[Phosphatidylserine and memory disorders in the aged].
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Biomedical subjects
Publications and source records attributed to A Magnani.
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Electroconvulsive therapy (ECT) is often efficacious in severe depression, and it is occasionally used in the treatment of schizophrenia. The mechanism of action of ECT is still poorly understood. We evaluated thyroid-stimulating hormone (TSH) and prolactin responses to thyrotropin-releasing hormone (TRH) after a first ECT and at the end of a series of seven ECTs in eight unipolar depressed patients with blunted basal TSH/TRH response, eight unipolar depressed patients with normal TSH/TRH response, and eight schizophrenic patients. The hormone patterns obtained after the first ECT showed an increase in prolactin and a decrease in TSH in all groups of patients, suggesting a nonspecific response. At the end of the therapeutic course, TSH responses increased in both groups of depressed patients, and the elevation was more relevant in depressed patients with normal TSH/TRH. Our data suggest that the mechanism of action of ECT becomes more specific when it is performed chronically and differs according to the organic substrate underlying different mental disorders. Moreover, an aminergic activation in the two groups of depressed patients seems to take place.
Dual chamber DDD pacing is fully physiologic when chronotropic response of sinus node to exercise is normal and when retrograde ventriculo-atrial conduction is absent. Comparison of results from exercise test with increasing work load showed that atrial-triggered ventricular pacing provides a significant functional benefit (delta VO2 15%) P less than 0.01, if compared with fixed rate ventricular pacing. The benefit is closely related with the amount of sinus rate increase during exercise. In patients with sinus node syndrome the atrial triggered ventricular pacing rate did not show significant increase during exercise and exercise capability was similar to that observed with fixed ventricular pacing. Retrograde ventriculo-atrial conduction was observed in 56% of patients with sick sinus syndrome and 28% of patients with complete AV block and was the reason for endless loop tachycardias (ELTs). ELTs can be eliminated by lengthening atrial refractory period (ARP). In patients with ARP greater than or equal to 250 ms (47%), mild (8:7, 4:3) or important (2:1) AV block appeared during exercise test, with sudden drop of pacing rate and cardiac output at highest work load. Among other "physiologic" pacing modes, respiration traced ventricular stimulation showed high physiologic sensitivity (90%) and haemodynamic benefit comparable to that obtained during dual chamber pacing and without the related disadvantages.
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Dual chamber pacemakers, with coordinate atrial and ventricular sensing and stimulation (DDD), even if allowing "physiological" pacing, exhibited new and complicated arrhythmic manifestations, whose real frequency is still unascertained. In 65 patients (mean age 68 +/- 12 years), implanted with a DDD multiprogrammable device (15 pts. Medtronic Versatrax 7000 A, 50 pts. Pacesetter AFP 283), we carried out a 24 hours Holter monitoring while pacemaker was programmed with standard parameters. In a subset of 15 patients Holter monitoring was performed before and after pacemaker implantation. We evidenced: a) atrial sensing and/or pacing malfunction in 3 patients (4.5%); b) pacer-unrelated arrhythmias in 49 patients (75%): atrial extra beats 35 patients (54%), ventricular extra beats 23 patients (35%), non-sustained ventricular tachycardias 10 patients (15%), atrial tachyarrhythmias 8 patients (12%); c) supraventricular arrhythmias with PM-mediated high rate ventricular pacing in 12 patients (18%); d) PM induced and sustained endless loop tachycardias in 31 patients (47%); e) arrhythmias depending on over-sensing in 11 patients (17%): myopotential interferences 9 patients (14%), cross-talk ventricular pacing inhibition 2 patients (3%). The prevalence of ventricular arrhythmias was not different before and after the pacemaker implantation. The prevalence of atrial extrasystoles (53% versus 40%) and atrial tachyarrhythmias (26% versus 6%) decreased after the pacemaker implantation. Aimed reprogramming with progressive extension of atrial refractory period (from 250 to 400 msec and DDX) achieved disappearance of PM-endless loop tachycardias in 95%. Use of multi-programmability lowered the incidence and symptoms of most PM-related arrhythmias. Drug therapy was of choice in clinical arrhythmias unrelated to pacer.
Clinical and prognostic significance of ventricular repolarization anomalies in sportsmen is still uncertain, even if they are most commonly regarded as benign. We studied a patient in whom those manifestations didn't show any progression within 30 years even after interruption of athletics and were related to idiopathic hypertrophic cardiomyopathy. Anatomical findings were combined with cardiac rhythm and conduction disturbances (paroxysmal atrial flutter, premature contractions, 2nd degree AV block). In our patient ventricular repolarization anomalies, even though without a negative prognosis, can't be related to "athlete's heart" but rather to organic cardiomyopathy.
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Time and costs involved in electrophysiologic study for sino-atrial and/or atrio-ventricular blocks were evaluated in 42 patients. Analysis of charge for staff, specific electrophysiologic equipment and disposable items reveals an operating cost of 540.000 lire per study. An electrophysiologic study is the only method of diagnosing with certainty the level of A-V block and of assessing the prognosis of patients with infranodal conduction disease. It also allows a careful choice of permanent pacing mode. The potential risk, although small involved in this procedure, its cost and the need of a high operating standard suggest however that the number of electrophysiology laboratories should not indiscriminately increase.
