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Biomedical subjects

G Baldi

Publications and source records attributed to G Baldi.

At least 19 recordsLinked to original sources
PubMed2000

Risk of hydrocyanic acid release in the electroplating industry.

This paper suggests assessing the consequences of hydrocyanic acid (HCN) release into the air by aqueous cyanide solutions in abnormal situations such as the accidental introduction of an acid, or the insertion of a cyanide in a pickling bath. It provides a well-defined source model and its resolution by methods peculiar to mass transport phenomena. The procedure consists of four stages: calculation of the liquid phase concentration, estimate of the HCN liquid-vapour equilibrium, determination of the mass transfer coefficient at the liquid-vapour interface, evaluation of the air concentration of HCN and of the damage distances. The results show that small baths operating at high temperatures are the major sources of risk. The building up of lethal air concentrations, on the other hand, is governed by the values of the mass transfer coefficient, which is itself determined by the flow dynamics and bath geometry. Concerning the magnitude of the risk, the fallout for external emergency planning is slight in all the cases investigated.

Air Pollution↗
PubMed2000

Certification of an emergency department according to UNI EN ISO 9002 criteria.

Over the past decade, the philosophy of total quality has appeared in all fields of industry in Japan and the USA. This philosophy is now present all over Europe as well, Italy included. In 1993 the Arcispedale Santa Maria Nuova of Reggio Emilia, a town in Northern Italy, began to apply the total quality management philosophy, thus embarking on a course of continuous quality improvement. The present article describes the main steps which led to an external accredited team granting the emergency department of this hospital a quality system certificate in 1997 according to the international quality system requirements UNI EN ISO 9002. The importance of this work lies in the fact than an industrial quality standardization system, whose requirements have little in common with a traditional view of medical practice, can nevertheless be applied to a public health care department.

Accreditation↗
PubMed1999

Glucocorticoid receptors in anorexia nervosa and Cushing's disease.

BACKGROUND: Patients with anorexia nervosa do not display cushingoid features in spite of elevated cortisol plasma levels. Whether a cortisol resistance or a reduced availability of the metabolic substrates necessary to develop the effect of glucocorticoids is responsible for this has not been established. METHODS: Twenty-two patients with severe restrictive anorexia nervosa, 10 patients with active Cushing's disease, and 24 healthy volunteers without psychiatric disorders or mood alterations were investigated. Glucocorticoid receptor characteristics were examined on mononuclear leukocytes by measuring [3H]dexamethasone binding and the effect of dexamethasone on [3H]thymidine incorporation, which represents an index of DNA synthesis. RESULTS: The number of glucocorticoid receptors on mononuclear leukocytes (MNL) was comparable in patients with anorexia nervosa, patients with active Cushing's disease, and normal subjects (binding capacity 3.3 +/- 0.23 vs. 3.7 +/- 0.30 and 3.5 +/- 0.20 fmol/10(6) cells). Conversely, glucocorticoid receptor affinity was significantly decreased in anorexia nervosa as well as in Cushing's patients compared to control subjects (dissociation constant 4.0 +/- 0.31 and 4.1 +/- 0.34 vs. 2.9 +/- 0.29 nmol/L, p < .001) and inversely correlated with the levels of urinary free cortisol in both groups of patients. Basal [3H]thymidine incorporation in MNL was significantly reduced in anorexia nervosa as well as in Cushing's patients compared to control subjects (p < .001) and was diminished by dexamethasone to an extent similar to control subjects in patients with anorexia nervosa, but significantly (p < .001) less in those with Cushing's disease. In patients with anorexia nervosa, the incorporation of [3H]thymidine into the MNL was inversely correlated with urinary free cortisol levels. CONCLUSIONS: These data indicate that the lack of cushingoid features in patients with anorexia nervosa is not ascribable to a reduced sensitivity to glucocorticoids but is more likely due to the paucity of metabolic substrates.

