scholarly journals Stimulation of Haemopoetic Activity in Bone Marrow and Deformation of Red Blood Cells in Albino Mice, Mus musculus Exposed to Radiations from GSM Base Stations

2011 ◽  
Vol 2 (2) ◽  
Author(s):  
AA Otitoloju ◽  
VO Osunkalu ◽  
MM Akogun ◽  
IA Obe ◽  
OA Adewale ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Mus Musculus ◽  
Blood Cells ◽  
Base Stations ◽  
Albino Mice ◽  
Stimulation Of

Evaluation of acute toxicity and effects of sub-acute concentrations of copper oxide nanoparticles (CuO-NPs) on hematology, selected enzymes and histopathology of liver and kidney in Mus musculus

2017 ◽  
Author(s):  
Atif Yaqub ◽  
Khalid Anjum ◽  
Amnah Munir ◽  
Hamid Mukhtar ◽  
Waseem Khan
Keyword(s):  
Acute Toxicity ◽  
Copper Oxide ◽  
Red Blood Cells ◽  
Mus Musculus ◽  
Blood Cells ◽  
Copper Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Cuo Nps ◽  
Liver And Kidney ◽  
Albino Mice

Industrial use of nanoparticles and their accumulation during the recent decade have created an urgent need to assess their environmental implications. The current study deals with the evaluation of acute toxicity of copper oxide nanoparticles (CuO-NPs) in the albino mice (Mus musculus). Lethal dose of these nanoparticles in albino mice injected via intravenous route were found to be 550 mg/kg body weight (BW). Exposure of the albino mice to sub-lethal concentrations of these nanoparticles resulted in altered hematological parameters such as a significant increase in white blood cells (WBCs), a significant decrease in red blood cells (RBCs), hemoglobin (Hb) and platelets count. NPs significantly elevated the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and creatinine. Histopathological examination of liver and kidney showed that sub-lethal doses of CuO-NPs, in liver, led to rupture of hepatocytes, dilation of sinusoid space, hemorrhaging in hepatic tissues, and congestion of the central vein with red blood cells leading towards ultimate rupture. On the other hand, the kidney showed ruptured renal capsule, loss of urinary space, swelling in glomerulus, degeneration in podocysts, and cytoplasmic vacuolization

Normalized levels of red blood cells expressing phosphatidylserine, their microparticles, and activated platelets in young patients with β-thalassemia following bone marrow transplantation

2017 ◽  
Vol 96 (10) ◽  
pp. 1741-1747 ◽  
Author(s):  
Phatchanat Klaihmon ◽  
Sinmanus Vimonpatranon ◽  
Egarit Noulsri ◽  
Surapong Lertthammakiat ◽  
Usanarat Anurathapan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Marrow Transplantation ◽  
Young Patients ◽  
Activated Platelets

Early erythropoiesis in foetal rat bone marrow: evidence for a liver-to-bone marrow relay

Development ◽  
1981 ◽  
Vol 64 (1) ◽  
pp. 275-293
Author(s):  
M. D. Nagel ◽  
J. Nagel ◽  
R. Jacquot
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Mechanism ◽  
Erythropoietic Activity ◽  
Intrauterine Life ◽  
Foetal Rat ◽  
Stimulate Bone Marrow ◽  
Rat Bone

Erythropoietic activity of foetal rat femoral marrow was examined during the last four days of intra-uterine life. Insignificant at day 18, it develops slowly thereafter until birth. In the non-suckled neonate (not older than two hours), it appears notably enhanced. In order to test the potential of the foetal marrow to develop precocious or increased erythropoiesis, the activity of the erythropoietic organ predominant at this time, the liver, was altered by modifying the level of circulating corticosteroids which govern its function. Maturation and involution of the hepatic erythron were prevented by corticosteroid deprivation of the foetus (maternal adrenalectomy and foetal hypophysectomy). Precocious maturation and exhaustion of the hepatic erythron was induced by submitting foetuses to corticosteroids excess from day 14. Both corticosteroid deprivation and excess increase the erythropoietic activity of the femoral marrow. This activity can reach and even exceed by day 20 of intrauterine life that in neonatal marrow. Foetal hepatic erythron misfunction can therefore initiate and stimulate bone marrow erythropoiesis. The study of circulating red blood cells demonstrates that: (1) anaemia initiates medullary erythropoietic activity; (2) this anaemia is largely corrected by the bone marrow. The regulatory mechanism is presumably erythropoietin mediated.

scholarly journals CELLS INVOLVED IN THE IMMUNE RESPONSE

1969 ◽  
Vol 129 (4) ◽  
pp. 757-774 ◽  
Author(s):  
Nabih I. Abdou ◽  
Maxwell Richter
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Bone Marrow Cells ◽  
Allogeneic Bone Marrow ◽  
Red Cells ◽  
Allogeneic Bone ◽  
Sheep Red Blood Cells ◽  
Sheep Red Cells

