scholarly journals The effect of fixed oil extracts of Nigella sativa on sickle cells: An in-vitro study in Khartoum state -Sudan

2021 ◽  
Vol 10 (3) ◽  
pp. 317-321
Author(s):  
Eman Ali Abuagla Dafaalla ◽  
Amira Ahmed Khalid Humeida
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Antioxidant Activities ◽  
Nigella Sativa ◽  
Venous Blood ◽  
In Vitro Study ◽  
Hemoglobin Concentration ◽  
Inherited Disorders ◽  
P Values

In Sudan, sickle cell anemia (SCA) is one of the most common inherited disorders of hemoglobin that has complications and becomes world problem. Nigella sativa NS (black seed) has been reported to have calcium antagonist and antioxidant activities, both of which play a role in the management of sickle cell anemia. The aim of the current study was to evaluate of the anti-sickling activity of the NS extracts, forty patients with sickle cell anemia were recruited for the study. A total of 3ml of venous blood was collected from each patient after obtaining the consent and the ethical approval, the blood was treated with Nigella sativa (NS) extract, and sickling test was performed. Descriptive study and p-values were used, and the correlation was evaluated, data was analyzed by SPSS. Recent study found that the sickling test after treating blood with Nigella sativa extract showed a negative result in 75% of patients and a 25% of patients showed persistently positive sickling test result. The anti-sickling effect in relation to various hemoglobin concentration, gender and age group showed p values of 0.007, 0.672 and 0.853 respectively indicating significant relationship with Hb concentration. Our study concluded that the fixed oil extract from Nigella sativa has an in-vitro anti-sickling activity on patients with SCA and this finding could indicate the use of this extract in treatment.

scholarly journals A New Inherited Abnormality of Hemoglobin and Its Interaction with Sickle Cell Hemoglobin

Blood ◽  
1951 ◽  
Vol 6 (12) ◽  
pp. 1240-1259 ◽  
Author(s):  
EUGENE KAPLAN ◽  
WOLF W. ZUELZER ◽  
JAMES V. NEEL
Keyword(s):  
Hemolytic Anemia ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Sickle Cell Trait ◽  
Asymptomatic Carrier ◽  
Hemoglobin Concentration ◽  
Clinical Genetic ◽  
Atypical Form ◽  
Erythroid Hyperplasia

Abstract Through clinical, genetic and physicochemical studies a new inherited abnormality of hemoglobin has been recognized in American Negroes. The new hemoglobin, provisionally called hemoglobin III, can be separated from both normal and sickle cell hemoglobin by electrophoretic analysis. The structural anomaly of the hemoglobin molecule is determined by a gene inherited as a simple Mendelian dominant. A distinct hemolytic syndrome which is intermediate between the benign sickle cell trait and sickle cell anemia results from the combination of the new hemoglobin with sickle cell hemoglobin. A tentative characterization of the syndrome is presented. In contrast to classical sickle cell anemia this form of sickle cell disease is characterized by a mild hemolytic anemia with slowly progressive splenomegaly in the absence of cardiac or musculo-skeletal manifestations. In vitro, the erythrocytes sickle like those of sickle cell anemia. The bone marrow shows erythroid hyperplasia, fecal urobilinogen excretion is increased, and the survival time of the erythrocytes in normal recipients is shortened, but in the patients the red cell count and hemoglobin concentration are only slightly depressed. Reticulocytosis is slight and icterus is not observed. Whereas in sickle cell anemia both parents are expected to have the sickle trait, only one parent of these individuals shows sickling, while the nonsickling parent is a carrier of the hemoglobin III. The new syndrome does not appear to be identical with that resulting from the simultaneous presence of the sickling gene and the thalassemiagene. The presence of hemoglobin III when combined with structurally normal hemoglobin is expressed as an asymptomatic carrier state. The erythrocytes do not sickle but have a high incidence of target cell deformity and increased resistance to hypotonic saline. Although there is no evidence of hemolysis in such individuals their erythrocytes are eliminated with abnormal rapidity from the circulation of normal recipients. The homozygous state with respect to this new hemoglobin has not yet been identified but may well be some already recognized atypical form of chronic hemolytic anemia. Studies are now in progress to determine the incidence of this new molecular abnormality of hemoglobin.

scholarly journals THE PHYSICAL STATE OF HEMOGLOBIN IN SICKLE-CELL ANEMIA ERYTHROCYTES IN VIVO

1968 ◽  
Vol 127 (4) ◽  
pp. 711-716 ◽  
Author(s):  
Johanna Döbler ◽  
John F. Bertles
Keyword(s):  
Electron Microscopy ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Physical State ◽  
Venous Blood ◽  
Significant Loss ◽  
Filamentous Form ◽  
Hb S

Venous blood removed anaerobically from patients with sickle-cell anemia was transferred immediately into fixative, thus precluding significant loss or gain of oxygen by the cells. Electron microscopy demonstrated an intraerythrocytic fibrillar fine structure similar to that described in prior studies on erythrocytes sickled by deoxygenation in vitro. Observations reported here lead to these conclusions: (a) explanations of the sickling process derived from in vitro experimentation may with validity be applied to sickling in vivo; and (b) the term "sickled" must be used with caution: a sickle-shaped membrane does not necessarily endose Hb S in filamentous form.