Adolescent↗
PubMed1999

Bioequivalence of levothyroxine tablets administered to a target population in steady state.

Two parallel trials were carried out with levothyroxine sodium salt in 50 and 100 microg strengths, respectively, giving 100 microg day-1(50x2 microg day-1 or 100x1 microg day-1) in both trials in a repeated dose regimen. Twenty patients suffering from primary hypothyroidism under treatment with 100 microg day-1 of thyroxine sodium salt were enrolled in each trial. They were clinically and chemically euthyroid. Each trial lasted 114 days, with 57 days being devoted to the first treatment (test or reference) and 57 days to the other (reference or test), according to a two-period, two-sequence, two-formulation design in a steady state without wash-out. The test formulation was prepared with a technological improvement and is being produced to replace that at present on the market. Serum concentrations of free and total levothyroxine, and free and total levotriiodothyronine were assayed repeatedly during the treatment and in timed samples after the last dose of each formulation, using radioimmunoassays. Cmax and AUCss,tau were considered to be target parameters for bioequivalence which was assessed through 90% confidence intervals in the 0.80-1.25 range, as required by EU and US FDA operating guidelines. The results have shown that of these hormones, the free and total parent compound thyroxine is that which most clearly showed a peak after dosing, whereas its metabolite, free and total triiodothyronine, fluctuated around pre-dose concentrations. Bioequivalence was fully assessed with Cmax and AUCss,tau, with all four hormones tested and at both strengths administered. The two test formulations in 50 and 100 microg are thus bioequivalent with the two reference preparations. Tolerability was very good in all cases.

Adult↗
PubMed1999

Differential expression of the retinoblastoma gene family members in choroidal melanoma: prognostic significance.

We evaluated 55 samples of choroidal melanoma managed by enucleation. Knowing that the immunohistochemical expression of the retinoblastoma gene family members Rb/p105, p107, and pRb2/p130 was inversely correlated with the degree of malignancy in at least some histological types, we investigated the expression of these three proteins in choroidal melanoma. We focused on the relationship between patient survival and the immunohistochemical detection of the retinoblastoma proteins. No correlation with clinical outcome was found for Rb/p105 and p107. However, we found pRb2/p130 to be an independent prognostic factor correlating positively or directly with patient survival times and indirectly or inversely with the degree of malignancy. Demonstration of the prognostic value of the immunohistochemical expression of pRb2/p130 is of significance, even if additional studies are required to confirm these data and to compare the prognostic value of pRb2/p130 immunodetection to that of other recently proposed markers, such as p53.

Choroid Neoplasms↗
PubMed1998

Prognostic factors for survival after enucleation for choroidal melanoma.

To evaluate the prognostic value of DNA content-ploidy, agoraphilic nucleolar organizing regions (AgNORs) and proliferating cell nuclear antigen (PCNA) for survival among patients with choroidal melanoma choroidal melanomas managed by enucleation in 55 patients with a follow-up of 5 years were studied. AgNor counts were evaluated by two examiners after sections were specifically processed. Immunohistochemistry was performed to evaluate PCNA expression. Kaplan-Meier estimation of survival curves, the log-rank test, and Cox regression analysis were used to compare survival according to the above mentioned factors. Five years after enucleation 62% of patients had died. Patients with spindle cell type melanomas had the best and those with epithelioid cell type had the worst survival (p=0.004). Patients with small tumors had better survival than those with medium or large tumors (p=0.02). Patients having tumors with aneuploid nuclear DNA content had worse survival than those having tumors with diploid DNA content (p=0.004). A high PCNA level correlated with lower survival rates (p=0.02). Patients having a high AgNor count had a worse survival than those with lower counts (p=0.02). DNA content, PCNA level, and AgNOR count each showed a clinically significant influence on patient survival. However, each of these new evaluated prognostic factors was strongly related to one or both of the classic prognostic factors. It is therefore difficult to separate the effects of the two categories of prognostic factors. Results of the Cox regression analysis suggested that these newer evaluated prognostic factors provided little additional information about patient prognosis.

