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Biomedical subjects

M Bigazzi

Publications and source records attributed to M Bigazzi.

62 records · Page 4Linked to original sources
PubMedDate not supplied

Inherited X chromosome linked thyroxine-binding globulin (TBG) deficiency in a homozygous female.

Of the 37 families with TBG deficiency so far described, 31 were shown to be compatible with X chromosome linked mode of inheritance, and in 5 of the remaining 6 this mode of transmission was suspected. Difficulties in proving X chromosome linkage in some families was usually due to the inability to identify the heterozygous female carriers when affected males were only partially TBG deficient. This work describes a new family with inherited TBG deficiency which on first glance showed inconsistencies with X chromosome linked inheritance. More specifically, there was an apparent male to male transmission of the trait and the presentation in one female of low TBG, phenotypically indistinguishable from the affected males. Studies on three generations identified TBG deficiency on both the maternal and paternal branches of the family. We were thus able to prove that the affected male inherited the trait from his heterozygous mother, rather than from his father, and that the female with more severe TBG deficiency was homozygous for the trait through acquisition of a defective X chromosome from both mother and father. The latter explained her phenotype presentation indistinguishable from that in affected hemizygous males. Thus, unless proven otherwise, all inherited TBG abnormalities in man appear to be X chromosome linked. Because of the relatively common prevalence of inherited TBG defects, marriages among such individuals are expected to give rise to a progeny with an unusual phenotypic presentation. All members of the family were clinically euthyroid and affected members showed a normal TSH response to TRH.

Adolescent↗
PubMedDate not supplied

Age- and sex-related variations of serum thyroxine binding globulin.

Measurements of serum thyroxine binding globulin (TBG) by a ligand partitioning sandwich assay were performed in 173 healthy subjects between three months and 92 yr of age. Significant sex-related differences were observed in subjects aged 21 to 50 yr. In males, serum TBG declined progressively reaching a nadir in the fourth decade and then increased with advancing age. In contrast, no significant age-related variation was observed in females.

Adolescent↗
PubMedDate not supplied

Relaxin, a potent microcirculatory effector, is not angiogenic.

The ability of relaxin (RLX), which is a potent microcirculatory effector in many species including the rat, to induce de novo angiogenesis in vascularized mammalian tissue was tested using the rat mesenteric-window angiogenesis assay. RLX was administered intraperitoneally on days 1-5 at doses of 0.33, 3.3 and 33 nM. Controls received the vehicle by the same route. Groups of animals were sacrificed at the end of the 1st, 2nd and 3rd weeks. Using computer-aided microscopic morphometry including image analysis, the response was quantified by sensitive, technically independent, highly reproducible methods in terms of the vascularized area (VA), a measure of microvascular spatial extension, and the microvascular length (MVL), a measure of microvascular density. The total MVL was computed from VA x MVL. The results obtained show that RLX did not cause significant changes in any of the variables tested, regardless of dose and observation time. These findings indicate that RLX is apparently unable to mediate significant de novo angiogenesis in the system used in contrast to previously tested angiogens such as basic fibroblast growth factor, vascular endothelial growth factor, isoform 165, and tumor necrosis factor-alpha. In previous studies, RLX has been shown to exert antitumor activity on breast cancer cells in vitro. In the search for a possible role for RLX as an anticancer agent in vivo, it is important to know that this peptide is not angiogenic, since de novo angiogenesis is known to be a prerequisite for tumor growth and metastatic spread.

Animals↗
PubMedDate not supplied

Hyperprolactinemia and 5-alpha-reductase activity.

A number of experimental data indicate that hyperprolactinemia inhibits the activity of 5-alpha-reductase; however, no information is available about the time required for this enzyme to re-activate after prolactinemia has returned to normal values. In the present study, five normal caucasian men, whose fertility had previously been proven, were given HCG (5000 IU/day by intramuscular route for three days) both in basal conditions and after sulpiride-induced hyperprolactinemia (dosage = 200 mg/day for ten days). In both conditions, the plasma levels of prolactin (PRL), testosterone (T), dihydro-testosterone (DHT), 17-beta-estradiol (E2), and dehydroepiandrosterone sulfate (DHAS) were monitored during the treatment with HCG and for an additional 24 hrs after HCG discontinuation. All hormones were assayed by RIA. Our results demonstrate that hyperprolactinemia causes a marked decrease (58%) of DHT, a less marked decrease (39%) of T, an increase (43%) of DHAS whereas only a small increase (2%) of E2 was observed. Steroids were shown to behave differently after the HCG tests performed in the two experimental conditions. In particular, the levels of DHT had a much more pronounced increased after HCG in the second test than in the first; in contrast, both DHAS and E2 had a less marked response after the second test. Our data, on the one hand, confirm that 5-alpha-reductase is inhibited by hyperprolactinemia; on the other hand, the hyperprolactinemia-induced block of this enzyme appears to be rapidly reversible because the enzyme is reactivated within 48-72 hrs after normalization of prolactin levels. (Normal values of prolactin were on the average achieved on the 4th day after sulpiride discontinuation).(ABSTRACT TRUNCATED AT 250 WORDS)

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMedDate not supplied

The response of serum and seminal plasma prolactin to bromocriptine in normal men.

The Authors describe their experience with a group of twelve volunteer healthy men in order to evaluate if the bromocriptine inhibition of serum prolactin concentration also modifies seminal plasma PRL values. The results of this study lead us to suppose that PRL in semen could arrive from serum by a filtration process through the prostatovescicular apparatus.

Adult↗