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Biomedical subjects

G M Molinatti

Publications and source records attributed to G M Molinatti.

At least 19 recordsLinked to original sources
PubMed1992

Influence of estrogens on calcitonin secretion.

In this study we investigated the calcitonin (CT) pattern both in basal conditions and after calcium infusion before and one month after oophorectomy in 17 premenopausal women. In addition, 13 oophorectomized women were randomly allocated to two groups, one given hormone replacement treatment and the other untreated, and CT response to hypercalcemia was reevaluated one year later. CT response to calcium infusion was significant only before oophorectomy and one year after estrogen-progestogen treatment, whereas there was no response one month after oophorectomy or after one year without hormone replacement therapy. Our data indicate that both estrogen secretion and replacement treatment may be important factors in CT response.

Adult↗
PubMed1992

Effect of testosterone on bone in hypogonadal males.

Bone mineral content (BMC) and testosterone levels were evaluated and compared in 10 hypogonadal males and 10 normal, age-matched controls. In 6 of the subjects an investigation was also carried out into the effects of testosterone administration on lumbar BMC, calcitonin (CT) response to hypercalcaemia, osteocalcin (BGP) and the fasting urinary calcium/creatinine and hydroxyproline/creatinine ratios. Our results confirm that male hypogonadism is characterized by a low BMC and that testosterone administration is able to improve this parameter and to increase both basal BGP and CT response to hypercalcaemia. Testosterone therefore probably acts on bone tissue through both a direct action on osteoblast cells and an improvement in CT secretion.

Adult↗
PubMed1992

Delayed replication of human umbilical vein endothelial cells in high glucose is corrected by L-tyrosine.

Human umbilical vein endothelial cells (HUVEC) cultured in high glucose exhibit delayed replication and colchicine-resistant microtubules. Tubulin dysfunction and stabilization, brought about by acetylation of the NH2-terminal residues, loss of the C-terminal tyrosine and binding of microtubular-associated proteins (MAPs) may be involved in the above phenomenon. The effects of L-tyrosine on HUVEC replication in high glucose were tested and the hypothesis that non-enzymatic glycosylation might impair tubulin depolymerization was also checked by growing the cells in the presence of L-glucose, which binds to intracellular proteins but remains metabolically inactive. After 18 days in culture, the number (mean +/- SEM, n = 7) of HUVEC grown in 28.0 mmol/l D-glucose (435.7 +/- 59.1 x 10(3)) was lower than in 5.6 mmol/l D-glucose (818.3 +/- 75.2 x 10(3)), p < 0.0001. The addition of L-tyrosine 1.7 mmol/l corrected such growth inhibition (623.3 +/- 81.7 x 10(3)), p < 0.0001 vs. D-glucose 28.0 mmol/l, but the cells recovered were less numerous than in physiological glucose alone (p = 0.016). The addition of L-tyrosine to D-glucose 5.6 mmol/l (731.0 +/- 63.2 x 10(3)) did not modify the cell number significantly. HUVEC in extra L-glucose (687.4 +/- 72.0 x 10(3)) were less numerous than in 5.6 mmol/l D-glucose, p = 0.028, but more than in D-glucose 28 mmol/l, p < 0.0001, and were not modified by the addition of L-tyrosine (729.4 +/- 67.1 x 10(3)). HUVEC grown in physiologic and high glucose exhibited specific immunofluorescence for acetylated tubulin and MAPs.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Division↗
PubMed1990

Primary pigmented micronodular disease of the adrenals.

Primary pigmented micronodular disease is a peculiar form of ACTH-independent Cushing's syndrome characterized by the familial occurrence, the frequent association with malformations and the pathological adrenocortical picture consisting in micronodules with cellular deposition of lipofuscinic pigment. We describe here a case occurring in a 14-year-old girl.

Adipose Tissue↗
PubMed1990

Vertebral bone loss in menopause.

A direct correlation between loss of ovarian function and reduction of bone mass is well established. The incidence of fractures sharply increases with age starting from the menopause. Therefore, it is very important to know the rate of bone loss occurring after menopause, at both trabecular and cortical levels. Several factors may contribute to the reduction of bone mass in menopause. Reduced estrogen secretion results in reduced intestinal calcium absorption, increased bone resorption, and probably a deficient production of calcitonin. Furthermore, in vivo and in vitro experimental data confirm that estrogen failure is associated with histologic changes, mirroring the biochemical changes described in postmenopausal osteoporosis.

Aged↗
PubMed1990

[Effect on phospho-calcium metabolism of testosterone administration in hypogonadal males].

