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Biomedical subjects

A Castelli

Publications and source records attributed to A Castelli.

At least 19 recordsLinked to original sources
PubMed1995

Low-dose ovine corticotropin-releasing hormone stimulation test in diabetes mellitus with or without neuropathy.

The function of the hypothalamic-pituitary-adrenal (HPA) axis was evaluated in insulin-dependent diabetics without (group I, n = 10) or with (group II, n = 10) established symptomatic neuropathy and in age- and weight-matched normal controls (n = 11). Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. Experiments started at 8:30 AM, when CRH was injected after two basal blood samples were withdrawn, and lasted 2 hours. Basal serum levels of ACTH were similar in the three groups. Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. Furthermore, a significantly lower ACTH response was observed in group II than in group I. In contrast, basal and CRH-induced cortisol levels were significantly higher in diabetics than in normal controls. Comparisons between diabetic groups showed that both basal and stimulated cortisol secretion was significantly higher in group II than in group I. When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). These data show that even uncomplicated diabetes mellitus is associated with adrenal hyperfunction. Such an alteration is more pronounced in the presence of neuropathy.

Adrenocorticotropic Hormone↗
PubMed1995

Prolonged treatment with ursodeoxycholic acid for primary biliary cirrhosis.

Eighteen patients affected with biopsy-proved primary biliary cirrhosis (PBC) (histological stage III and IV) received ursodeoxicholic acid (UDCA) 600 mg for 1 year. Signs and symptoms and biochemical tests (glutamic and oxalcetic transaminase, glutamic and pyruvic transaminase, bilirubine, gamma-glutamyl transpeptidase, alkaline phosphatase, leucine aminopeptidase, bile acids, plasma proteins electrophoresis, immunoglubulins A, G and M) and antimitochondrial antibodies were evaluated before the treatment and every four months during the treatment. The results were compared with those obtained in 8 untreated patients affected PBC. The control group of patients were comparable (as far as age, histological stage, biochemical tests are concerned) to the group who received UDCA. Bilirubine, ALP, gamma-GT and LAP decreased during the treatment with UDCA and remained lower than baseline values until the end of the observation (12 months), while no changes occurred in the untreated patients. Both in the treated and untreated group plasma protein electrophoresis, serum immunoglubulins A, G and M remained unchanged, as well as anti-mitochondrial antibody. A moderate reduction of transaminases and bile acids was observed in the group of patients receiving UDCA but it did not reach statistical significance. In 16 out of the 18 treated patients pruritus disappeared and resulted diminished in the remaining 2 patients. No significant amelioration of pruritus was observed in the patients who did not receive UDCA. In conclusion, our data show that prolonged treatment with UDCA drastically reduces pruritus and improves cholestasis biochemical tests in patients affected with symptomatic PBC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Insulin therapy in uremic diabetic patients on continuous ambulatory peritoneal dialysis; comparison of intraperitoneal and subcutaneous administration.

OBJECTIVE: To compare, in diabetic uremic patients on continuous ambulatory peritoneal dialysis (CAPD), the effects of two patterns of insulin administration, four times daily subcutaneous (SC) injections and intraperitoneal (IP) route, on blood glucose, insulin, lactate, beta-hydroxybutyrate and glycerol levels. PATIENTS AND METHODS: We examined 6 uremic insulin-dependent diabetic patients on CAPD. The two insulin regimens, SC and IP, were tested successively in randomized sequence in each patient. At the end of each treatment period we determined the 24-hour profiles of blood glucose, free insulin, lactate, beta-hydroxybutyrate, and glycerol. RESULTS: Mean blood glucose over 24 hours (SC 7.21 +/- 0.61 mmol/L, IP 7.49 +/- 0.93 mmol/L), Schlichtkrull's M value, an index of glycemic control and stability (SC 10 +/- 3, IP 10 +/- 5), and the blood intermediate metabolites beta-hydroxybutyrate, lactate, and glycerol were similar in both groups. Mean serum free insulin was significantly higher during subcutaneous treatment (SC 257.4 +/- 127.2 pmol/L, IP 170.4 +/- 83.4 pmol/L, p < 0.001). Insulin requirements were 2.5 times greater for the intraperitoneal route (SC 51 +/- 4 U/24 hours, IP 130 +/- 43 U/24 hours). CONCLUSIONS: In uremic diabetic patients on CAPD, good glycemic control may be achieved either with subcutaneous intensive insulin therapy or with intraperitoneal insulin administration. The latter method allows reduction of circulating free insulin levels, but requires a higher dose of insulin per day.

