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The concentration of lactoferrin, a non-heme iron binding glycoprotein, was determined in more than 1500 EDTA plasma samples by a 2-site solid phase immunoradiometric assay to assess the significance of lactoferrin in plasma and to investigate applications for this assay. The use of commercially available antibody and antigen and a relatively short assay time make this assay more suitable for use in routine clinical laboratories than previous methods. A normal range of 250-750 micrograms/l was established. There was a correlation between plasma lactoferrin concentration and the circulating blood neutrophil count in most patients except those with splenomegaly, post-splenectomy and undergoing intensive chemotherapy. Patients with gross splenomegaly usually had an increased and post-splenectomy patients a decreased lactoferrin/neutrophil ratio indicating a respective increase and decrease in the marginated pool. In patients with acute leukemia after chemotherapy or transplantation plasma lactoferrin levels increased 1 to 5 d before blood neutrophil counts rose. As plasma lactoferrin seems to be derived from neutrophils, its concentration is probably related to the size of the total blood granulocyte pool. Calculation of the lactoferrin/neutrophil ratio demonstrated variations in the size of the bone marrow reserve and the marginated neutrophil pool.

Specific glucocorticoid receptors were measured in circulating mononuclear leukocytes from 12 patients with anorexia nervosa and 21 healthy control subjects. Cells from patients were found to contain a significantly (p less than 0.01) lower level of glucocorticoid receptor (3830 +/- 210 sites/cell, mean +/- SE) than those from controls (4930 +/- 250 sites/cell). A partial glucocorticoid receptor defect may well explain the abnormal cortisol metabolism and glucocorticoid resistance commonly found in patients with anorexia nervosa.

Using the Crithidia assay 3.0 ng biopterin/ml blood was found, of which one third was present in the plasma. The erythrocyte fraction comprised 1.7 ng and the buffy coat 0.33 ng. After Ficoll separation 0.050 ng were found in the lymphocyte layer of 1 ml blood. During blast crisis of chronic myelocytic leukemias increased amounts of biopterin were found in the erythrocyte fraction and in the buffy coat. The high biopterin concentration per unit of protein in the white cell fraction indicated the presence of blasts. In Polycythemia vera increased amounts of biopterin in both the red cell fraction and in the buffy coat were also found but the percentage distribution within total cellular biopterin was markedly shifted toward the erythrocyte fraction. In cases of chronic and acute lymphocytic leukemias the low amounts of biopterin in the red cell fraction agreed with the current view of partial extinction of the erythropoietic line. The isolated lymphoblasts were characterized by high biopterin concentrations per unit of protein. During remission the biopterin patterns approached normal levels.

Neutral glycosphingolipids and gangliosides were isolated from the malignant cells of a patient with acute myelomonoblastic leukemia. Structural analyses were performed by gas-liquid chromatography and by high-performance liquid chromatography combined with enzymatic hydrolysis of glycosphingolipids using glycosidases. We found that, in contrast to normal leukocytes and chronic leukemia cells which have only a single tetraosylceramide species, these acute myelomonoblastic leukemia cells have approximately equal amounts of both globo- and neolactotetraosylceramide. This is the first population of human leukocytes in which we found two families of neutral glycosphingolipids to be present. The ganglioside fraction was composed of appreciable quantities of both NeuAc alpha 2 leads to 3Gal beta 1 leads to 4Glc beta 1 leads to 1Cer (GM3, hematoside) and NeuAc alpha 2 leads to 3Gal beta 1 leads to 4GlcNAc beta 1 leads to 3Gal beta 1 leads to 4Glc beta 1 leads to 1Cer (sialoparagloboside). These cells did not have the 'leukocyte-specific' N-acetylneuraminosyllactotriaosylceramide found in normal human lymphocytes and neutrophils. These results are discussed in relation to normal leukocyte differentiation and acute leukemia. The present study also illustrates the usefulness of combining enzymatic degradation with high-performance liquid chromatography for glycosphingolipid structural determination.

