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Biomedical subjects

A Fantoni

Publications and source records attributed to A Fantoni.

At least 19 recordsLinked to original sources
PubMed1992

Control of human coagulation by recombinant serine proteases. Blood clotting is activated by recombinant factor XII deleted of five regulatory domains.

The availability of engineered serine proteases allows one to study the activation, substrate specificity and regulation of human coagulation and fibrinolytic activities. Human coagulation factor XII is composed of the protease catalytic region at the C-terminus, a hinge proline-rich region and regulatory domains at the N-terminus. From cDNA clones coding for factor XII, two DNA molecules were constructed, one being full length and the other being deleted of exons coding for the regulatory domains. Engineered factor-XII cDNA species were inserted by a homologous recombination technique into vaccinia viruses, which were used to infect the human hepatoma cell line HepG2. Two recombinant proteins were prepared from the culture media and identified by their antigenic properties and electrophoretic mobilities. The recombinant protein of larger size was identified as the full-length factor XII of 80 kDa and its specific activities and activation patterns, determined both by the coagulation and the amidolytic assays, are very similar to these of native human factor XII. The recombinant protein of smaller size was identified as a 319-amino-acid-deleted factor-XII protein of 32 kDa, containing only the entire protease region and part of the proline-rich hinge. This protein was expected to be the 'minimal' portion of factor XII able to sustain protease but unable to recognize substrates and surfaces necessary to activate the contact phase of coagulation. However, this 'minimal' factor-XII protein displays a marked protease activity and, although lacking five regulatory domains of factor XII, is bound and activated by negative charges and promotes coagulation with high efficiency.

Base Sequence↗
PubMed1992

[Thoraco-abdominal binding in the treatment of overdistention of the lung bases in children].

In the patient with homogeneously or inhomogeneously distributed atelectasis, localized primarily in the apices, overdistension of the non-dependent portion of the lung bases, only partially surrounded by the rib cage, is generally observed during mechanical ventilation. This phenomenon is even more pronounced in the neonate and in the infant because their rib cage compliance is almost infinite. In order to protect the lung bases in the event of their overdistension and/or to reexpand the atelectasis of the upper lobes we apply an external resistance, in form of thoracoabdominal binding, to limit the movement of the diaphragm. The degree of the binding's tension is regulated according to the degree of the distension of the lung bases detected on chest x-ray. This restriction was so far applied in 12 children using elastic bandages. We have used the thoraco-abdominal binding with good result in the treatment of atelectasis of the upper lobes, in extensive atelectasis as well as in the treatment of primitive lung bases overdistension, as described in 3 cases reports. We suggest this technique in order to obtain an homogeneous ventilation along the longitudinal axis of the lung. This method does not interfere with prone-supine postural changes, systematically applied in our department, and therefore, the homogeneous ventilation along the vertical axis is also provided.

Abdomen↗
PubMed1990

Carrier detection for hemophilia B: evaluation of multiple polymorphic sites.

DNA analysis was performed in families with hemophilia B. Restriction fragment length polymorphisms (RFLPs) produced by endonucleases Taql, Xmnl, and Ddel were studied by two factor IX genomic probes, F9(VIII) and F9(XIII). Fifty-seven subjects from ten families were investigated; of them, 31 were carriers (11 obligate and 20 potential). Of the potential carriers, ten displayed laboratory features allowing for a phenotypic diagnosis of heterozygosity. Segregation analysis of the markers was informative in 19/20 potential carriers, which belong to nine of the ten studied families. Among the potential carriers, Taql allowed the carriership assessment in 15 (78.9%), Xmnl in 15 (94.7%), and Ddel in two (10.4%). Diagnosis was not possible in one family since a homozygosity in the key individuals with all the employed enzymes (Taql, Xmnl, Ddel, + BamHI) was found. Hemophilia B syndrome in two families likely results from a new mutation. In one family, a first-trimester prenatal diagnosis was performed. The use of RFLP analysis allowed us to improve genetic counseling as compared with the phenotypic evaluation by clotting factor assays. Indeed, evaluation of RFLP increased by 26% the carriership assessment of the potential carriers of the hemophilia B trait.

DNA Probes↗
PubMed1990

Effect of nifedipine on morphine-induced analgesia.

Experimental data show that opiates interfere with calcium influx in the cell and that some calcium-channel blockers are analgesic. We therefore studied the effect of the calcium-receptor blocker nifedipine on the analgesic effect of morphine in the rat, using tail-flick responses, and in humans, using measurements of the intensity of postoperative pain. In both the experimental animals and humans nifedipine significantly (P less than 0.001) increased the analgesic effect of morphine independently of any effect on the metabolism of morphine. Respiratory and cardiovascular functions were not significantly changed by nifedipine. The data indicate that Ca2+ is important in mediating the analgesic effects of opiates and suggest that calcium-receptor blockers might find a place in the treatment of pain.

Adult↗
PubMed1990

[Tumor marker ca. 125 in acute pelvic inflammations].

The paper reports a case of acute pelvic inflammatory disease (PID): the symptoms, diagnostic treatment and therapy, which was carried out according to standard protocols, the operation and the postoperative period were all fully correlated with serum concentrations of the marker ca. 125. Above all, a close interdependence was observed between the clinical regression of disease and the parallel reduction of marker serum levels. The graphic curve of ca. 125 was compared during the postoperative period to the curves expressed by the levels of GB and VES values. The method of monitoring highlighted the parallelism of the three curves with a particular affinity between the ca. 125 and GB curves.

Acute Disease↗
PubMed1990

[Clinical patterns of fibrocystic mastopathy in relation to parity and age].

Two thousand five hundred and twenty cases of fibrocystic mastopathy (FCM) were chosen from a vast population of patients examined during the period from 1980 to 1989. The main clinical symptoms of FCM were assessed in relation to their evolution according to age and parity. Correlations were observed between the clinical symptoms examined and the age range of patients. Parity was also significantly correlated to clinical symptoms of FCM.

Adolescent↗
PubMed1988

Assignment of human coagulation factor XII (fXII) to chromosome 5 by cDNA hybridization to DNA from somatic cell hybrids.

Human coagulation factor XII (fXII), a serine protease synthesized in liver and active in plasma, is involved in a wide variety of functions, including blood coagulation, fibrinolysis, bradykinin and complement activation. A complementary DNA (597 bp) encoding amino acid -16 to amino acid 183 of fXII protein was used to determine the chromosomal location of the fXII gene. DNAs from hamster-human somatic cell hybrids were digested with restriction enzymes and hybridized with the fXII cDNA. By the Southern method it was shown that restriction fragments able to hybridize to fXII cDNA are present only in DNA extracted from clones retaining human chromosome 5.

Animals↗
PubMed1987

Factor XII gene alteration in Hageman trait detected by TaqI restriction enzyme.

A cDNA for coagulation factor XII has been used to investigate the presence of gene lesions and restriction fragment length polymorphisms in two brothers with Hageman trait and their family. A TaqI polymorphic fragment has been found in the two propositi and in 11 members of the paternal lineage. This polymorphism, absent in the normal population, is correlated with the reduction of factor XII activity and enables the identification of heterozygous factor XII deficiency. Factor XII gene deletion as the cause of Hageman trait in this family has been excluded. A restriction map has been constructed, and the TaqI polymorphic site has been localized within the 5' portion of the gene. The mutation in the polymorphic site is probably the cause of the factor XII deficiency. Data suggest the presence of one factor XII gene per haploid genome.

Collodion↗