Biomedical subjects
Publications and source records attributed to A Lecchi.
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We have done a comprehensive study in normal volunteers of the in vitro and ex vivo effects of the antiplatelet agent indobufen on platelet aggregation, the release reaction and thromboxane B2 (TxB2) production as induced by different concentrations of aggregating agents. At low concentrations (10 microM), indobufen completely inhibited secondary platelet aggregation, the release reaction and TxB2 production stimulated by ADP, epinephrine and low concentrations of platelet-activating factor (PAF acether). Higher concentrations of indobufen (100 microM) completely inhibited TxB2 production, platelet aggregation and ATP release induced by arachidonic acid (1 mM) or collagen (2 micrograms/ml). The inhibitory effect was partially overcome by higher concentrations of arachidonic acid (2 mM). Data obtained ex vivo 2 h after the oral administration of 200 mg indobufen to 8 normal volunteers were in keeping with those of the in vitro study. We conclude that indobufen inhibits platelet aggregation and the release reaction by inhibiting the platelet arachidonate pathway.
Platelets from two afibrinogenemic patients were used to determine whether fibrinogen is essential for platelet aggregation and to examine whether released fibrinogen contributes to the stabilization of platelet aggregates when platelets have been induced to aggregate and release their granule contents by stimulation with thrombin. The addition of adenosine diphosphate (ADP) to platelet-rich plasma (PRP) or to suspensions of washed platelets from the afibrinogenemic patients caused the formation of small aggregates, which was either not inhibited or only slightly inhibited by the F(ab')2 fragments of an antibody to fibrinogen but was inhibited by an antibody (10E5) to glycoprotein IIb/IIIa. Thus there is a component of ADP-induced platelet aggregation that is not dependent on fibrinogen or other plasma proteins but is dependent on glycoprotein IIb/IIIa. There was little difference in the extent of aggregation and the release of granule contents of normal and afibrinogenemic platelets in response to the release-inducing agents collagen, platelet-activating factor (PAF), sodium arachidonate, or thrombin. With normal or afibrinogenemic platelets, aggregation by thrombin (0.2 U/mL or higher) was not inhibited by the F(ab')2 fragments of an antibody to human fibrinogen. Deaggregation by combinations of inhibitors of platelets aggregated by 1 U/mL thrombin showed no difference between platelets from afibrinogenemic and control subjects, indicating that released fibrinogen does not make a major contribution to the stabilization of platelet aggregates formed by thrombin stimulation.
OBJECTIVES: To determine frequency and type of respiratory and allergic symptoms in textile workers employed in early stages of wool processing. METHODS: A cross-sectional study was carried out in four wool textile mills. 202 subjects (n. 148 males, 54 females, mean age 38.9 yrs, SD 9.5) employed in early stages (combing, n. 138, carding, n. 64) of wool processing were examined and an environmental survey was carried out to determine the level of wool dust exposure. All subjects were submitted to clinical interview, spirometry and measurement of serum specific IgE (s-IgE) against extracts of two wool lots (Australia and New Zealand) by means of RAST. In the subjects with a positive questionnaire for allergic symptoms serum specific IgE for common pneumoallergens were measured (PHADIATOP test). RESULTS: We found higher air dust concentrations during carding operations (inspirable fraction-IF-: range 1.6-20 mg/m3; respirable fraction (RF): 0.5-6.9 mg/m3) and lower concentrations during combing (IF 0.3-0.7 mg/m3, RF 0.1-0.3 mg/m3). 70 out of 202 subjects (34.7%, n. 26 employed in carding and n. 44 in combing operations) reported work-related symptoms. Cutaneous itching was reported by 30 subjects, upper airway irritation by 24, ocular irritation by 17 and dyspnoea by 5. Globally 27 subjects (13.4%) had respiratory work-related symptoms. 12 subjects reported only seasonal respiratory symptoms not related to work. Within the group of 82 symptomatic subjects, 62 (75.6%) had serum specific IgE for common pneumoallergens. In the whole group (n. 202) mean basal FEV-1 was L 3.6, SD 0.9 (103.6% of predicted values). No significant difference was found in basal FEV-1 between carding and combing workers. No s-IgE against the two wool extracts was detectable in any of the 202 examined subjects. CONCLUSIONS: Our data show that in early stages of wool processing: 1) the overall frequency of respiratory work-related symptoms is low and does not seem to be related to the stages of processing, 2) symptoms are mainly nasal and/or ocular; 3) serum s-IgE against wool extracts are not detectable. We conclude that respiratory allergy risk in wool textile mills is low.
Polycythemia and hyperhomocysteinemia are risk factors for thrombosis. Since red blood cells actively metabolize methionine to homocysteine, we investigated whether or not patients with polycythemia have increased plasma levels of homocysteine, which might contribute to their increased thrombotic risk. In ten patients with polycythemia, the plasma homocysteine levels were measured before phlebotomy, three days after the procedure and 1-2 months later. The baseline mean plasma homocysteine levels in patients (9.7 +/- 1.6 mumol/L [+/-SD]) did not differ significantly from that found in 30 sex- and age-matched healthy controls (12.2 +/- 6.9). Despite a fall in the patients' mean [+/-SD] hematocrit from 0.50 +/- 0.02 at baseline to 0.47 +/- 0.03 three days after phlebotomy (significant at 95%) and to 0.48 +/- 0.02 after 1 to 2 months (not significant), the mean plasma homocysteine levels did not change significantly (9.9 +/- 2.3 mumol/L at 3 days and 9.7 +/- 2.1 mumol/L at 1-2 months). It is unlikely that high plasma homocysteine levels contribute to the increased thrombotic risk of polycythemic patients.