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Biomedical subjects

A Albertini

Publications and source records attributed to A Albertini.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Various immune functions (with particular attention to NK cells) in young people with frequent episodes of pharyngitis].

In four girls, selected during three years of ambulatory observations, the evolution of repeated upper respiratory tract infection events, under the immunologic aspect, has been studied. The group of girls, with age between 13 and 16 years, practically formed a small casuistry, as an experimental recruitment. With the aim to find the causes of the told infectious events, firstly were checked numerous immune functions, successively were evaluated only the ones that had resulted altered (percentage number of "NK" cells, complement "C3" fraction and "T4" lymphocytes). Particularly significative variations, toward diminution, of the "NK" cells number related to the most compelling school attendance periods were recognized. What observed could let hypothesize that stress and emotions , correlated to scholastic events negatively influence some immune functions, peculiarly the number of "NK" cells. To the lowering of these cells could correspond a facilitation and higher frequency of upper respiratory tract infections (with pharynx as an epicenter), likely by viral aetiology. The subsequent vicarious and/or compensatory intervention by other immune functions could allow, however, the spontaneous recovery, without chemotherapeutic recourse, of the infectious events, that could arise with higher frequency but, most likely, with lower seriousness than could happen when "NK" cells normally act.

Adolescent↗
PubMed1989

Improved radioimmunoassay of atrial natriuretic peptide in plasma.

We describe a radioimmunoassay (RIA) for measurement of atrial natriuretic peptide (ANP), based on one-step incubation and a simplified extraction procedure. The extraction was performed on a "Supelclean LC 18" column, with 2-mL plasma samples. Use of a diiodinated tracer improved the sensitivity of the RIA method. The minimal detectable value was 5 ng/L. Simplification of the extraction procedure and simultaneous incubation of the reagents provide a method more suitable for routine standard assay of ANP than those currently available. Intra- and interassay CVs were 6% (n = 12) and 11% (n = 10), respectively. The mean concentration of ANP in plasma of 32 healthy volunteers was 33 (SEM 4) ng/L. The ANP values for plasma after one-step incubation correlated well with those determined by a commercial RIA kit: r = 0.971, slope = 1.099, intercept = 1.949 ng/L (n = 25).

Atrial Natriuretic Factor↗
PubMed1989

[Potentiating effect of a supine position on ischemia induced by exercise].

Though sitting bicycle and treadmill are the commonest devices used in exercise stress testing, supine ergometric test shows some advantages, especially in research investigations. The latter allows better ECG and blood pressure recordings during exercise. Recently, a greater frequency of ST-segment depression has been reported with supine vs upright exercise, but some doubt as to the ischemic significance of this result has been raised. Thus, we compare the ECG and hemodynamic pattern during upright and supine bicycle exercise in 50 subjects with chest pain, without prior myocardial infarction: 31 had documented coronary artery disease (CAD) and 19 had normal coronary vessels. In a subgroup (22 CAD patients and all subjects without CAD) a measurement of myocardial perfusion was performed during exercise using thallium-201 radionuclide ventriculography. Initial work-load and the further graded increases were identical for both postures. The frequency of ST-segment depression was higher during supine exercise (84% vs 74%). The increase in sensitivity (+7% vs CAD) was wider if a more direct measurement of myocardial ischemia was adopted as gold standard (+13% vs TI-201 responses) and was not associated with a decreased specificity (Tab. II). In the supine position the threshold of exercise-induced ST-segment depression was significantly lower. Chest pain appeared more frequently and at a lower work-load. Accentuation and precocity of exercise-induced ischemia in the supine-position could be attributed to an increased imbalance between supply and demand of MVO2 at equivalent work-load, heart rate changes, systolic blood pressure and double product were significantly higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Mechanism of ferritin iron uptake: activity of the H-chain and deletion mapping of the ferro-oxidase site. A study of iron uptake and ferro-oxidase activity of human liver, recombinant H-chain ferritins, and of two H-chain deletion mutants.

