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Biomedical subjects

P Dall'Aglio

Publications and source records attributed to P Dall'Aglio.

At least 19 recordsLinked to original sources
PubMed2000

HTLV-II down-regulates HIV-1 replication in IL-2-stimulated primary PBMC of coinfected individuals through expression of MIP-1alpha.

The influence of human T-cell leukemia/lymphoma virus type II (HTLV-II) in individuals also infected with HIV-1 is poorly understood. To evaluate the reciprocal influence of HTLV-II and HIV-1 infection, primary peripheral blood mononuclear cell (PBMC) cultures from coinfected individuals were established in the presence of interleukin 2 (IL-2). In these cultures, the kinetics of HTLV-II replication always preceded those of HIV-1. Noteworthy, the kinetics of HIV-1 production were inversely correlated to the HTLV-II proviral load in vivo and its replication ex vivo. These observations suggested a potential interaction between the 2 retroviruses. In this regard, the levels of IL-2, IL-6, and tumor necrosis factor-alpha (TNF-alpha) were measured in the same coinfected PBMC cultures. Endogenous IL-2 was not produced, whereas IL-6 and TNF-alpha were secreted at levels compatible with their known ability to up-regulate HIV-1 expression. The HIV-suppressive CC-chemokines RANTES, macrophage inflammatory protein-1alpha (MIP-1alpha), and MIP-1beta were also determined in IL-2-stimulated PBMC cultures. Of interest, their kinetics and concentrations were inversely related to those of HIV-1 replication. Experiments were performed in which CD8(+) T cells or PBMCs from HTLV-II monoinfected individuals were cocultivated with CD4(+) T cells from HIV-1 monoinfected individuals separated by a semipermeable membrane in the presence or absence of antichemokine neutralizing antibodies. The results indicate that HTLV-II can interfere with the replicative potential of HIV-1 by up-regulating viral suppressive CC-chemokines and, in particular, MIP-1alpha. This study is the first report indicating that HTLV-II can influence HIV replication, at least in vitro, via up-regulation of HIV-suppressive chemokines. (Blood. 2000;95:2760-2769)

Acquired Immunodeficiency Syndrome↗
PubMed1999

Synthesis, structure, spectroscopic properties and biological activity of mixed diorganotin(IV) complexes containing pyridine-2-carbaldehyde thiosemicarbazonato and diphenyldithiophosphinato ligands.

Reaction of the title ligands (HPyTSC and HS(S)PPh2, respectively) with R2SnO (R = Me, Et, Bu) in ethanol (EtOH) afforded the complexes [SnMe2(PyTSC) (S2PPh2)].EtOH (1) and [SnR2(PyTSC) (S2PPh2)] (R = Et (2), Bu (3)). The structures of 1 and 2 were determined by single-crystal X-ray diffractometry. In both these complexes the tin atom is coordinated to an N,N,S-dentate thiosemicarbazonate ligand, an anisobidentate dithiophosphinato ligand and the two R groups. The coordination polyhedrons can be described as distorted pentagonal bipyramids. A comparative study of the IR spectra of 1, 2 and 3 indicates that the butyl complex has a similar structure. Multinuclear (1H, 13C, 31P and 119Sn) NMR data suggest that the structures of 1 and 2 probably remain in CDCl3 (or DMSO-d6) solution but compound 3 partially decomposes in these media. Preliminary results on the effects of the complexes on the proliferation and differentiation of FLC, CEM, U937, K562 and TOM-1 leukaemia cells, and on the clonogenic activity of K562 cells are also described.

Cell Differentiation↗
PubMed1999

Disruption of nocturnal melatonin rhythm and immunological involvement in ischaemic stroke patients.

The aim of this study was to evaluate nocturnal and diurnal urinary melatonin excretion in a group of ischaemic stroke patients, and to verify if a possible impairment of this excretion could be linked with some changes of immunological and neuro-psychic status. We assessed 13 ischaemic stroke patients and five healthy controls for nocturnal urinary melatonin excretion, which was found to be impaired in stroke patients (patients, 0.05 +/- 0.01 ng/ml; controls, 30 +/- 3.0 ng/ml; P < 0.001). No differences were found between the groups with regard to diurnal excretion. Patients with impaired nocturnal melatonin excretion presented: a decreased cell-mediated immunity (assessed by a skin-test); a prevalence of anergic status (69% of patients were anergic compared with 0% of controls; P < 0.05); a slight (but not significant) enhancement of plasma cortisol levels; and some changes in lymphocyte subsets (an overall decrease in CD3 lymphocyte number). In almost all the ischaemic stroke patients there was an impairment of cortisol/melatonin ratio (a marker of depression) and an altered sleep rhythm with mood disorders. Our data suggest that ischaemic stroke patients had an impairment of nocturnal urinary melatonin excretion, which was associated with an impaired cell-mediated immunity and some changes of lymphocyte subsets. In addition, reduced melatonin excretion might be associated with neurological and psychical symptoms.

