Search PubMed⌕ Search

Biomedical subjects

M Ferrari

Publications and source records attributed to M Ferrari.

At least 253 records · Page 14Linked to original sources

A new pericardium vascular prosthesis: mechanical behavior, SEM analyses and clinical indications.

This study deals with the mechanical characterization of a new vascular prosthesis. The prosthesis, made from a single portion of pericardial tissue, is bifurcated, crimped and not porous. The clinical use of this graft could increase hemocompatibility of the device compared to polymeric grafts and reduce the compliance mismatch between the natural vessel and the graft. Several mechanical analyses were performed to evaluate the load-displacement and the cyclic loading characteristics of the graft. Scanning electron microscopy was used to evaluate the tissue and suture line morphology before and after mechanical failure. The preliminary results of some clinical cases are also reported. The results point out that the prostheses, developed using correct technological procedures, show a mechanical behavior similar to that of natural arteries and could be successfully used in selected patients.

Aged↗

[High risk PTCA: prevention and treatment of cardiogenic shock with mechanical assist systems].

Vessel occlusion during of after PTCA integrates the risk of pump failure if the ischemia volume is great as compared to the remaining myocardium. In so-called high-risk PTCA a risk stratification by means of risk scores such as "Bergelson Score" is mandatory. To encounter the risk of pump failure the application of mechanical cardiac assist devices such as balloon pumps, Hemopump or percutaneous applicable cardio-pulmonary support (pCPS) can be considered. To counteract ischemia during balloon inflation active perfusion balloons can be applied. The latter systems are simple and effective, however the duration of application is restricted to the balloon inflation period. Cardiac assist devices are more aggressive. While the results of intaaortic ballon pump in combination with high-risk PTCA are unsatisfying, Hemopumps and pCPS were alternatives, although the Hemopump is still under investigation. Our own results on 42 patients with high-risk PTCA demonstrate an acceptable 8.6% hospital mortality rate, however an unsatisfying intermediate survival rate since a complete revascularisation in this subset of patients with extensive coronary disease and, frequently, total vessel occlusion is mostly impossible.

Angioplasty, Balloon, Coronary↗

Genotype-phenotype correlation in cystic fibrosis patients.

Cystic fibrosis (CF) is the most common severe recessive disease in Caucasians. The gene responsible for the disease encodes a protein named cystic fibrosis transmembrane conductance regulator, which is predicted to function as a cAMP-regulated chloride channel. Reduced chloride secretion is at the basis of insufficient hydratation of ductural mucus in the airways, reproductive system and pancreas, leading to progressive obstructive damage. The clinical expression of the disease is heterogeneous but most CF patients typically present with chronic obstructive lung disease, elevated electrolyte concentration in sweat and insufficient pancreatic exocrine function. Approximately 10-15% of CF patients have pancreatic sufficiency, 2 to 5% of patients have liver disease and infertility is present in almost all adult males, due to congenital bilateral absence of the vas deferens, and frequently in females. To date, over 500 mutations have been identified in the CFTR gene. A genotype-phenotype correlation has been observed only with pancreas status, while severity of lung involvement is not clearly related to the CFTR genotype, suggesting that this phenotype might be modulated by additional genetic or environmental factors; liver disease in general is not genetically determined. A large proportion of sterile healthy men with congenital bilateral absence of the vas deferens carry a mutation in at least one of their CFTR genes. The data collected so far suggest that the relationship between the CFTR genotype and the clinical manifestation is multiple and complex.

Adult↗

Sealing performance of Scotchbond Multi-Purpose-Z100 in Class II restorations.