Many authors have shown that osteoporosis is an important complication in male hypogonadism, due to the chronic lack of androgens; but in hypogonadal males the pathogenesis of osteopenia isn't completely explained. In this work we examined in 10 hypogonadal males (4 with Klinefelter's Syndrome and 6 with Hypogonadotropic Hypogonadism) lumbar bone mineral content (BMC) and the effects of testosterone (Sustanon) administration on BMC and other phosphocalcium parameters. We evidenced lower BMC levels in hypogonadal subjects if compared to those observed in the control age-matched group; moreover after 3 months of treatment a statistically significant increment of plasma bone gla protein, calcitonin and lumbar BMC was observed. On the contrary no significant variation was observed in osteoclastic indexes (PTH-MM, OHPU/CrU, CaU/CrU) after treatment. In addition both calcitonin basal levels and secretory reserve, measured with calcium infusion, were significantly increased after treatment. Our data confirm the hypothesis that androgen acts on bone principally directly at osteoblastic level, in a stimulatory manner, and indirectly, with calcitonin mediation, with inhibition of osteoclasts.

Adolescent↗
PubMed1989

Calcitonin and lumbar bone mineral content during oestrogen-progestogen administration in post-menopausal women.

It now appears to be accepted that oestrogens and progestogens can help to prevent post-menopausal bone loss. This study accordingly evaluated vertebral bone mineral content (BMC) patterns and changes in calcitonin (CT) secretion in 12 women who had been ovariectomized in the previous 6 mth and in 12 others who had had a natural menopause, all of whom received oestrogen-progestogen replacement therapy for 12 mth. We also studied 12 oophorectomized and 21 normal-menopause women who did not receive any treatment and hence constituted the corresponding control groups. A significant difference was found between the lumbar BMC in the treated women and the controls. Moreover, the CT levels rose significantly after replacement therapy in both the oophorectomized and the natural-menopause subjects. It was concluded that combined oestrogen-progestogen treatment can prevent post-menopausal bone loss and increase CT secretion.

Bone Density↗
PubMed1988

Diagnostic notes--lumbar BMC reproducibility as evaluated by means of dual photon absorptiometry.

Three evaluations of lumbar bone mineral content (BMC) were carried out at different times at intervals of a few days in 10 normal volunteers aged between 18 and 60. The dual photon absorptiometry technique was employed (using gadolinium-153 as radioactive isotope). Data on 20 subjects aged from 23 to 62 were recorded on magnetic tape and processed ten times by the same operator. The data for individual subjects proved satisfactorily reproducible and the repeated processing of a single scan by the same investigator gave very satisfactory results. The findings demonstrate that the evaluation of lumbar BMC by dual photon absorptiometry can provide highly reproducible and acceptably accurate data.

Adult↗
PubMed1988

[Endothelium and its morphofunctional changes in the pathogenesis of diabetic microangiopathy].

Recent advances in our knowledge of endothelial function in health and in the presence of generalized microvascular damage, such as found in diabetic microangiopathy, are discussed in this review article. In microangiopathy there are no typical morphological signs of endothelial stress, apart from ubiquitous thickening of the basement membrane and the finding of both hyper- and acellular capillaries, whereas important derangements of endothelial function may occur in the early stages of the disease, like accelerated turnover, intracellular accumulation of potentially toxic intermediate metabolites, hyperpermeability of the vessel wall, altered synthesis of some haemostatic factors, expression of angiogenetic potentialities in inappropriate situations. The possible pathogenetic mechanisms underlying such alterations are reviewed, with special emphasis on the shortcomings of the experimental models available for laboratory investigation and on the in vivo situation.

Animals↗
PubMed1988

High glucose concentrations inhibit DNA synthesis and replication without causing death or impairing injury repair in cultured human endothelial cells.

Endothelial cells are directly exposed to the metabolic derangements of diabetes mellitus and may be damaged early, if not primitively, in the pathogenesis of diabetic microangiopathy. Cultured human umbilical vein endothelial cells were subjected to equimolar concentrations of glucose or mannitol for the evaluation of 3H-thymidine uptake, cell replication, cell death and repair of standard mechanical lesions. 3H-thymidine uptake was inhibited dose-dependently and to a similar extent by both glucose and mannitol. The former reduced cell replication whereas the latter did not (p less than 0.01 at 27.8 mmol/l, p less than 0.001 at 50.0 mmol/l). Neither caused excess cell death nor interfered with lesion repair. These results suggest that supra-physiological amounts of glucose inhibit DNA synthesis with osmotic mechanisms, delay cell replication through at least partially non osmotic effects, do not cause excess cell death and do not impair local injury repair. The above effects may play a role in the pathogenesis of long-term complications of diabetes.

Cell Count↗
PubMed1988

Effect of cortisol on the native and in vitro induced non-MHC restricted cytotoxicity of large granular lymphocytes.

