Tactoid formation in deer hemoglobin

1960 ◽  
Vol 199 (1) ◽  
pp. 190-192 ◽  
Author(s):  
John H. Moon
Keyword(s):  
Odocoileus Virginianus ◽  
Sickle Cell ◽  
Moving Boundary ◽  
Paper Electrophoresis ◽  
Free Hemoglobin ◽  
Hemoglobin Solution ◽  
Hunting Season ◽  
Phase Microscopy ◽  
Veronal Buffer ◽  
Kinetics Of

Sickle cell preparations were made on eight Virginia white-tail deer ( Odocoileus virginianus) killed during the 1958–59 hunting season. All preparations showed sickling. Paper electrophoresis of carboxyhemoglobin from these animals revealed identical mobilities and a single hemoglobin component present at pH 8.6. Alkali denaturation of the deer carboxyhemoglobin solution showed that it was markedly resistant to alkali denaturation and that the kinetics of the denaturation were different from that of human cord hemoglobin. Deer carboxyhemoglobin migrated 0.6 x 10–5 cm2/volt/sec.–1 faster than human carboxyhemoglobin A in moving boundary electrophoresis in veronal buffer at pH 8.2. Tactoids were demonstrated in free hemoglobin solution with phase microscopy after concentration of the solution. These particles are very similar morphologically to these prepared from hemoglobin solution containing hemoglobin S.

scholarly journals EVALUATION OF A STROMA-FREE HEMOGLOBIN SOLUTION FOR USE AS A PLASMA EXPANDER

1967 ◽  
Vol 126 (6) ◽  
pp. 1127-1142 ◽  
Author(s):  
S. Frederick Rabiner ◽  
J. Raymond Helbert ◽  
Harry Lopas ◽  
Lila H. Friedman
Keyword(s):  
Carrying Capacity ◽  
Vital Signs ◽  
Free Hemoglobin ◽  
Hemoglobin Solution ◽  
Plasma Expander ◽  
Chronic Effects ◽  
Coagulant Activity ◽  
Methemoglobin Formation ◽  
Oxygen Carrying Capacity ◽  
Acute And Chronic Effects

The preparation of large quantities of a stable, stroma-free hemoglobin solution without coagulant activity is described. Following infusion of this solution into phlebotomized dogs, there is no methemoglobin formation, no adverse effects on vital signs, and no demonstrable activation of blood coagulation. The hemoglobin maintains its oxygen-carrying capacity and liberates oxygen into tissues. Acute and chronic effects on renal function following infusion of this preparation were also studied and no effect on clearance of urea, creatinine, or P.A.H. could be demonstrated. There was no change in urinary output and histological sections revealed no lesions attributable to hemoglobin toxicity. It is concluded that a stroma-free hemoglobin solution may have use as a plasma expander.

scholarly journals Influence of Haptoglobin Polymorphism on Stroke in Sickle Cell Disease Patients

Genes ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 144
Author(s):  
Olivia Edwards ◽  
Alicia Burris ◽  
Josh Lua ◽  
Diana J. Wilkie ◽  
Miriam O. Ezenwa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Blood Cells ◽  
Cell Disease ◽  
Free Hemoglobin ◽  
Cerebral Tissue ◽  
Sickle Hemoglobin ◽  
Haptoglobin Polymorphism

This review outlines the current clinical research investigating how the haptoglobin (Hp) genetic polymorphism and stroke occurrence are implicated in sickle cell disease (SCD) pathophysiology. Hp is a blood serum glycoprotein responsible for binding and removing toxic free hemoglobin from the vasculature. The role of Hp in patients with SCD is critical in combating blood toxicity, inflammation, oxidative stress, and even stroke. Ischemic stroke occurs when a blocked vessel decreases oxygen delivery in the blood to cerebral tissue and is commonly associated with SCD. Due to the malformed red blood cells of sickle hemoglobin S, blockage of blood flow is much more prevalent in patients with SCD. This review is the first to evaluate the role of the Hp polymorphism in the incidence of stroke in patients with SCD. Overall, the data compiled in this review suggest that further studies should be conducted to reveal and evaluate potential clinical advancements for gene therapy and Hp infusions.

scholarly journals Transmembrane mobility of phospholipids in sickle erythrocytes: effect of deoxygenation on diffusion and asymmetry