Cysteamine is the most effective agent known for the reduction of the elevated cystine content of cells from patients with cystinosis. A defect in endogenous cysteamine generation could account for many of the metabolic features of this disorder. To test this hypothesis, we have developed improved methods for measuring pantetheinase (cysteamine-generating) activity and intracellular cysteamine levels and used these methods to measure such parameters in cystinotic and normal leukocytes and cultured skin fibroblasts. Pantetheinase activity as defined in the test was similar in extracts of cystinotic and normal cells [leucocytes, normal, 78 +/- 15 (S.E.), cystinotic, 56+/- 6.4; fibroblasts, normal, 9.4 +/- 1.5; cystinotic, 7.7 +/- 1.7]. Cysteamine levels were normal in leukocytes from cystinotics receiving no cysteamine or doses of oral cysteamine too low to reduce leukocyte cystine content. The results indicate that the cause of cystinosis is unlikely to be related to a failure to generate of sustain normal intracellular cysteamine levels.

DNA was isolated from the white cells of a subject with the Hb S-Kenya-G gamma-HPFH condition, and digested with the restriction endonucleases Bg1 II, Xba I, and Eco RI. The resulting fragments were identified by standard techniques using [32P] labelled probes which are specific for the second intervening sequences of the beta gene and the gamma genes, respectively. A comparison with data for normal DNA indicated the presence of one additional fragment in each of the three digests, namely a 10.5 kb Bg1 II fragment, a 7.8 kb Xba I fragment, and a 2.9 kb Eco RI fragment. These observations are believed to show a large (approximately 22.5 kb) deletion in the DNA of the Kenya chromosome which includes the 3' section of the A gamma gene, the delta gene, and the 5' section of the beta gene. These results are consistent with the original hypothesis which was based on structural data for the different hemoglobin chains.

In both cases, the interferon is significantly increased. This could explain the immunological alterations of the efferent or the afferent ways described in the psoriasis. The interferon anti-proliferative action would not be produced by a failure in the receptors of the cellular membrane at the psoriasis epidermis. In some psoriasis, interferon inductors activated or not by viruses could be associated to the etiology of the disease.

Prenatal diagnosis by restriction enzyme analysis is now available in South Africa for globin-related disorders. An Indian couple at risk for sickle-cell anaemia requested prenatal diagnosis which was carried out by restriction enzyme analysis of DNA from cultured amniotic cells. In the case of the sickle-cell mutation a restriction enzyme, Mst II, is available for direct detection of the mutant gene. Mst II together with linked restriction fragment polymorphisms were used to make the diagnosis in this family. The fetus was found to be homozygous for the normal allele and this was confirmed postnatally by placental DNA analysis.

Previous work has shown that plasma and tissue concentrations of histamine are elevated in rats with experimental diabetes mellitus and that leucocytes and platelets from patients with peripheral vascular disease have a higher histamine content than those from controls. In the present study, we have measured: (a) plasma histamine concentrations; (b) leucocyte and platelet histidine decarboxylase (the enzyme responsible for the biosynthesis of histamine) in patients with diabetes mellitus (Types I and II) and peripheral vascular disease; and (c) platelet and leucocyte histamine content. Plasma histamine concentration was significantly higher in patients with diabetes and peripheral vascular disease respectively than that in age-matched controls. Leucocyte histidine decarboxylase activity in diabetic and peripheral vascular disease patients was similar to that in controls, while platelets had no histidine decarboxylase activity. The leucocyte and platelet content of histamine were greater in patients with peripheral vascular disease than those in controls, but they were not altered in diabetic patients. There was no correlation between plasma histamine concentration, leucocyte and platelet histamine content, and histidine decarboxylase activity. We conclude that plasma histamine is elevated in diabetics and in patients with peripheral vascular disease and that platelet and leucocyte histamine content is increased in the latter. This increase in platelet and leucocyte histamine content is not due to an increase in histidine decarboxylase activity of these cells. The increase in plasma and cellular histamine content may contribute to the pathogenesis of increased endothelial permeability in diabetes and to the pathogenesis of intimal damage in atherosclerosis.