Natural Killer (NK) activity has been shown to be depressed under stressful conditions. Glucocorticoids, which are known to increase during stress, seem to negatively regulate the activity of NK cells. In the present study we have explored the effect of cortisol (hydrocortisone, HC) on NK activity. A significant inhibitory effect could be observed as early as 6 hr after the addition of HC at the concentration of 0.5 microM, corresponding to the upper physiological circulating level. Both the lysis and the binding of the K562 target cells were affected by HC, indicating that the hormone acts on the target recognition phase. The HC-mediated inhibition of the NK activity was fully reversed after 6 hr incubation in a HC-free medium. The observation of comparable levels of NK-inhibition using unseparated PBL or purified LGL, show that HC acts directly on LGL to inhibit their cytotoxic function. The effect of HC on the responsiveness of NK cells to the modifiers beta-interferon (beta-IFN) and recombinant interleukin 2 (rIL2) was also studied. Pre-incubation with HC did not alter the enhancement of the activity induced by beta-IFN, demonstrating that the HC- and beta-IFN-mediated effects occur in separate NK subsets. By contrast the increase of NK cytotoxicity induced by rIL2 was lower in the HC-treated compared to the untreated cell cultures (35.8 +/- 6.2 and 20.7 +/- 4.3% respectively, p less than 0.05) which could indicate that a portion of the cells triggered by rIL2 belong to the HC-sensitive NK subpopulation.

Cell Line, Transformed↗
PubMed1988

[Treatment of differentiated carcinoma of the thyroid gland].

In this paper the Authors, after a description of the prognostic factors in patients with differentiated thyroid carcinoma, propose a rationale for the therapy. The role of surgery, radioiodine treatment, endocrine therapy, radiotherapy and chemotherapy is described. The follow-up for the disease is briefly outlined. The authors suggest that treatment and follow-up protocols should be in accordance with the prognostic factors.

Adenocarcinoma↗
PubMed1988

[Recent diagnostic and therapeutic findings on postmenopausal and senile osteoporosis].

The incidence of osteoporosis in the West is considerable and its complications are such as to make it a common and disabling problem. Recent developments in the classification, pathogenesis and diagnosis of the disease are reported. Certain laboratory techniques have recently been developed that can provide adequate information about the degree of demineralisation present. Furthermore the accurate in vivo assessment of bone density is made possible by the development of double beam photon osteodensitometry that measures bone mineral content (BMC) with sensitivity and accuracy. On the treatment side, the various drugs available are reviewed with particular reference to estrogen, vitamin D, anabolisers (recently reassessed in radiogrammometric and densitometric studies) fluorides and calcitonin. Finally certain treatment protocols for post-menopausal and senile osteoporosis are proposed that should produce good results in a reasonably short space of time.

Aged↗
PubMed1987

Antiandrogens and hirsutism.

The clinical appearance of female idiopathic hirsutism and its pathophysiological aspects and the antiandrogen drugs in relation to the therapy of hirsutism are discussed. Two compounds have been widely employed, namely cyproterone acetate, mainly in the 'reverse sequential regimen', and spironolactone, with or without the association of a contraceptive pill containing cyproterone acetate and ethinylestradiol. The ability to compete with dihydrotestosterone in skin androgen receptors, shared by these two compounds, has led to excellent clinical results for many years. A topical antiandrogen therapy would be a further advantage for these patients.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Levels of serum angiotensin-converting enzyme before and after forearm venous stasis in diabetic microangiopathy.

The levels of angiotensin-converting enzyme and Factor VIII-related antigen, 2 endothelial synthesized glycoproteins, were measured in basal conditions and after forearm venous stasis in 12 healthy controls and 12 patients with diabetic microangiopathy. Angiotensin-converting enzyme levels were similar in the controls and in the patients both basally (185 +/- 17 nm/ml/min (SEM) and 192 +/- 15, respectively) and after stasis (238 +/- 17 and 220 +/- 15), whereas Factor VIII-related antigen was lower in the former basally (101 +/- 13% vs 184 +/- 16%, p less than 0.001) and after stasis (140 +/- 21% and 243 +/- 21%, p less than 0.01). It is concluded that Factor VIII-related antigen is a more sensitive indicator of endothelial cell damage in diabetic microangiopathy than angiotensin-converting enzyme.

Antigens↗
PubMed1986

[Lactic acidosis].

Lactic acidosis is a metabolic disturbance characterized by an increase of the production/clearance ratio of lactate. Lactate is a catabolite of glycolysis when this takes place under anaerobic conditions. Clinically LA is characterized by: signs of acidosis, venous blood lactate greater than 5 mMol/l, arterial pH less than 7.25. LA is classified in type A, due to shock, and type B which, in turn, can be divided according to its pathogenesis in B1 correlated to particular pathologies, B2 due to exogenous substances and B3 caused by congenital metabolic diseases. LA is of particular interest in type II diabetes mellitus treated by phenformin. Current therapeutic directions, although suboptimal, are: to eliminate the causes of lactate hyperproduction by maintaining a sufficient efficiency of the cardio-vascular apparatus, to correct acidosis by using alkalinizing solutions, to remove pharmacologically or by dialysis the excess of lactate.

Acidosis↗