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1

Walski, Tomasz, Ludmiła Chludzińska, Małgorzata Komorowska, and Wojciech Witkiewicz. "Individual Osmotic Fragility Distribution: A New Parameter for Determination of the Osmotic Properties of Human Red Blood Cells." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/162102.

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The aim of our experiments was to characterise and to validate the osmotic fragility test when applied to human blood samples with no significant alterations of osmotic fragility but with a differentiating shape of the haemolysis curve. All experiments were carried out on human erythrocytes taken from the Regional Centre of Blood Donation and Blood Therapy in Wrocław. The washed erythrocytes were exposed to near-infrared radiation (NIR) or ozonated, and the osmotic fragility test was applied. The osmotic fragility, calculated from the experimental haemolysis curve for the control and cells irradiated for 15 min, is the same within the empirical error. Calculation of the first derivative of the haemolysis curve allowed us to visualise the changes in osmotic fragility distribution after exposure to NIR. By contrast, significant changes both to the osmotic fragility value and the distribution of osmotic properties were observed after an erythrocytes ozonation procedure. Description of cell osmotic properties requires at least two parameters—the value of osmotic fragility and the slope of the haemolysis curve in the region where absorbance sharply increases due to cell haemolysis.
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2

Garganeeva, A. A., V. A. Aleksandrenko, E. A. Kuzheleva, V. V. Ryabov, T. Yu Rebrova, and S. A. Afanasiev. "Association between the osmotic fragility of erythrocytes and the course of acute myocardial infarction." Complex Issues of Cardiovascular Diseases 10, no. 3 (September 25, 2021): 6–14. http://dx.doi.org/10.17802/2306-1278-2021-10-3-6-14.

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Aim. To investigate the relationship between the osmotic fragility of erythrocytes and the course of acute myocardial infarction (MI).Methods. An analysis of the osmotic fragility of erythrocytes was conducted using beta-blocker-based osmotic fragility test in sixty-two patients within the first 6 hours after onset of MI symptoms.Results. The results revealed that the patients with increased erythrocyte osmotic fragility experienced more complications after acute MI, such as left ventricular failure and cardiac arrhythmias (ventricular extrasystoles and ventricular tachycardia) (p = 0.026). Moreover, these patients exhibited greater myocardial injury - the concentration of biomarkers of myocardial necrosis, such as creatine phosphokinase, creatine phosphokinase MB and Troponin I was increased - p = 0.009, p = 0.032 and p = 0.001, respectively. In addition to that, the patients with high osmotic fragility had a larger number of hypokinetic and akinetic segments, high impaired myocardial contractility index, and low ejection fraction. The impaired myocardial contractility index was significantly higher in patients with increased erythrocyte osmotic fragility (1.5 (1.22; 1.75) vs 1.12 (1.0; 1.56), U = 157.5, p = 0.032).Conclusion. Increased erythrocyte osmotic fragility in patients was associated with greater myocardial injury, manifesting through the higher concentration of biomarkers of myocardial necrosis in blood, as well as higher number of hypokinetic segments.
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3

Tao, Yi-Feng, Zeng-Fu Deng, Lin Liao, Yu-Ling Qiu, Xue-Lian Deng, Wen-Qiang Chen, and Fa-Quan Lin. "Evaluation of a Flow-Cytometric Osmotic Fragility Test for Hereditary Spherocytosis in Chinese Patients." Acta Haematologica 135, no. 2 (October 28, 2015): 88–93. http://dx.doi.org/10.1159/000438738.