Connectin is known to be an anchoring protein of actomyosin filaments in skeletal muscle. Attempts were made to extract this protein from white blood cells and platelets in order to investigate its properties. The purified connectin-like protein obtained had a rubbery appearance and was insoluble in water and immobile on SDS gel-electrophoresis. Amino acid composition and electron microscopic features of the protein were similar to those of skeletal muscles. FITC-labeled antibody to the protein showed a positive reaction to the membrane fractions of red cells, white cells and platelets. In moving cells fluorescence was observed not only in pseudopod, but also in whole cytoplasm. No changes in the fluorescence patterns were observed with respect to moving stages or cell types. The presence of the protein beneath the cell membrane was also confirmed electron micrographically.

Autonomic system dysfunction could be the cause of postural hypotension seen in patients on continuous ambulatory peritoneal dialysis (CAPD). To verify this hypothesis, we examined the alpha 2- and beta 2-adrenoceptors on blood cells after 1/2 h in the resting supine position with the peritoneal cavity filled for 2-3 h, as well as the response of plasma norepinephrine (NE), heart rate (HR) and mean arterial blood pressure (MAP) to 10 min of standing. Supine free and particularly conjugated NE levels were significantly higher in all uremic patients compared with controls. The postural test induced similar increases of MAP and HR in 8 diabetic, 11 nondiabetic patients and 23 controls, whereas 4 diabetic patients became hypotensive. Orthostasis caused a mean free NE increment of only 0.5 nmol/l in the latter patient group with mean NE responses of 1.45-1.65 nmol/l in the former 3 groups. The densities of platelet alpha 2-adrenoceptors (assessed by [3H] yohimbine binding) and of mononuclear leucocyte (MNL) beta 2-adrenoceptors determined by (-) (125I) iodocyanopindolol binding amounted to 160 +/- 50 and 1600 +/- 520 binding sites/cell, respectively, in controls and were unchanged in patients without postural hypotension. The 4 diabetic patients suffering from postural hypotension showed numerically higher beta 2-receptor numbers (2080 binding sites/cell), significantly increased alpha 2-receptor densities (280 binding sites/cell, p less than 0.05) and significantly increased MNL isoproterenol-stimulated adenylate cyclase activities (38 vs 24 pmol cAMP/10(6) MNL/10 min in controls, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of osteoclast activating factor (OAF) released by normal human peripheral blood leukocytes cultured with phytohemagglutinin have been examined in organ culture. Like parathyroid hormone (PTH), OAF causes a rapid increased in the release of previously incorporated 45Ca from fetal rat bone after brief or continuous exposure; the bones also lose stable calcium and collagen content. The resorption response to OAF also resembles that of PTH in having a steep dose response curve and being only transiently inhibited by calcitonin and partially inhibited by increasing medium phosphate concentration. OAF-stimulated resorption was inhibited more effectively by cortisol than was PTH stimulation. The response to maximally effective doses of OAF was not enhanced by PTH or prostaglandin E2, but submaximal doses gave additive effects. Both OAF and PTH inhibit collagen synthesis in fetal rat calvaria at the concentrations that stimulate bone resorption.

Leukocyte-depleted blood products are being used with increasing frequency in hopes of preventing or delaying platelet alloimmunization. However, accurately monitoring the efficiency of leukocyte (WBC) removal is a difficult problem because electronic cell counters are not accurate at very low WBC numbers and hemocytometer counts are tedious and time consuming. A simple flow cytometric technique was developed which accurately and rapidly measures extremely low WBC counts. Using a propidium iodide solution which causes DNA to fluoresce, the residual WBC count was measured in 42 units of blood products after leukocyte depletion using a commercial filter. There was a significant correlation with simultaneous hemocytometer counts, r = 0.672, but residual WBC could be identified in every unit using the flow cytometer, whereas in 19% of the units no WBC were seen using the hemocytometer. Extremely low counts, as low as a single WBC/4 microliters could be reproducibly obtained. In addition, serial dilution studies yielded a correlation coefficient of 0.997. Because most clinical laboratories now have access to flow cytometers, this technique can be widely used.

