Relevant bibliographies by topics / Red cells disorder

Academic literature on the topic 'Red cells disorder'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Red cells disorder"

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Francis, David M., Sheryl A. Barringer, and Robert E. Whitmoyer. "Ultrastructural Characterization of Yellow Shoulder Disorder in a Uniform Ripening Tomato Genotype." HortScience 35, no. 6 (October 2000): 1114–17. http://dx.doi.org/10.21273/hortsci.35.6.1114.

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Yellow shoulder disorder (YSD) is characterized by sectors of yellow or green tissue under the peel of uniform ripening tomato (Lycopersicon esculentum Mill.) fruit. Tissues excised from sectors of fruit expressing YSD, from adjacent red sectors, and from mature green fruit were used to compare the ultrastructural alterations in cells and tissue affected by YSD and to determine whether the disorder is caused by delayed fruit maturation or by aberrant development. Cells from YSD sectors were smaller than those from both adjacent red-ripe tissue and mature green fruit. The smaller cells from the YSD sectors were at a different developmental stage than cells of the adjacent red-ripe tissue. Chromoplasts in red-ripe tissue were more advanced in development than those in YSD sectors or mature green fruit. Using the transition from chloroplast to chromoplast and the degradation of the middle lamella between adjacent cells as developmental markers, the maturity of tissue from YSD sectors appeared to be equal or greater than that of tissue from mature green fruit. However, cell enlargement, which takes place early in fruit development, was retarded in YSD sectors. Therefore, the ultrastructural features of YSD are not compatible with a delayed ripening model for this blotchy ripening disorder. These observations provide a basis for comparing YSD in uniformly ripening tomatoes with other blotchy ripening disorders.
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Yektas, Cigdem, Ali Tufan, Onder Kilicaslan, Merve Yazici, Sumeyra Karakaya, and Enes Sarigedik. "Elevated Monocyte Levels Maybe a Common Peripheral Inflammatory Marker in Specific Learning Disorders and Attention Deficit/Hyperactivity Disorder." Psychiatry and Behavioral Sciences 12, no. 3 (2022): 125. http://dx.doi.org/10.5455/pbs.20210518080022.

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Aim: the primary aim of this study was to determine whether the neutrophil / lymphocyte ratio, mean platelet volume, monocyte/ lymphocyte ratio and distribution width of red blood cells are different in children with specific learning disorders compared to healthy controls. The second aim of the study is to investigate the relationships of those inflammatory markers with SLDs clinical severity. Methods: A total of 100 drug-naive participants, aged 7-12 years, who were newly diagnosed as having specific learning disorders according to the DSM-5 criteria were compared with a healthy control group of 75 age, sex matched children. the neutrophil / lymphocyte ratio, mean platelet volume, monocyte/ lymphocyte ratio and distribution width of red blood cells were measured according to the complete blood count. Results: specific learning disorders significantly affected monocyte levels and tended to affect monocyte/ lymphocyte ratio and neutrophil levels while attention deficit hyperactivity disorder diagnosis significantly affected monocyte levels and mean platelet volume and also tended to affect distribution width of red blood cells. Specific learning disorders symptom severity did not correlate significantly with peripheral inflammatory markers. Conclusions: This study is the first to investigate the effect of peripheral inflammatory markers in a large specific learning disorders sample by controlling attention deficit hyperactivity disorder comorbidity. The findings demonstrated that the monocyte levels are higher in both specific learning disorders and attention deficit hyperactivity disorder groups suggesting that elevated monocyte levels may be a common marker in the inflammatory pathophysiology.
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Yang, Yang, Xiaopeng Zhao, Hui Liu, and Jiankai Xiang. "Blue–green–red light left-handed metamaterials from disorder dendritic cells." Journal of Materials Science: Materials in Electronics 24, no. 9 (May 1, 2013): 3330–37. http://dx.doi.org/10.1007/s10854-013-1251-x.

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Izzati Binti Che Marzuki, Nurhanis Izzati Binti Che Marzuki, Nasrul Humaimi bin Mahmood Humaimi bin Mahmood, and Mohd Azhar bin Abdul Razak. "Identification of Thalassemia Disorder using Active Contour." Indonesian Journal of Electrical Engineering and Computer Science 6, no. 1 (April 1, 2017): 160. http://dx.doi.org/10.11591/ijeecs.v6.i1.pp160-165.

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Thalassemia was known as the red blood cell (RBC) morphology disorder. This disease mostly affects the shape of the red blood cells. Thalassemia becomes the major public health problem when one of the people becomes the carrier of the disease. It can occur within a months after birth or even before birth and results in inappropriate growth and development of babies. Sometimes the affected babies will die shortly after birth. In order to screen thalassemia, there are a few tests need to be done. Firstly by performed Complete Blood Count (CBC) and secondly continued with hemoglobin electrophoresis test. This CBC test will identify the morphology of RBC. Hence, this paper will discuss the methods on identifying the morphology of thalassemia blood cells by using active contour technique. From the result of 16 normal and abnormal blood cell images, the active countour methods able to identifyThalassemia blood cells with accuracy of 90% from the abnormal cell images.
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Ciccoli, Lucia, Claudio De Felice, Silvia Leoncini, Cinzia Signorini, Alessio Cortelazzo, Gloria Zollo, Alessandra Pecorelli, Marcello Rossi, and Joussef Hayek. "Red blood cells in Rett syndrome: oxidative stress, morphological changes and altered membrane organization." Biological Chemistry 396, no. 11 (November 1, 2015): 1233–40. http://dx.doi.org/10.1515/hsz-2015-0117.