Adult↗
PubMed1997

Galparan induces in vivo acetylcholine release in the frontal cortex.

The chimeric peptide galparan (galanin(1-13)-mastoparan) induced the in vivo release of acetylcholine in the frontal cortex of rats when injected intracerebroventricularly, i.c.v. The ACh-releasing effects of galparan are reversible, dose-dependent, and not exerted at galanin receptors or at sites where mastoparan acts. Pertussis toxin pretreatment (i.c.v.) of the rats for 96 h prior to injection of galparan or of mastoparan completely prevented the ACh-releasing effects of both galparan and mastoparan. It appears that galparan acts at a novel site in the release of ACh in the cerebral cortex in vivo.

Acetylcholine↗
PubMed1997

Spontaneous nocturnal growth hormone secretion in anorexia nervosa.

In anorexia nervosa, serum GH levels are increased under basal conditions and respond abnormally to provocative stimuli. We report here, for the first time, an analysis of pulsatile GH secretion in these patients performed by Cluster algorithm. Seven anorectic and six normal weight, healthy women underwent serial blood sampling at 20-min intervals form 2030-0830 h for GH estimation. The total area under the curve (AUC; micrograms per L/min) was elevated 4-fold in anorectic patients compared to controls (4743.0 +/- 1520.09 vs. 1148.6 +/- 519.27; P < 0.01), largely due to an increase in the non-pulsatile fraction (3212.5 +/- 990.45 vs. 378.7 +/- 123.27; P < 0.01). Accordingly, the valley mean value was higher in anorectic than in control subjects (5.9 +/- 2.25 vs. 1.0 +/- 1.30 micrograms/L; P < 0.01). Furthermore, pulsatile AUC was also greater in anorectic patients (1530.4 +/- 654.72 vs. 769.8 +/- 404.02; P < 0.01) due to a significant increase in GH peak frequency (5.0 +/- 0.81 vs. 3.0 +/- 0.89; P < 0.01). No correlations were observed in these patients between body mass index and any of the parameters of spontaneous GH release, whereas a positive correlation was found between insulin-like growth factor I levels and pulsatile AUC (r2 = 0.583; P < 0.05), peak height (r2 = 0.743; P = 0.01), peak increment (r2 = 0.801; P < 0.01), and GH valley mean (r2 = 0.576; P < 0.05). In conclusion, it appears that the enhanced GH secretion in anorexia nervosa is the result of an increased frequency of secretory pulses superimposed on enhanced tonic GH secretion. Although this latter is consistent with a reduction of hypothalamic SRIH tone, the former may be accounted for by an increased number of GHRH discharges. Considering that in normal weight and obese subjects parameters of GH release are negatively correlated with adiposity indexes, the lack of such a negative correlation in our patients suggests that the enhancement of spontaneous GH release in anorectic patients is not merely the consequence of malnutrition-dependent impairment of insulin-like growth factor I production, but reflects a more complex hypothalamic dysregulation of GH release.

Adolescent↗
PubMed1996

A critical role for D1 receptors in the 5-HT1A-mediated facilitation of in vivo acetylcholine release in rat frontal cortex.

Subcutaneous administration of 8-OH-DPAT dose-dependently increased acetylcholine (ACh) output in frontal cortex of awake rats. The maximal effect of 8-OH-DPAT (0.5 mg/kg, s.c.) was prevented by the 5-HT1A antagonist WAY 100635 (1 mg/kg, s.c.) and by the D1 antagonists SCH 23390 or SCH 39166 (both 0.3 mg/kg, s.c.) but not seven days after chemical lesion of the raphe serotoninergic neurons. It is postulated that the 8-OH-DPAT activation of postsynaptic 5-HT1A receptors enhances the release of dopamine which, by acting at D1 receptors, stimulates the release of ACh in the frontal cortex.

