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Biomedical subjects

G Fontana

Publications and source records attributed to G Fontana.

At least 37 records · Page 2Linked to original sources
PubMed1997

Neuropeptide Y release from cultured hippocampal neurons: stimulation by glutamate acting at N-methyl-D-aspartate and AMPA receptors.

L-Glutamate, N-methyl-D-aspartate, DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and kainate increased the release of neuropeptide Y-like immunoreactivity from primary cultures of rat hippocampal neurons incubated in Mg2+(1.2 mM)-containing medium. The neuropeptide Y-like immunoreactivity released by 100 microM glutamate was mainly accounted for by neuropeptide Y (1-36), but consisted in part (about 20%) of peptide YY. The effect of 100 microM glutamate on neuropeptide Y-like immunoreactivity release was largely (about 70%) prevented by the N-methyl-D-aspartate receptor antagonist dizocilpine maleate (10 microM), while the remainder (about 30%) was sensitive to the AMPA/ kainate receptor antagonist 6-nitro-7-sulphamoylbenzo(f)quinoxaline-2-3-dione (10 microM). The AMPA(100 microM)-evoked release of neuropeptide Y-like immunoreactivity was strongly antagonized by 6-nitro-7-sulphamoylbenzo(f)quinoxaline-2-3-dione and by 1-aminophenyl-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine, but it was in part (15-20%) sensitive to dizocilpine. The releases of neuropeptide Y-like immunoreactivity elicited by glutamate, N-methyl-D-aspartate, AMPA and kainate were all strongly Ca(2+)-dependent. Tetrodotoxin (1 microM) abrogated the N-methyl-D-aspartate-evoked release and partly inhibited the release caused by glutamate, but did not modify significantly AMPA- or kainate-evoked release. Removal of Mg2+ from the medium caused increase of neuropeptide Y-like immunoreactivity release, an effect prevented by dizocilpine maleate or 7-Cl-kynurenate. Cyclothiazide (10 microM), a drug known to prevent AMPA receptor desensitization, enhanced the neuropeptide Y-like immunoreactivity release elicited by 100 microM AMPA, but not that caused by 100 microM kainate. However, when used at a lower concentration (50 microM), kainate elicited a response that was potentiated significantly by cyclothiazide. It is concluded that glutamate can stimulate Ca(2+)-dependent release of neuropeptide Y from hippocampal neurons mainly through N-methyl-D-aspartate receptors and, less so, by activating cyclothiazide-sensitive receptors of the AMPA-preferring type.

Animals↗
PubMed1997

Activation of brain nitric oxide synthase in depolarized human temporal cortex slices: differential role of voltage-sensitive calcium channels.

1. Nitric oxide (NO) synthase activity was studied in slices of human temporal cortex samples obtained in neurosurgery by measuring the conversion of L-[3H]-arginine to L-[3H]-citrulline. 2. Elevation of extracellular K+ to 20, 35 or 60 mM concentration-dependently augmented L-[3H]-citrulline production. The response to 35 mM KCl was abolished by N(G)-nitro-L-arginine (100 microM) demonstrating NO synthase specific conversion of L-arginine to L-citrulline. Increasing extracellular MgCl2 concentration up to 10 mM also prevented the K+ (35 mM)-induced NO synthase activation, suggesting the absolute requirement of external calcium ions for enzyme activity. 3. However, the effect of high K+ (35 mM) on citrulline synthesis was insensitive to the antagonists of ionotropic and metabotropic glutamate receptors dizocilpine (MK-801), 6-nitro-7-sulphamoylbenzo(f)-quinoxaline-2-3-dione (NBQX) or L-2-amino-3-phosphonopropionic acid (L-AP3) as well as to the nicotinic receptor antagonist, mecamylamine. 4. The 35 mM K+ response was insensitive to omega-conotoxin GVIA (1 microM) and nifedipine (100 microM), but could be prevented in part by omega-agatoxin IVA (0.1 and 1 microM). The inhibition caused by 0.1 microM omega-agatoxin IVA (approximately 30%) was enhanced by adding omega-conotoxin GVIA (1 microM) or nifedipine (100 microM). Further inhibition (up to above 70%) could be observed when the three Ca2+ channel blockers were added together. Similarly, synthetic FTX 3.3 arginine polyamine (sFTX) prevented (50% at 100 microM) the K+-evoked NO synthase activation. This effect of sFTX was further enhanced (up to 70%) by adding 1 microM omega-conotoxin GVIA plus 100 microM nifedipine. No further inhibition could be observed upon addition of MK-801 or/and NBQX. 5. It was concluded that elevation of extracellular [K+] causes NO synthase activation by external Ca2+ entering cells mainly through channels of the P/Q-type. Other Ca2+ channels (L- and N-type) appear to contribute when P/Q-channels are blocked.