Effect of black seeds (Nigella sativa) volatile oil on the cervical cancer: In vitro study, on Hela cell lines

2019 ◽  
Vol 7 (4) ◽  
pp. 91-96
Author(s):  
Isra'a Al-sobhi ◽  
◽  
Rawan Al-Ghabban ◽  
Soad Shaker Ali ◽  
Jehan Al-Amri ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Hela Cell ◽  
Cell Lines ◽  
Nigella Sativa ◽  
In Vitro Study ◽  
Volatile Oil ◽  
Vitro Study ◽  
Hela Cell Lines ◽  
Black Seeds

AUREOMYCIN IN STAPHYLOCOCCIC MENINGITIS COMPLICATING SUBARACHNOID HEMORRHAGE IN SICKLE CELL ANEMIA

PEDIATRICS ◽  
1949 ◽  
Vol 3 (6) ◽  
pp. 764-768
Author(s):  
JOHN R. ALMKLOV ◽  
ARILD E. HANSEN
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Therapeutic Agent ◽  
In Vitro Studies ◽  
Neurologic Complications ◽  
Rare Occurrence ◽  
Laboratory Findings ◽  
Spontaneous Subarachnoid Hemorrhage

The rare occurrence of a spontaneous subarachnoid hemorrhage in an 11 year old Negro boy with sickle cell anemia is recorded. Of the eight reported cases five have occurred in children. In the study of sickle cell anemia it is evident there is an increasing awareness of this as well as other neurologic complications. This patient developed staphylococcus albus meningitis which for 12 days resisted combined penicillin, streptomycin and sulfadiazine therapy. The response to aureomycin as a sole therapeutic agent was dramatic, and this represents the first reported case of meningitis treated with this drug. The use of aureomycin as the only antibiotic in this staphylococcic infection seems to have been fortunate in view of the laboratory findings. In vitro studies disclosed that when penicillin and aureomycin or streptomycin and aureomycin were combined, the result was a decrease in the effectiveness of either drug on staphylococci.

scholarly journals Sickle Cell Anemia and Babesia Infection

Pathogens ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1435
Author(s):  
Divya Beri ◽  
Manpreet Singh ◽  
Marilis Rodriguez ◽  
Karina Yazdanbakhsh ◽  
Cheryl Ann Lobo
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Current Knowledge ◽  
Globin Gene ◽  
Environmental Niche ◽  
Parasite Resistance ◽  
The Usa ◽  
Human Infections

Babesia is an intraerythrocytic, obligate Apicomplexan parasite that has, in the last century, been implicated in human infections via zoonosis and is now widespread, especially in parts of the USA and Europe. It is naturally transmitted by the bite of a tick, but transfused blood from infected donors has also proven to be a major source of transmission. When infected, most humans are clinically asymptomatic, but the parasite can prove to be lethal when it infects immunocompromised individuals. Hemolysis and anemia are two common symptoms that accompany many infectious diseases, and this is particularly true of parasitic diseases that target red cells. Clinically, this becomes an acute problem for subjects who are prone to hemolysis and depend on frequent transfusions, like patients with sickle cell anemia or thalassemia. Little is known about Babesia’s pathogenesis in these hemoglobinopathies, and most parallels are drawn from its evolutionarily related Plasmodium parasite which shares the same environmental niche, the RBCs, in the human host. In vitro as well as in vivo Babesia-infected mouse sickle cell disease (SCD) models support the inhibition of intra-erythrocytic parasite proliferation, but mechanisms driving the protection of such hemoglobinopathies against infection are not fully studied. This review provides an overview of our current knowledge of Babesia infection and hemoglobinopathies, focusing on possible mechanisms behind this parasite resistance and the clinical repercussions faced by Babesia-infected human hosts harboring mutations in their globin gene.

Low non-carbonic buffer power amplifies acute respiratory acid-base disorders in septic patients: an in-vitro study

2021 ◽  
Author(s):  
Thomas Langer ◽  
Serena Brusatori ◽  
Eleonora Carlesso ◽  
Francesco Zadek ◽  
Paolo Brambilla ◽  
...  
Keyword(s):  
Whole Blood ◽  
In Vitro Study ◽  
Blood Gases ◽  
Hemoglobin Concentration ◽  
Strong Ion Difference ◽  
Strongly Correlated ◽  
Acid Base ◽  
Buffer Power ◽  
Ph Variations