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Background: Osmotic fragility testing based on flow cytometry was recently introduced for the screening of hereditary spherocytosis (HS). This study was undertaken to evaluate the clinical diagnostic value of a flow-cytometric osmotic fragility test for HS. Methods: Peripheral blood was collected from 237 subjects at the First Affiliated Hospital of Guangxi Medical University, including 56 HS patients, 86 thalassemia patients and 95 healthy controls. The samples were examined by flow-cytometric osmotic fragility test and the percentage of residual red blood cells was used to determine HS. Peripheral blood smears were performed to examine the red blood cell morphology. Results: With clinical diagnosis of HS as the gold standard and the percentage of residual red blood cells <23.6% as the diagnostic threshold in the flow-cytometric osmotic fragility test, the sensitivity of the flow-cytometric osmotic fragility test for HS was 85.71% and the specificity was 97.24%. Conclusion: The flow-cytometric osmotic fragility test combined with a red blood cell morphology test by peripheral blood smear could be a simple, practical and accurate laboratory screening method for HS.
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4

Zgodzińska, Agata, and Olga Ciepiela. "Osmotic fragility of red blood cells – a review of diagnostic methods." Diagnostyka Laboratoryjna 51, no. 3 (October 11, 2015): 229–34. http://dx.doi.org/10.5604/01.3001.0008.2263.

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Osmotic Fragility Test (OFT) is widely considered as a sensitive indicator of red blood cells sensitivity to the hypotonic solution. Traditional osmotic fragility test (Dacie and Lewis) is time and work-consuming, and need relatively large minimum volume of peripheral blood for proper test performance. It does not belong to the most popular tests in a daily laboratory practice. The purpose of this article is to underline the diagnostic value of the Osmotic Fragility Test as well as present the latest methods that improves the traditional technique, such as Acidified Glycerol Lysis Test (AGLT 50), Pink Test, or Flow Cytometric Osmotic Fragility Test (FCM OF Test). Perhaps a new, fresh view at the issue in the nearest future will contribute to reconsider the osmotic fragility test for routine diagnostic screening of red blood cell disorders in children and adults.
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5

Dobrynina, Larisa A., Alla A. Shabalina, Kamila V. Shamtieva, Elena V. Gnedovskaya, Alexander B. Berdalin, and Marina V. Krotenkova. "The Predictive Value of Salt Sensitivity and Osmotic Fragility in the Development of Cerebral Small Vessel Disease." International Journal of Molecular Sciences 21, no. 6 (March 16, 2020): 2036. http://dx.doi.org/10.3390/ijms21062036.

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Increased salt intake in food probably affects the progression of cerebral small vessel disease (CSVD), which justifies the study of disturbances in sodium homeostasis associated with the development of CSVD. We aimed to clarify the role of salt sensitivity and osmotic fragility in the development of CSVD. Erythrocyte salt sensitivity was measured using the modified salt blood test, and osmotic fragility was measured using the classic osmotic fragility test in 73 patients with CSVD (48 women; 60.1 ± 6.5 years) and 19 healthy volunteers (14 women; 56.9 ± 6.4 years). Salt sensitivity and osmotic fragility exhibited a predictive value in relation to CSVD. These parameters were associated with an increase in white matter hyperintensities (p = 0.019 and 0.004, respectively). Their simultaneous use increased their predictive ability for CSVD (p < 0.000001; AUC (95% CI), 0.824 (0.724–0.923)). The possibility of predicting CSVD using erythrocyte salt sensitivity and osmotic fragility indicates the value of the individual glycocalyx buffer capacity in relation to sodium and the activity of sodium channels in the development of CSVD. Increased salt sensitivity and osmotic fragility seem to be risk factors for CSVD.
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6

Lima-Filho, Guilherme L., Glaydes M. T. Lima, Silvana R. F. Moreno, Luiz C. M. Aleixo, Sebastião D. Santos-Filho, Rosimeire S. Freitas, Vilma G. B. Melo, and Mario Bernardo-Filho. "Physiological (osmotic fragility) and morphological effects on red blood cells: action of phytic acid and stannous fluoride." Canadian Journal of Physiology and Pharmacology 82, no. 12 (December 1, 2004): 1091–95. http://dx.doi.org/10.1139/y04-110.