Alanine↗
PubMed1997

[Anesthesia in Apert syndrome].

The anaesthetic technique chosen for a laparohysterectomy in a woman affected by Apert's acrocephalosyndactilia is described. Difficulties in performing tracheal intubation were overcome by mean of loco-regional anesthesia (LRA). In order to minimize the anaesthetic risk, a standardised preoperative evaluation and assessment integrating the usual investigations and the possibility of employing intubation techniques as alternative to direct laryngoscopy are suggested.

Acrocephalosyndactylia↗
PubMed1997

[Adenomatoid tumor of the testicle. Description of a case].

The authors report a case of adenomatoid tumour of the right testicle which was referred to their attention in a 40-year-old, asymptomatic male. During the course of the urological examination, a chance discovery was made of a fibrous area at the lower extremity of the testicle. The scan showed a small hyperechogenic, slightly dishomogenous and clearly delimited area with a diameter of 4 x 6 mm. Testicular markers were negative. During the course of surgical exploration, an extensive area of the suspect testicle was removed given that extemporary diagnosis revealed that the lesion was benign. The final diagnosis was adenomatoid tumour. Control scans performed over time exclude local recurrence, thus confirming the value of conservative surgery in this type of neoplasia.

Adenomatoid Tumor↗
PubMed1997

[Transurethral tissue vaporization: indications and limitations of the technique. Our experience in 105 cases].

INTRODUCTION: Laser vaporisation of the prosthesis (LP) is now regarded as the most valid alternative to endoscopic resection (TUR). It is a safe, relatively non-invasive and clinically effective method but requires the use of very expensive instruments. AIM: In order to obtain the same results but at a lower cost, an innovative technique has recently been introduced: "prostatic electrovaporisation" which uses a combination of coagulation and electrosurgical tissue vaporisation, and achieves the same biological effect as laser treatment using equipment already available for standard TUR merely by modifying the operator electrode. METHODS: From February to September 1995, a total of 105 patients (38 with benign prostatic hypertrophy, 7 with advanced prostate carcinoma, 60 with multifocal superficial vescical carcinoma with a mean diameter of 2.5 cm) underwent transurethral tissue vaporisation using a rotary, constant flow ACMI resector with a grooved roller ball which enables the contemporary coagulation and vaporisation of tissues. RESULTS: In terms of benign and malignant prostate pathology, surgery is slightly shorter than TUR (5-10 minutes on average), blood loss is minimum (hemotransfusion is never required), the post-TVP catheter stage is comparable to that of TUR; late hematuria never occurs caused by scab removal and there are no episodes of urinary incontinence. Cervical deobstruction has always proved valid when controlled by RT scan, micturitional cystography and uroflowgraph with very slight irritative symptoms following the recovery of spontaneous micturition. In the case of vescical neoplasia it has always shown a good destructive effect on the oncotic mass with an oncological radicality comparable to that of TUR. There is a very low risk of accidental perforation of the vescica, and the intensity of the obturating reflex is also considerably diminished; bleeding is almost absent. This has led to a shorter hospital stay and a marked reduction in hospitalisation costs. Like LP, TVP does not allow a precise histological evaluation. In order to avoid this drawback, prior to tissue vaporisation treatment it is worth carrying out a clinical study to exclude malignant pathology (transrectal prostate ecotomography, PSA and/or PSA density and/or preoperative prostate biopsy), and intraoperative biopsy resection. CONCLUSION: In short, with due respect for the clinical indications, tissue vaporisation should be preferred: a) to standard TUR, essentially on account of limited bleeding and consequent drastic reduction in hospital stay; b) to laser treatment, basically because of the reduced costs and scarcity (or absence) or post-treatment irritative disorders.