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Abstract In this review, we summarize the current evidence on the erythrocyte as a previously unrecognized target cell in Rett syndrome, a rare (1:10 000 females) and devastating neurodevelopmental disorder caused by loss-of-function mutations in a single gene (i.e. MeCP2, CDKL5, or rarely FOXG1). In particular, we focus on morphological changes, membrane oxidative damage, altered membrane fatty acid profile, and aberrant skeletal organization in erythrocytes from patients with typical Rett syndrome and MeCP2 gene mutations. The beneficial effects of ω-3 polyunsaturated fatty acids (PUFAs) are also summarized for this condition to be considered as a ‘model’ condition for autism spectrum disorders.
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H. Al-khafaji, Kawther, and Athraa H. Al-khafaji. "Diagnoses of Blood Disorder in Different Animal Species Depending on Counting Methods in Blood Cell Images." International Journal of Engineering & Technology 7, no. 4.36 (December 9, 2018): 660. http://dx.doi.org/10.14419/ijet.v7i4.36.24218.

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Counting of red blood cells (RBCs) in microscope blood cell images, can give the pathologists valuable information regarding various hematological disorders, like anemia, leukemia,....etc. in several animal species, in this paper, an automated vision system has been developed which is capable of counting of red blood cells, in blood samples by applying different algorithms, based on red blood cellshape, the difference in the red blood cell shape of animal species make it difficult to use a one algorithm, therefore, for each animal species used specific algorithm which was capable of counting of RBCs effectively.
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Chakmakjian, Carl, and Ed Rappaport. "RBC Histogram Predictive of HE." Blood 106, no. 11 (November 16, 2005): 3706. http://dx.doi.org/10.1182/blood.v106.11.3706.3706.

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Abstract Hereditary elliptocytosis (HE) encompasses a family of inherited erythrocyte disorders characterized by red blood cells with an oval, elongated shape. Diagnosis is most commonly made upon peripheral smear examination. Although the disorder is usually clinically silent, these patients may have some degree of chronic hemolysis that may necessitate splenectomy on occasion. We report a consistent finding in HE common to most electronic cell counters. The red blood cell histogram reliably has a two to three millimeter elevation above baseline at the extreme left of the graph. This “foot” on the histogram is predictive of possible red blood cell elliptocytes. Please see example. Figure Figure
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Vlachaki, Efthymia, Michael D. Diamantidis, Philippos Klonizakis, Styliani Haralambidou-Vranitsa, Elizabeth Ioannidou-Papagiannaki, and Ioannis Klonizakis. "Pure Red Cell Aplasia and Lymphoproliferative Disorders: An Infrequent Association." Scientific World Journal 2012 (2012): 1–7. http://dx.doi.org/10.1100/2012/475313.

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Pure red cell aplasia (PRCA) is a rare bone marrow failure syndrome defined by a progressive normocytic anaemia and reticulocytopenia without leukocytopenia and thrombocytopenia. Secondary PRCA can be associated with various haematological disorders, such as chronic lymphocytic leukaemia (CLL) or non-Hodgkin lymphoma (NHL). The aim of the present review is to investigate the infrequent association between PRCA and lymphoproliferative disorders. PRCA might precede the appearance of lymphoma, may present simultaneously with the lymphoid neoplastic disease, or might appear following the lymphomatic disorder. Possible pathophysiological molecular mechanisms to explain the rare association between PRCA and lymphoproliferative disorders are reported. Most cases of PRCA are presumed to be autoimmune mediated by antibodies against either erythroblasts or erythropoietin, by T-cells secreting factors selectively inhibiting erythroid colonies in the bone marrow or by NK cells directly lysing erythroblasts. Finally, focus is given to the therapeutical approach, as several treatment regimens have failed for PRCA. Immunosuppressive therapy and/or chemotherapy are effective for improving anaemia in the majority of patients with lymphoma-associated PRCA. Further investigation is required to define the pathophysiology of PRCA at a molecular level and to provide convincing evidence why it might appear as a rare complication of lymphoproliferative disorders.
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Koju, Surendra, and Ramesh Makaju. "Hereditary Spherocytosis." Journal of Lumbini Medical College 6, no. 1 (June 22, 2018): 41–43. http://dx.doi.org/10.22502/jlmc.v6i1.202.

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Introduction: Hereditary spherocytosis is a red cell membrane disorder that causes hemolytic anemia. Due to defective cell membrane, red cells are spherical shaped and result in their early lysis. Osmotic fragility of spherocytic red cell is increased. Case report: A 22 year old female presented with chief complain of abdominal pain. Initially she was diagnosed as cholelithiasis. Under laboratory evaluation she was found to be anemic with reticulocytosis. In peripheral blood smear, spherocytes were moderately distributed. Antihuman globulin test was negative but osmotic fragility was high. Hence, she was confirmed as case of hereditary spherocytosis. Conclusion: Hereditary spherocytosis is a rare red cell disorder and its diagnosis can be made by osmotic fragility test.
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Zhu, Yiwen, Chris Paszty, Tikva Turetsky, Susan Tsai, Frans A. Kuypers, Gloria Lee, Philip Cooper, et al. "Stomatocytosis Is Absent in “Stomatin”-Deficient Murine Red Blood Cells." Blood 93, no. 7 (April 1, 1999): 2404–10. http://dx.doi.org/10.1182/blood.v93.7.2404.