Blood Glucose↗
PubMed1992

Effects of mexiletine, propafenone and flecainide on signal-averaged electrocardiogram.

The effects of mexiletine, propafenone and flecainide on the parameters of signal-averaged electrocardiogram in 40 subjects with symptomatic and repetitive ventricular arrhythmias were studied. Mexiletine (n = 16) suppressed ventricular arrhythmias in 10 patients and did not produce any significant changes in filtered QRS duration (fQRS), root mean square voltage of the final 40 ms of filtered QRS (RMS40) or low amplitude terminal component duration (LAS40). Acute (n = 8, 450 mg) and chronic (n = 16, 600-1200 mg.day-1) administration of propafenone determined a significant increase in fQRS (from 123 +/- 2.2 to 139 +/- 3 ms) and a reduction in RMS40 (from 54 +/- 8.8 to 34 +/- 6.7 microV); as a consequence the incidence of ventricular late potentials rose from 43 to 62%. The observed effects were independent of anti-arrhythmic efficacy, which was 86% for this drug. Acute (n = 8, 200 mg) and chronic (n = 13, 200-300 mg.day-1) administration of flecainide was associated with a marked prolongation in fQRS (from 123 +/- 2.8 to 138 +/- 4.1 ms) and a reduction in RMS40 (from 69 +/- 11.5 to 47 +/- 11 microV); thus determining an increase in the incidence of ventricular late potentials from 29 to 48%. Changes in signal-averaged electrocardiogram were not related to drug efficacy, which was 81%. These data indicate that 1c anti-arrhythmic drugs consistently modified the parameters of signal-averaged electrocardiogram; the observed changes might reflect an inhomogeneous slowing of intramyocardial impulse propagation.

Adult↗
PubMed1991

Luteinizing hormone responses to gonadotropin-releasing hormone and naloxone in menstruating women with type I diabetes of different duration.

Luteinizing hormone (LH) responses to gonadotropin-releasing hormone (GnRH) (100 micrograms injected intravenously (IV)) or naloxone (4 mg injected plus 8 mg infused in 2 hours IV) were evaluated in 29 women with insulin-dependent diabetes mellitus (IDDM) (duration, group I (n = 15): less than 10 years, range 3 to 9 years; group II (n = 14): greater than 10 years, range 11 to 20 years) and in 15 normal controls, on the 22nd days of normal menstrual cycles. Both GnRH- and naloxone-induced LH responses were similar in group I diabetics and normal controls, whereas they were significantly lower in group II than in group I diabetics or normal controls. Positive correlations were found between LH responses to GnRH and naloxone, whereas negative correlations were observed between maximal LH peaks in response to GnRH or naloxone and duration of diabetes. These data indicate that a hypothalamic pituitary disorder affects LH secretion with time after the onset of IDDM.

Adult↗
PubMed1991

Reduction of baclofen-, but not sodium valproate-induced growth hormone release in type I diabetic men.

The effects of sodium valproate (a drug enhancing endogenous gamma aminobutyric acid (GABA)-ergic activity) and of the GABA analog baclofen (a GABA B receptor agonist) on serum GH levels was tested in 8 type I diabetic men and 8 normal controls. Sodium valproate (800 mg) or baclofen (10 mg) were given by mouth at 08.30 h on the experimental day. Control tests with a placebo were performed on different occasions. Basal GH levels were similar in controls and diabetic patients. Sodium valproate induced a 7 fold increase in serum GH concentrations in both groups. In contrast, baclofen-induced GH rise was significantly higher in normal controls (mean peak was 3.4 times higher than baseline) than in diabetic patients (mean peak was only 2.1 times higher than basal value). Serum GH levels did not change after placebo administration in any groups. These data suggest the presence of diabetes-induced alterations of a GABAergic pathway mediated by B receptors in the control of GH secretion. Alternatively, the data might indicate a change in diabetic men of other baclofen-sensitive neurotransmissions, different from GABA.

Adult↗
PubMed1991

Juvenile pemphigus vulgaris: efficacy of moderate doses of deflazacort.

A 13-year-old girl with pemphigus vulgaris (PV) had clinical features of chronic stomatitis. The histologic and immunologic findings were typical of a diagnosis of PV. Good therapeutic results were obtained with moderate doses of deflazacort, 1 mg/kg/day slowly tapered to 0.1 mg/kg every other day. The patient had no significant side effects.