Irradiated rabbits given allogeneic bone marrow cells from normal adult donors responded to an injection of sheep red blood cells by forming circulating antibodies. Their spleen cells were also capable of forming many plaques using the hemolysis in gel technique, and were also capable of undergoing blastogenesis and mitosis and of incorporating tritiated thymidine upon exposure to the specific antigen in vitro. However, irradiated rabbits injected with allogeneic bone marrow obtained from rabbits injected with sheep red blood cells 24 hr prior to sacrifice (primed donors) were incapable of mounting an immune response after stimulation with sheep red cells. This loss of reactivity by the bone marrow from primed donors is specific for the antigen injected, since the immune response of the irradiated recipients to a non-cross-reacting antigen, the horse red blood cell, is unimpaired. Treatment of the bone marrow donors with high-titered specific antiserum to sheep red cells for 24 hr prior to sacrifice did not result in any diminished ability of their bone marrow cells to transfer antibody-forming capacity to sheep red blood cells. The significance of these results, with respect to the origin of the antigen-reactive and antibody-forming cells in the rabbit, is discussed.

Adenosine causes cAMP-dependent activation of chick embryo red cell carbonic anhydrase and 2,3-DPG synthesis

1996 ◽  
Vol 271 (4) ◽  
pp. R973-R981 ◽  
Author(s):  
S. Glombitza ◽  
S. Dragon ◽  
M. Berghammer ◽  
M. Pannermayr ◽  
R. Baumann
Keyword(s):  
Carbonic Anhydrase ◽  
Red Blood Cells ◽  
Adenylyl Cyclase ◽  
Adenosine Receptor ◽  
Blood Cells ◽  
Cell Protein ◽  
Red Cell ◽  
Receptor Stimulation ◽  
2,3 Dpg ◽  
Stimulation Of

In late chick embryos, coordinate activation of red cell carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis is initiated by hypoxia. The effects are mediated by unidentified hormonal effectors resident in chick plasma. In the present investigation, we have analyzed the effect of adenosine receptor stimulation on embryonic red cell CAII and 2,3-DPG synthesis. We find that primitive and definitive embryonic red blood cells from chick have an A2a adenosine receptor. Stimulation of the receptor with metabolically stable adenosine analogues causes a large increase of red cell adenosine 3',5'-cyclic monophosphate (cAMP) and subsequent activation of red cell CAII and 2,3-DPG production in definitive red blood cells and of CAII synthesis in primitive red blood cells. Direct stimulation of adenylyl cyclase with forskolin has the same effect. Analysis of red cell protein pattern after labeling with [35S]methionine shows that stimulation of red cell cAMP levels activates synthesis of several other proteins aside from CAII. Presence of actinomycin D inhibits cAMP-dependent changes of protein synthesis, indicating that cAMP-dependent transcriptional activation is required. In contrast to the stable adenosine receptor analogues, adenosine itself was a very weak agonist, unless its metabolism was significantly inhibited. Thus, besides adenosine, other effectors of the adenylyl cyclase system are likely to be involved in the O2 pressure-dependent regulation of red cell metabolism in late development of avian embryos.

scholarly journals Peripheral Red Blood Cell Split Chimerism as a Consequence of Intramedullary Selective Apoptosis of Recipient Red Blood Cells in a Case of Sickle Cell Disease

2014 ◽  
Vol 6 (1) ◽  
pp. e2014066 ◽  
Author(s):  
Marco Marziali ◽  
Antonella Isgrò ◽  
Pietro Sodani ◽  
Javid Gaziev ◽  
Daniela Fraboni ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Blood Cells ◽  
Marrow Transplant ◽  
Mixed Chimerism ◽  
Radical Cure ◽  
Hematopoietic Stem ◽  
Hematopoietic Chimerism

Allogeneic cellular gene therapy through hematopoietic stem cell transplantation is the only radical cure for congenital hemoglobinopathies like thalassemia and sickle cell anemia. Persistent mixed hematopoietic chimerism (PMC) has been described in thalassemia and sickle cell anemia. Here, we describe the clinical course of a 6-year-old girl who had received bone marrow transplant for sickle cell anemia. After the transplant, the patient showed 36% donor hematopoietic stem cells in the bone marrow, whereas in the peripheral blood there was evidence of 80%  circulating donor red blood cells (RBC). The analysis of apoptosis at the Bone Marrow  level suggests that Fas might contribute to the cell death of host erythroid precursors. The increase in NK cells and the regulatory T cell population observed in this patient suggests that these cells might contribute to the condition of mixed chimerism.

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