Adenocarcinoma↗
PubMed1997

Screening of gestational diabetes in Tuscany: results in 2000 cases.

According to the guidelines of the "Third international workshop conference on GDM", we have examined 2000 pregnant women. The glucose challenge test (GCT) was positive in 408 cases (20.4%) and negative in 1592 (79.6%). The OGTT (Carpenter and Coustan's criteria) was performed in 647 pregnant women. GDM and IGGT prevalence was of 6.25% and 5.5% respectively and normal glucose tolerance (NGT) 88.25%. The GCT effectiveness for GDM and IGGT diagnosis is: sensibility 75.1%, specificity 44%, positive predictive value 46.4% and negative predictive value 74%. GDM and IGGT compared with NGT women were significantly older (p < 0.05) and prepregnancy BMI was higher (p < 0.01); the prevalence of previous macrosomia (p < 0.01), previous gestational diabetes (p < 0.01) and family history for diabetes mellitus (p < 0.05) was greater in GDM and IGCT. The prevalence of preterm delivery was higher in both GDM and IGCT (GDM 12.5% and IGGT 15.4% vs NGT 6%; p < 0.01), as well as the prevalence of cesarean sections (GDM 31.6% vs IGGT 23.5% and NGT 20.3%; p < 0.02), and the occurrence of macrosomia (GDM 27.6%, IGGT 16.6% and NGT 16.2%). In addition a higher prevalence (p < 0.01) of hyperbilirubinaemia, hypoglycemia and hypertrophy cardiomyopathy was observed in newborns from GDM women. Our data show that: GCT has a good specificity for GDM diagnosis, prevalence of GDM in our population is about 6%, GDM is still correlated to an elevated maternal and neonatal morbility.

Adult↗
PubMed1997

[Recurrent urinary tract infections. Biological suppositions and clinical treatment with thymopentin].

BACKGROUND: Urinary tract infections (UTI) are a common usual pathological event. They relapse often due to the periurethral colonization of microorganisms from the intestinal bacterial flora. They also constitute an important and considerable social and clinical problem. The absence of inducing organic conditions or an infective focus at the base of the pathogenetic mechanism suggests the existence of alterations of the immune response of the subject. MATERIALS AND METHODS: In this work we wanted to verify if, in those subjects with relapsing UTI (more than four events every year) cure with "biological" response modifiers, particularly "thymopentin", meaningfully reduced the number of events. RESULTS: The results obtained confirm that for those cases in which the chemo-antibiotic therapy did not have the expected results, it is rational to support it with an immune-modulating drug (thymopentin). In fact the post-therapy reduction of UTI observed during two years of follow-up is statistically significant when compared to the average of UTI before therapy. CONCLUSIONS: The "cost-benefits" analysis should prove to be a saving in favour of the use of thymopentin, taking into consideration the reduction of chemo-antibiotics consumption and the lower number of working hours lost every year.

Adjuvants, Immunologic↗
PubMed1996

Ectocellular in vitro and in vivo metabolism of cADP-ribose in cerebellum.