B-Lymphocytes↗
PubMed1998

Fasting and post-methionine load homocyst(e)ine values are correlated with microalbuminuria and could contribute to worsening vascular damage in non-insulin-dependent diabetes mellitus patients.

The study aim was to assess the relationship between homocyst(e)inemia and microalbuminuria in non-insulin-dependent diabetes mellitus (NIDDM) patients. The study was performed on 33 NIDDM patients (16 males and 17 females), and 16 healthy control subjects (seven males and nine females). Plasma fasting and post-methionine load homocyst(e)ine (tHcy), together with other parameters that could modify tHcy levels, were assessed. There were no significant differences between NIDDM patients and controls for fasting tHcy (8.12 +/- 3.17 v 7.19 +/- 2.40 micromol/L) and post-methionine load tHcy (26.51 +/- 11.50 v 25.06 +/- 10.76 micromol/L). Moreover, there was a significant correlation between urinary albumin excretion (UAE) and fasting tHcy (r = .340, P = .05) and post-methionine load tHcy (r = .502, P = .004) in NIDDM patients. Fasting tHcy was correlated both with post-methionine load tHcy (r = .429, P = .01) and with vitamin B12 (r = -.349, P = .04) in NIDDM patients. Microalbuminuric NIDDM patients had higher fasting tHcy (9.05 +/- 3.83 micromol/L) than normoalbuminurics (7.12 +/- 1.95 micromol/L). In addition, NIDDM patients with complications presented higher fasting tHcy values than the group without complications (9.61 +/- 3.34 v 6.53 +/- 2.09 micromol/L, Kolmogorov-Smirnov two-sample test for nonparametric data [KS] = 1.794, P = .003), without any other significant differences in the parameters considered. tHcy could be an important risk factor worsening the prognosis in NIDDM patients, especially microalbuminuric patients. Microalbuminuric NIDDM patients could be particularly prone to hyperhomocyst(e)inemia, probably due to endothelial or renal dysfunction with a reduction in the scavenging of tHcy.

Aged↗
PubMed1998

Dopamine-2 receptor blockade potentiates the renal effects of nitric oxide inhibition in humans.

In eight young healthy subjects on a 240 mM Na diet mean arterial pressure (MAP), renal hemodynamics and renal handling of Na and exogenous Li were measured at baseline and during acute nitric oxide (NO) inhibition with 90-minute infusion of 3.0 microg/kg x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The same experiment was repeated with infusion of 50 microg/kg x min(-1) of DA2 receptor blocker L-Sulpiride (L-SULP) alone and, finally, with simultaneous infusion of both L-NAME and L-SULP. L-SULP alone did not elicit any effect. L-NAME alone produced no changes in MAP from 0 to 45 minutes (P1) and a 6.6% increase at 45 to 90 minutes (P2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 10.2% and 7.6%, respectively, in P1 and by 15.3% and 11.5% in P2. Filtration Fraction (FF) rose by 4.2% in P2. Calculated renal vascular resistance (RVR) increased by 13.0% to 25.6%. Fractional excretion of Na (FENa) and Li (FELi) fell by 20.0% and by 16.0%, respectively, in P1 and by 40.0% and 25.1% in P2. All these variations, except for MAP and GFR, were significantly greater during coinfusion of L-NAME and L-SULP. ERPF declined by 17.8% to 33.7%, FENa by 26.7% to 53.3%, FELi by 13.8% to 34.8%, while RVR rose by 22.5% to 59.1% and FF by 10.1% to 29.3%. The present data confirm that NO blockade with low-dose systemic infusion of L-NAME produces renal vasoconstriction, reduced GFR with slight increase in FF, and enhanced tubular Li, and Na reabsorption. Since increase in RVR and FF and decrease in FENa and FELi are markedly potentiated by the simultaneous infusion of DA2 blocker L-SULP, which exerts no effects by itself, we suggest that DA interactions between DA system at the level of DA2 receptors and basal NO production play a physiological role in the regulation of renal function in humans.

Adult↗
PubMed1997

Angiotensin II blockade does not prevent renal effects of L-NAME in sodium-repleted humans.