In this study, we describe a simple strategy to detect beta-thalassaemia mutations in prospective parents and to make prenatal diagnosis in pregnancies at risk in the Mediterranean population. Screening of prospective parents is carried out by dot blot analysis on enzymatically amplified DNA with a set of oligonucleotide probes complementary to the most common mutations in this population. Prenatal diagnosis is accomplished by the same procedure on enzymatically amplified amniocyte or trophoblast DNA. The main advantages of this procedure are the simplicity, sensitivity (0.05 micrograms of DNA), and rapidity (12-24 h). Further simplification is obtained by amplification of the DNA from crude amniotic cell lysate. The very low amount of fetal material necessary for this analysis eliminates the need to culture amniotic fluid cells and may decrease the fetal loss rate associated with trophoblast sampling. The number of specific DNA sequences obtained by the amplification procedure allowed us to use non-radioactive labelled oligonucleotide probes, which have several advantages compared to radioactive probes.

A sensitive and quantitative amidolytic assay for thromboplastin (tissue factor) coupled to thrombin formation was established. A fluogenic peptide substrate, Boc-Val-Pro-Arg-MCA, was found to be suitable for the coupled amidolytic assay. The amidolytic assay was applied to measure TF activity of endotoxin-stimulated mononuclear leukocytes and monocytes. The amidolytic assay showed good correlation of 0.97 with the currently used clotting assay upon measuring TF activity of the cellular samples.

A new method of assessing disease activity in ulcerative colitis has been developed utilizing indium-111-labelled granulocytes. Faecal 111In excretion after intravenous administration of labelled granulocytes ranged from 1.1% to 45% of the injected dose in patients with ulcerative colitis, showing significant differences between mild, moderate, and severely active groups. There was a significant correlation between faecal 111In excretion and a clinical index based on the Crohn's disease activity index (r = 0.79, p less than 0.001) and the erythrocyte sedimentation rate (r = 0.73, p less than 0.001). Quantitative faecal 111In-labelled granulocyte excretion is an objective and specific method of assessing disease activity in ulcerative colitis.

Activity promoting the growth of carp T-like cells has been found in supernatants of mitogen (PHA)- and alloantigen (MLR)-stimulated carp leukocyte cultures. Activity level in culture supernatants was elevated by phorbol myristate acetate. Proliferation of carp T-like lymphoblasts was also promoted in the presence of Il-2-containing supernatants of mammalian origin. The significance of these findings is discussed.

Protein with a molecular mass of 53000 daltons undetectable in healthy persons was identified by electrophoresis in peripheral blood leukocytes of patients with Down's syndrome. The protein was completely extracted with 0.4 N HCl from leukocyte homogenates and was found to be identical, as regards electrophoretic mobility, to protein detected in two patients with chronic myeloblastic leukemia. The causes of discrepancy between theoretically expected and electrophoresis-revealed differences in protein composition of normal and trisomal cells.

The triad of severe pre-eclampsia is often described as a combination of hypertension, oedema and proteinuria. Hypertension alone arising in the second half of pregnancy however is not associated with any greater perinatal mortality or low birthweight than normotensive primigravidae and it is probable that this hypertension may be either physiological or a manifestation of essential hypertension or, in some cases, a mild form of pre-eclampsia. Oedema also does not necessarily signify abnormality. High weight gain, fluid retention or oedema is associated with a lower incidence of small babies, but with a higher incidence of pre-eclampsia. Considerable amounts of water retention can occur in normal pregnancy, either measured as an increase during pregnancy, or as a fall after delivery. The diuretics cyclopenthiazide, spironolactone and clopamide given prophylactically to high weight gain primigravidae did not prevent the onset of proteinuric pre-eclampsia, but caused the babies to be lighter in weight than those of controls. Sodium potassium and water content of leucocytes from primigravidae with proteinuric pre-eclampsia is the same as in mild pre-eclampsia and normal pregnancy. Although salt and water retention are common features of pre-eclampsia, they do not cause the condition and are not an essential part of it.