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Abstract To examine the relationship between erythrocyte membrane protein 7.2b deficiency and the hemolytic anemia of human hereditary stomatocytosis, we created 7.2b knock-out mice by standard gene targeting approaches. Immunoblots showed that homozygous knock-out mice completely lacked erythrocyte protein 7.2b. Despite the absence of protein 7.2b, there was no hemolytic anemia and mouse red blood cells (RBCs) were normal in morphology, cell indices, hydration status, monovalent cation content, and ability to translocate lipids. The absence of the phenotype of hereditary stomatocytosis implies that protein 7.2b deficiency plays no direct role in the etiology of this disorder and casts doubt on the previously proposed role of this protein as a mediator of cation transport in RBC.
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Dissertations / Theses on the topic "Red cells disorder"

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DE, ROSA GIANLUCA. "UNRAVELING THE MOLECULAR PATHOGENESIS OF INEFFECTIVE ERYTHROPOIESIS IN CONGENITAL DYSERYTHROPOIETIC ANEMIA TYPE II: IN VITRO EVALUATION OF RAP-011 TREATMENT." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/697529.

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Congenital Dyserythropoietic Anemias (CDAs) are subtypes of bone marrow failure syndromes, hallmarked by ineffective erythropoiesis. The most common form is CDA type II (CDAII), showing moderate/severe anemia, relative reticulocytopenia, jaundice, splenomegaly, and iron overload. It is inherited as an autosomal recessive disorder due to loss-of-function mutations in the SEC23B gene. Molecular pathogenesis of CDA II still has to be investigated because the described animal models did not recapitulate the clinical features observed in humans. To date, treatments for CDAII patients consist of supportive therapy, such as erythrocyte transfusions, or bone marrow transplantation or splenectomy in transfusion-dependent cases. Recently, members of TGF-β superfamily have been studied as potential regulators of erythropoiesis, especially the growth differentiation factor 11 (GDF11). Through the binding of specific receptors, GDF11 leads to an inhibited late-stage erythropoiesis. Indeed, two GDF11 inhibitors, ACE-011 and ACE-536, have been associated with an improvement of hematologic parameters. Studies with the mouse counterpart of ACE-011, RAP-011, on a mouse model of β-thalassemia showed increased differentiation of erythroid cells, improvement of the anemic condition and reduced iron overload in treated mice. The first aim of our study was the establishment of a cellular model of CDA II, that could reproduce the main defects of the disease, such as the lack of the erythroid differentiation due to the low or absent expression of SEC23B gene. For this aim, we selected the K562 cell line and, through short-hairpin RNA-based strategy, we obtained two different clones of K562 showing a stable silencing of SEC23B. Then, we decided to assess the effects of RAP-011 on this CDA II model, by investigating the pathway involved in the GDF11 signaling. This treatment simulated the ligand trap function played by RAP-011 towards GDF11. The administration of RAP-011 resulted in a reduction of SMAD2 phosphorylation induced by GDF11 and, moreover, in an increase of different erythroid differentiation markers.
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Mundee, Yuttana. "Red cell adhesion molecules, foetal haemoglobin and endothelial factors in sickle cell disorders." Thesis, University College London (University of London), 2001. http://discovery.ucl.ac.uk/1317695/.

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Sickle cell anaemia (SS) is a haemoglobinopathy involving production of sickle haemoglobin (HbS, β⁶Glu-->Val), which is able to polymerise leading to vaso-occlusion. Hydroxyurea (HU) treatment increases foetal haemoglobin (HbF) levels but decreases vaso-occlusion and red cell adhesion molecule (AM) expression, and therefore improves clinical symptoms. In this thesis, the contribution of AMs, HbF and endothelial factors to the severity of sickle cell disease has been studied. Flow cytometry for measurement of HbF-containing red cells (F⁺cells), AM-expressing red cells (AM⁺cells) and reticulocytes (retics) was developed and validated using single-, double- and triple-colour staining procedures. The AMs examined were CD36, CD41 and CD49d. F⁺cells are increased in SS patients over normal control subjects. In the controls, the percentage of F⁺mature red cells (%F⁺MRCs) is equal to %F⁺retics leading to an enrichment ratio (ER = %F⁺MRCs / %F⁺retics) close to 1.0, indicating no survival advantage of F⁺cells. However in SS patients, the ER is about 1.5-2.5 indicating a survival advantage of F⁺cells. AM⁺cells in SS patients are also increased over the controls. In both the controls and SS patients, the AM⁺cell depletion ratio (AMDR = %AM⁺MRCs / %AM⁺retics) is decreased to less than 0.05, indicating a rapid shedding of AMs from reticulocytes during maturation. This shedding is confirmed by a reduction of %AM⁺cells to undetectable levels after 5 days of reticulocytes in culture. In HU-treated SS patients, F⁺cell increment and AM⁺cell reduction are found. The %AM⁺retics for pre- and post-HU treatment is not different, suggesting that AM⁺cell reduction is dependent on the reduction of reticulocytes. In the controls, proportion of F⁺cells expressing AMs is higher than F⁺cells, indicating that F⁺cells are more primitive. In SS patients, these proportions are similar. However, in HU-treated SS patients, the proportion of F⁺cells expressing AMs is lower than F⁺cells, confirming that F⁺cells survive longer so that they have more time to shed more AMs. This finding is similar in both reticulocyte and MRC populations. Vascular endothelial growth factor (VEGF) may be involved in vasoocclusion. It is significantly increased in SS patients. VEGF is able to induce nitric oxide metabolite (NOx) release. However in this thesis, NOx levels were not increased in SS patients and no correlation was found between NOx and VEGF levels. No relationship was observed between VEGF and either erythropoietin or Hb levels, suggesting that VEGF increment may not be due to generalised anaernia. Increases in soluble endothelial selectin (sE-Selectin) and soluble vascular cell adhesion molecule 1 (sVCAM-1) found in SS patients indicate endothelial activation. Beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were also increased in SS patients, due to local platelet activation in vivo. Platelets as well as endothelial cells contain VEGF, therefore the increased VEGF levels in SS could be a consequence of local ischaernia resulting from vaso-occlusion and local platelet and endothelial cell activation.
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Huang, Sha Ph D. Massachusetts Institute of Technology. "The relevance of red blood cell deformability in the pathophysiology of blood disorders." Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/93062.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 136-144).
Red blood cells (RBCs) play a crucial role in delivering oxygen to the body tissues. During the 120 days of their lifespan, average RBCs would circulate for approximately 500,000 times and undergo repeated deformations in small blood capillaries and splenic cords. Increased RBC clearance in the spleen is considered as one of the direct consequences of reduced RBC deformability. On the other hand, deformability is also indirectly impacting on RBC functionality through its complex connections with underlying molecular mechanisms. With the aid of microfabrication and microfluidic, we are able to perform high-throughput single cell deformability measurement. Overall, we established RBC deformability as an important biomarker for several blood related real world problems such as malaria and blood storage lesion. The ultimate goal is through our quantitative assessment of population-wide single cell deformability, we could aid in the decision-making of various clinical scenarios including drug screening and blood transfusion. Malaria is the most deadly parasitic disease affecting hundred millions of people worldwide. Infected RBCs are found to be less deformable and therefore more susceptible to splenic RBC clearance. In this thesis, we identified several clinically used anti-malarial drugs that are capable of altering RBC deformability and ultimately modifying RBC retention in spleen. We also employed a rodent malarial model, confirming the important connection of RBC deformability with splenic RBC retention and consequently malarial anemia in vivo. Blood storage lesion is another important application of our work. Taking the advantage of device high-throughput, we profiled hundreds of single RBC deformability from a large population and identified subpopulations that are less deformable. These subpopulations also exhibited higher osmotic fragility and were therefore predicted to pose higher transfusion risk according clinical standard. Furthermore, a deformability based sorting device was also developed to filter the less deformable blood subpopulations, improving overall blood quality.
by Sha Huang.
Ph. D.
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Liesner, Raina Joan. "The control of thrombin generation in haemoglobinopathies and other haemolytic red cell disorders in children." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417831.

