Qualitative bedside assay of increased human serum myoglobin by sandwich dot-immunogold filtration for the diagnosis of acute myocardial infarction.

We isolated and purified myoglobin (MYO) from human fresh skeletal muscle and prepared monoclonal and polyclonal antibody from it. A sandwich dot-immunogold filtration assay (DIGFA) for the detection of MYO was developed by using affinity purified sheep anti-MYO antibody as the first antibody for coating nitrocellulose membranes (NCMs; the support) and colloidal gold labelled monoclonal antibody (H3) as the second antibody (an indicator). The test can be completed in 3 min without incubation or any equipment. A reddish dot, indicating positivity, is obvious to the naked eye. No interferences from bilirubin, hemoglobin, rheumatoid factors and lipid were found. In order to use undiluted serum, the detection limit was set at 100 microg of MYO/l. Concentrations up to 30,000 microg/l can be measured without getting a "hook" effect. Serum MYO levels in 53 patients with acute myocardial infarction (AMI), 100 healthy individuals, seven patients with chest pain but without myocardial ischemia and in 39 patients with renal insufficiency were measured simultaneously by DIGFA and enzyme-linked immunosorbent assay (ELISA). All serum samples from patients had MYO concentrations above 100 microg/l by ELISA and were positive by DIGFA. Serum creatinine values were related to MYO test results. Healthy individuals had MYO levels below 85 microg/l by ELISA and were negative by DIGFA.

Coordination of copper with aspirin enhances its anti-platelet aggregation activity.

Anti-platelet aggregation of copper aspirinate, a copper complex of aspirin, has been studied in vitro and in vivo. The result shows that copper aspirinate is much more effective than aspirin against AA-, ADP- and PAF-induced platelet aggregation. Its mechanism is related to the inhibition of platelet cyclooxygenase and release of active substances from platelets, and to the promotion of PGI(2) level in plasma.

Epstein-Barr virus in nasal T-cell lymphomas (polymorphic reticulosis/midline malignant reticulosis) in western China.

Polymorphic reticulosis (PR) or midline malignant reticulosis (MMR) is considered to be malignant, or at least pre-malignant T-cell proliferations of the nose or midline area. Recent reports of small series of nasal T-cell lymphomas have shown a strong association with Epstein-Barr virus (EBV). Furthermore, a peculiar phenotype is described, with expression of CD56 and not of CD3, suggesting a possible origin from natural killer (NK) cells. We have analysed a series of 38 cases of PR/MMR for the presence of EBV by in situ hybridization (ISH) of the EBV-encoded RNAs 1 and 2 (EBER). Twenty cases were tested for expression of EBV-encoded latent membrane protein 1 (LMP-1). Special attention was also paid to the expression of CD3 and the NK cell-related marker CD56. Thirty-two cases (84 per cent) showed positive EBER ISH. In 5 of 20 cases, LMP-1 expression was detected. In three cases, a few scattered cells were positive, and in two cases, LMP-1 was detected in clusters of atypical cells. Most of the neoplasms showed expression of CD3 (89 per cent) and in 27 cases (71 per cent), CD56 was detected. These results are consistent with an aetiopathogenetic role for EBV in most, but not all, cases of PR/MMR. Our findings are less supportive of a major role for LMP-1 in tumour genesis. CD3 expression in most of the cases of PR/MMR underlines the T-cell origin of these neoplasms, often with aberrant expression of CD56.