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Phytic acid occurs in foods derived from plants. We have investigated the possibility that phytic acid and stannous fluoride are capable of altering the physiological properties (osmotic fragility) and morphological properties of red blood cells (RBC). Osmotic fragility was unchanged by the presence of phytic acid and stannous fluoride in the studied concentrations, but RBC morphology was modified in the presence of the studied substances. In conclusion, the alterations to RBC morphology were not sufficient to promote modifications in osmotic fragility. Our results suggest that the chelating properties of phytic acid could be responsible for the observed effects.Key words: phytic acid, stannous fluoride, morphology, osmotic fragility.
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7

Sprandel, U., and N. Zöllner. "Osmotic fragility of drug carrier erythrocytes." Research in Experimental Medicine 185, no. 1 (January 1985): 77–85. http://dx.doi.org/10.1007/bf01851531.

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8

Radisic, Rebecca, Sean D. Owens, Charles A. Manire, Nicole Montgomery, Doug Mader, Bette Zirkelbach, and Nicole I. Stacy. "Red blood cell osmotic fragility in healthy loggerhead and green sea turtles." Journal of Veterinary Diagnostic Investigation 32, no. 6 (September 30, 2020): 908–11. http://dx.doi.org/10.1177/1040638720957117.

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Loggerhead ( Caretta caretta; Cc) and green sea ( Chelonia mydas; Cm) turtles admitted to rehabilitation facilities may require blood transfusions for supportive treatment of disorders resulting in life-threatening anemia, but, considering the unique erythrocyte chemistry of sea turtles, standardized donor red blood cell (RBC) storage protocols have not been established. Prolonged cold storage and the effects of various anticoagulant-preservative solutions have been associated with increased RBC osmotic fragility across a broad range of species. Increased RBC fragility in stored RBC products has been associated with acute transfusion reactions. The osmotic fragility test is used to measure erythrocyte resistance to hemolysis while being exposed to a series of dilutions of a saline solution. We obtained baseline measurements for osmotic fragility in healthy Cc and Cm. Osmotic fragility testing was performed on samples from 10 Cc to 10 Cm. Fifty percent (50%) RBC hemolysis was identified at a mean NaCl concentration of 0.38% in both species. Results of our study will help guide future studies evaluating optimal storage solutions for sea turtle blood products.
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9

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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10

Santoro, Marcelo L., Marcia M. Kogika, Mitika K. Hagiwara, Regina M. S. Mirandola, and Izaura L. C. G. Castelar. "Decreased erytrocyte osmotic fragility during canine leptospirosis." Revista do Instituto de Medicina Tropical de São Paulo 36, no. 1 (February 1994): 1–5. http://dx.doi.org/10.1590/s0036-46651994000100001.

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Erythrocyte osmotic fragility (EOF) was carried out in nineteen dogs naturally infected by Leptospira interrogans serovar icterohaemorrhagiae/copenhagi. A decreased EOF was observed, suggesting a modification of erythrocyte components secondary to disturbances that occur during canine leptospirosis, such as renal damage and hepatic disease.
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11

Massaldi, H. A., G. V. Richieri, and H. C. Mel. "Osmotic fragility model for red cell populations." Biophysical Journal 54, no. 2 (August 1988): 301–8. http://dx.doi.org/10.1016/s0006-3495(88)82960-6.

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12

Heistø, H., and H. C. Godal. "Osmotic Erythrocyte Fragility and ABO Blood Groups." Scandinavian Journal of Haematology 28, no. 5 (April 24, 2009): 456–58. http://dx.doi.org/10.1111/j.1600-0609.1982.tb00552.x.

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13

Norman, N. Kathleen, and Michael J. Dewey. "Genetic control of red cell osmotic fragility." Journal of Heredity 76, no. 1 (January 1985): 31–35. http://dx.doi.org/10.1093/oxfordjournals.jhered.a110013.

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14

Korones, David, and Howard A. Pearson. "Normal erythrocyte osmotic fragility in hereditary spherocytosis." Journal of Pediatrics 114, no. 2 (February 1989): 264–66. http://dx.doi.org/10.1016/s0022-3476(89)80794-2.

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15

SARKAR, M., and DB MONDAL. "Osmotic fragility of erythrocytes in periparturient yaks." Australian Veterinary Journal 77, no. 12 (December 1999): 821. http://dx.doi.org/10.1111/j.1751-0813.1999.tb12957.x.