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Daar, Shahina Firdos. "Haemoglobinopathies in the Sultanate of Oman : a study of clinically significant beta globin gene mutations." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340440.

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Wang, Qin. "Short Term Trend Analysis of Hospital Admissions Due to Red Blood Cell Disorders: Big Data Perspective." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428070351.

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Lee, Sherman. "The effect of acute cigarette smoke exposure on regional pulmonary blood flow, volume, red cell transit and polymorphonuclear leukocyte retention in the rabbit lung." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24840.

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Regional pulmonary blood flow and volume was measured in ten rabbits anesthetized with pentobarbital (30 mg/kg). Tracheostomy was performed and catheters were placed into the jugular vein and carotid artery. The cardiac ⁹⁹mtc output was measured using the indicator-dilution technique using Tc labelled RBC followed by an injection of radiolabelled macroaggregates (MAA) to mark regional blood flow. Measurements were made both before and after either exposure to cigarette smoke (3 cigarettes for ten minutes at 4 puffs/minute) or sham exposure to air. The animals were sacrificed and the lungs were removed with the vessels tied. The lungs were then inflated and rapidly frozen over liquid nitrogen. The lungs were sampled into slices by vertical height, each slice was further sampled and then gamma counted for the injected isotopes. Regional pulmonary blood flow was calculated by setting the total lung MAA counts for each MAA equal to the cardiac output so that the sample flow was calculated as the fraction of sample counts to total counts times the cardiac output. The blood volume was marked by the labelled RBC and RBC transit was calculated as blood volume (ml) divided by blood flow (ml/sec). In a second series of experiments (N=10) , ⁵¹Cr PMN were injected as a bolus along with ⁹⁹mtc RBC in an indicator-dilution run. Following the injection of the cells, the blood flow was marked with MAAs and then the same sham or smoke treatments were given as in the previous experiments. At the end of ten minutes, the animals were sacrificed and the lungs were processed the same as before. Regional PMN retention was calculated as the [formula omitted]. The data show that smoke exposure increased pulmonary blood volume (p<.01), pulmonary transit time (pMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Meng, Shu. "HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/234268.