Rationale: Septic patients have typically reduced concentrations of hemoglobin and albumin, the major components of non-carbonic buffer power(β). This could expose patients to high pH variations during acid-base disorders. Objectives: To compare, in-vitro, non-carbonic β of septic patients with that of healthy volunteers, and evaluate its distinct components. Methods: Whole blood and isolated plasma of 18 septic patients and 18 controls were equilibrated with different CO2 mixtures. Blood gases, pH and electrolytes were measured. Non-carbonic β and non-carbonic β due to variations in Strong Ion Difference (βSID) were calculated for whole blood. Non-carbonic β and non-carbonic β normalized for albumin concentrations (βNORM) were calculated for isolated plasma. Representative values at pH=7.40 were compared. Albumin proteoforms were evaluated via two-dimensional electrophoresis. Measurements and Main Results: Hemoglobin and albumin concentrations were significantly lower in septic patients. Septic patients had lower non-carbonic β both of whole blood (22.0±1.9 vs. 31.6±2.1 mmol/L, p<0.01) and plasma (0.5±1.0 vs. 3.7±0.8 mmol/L, p<0.01). Non-carbonic βSID was lower in patients (16.8±1.9 vs. 24.4±1.9 mmol/L, p<0.01) and strongly correlated with hemoglobin concentration (r=0.94, p<0.01). Non-carbonic βNORM was lower in patients (0.01 [-0.01 - 0.04] vs. 0.08 [0.06 - 0.09] mmol/g, p<0.01). Septic patients and controls showed different amounts of albumin proteoforms. Conclusions: Septic patients are exposed to higher pH variations for any given change in CO2 due to lower concentrations of non-carbonic buffers and, possibly, an altered buffering function of albumin. In both septic patients and healthy controls, electrolyte shifts are the major buffering mechanism during respiratory acid-base disorders.

scholarly journals The Effects of Cyanate In Vitro on Red Blood Cell Metabolism and Function in Sickle Cell Anemia

1972 ◽  
Vol 51 (3) ◽  
pp. 566-574 ◽  
Author(s):  
Frank G. De Furia ◽  
Denis R. Miller ◽  
Anthony Cerami ◽  
James M. Manning
Keyword(s):  
Blood Cell ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Red Blood Cell ◽  
Cell Metabolism ◽  
And Function

scholarly journals Effects of glucose-6-phosphate dehydrogenase deficiency upon sickle cell anemia

Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 748-752 ◽  
Author(s):  
MH Steinberg ◽  
MS West ◽  
D Gallagher ◽  
W Mentzer
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
G6pd Deficiency ◽  
Electrophoretic Pattern ◽  
Hemoglobin Concentration ◽  
Wild Type ◽  
Standardized Protocol ◽  
Cellulose Acetate Membranes ◽  
Male Patients ◽  
Glucose 6 Phosphate Dehydrogenase

Abstract We studied the interactions of the A- variety of glucose-6-phosphate dehydrogenase (G6PD) deficiency and sickle cell anemia (HbSS) to see if G6PD deficiency influenced laboratory and clinical features of HbSS. A total of 801 male patients over age 2 had G6PD electrophoresis on cellulose acetate membranes. Assays of both G6PD activity and hexokinase activity were then done on all samples that had an electrophoretic pattern other than the normal wild type (GdB). The collection of clinical data used a standardized protocol. Using cluster analyses we classified 10.4% males to be G6PD deficient, while 18.4% had the functionally normal GdA+ enzyme. The prevalence of G6PD deficiency did not change significantly when age was stratified by decade, suggesting little survival advantage or disadvantage of the combination of G6PD deficiency and HbSS. Compared to patients who were not G6PD deficient, there were no significant differences in the hemoglobin concentration, mean corpuscular volume, reticulocyte count, bilirubin, or SGOT level in patients with HbSS who had G6PD deficiency. The incidence of painful episodes, sepsis, or acute anemic episodes was similar in both groups. Our results are consistent with recent studies of smaller numbers of patients that have found little influence of G6PD deficiency upon HbSS. Specifically, we found no evidence that G6PD enhanced the severity of hemolysis or increased the incidence of acute anemic episodes or sepsis in HbSS.

scholarly journals Genetic Correction of Sickle Cell Anemia and β-Thalassemia: Progress and New Perspective

2010 ◽  
Vol 10 ◽  
pp. 644-654 ◽  
Author(s):  
Ajay Perumbeti ◽  
Punam Malik
Keyword(s):  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Globin Genes ◽  
Induced Pluripotent Cells ◽  
Substantial Progress ◽  
Lentivirus Vectors ◽  
New Perspective ◽  
Induced Pluripotent ◽  
New Strategies

Gene therapy for β-globinopathies, particularly β-thalassemia and sickle cell anemia, holds promise for the future as a definitive corrective approach for these common and debilitating disorders. Correction of the β-globinopathies using lentivirus vectors carrying the β- or γ-globin genes and elements of the locus control region has now been well established in murine models, and an understanding of "what is required to cure these diseases" has been developed in the first decade of the 21st century. A clinical trial using one such vector has been initiated in France with intriguing results, while other trials are under development. Vector improvements to enhance the safety and efficiency of lentivirus vectors are being explored, while new strategies, including homologous recombination in induced pluripotent cells, for correction of sickle cell anemia have shown proof-of-conceptin vitro. Here, a review is provided of the current substantial progress in genetic correction of β-globin disorders.

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