CD38, a type II transmembrane glycoprotein predominantly expressed in blood cells, is a bifunctional ectoenzyme directly involved in the metabolism of cADP-ribose (cADPR). This is a potent Ca2+ mobilizer in several types of cells. The relationship between the ectocellular site of cADPR production and its intracellular calcium-related functions is poorly understood. Cultured rat cerebellar granule cells showed both enzymic activities of CD38, ADP-ribosyl cyclase and cADPR hydrolase, at a ratio of 16 to 1 respectively, and were immunostained by the anti-(human CD38) monoclonal antibody IB4. In these cells externally added cADPR and beta-NAD+ (the precursor of cADPR), but not alpha-NAD+ or ADP-ribose, enhanced the peak of the depolarization-induced rise in intracellular Ca2+ concentration. This effect was inhibited by 1 microM ryanodine, suggesting a potentiation of calcium-induced calcium release by cADPR. CD38 ectoenzyme activities, ADP-ribosyl cyclase and cADPR hydrolase, were also demonstrated in vivo by microdialysis of adult rat cerebellum, where IB4 bound to granule neurons selectively. Trace amounts (11.5 +/- 3.8 nM) of NAD+ were detected by microdialysis sampling and sensitive assays in the basal interstitial fluid of the cerebellum. These results provide a link between ectocellular cADPR turnover and intracellular calcium mobilization in cerebellum.

ADP-ribosyl Cyclase↗
PubMed1996

Characterization of the glutamate receptors mediating release of somatostatin from cultured hippocampal neurons.

L-Glutamate, NMDA, DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and kainate (KA) increased the release of somatostatin-like immunoreactivity (SRIF-LI) from primary cultures of rat hippocampal neurons. In Mg(2+)-containing medium, the maximal effects (reached at approximately 100 microM) amounted to 737% (KA), 722% (glutamate), 488% (NMDA), and 374% (AMPA); the apparent affinities were 22 microM (AMPA), 39 microM (glutamate), 41 microM (KA), and 70 microM (NMDA). The metabotropic receptor agonist trans-1-aminocyclopentane-1,3-dicarboxylate did not affect SRIF-LI release. The release evoked by glutamate (100 microM) was abolished by 10 microM dizocilpine (MK-801) plus 30 microM 1-aminophenyl-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466). Moreover, the maximal effect of glutamate was mimicked by a mixture of NMDA+AMPA. The release elicited by NMDA was sensitive to MK-801 but insensitive to GYKI 52466. The AMPA- and KA-evoked releases were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX) or by GYKI 52466 but were insensitive to MK-801. The release of SRIF-LI elicited by all four agonists was Ca(2+) dependent, whereas only the NMDA-evoked release was prevented by tetrodotoxin. Removal of Mg2+ caused increase of basal SRIF-LI release, an effect abolished by MK-801. Thus, glutamate can stimulate somatostatin release through ionotropic NMDA and AMPA/KA receptors. Receptors of the KA type (AMPA insensitive) or metabotropic receptors appear not to be involved.

Animals↗
PubMed1996

Role of external and internal calcium on heterocarrier-mediated transmitter release.

Release-regulating heterocarriers exist on brain nerve endings. We have investigated in this study the mechanisms involved in the neurotransmitter release evoked by GABA heterocarrier activation. GABA increased the basal release of [3H]acetylcholine and [3H]noradrenaline from rat hippocampal synaptosomes and of [3H]dopamine from striatal synaptosomes. These GABA effects, insensitive to GABA receptor antagonists, were prevented by inhibiting GABA uptake but not by blocking noradrenaline, choline, or dopamine transport. Lack of extracellular Ca2+ or addition of tetrodotoxin selectively abolished the GABA-evoked release of [3H]noradrenaline, leaving unaffected that of [3H]acetylcholine or [3H]dopamine. 1,2-Bis(2-aminophenoxyl)-ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM) or vesamicol attenuated the release of [3H]acetylcholine elicited by GABA. Reserpine, but not BAPTA-AM, prevented the effect of GABA on [3H] dopamine release. Autoreceptor activation inhibited the GABA-evoked release of [3H]noradrenaline but not that of [3H]acetylcholine or [3H]dopamine. It is concluded that (a) the release of [3H]noradrenaline consequent to activation of GABA heterocarriers sited on noradrenergic terminals meets the criteria of a conventional exocytotic process, (b) the extracellular [Ca2+]-independent releases of [3H]acetylcholine and [3H]dopamine appear to occur from vesicles possibly through involvement of intraterminal Ca2+, and (c) autoreceptor activation only affects heterocarrier-mediated vesicular release linked to entry of extracellular Ca2+.

