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Biomedical subjects

V Martinelli

Publications and source records attributed to V Martinelli.

At least 127 records · Page 7Linked to original sources

Electrophysiological and MRI evaluation of neurological involvement in Behçet's disease.

Eight patients with stable Behçet's disease were studied by means of multimodality evoked potentials and magnetic resonance imaging to evaluate the possibility of an earlier and objective demonstration of clinical and subclinical Central Nervous System (CNS) involvement. It was shown that both diagnostic techniques are useful for quantitative evaluation of neurological involvement in Behçet's disease; of particular interest was the demonstration of subclinical CNS changes.

Adult↗

Proliferative pathways in CD1- CD3+ CD4+ CD8+ T-prolymphocytic leukemic cells: analysis with monoclonal antibodies and cytokines.

The antigenic profile and the proliferative pathways in leukemic cells from the patient TRT with T-prolymphocytic leukemia (T-PLL) were analyzed using monoclonal antibodies (MoAbs) and cytokines. T-PLL cells expressed the phenotype CD1- CD3+ CD4+ CD8+. Incubation with the differentiating agent phorbol-12-myristate-13-acetate markedly increased the percentage of cells with the CD4- CD8+ phenotype, suggesting that leukemic cells were already committed towards a differentiated element with the CD4- CD8+ phenotype. T-PLL cells were induced to proliferate by anti-CD2 MoAb 9-1 + 9.6 and by anti-CD3 MoAb OKT3. The two pathways exhibited normal functional interactions and were susceptible to modulation by anti-HLA class I MoAbs. These results indicate that regulation of cell proliferation was preserved to a significant extent in the T-PLL cells analyzed. At variance with normal resting T cells that require previous activation to proliferate when incubated with interleukin-1 (IL-1) or interleukin-2 (IL-2), T-PLL cells proliferated vigorously when incubated with either interleukin. Furthermore, T-PLL cells proliferated when incubated with immune interferon (IFN-gamma). The latter finding parallels the enhancement by IFN-gamma of the proliferative response of lectin-activated murine T lymphocytes. These results suggest that T-PLL cells, which express a high constitutive level of c-myc mRNA, may be in an activated state. The antigenic phenotype and the characteristics of the proliferative pathways of T-PLL cells from the patient TRT are compatible with the possibility that they may be derived from an intermediate thymocyte.

Antibodies, Monoclonal↗

Differential regulatory role of monomorphic and polymorphic determinants of histocompatibility leukocyte antigen class I antigens in monoclonal antibody OKT3-induced T cell proliferation.

Monoclonal antibodies (mAb) to monomorphic and polymorphic determinants on the heavy chain of histocompatibility leukocyte antigen (HLA) class I antigens inhibit mAb OKT3-induced T cell proliferation, whereas the anti-beta 2-microglobulin mAb NAMB-1 does not affect it. The inhibitory effect of anti-HLA class I mAb is specific, is not an Fc-mediated phenomenon, does not require accessory cells, and does not involve early stages of T cell activation. Distinct determinants of HLA class I antigens regulate T cell proliferation by different mechanisms, because the anti-HLA-A2, A28 mAb CR11-351, and the mAb W6/32 to a framework determinant of HLA class I antigens block interleukin 2 (IL-2) secretion and IL-2 receptor expression, whereas the mAb CR10-215 to a monomorphic determinant blocks only IL-2 receptor expression. The mAb CR10-215 and W6/32 induced a 50% of maximal inhibition of T cell proliferation, when added after 27 and 12 hr, respectively, of incubation of peripheral blood mononuclear cells with mAb OKT3. On the other hand, the mAb CR11-351 inhibited T cell proliferation even when added after 38 hr of incubation of peripheral blood mononuclear cells with mAb OKT3 and was the only one to inhibit proliferation of cycling T lymphocytes. It is suggested that HLA class I antigens regulate T cell proliferation by interacting with cell-surface molecules involved in T cell activation. The differential inhibitory activity of the anti-HLA class I monoclonal antibodies tested may reflect the different ability of the corresponding determinants to interact with activation molecules.

Antibodies, Monoclonal↗

The rapid assessment of visual dysfunction in multiple sclerosis.

A consecutive series of patients with normal activity and a diagnosis of multiple sclerosis (10 male and 31 female) underwent extensive ophthalmological examination including visual evoked potentials (VEPs) and a new test of contrast sensitivity, which is described in detail. Seventy three per cent of patients had abnormal contrast sensitivity and 83% had abnormal VEPs. There was no association between abnormalities of the two types, but patients who had impaired contrast sensitivity and normal VEPs were younger than those whose contrast sensitivity was normal but whose VEPs were not. The test of contrast sensitivity (which took less than 5 minutes to administer) was the only examination to reveal visual abnormalities in all nine patients with a history of optic neuritis, and would be a useful supplementary test in the examination of patients with suspected multiple sclerosis.

Adolescent↗

Assessment of visual function in MS patients: comparative study of some diagnostic tests.

Optic pathways are frequently involved in Multiple Sclerosis (MS). However, in some cases the involvement is asymptomatic or gives rise to only slight visual disturbances without alterations of visual acuity or of clinically evident visual field defects. In these cases several diagnostic tests permit an objective evaluation of the visual dysfunction. The aim of this study is to compare the value of contrast sensitivity test (CST), pattern reversal visual evoked potential (VEP), ophthalmoscopy, Goldmann perimetry in 45 MS patients with normal visual acuity. Examination of contrast sensitivity was carried out with a simple two-alternative forced choice test estimating the spatial frequency of 4 cycles/degree. The VEP was performed with a pattern reversal checkerboard at a spatial frequency of 1 and 2 cycles/degree. Fundus examination was abnormal in 12 patients; visual field defects were detected in 16 patients. 32 patients (71.1%) had abnormal CST in one or both eyes. VEP for the 30' checks was abnormal in 32 cases (71.1%) and that for the 15' checks in 36 cases (80.0%). All but 4 patients (91.2%) had one or more abnormal tests. All patients with abnormal perimetry and/or fundus examination had also CST and/or VEP altered. It is apparent that CST and VEP reveal a significant proportion of abnormalities in the visual system that have not been revealed by routine neuroophthalmological examination.

Adolescent↗

Visual evoked potentials in diabetic teen-agers: influence of metabolic control and relationship with peripheral neuropathy.

85 type 1 diabetics aged between 8 and 20 years (mean: 15.06) performed Pattern Reversal Visual Evoked Potentials (PRVEP). In addition all of them were investigated for peripheral neuropathy and 63 subjects for retinopathy. Our study disclosed a subclinical involvement of optic nerve pathways in about 1/4 of diabetic teen-agers. P100 mean latency was delayed in diabetics for both 30' (112.8 +/- 7.7 msec versus 109.1 +/- 4.8 msec) and 15' check size (119.1 +/- 10.5 msec versus 112.8 +/- 5.2 msec). The N75-N140 interpeak latency was also significantly delayed and the mean N75-P100 amplitude was significantly reduced in diabetics. No correlation was found between PRVEPs latency and age, HbA1, and insulin requirement. The mean P100 latency significantly increased with the duration of diabetes. A negative correlation was found at the 30' check size between P100 latency and motor and sensory conduction velocity in all the examined nerves. 10 out of 63 patients, who had been examined with fluorangiography, showed abnormalities; only 2 of these 10 subjects had abnormal PRVEP. The association of prolonged P100 latency, prolonged N75-N140 interpeak latency and reduced N75-P100 amplitude can be considered consequent to a desincronisation of the impulses travelling along the optic pathways.

Adolescent↗