The degree of 5-methylcytosine formation in DNA sequences differing in reassociation rate and susceptibility to DNase II digestion has been investigated in human chronic myelogenic leukemia and acute leukemia leukocytes, human PHA-stimulated lymphocytes and murine L5178Y lymphoblasts cultured in various phases of growth. The results indicate that in all forms of cells studied by us the general pattern of intragenomic 5-methylcytosine distribution is similar, with two preferentially methylated regions: the sequences fast reassociating and rendered Mg++-soluble after DNase II digestion of nuclei. The most variable fraction as regards the level of methylation seemed to be DNA of Mg++-soluble fraction of DNase II digest, which in acute leukemia leukocytes, PHA-stimulated lymphocytes and exponentially growing L5178Y cells revealed about twice greater relative proportion of methylated cytosines than in leukocytes of chronic myelogenic leukemia and L5178Y cells maintained at saturation density.

We tested the effect of human leukocyte interferon on early localized herpes zoster infections in three placebo-controlled, randomized double-blind trials involving 90 patients with cancer. There were no significant differences in pretreatment severity of infection or nature of underlying disease in the groups. Higher dosages of more purified interferon in the second and third trials produced a significant (P less than or equal to 0.01) decrease in cutaneous dissemination. No dissemination occurred in those receiving the highest dosage (5.1 x 10(5) U per kilogram per day) (P less than or equal to 0.025). The number of days of new-vesicle formation in the primary dermatome decreased (mean, 2.3 days, P less than or equal to 0.05) in this group. Treated patients had a trend toward less acute pain, and significantly (P less than or equal to 0.05) diminished severity of post-herpetic neuralgia, at the two highest dosage levels. Visceral complications were six times less frequent in interferon recipients. High-dosage interferon appeared effective in limiting cutaneous dissemination, visceral complications and progression within the primary dermatome.

The physiologic and cyclic adenosine monophosphate (cAMP) response to beta adrenergic stimulation in lymphocytes and granulocytes was examined in atopic eczema. These cells were isolated by Ficoll-Hypaque gradient from 10 patients with atopic eczema, and their responses were compared to 10 normal subjects. In eczema, basal concentrations of cAMP were normal in both lymphocytes and granulocytes. Lymphocyte cAMP response in eczema was decreased both to epinephrine (10-5 M) and to isoproterenol (10-5 M) but normal to prostaglandin E1 (PGE1). It was also noted that the glycogenolysis response to isoproterenol was significantly less at 10-5 M in eczema, but the fall in glycogen was normal with PGE (10-5 M and 10-7 M). The inhibition of lysosomal enzyme release from granulocytes after zymosan stimulation was significantly less (p less than 0.01) in eczema with all concentrations of isoproterenol tested. There was also a decrease in cyclic AMP response to isoproterenol in the polymorphonuclear leukocytes. PGE1 inhibited lysosomal enzyme release and stimulated cAMP normally. In eczema, both lymphocytes and polymorphonuclear leukocytes have a decreased beta adrenergic response.

Morning plasma and leucocyte vitamin C concentrations were measured in 178 healthy men aged 17-68 years. In the youngest age group (17-29 years), smokers had significantly lower plasma (P less than 0.01) and leucocyte (P less than 0.001) vitamin C levels than non-smokers. With advancing age plasma and leucocyte vitamin C levels of non-smokers appeared to decline. The lower levels in younger smokers did not significantly alter in the later decades. There was no significant difference between the plasma or leucocyte vitamin C levels of smokers and non-smokers in the decade 60-69 years.