PURPOSE: To evaluate the sealing ability of Class II Scotchbond Multi-Purpose/Z100 composite restorations placed under in vivo and in vitro conditions. MATERIALS AND METHODS: For the in vivo part, Class II preparations were cut in posterior teeth which were scheduled for extraction for periodontal reasons. The cervical margins ended in dentin-cementum, 1 mm below the CEJ. The teeth were extracted after 2-3 months of clinical service. The in vitro part was performed in extracted posterior teeth, free from restorations and caries, following the same in vivo protocol. The in vivo and in vitro samples were processed and evaluated for marginal leakage. RESULTS: Leakage by dye penetration was observed at the cervical margins in 70% of the in vivo and in 50% of the in vitro specimens. All in vivo samples with no leakage at the cervical margin were restored where the adjacent interproximal tooth was missing. In more than 40% of the restorations placed in vivo, leakage was also found at the occlusal margins. Statistically significant differences were found at the cervical margins between in vivo and in vitro groups (P < 0.05). The in vitro samples can be of only limited value in predicting clinical performances of an enamel-dentin bonding system in Class II restorations.

Aged↗

Dentin contamination protection after mechanical preparation for veneering.

PURPOSE: To evaluate in vivo the efficacy in preventing post-operative sensitivity and bacterial invasion of primed dentin that was left unprotected for 4 days after laminate veneer preparation. MATERIALS AND METHODS: Twelve vital, periodontically involved anterior teeth were prepared for experimental laminate veneers and divided into three groups: (1) Control group, in which the prepared surfaces were left unprotected after preparation; (2) Prepared dentin surfaces were cleaned with Tubulicid Red Label and covered with Tubulitec Primer; (3) All-Bond 2 Primer was applied to the prepared dentin surface. Post-operative sensitivity was evaluated immediately and a second appointment, 4 days later. The teeth were then extracted and examined by SEM. RESULTS: The application of a primer (Groups 2 and 3) prevented all sensitivity. After 4 days, the teeth in Group 1 were still sensitive to air blasts. Bacterial penetration into the unprotected tubules was observed in Group 1, but not in Groups 2 and 3.

Adult↗

Dentin infiltration by three adhesive systems in clinical and laboratory conditions.

PURPOSE: To evaluate in vivo and in vitro the formation of hybrid layer, resin tags and adhesive lateral branches, by use of three different enamel dentin bonding systems. MATERIALS AND METHODS: The dentin adhesives were tested on flat dentin preparations made on buccal surfaces of vital, periodontally compromised teeth. The samples were randomly divided in four groups: Group 1: Prime & Bond 2.0; Group 2: Scotchbond Multi-Purpose Plus; Group 3: Clearfil Liner Bond 2 (the self-etching primer was applied for 30 seconds on the enamel and dentin); Group 4: Clearfil Liner Bond 2 (the self-etching primer was applied for 60 seconds on the enamel and dentin). The sample teeth were extracted immediately after the bonding was cured. The same procedure described for the in vivo samples was performed in vitro on extracted molars. All the samples were split-fractured along their long axis. Half of the samples were used to visualize the hybrid layer and the other half to observe the morphology of resin tags by use of scanning electron microscopy. RESULTS: All the tested products formed a hybrid layer, both in vivo and in vitro. In many areas of the samples of Groups 1, 2 and 4, characteristic reverse cone-shaped tags with their corresponding adhesive lateral branches were evident. In contrast to this, resin tags found in samples of Group 3 were narrower at the tubule orifices, and adhesive lateral branches were scarce. The length of the resin tags observed in the samples of Groups 1 and 2 were longer than those found in Groups 3 and 4. The morphology of the hybrid layer of the in vivo samples was similar to that of the in vitro samples.

Bisphenol A-Glycidyl Methacrylate↗

Identification of protein tyrosine phosphatase-like IA2 (islet cell antigen 512) as the insulin-dependent diabetes-related 37/40K autoantigen and a target of islet-cell antibodies.

