The B19 parvovirus is a remediable cause of severe chronic anemia in HIV-infected patients. Recognition of and therapy for parvovirus in this population will avoid erythrocyte transfusion and should prevent transmission of the virus to other persons, including immunosuppressed persons and women of child-bearing age.

(4) and normal and malignant tissues (6, 7) showed that R24 reacts with melanocytes, astrocytes, melanomas, astrocytomas, and a subset of sarcomas. R24 also mediates a variety of biological effector functions, including tumor cell aggregation, human complement-mediated cytotoxicity, and antibody-dependent cell-mediated cytotoxicity with human effector cells (refs. 8-10; unpublished work).In the present study, we have investigated the response of melanoma patients to R24 with regard to different dose levels, toxicity, serological parameters, and tumor response. MATERIALS AND METHODSPatients. Patients' tumors were shown to express GD3 by indirect immunofluorescence tests on frozen sections prior to treatment. All patients had objectively measurable disease, a performance status (Karnofsky scale) of at least 60, and had been off anticancer therapy for at least 4 weeks. No concurrent anticancer therapy was given during evaluation. Patients were considered evaluable 6 weeks after initiation of therapy; 10 patients are evaluable and 2 have not yet reached the 6-week mark.Preparation and Administration of R24. R24 was prepared from ascites of (BALB/c x C57BL/6)F1 mice and purified by ammonium sulfate precipitation, chromatography over protein A-Sepharose and Sephadex G-25 columns, and filtration. Each R24 batch was tested for antibody reactivity and assayed for nucleic acids, 16 mouse viruses, bacteria, fungi, and mycoplasma. Preparations underwent standard safety testing in mice and guinea pigs and pyrogenicity testing in rabbits.R24 was administered by i.v. infusion in 100-200 ml of 0.9% saline/5% human serum albumin. Skin tests with 0.1 ,ug of R24 were done before the first treatment. The schedule of treatment was 1 or 10 mg/M2 every other day for eight treatments or 30 mg/M2 per day by continuous infusion on days 1-5 and 8-12.Serological Tests. R24 antibody titers were determined by testing serum samples in protein A mixed hemadsorption assays (11) against the melanoma target cell line SK-MEL-28. R24 concentrations were measured by an enzyme-linked immunoassay. Falcon 3034 plates were precoated with purified R24 at 125 ,g/ml. Rabbit anti-mouse IgG3 (Bionetics, Kensington, MD) diluted 1:100 was mixed (1:1, vol/vol) with patients' serum samples diluted 1:4 and incubated for 120 min. The mixture was transferred to the precoated wells and incubated for 60 min, and wells were washed with phosphatebuffered saline. Wells were incubated with goat anti-rabbit IgG linked to alkaline phosphatase (Sigma) for 60 min. Alkaline phosphatase activity was determined using p-nitrophenyl disodium phosphate substrate (12). R24 concentrations were determined by comparison with standards using different concentrations of purified R24 diluted in a pretreatment serum sample from the patient.Human IgG antibody against mouse Ig was detected by enzyme-linked immunoassays. Falcon 3034 plates precoated with R24 at 50 ug/ml were incubated with patients' serum samples diluted 1:50 for 60 min and washed with'phosphatebuffered saline. Anti-human I...

Background-Cocaine has been implicated as a trigger of acute myocardial infarction in patients with and those without underlying coronary atherosclerosis. However, the magnitude of the increase in risk of acute myocardial infarction immediately after cocaine use remains unknown. Methods and Results-In the Determinants of Myocardial Infarction Onset Study, we interviewed 3946 patients (1282 women) with acute myocardial infarction an average of 4 days after infarction onset. Data were collected on the use of cocaine and other potential triggers of myocardial infarction. We compared the reported use of cocaine in the hour preceding the onset of myocardial infarction symptoms with its expected frequency by using self-matched control data based on the case-crossover study design. Of the 3946 patients interviewed, 38 (1%) reported cocaine use in the prior year and 9 reported use within the 60 minutes preceding the onset of infarction symptoms. Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, Pϭ0.01), current cigarette smokers (84% vs 32%, PϽ0.001), younger (44Ϯ8 vs 61Ϯ13 years, PϽ0.001), and minority group members (63% vs 11%, PϽ0.001). The risk of myocardial infarction onset was elevated 23.7 times over baseline (95% CI 8.5 to 66.3) in the 60 minutes after cocaine use. The elevated risk rapidly decreased thereafter. Conclusions-Cocaine use is associated with a large abrupt and transient increase in the risk of acute myocardial infarction in patients who are otherwise at relatively low risk. This finding suggests that studying the pathophysiological changes produced by cocaine may provide insights into the mechanisms by which myocardial infarction is triggered by other stressors. (Circulation. 1999;99:2737-2741.)

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