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Pharmacology
Ph.D.
Background: Hyperhomocysteinemia (HHcy) is an established risk factor for thrombotic diseases yet the underlying mechanism remain unclear. In this study we investigated the effect of HHcy on endothelial cell-platelet interaction and its role in thrombosis. Methods and Results: We used a novel mouse model of HHcy (plasma homocysteine, Hcy 80 micromolar) in which a Zn2+ inducible human cystathionine beta-synthase (CBS) transgene was introduced to circumvent the neonatal lethality of the Cbs gene deficiency (Tg-hCBS Cbs-/- mice). Hcy-lowering therapy was performed by giving ZnSO4 water to induce human CBS transgene expression in adult mice. Thrombus formation was examined by photo dye-induced cremaster microvasculature thrombosis using intravital microscopy, in which endothelium was preserved, and by FeCl3-induced carotid artery thrombosis, which denudated the endothelium. HHcy accelerated cremaster arteriolar thrombosis and decreased blood flow cessation time from 41.8 min in control mice to 30.5 min in TghCBS Cbs-/- mice. Venular blood flow cessation time was slightly decreased from 5.6 to 5.0 min. Hcy-lowering therapy reduced Hcy level from 80 micromolar to 6.8 micromolar after 2 weeks of ZnSO4 water and prolonged arteriolar blood cessation time from 30.5 to 37.8 min. Interestingly, FeCl3-induced carotid artery thrombosis did not change the occlusion time. Hcy did not potentiate the aggregation and secretion function in washed human platelets from healthy donor treated with Hcy (50, 100 micromolar) or from Tg-hCBS Cbs-/- mice. However, inter-cellular adhesion molecule 1 (ICAM-1) levels, but not vascular adhesion molecule 1 (VCAM-1), were increased in cremaster tissues from Tg-hCBS Cbs-/- mice by western blot. In cultured human umbilical vein ECs (HUVEC), Hcy (100 micromolar, 24h) promoted human platelet adhesion by 200% in static adhesion assay. Using western blot, FACS and RT-PCR, we found that Hcy increased protein and mRNA levels of ICAM-1, but not that of VCAM-1, in HUVEC. ICAM-1 blocking antibody partially reversed Hcy increased platelets adhesion to HUVEC. Hcy induced ICAM-1 expression and reduced DNA methylation on ICAM-1 promoter, which were mimicked by DNA methyltransferase inhibitor azacytidine, and histone deacetylase inhibitors sodium butyrate and trichostatin A. Hcy treatment also increased intracellular Hcy, Sadenosylhomocysteine (SAH) accumulation and decreased SAM/SAH ratio in HUVECs. Hcy decreased methyl CpG binding protein 2 (MeCP2) binding and increased acetylated histone H3 (AcH3) binding to ICAM-1 core promoter region using chromatin immunoprecipitation. Pyrosequencing of ICAM-1 core promoter and adjacent region shows a decreased DNA methylation by Hcy treatment. In high methionine diet-induce HHcy in WT and Icam-/- mice, Icam-/- mice fed with HM diet only show moderately accelerated venular and barely accelerated arteriolar occlusion time compared with WT mice with CT diet using photo dye-induced thrombosis model. Conclusion: HHcy accelerates arteriolar thrombosis and increases EC-platelet interaction via ICAM-1 induction partially through DNA hypomethylation.
Temple University--Theses
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Kietrys, David. "The Effects of High Repetition Low Force Motion on Tendon Integrity and Motor Behavior in an Animal Model of Work-related Musculoskeletal Disorders." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/73145.

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Physical Therapy
Ph.D.
The National Occupational Research Agenda stresses the importance of identifying work-related musculoskeletal disorder (WMSD) risk factors, understanding their exposure dependent nature, and identifying strategies to reduce their incidence and severity. We first examined behavioral changes after exposure to a low repetition low force (LRLF) reaching task for 12 weeks in young rats. We observed increased movement reversals in LRLF - week 8, indicative of a decline in fine motor control, and a small decrease in voluntary task participation in LRLF - week 12, compared to controls. This decline was associated temporally with a low-grade increase of macrophages in peripheral nerve and distal forelimb bones that correlated with nociceptive neurochemical increases in the spinal cord. We next examined motor behavior changes in young rats exposed to either a food retrieval high repetition negligible force (HRNF) task or a lever pulling high repetition low force (HRLF) reaching task. We found that both tasks led to motor declines, with more marked declines in fine motor control in the HRNF group. Thus, repetition, rather than the difference in force magnitude between the 2 tasks, appears to be the key factor in the induction of motor declines associated with repetitive motion injuries (RMIs). Also, these findings indicate that activities involving negligible force do not necessarily pose a lower risk than activities involving low force. Factors such as fine motor coordination requirements may even pose greater risks. Also, compared to the LRLF task, the high repetition tasks resulted in more motor performance declines, thus confirming exposure-dependency in the context of RMI. We also explored the effects of HRNF and HRLF tasks on supraspinatus tendon of young adult rats in 6 and 12 weeks. We found a small but non-significant elevation of ED1+ macrophages in 6 weeks. The supraspinatus tendon does not appear to develop as many pathological changes as forelimb flexor tendons (Barbe, et al., 2003) with task performance. Lastly, we examined the effects of performing HRLF tasks in aged rats. We found that aged rats demonstrate both declines in motor performance and pathological tissue changes over the course of 12 weeks of exposure to the HRLF lever pulling task. The observed declines in grip strength in aged trained control and HRLF rats over time suggest that both age and cumulative exposure to the repetitive task are factors in the development of WMSDs. Our findings suggest that additional study of exposure-dependency and risk factors is warranted. Deeper understanding of the relative contributions of various risk factors can help inform prophylactic programs and/or interventions for individuals who are at risk for, or suffer from, WMSDs.
Temple University--Theses
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Costessi, Luisa. "Analysis of the β-adducin gene: new insights into gene structure and function." Doctoral thesis, Scuola Normale Superiore, 2008. http://hdl.handle.net/11384/85941.

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Adducins are a family of membrane skeleton proteins encoded by three related genes (ADD1, ADD2 and ADD3 or a-, b- and g-adducin genes). Both ADD1 and ADD3 are ubiquitously expressed, while the b-adducin gene shows a pattern of expression restricted to brain and haematopoietic tissues. Adducin is found as either a heterodimer or heterotetramer of a/b or a/g subunit composition in most tissues. Human erythrocytes mainly contain a/b heterodimers, whereas the g-subunit is also found at low levels in mouse red blood cells (RBCs). [...]
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Books on the topic "Red cells disorder"

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L, Nagel R., ed. Genetically abnormal red cells. Boca Raton, Fla: CRC Press, 1988.

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A, Tanner M. J., and Anstee D. J, eds. Red cell membrane disorders. London: Baillière Tindall, 1999.

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A, Zanella, ed. Inherited disorders of red cell metabolism. London: Baillière Tindall, 2000.

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R, Bridges Kenneth, and Pearson Howard A, eds. Anemias and other red cell disorders. New York: McGraw-Hill, 2007.