5,7-Dihydroxytryptamine↗
PubMed1996

The cerebral cortex and parafascicular thalamic nucleus facilitate in vivo acetylcholine release in the rat striatum through distinct glutamate receptor subtypes.

Electrical stimulation (ten pulses of 0.5 ms, 10 V applied over 10 s at 10 Hz, 140 microA) delivered bilaterally to the prefrontal cortex or the parafascicular thalamic nucleus of freely moving rats facilitated acetylcholine release in dorsal striata, assessed by trans-striatal microdialysis. The facilitatory effects were blocked by coperfusion with 5 microM tetrodotoxin, suggesting that the release was of neuronal origin. The response of the striatal cholinergic neurons to prefrontal cortical stimulation was short-lived and required a longer period of stimulation (20 min) that the response to thalamic stimulation (4 min) to reach maximal effect. The alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate glutamatergic receptor antagonist 6,7-dinitroquinoxaline-2,3-dione [DNQX; 12 nmol per side, intracerebroventricularly (i.c.v.)] and the AMPA antagonist 6-nitro-7-sulphamoylbenzo(f)quinoxaline-2,3-dione (NBQX; 12 nmol per side, i.c.v. or 12.8 microM infused into the striatum), but not the NMDA-type receptor antagonist MK-801 (0.2 mg/kg, i.p.), abolished the facilitatory effect on striatal acetylcholine release evoked by stimulation of the prefrontal cortex. By contrast, DNQX or NBQX did not prevent the increase in striatal acetylcholine release evoked by parafascicular nucleus stimulation, but MK-801, in accordance with previous results, did so. MK-801 by itself lowered striatal acetylcholine output while DNQX and NBQX did not. The results provide in vivo evidence that the cerebral cortex facilitates cholinergic activity in the dorsal striatum apparently through the non-tonic activation of AMPA-type glutamatergic receptors while the parafascicular nucleus does this through tonic activation of NMDA receptors. Both glutamate receptor types are probably located in the striatum. The overall results suggest that the two pathways operate independently to regulate striatal cholinergic activity through distinct mechanisms.

Acetylcholine↗
PubMed1996

Endogenous serotonin facilitates in vivo acetylcholine release in rat frontal cortex through 5-HT 1B receptors.

We characterized the role of endogenous serotonin (5-HT) in regulating in vivo acetylcholine (ACh) output in frontal cortex of freely moving rats using the microdialysis technique. Systemic (0.63, 1.25 and 2.5 mg/kg, i.p.) or local (20 and 40 microM, reverse dialysis) administration of the 5-HT releaser and uptake inhibitor, d-norfenfluramine, dose-dependently enhanced frontal cortex ACh output. The d-norfenfluramine-induced increase in cortical ACh release was tetrodotoxin sensitive and completely prevented by a 7-day chemical degeneration of the serotonergic afferents to the frontal cortex. Investigating the 5-HT receptors that might mediate the d-norfenfluramine cholinergic effect, we found that the 5-HT4 (GR 125487) and 5-HT2A/2C (ritanserin) receptor antagonists, at doses effective in other in vivo tests, did not prevent the increase in cortical ACh output induced by the maximal effective does of d-norfenfluramine. However, the 5-HT1A/1B receptor antagonists (-)-pindolol (8 mg/kg, s.c.) or (-)-propanolol (8.8 mg/kg, i.p.) antagonized the increasing effect of d-norfenfluramine although the selective 5-HT1A receptor antagonist WAY-100635 (1 and 2 mg/kg, s.c.) did not. In accordance with an involvement of the 5-HT1B receptor in the ACh facilitation induced by d-norfenfluramine is the finding that the selective 5-HT1B agonist, CP-93,129, given locally (2, 4 and 8 micrograms/side) does-dependently raised cortical ACh release. In conclusion, the overall regulatory control exerted by endogenous 5-HT in vivo is to facilitate frontal cortex ACh release through 5-HT1B receptors located in the frontal cortex. The 5-HT1B receptors may act indirectly to facilitate ACh release probably by inhibiting cortical inhibitory inputs onto the cholinergic neurons.

