PubMed Health⌕ Search

Biomedical subjects

L S Lessin

Publications and source records attributed to L S Lessin.

At least 37 records · Page 2Linked to original sources
PubMed1984

Erythrocyte density distribution in sickle cell anemia.

Density distributions were determined for sickle cell erythrocytes from 27 patients with HbSS genotype using the phthalate ester microcapillary differential flotation method of Danon and Marikovsky. Mean density distribution curves showed HbSS erythrocytes to have trimodal populations with significant increases in both dense and light cell fractions when compared to 20 normal controls of HbAA genotype (p less than 0.05). Irreversibly sickled cell (ISC) and reticulocyte counts were compared with density distributions. Integrated unit areas under the dense cell population curves correlated with ISC percentages, while corresponding unit areas for light populations correlated to a lesser extent with reticulocyte percentages. Mean cell density, D50, varied widely among patients and correlated poorly with the ISC or reticulocyte percentage; however, D50 did correlate with the net change in integrated unit areas. Several patients had repeated density distributions over a 2-year time period. All HbSS patients showed increased but variable dense cell fractions which could not be definitively correlated with the clinical state of the patient. Transfusion reproducibly resulted in a lowering of the dense cell fraction. Erythrocytes from the HbSC patients showed a uniform increase in density and absence of the large dense cell fraction seen in most HbSS patients. This method provides a simple means for quantitation of the light and dense cell fraction in blood of patients with sickling disorders and displays the profile of erythrocyte density heterogeneity for the individual sickle cell patient.

Anemia, Sickle Cell↗
PubMed1984

Freeze-etching and biochemical analysis of human fetal erythrocyte membranes.

In order to test the hypothesis that there are ultrastructural and supramolecular differences between fetal and adult erythrocyte membranes that are manifested in their functional characteristics, the cells were studied by freeze-etching and transmission microscopy and biochemical methods. Freeze-etching and transmission electron microscopy of fetal erythrocyte membranes showed that the protoplasmic and exoplasmic fracture faces have 24% and 45% greater intramembrane particles respectively compared to adult cells (p less than 0.01). The apparent diameters of the intramembrane particles estimated on the exoplasmic fracture face averaged as follows: 4.84, 7.74, 11.42, and 15.64 nm, which are similar to estimates in adult cell membranes, suggesting similar dimensions for the presumptive glycoprotein structures in the fluid mosaic complex of the cell membranes. The average total cholesterol, phospholipid, and protein content per fetal erythrocyte ghost as well as ratios of protein/lipid, protein/cholesterol, and protein/phospholipids were all significantly greater than in the adult ghost (p less than 0.01). Analysis of fetal and adult ghost proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed similar qualitative and quantitative polypeptide and glycopeptide bands except for the intense appearance of bands 4.5 and 8 in the fetal samples. Polypeptide chains per ghost membrane were significantly greater in fetal ghosts than in adult ghosts. However, the molar ratios of the major polypeptides relative to band 3, the predominant protein in the ghost membrane, are comparable for the two cell types except for bands 4.5 and 8. These findings suggest that the molecular characteristics of the erythroid plasma membrane vary with the developmental age.

Blood Protein Electrophoresis↗
PubMed1983

Acquired pure red cell aplasia associated with chronic lymphocytic leukemia.

Pure red cell aplasia (PRCA) represents selective failure of erythropoiesis in the absence of abnormalities in leukopoiesis or thrombocytopoiesis. Acquired PRCA has occurred uncommonly in chronic lymphocytic leukemia (CLL). We report six patients with non-T-cell CLL in which nine episodes of PRCA were observed. In six of the nine episodes, the patients had received recent oral alkylating agents; conversely, recovery from aplasia occurred in some while on alternate alkylator therapy and two patients had no pretreatment. Spontaneous occurrence and recovery, therefore, could not be excluded. Onset of PRCA may be suggested by macrocytosis, but discontinuance of therapy at its development may not prevent PRCA if, indeed, therapy is one of the causes. Supportive therapy or alkylators and prednisone permitted recovery without mortality in all six patients. The interval between onset of CLL and the recognition of first PRCA episode varied from one month to nine years (mean, 5.3 years); the duration of PRCA ranged from three to nine months (mean, 4.7 months). In addition to previously better understood causes of anemia in CLL, the uncommon occurrence of PRCA is an additional consideration in the differential diagnosis of sudden anemia in CLL.

Aged↗
PubMed1982

Bone marrow mast cell content in preleukemic syndrome.

