SummaryA family with a high incidence of spontaneous thromboembolism has been investigated and those members affected were found to have significantly depressed levels of plasma and serum heparin cofactor activity; i.e., antithrombin III and anti-Xa activity. Further studies revealed that despite a marked diminution of antithrombin III activity in these patients measurement of antithrombin III by immunological techniques showed the levels to be normal. It is concluded that this anomaly represents a defect in the synthesis of the antithrombin III molecule. The abnormality appeared to be inherited but the mode of inheritance could not be determined with the available data.

These findings indicate that, except for regulation of the negative APPs by TNF-alpha, the mechanism of APP regulation is different under the conditions of the short-term and the chronic, long-lasting 'acute-phase reaction'.

Summary.Immunophenotyping is considered to be less valuable in the diagnosis of acute myeloid leukaemias (AML) compared with acute lymphoid leukaemias. Here, we present data on the use of quantitative flow cytometry (QFC) of P-selectin glycoprotein ligand 1 (PSGL-1, CD162) and three-colour immunophenotyping including CD162 staining in the identification of myeloid precursors in AML. Analysis of normal peripheral blood (n 20) and normal bone marrow (n 5) samples and on 20 samples from de novo M1, M2, M4 and M5 AML patients demonstrated that PSGL-1 is differentially expressed on various mature and immature leucocyte subsets. It was found by QFC that neutrophils expressed 26500^4500 and monocytes 47200^9900 copies of PSGL-1 on their surface, whereas AML blasts from M1 and M2 AML patients expressed significantly less PSGL-1 (12 000^5300) than mature neutrophils (P , 0´001). In M4 and M5 leukaemias, however, the amount of PSGL-1 on monocytic precursors is displayed in a fairly broad range that is not significantly different from that of mature monocytes (P 0´084). Using three-colour immunophenotyping PSGL-1-dim staining was co-expressed with CD7 and C34 positivity and PSGL-1 staining intensity on immature myeloid cells paralleled with CD45 expression. This would imply a differential expression of PSGL-1 during myeloid haematopoietic development and suggests that quantification of surface PSGL-1 may aid in differentiating myeloblasts from monoblasts by immunophenotyping in different AML subsets.

In the present study we describe the relationship between laboratory values obtained with routinely used laboratory analytical methods and near infrared (NIR) spectral data of 126 whole blood and 228 blood serum samples. Spectra were measured with a SPECTRALYZER 1025 (PMC) computerised research analyser. The relationship among laboratory data and values of the second derivative of the log (1/R) spectra measured at different wavelengths was determined by multiple linear regression (MLR) using three and four term linear summation equations, principal component regression (PCR) and partial least-squares (PLS) regression methods.Along with examples for qualitative detection of protein and lipid in human sera, as well as distinction of albumin and globulin dissolved in physiological saline solution, we describe mathematical models and evaluate their performance for the determination of protein and beta-lipoprotein (β-LP) content of serum as well as oxygen saturation and carbon dioxide pressure in whole blood. Validation of our results yielded a standard error of performance (SEP) of 2.47 g L -1 for protein content and 0.79 TU for β-LP content in blood serum, whereas SEP values of 5.41% for oxygen saturation and 5.27 mm Hg for carbon dioxide pressure in whole blood were found. Our results presented in this preliminary study indicate that NIR measurements can be related to analytical data of whole blood and serum. NIR spectroscopy is a rapid, accurate, cost effective method for determining quality parameters of whole blood and serum and might be a promising new tool in the field of automated clinical laboratory analysis.

Large numbers of papers have been published on the relationship of different diseases and human blood-groups. Comparing blood-group distribution of a great number of patients suffering from acute leukaemia (AL) to that of control persons, no significant differences could be detected (Shirley & Desai, 1965; Vogel & Helmbold, 1972; Harris et al, 1977).We found blood-group 0 frequency surprisingly high among female patients with AL treated in our clinic between 1974 and 1980. Therefore blood-group distribution of patients related to sex was studied. Data of 45 female and 69 male patients are summarized in Table 1. Women suffering from AL have significantly more blood-group 0 than men (51 % and 22%, respectively; x2 = 11.1 1, significant difference). Blood-group A occurred more often (46%) in men with AL than in women (33%). When comparing different types of AL-though our case-number is rather limited-it could be pointed out that blood-group 0 was in highest frequency in women with acute lymphoid leukaemia (62%), while it was less often present in men with acute myeloid leukaemia (21%).These results were compared to blood-group frequency in Hungary. Blood-group 0 occurs in 30-32% of the whole Hungarian population without considerable differences among the different regions (Rex-Kiss & Szabit, 1979). There was no difference when a comparison was made between blood-group distribution of patients with AL and that of a healthy population. However, in group 0 a sex-linked difference was evident. A similar difference in blood-group frequency of a healthy population seems to be rather improbable and no data supporting it are available in the literature.The probable importance of sex differences in blood-group distribution of patients with AL has not been emphasized yet. However, studying retrospectively Mustacchi's earlier report (1960) on 570 patients with AL a similar distribution could be detected. 41 % ofpatients Changes in blood-group characteristics of patients with AL in the course ofdisease are well known but it cannot be used for explaining sex differences in blood-group distribution.