Among 87 cases of different non-Hodgkin lymphomas studied with morphologic, enzymehistochemical, and immunologic techniques, ten were found with a positive alkaline phosphatase staining reaction of the cell membranes. The ages of the seven adult patients included in this report varied between 48-85 years. Studies of cell suspensions or cryostat sections demonstrated the presence of monoclonal membrane immunoglobulins indicating a B-cell origin of these lymphomas. Investigation of peripheral blood of six patients revealed the presence of a corresponding monoclonal lymphocyte population in four. According to Rappaport's classification, lymphoblastic, poorly differentiated, and well-differentiated lymphocytic as well as histiocytic lymphoma were encountered. According to the "Kiel" classification, most lymphomas were classified in the group of follicle-center cell tumors. The clinical course of the patients was variable. Non-Hodgkin lymphomas with alkaline phosphatase positive staining do not constitute a separate entity.

Cysteamine (beta-mercaptoethylamine, MEA) is currently used to treat children with nephropathic cystinosis. In this study MEA was compared to phosphocysteamine (MEAP), a phosphorothioester that tastes and smells better than MEA, with respect to its ability to elevate plasma MEA and deplete leukocytes of cystine. Studies were performed in six children with nephropathic cystinosis ranging in age from 2 to 10 yr. After equimolar oral doses of either MEA or MEAP plasma cysteamine was determined at various times for 6 h. MEA was determined by sodium borohydride reduction followed by high-performance liquid chromatography separation and electrochemical detection. Leukocyte cystine was measured before and 1 and 6 h after drug administration. Peak plasma MEA was obtained 30 min to 1 h after a dose and was not significantly different when MEA (48.6 +/- 10.7, mean +/- SD) or MEAP (54.1 +/- 20.2) was given. Significant plasma MEA concentrations were seen as early as 15 min after an oral dose, indicating rapid absorption. Analysis of vomitus indicated that hydrolysis of the phosphate group of MEAP occurs in the stomach. The percent decrease in leukocyte cystine content obtained with MEA administration (61.9%) was not significantly different from the decrease observed when MEAP was administered (65.3%). MEA and MEAP appear to be equally effective in their cystine-depleting properties.

We describe a method for measuring plasma, erythrocyte, and leukocyte sodium (Na+), potassium (K+), and magnesium (Mg2+) concentrations in 10-mL blood specimens. After separating cells with Ficoll-Hypaque and washing with isotonic choline chloride, erythrocytes and leukocytes are counted, so that results can be expressed as amount of substance per cell and also to monitor cell integrity and possible contamination. Plasma and cell lysates were analyzed (CV less than or equal to 7.0%) with flame photometry and atomic absorption spectrometry. Reference intervals for an elderly population with values for plasma electrolytes within reference intervals are similar to those for younger healthy subjects. From data on biological variation, reference values for erythrocyte cations are not of much use, and analytical goals for precision are not met, but the results might be useful for monitoring disease progression in individual patients. In contrast, reference values for leukocyte cations are theoretically of use and goals are achieved, but large changes are required before consecutive results can confidently be said to be significantly different.

Based on the main data from the specialty literature and on their own experience in the field, the authors present the principles and some details of the classical and the modern techniques used to identify and study the various leukocytes and especially the leukemic ones. These different methods of investigation are included into the wide categories of histologic, cytomorphologic, cytochemical, cytoenzymatic, cytoimmunological, cytogenetic, cell culture and other complementary techniques. The great progress achieved in this domain was favoured by the development of light, contrast phase and fluorescent microscopy and of the new techniques of transmission and scanning electron microscopy--whose utility for the study of the white blood cells, and particularly of the leukemic ones, is demonstrated in this paper by numerous suggestive illustrations.