In seven healthy, young subjects on a 240 mmol sodium diet, mean arterial pressure (MAP), renal hemodynamics, and renal handling of Na and exogenous Li were measured at baseline and during short-term nitric oxide (NO) blockade with a 90-minute infusion of 3.0 microg x kg(-1) x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The infusion was performed twice: after a 3-day pretreatment with either placebo or 50 mg losartan to block Ang II receptors. With placebo, L-NAME produced no change in MAP from 0 to 45 minutes (period 1) and only a 5% increase at 45 to 90 minutes (period 2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 11.7% and 8.0%, respectively in period 1 and by 14.6% and 11.6%, respectively, in period 2. Calculated renal vascular resistance (RVR) increased by 13.0% to 20.6%. Fractional excretion of Na (FE(Na)) and Li (FE(Li)) fell by 30.0% and 21.0%, respectively, in period 1 and by 44.2% and 31.1% in period 2. All these variations were significant versus baseline. With losartan, the rise in MAP at 45 to 90 minutes was completely abolished, whereas all changes in ERPF, GFR, RVR, FE(Na), and FE(Li) in response to L-NAME were the same as those observed with placebo. The present data show that NO blockade with low-dose systemic infusion of L-NAME produces renal vasoconstriction, reduced GFR, and increased tubular Na reabsorption independent of changes in MAP. Reduced FE(Li) indicates an effect of NO on the proximal tubule. Since these changes are not prevented by losartan, we conclude that in Na-repleted humans, renal vasoconstriction and Na-retaining effects of inhibition of basal NO production are not due to the unopposed action of endogenous Ang II.

Adult↗
PubMed1997

[Doppler echocardiographic study of left ventricular function in patients with systemic lupus erythematosus].

This study was aimed at investigating abnormalities in left ventricular size and function in patients with systemic lupus erythematosus without overt cardiovascular manifestations, in order to detect a very early impairment in myocardial function. Seventeen females and 1 male with systemic lupus erythematosus of 4 to 20 year duration and without clinical evidence of heart disease were studied. Twelve healthy volunteers, matched for age, sex and quatelet index, were utilized as controls. Each patient had a two-dimensional M-mode echocardiographic and Doppler examination. In patients with systemic lupus erythematosus there was an increase in left ventricular ejection fraction (p < 0.001), a slight reduction of end-diastolic volume index and a significant decrease of end-systolic volume index (p < 0.001). In the same patients we also found prolongation of the isovolumic relaxation time (p < 0.02), a clear impairment of diastolic filling parameters. Peak E velocity was lower (p < 0.01), peak A velocity was higher (p < 0.01), with a clear lowering, of the corresponding E/A ratio (p < 0.001) in patients with systemic lupus erythematosus.

Adult↗
PubMed1996

BCL2 oncogene protein expression in human hematopoietic precursors during fetal life.

BCL2 proto-oncogene encodes a 25-kD protein that is characteristically localized in the inner mitochondrial membrane of the cell. It has been reported that BCL2 protein has the unique functional role of blocking programmed cells death without affecting proliferation. We have analyzed the expression of the BCL2 protein in fetal hematopoietic tissues from the 10th week of gestational age onward. Fetal thymus, liver, and bone marrow and cord blood were investigated. The experiments were performed by the alkaline-antialkaline phosphatase (APAAP) technique by staining air-dried acetone-fixed cytospins and by dual-color immunofluorescent assay by staining mononuclear cell suspensions with monoclonal antibodies detecting BCL2 protein and antigens expressed by different hematopoietic subsets. Flow cytometric analyses were performed on FACSort's Comsort 32 (Becton Dickinson, San Jose, CA). The results have shown that the BCL2 protein is expressed in human fetal ontogenesis at the earliest stages examined. The major conceptual aspects of the results are 1) BCL2 is largely expressed in the hematopoietic cells during ontogenesis. BCL2+ cells include both immature and more differentiated subsets. Moreover, the 25-kD protein is expression in cell subsets well known to be high proliferating. This behavior suggests that BCL2 could have more complex functions than those previously described. 2) The expression in the major part of CD34+ cells suggests that BCL2 could play a role in stem cell survival. 3) BCL2 is expressed in not only medullary but also cortical thymocytes, where it could cooperate in positive selection processes. 4) The involvement of BCL2 in the immunosurveillance is indicated not only by its role in B and T cell lineages but also by its expression in particular subsets like that of the cytoplasmic CD3+ fetal liver NK cells. 5) The discrepancy observed between the results of transgenic mice analysis and in vitro inhibition experiments by antisense oligonucleotides performed for understanding BCL2 functions must stress the importance of the direct immunologic analysis of BCL2 in human hematopoietic cells.

Bone Marrow↗
PubMed1985

In vitro immunoglobulin synthesis: T-cell requirement in pokeweed and staphylococcus aureus B-cell activation.

