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Biomedical subjects

M Grilli

Publications and source records attributed to M Grilli.

At least 55 records · Page 3Linked to original sources
PubMed1994

Abnormally high circulation levels of tissue plasminogen activator and plasminogen activator inhibitor-1 in patients with a history of ischemic stroke.

We evaluated 106 subjects with and 109 subjects without a history of ischemic stroke. All were attending a metabolic ward. The two groups were compared for major risk factors for ischemic events. A positive family history for ischemic complications of atherosclerosis was more common in subjects with a history of stroke than in those without; moreover, plasma levels of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (TPA) were higher in patients with documented previous events. A strong positive significant correlation was found between TPA and PAI-1 levels, and an interaction between age and TPA was observed when the sample was stratified according to ages being above or below 70 years. When the patient population was analyzed according to the number of ischemic events, it was found that 62 of the 106 subjects with a history of stroke had experienced more than one ischemic event. Under these conditions, the levels of TPA and PAI-1 still correlated with the occurrence of previous ischemic episodes. As in the whole patient sample, TPA was the strongest discriminator. We conclude that in subjects attending a metabolic ward, TPA and PAI-1 levels consistently help identify subjects with a history of cerebral ischemic episodes and that TPA is the strongest discriminator.

Adult↗
PubMed1993

Tumor necrosis factor alpha mediates a T cell receptor-independent induction of the gene regulatory factor NF-kappa B in T lymphocytes.

We investigated the molecular basis of the ability of DCEK experimental antigen-presenting cells (APCs) to induce the nuclear form of the transcription factor NF-kappa B in T lymphocytes without engagement of the T cell receptor. We found that NF-kappa B induction did not require contact between the APCs and T lymphocytes and could be achieved by medium conditioned by the APCs. The APCs were found to express low levels of mRNA for TNF alpha. The addition of antibody against TNF alpha blocked the ability of APCs to induce NF-kappa B. These observations were extended by the finding that NF-kappa B was also induced in T lymphocytes separated by a membrane from a mixture of T lymphocytes, splenic APCs and antigen by a TNF alpha-dependent mechanism. Together, these findings suggest that induction of NF-kappa B in antigenically stimulated or 'bystander' T cells may take place through stimulation by TNF alpha as well as in response to T cell receptor occupancy.

Animals↗
PubMed1993

[Acute viral myocarditis with transient concentric pseudohypertrophy of the left ventricle complicated by cardiogenic shock].

The authors report the case of a 38-year-old woman with acute influenza myocarditis, cardiogenic shock and multiorgan injuries. The echocardiogram showed symmetric thickening and severe hypokinesis of the ventricular wall, with a concomitant reduction of the left ventricular cavity due to myocardial edema and cellular infiltration. The myocardial thickening gradually decreased and the ejection fraction improved, as shown by serial echocardiographic evaluations. Blood levels of cardiospecific enzymes were slightly elevated and ECG showed little change. The myocarditis resolved without sequelae. The hemodynamic implications of this transient myocardial thickening and its relationship to steroid therapy are discussed.

Acute Disease↗
PubMed1992

NF-kappa B subunit regulation in nontransformed CD4+ T lymphocytes.

Regulation of interleukin-2 (IL-2) gene expression by the p50 and p65 subunits of the DNA binding protein NF-kappa B was studied in nontransformed CD4+ T lymphocyte clones. A homodimeric complex of the NF-kappa B p50 subunit was found in resting T cells. The amount of p50-p50 complex decreased after full antigenic stimulation, whereas the amount of the NF-kappa B p50-p65 heterodimer was increased. Increased expression of the IL-2 gene and activity of the IL-2 kappa B DNA binding site correlated with a decrease in the p50-p50 complex. Overexpression of p50 repressed IL-2 promoter expression. The switch from p50-p50 to p50-p65 complexes depended on a protein that caused sequestration of the p50-p50 complex in the nucleus.

Animals↗
PubMed1991

Characterization of [3H]dopamine uptake sites and [3H]cocaine recognition sites in primary cultures of mesencephalic neurons during in vitro development.

[3H]Dopamine uptake and [3H]cocaine binding sites were studied in primary cultures of ventral mesencephalon from 14-day-old rat embryos. Specific binding sites for [3H]cocaine and [3H]mazindol were detected only in intact cell cultures of ventral mesencephalon, and were absent in sonicated, washed membranes prepared from these cell cultures. [3H]Cocaine was not taken up by the cells through an active transport process because [3H]cocaine binding occurred also at 4 degrees C. Moreover, the possibility of [3H]cocaine entering the cells by passive diffusion and ion trapping was also excluded because extensive washing failed to remove [3H]cocaine from the cells. [3H]Cocaine binding was reduced to 6% of control when cells were permeabilized with streptolysin O (0.2 U/ml, 5 min). Taken together, these results suggest that in cultured mesencephalic neurons, [3H]cocaine may enter the cell by passive diffusion and then be sequestered by a cytosolic compartment that is lost in the process of permeabilization or sonication and washing of membrane preparations. Permeabilization of cultured neurons failed to alter the storage of [3H]dopamine. When cells were permeabilized with streptolysin O (0.2 U/ml; 5 min) after [3H]dopamine was taken up, [3H]dopamine was retained by the cells and did not leak into the incubation medium, indicating that [3H]dopamine was stored in sites that could not pass through the perforated membranes. In contrast, [3H]dopamine uptake into already permeabilized cells was reduced by 33%, suggesting that a cytosolic protein that had leaked out may play a functional role in the uptake process. In contrast to striatal membrane preparations of adult rats, [3H]cocaine binding in intact mesencephalic cell cultures was Na+ independent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