Bone-marrow reactions. I. The blood count in the albino rat: Erythrocytes and hemoglobin

1930 ◽  
Vol 44 (4) ◽  
pp. 335-347 ◽  
Author(s):  
Stuart L. Vaughan ◽  
Francis D. Gunn
1930 ◽  
Vol 45 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Francis D. Gunn ◽  
Stuart L. Vaughan

2020 ◽  
pp. 5181-5188
Author(s):  
Wendy N. Erber

The diagnosis of haematological malignancies requires an understanding of the diseases and the uses and limitations of the range of available investigations. The relative importance of different investigations varies by disease entity. The blood count is one of the most widely used tests in all of medicine and often the first indication of an underlying haematological malignancy. Some blood count features are ‘diagnostic’ and others may give an indication of a bone marrow defect. Morphological assessment of a stained blood film adds value to an abnormal blood count. It may identify abnormal morphology of red cells, leucocytes, or platelets which may be specific and diagnostic, or give clues suggesting a diagnosis. Bone marrow aspirate (liquid sample) gives cytological detail, and trephine biopsy provides information about marrow cellularity, architecture, cellular distribution, and extent of fibrosis. Immunophenotyping detects cellular antigens in clinical samples and is essential in the diagnosis and classification of haematological malignancies. It is also used for disease staging and monitoring, to detect surrogate markers of genetic aberrations, identify potential immunotherapeutic targets, and to aid prognostic prediction. Cytogenetics assesses the number and structure of whole chromosomes and chromosomal regions in neoplastic cells and is performed to diagnose and classify some haematological malignancies. Molecular genetic methods facilitate the detection of mutations, rearrangements, or translocations in genes. Applications in malignant haematology include confirming clonality, detecting disease-associated genotypes, determining prognosis, disease monitoring following therapy, predicting imminent clinical relapse, and identifying patients who are likely (or not) to respond to new targeted inhibitor therapies.


Blood ◽  
1948 ◽  
Vol 3 (3) ◽  
pp. 292-294 ◽  
Author(s):  
D. G. CAMERON ◽  
G. M. WATSON

Abstract A technic for repeated femoral bone marrow biopsy in the rat is detailed. Differential counts confirmed the distribution of the cellular elements as described by other authors.


Blood ◽  
1952 ◽  
Vol 7 (10) ◽  
pp. 1005-1016 ◽  
Author(s):  
ROSANNA N. CHUTE ◽  
SHELDON C. SOMMERS

Abstract Disharmoniouns parabiotic rats were studied, which had clinical, hematologic, pathologic and serologic evidences of blood incompatibility, isohemagglutinin hypersensitization and hemolytic anemia. Spherocytosis and increased incomplete isohemagglutinin antibodies, demonstrated by indirect Coombs-type agglutinations and with trypsinized rat erythrocytes, were found in both parabionts. One partner became anemic with reticulocytosis, erythroblastosis, bone marrow necrobiosis, reactive hematopoietic hyperplasia and enhanced extramedullary hematopoiesis. The other parabiont showed lymphoid and reticulo-endothelial hyperplasia, leukocytoid lymphocytosis and erythrophagocytosis. It was plethoric with polycythemia, increased blood volume and high blood pressure. The polycythemia was explained by mechanical trapping of sludged antibody-coated incompatible erythrocytes, which the reticulo-endothelial system was inadequate to process. Complicating hemoglobinemia and hemoglobinuric nephrosis developed. Other manifestations of parabiosis intoxication are briefly discussed.


Blood ◽  
1959 ◽  
Vol 14 (5) ◽  
pp. 548-557 ◽  
Author(s):  
J. W. HOLLINGSWORTH ◽  
Mary C. Perfetto

Abstract 1. Humoral antibody production has been studied in severely irradiated mice treated with isologous (same strain) or homologous (different strain) bone marrow. 2. The two methods of study involved functional end points of humoral antibody production as evidenced by in vivo lysis of rat erythrocytes or by regression of mouse leukosis E.L. 4 in histoincompatible mouse recipients. 3. Humoral antibody production was lost after irradiation and isologous marrow treatment, but recovered partially in two weeks and almost completely in four weeks. 4. Established immunity was not abruptly terminated after irradiation and treatment with either isologous or homologous marrow, although there was premature loss of immunity to rat erythrocytes by the irradiated, isologous marrow-treated mouse. 5. Permanent immunity could not be transferred by isologous marrow or spleen from immunized donors to irradiated recipients. 6. Treatment of mice histoincompatible to E.L. 4 leukosis with histocompatible donor bone marrow failed to establish rejection of the tumor. 7. These studies support the concept that humoral antibody production in irradiated, marrow-treated mice remains a function of the host rather than of the transplanted tissues. 8. These studies failed to clarify the conflicting evidence concerning the mechanism of the late illness that occurs after treatment of the irradiated mouse with bone marrow from a different strain or species.