Blood ◽  
1991 ◽  
Vol 77 (4) ◽  
pp. 849-854 ◽  
Author(s):  
N Blumenfeld ◽  
A Zachowski ◽  
F Galacteros ◽  
Y Beuzard ◽  
PF Devaux
Keyword(s):  
Sickle Cell ◽  
Blood Cells ◽  
Cell Disease ◽  
Aminophospholipid Translocase ◽  
Outer Leaflet ◽  
First Case ◽  
Sickle Erythrocytes ◽  
Dependent Transport ◽  
The Relationship ◽  
Kinetics Of

Abstract We studied the effect of sickling on the transmembrane reorientation and distribution of phospholipids in the red blood cells of patients homozygous for sickle cell anemia (SS). To this purpose, we followed the redistribution kinetics of trace amounts of spin-labeled analogues of natural phospholipids first introduced in the membrane outer leaflet of normal or sickle erythrocytes exposed to air or nitrogen. Deoxygenation had no effect on the lipid redistribution kinetics in normal (AA) cell membranes. At atmospheric pO2, unfractionated SS cells were not different from normal cells. However, on deoxygenation inducing sickling, phosphatidylcholine passive diffusion was accelerated and the rate of the adenosine triphosphate-dependent transport of aminophospholipids was reduced, especially for phosphatidylserine. The stationary distribution of the aminophospholipids between the two leaflets was slightly less asymmetric, a phenomenon more pronounced with phosphatidylethanolamine. These changes were rapidly reversible on reoxygenation. When SS cells were separated by density, both dense and light cells exhibited the properties cited above. However, dense cells exposed to air possessed a lower aminophospholipid transport rate. These data favor the relationship between aminophospholipid translocase activity and phospholipid transmembrane asymmetry. Sickle cell disease is the first case of aminophospholipid translocase pathology.

scholarly journals Evidence Concerning the Inadequacy of Mutation as an Explanation of the Frequency of the Sickle Cell Gene in the Belgian Congo

Blood ◽  
1955 ◽  
Vol 10 (4) ◽  
pp. 341-350 ◽  
Author(s):  
J. M. VANDEPITTE ◽  
WOLF W. ZUELZER ◽  
JAMES V. NEEL ◽  
J. COLAERT
Keyword(s):  
Natural Selection ◽  
Sickle Cell ◽  
Spontaneous Mutation ◽  
Genetic Modifier ◽  
Paper Electrophoresis ◽  
Preliminary Calculation ◽  
Spontaneous Mutation Rate ◽  
Balanced Polymorphism ◽  
Belgian Congo ◽  
Cell Gene

Abstract It is pointed out that there are two outstanding (and not mutually exclusive) possible explanations for the persistence of the sickle cell gene in the face of strong negative natural selection. These are (1) "balanced polymorphism," and (2) a high spontaneous mutation rate. In Léopoldville, Belgian Congo, approximately 25 per cent of the natives exhibit the sickling phenomenon. Over a two and one-half year period 261 patients with sickle cell disease, distributed among 243 families, were seen at the Institute of Tropical Medicine in Léopoldville. A total of 233 of the 243 mothers of the patients in this series was tested for the sickling phenomenon. Only two failed to sickle. Hemoglobin from these two women was normal on paper electrophoresis. The occurrence of these two exceptional mothers can be explained on the basis of mutation at some stage of oogenesis resulting in a sickle cell gene. Alternate possible explanations include (1) transmission by the mother of some other abnormal gene affecting hemoglobin synthesis, (2) occurrence in the mother of a genetic modifier of the effects of the sickle cell gene, (or its normal allele), and (3) unreported adoption. These data make possible a preliminary calculation of the extent to which mutation may be responsible for maintaining the sickle cell gene. Calculations based on the assumption that both these exceptional mothers indicate the occurrence of a mutation will lead to maximal estimates of the rate of mutation of the sickle cell gene. This maximal estimate is 1.7 x 10-3 per gene per generation. This rate, although very high by the usual standards of human mutation rates, is only approximately one-tenth that necessary to offset natural selection in a population with 25 per cent sickling.

scholarly journals Paper Electrophoresis of Abnormal Hemoglobins and Its Clinical Applications

Blood ◽  
1954 ◽  
Vol 9 (9) ◽  
pp. 897-910 ◽  
Author(s):  
ARNO G. MOTULSKY ◽  
MILTON H. PAUL ◽  
E. L. DURRUM
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Trait ◽  
Fetal Hemoglobin ◽  
Paper Electrophoresis ◽  
Clinical Applications ◽  
Hemoglobin C ◽  
Hemoglobin Type ◽  
Cell Life ◽  
Practical Tool ◽  
Adult Hemoglobin