Adolescent↗
PubMed1990

Increase by naloxone of arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia in obese men.

The present study was carried out to establish whether the low arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia observed in obese men was due to alteration of the opioid control of posterior pituitary function. For this purpose, the AVP and OT releasing effect of insulin (0.15 IU/kg bw)--induced hypoglycemia was tested in eight normal weight men and in 10 age-matched obese subjects, without and with the previous treatment with the specific opioid receptor antagonist naloxone (3 mg in an iv bolus). In a control study, naloxone was given alone to the same subjects. Obese men showed similar basal glucose, AVP and OT levels, which remained unmodified after treatment with naloxone alone. Insulin induced a similar decrement of blood glucose levels in all subjects, with a nadir at 30 min. Plasma levels of AVP and OT rose strikingly in normal and obese subjects with mean peak responses at 30 min for AVP and at 45 min for OT. However, both AVP and OT responses were significantly lower in obese than in control subjects. Pretreatment with naloxone did not modify the AVP and OT responses to hypoglycemia in normal weight subjects, whereas it significantly enhanced both hormonal responses in obese subjects. In the presence of naloxone normal controls and obese subjects showed similar responses of both AVP and OT to hypoglycemia. These data indicate that an abnormal activity of endogenous opioids might account for the hypothalamic posterior pituitary dysfunction, which is responsible for the low AVP and OT responses to insulin-induced hypoglycemia in obesity.

Adult↗
PubMed1989

Time-resolved fractionation of bone and liver alkaline phosphatase activities with a 'peeling-off' method.

A procedure for the selective fractionation of the bone and liver alkaline phosphatase activity in tissue extracts and human sera is proposed. Optimized conditions of the assay are: urea 3.7 mol/l in 0.5 mol/l DEA buffer, pH 9.8; 0.5 mmol/l MgCl2; 10.0 mmol/l p-nitrophenyl phosphate. The sample is diluted 1:20 in the reagent solution and the activity is recorded for 10 min at 37 degrees C. By means of a computerized or manual graphic analysis, based on 'peeling-off' the exponentials, the two differently urea-sensitive subforms are identified and the slow-(liver) and the fast-decaying (bone) activities are easily discriminated and their respective values calculated. Interference due to the intestinal isoenzyme can be also accounted for. The analytical variability is very satisfactory (within run CV = 7.5 and 4.5% for osseous and hepatic form, respectively; day-to-day CV less than 10% for both). The lower limits of detection are about 10 U/l and the serum or plasma reference values together with the influence on the assay of hemoglobin and protein content are also investigated.

Adult↗
PubMed1989

Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression.

The present study was undertaken in order to establish whether muscarinic cholinergic receptors are involved in the anomalous GH response to GnRH in men with insulin-dependent diabetes mellitus and in male patients with major depression. For this purpose, 16 male diabetics, 18 depressed men and 9 normal controls were tested with GnRH (25 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before GnRH). Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. The administration of GnRH stimulated GH release in 12 out of the 16 diabetics and in 8 out of the 18 depressed patients, but not in the normal controls. Control and diabetic non-responders to GnRH did not respond to TRH. In contrast, all diabetic responders to GnRH, except 2, showed paradoxical GH responses to TRH. All depressed responders to GnRH and 3 of the non-responders, were responsive to TRH. The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression.

Acetylcholine↗
PubMed1989

[Naloxone doesn't determine the response of growth hormone to clonidine in obese patients].

The effect of naloxone (opioid receptor blocker) on the impairment of growth hormone (GH) release after clonidine (alfa 2-adrenergic agonist) was investigated in 10 volunteer obese subjects. The patients (4 males and 6 females, 16-22 year old) with fat excess (15 +/- 2 kg) estimated by bioelectrical impedance analysis (BIA) were studied repeatedly. The patients, were perfused by a slow saline infusion. 30 min later they received a bolus dose of clonidine (150 micrograms p.o.), followed 30 min later by a bolus dose of naloxone (10 mg i.v.) or a corresponding volume of isotonic sodium cloride (I.S.) for control. No significant changes occurred in blood GH concentration after clonidine administration and naloxone did not induce GH response at clonidine. These results suggest that in obese subjects the impairment of GH release after clonidine is not mediated via receptors sensitivity to naloxone.