Acetylcholine↗
PubMed1996

Use of pleural catheter for the management of simple pneumothorax.

STUDY OBJECTIVE: We assessed the use of a pleural catheter (Thoracic Vent) to determine its effectiveness in treating simple pneumothorax (PTX) and in preventing recurrent PTX. DESIGN: A retrospective review was conducted of 84 patients treated with a pleural catheter for iatrogenic (52) and spontaneous (11 primary, 21 secondary) PTX between 1989 and 1994. PATIENTS: There were 45 men and 39 women with a mean age of 50.4 years (range, 18 to 85 years). RESULTS: Mean time to lung reexpansion was 0.5 +/- 0.1 days. Forty-five (57%) patients manifested an air leak after catheter placement for 2.0 +/- 0.2 days. The duration of time to catheter removal was 3.3 +/- 0.2 days. Seventy-one (85%) patients had resolution of PTX with this therapy alone. Thirteen patients (15%) failed to resolve their PTXs and required subsequent tube thoracostomy alone (6) or surgical therapy (7). Four of 11 patients who required tube thoracostomy also failed to respond to this therapy. Treatment failure was more common among patients with spontaneous PTX than with iatrogenic PTX (34% vs 4%; p < 0.005). During a mean follow-up of 3.0 +/- 0.2 years, 6 (7%) patients suffered recurrent PTX an average of 23 days after initial therapy. CONCLUSION: This pleural catheter is effective in the management of simple iatrogenic and spontaneous PTX.

Adolescent↗
PubMed1995

Transmitter release associated with long-term synaptic depression in rat corticostriatal slices.

Using a corticostriatal slice preparation, we have recently shown that tetanic stimulation of the corticostriatal pathway produces long-term depression (LTD) of striatal excitatory synaptic transmission. In the present study we have analysed the relationship between LTD and the striatal release of different endogenous transmitters. Samples of perfusate were collected via a small cannula placed just above the surface of the striatal slice close to the recording electrode, and were analysed by HPLC. The high-frequency stimulation (100 Hz, three trains, 3 s duration, 20 s interval) used to induce LTd caused a significant but transient increase in the release of both excitatory (aspartate and glutamate) and inhibitory (glycine and GABA) amino acid transmitters. Tetanic stimulation also produced a significant, but transient increase in the release of endogenous dopamine. We conclude that the tetanic stimulation of the corticostriatal pathway is able to induce a large but transient release of excitatory amino acids and of dopamine, whose participation in the induction of striatal LTD has been demonstrated previously. Moreover, the maintenance of this form of synaptic plasticity does not seem to require a sustained change in transmitter release.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1995

Kinetic properties of the sodium-calcium exchanger in rat brain synaptosomes.

