in the fibrinogen beta-chain gene is associated with the risk of familial myocardial infarction by increasing plasma fibrinogen levels. A case-control study in a sample of GISSI-2 patients.

The aim of this study was to investigate the association of the Bcl I beta-chain fibrinogen polymorphism with the risk of acute myocardial infarction (AMI) and its relationship with fibrinogen levels in the Italian population. We studied 102 AMI patients, selected within the framework of the GISSI-2 trial, who had a familial history of arterial thrombosis (at least one first-degree relative suffering from AMI or stroke before 65 years) and 173 control subjects (with neither AMI nor personal or familial history of arterial thrombosis). All subjects were Italian. Patients showed fibrinogen levels higher than control subjects. There was a highly significant difference in allele frequency in cases versus control subjects, the B2 allele frequencies being respectively 0.28 versus 0.17 (P = .002). In multivariate analysis, adjusted for sex, age, smoking habits, and history of hyperlipidemia, hypertension, or diabetes, the (B1B2 + B2B2) genotype was associated with a higher risk of AMI (odds ratio 2.4, 95% confidence interval, 1.2 to 4.6). The Bcl I genotype was also associated with fibrinogen levels, independently of gender and smoking habits, the (B1B2 + B2B2) subjects showing the highest levels in both cases and control subjects. The difference in fibrinogen levels between cases and control subjects was significantly influenced by the genotype (significant interaction, P = .042). The B2 allele of the Bcl I polymorphism in the beta-chain of the fibrinogen gene is a new factor associated with the risk of familial AMI through its association with fibrinogen levels. These data provide evidence for a causal role of fibrinogen in familial AMI.

Case-Control Studies↗
PubMed1996

Inhibitors of acyl CoA:cholesterol acyltransferase.

Conformational restriction of previously disclosed acyclic (diphenylethyl)diphenylacetamides led to the discovery of several potent inhibitors of acyl CoA:cholesterol acyltransferase (ACAT). cis-[2-(4-Hydroxyphenyl)-1-indanyl]diphenylacetamide (4a) was the most potent ACAT inhibitor identified (IC50 = 0.04 microM in an in vitro rat hepatic microsomal ACAT assay, ED50 = 0.72 mg/kg/day in cholesterol-fed hamster.

Animals↗
PubMed1995

Human endothelial cell damage by neutrophil-derived cathepsin G. Role of cytoskeleton rearrangement and matrix-bound plasminogen activator inhibitor-1.

Cathepsin G, a major protease released by activated neutrophils, induces functional and morphological damage to human endothelial cells. We studied the mechanisms involved and ways to reverse this damage. Cathepsin G induced a concentration- and time-dependent injury to human umbilical vein endothelial cell (HUVEC) morphology simultaneous with cytoskeleton rearrangement. Preincubation of the endothelial monolayer with phallacidin completely prevented damage to cell morphology by cathepsin g, whereas preincubation with cytochalasin b potentiated its activity. Damage to cell shape and F-actin cytoskeleton were prevented by eglin C, and inhibitor of the active site of cathepsin G. Furthermore, cathepsin G increased transcellular permeability to albumin and induced a time-dependent detachment of PAI-1 from the extracellular matrix of a cell-free system. The inhibition of matrix-bound PAI-1 activity by specific antibodies induced matrix-bound PAI-1 activity by specific antibodies induced changes in HUVEC monolayers similar to those observed after cathepsin G. However, although stabilization of F-actin microfilaments by phallacidin prevented changes in cell shape, it did not prevent the ability of cathepsin G to increase cell permeability and release matrix PAI-1. The damage of cathepsin G to cell morphology and cytoskeleton arrangement was reversed within 12 hours if the deendothelialization area was < 50% to 55% and the subendothelial matrix was still able to bind the newly synthesized PAI-1. Thrombin, whose role in the thrombotic process is well known, also induced changes in cell morphology and cytoskeleton arrangement of HUVEC. Cathepsin G reaches the subendothelial matrix through an increase in cell permeability and injures endothelial cell morphology by detaching matrix-bound PAI-1. These events expose a highly thrombogenic surface to which platelets can adhere, become activated, attract further neutrophils, and trigger thrombus formation.

Cathepsin G↗
PubMed1995

[Hemostatic factors and family history of thrombosis in patients with a myocardial infarct: a case-control study. The participants in GISSI-2-Efrim. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico].

We studied a series of hemostasis factors in a group of patients selected from a cohort of 916 patients affected by MI from the GISSI-2 study population. Following a case-control design, 73 patients with a family history of thrombosis (the presence of at least two first degree relatives affected by MI and/or stroke before 65 years) were matched with MI patients with no family history of thrombosis. Blood collection could be performed 6 +/- 1 months after the acute phase following MI in 53 pairs of such patients. The presence of mixed disulphides (MDS) was significantly higher in patients with family history than in controls; MDS were detected in 7 cases and only in 1 control. No difference was found in contrast in the distribution of fibrinogen, factor VII, factor VIII, vWF, protein C, protein S, AT III, HC II, PAI-1, lipoprotein (a). Nevertheless, independently from the family history, in the whole population of MI patients studied, 21 cases of suspected deficiency of protein C were found. Sixteen out of 53 patients with family history of MI and/or stroke had a family history of MI only. In patients with family history of MI the t-PA antigen levels were significantly lower than in the control group (7.5 +/- 4.4 vs 11.1 +/- 3.5 ng/ml, t = -2.6, p < 0.02). In the whole population of MI patients and in patients with a family history of thrombosis t-PA antigen was positively correlated with PAI-1 antigen and vWF. The correlation with PAI-1 was lost in patients with family history of MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