The T-cell requirement for the B-lymphocyte immunoglobulin synthesis induced by Pokeweed mitogen (PWM) and by Staphylococcus aureus Cowan I (SAC) was investigated. We found that the PWM induced B-cell activation was controlled by an absolute Mitomycin-C resistant T-cell helper activity and by a Mitomycin-C sensible T-cell suppressor activity. On the other hand the SAC induced B-cell activation was less thymus dependent and was not influenced by Mitomycin-C treated or irradiated T cells. The different T-cell requirement could be an expression of different responding B-cell subpopulations.

Adult↗
PubMed1984

Altered expression of B lymphocyte surface immunoglobulins in minimal change nephrotic syndrome and focal glomerulosclerosis.

In 20 patients with nephrotic syndrome (10 minimal change glomerulonephritis, MCN; 10 focal glomerulosclerosis, FGS) the peripheral blood lymphocytes showed a statistically significant increase in IgG-bearing cells (SIgG-C) in comparison with 30 patients with other histological types of primary glomerulonephritis with and without nephrotic syndrome (14 and 16, respectively). In the same MCN and FGS patients the serum IgG levels were slightly decreased. Furthermore, 5 cases of MCN in sustained remission for 1 year after steroid therapy showed normalization of the SIgG-C and the serum IgG levels. The possible significance of these phenomena in the pathogenesis of the hypo-IgG-globulinemia in MCN and FGS is discussed.

Adolescent↗
PubMed1983

Minimal change glomerulonephritis and focal glomerulosclerosis markers and 'in vitro' activity of peripheral blood mononuclear cell.

Serum concentrations of IgG, IgA and IgM and PBMC were investigated in 11 prevalently adult patients with idiopathic glomerulonephritis, five minimal change glomerulonephritis (MCGN) and six focal glomerulosclerosis (FGS) and nephrotic syndrome. Among the peripheral blood mononuclear cells (PBMC) E rosette forming cells (T-cells), surface immunoglobulin bearing cells (B-cells), and T-cells with IgG Fc receptor (T gamma) were determined. In the culture supernatants of PBMC stimulated with PWM, the concentration of secreted IgG, IgA and IgM was determined by a solid phase immunofluorescence assay. After stimulation with PWM and PHA, the 3H-TdR uptake from PBMC was evaluated. In patients only the serum values of IgG were found significantly decreased. No difference was observed between patients and healthy age and sex matched controls, in percentage and absolute number of T and B-cells, whereas an increased number of T gamma was present in patients. In these patients after stimulation with PWM the production of IgG and IgA, but not IgM, and the 3H-TdR incorporation, were significantly lower than in healthy controls. These results suggest an imbalance in the cellular co-operation or an intrinsic B-cell defect in the synthesis or secretion of Ig in MCGN and FGS.

Adolescent↗
PubMed1980

Mesangioproliferative glomerulonephritis.

UNLABELLED: The clinical and bioptic aspects of 211 cases of primary mesangioproliferative glomerulonephritis with urinary abnormalities lasting mre than 1 year were reviewed. We observed the following clinical syndromes: 1) Persistent proteinuria, isolated or with microhematuria: - a) with latent onset: 39% with hypertension (H); 10% with renal failure (RF); - b) with acute nephritic syndrome at onset: 31% with H; 6% with RF; 2) Recurrent macroscopic hematuria: 26% with H; 10% with RF; 3) Nephrotic syndrome: 70% with H; 29% with RF. The histological lesions, diffuse in all cases, appeared unrelated to the clinical syndromes and/or immunofluorescent patterns. In 65 cases with prevalent mesangial deposits of IgA, 46% showed persistent proteinuria with latent onset, 23% persistent proteinuria with acute nephritic syndrome at onset, 28% recurrent hematuria and 3% nephrotic syndrome. 37% of such patients developed H, 14% RF and 6% remission (R). On the other hand in 65 patients with other deposits the clinical aspects were as follows: persistent proteinuria with latent onset: 46%; persistent proteinuria with acute nephritic syndrome at onset: 31%; recurrent hematuria: 17%; nephrotic syndrome: 6%. 35% of these cases displayed H; 9% RF and 8% R. CONCLUSION: primary mesangioproliferative glomerulonephritis appears to represent a heterogeneous group with only the morphological aspects in common and associated with one of the three above-mentioned clinical syndromes. Immunohistology shows different Ig and/or complement which bear no specific relationship with clinical courses. In particular IgA deposits are present in 50% of the cases and are only related to higher incidence of recurrent hematuria and abnormal IgA serum levels.

Adolescent↗