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Biomedical subjects

E Nobile Orazio

Publications and source records attributed to E Nobile Orazio.

7 recordsLinked to original sources

Low levels of LTB4 in cerebrospinal fluid of AIDS patients with cryptococcal meningitis.

In this study we evaluated the release of leukotriene B4 (LTB4) in the cerebrospinal fluid (CSF) of 12 patients with Acquired Immunodeficiency Syndrome (AIDS), which disease was complicated by Cryptococcal Meninigitis and in CSF of 12 control subjects with inflammatory and degenerative pathologies of the Central Nervous System (CNS). We obtained low levels of LTB4 in all the AIDS patients (mean 60.5 pg/ml), while the HIV negative subjects with degenerative and inflammatory pathologies of CNS showed a mean of 91.5 pg/ml. The finding of low levels of this inflammatory reaction mediator agrees with the limited clinical symptoms of cryptococcal meningoencephalitis in patients affected by AIDS.

Acquired Immunodeficiency Syndrome↗

NK cells in patients with peripheral neuropathy and IgM monoclonal protein reacting with the myelin-associated glycoprotein (MAG).

We studied Leu 7+ cell distribution and natural killer (NK) activity in the peripheral blood of six patients who had peripheral neuropathy and monoclonal IgM protein directed against myelin-associated glycoprotein (anti-MAG IgM). We did not find any difference between patients and control subjects (healthy or polyneuropathic, some with IgM monoclonal paraprotein but without anti-MAG activity). The presence of autologous sera did not interfere with these results. We noted an increase in Leu 11+ cell percentages after pre-incubation of the patient cells with autologous sera but the phenotypes of cells from control subjects did not change after incubation with autologous or patient sera.

Aged↗

Protein C in acute stroke.

The plasma concentrations of protein C, an anticoagulant protein, and fibrinopeptide A were measured in 37 patients with acute hemispheric stroke and in age-matched controls with nonvascular neurologic diseases. In 11 stroke patients who died within 15 days after the onset (nonsurvivors) protein C antigen concentration on admission was lower than in the control group (p less than 0.005), with a mean value of 63% of the concentrations found in the 26 survivors (p less than 0.001). The difference in protein C concentrations was not associated with different prothrombin time ratios and serum albumin concentration in survivors and nonsurvivors of stroke and was independent of the size of the cerebral lesion. Increased fibrinopeptide A concentration on admission was found in all stroke patients (p less than 0.001), but it was higher in nonsurvivors than in survivors (p less than 0.01), suggesting that lower protein C concentrations in nonsurvivors might be due to increased thrombin-dependent protein C activation. In survivors, protein C concentration was slightly but significantly higher than in controls (p less than 0.05) and was unchanged 2 months after stroke, a time when fibrinopeptide A concentrations had returned to normal. These results show that protein C is involved in the hemostatic derangement caused by stroke and provide a rationale for clinical trials evaluating the therapeutic supplementation with protein C of patients with acute ischemic stroke.

Acute Disease↗

Hypercoagulability in acute stroke: prognostic significance.

To evaluate the clinical significance of hemostatic abnormalities in acute stroke, we studied coagulation and platelet function in 70 patients with recent cerebral infarction or hemorrhage and in 45 age-matched controls. Higher levels of one-stage factor VIII coagulant activity, fibrinopeptide A (FPA), and beta-thromboglobulin were associated with the occurrence of stroke. All hemostatic test results were remarkably similar in patients with ischemic and hemorrhagic stroke. FPA levels and size of the lesion on CT were the only variables independently predicting mortality in a multivariate regression analysis. Our findings demonstrate that hypercoagulability is an important prognostic factor in stroke and lend support to clinical trials of drugs interfering with the coagulation system in the early phase of cerebral ischemia.

Acute Disease↗

Idiopathic inflammatory polyradiculoneuropathy: evaluation of clinical and laboratory data and therapeutic considerations.

The clinical, immunological and neurophysiological data on 54 patients with idiopathic inflammatory polyradiculoneuropathy (IIP) are reviewed in order to reach a correct diagnostic and therapeutic approach. 49 of these patients presented acute and 5 recurrent IIP. Of the acute cases 10 patients had a severe course with paralysis of all limbs and respiratory insufficiency, and 3 died. An increase in CSF total proteins and impairment of nerve motor conduction velocities proved to be valuable tests for the diagnosis of IIP; these tests usually become more significant after 2 or 3 weeks of illness. Steroid treatment did not prove to be effective, while two patients with acute and progressive IIP, subjected to plasmapheresis, showed rapid and steady improvement. In these two patients the plasmapheresis was associated with azathioprine.

Adolescent↗

A sporadic, atypical case of desminopathy: morphological and immunological characterization.

Recently, abnormal expression of cyclin-dependent kinases was proposed as a possible cause of desminopathy. We describe an atypical case clinically characterized by severe respiratory distress. Muscle biopsy showed subsarcolemmal and intracytoplasmic accumulation areas, which intensively stained with anti-desmin antibodies and contained electrondense filamentous material at ultrastructural level. WB analysis showed 30% increased desmin signal compared to controls. Positive immunostain for CDC2 kinase, CDK2 and emerin and nuclear matrix-associated protein were, found in desmin-positive fibres.

Adult↗