2019 ◽  
Vol 12 (3) ◽  
pp. e227821
Author(s):  
Adele Beck ◽  
Hannah Hunter ◽  
Simon Jackson ◽  
David Sheridan

A 17-year-old man with no significant past medical history presented with a 2-week history of worsening jaundice, lethargy, anorexia and progressive right upper quadrant abdominal pain. There were no stigmata of chronic liver disease. Initial investigations were suggestive of cholangitis with large intrahepatic and extrahepatic bile duct strictures but otherwise normal hepatic and splenic appearances. A percutaneous transhepatic cholangiogram with the positioning of drains was performed to alleviate the obstructive jaundice. Within 2 weeks of the first presentation, full blood count revealed a significantly raised white blood count and a subsequent peripheral blood smear and bone marrow were consistent with a diagnosis of acute myeloid leukaemia. Chemotherapy was started after partial improvement of his obstructive jaundice. Complete morphological and cytogenetic remission was obtained 4 weeks after the first cycle of chemotherapy (half dose of daunorubicin and full dose of cytarabine, treated off trial) on control bone marrow. The patient remains in remission.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4192-4192
Author(s):  
Gina Zini ◽  
Mariagrazia Garzia ◽  
Antonella Di Mario ◽  
Elena Rossi ◽  
Giuliana Farina ◽  
...  

Abstract Bone marrow (BM) analysis is conventionally performed by microscope examination on films of about 0.3ml of aspirated bone marrow fluid, stained with Romanowsky dyes. Until 1996 the simple automated screening of marrow composition was made very difficult by a number of factors, mainly the lack of the erythroblasts quantitation and the fat interference. From 1996 last generation automated hematology analyzers provide accurate and precise erythroblasts counts; moreover same systems have improved their software reducing the problem of fat interference. We have analyzed data from 100 normal BM samples from patients submitted for diagnostic and/or follow up purposes in our Hematology Day Hospital. BM fluid was harvested from the superior posterior iliac crest. The first 0,3–0.5 ml were used for smears, while the next 1–2 ml of BM, collected into K3-EDTA, were analysed with Coulter LH 750, a fully automated hematology analyzer which provides Complete Blood Count, White Blood Count Differential included Nucleated Red Blood Cells (NRBC) and Reticulocytes count. We used the microscope examination conventionally performed on films stained with Romanowsky dyes as reference method. Quantitative detection BM cellularity was obtained by semi quantitative evaluation based on the evaluation of hematopoietic cells in several marrow particles: physiological differences age related were also taken in account. If hematopoietic cells occupy less than 25% or more than 85% the sample is defined respectively hypocellular or hypercellular (none of our sample was as). Differential cell count was usually performed on two different slides counting 500 cells (1000 when hypercellular, but none of our sample was as). We found a strict correlation between microscope semi-quantitative cellularity evaluation and the instrumental cell count as sum of WBC plus NRBC, the Total Nucleted Cell Count (TNCC). The mean value of the TNCC in normal PM samples was 29,48 x109/L with a range 25,9–54,9 x109/L. These results are in good agreement with normal BM cell count reported in the literature using a cytofluorimetric method, which is 34,5 x109/L (SD28.0). The instrumental mean percentage of BM granulocytes corrected for TNNC was 62% (range: 23,5–93,7) versus a mean microscope percentage of 58,42% (range: 40–72). The automated NRBC BM count corrected for TNCC was 11,38% (range: 2,7 – 39,17) versus a microscopic mean value of 28% (range: 9–45). These results, including the slight NRBC underestimation probably due to partial mature cell lysis, are in line with the data of the literature. This study confirms the feasibility of routine automated cell count using a hematology in normal BM fluid samples. Automated methods will support morphologists quickly providing accurate and precise quantitative information such as TNCC and myeloid/erythroid ratio.


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