The majority of patients with insulin-dependent diabetes (IDDM) have Abs to 40- and/or 37-kDa tryptic fragments (37/40K-Abs) deriving from an unidentified islet cell membrane protein distinct from glutamate decarboxylase (GAD). Recently, autoantibodies against ICA512, which has identity with the protein tyrosine phosphatase-like protein IA2, were reported. In this study we have examined whether IA2/ICA512 is the Ag specificity of 37/40K-Abs, and one of the determinants of islet cell Abs (ICA) detected by immunofluorescence. Serum from 51 of 100 new onset IDDM patients immunoprecipitated 40- and/or 37-kDa insulinoma polypeptides, and 53 immunoprecipitated in vitro translated rIA2; 49 had both 37/40K-Abs and rIA2 Abs. There were strong correlations between the levels of Abs to rIA2 and both 40 kDa (r = 0.85, p < 0.0001) and 37 kDa (r = 0.70, p < 0.0001) insulinoma polypeptides. Trypsin treatment of immunoprecipitated rIA2 yielded 40- and 37-kDa fragments, and preincubation of sera with rIA2 completely inhibited binding to the insulinoma 40- and 37-kDa polypeptides. IA2 Ab levels also correlated with ICA titer in GAD-Ab negative sera, and preincubation with rIA2 reduced ICA staining intensity in sera with ICA and IA2 Abs, but not in sera with ICA in the absence of IA2 Abs. These results provide clear evidence for the identification of IA2/ICA512 as the precursor of the islet 40- and 37-kDa polypeptide autoantigens and as one of the ICA specificities. Combined detection of Abs to IA2 and GAD65 in a single radio-binding assay identified Abs in 88 of 100 IDDM patients, and potentially facilitates population screening for IDDM risk assessment.

Adolescent↗

CAG triplet analysis in families with androgen insensitivity syndrome by capillary electrophoresis in polymer networks.

The potential use of capillary zone electrophoresis in polymer networks (linear polymers above the entanglement threshold, added to the background electrolyte for sieving purposes) for analysis of DNA fragments amplified by a polymerase chain reaction, is shown. In typical runs, the capillary is filled with Tris-borate-EDTA buffer, at pH 8.3, containing 6% linear polyacrylamide as a dynamic sieving matrix. Such formulations allow replenishing the capillary with fresh sieving solution when resolution decays after prolonged use (typically > 30 injections per capillary are obtained). The DNA fragments are detected by their intrinsic absorbance at 254 nm. This system has been applied to the analysis of CAG triplet polymorphism in families carrying the androgen insensitivity syndrome. While easy separation is obtained for fragments 139 base pairs (bp) and 160 bp (in families carrying a difference of 7 CAG repeats) even more difficult cases (such as those of families exhibiting fragments of 136 and 139 bp, thus differing by only one CAG repeat) are resolved with precision and diagnostic value.

Androgen-Insensitivity Syndrome↗

Pulmonary and left ventricular decompression by artificial pulmonary valve incompetence during percutaneous cardiopulmonary bypass support in cardiac arrest.

BACKGROUND: In cardiac arrest, use of percutaneous cardiopulmonary bypass support (PCPS) may lead to left ventricular loading, with deleterious effects on the myocardium, and is often accompanied by an increase in pulmonary artery pressure. The present study was designed to assess the potential of artificially induced pulmonary valve incompetency to retrogradely decompress the left ventricle during PCPS in ventricular fibrillation. METHODS AND RESULTS: Studies were performed using a standardized experimental animal model in sheep (n = 12; body weight, 77 to 112 kg). When PCPS was used during fibrillation, an increase in left ventricular pressure (from 21.4 +/- 5.0 mm Hg after 1 minute to 28.4 +/- 9.5 mm Hg after 10 minutes of fibrillation) was observed in all animals, with a simultaneous increase in pulmonary artery pressure in 6 animals, from 15.5 +/- 3.8 to 24.3 +/- 5.4 mm Hg (group A). In these animals, artificial pulmonary valve incompetency, which was induced by a special "pulmonary valve spreading catheter," led to effective decompression of both the pulmonary circulation (decrease in pulmonary artery pressure from 24.3 to 11.3 mm Hg) and the left ventricle (decrease in left ventricular pressure from 30.5 to 17.7 mm Hg). We simultaneously measured a decrease in the myocardial release of lactate (increase in arterial coronaryvenous difference in lactate content from -0.01 to 0.14 mmol/L), demonstrating the myocardial protective effect of the procedure. In contrast, in 6 animals without an increase in pulmonary artery pressure during PCPS (group B), artificial pulmonary valve incompetency did not reduce left ventricular loading, which was probably because of competent mitral valves in these animals. CONCLUSIONS: In case of increasing pulmonary artery pressure during PCPS in cardiac arrest, artificial pulmonary valve incompetency might be a useful tool for effective pulmonary and retrograde left ventricular decompression.