Abstract 1. Paper electrophoresis of abnormal hemoglobins is a simple and convenient technic for the study of the hereditary hemoglobinopathies. 2. A semiquantitative paper electrophoretic technic is described, which allows rather accurate quantitation of the various hemoglobin components by inspection alone. 3. For exact results, the more elaborate technics of elution or photoelectric scanning may be employed. The accuracy of these quantitative technics is illustrated by artificial mixture experiments. 4. The clinical applications of the method in the study of sickle cell disease and hemoglobin C abnormalities are discussed. Apart from the more common hemoglobin abnormalities (such as sickle cell trait, sickle cell anemia, C trait, sickle cell-hemoglobin C disease), a patient with 100 per cent hemoglobin C (homozygous hemoglobin C disease) and a Negro patient with sickle cell-thalassemia disease were discovered. Normal adult hemoglobin (hemoglobin A) was found in all other hereditary and acquired anemias studied. Slightly increased amounts of fetal hemoglobin were detected in cases of hereditary nonspherocytic hemolytic disease and aregenerative anemia. 5. This technic may be used for red cell life span determinations by serially following the disappearance of a certain hemoglobin type transfused into a patient with a different hemoglobin variety. Further applications of the technic are suggested. 6. The combination of the technics of paper electrophoresis and alkali denaturation offer an adequate, simple, and practical tool for diagnosis and investigation of hereditary hemoglobinopathies. 7. Identical apparatus and buffer may be used for serum protein electrophoresis.

Quantitative Electrophoresis of Serum Proteins on Paper

1956 ◽  
Vol 2 (5) ◽  
pp. 303-319 ◽  
Author(s):  
Moses Wurm ◽  
Frederick H Epstein
Keyword(s):  
Protein Concentration ◽  
Moving Boundary ◽  
Serum Proteins ◽  
Paper Electrophoresis ◽  
Bromphenol Blue ◽  
Good Resolution ◽  
Confidence Limits ◽  
Protein Patterns ◽  
Electrophoretic Patterns ◽  
Normal Human

Abstract 1. A procedure for paper electrophoresis has been described which gives highly reproducible protein patterns with good resolution and freedom from distortions. 2. Densitometry of protein bands on paper stained with bromphenol blue or Amidoschwarz 10B reveals that the logarithm of protein concentration is proportional to optical density and that Beer's law does not apply. Electrophoretic patterns of normal human serum evaluated in this manner give values in close agreement with those obtained by moving-boundary electrophoresis. 3. Confidence limits were determined for both methods.

scholarly journals Kinetics of sickle cell biorheology and implications for painful vasoocclusive crisis

2015 ◽  
Vol 112 (5) ◽  
pp. 1422-1427 ◽  
Author(s):  
E Du ◽  
Monica Diez-Silva ◽  
Gregory J. Kato ◽  
Ming Dao ◽  
Subra Suresh
Keyword(s):  
Disease Severity ◽  
Cell Density ◽  
Sickle Cell ◽  
Hematological Parameters ◽  
Diagnostic Tools ◽  
Hypoxic Conditions ◽  
Vitro Model ◽  
Kinetics Of

We developed a microfluidics-based model to quantify cell-level processes modulating the pathophysiology of sickle cell disease (SCD). This in vitro model enabled quantitative investigations of the kinetics of cell sickling, unsickling, and cell rheology. We created short-term and long-term hypoxic conditions to simulate normal and retarded transit scenarios in microvasculature. Using blood samples from 25 SCD patients with sickle hemoglobin (HbS) levels varying from 64 to 90.1%, we investigated how cell biophysical alterations during blood flow correlated with hematological parameters, HbS level, and hydroxyurea (HU) therapy. From these measurements, we identified two severe cases of SCD that were also independently validated as severe from a genotype-based disease severity classification. These results point to the potential of this method as a diagnostic indicator of disease severity. In addition, we investigated the role of cell density in the kinetics of cell sickling. We observed an effect of HU therapy mainly in relatively dense cell populations, and that the sickled fraction increased with cell density. These results lend support to the possibility that the microfluidic platform developed here offers a unique and quantitative approach to assess the kinetic, rheological, and hematological factors involved in vasoocclusive events associated with SCD and to develop alternative diagnostic tools for disease severity to supplement other methods. Such insights may also lead to a better understanding of the pathogenic basis and mechanism of drug response in SCD.

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