To study the functional differences between human ferritin H- and L-chains and the role of the protein shell in the formation and growth of the ferritin iron core, we have compared the kinetics of iron oxidation and uptake of ferritin purified from human liver (90% L) and of the H-chain homopolymer overproduced in Escherichia coli (100% H). As a control for iron autocatalytic activity, we analyzed the effect of Fe(III) on the iron uptake reaction. The results show that the H-chain homopolymer has faster rates of iron uptake and iron oxidation than liver ferritin in all the conditions analyzed and that the difference is reduced in the conditions in which iron autocatalysis in high: i.e. at pH 7 and in presence of iron core. We have also analyzed the properties of two engineered H-chains, one lacking the last 22 amino acids at the carboxyl terminus and the other missing the first 13 residues at the amino terminus. These mutant proteins assemble in ferritin-like proteins and maintain the ability to catalyze iron oxidation. The deletion at the carboxyl terminus, however, prevents the formation of a stable iron core. It is concluded that the ferritin H-chain has an iron oxidation site which is separated from the sites of iron transfer and hydrolysis and that either the integrity of the molecule or the presence of the amino acid sequences forming the hydrophobic channel is necessary for iron core formation.

Chromosome Deletion↗
PubMed1988

Assessment of ventricular function in arterial hypertension with radionuclide ventriculography.

Diastolic function of the left ventricle was assessed in 29 untreated patients with mild to moderate hypertension and in 21 normotensive control subjects using gated radionuclide ventriculography. In hypertensive patients, the time to peak filling rate was significantly longer (p less than 0.01) than that in control subjects, and first-third filling fraction and peak filling rate were significantly reduced (p less than 0.001). The ejection fraction and peak ejection rate were also significantly reduced in hypertensive patients (p less than 0.001). No relation was observed between diastolic functional impairment and age, cardiac hypertrophy, or severity of hypertension. Thus, early impairment of ventricular filling is present in hypertension, even in young patients without evidence of cardiac hypertrophy.

Adult↗
PubMed1988

Inhibition of the aldosterone response to sodium depletion in man by stimulation of dopamine DA2 receptors.

In this study we have investigated the effect of co-dergocrine, a selective DA2-agonist, on plasma aldosterone concentrations (PAC) in twelve patients with essential hypertension both in basal conditions and during sodium depletion. Sodium depletion resulted in an increase of PAC from 38 (13) pg/ml to 297 (21) pg/ml. The PAC response to sodium depletion was reduced to 155 (29) pg/ml by co-dergocrine. No significant PAC changes were found in patients maintained on a normal sodium intake. In addition the drug did not significantly modify plasma renin activity (PRA) in either experimental group. These results suggest that the dopaminergic inhibition of aldosterone secretion in man is mediated by DA2 receptors in the adrenal cortex.

Aged↗
PubMed1988

Metabolic changes during post-ischaemic reperfusion.

We attempted to identify the nature and time-course of metabolic changes occurring during ischaemia followed by reperfusion either in coronary artery disease patients undergoing intracoronary thrombolysis or in isolated and perfused rabbit hearts. Arterial and coronary sinus differences for oxygen, lactate, glucose, free fatty acid and creatine kinase were measured in patients undergoing successful intracoronary thrombolysis of left anterior descending occlusion. Early reperfusion (after 160 mins of ischaemia) restored aerobic metabolism and myocardial contractility. In contrast, reperfusion after more prolonged ischaemia (335 mins) did not restore mitochondrial function or contractile activity of the myocytes. Results obtained using isolated and perfused rabbit hearts also confirm that the likelihood of recovery during reperfusion depends on the rapidity of recanalization. Furthermore the data reported indicate that on reperfusion after prolonged ischaemia (90 mins) cell damage occurs, leading to a breakdown of the permeability barrier to ions and to larger molecules such as creatine phosphokinase. As a consequence, reperfusion produces a large increase of intracellular calcium, whilst the intracellular magnesium content is severely reduced. Under these conditions, with the observed loss of magnesium from the cell, mitochondrial calcium transport is highly stimulated and the equilibrium between ATP synthesis and calcium influx is shifted towards calcium influx. This sequence of events leads to mitochondrial calcium overload with subsequent damage of mitochondrial structure and loss of the ability to synthesize ATP. Reperfusion of the isolated rabbit hearts with solutions containing high magnesium and low calcium for 10 mins reduced mitochondrial calcium overload. This, in turn, resulted in maintenance of ATP synthesis and, on return to normal perfusate, in partial recovery of developed pressure and myocardial ATP content. These findings may be of importance in the restoration of blood flow to ischaemic heart muscle during thrombolysis.

Adenosine Triphosphate↗
PubMed1988

Protective effect of a prostacyclin-mimetic on the ischaemic-reperfused rabbit myocardium.