Adolescent↗
PubMed1988

Mixed function oxidation and enzymes: kinetic and structural properties of an oxidatively modified alkaline phosphatase.

No major structural alteration of alkaline phosphatase can be observed in the early stages of enzyme oxidative inactivation by the ascorbate model system. Fluorescence changes of protein-bound 8-anilino-1-naphthalenesulfonic acid suggest, however, that localized modifications take place. Oxidized alkaline phosphatase displays less catalytic efficiency (decrease of Vmax), while retaining the other kinetic properties, including the same affinity for substrates and inhibitors and the same activation energy of the native enzyme. Typical features of the modified protein are a decreased thermal stability and a biphasic heat inactivation profile, which make the oxidized form quite similar to aged enzymes. The lower response to Mg2+ activation indicates that the magnesium binding sites of alkaline phosphatase are probably the targets of the ascorbate system oxidative modifications.

Alkaline Phosphatase↗
PubMed1988

Metergoline, naloxone, and sodium valproate did not modify arginine vasopressin response to insulin-induced hypoglycemia in man.

The present study was carried out in order to determine whether insulin-induced hypoglycemia exerts its stimulatory effect on plasma concentrations of arginine vasopressin (AVP) by interacting with a serotonergic, a GABA-ergic or an opioid pathway. For this purpose, the effect of the serotonergic antagonist metergoline (10 mg/day for 4 days po), the GABA-ergic agonist sodium valproate (600 mg in three divided doses po) and the opioid-receptor blocker naloxone (10 mg in a iv bolus) on the AVP response during an insulin (0.15 IU/kg bw) tolerance test (ITT) was evaluated in three groups of 6 normal men each. In all men, control ITTs were performed without drug treatments. Basal and ITT-stimulated AVP secretion was not modified by drug administration, suggesting that serotonergic, GABAergic and naloxone-sensitive opioid receptors are not involved in the regulation of AVP secretion in response to insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗
PubMed1987

Early conformational changes and activity modulation induced by guanidinium chloride on intestinal alkaline phosphatase.

Moderate concentrations of guanidinium chloride induce both instantaneous and time-dependent modifications of the catalytic and optical properties of intestinal alkaline phosphatase, which undergoes consecutive conformational transitions at about 0.05 M, 0.25 M and 1.0 M denaturant. A paradoxical activation is observed up to 1.0 M-guanidine, with a maximum at 0.25 M- and a mid-point around 0.5 M-guanidine. Difference absorbance and fluorescence spectra imply a change in the state of ionization of the protein residues, with variation in molecular size suggested by light-scattering. Random-coil formation is indicated by a lower fluorescence yield, a more polar environment of the aromatic residues and another separate tryptophan emission. Iodide quenching confirms the alterations of conformation. Deprotonation favours the loss of the intramolecular constraints and the enhancement of the structure disruption by guanidine.

Alkaline Phosphatase↗
PubMed1987

Alkaline phosphatase inactivation by mixed function oxidation systems.

Alkaline phosphatase is inactivated by mixed function oxidation systems. OH. radicals, generated via an ascorbate-modified Haber-Weiss cycle or a Fenton-type reaction, seem to be responsible for the protein oxidative damage. Experiments with hydroxyl radical scavengers, enzyme substrates, products, and metal cofactors suggest that a "site-specific" radical attack takes place at or near the active center. Vitamin E fails to protect alkaline phosphatase; uric acid, instead, is particularly effective in shielding the protein against covalent modifications.

Alkaline Phosphatase↗
PubMed1986

The relationship between the optical properties and the kinetic behaviour of ascorbate-inhibited alkaline phosphatase.

Aromatic residues of bovine kidney alkaline phosphatase appear to be involved in the interaction with ascorbate, as shown by the strong quenching of intrinsic fluorescence and absorption. Difference u.v.-absorption spectra clearly indicate that conformational changes also occur. The pH value at which the greatest fluorescence deactivation is found is close to that necessary for optimal catalytic activity and for maximal inhibition by ascorbate. A protective effect against ascorbate is afforded by Pi. Time profiles of inactivation on one side and of absorbance and emission quenching on the other display opposite behaviours. Attempts to reverse the effects by the use of KOH fail to restore enzyme activity or to modify the spectral effects of ascorbate. The protein alterations are related, directly or indirectly, to the enzyme active centre and can be probably ascribed to the redox and chelating properties of ascorbate.

Alkaline Phosphatase↗