His bundle study with long term follow-up (mean 42 months) was performed in 155 patients (107 with previous syncope, 48 without or with few symptoms). The electrocardiogram showed various conduction abnormalities, but in some cases it was normal. Patients were excluded at the beginning of the study, if they showed sick sinus syndrome, recorded 3rd degree atrioventricular block, angina pectoris, recent myocardial infarction, congenital or surgical cardiac block. In previous studies the diagnostic sensibility and specificity of ajmaline (1 mg/kg/1' i.v.) and overdriving tests have been evaluated. In this study the prognostic meaning of these tests has been evaluated. During a mean 42 months follow-up, 17 patients (10.9%) developed advanced atrioventricular block. A higher risk of developing advanced atrioventricular block below the AV node was detected in patients who showed: basal HV greater than or equal to 65 ms (33% developed advanced atrioventricular block vs 4.7% of patients with basal HV less than 65 ms; p less than 0.001); HV value greater than or equal to 120 ms or 2nd-3rd degree atrioventricular block during ajmaline test (40% progressed to advanced atrio-ventricular block vs 0.85%; p less than 0.001); HV prolonged greater than 10 ms or 2nd-3rd degree atrioventricular block during atrial pacing (40% progressed to a atrioventricular block vs 3.4%; p less than 0.001) regardless of previous syncope.(ABSTRACT TRUNCATED AT 250 WORDS)
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3-Mercapto-4-methylpicolinic acid one of very few compounds derived from 3-mercaptopicolinic acid (3-MPA) to have hypoglycemic activity. In an effort to find compounds with greater potency than 3-MPA, several 4-substituted 3-mercaptopicolinic acids (4-OMe, OC6H5, SMe, SH, Cl, NH2, Et; 1-7) were prepared and tested in 48-h fasted rats. None was hypoglycemic in this test system after oral dosing of 150 mg/kg.
Sulphated hyaluronic acids having a sulphation degree of 3.5 per disaccharide unit, HyalS3.5, were prepared with different molecular weights corresponding to 21 x 10(3), 320 x 10(3) and 3500 x 10(3). The thrombin inhibition in plasma and in the presence of purified molecules, i.e. fibrinogen, antithrombin III (AT III) and heparin cofactor II (HC II), were studied for the three different MW compounds at different concentrations. The thrombin time in plasma depended on the length of the chain, and the two lower MW HyalS3.5 inhibited thrombin both by direct aspecific interaction and via HC II, whereas the activity of the highest MW compound was mainly related to the electrostatic interaction with HC II. The inactivation of FXa serine protease was only attributed to HyalS3.5-AT III complex.
Anticoagulant polymer sulfated hyaluronic acid was patterned immobilized on a poly(ethylene terephthalate) (PET) film in a specific pattern by photolithography. Hyaluronic acid was sulfated by a sulfur trioxide-pyridine complex. The polymer was coupled with azidoaniline. The derivatized polymer was cast on a PET film from aqueous solution. After drying, the film was photoirradiated in the presence or absence of a photomask. The micropatterning was confirmed by staining with a dye, brilliant green. Since the anticoagulant polymer has negative charges, the cationic dye was adsorbed on the regions where the anticoagulant polymer was immobilized. Platelet adhesion was reduced on the sulfated hyaluronic acid-immobilized areas. The immobilized sulfated hyaluronic acid significantly reduced thrombus formation.
The effect of fibronectin protein (Fn) coating onto polysaccharide layers of hyaluronic acid (Hyal) and its sulfated derivative (HyalS) on fibroblast cell adhesion was analyzed. The Hyal or HyalS were coated and grafted on the glass substrate by a photolithographic method. The Fn coating was achieved by two different routes: the immobilization of Fn by covalent bond to the polysaccharide layers and the simple adsorption of Fn onto Hyal and HyalS surfaces. AFM, SEM, and ATR-FTIR techniques were used for the chemical and topographical characterization of the surfaces. According to AFM and SEM data, the surface topography was dependent on the method used to cover the polysaccharide layers with the protein. ATR-FTIR analysis supplied information about the rearrangement of Fn after the interaction (adsorption or binding) with the Hyal and the HyalS. The conformational changes of the Fn were minimal when it was simply adsorbed on HyalS surfaces and larger once bound, whereas on the Hyal layer the protein underwent a bigger conformational change once adsorbed and covalently grafted. Then, the biological characterization was carried out by analyzing the human diploid skin fibroblasts adhesion on these surfaces. The morphology of fibroblasts was evaluated by SEM, whereas the dynamics of fibroblasts movement were recorded by a time-lapse system. Cell variations in area, perimeter, and length were analyzed at 2, 4, and 6 h. It was found that the addition of Fn (covalently bound or merely adsorbed) was fundamental in the promotion of fibroblasts adhesion and spreading. The greatest adhesion occurred onto HyalS layers covered by the adsorbed Fn.
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