1. The kinetic properties of the internal Na+ (Na+i)- dependent 45Ca2+ influx and external Na+ (Na+o)-dependent 45Ca2+ efflux were determined in isolated rat brain nerve terminals (synaptosomes) under conditions which the concentrations of internal Na+ ([Na+]i), external Na+ ([Na+]o), external Ca2+ (Ca2+]o), and external K+ ([K+]o) were varied. Both fluxes are manifestations of Na(+)-Ca2+ exchange. 2. Ca2+ uptake was augmented by raising [Na+]i and / or lowering [Na+]o. The increase in Ca2+ uptake induced by removing external Na+ was, in most instances, quantitatively equal to the Na+i-dependent Ca2+ uptake. 3. The Na+i-dependent Ca2+ uptake (measured at 1 s) was activated with an apparent half-maximal [Ca2+]o (KCa(o)) of about 0.23 mM. External Na+ inhibited the uptake in a non- competitive manner: increasing [Na+]o from 4.7 to 96 mM reduced the maximal Na+(i)-dependent Ca2+ uptake but did not affect KCa(o). 4. The inhibition of Ca2+ uptake by Na+o was proportional to ([Na+]o)2, and had a Hill coefficient (nH) of approximately 2.0. The mean apparent half-maximal [Na+]o for inhibition (KI(Na)) was about 60mM, and was independent of [Ca2+]o between 0.1 and 1.2mM; this, too, is indicative of non-competitive inhibition. 5. Low concentrations of alkali metal ions (M+) in the medium, including Na+, stimulated the Na+i-dependent uptake. The external Na+ and K+ concentrations required for apparent half-maximal activation (KM(Na) and KM(K), respectively) were 0.12 and 0.10mM. Thus, the relationship between Ca2+ uptake and [Na+]o was biphasic: uptake was stimulated by [Na+]o < or = 10 mM, and inhibited by higher [Na+]o. 6. The calculated maximal Na+i-dependent Ca2+ uptake (Jmax) was about 1530 pmol (mg protein) -1s-1 at 30 degrees C saturating [Ca2+]o and external M+ concentration ([M+]o), and with negligible inhibition by external Na+. 7. Internal Na+ activated the Ca2+ uptake with an apparent half-maximal concentration (KNa(i)) of about 20 mM and a Hill coefficient, nH, of approximately 3.0. 8. The Jmax for the Na+o-dependent efflux of Ca2+ from 45Ca(2+)-loaded synaptosomes treated with carbonyl cyanide p-trifluormethoxy-phenylhydrazone (FCCP) and caffeine (to release stored Ca2+ and raise the internal Ca2+ concentration ([Ca2+]i) was about 1800-2000 pmol (mg protein -1s-1 at 37 degrees C. 9. When the membrane potential (Vm) was reduced (depolarized) by increasing [K+]o, the Na+i-dependent Ca2+ influx increased, and the Na+o-dependent Ca2+ efflux declined. Both fluxes changed about 2-fold per 60 mV change in Vm. This voltage sensitivity corresponds to the movement of one elementary charge through about 60% of the membrane electric field. The symmetry suggests that the voltage-sensitive step is reversible. 10. The Jmax values for both Ca2P influx and efflux correspond to a Na+-Ca2+ exchange-mediated flux of about 425-575 jumol Ca2P (1 cell water)-' s-' or a turnover of about one quarter of the total synaptosome Ca2P in 1 s. We conclude that the Na+-Ca2P exchanger may contribute to Ca2P entry during nerve terminal depolarization; it is likely to be a major mechanism mediating Ca2P extrusion during subsequent repolarization and recovery.

Animals↗
PubMed1995

In vitro cytotoxicity of fenthion and related metabolites in human neuroblastoma cell lines.

The aim of our research was the evaluation in vitro of the neurotoxic effects of fenthion and its metabolites on human neuroblastoma cells, as a model for their toxicity in humans. The results indicate that 24 hours exposure was sufficient to produce dose related effects on SK-N-BE and IMR 32 cell viability causing detachment and loss of cells at the effective doses. In the two cell lines fenthion metabolites display an increased cytotoxicity respect to the parent compound with a distinct pattern of toxicity on neurons. Our data suggest that cultured neuronal cells of human origin are discriminating experimental systems, sensitive to minor differences, of correlating in vivo and in vitro neurotoxicants.

Cell Survival↗