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Alberto, Zanella, ed. Inherited disorders of red cell metabolism. London: Baillière Tindall, 2000.

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Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.

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1915-, Finch Clement A., ed. Red cell manual. 7th ed. Philadelphia: F.A. Davis, 1996.

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1915-, Finch Clement A., ed. Red cell manual. 5th ed. Philadelphia: F.A. Davis, 1985.

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Hillman, Robert S. Red cell manual. 6th ed. Philadelphia: F.A. Davis, 1992.

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Tsuyoshi, Ohnishi S., and Ohnishi Tomoko, eds. Membrane abnormalities in sickle cell disease and in other red blood cell disorders. Boca Raton, Fla: CRC Press, 1994.

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Book chapters on the topic "Red cells disorder"

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Shamsi, Tahir S. "Red Cell Disorders." In Hemostasis and Thrombosis in Obstetrics & Gynecology, 12–27. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444328332.ch2.

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Morrison, John C. "Red Blood Cell Disorders." In Principles of Medical Therapy in Pregnancy, 1177. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2415-7_177.

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Mallouh, Ahmad A. "Red Blood Cell Membrane Disorders." In Textbook of Clinical Pediatrics, 2985–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_322.

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Zanella, Alberto, and Edward C. Gordon-Smith. "Disorders of Red Cell Metabolism." In Postgraduate Haematology, 140–57. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323160.ch9.

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Tang, Amy. "Red Blood Cell Membrane Defects." In Benign Hematologic Disorders in Children, 105–12. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49980-8_8.

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Bianchi, Paola, and Narla Mohandas. "Hereditary Disorders of the Red Cell Membrane and Disorders of Red Cell Metabolism." In Postgraduate Haematology, 114–37. Oxford, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118853771.ch8.

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Ford, Jason C. "Approach to Disorders of Red Blood Cells." In Non-Neoplastic Hematopathology and Infections, 45–64. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118158562.ch3.

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Delaunay, Jean. "Disorders of the Red Cell Membrane." In Principles of Molecular Medicine, 191–95. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_21.

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Patrinos, George P., and Frank G. Grosveld. "Transgenic Models of Red Cell Disorders." In Red Cell Membrane Transport in Health and Disease, 643–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8_28.

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Arese, Paolo, and Evelin Schwarzer. "Metabolic Disorders." In Red Cell Membrane Transport in Health and Disease, 525–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8_22.

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Conference papers on the topic "Red cells disorder"

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Erjavec, Vladimira, and Alenka Nemec Svete. "Brachycephalic Dogs with Brachycephalic Obstructive Airway Syndrome Have Increased Variability in Red Blood Cell Size." In Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d8.

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Brachycephalic obstructive airway syndrome (BOAS) is a conformation-related respiratory disorder of dog breeds with congenitally flattened facial and skull anatomy. BOAS is characterized by chronic shortness of breath and subsequent difficulty in exercising, a tendency to overheat, increased and abnormal respiratory noise, and low oxygen levels. The aim of our retrospective study was to inves-tigate the level of red blood cell distribution width (RDW), a biomarker of chronic hypoxemia, in groups of BOAS patients with different degrees of BOAS and a group of healthy non-brachycephalic dogs. Red blood cell distribution width provides information on the variability in the red blood cell volume. It is a simple and inexpensive variable included in the complete blood count report. Seventy-two BOAS patients and 24 non-brachycephalic dogs were included in this retrospective study. Pa-tients with BOAS were classified into grade 1 (13 dogs), grade 2 (27 dogs), and grade 3 (32 dogs) according to the severity of the disease. In our study, a significantly (p < 0.05) higher RDW was found in all groups of BOAS patients compared to the non-brachycephalic dog group. However, we found no significant difference in RDW between the groups of BOAS patients. Thus, we may conclude that BOAS patients have increased variability in the size of red blood cells compared with healthy non-brachycephalic dogs. Our results warrant further studies to determine the potential utility of RDW in BOAS and to clarify the role of RDW in BOAS patients in relation to the severity of BOAS and cardiovascular risk. Keywords: Brachycephaly; Brachycephalic obstructive airway syndrome; Dogs; Haematology; Erythrocytes; Red blood cell distribution width
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Acharya, Vasundhara, and Preetham Kumar. "Identification and red blood cell classification using computer aided system to diagnose blood disorders." In 2017 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2017. http://dx.doi.org/10.1109/icacci.2017.8126155.

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kariyone, S., H. kambayashi, T. satoh, T. uchida, H. ohto, and H. maeda. "A NEW MONOCLONAL ANTIBODY TO PLATELET MEMBRANE GLYCOPROTEINIV: EXPRESSION OF GLYCOPROTEIN IV ON PLATELETS, MEGAKRYOCYTES AND ERYTHROBLASTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643531.

