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Biomedical subjects

A Bertagna

Publications and source records attributed to A Bertagna.

11 recordsLinked to original sources

Vertebral bone density in non-amenorrhoeic hyperprolactinaemic women.

Recently, a decrease in bone mineral content (BMC) in hyperprolactinaemic women with long-lasting amenorrhoea has been reported, and attributed either to a direct effect of PRL on bone or secondary to the oestrogen deficiency. To verify if PRL by itself has a direct effect on bone, we have studied BMC at the lumbar level by double-photon absorptiometry in 22 patients with hyperprolactinaemia, selected on the basis of normal or near-normal oestradiol levels. The results were compared with those obtained in 28 healthy closely-matched women, and seven hyperprolactinaemic patients with long-lasting amenorrhoea and oestrogen deficiency. No significant difference in BMC was observed between hyperprolactinaemic patients with normal oestrogen levels (mean +/- SEM = 3.87 +/- 0.10 gHA/cm) and normal subjects (mean +/- SEM = 3.76 +/- 0.10 gHA/cm). Moreover, no significant change was observed during a 6 month follow-up in 13 patients. On the other hand, a significant difference (P less than 0.05) was detected in BMC between the hyperprolactinaemic patients with normal oestradiol levels and those with long-lasting amenorrhoea and oestrogen deficiency (mean +/- SEM = 3.39 +/- 0.18). These results suggest that hyperprolactinaemia by itself is not a risk factor for the development of osteoporosis.

Adult

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

Growth hormone responses to pyridostigmine in normal adults and in normal and short children.

There is evidence indicating that the cholinergic system positively modulates GH release probably by inhibiting somatostatinergic tone. In the present study, the effects of cholinergic enhancement by pyridostigmine, (PD), a cholinesterases inhibitor, on GH release in normal adults (n = 14) (NA) and in both normal (n = 5) (NC) and short children (n = 19) (SC) with familial short stature (n = 7) or constitutional growth delay (n = 12) were studied. In SC the insulin hypoglycaemia (IH)-induced GH increase was also studied. In both NC and SC 60 mg orally PD induced a significant GH increase with mean peak at 90 min (mean +/- SEM 11.0 +/- 2.2 ng/ml in NC and 11.2 +/- 2.3 ng/ml in SC). The GH areas under response curve (AUC) were 379.3 +/- 76.6 and 327.8 +/- 43.2 ng/ml/h in NC and SC respectively. In NA 120 mg orally PD induced a significant GH increase with mean peak at 120 min (5.1 +/- 1.1 ng/ml) which was significantly lower (P less than 0.05) than that observed in both NC and SC. This statistical difference was strengthened by evaluating AUC (NA:205.6 +/- 33.7 ng/ml/h, P less than 0.05 vs NC and SC). The correlation of drug dosage with body area ruled out that this difference could be related to the different PD dose in adults and children. In SC, IH induced a GH increase significantly lower than that observed after PD (GH peak 7.8 +/- 0.6 vs 16.4 +/- 1.9 ng/ml P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

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

Effect of metoclopramide, domperidone and apomorphine on GH secretion in children and adolescents.

The way in which the dopaminergic system controls GH secretion in infancy and adolescence was investigated by studying the effects on GH of a specific dopaminergic agonist apomorphine, and two antagonists, metoclopramide (MC), which can and domperidone (DOM), which cannot cross the blood-brain-barrier, (BBB), in 14 males and 6 females aged 8-17 years. Treatment with both antagonists was followed by a marked increase in Prl, whereas only MC stimulated GH secretion, suggesting that this action must occur inside the BBB if it is linked to antidopaminergic properties. GH secretion was also stimulated by apomorphine, which acts at the central level. The paradox posed by the presence of a central effect on GH secretion derived from both an agonist and an antagonist of the dopaminergic receptors is discussed.

Adolescent

[Determination of LH and FSH levels before and after prostatic adenomectomy (author's transl)].

Plasma testosterone, LH, and FSH levels were measured in 29 patients with adenoma of the prostate, before and after adenomectomy. Blood testosterone levels showed significant variations which were probably related to operation stress, as after a moderate reduction--they returned to pre-operative levels. No significant modifications in plasma LH or FSH levels were observed.

Aged