Animals↗

Interaction of the anthracycline 4'-iodo-4'-deoxydoxorubicin with amyloid fibrils: inhibition of amyloidogenesis.

All types of amyloidosis are structurally characterized by the cross beta-pleated sheet conformation of the fibrils, irrespective of their biochemical composition. The clinical observation that the anthracycline 4'-iodo-4'-deoxy-doxorubicin (IDOX) can induce amyloid resorption in patients with immunoglobulin light chain amyloidosis was the starting point for this investigation of its possible mechanism of action. IDOX binds strongly to all five types of natural amyloid fibrils tested: immunoglobulin light chains, amyloid A, transthyretin (methionine-30 variant), beta-protein (Alzheimer), and beta 2-microglobulin. Quantitative binding studies showed that IDOX, but not doxorubicin, binds strongly to amyloid fibrils. This binding is saturable and involves two apparently distinct binding sites with Kd values of 5.9 x 10(-11) M and 3.4 x 10(-9) M. IDOX inhibited in vitro insulin amyloid fibrillogenesis. In vivo studies using the experimental amyloid murine model confirmed the specific targeting of IDOX to amyloid deposits. Preincubation of amyloid enhancing factor with IDOX significantly reduced the formation of amyloid deposits. It is hypothesized that IDOX exerts its beneficial effects through the inhibition of fibril growth, thus increasing the solubility of existing amyloid deposits and facilitating their clearance. IDOX may represent the progenitor of a class of amyloid-binding agents that could have both diagnostic and therapeutic potential in all types of amyloidoses.

Amyloid↗

Mutational analysis of muscle and brain specific promoter regions of dystrophin gene in DMD/BMD Italian patients by denaturing gradient gel electrophoresis (DGGE).

In order to characterize the nature of mutations occurring in non-deleted Duchenne (DMD) and Becker muscular dystrophy (BMD) affected males, a total of 40 unrelated Italian patients was studied for the presence of point mutations within the muscle-specific regulatory region of the dystrophin gene. We decided to investigate the dystrophin promoter sequences because nucleotide variations in these regions could impair the expression of the gene and be the underlying molecular defect in some forms of the disease. In four patients suffering from mental retardation, the brain promoter region was also studied. To screen for point mutations, we applied molecular analysis by parallel denaturing gradient gel electrophoresis (DGGE). No sequence alterations were found in either the muscle or the brain promoters, suggesting that mutations in these regions do not represent a common mechanism of mutation in DMD/BMD.

Base Sequence↗

Search for mutations in pancreatic sufficient cystic fibrosis Italian patients: detection of 90% of molecular defects and identification of three novel mutations.

A cohort of 31 cystic fibrosis patients showing pancreatic sufficiency and bearing an unidentified mutation on at least one chromosome was analyzed through denaturing gradient gel electrophoresis of the whole coding region of the cystic fibrosis transmembrane conductance regulator gene, including intron-exon boundaries. Three new and 19 previously described mutations were detected. The combination of these with known mutations detected by other methods, allowed the characterization of mutations on 56/62 (90.3%) chromosomes. Among those identified, 17 can be considered responsible for pancreatic sufficiency, since they were found in patients carrying a severe mutation on the other chromosome. Among these presumed mild mutations, eight were detected more than once, R352Q being the most frequent in this sample (4.83%). Intragenic microsatellite analysis revealed that the six chromosomes still bearing unidentified mutations are associated with five different haplotypes. This may indicate that these chromosomes bear different mutations, rarely occurring among cystic fibrosis patients, further underlying the molecular heterogeneity of the genetic defects present in patients having pancreatic sufficiency.

Adolescent↗

Failure to detect Glut4-Ile383 and IR-Gln1152 variants in NIDDM (non-insulin dependent diabetes mellitus) and control subjects in an Italian population.