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A New monoclonal antibody, designated as TP85, was produced by fusion of the X63.Ag8.653 murine myeloma cell line with splenocytes from BALB/C mice immunized with washed human platelets. TP85 monoclonal antibody precipitated a single petide of 97,000 daltons in both reduced and nonreduced states by immune precipitation of 125I-labelled solubilized membrane. An isoelectric point was around pH 5.0. The antibody was IgG2b in isotype, as determined by the Ouchterlony immunodiffusion method.The reactivity of TP85 was examined by using indirect immuno-fluorescent assays and ABC immunoperoxidase method. TP85 reacted with platelets, megakaryocytes and erythroblasts from normal human and patients with myeloproliferative disorders, but not with lymphocytes, granulocytes and other bone marrow cells. In a panel of cultured cell line, only 5-10% cells of K652 myeloid/ erythroid cell line were positive, but other cell lines, including common ALL(Reh), T lymphoid(Molt-3, CCRF-CEM), B lymphoid(Raji ,Daudi), myeloid(KG-l, HL-60) and monoblastoid(U937, THP-l) cell lines, were all negative.TP85 did not inhibit platelet aggregations induced by ADP, collagen, epinephrine and ristocetin while TP80 which was an antibody for GPIIb/IIIa inhibited these aggregations except induced by ristocetin.It is concluded that glycoprotein IV, which is immunoprecipitated by TP85, may exist not only on platelet membrane, but also on megakaryocytes and erythroblasts, and has no role on platelet aggregation.
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Yamaguchi, T., H. Kondo, Y. Imai, and T. Ishikawa. "Microvascular disorders induced by malaria infected red blood cells: a computational mechanical study using the biological particle method." In BIOMED 2009. Southampton, UK: WIT Press, 2009. http://dx.doi.org/10.2495/bio090051.

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Lima, Rui, Takuji Ishikawa, Motohiro Takeda, Shuji Tanaka, Yo-suke Imai, Ken-ichi Tsubota, Shigeo Wada, and Takami Yamaguchi. "Measurement of Erythrocyte Motions in Microchannels by Using a Confocal Micro-PTV System." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175969.

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Detailed knowledge on the motion of individual red blood cells (RBCs) flowing in microchannels is essential to provide a better understanding on the blood rheological properties and disorders in microvessels. Several studies on both individual and concentrated RBCs have already been performed in the past [1, 2]. However, all studies used conventional microscopes and also ghost cells to obtain visible trace RBCs through the microchannel. Recently, considerable progress in the development of confocal microscopy and consequent advantages of this microscope over the conventional microscopes have led to a new technique known as confocal micro-PIV [3, 4]. This technique combines the conventional PIV system with a spinning disk confocal microscope (SDCM). Due to its outstanding spatial filtering technique together with the multiple point light illumination system, this kind of microscope has the ability to obtain in-focus images with optical thickness less than 1 μm, a task extremely difficult to be achieved by using a conventional microscope.
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Bellan, M., M. Sguazzotti, C. Piccinino, A. Giubertoni, J. Zanaboni, A. Dimagli, M. Gravellona, P. Marino, M. Pirisi, and P. P. Sainaghi. "AB0785 Red cell distribution width is a promising marker of pulmonary arterial hypertension in scleroderma-related disorders." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5756.

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Grabowski, F. E. "RHEOLOGY AND PRIMARY HEMOSTASIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643986.

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Overview The adhesion-aggregation of platelets to a site of vessel wall injury is a quintessential blood flow phenomenon. Firstly, platelets are driven to the vicinity of the vessel wall by a form of convective diffusion in which red cells both mechanically augment the effective platelet diffusivity (Turitto et al., Ind. Eng. Chem. Fund. 11:216-223, 1972; Grabowski et al., Ind. Eng. Chem. Fund. 11:224-232, 1972) and enhance the near-wall piatelet concentration (Ti11es and Eckstein, Microvasc Res., In press, 1987). Secondly, red cells subjected to physiologic shear forces are capable of secreting sufficient adenine nucleotides to induce primary platelet aggregation without themselves undergoing frank lysis (Reimers et al, Blood 64:1200-1206, 1984). This "humoral" effect of erythrocytes is likely to contribute to primary hemostasis in a shear stress-dependent manner. Thirdly, endothelial cells are able to modulate platelet aggregation at a site of vessel injury by producing prostacyclin (and perhaps other antithrombotic substances) in a manner which increases with vessel shear rate (Grabowski et al, Blood 62:301a, 1983); production for a large range of arterial shear rates appears to be limited by plasma-borne substrate (arachidonate). This manner of production ensures a concentration of prostacyclin in the near-wall region which remains relatively independent of shear rate.Imaging primary hemostasis. In our work, epi-fluorescence videomicroscopy has allowed real time imaging of platelet adhesion-aggregation to a simulated vessel wall injury. The injury model is an endothelial cell monolayer (ECM) across which, prior to ECM exposure to flowing blood, a 6-0 sterile suture is drawn in a direction transverse to flow. Microinjuries result which measure 70 ± 15μm (Mean ± SD) in width. The fluorescent label is the TAB murine monoclonal antibody (courtesy of Dr. R.P. McEver) directed against human platelet GPIIB, together with a fluorescein-conjugated goat F(ab')2 against murine inmunoglobulin. The injured ECM's, grown to confluence on rectangular cover glasses precoated with microfibrillar collagen, comprise one wall of a flow chamber mounted on a vertical microscope stage. On microinjury sites and at shear rates of 100 to 700 sec-1, computer-enhanced video images show adherence, remodelling and growth of chains of platelet aggregates. Aligned with the flow direction, these chains have a spacing of approximately 30)im, a length similar to the average endothelial cell diameter. One may speculate that such chains provide a scaffold for wound healing insofar as they are likely rich in agents chemotactic for leukocytes and in platelet-derived growth factor.Modulatory role of endothelium. When the ECM's are pre treated with 1.0 mM FC lysine acetyl sal icy late (LA), aggregate length increases (P<0.001) up totwo-fold, outflow levels by RIA of serum thromboxane B2 increase (8 of 8 paired runs), and outflow levels of prostacyclin by RIA for 6-Keto PGFiot decrease (5 of 7 paired runs). The Table gives data for one of four similar experiments at 270 sec-1 and following five minutes of flow. These data imply that products of ECM which are inhibitable by aspirin modulate local adhesion-aggregation; their inhibition, as by vasculitis or drugs, may give rise to thrombotic states.Bleeding disorders. Aggregate length is reduced in von Willebrand's disease (4 patients), Hermansky-Pudlak syndrome (2 patients), and after 300 mg oral aspirin (Tablet 4 donors). The reduction in the first two, however, is greater (P<0.01) than that for oral aspirin. With oral aspirin, further, there is a paradoxic increase in the percent platelet coverage of the injury area. Summary. Rheology has profound effects on the rate, structure, and modulation of primary hemostasis. Many of these effects can be studied via real-time, epi-fluorescence videomicroscopy of platelet adhesion-aggregation to a site of injury to an endothelial cell monolayer exposed to flowing blood. The model described has application to the study of thrombotic and hemostatic disorders and unstable angina.
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Crawford, N., M. Crook, J. Dawes, and C. R. W. Gray. "THE SOLE USE OF MAGNESIUM CHLORIDE FOR BLOOD ANTICOAGULATION: PRESERVATION OF PLATELET SURFACE-BOUND “PROTEINACEOUS HALO”!" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643708.