Bone marrow mast cell content was evaluated by a semiquantitative method in 22 marrow specimens from 20 patients with preleukemic syndrome and was compared with 21 marrow specimens from iron-deficient control subjects. Results indicate a statistically significant increase of bone marrow mast cell content in patients with preleukemic syndrome in comparison to control subjects (p less than or equal to 0.0005). Two of 20 preleukemic patients converted to acute myeloblastic leukemia and conversion was accompanied by a significant decrease of bone marrow mast cell content. Our findings indicate that bone marrow mast cell content can be reproducibly quantitated and represents an additional morphologic criterion for diagnosis of the preleukemic syndrome.

Adolescent↗
PubMed1982

Platelet to leukocyte adherence phenomena. (Platelet satellitism) and phagocytosis by neutrophils associated with in vitro platelet dysfunction.

Platelet to leukocyte adhesion phenomena (PLAP) and the phagocytosis of platelets by neutrophils from the EDTA anticoagulated blood samples are described. PLAP was transferable to a normal blood specimen by patient's plasma or serum with or without complement. Further studies revealed in vitro evidence of hereditary platelet dysfunction. In vivo study of platelet survival and in vitro analysis of platelet membrane glycoproteins were normal. We conclude that PLAP can be seen in an asymptomatic individual with in vitro evidence of hereditary platelet dysfunction.

Adolescent↗
PubMed1982

Rheological assessment of antisickling effects of pyridoxine and pyridoxal.

The antisickling effects of pyridoxine and pyridoxal on intact sickle erythrocytes (SRBCs) were assessed by microviscometry of cell suspensions at shear rates of 1.15 to 230.0/s, measurement of cellular deformability by cell filtration and scanning and transmission electron microscopy (EM). Incubation of fresh SRBCs in albuminated (0.1%) phosphate buffered saline, pH 7.4, with 5 to 30 mM, pyridoxine or pyridoxal at 37 degrees C for 90 min followed by deoxygenation to pO2 = 25 mmHg, decreased the percentage of sickled cells observed as a function of vitamin concentration. EM of fresh SRBCs incubated with 20 mM pyridoxine or pyridoxal at 25 mmHg pO2 showed mostly discocytes without intracellular fibers indicating absence of hemoglobin polymerization. Determination of fluidity (viscosity-1) versus shear stress showed that both pyridoxine and pyridoxal significantly (P less than 0.01) increased the fluidity of a deoxygenated suspension of SRBCs. The estimated apparent yield stress from Casson plots for the vitamin-treated deoxygenated cells and the deoxygenated control cells were 0.11 and 0.18 dynes/cm2 respectively. The relative resistance of 0.2% cell suspension to flow through 5 microns Nuclepore filters indicated a significant increase (greater than 75%) in the deformability of the vitamin-treated deoxygenated sickle cells. The ultrastructure of the SRBCs through the filter pores further suggested that the fluidity of the intracellular milieu of the vitamin-treated deoxygenated cells was higher than that of the deoxygenated controls. These data support the hypothesis that pyridoxylation of sickle hemoglobin inhibits sickling, increases the fluidity of sickle hemoglobin under low pO2, and thereby enhances the deformability of SRBCs in models of capillary blood flow.

Anemia, Sickle Cell↗
PubMed1981

Aggregation of intramembrane particles in erythrocyte membranes treated with diamide.

Treatment of erythrocytes with diamide (diazene dicarboxylic acid bis-(N,N-dimethylamide)) results in oxidation of sulfhydryl groups of the membrane, and cross-linking of membrane proteins into high molecular weight complexes. Concomitant freeze-etching studies show aggregation of intramembrane particles on the protoplasmic fracture face of erythrocyte ghost membranes treated with the oxidant. Furthermore, after a 3 h incubation of erythrocytes with 10 mM diamide at 37 degrees C, cellular energy levels declined to about 70% of control values. The data suggest that disulfide cross-linking of the major membrane proteins releases the apparent physical occlusion of the band 3 proteins within the interstices of the cytoskeletal shell. This results in the translational mobility of band 3 proteins which is reflected ultra-structurally in the freeze-etch images.

Adenosine Triphosphate↗
PubMed1978

Deformability characteristics of sickle cells by microelastimetry.

Deformability of normal and sickle erythrocytes was measured by means of micropipette elastimetry with determination of intrinsic membrane rigidity (P) and total cell deformability (Pt). In the elastimetric technique employed, negative pressure at the pipette tip was generated and measured continuously. Membrane rigidity is defined as the negative pressure, in mm H2O, required to induce a hemispherical projection of the cell surface into the micropipette, and total cell deformability as the negative pressure required to aspirate the entire cell into the pipette lumen. Membrane rgidity for oxygenated sickle discocytes was not statistically different from that of control normal discocytes, but Pt measurements were significantly higher for sickle than normal discocytes. Irreversibly sickled cells (ISCs) had markedly increased membrane rigidity and whole cell deformability when compared to control normal cells. Mildly deformed ISCs and severely deformed ISCs at ambient pO2, both showed significantly higher mean membrane rigidity values than sickle discocytes and reversibly sickled cells. Sickle and normal discocytes both showed membrane elasticity with reversion to original cell shape following release of the cell from its aspirated position at the pipette tip. ISCs, however, exhibited elastic deformation of the membrane. These studies provide further evidence of progressive alteration of the sickle cell membrane induced by the sickling-unsickling process, culminating in formation of the ISC, and suggest a role for the ISC membrane abnormality in the pathologic rheology of sickle cell disease.