To assess whether the administration of the stable prostacyclin-mimetic ZK 36374 (iloprost) protects the myocardium in a dose-dependent manner against ischaemia and reperfusion, isolated rabbit hearts were infused with three different concentrations of iloprost: 2.7, 27 and 270 nM. Diastolic and developed pressures were monitored; coronary effluent was collected and assayed for creatine phosphokinase (CPK) activity and for noradrenaline concentration; mitochondria were harvested and assayed for respiratory activity; ATP production and calcium content and tissue concentration of adenosine triphosphate (ATP) and creatine phosphate (CP) were determined. Treatment with iloprost altered neither developed pressure under normoxic conditions nor the rate and extent of depletion of ATP and CP during ischaemia. The ischaemic-induced deterioration of mitochondrial function, however, was attenuated. On reperfusion, hearts treated with iloprost recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores and mitochondrial function. The reperfusion-induced mitochondrial calcium overload and release of CPK and of noradrenaline were also significantly reduced. The effect of iloprost was dose-dependent. The lower concentration (2.7 nM) failed to modify ischaemic and reperfusion damage. The best protective effect was found at 27 nM. An increase of the dose to 270 nM did not result in further protection. It is concluded that iloprost infusion provides a dose-dependent protection of the heart against some of the deleterious effects of ischaemia and reperfusion and, in particular, prevents mitochondrial calcium overload and maintains mitochondrial function. Because this protection occurred in the absence of negative inotropic effect during normoxia or of a coronary dilatory effect during ischaemia, it cannot be attributed to an energy sparing effect or to improvement of oxygen delivery. Therefore, alternative mechanisms of action are to be considered.

Adenosine Triphosphate↗
PubMed1988

Neonatal T4+ lymphocytes: analysis of the expression of 4B4 and 2H4 antigens.

Using monoclonal antibodies anti-2H4 and anti-4B4 we investigated by double immunofluorescence and immunorosette technique the presence of cells displaying the helper-inducer and the inducer of suppression phenotype among T4+ cord blood cells. The analysis of the estimated frequencies of subpopulations of T4+ cells shows that a high percentage of T4+ cord blood cells can coexpress both antigens in comparison to adult. Furthermore the percentage of T4+ cells with helper-inducer phenotype (2H4-4B4+) is significantly lower than that in the adult, while the percentage of T4+ cells with suppressor-inducer phenotype (2H4+4B4-) although higher, is not significantly different. These findings suggest that the relative immunoincompetence observed in the newborn may result from a variety of mechanisms including a low percentage of helper-inducer (4B4+2H4-) T4+ lymphocytes possibly also associated to an increased number of suppressor-inducer T4+ cells (2H4+4B4-).

Antibodies, Monoclonal↗
PubMed1988

The role of glutathione status in the protection against ischaemic and reperfusion damage: effects of N-acetyl cysteine.

It is known that myocardial ischaemia causes a marked decline of cellular thiol pool and of protein sulphydryl groups content. Reperfusion under these conditions results in oxydative damage which is concomitant with poor recovery of mechanical function. We have evaluated the role of glutathione status in the protection against ischaemic and reperfusion damage by treating the isolated rabbit hearts with N-acetylcysteine (10(-6) M), a sulphydryl group donor. Ischaemic and reperfusion damage was determined in terms of mechanical function, rate of lactate and creatine kinase (CPK) release, mitochondrial function and tissue content of reduced (GSH) and oxidized (GSSG) glutathione and of protein sulphydryl groups (SH). After 60 mins of ischaemia (induced by reducing coronary flow from 24 to 1 ml/min) followed by 30 mins of reperfusion there was an increase of diastolic pressure to 51.6 +/- 3.5 mmHg with only a 22% recovery of systolic pressure, massive CPK release and a deterioration in mitochondrial function. Tissue contents of GSH and of protein SH were severely decreased, while those of GSSG were increased. The GSH/GSSG ratio was reduced from the aerobic value of 50 to 13.4, suggesting that an oxidative stress has occurred. N-acetylcysteine infused for 60 mins before ischaemia determined a 38% increase in tissue content of GSH with no major changes of GSSG or protein SH. The ischaemic-induced decrease of GSH and protein SH was also limited by pretreatment with N-acetylcysteine and there was no accumulation of GSSG after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1988

Effects of changes in intravascular volume on atrial size and plasma levels of immunoreactive atrial natriuretic peptide in uremic man.