Acetylcholine↗
PubMed1996

Influence of insulin on beta-endorphin plasma levels in obese and normal weight subjects.

OBJECTIVE: To establish the possible role of hyperinsulinemia in the elevation of plasma beta-endorphin (beta-EP) levels observed in obese patients after an oral glucose load. DESIGN: Oral glucose tolerance test (OGTT) and euglycemic-hyperinsulinemic clamp. SUBJECTS: Two groups of six (age: 22-39 y, BMI: 30-48 kg/m2) and eight obese men (age: 18-37 y, BMI: 35-45 kg/m2), respectively, and five normal weight healthy men (age: 22-30 y, BMI 22-23 kg/m2). MEASUREMENTS: Glucose, insulin and beta-EP levels at baseline and every 30 min until 180 min during the OGTT; glucose, insulin, C-peptide and beta-EP concentrations at baseline and in steady state condition (i.e. during the last 30 min of insulin infusion) in the euglycemic-hyperinsulinemic clamp studies. RESULTS: In the six obese patients undergoing the OGTT a significant elevation of beta-EP plasma levels was observed between 60 and 90 min after glucose ingestion. In the clamp studies no significant differences in beta-EP plasma levels, blood glucose and serum insulin were observed between obese and normal weight subjects both at baseline and at steady state. A markedly diminished insulin sensitivity along with a lower inhibition of C-peptide during insulin infusion was observed in obese patients compared to control subjects. CONCLUSION: A rise in serum insulin levels unaccompanied by a concomitant increase in blood glucose concentration is unable to elicit a beta-EP response in obese patients.

Adolescent↗
PubMed1995

Gene expression and in vitro release of galanin in rat hypothalamus during development.

The expression and distribution of the mRNA coding for galanin precursor, preprogalanin (ppGAL), were analysed in several rat hypothalamic nuclei (periventricular, paraventricular, supraoptic, dorsomedial and arcuate nuclei and the lateral hypothalamic area) during development by an in situ hybridization technique and computer-assisted grain counting over individual cells. ppGAL mRNA (expressed as number of grains/100 microns2) was detectable from postnatal day (PD) 1 in all the nuclei considered, and the amount of transcript per cell was 6-11 times less than in the adult. ppGAL mRNA progressively increased from PD8 to 14 to 21. The level of ppGAL mRNA in all the nuclei at PD21 was about half that in adulthood, except in the dorsomedial nucleus, where the difference was no more than 20%. As an index of the activity of galanin-containing neurons, we measured the basal and K(+)-evoked in vitro release of galanin-like immunoreactivity from hypothalamic slices of PD14, 21 and 90 rats by radioimmunoassay. Basal release of galanin-like immunoreactivity remained at the same level from PD14 to PD90, but the response to KCl (50 mM) stimulation was lower at PD14 (approximately 90%) and PD21 (> 200%) than at PD90 (350%). Basal and K(+)-evoked release was sensitive to tetrodotoxin, indicating a neuronal origin. This study provides the first evidence that the increase in ppGAL mRNA during the ontogeny of hypothalamic nuclei is associated with an increase in galaninergic neuronal function.

Age Factors↗
PubMed1995

Trans-synaptic modulation of striatal ACh release in vivo by the parafascicular thalamic nucleus.