Insulin receptor (IR) and insulin-responsive glucose transporter (Glut4) represent two candidate genes involved in the development of non-insulin dependent diabetes mellitus (NIDDM); detection of molecular alterations in these genes might explain their possible contribution to NIDDM. Recently, mutations within the coding region of IR and Glut4 have identified: they include the Glut4Ile383 and IRGln1152 variants which were found at low frequencies in diabetic Caucasian populations. In this study Italian NIDDM patients and control subjects were analysed and mutated alleles were not found. Therefore in our population these variants appear to have little relevance to the genetic susceptibility to NIDDM.

Base Sequence↗

HLA DQA1-DQB1-TAP2 haplotypes in IDDM families: no evidence for an additional contribution to disease risk by the TAP2 locus.

The TAP2 gene, located in the HLA class II region, encodes a subunit of a transporter involved in the endogenous antigen-processing pathway, and has been suggested to contribute to the genetic risk for insulin-dependent diabetes (IDDM). In order to determine whether the TAP2 locus modulates the risk conferred by HLA DQ loci, HLA DQA1-DQB1-TAP2 haplotypes were analysed in 48 IDDM probands, their first degree relatives, and in 62 normal control subjects. A decreased frequency of the TAP2B allele was confirmed in this IDDM cohort (12 vs 28% in control subjects, pc < 0.05). Analysis of 73 informative meiotic events in IDDM and control families demonstrated a recombination fraction between HLA DQB1 and TAP2 loci of 0.041 (Log of the odds score = 16.5; p < 10(-8)) indicating strong linkage between these loci. Family haplotype analysis demonstrated linkage disequilibrium between TAP2 and HLA DQA1-DQB1, and showed that the reduced frequency of TAP2B was associated with its absence on the IDDM susceptible DQA1*0301-DQB1*0302 haplotype, its low frequency on DQA1*0501-DQB1*0201, and the association of TAP2B with DQA1*0101-DQB1*0501 haplotypes which were less frequent in IDDM patients. Comparison of transmitted with non-transmitted haplotypes in IDDM families showed a slight but not significant decrease in TAP2B allele frequency on transmitted (3 of 37) vs non-transmitted (2 of 9) HLA DQA1*0501-DQB1*0201 haplotypes. No other differences were observed. Twenty-four unrelated DQA1*0501-DQB1*0201 haplotypes from non-diabetic families had a TAP2B allele frequency (4%) similar to that in IDDM haplotypes.(ABSTRACT TRUNCATED AT 250 WORDS)

ATP Binding Cassette Transporter, Subfamily B, Mem↗

HLA-DQ screening for risk assessment of insulin dependent diabetes in northern Italy.

Genetic markers may be used to improve the prediction of insulin-dependent diabetes mellitus (type 1) in individuals with islet autoantibodies. In order to develop a risk assessment strategy for the Lombardy region of northern Italy based on genetic and immunological markers, we analyzed HLA DQA1 and DQB1 alleles in 60 type 1 probands and their first-degree relatives and 65 unrelated control subjects from the same area using polymerase chain reaction (PCR) and oligonucleotide probes. The major risk haplotypes were DQA1 *0501-DQB1*0201 (39.1% of diabetic vs. 8.9% of non-diabetic haplotypes) and DQA1 *0301-DQB1*0302(20% of diabetic vs 7.1% of non-diabetic haplotypes). Stratified analysis showed DQA1*0102-DQB1*0502 also to be associated with type 1 susceptibility when found together with DQA1*0501-DQB1*0201 or DQA1*0301-DQB1*0302. One type 1 patient had the type 1-protective DQA1*0102-DQB1*0602 haplotype. Overall, 88% of patients and 20% of unrelated control subjects had either DQA1*0501-DQB1*0201 or DQA1*0301-DQB1*0302 in the absence of DQA1*0102-DQB1*0602. These data suggest that typing for markers identifying these three haplotypes in the Lombardy population will achieve a sensitivity of almost 90% and exclude 80% of children from subsequent islet autoantibody testing.

Adolescent↗