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European Patent No. 83901336 [C.R.W. GRAY & N. CRAWFORD] refers to the use of bivalent cations for blood anticoagulationand the preparation of plasma and cellular products. Both CaCl2 and MgCl2 are effective as sole anticoagulants although the concentration of Ca+2 to maintain blood fluid for >7 days exceeds the osmolarity limits for good preservation of cellular integrity. With MgCl2 ,however, [at final concentrations 25-30 mM and suitable blood/MgCl2 volume ratios] red cells show good preservation, granulocytes phagocytose well and platelets are discoid and respond to all conventional agonists [although higher than normal doses are required]. The concentrations of 6 thromboglobulin (βTG) in “MgCl2-plasma” aresubstantially lower than with Cacomplexing anticoagulants containing theophylline and PGE . Thrombospondin [TSP]another major granule protein, unlike 6TG, binds after release to the activated platelet surface in the presence of physiological [Ca+2+]1 RIA assays of TSP has revealed that “Mg platelets” have 3 times more surface bound TSP than “CPD-platelets”. Subpopulation profiling by continuousflow electrophoresis shows that formol-fixed platelets from Mg2 anticoagulated blood are substantial>ly less electronegative than "CPD platelets" similarly processed. We believe that plateletsfrom blood in which the extracellular[Ca2+] is undisturbed carrya surface-associatd “halo”ofnonspecific [electrostatically-associated] and Ca2+-linked adsorbed proteins. Released TSP is an example of the latter association. Since plasma 0TG levels are influenced by kidney clearancekinetics and other factors, the measurement of surface bound TSP on platelets from MgCl2-anticoagulatedbloodmay have clinical value as an indexof invivo release events and particularly in vascular disorders accompanied by renal damage where the findings with 0TGhave been equivocal(2)
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Pereira, Isabel Cristina Areia Lopes, Gabriela Emery Cavalcanti Santos, Isabella de Andrade Figueirêdo, Lívia Silas de Melo, and Ana Clara Araujo Miranda. "ROSAI-DORFMAN DISEASE OF THE BREAST: A CASE REPORT." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1073.

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Rosai-Dorfman disease (RDD) is a rare histiocytic disorder that was first described by Destombes in 1965 and subsequently classified by Rosai and Dorfman in 1969 as a distinct clinical and pathological condition. It is a self-limiting disease process characterized by a non-Langerhans cell benign proliferation that usually involves the lymph nodes, but can affect extranodal sites. Classic RDD most commonly presents as massive bilateral painless cervical lymphadenopathy, with associated fever and loss of weight in children and young adults. Despite the predilection for the head and neck lymph nodes, RDD may present extranodal case in 43% of cases and in rare instances (around 23% of extranodal cases) only extranodal involvement can be described. The more common extranodal sites include the skin, nasal cavity, bone, orbital tissue, and the central nervous system. RDD involving the breast tissue is extremely rare, with fewer than 50 reported cases and it is important to recognize because it can mimic malignancy. Patients with involvement of the breast can present with painless palpable mass and ill-defined sensation or abnormal mammogram. The radiologic presentation of RDD lesions can have a notable diversity, but commonly have an appearance that is indistinguishable from breast carcinoma on mammogram and US. Therefore, the main diagnostic modality is histopathologic evaluation, with the features of marked dilatation of sinuses due to accumulation of activated histiocytes that demonstrate variable degrees of emperipolesis, along with the immunohistochemical characteristics like S100+, CD68+, and CD1a−. Management of RDD depends on the symptoms and it can be conservative with observation, as long as some cases have spontaneous regression, especially in the classic nodal disease. Surgical excision may be indicated in unifocal extranodal disease, especially for symptomatic cases. A 14-year-old female adolescent visited a breast surgeon with a self-detected painless palpable mass in the left breast for 3 months, without systemic symptoms or significant family history. On examination, there was a firm 3.5-cm mass in the upper inner quadrant of the left breast. The mammogram revealed a focal distortion on axillary tail in the left breast, designated as BIRADS 4. US demonstrated two masses in the left breast, including a 3.4×2.6×1.5 cm hypoechoic, irregular mass at 11:00 and a 1×0.9×0.7 cm hypoechoic, irregular mass at 11:00, both near the infraclavicular region, accompanied by a 2.8×1 cm atypical lymph node in the left axillary region, designated BIRADS 4C. US-guided core biopsies of both masses were obtained, which showed a nonspecific chronic inflammatory process. A new core biopsy was performed but once more with nonspecific histopathological findings, as well as negative results from culture examinations. Following these indeterminate findings, the patient underwent excisional biopsy, which histopathologic conclusion finally elucidated the extranodal RDD diagnosis.
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