Samples from 49 cases of myeloproliferative diseases were tested by an immunocytochemical technique for leucocyte lysozyme and lactoferrin. The presence of these constituents in myeloid precursors from cases of acute and chronic myeloid leukaemia reflected the degree of cellular maturation, lysozyme appearing (as it does in normal myeloid cells) at the stage of primary granule production (in promyelocytes), while lactoferrin wad detectable only in more mature, secondary granule-containing myeloid cells. Auer rods stained positively for lysozyme, in keeping with their relationship to primary granules. Monocytes from five cases of leukaemia showing predominantly monocytic differentiation were indistinguishable from normal monocytes in their staining reactions for lysozyme despite the presence of raised serum and urinary lysozyme levels. In four cases of acute myeloid leukaemia circulating polymorphs deficient in lactoferrin were detected: in one of these cases a similar percentage of polymorphs was lysozyme negative.

The problems of assessment of human zinc status are reviewed, with particular emphasis on the limitations to each of the current available measurements. The advantages and limitations of leukocytes are then described. Methods of preparation and potential problems in the assay for zinc are described in detail. The data so-far produced by this method are reviewed.

Extracts of blood lymphocytes, polymorphonuclear neutrophils and B, T or monocytic cell lines were analyzed by two-dimensional gel electrophoresis and immunoradiometric assay after electro-transfer to nitrocellulose sheets with radiolabelled polyclonal or monoclonal antibodies specific for beta 2-microglobulin. Four different forms of the molecule were identified with an apparent Mr of 12,000 and pI values of 5.7, 5.3 and lower. Lymphocyte activation by phytohemagglutinin and concanavalin A, or incubation with recombinant alpha 2b interferon, resulted in an increased beta 2-microglobulin cell content and release of the protein in supernatants with a predominant elevation of the more acidic minor forms. Recombinant interleukin-2 and recombinant gamma interferon increased the expression of the molecule without significant shift in the relative proportion of beta 2-microglobulin forms. Tumor necrosis factor alpha did not increase cell beta 2-microglobulin (beta 2-m) content and release and did not alter the relative distribution of the different forms of the molecule. Several mechanisms may be considered for the generation of beta 2-m microheterogeneity, including intracytoplasmic post-translational modifications such as proteolysis or modification of the amide groups of internal amino acids.

The visualization of the specific granulation of leukocytes is useful in hematology to identify de cell type in leukemic diseases. The authors employed the acidic fluorochrome morin after testing its high affinity for the fluorescent reaction with morin in human and chicken peripheral blood smears, and in streak smears from rabbit spleen. The best results were obtained with a solution prepared either with 0.10 mg morin per ml of 50 per 100 ethanol, or with a saturated solution of morin in distilled water diluted to one fourth in 25 per 100 ethanol. When observed under blue-violet excited light (436 nm) the acidophilic granules of leukocytes produce a bright yellow fluorescence, while the cell nuclei show a faint greenish fluorescence. As for the mechanism of the reaction, it consists possibly in an interaction between morin and the basic components of the granules. Other acidic fluorochromes, as primulin and hematoxylin, produce similar fluorescent reactions with the acidophilic granules.

We observed postictal pleocytosis in 7 of 62 cerebrospinal fluid specimens obtained from 27 patients with epilepsy. Each patient had a known seizure disorder; none had any other cause for the pleocytosis. The maximum number of leukocytes was 12/mm3; the maximum number of erythrocytes was 190/mm3. Postictal pleocytosis was more common in samples obtained within 12 hours of the last seizure. Although previous studies have emphasized that pleocytosis is more common after repetitive generalized tonic-clonic seizures, we found increased leukocyte counts in cerebrospinal fluid after single simple, complex partial, or generalized tonic-clonic seizures.

The primary structures of three major species of human leukocyte interferon differ from the structure predicted from the DNA sequence of recombinants containing leukocyte interferon-coding regions. Compared to the recombinant interferon produced in bacteria, three of the purified natural proteins isolated from leukocytes lack the 10 COOH-terminal amino acids suggested by the DNA sequence.