Anemia, Sickle Cell↗
PubMed1978

Membrane alterations in irreversibly sickled cells: hemoglobin--membrane interaction.

Irreversibly sickled cells (ISCs) are sickle erythrocytes which retain bipolar elongated shapes despite reoxygenation and owe their biophysical abnormalities to acquired membrane alterations. Freeze-etched membranes both of ISCs produced in vitro and ISCs isolated in vivo reveal microbodies fixed to the internal (PS) surface which obscure spectrin filaments. Intramembranous particles (IMPs) on the intramembrane (PF) surface aggregate over regions of subsurface microbodies. Electron microscopy of diaminobenzidine-treated of ISC ghosts show the microbodies to contain hemoglobin and/or hemoglobin derivatives. Scanning electron microscopy and freeze-etching demonstrate that membrane--hemoglobin S interaction in ISCs enhances the membrane loss by microspherulation. Membrane-bound hemoglobin is five times greater in in vivo ISCs than non-ISCs, and increases during ISC production, parallelling depletion of adenosine triphosphate. Polyacrylamide gel electrophoresis of ISC membranes shows the presence of high-molecular-weight heteropolymers in the pre--band 1 region, a decrease in band 4.1 and an increase in bands 7, 8, and globin. The role of cross-linked membrane protein polymers in the generation of ISCs is discussed and is synthesized in terms of a unified concept for the determinants of the genesis of ISCs.

Adenosine Triphosphate↗
PubMed1978

Inhibition of erythrocyte sickling in vitro by pyridoxal.

To test the antisickling activity of pyridoxal, we compared the oxygen affinity and the percent sickling at low PO2 of untreated erythrocytes with values for cells from the same blood sample incubated with pyridoxal, glyceraldehyde, or pyridoxine. Pyridoxal increased oxygen affinity much more than glyceraldehyde. 20 mM pyridoxal and glyceraldehyde had equivalent antisickling activity. At PO2 levels above 20 mm Hg, both agents reduced sickling to less than 2%. In samples examined by electron microscopy, pyridoxal reduced the percent sickled cells and the percent cells that contain hemoglobin S fibers by the same amount (from 74 to 3%). Pyridoxine had no effect on oxygen affinity or sockling. Pyridoxal reacts with intracellular hemoglobin to increase oxygen affinity, which inhibits hemoglobin S polymerization and sickling.

Anemia, Sickle Cell↗
PubMed1978

Bone-marrow mast cells in lymphoproliferative disorders.

Increased bone-marrow mast-cell content and lymphoproliferative disorders have been previously linked. Using a semiquantitative method we examined bone-marrow mast-cell content in 120 marrow specimens from patients with multiple myeloma, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis. Results indicated a statistically significant increase of marrow mast-cell content in patients with chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis when compared with iron-deficient control subjects (p less than or equal to 0.0005). Patients with multiple myeloma had decreased marrow mast-cell content, clearly separating them from patients with lymphoproliferative disorders and reactive lymphocytosis. Linear regression plot of marrow mast-cell content against percentage of marrow lymphocytes showed a direct relation, indicating that marrow mast-cell density may be related more to the degree of lymphoid proliferation than to the specific lymphoproliferative process. Marrow mast-cell content may therefore be reproducibly determined and used to support the morphologic diagnosis of lymphoproliferative disorders and differentiate them from atypical myelomas.

Adolescent↗
PubMed1975

Multiple myeloma in a patient with sickel cell anemia. Interacting effects on blood viscosity.

Described here is a case of multiple myeloma in a patient with sickle cell anemia. Viscometric studies were made by comparing the patient's whole blood, plasma and washed red blood cells with those of a normal control subject and a patient with sickle cell anemia. Results showed that the increased viscosity of the patient's whole blood as compared with that of the control patient with sickle cell anemia was mainly due to erythrocytic interaction with the circulating abnormal immunoglobulin. It is postulated that the increased frequency of vaso-occlusive crisis that occurred in our patient in the months before the diagnosis and treatment of multiple myeloma, was due to this cell-protein interaction with the resulting enhancement of whole blood viscosity and the sickling phenomena.

Adult↗