Electrical stimulation of the parafascicular but not the ventrolateral or dorsomedial thalamic nucleus (ten 0.5 ms, 10 V pulses, 140 microA) of freely moving rats induced a frequency-dependent (2.5, 5, 10 and 20 Hz) increase in the extracellular acetylcholine (ACh) content of the dorsal striatum, assessed by trans-striatal microdialysis. The time-dependent effect of 10 Hz stimulation was studied. The peak increase, 39% above baseline, was attained during 4 min of stimulation. This was blocked by coperfusion with 5 microM tetrodotoxin, indicating that the release we measured represents a physiological process. The facilitatory effect of parafascicular nucleus stimulation does not appear to be associated with indirect action through the cerebral frontal cortex because acute lesion of the excitatory corticostriatal afferents, which by itself reduced basal ACh release by 40%, did not modify the effect of 10 Hz stimulation. The possible involvement of the fasciculus retroflexus in the facilitation of ACh release was also ruled out. The non-competitive NMDA-type receptor antagonist MK-801, applied by reversed dialysis (30 microM) or systemically injected (0.2 mg/kg), significantly reduced the basal ACh output and prevented the tetanus-evoked increase in ACh release. The results provide in vivo evidence that the activity of the cholinergic neurons in the dorsal striatum is trans-synaptically modulated by parafascicular nucleus excitatory afferents through activation of the NMDA subtype of glutamate receptors that is probably located in the striatum.

Acetylcholine↗
PubMed1994

Nimesulide decreases superoxide production by inhibiting phosphodiesterase type IV.

Nimesulide, the prototype of a new class of anti-inflammatory drugs, dose-dependently decreases the production of the superoxide anion (O2-.) in N-formyl-methionyl-leucyl-phenylalanine (fMLP)- and in phorbol myristate acetate (PMA)-stimulated polymorphonuclear leukocytes. The inhibition of O2-. is possibly related to its inhibitory effect on polymorphonuclear leukocyte cytosolic phosphodiesterase type IV (IC50 = 39 +/- 2 microM), to the related increase in cAMP (P < 0.01 at 1 microM) and the subsequent increase in protein kinase A activity. In fact H-89, a specific protein kinase A inhibitor, counteracts the inhibitory effect of nimesulide on O2-. production by fMLP and PMA. The activation of protein kinase A may prompt the phosphorylation of a number of substrates, thus inhibiting the assembly of NADPH-oxidase in the plasma membrane. Accordingly, nimesulide decreases PMA-induced assembly of NADPH-oxidase in polymorphonuclear leukocytes plasma membranes by about 35%. Protein kinase A activation may also interfere with chemotaxis. Nimesulide inhibits stimulated chemotaxis and the effect is decreased by H-89. Inhibition of phosphodiesterase type IV may explain many of nimesulide's effects.

Adenylyl Cyclases↗
PubMed1994

Impulse flow dependency of galanin release in vivo in the rat ventral hippocampus.

Using microdialysis and a sensitive RIA, we have studied the in vivo release of the neuropeptide galanin (GAL) from the ventral hippocampus of freely moving rats. The spontaneous outflow of GAL-like immunoreactivity (GAL-LI) (1.8 +/- 0.3 fmol per ml per 20 min) was dependent on the presence of extracellular Ca2+ and was inhibited by tetrodotoxin. Evoked release induced by infusion of KCl (60 mM) or veratridine (148 microM) was also Ca(2+)-dependent and sensitive to tetrodotoxin. Electrical stimulation of the ventral limb of the diagonal band nuclei induced a frequency-dependent (50-200 Hz) and tetrodotoxin-sensitive overflow of GAL-LI in the hippocampus. In vitro GAL-LI release (1.0 +/- 0.02 fmol per ml per 5 min), studied in slices of rat ventral hippocampus, was also Ca(2+)-dependent and was increased in a concentration-dependent manner by KCl depolarization. This study demonstrates the release of the neuropeptide GAL in the rat central nervous system. The in vivo release is related to the activity of the cholinergic GAL-LI-containing cells in the septal diagonal band nuclei. The results are discussed in relation to the coexistence of GAL and acetylcholine within the septal/diagonal band complex.

Animals↗