To study the trigger for the release of atrial natriuretic peptide (ANP) in man, we measured the atrial areas (AA) by 2-D echocardiography, the total blood volume (TBV) by 131I-serum albumin and plasma immunoreactive ANP (i-ANP) concentrations by radioimmunoassay, after prior plasma extraction, for 10 dialyzed uremic patients. Measurements were made when the patients were volume-loaded or volume-depleted by isoosmotic ultrafiltration and again 48 h later, when they were again volume-loaded. Analysis of plasma extracts by high-performance gel permeation chromatography revealed that the greatest amount of the i-ANP fraction was a peptide eluting like human synthetic alpha-ANP. Ultrafiltration consistently decreased the TBV, while spontaneous regain of body-fluids caused TBV to rise to pre-ultrafiltration levels. Changes in TBV were closely related in time to changes in both right (RAA) and left (LAA) atrial area and in plasma i-ANP concentrations. Significant direct relationships were found between TBV and RAA, TBV and i-ANP and between both LAA and RAA and i-ANP. Furthermore, the decreases and the increases in TBV, RAA and LAA were closely correlated with changes in i-ANP. Multiple regression analysis, however, revealed that the changes in plasma i-ANP were mainly related to the changes in RAA, with little or no relationship to the changes in TBV or LAA. These findings are evidence for a positive feed-back between the level of intravascular filing volume, extent of atrial distention and amount of i-ANP released into the blood stream.

Adult↗
PubMed1988

Monoclonals and allergy. A review, with experimental contribution.

The role of monoclonal antibodies in allergy has been explored. First the status of art of monoclonal research in general is reviewed, by outlining a monoclonals identikit and the relevant technologies employed for their development. The attention is then focused on the present impact of monoclonals in the allergological field, first considering a general outline, and then the important steps of standardization of monoclonal antibodies. A comprehensive hint is made concerning the monitoring of immunotherapy, with future extrapolations on developing anti-idiotype vaccines, of which same examples can already be found in the infectious field, thus leaving the way open in allergy as well. A second section deals with the experimental contribution of the Authors, with the description of the preparation of the allergenic extracts of D.F., with details of the relevant steps (rabbit immunization; extract characterization; techniques used for monoclonal screening and characterization). The results obtained are discussed in relation to the techniques employed, weighing the reciprocal advantages and drawbacks.

Animals↗
PubMed1988

Immunoreactivity to various peptides in the human carotid body.

Human carotid bodies, removed at routine necropsies, have been subjected to radioimmunoassay for various peptides. Average levels of immunoreactivity, expressed in pm/g, were: met-enkephalin 612, leu-enkephalin 162, bombesin 73, neurotensin 67, VIP 9 and substance P 16. No alpha-hANP immunoreactivity could be detected.

Carotid Body↗
PubMed1987

Mechanism of myocardial protective action of dilazep during ischaemia and reperfusion.

The aim of this study was to investigate if dilazep is able to reduce with a direct protective action on the myocardium the deleterious effects caused by ischaemia and reperfusion. For this purpose we used an isolated rabbit heart preparation. The hearts were either perfused aerobically or made totally ischaemic for 60 min (by abolishing coronary flow) or made ischaemic for 60 min and then reperfused for 30 min. Ischaemic and reperfusion damage was measured in terms of alteration in mechanical function, lactate and CPK release, mitochondrial function and tissue content of Adenosine Triphosphate (ATP), Creatine Phosphate (CP) and calcium. Dilazep (10(-5) M) was administered in the perfusate either 20 minutes before ischaemia or only during post-ischaemic reperfusion. Ischaemia induced a decline of the endogenous stores of ATP and CP, followed by an alteration of calcium homeostasis with increase of diastolic pressure, mitochondria calcium overload and impairment of the oxidative phosphorylating capacities. On reperfusion, tissue and mitochondrial calcium increase the capacity of the mitochondria to use O2 for state III respiration was further impaired and the ATP-generating capacity reduced. Diastolic pressure increased and there was only a small recovery of active tension generation associated with massive CPK release. Administration of dilazep before ischaemia induced a negative inotropic effect which, in turn, resulted in a slowing of the rate of CP and ATP depletion during ischaemia. This protected the hearts against the ischemic, and reperfusion-induced decline in the ATP-generating and O2-utilizing capacities of the mitochondria. In addition, there was a less marked increase in tissue and mitochondrial Ca++, CPK and lactate release were reduced and the recovery of developed pressure on reperfusion was significantly increased. Administration of dilazep during reperfusion failed to modify the exacerbation of ischaemic damage caused by the readmission of coronary flow. These data suggest that dilazep benefits the ischaemic myocardium via an ATP sparing action.

Adenosine Triphosphate↗