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16

Won, Dong Il, and Jang Soo Suh. "Flow cytometric detection of erythrocyte osmotic fragility." Cytometry Part B: Clinical Cytometry 76B, no. 2 (March 2009): 135–41. http://dx.doi.org/10.1002/cyto.b.20448.

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17

Řeháková, Kristína, Ivana Uhríková, Leona Raušerová-Lexmaulová, Jana Lorenzová, Ladislav Stehlík, Eva Jánová, Ondřej Škor, and Jaroslav Doubek. "Association of increased erythrocyte osmotic resistance with haematological and histopathological findings in dogs with a congenital extrahepatic portosystemic shunt." Acta Veterinaria Brno 82, no. 4 (2013): 393–98. http://dx.doi.org/10.2754/avb201382040393.

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The aim of the study was to investigate changes in erythrocyte osmotic resistance in relation to haematological and histological changes in dogs with a congenital portosystemic shunt. Osmotic fragility tests with complete blood counts and liver histological examinations were performed in 12 dogs with single extrahepatic portosystemic shunt confirmed by surgical exploration. Laboratory results were compared with those from 30 healthy dogs. Dogs with portosystemic shunt had a significantly increased erythrocyte osmotic resistance (P < 0.01) with 5%, 50% and 90% haemolysis corresponding to 0.45%, 0.35% and 0.30% NaCl solution, respectively. Statistical analyses revealed no correlation between haematological indicators and the osmotic fragility test results. Increased osmotic resistance was significantly associated with hepatic lipogranulomas. Based on these results, dogs with a congenital portosystemic shunt have a significantly increased erythrocyte osmotic resistance suggesting impaired red blood cell deformability. Osmotic resistance test that until now was not studied in canine hepatopathies seems to be independent of routinely performed haematological tests.
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18

Fitrianto, Agus, Moedrik Tamam, and Nyoman Suci Widyastiti. "Vitamin E effect on osmotic fragility in β thalassemia major." Paediatrica Indonesiana 54, no. 5 (October 30, 2014): 280. http://dx.doi.org/10.14238/pi54.5.2014.280-3.

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Background Blood transfusion remains the main therapy for anemia in β thalassemia major patients. However, frequent transfusions can cause oxidative stress in response to iron overload. Vitamin E is considered to be the best lipid-soluble exogenous antioxidant in humans. It can protect phospholipid membrane from peroxidarion. Erythrocyte osmotic fragility is a useful test to assess for the improvement of red blood cells in thalassemia patients after vitamin E supplementation.Objective To investigate the effect of vitamin E for improving erythrocyte osmotic fragility in β thalassemia major and for decreasing the need for frequent transfusions.Methods T his was a double blind placebo controlled randomized clinical trial on children aged 2-14 years with thalassemia major who received frequent blood transfusions. Fifty subjects were divided into 2 groups: group I with vitamin E supplementation and group II with placebo, as a control group, for a period of 1 month. Pre- and post-treatment data on erythrocyte osmotic fragility and hemoglobin level were analyzed with non-paired T-test.Results Improved erythrocyte osmotic fragility was found: in group I, pre-treatment 31.59 (SD 6.342)% to post-treatment 38.08 (SD 7.165)%, compared to the control group pre-treatment 34.40 (SD 6.985)% to post-treatment 29.26 (SD 9.011)% (P=0.0001). Comparison of the mean delta Hb level in group I was 0.94 (SD 0.605) gr% and that of group II was - 0.23 (SD 1.199) gr% (P=0.0001).Conclusion Vitamin E supplementation improves erythrocyte fragility and Hb level in β thalassemia major pediatric patients.
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19

Karabulut, Ismail, Z. Dicle Balkanci, Bilge Pehlivanoglu, Aysen Erdem, and Ersin Fadillioglu. "Effect of toluene on erythrocyte membrane stability under in vivo and in vitro conditions with assessment of oxidant/antioxidant status." Toxicology and Industrial Health 25, no. 8 (September 2009): 545–50. http://dx.doi.org/10.1177/0748233709346758.

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Toluene, an organic solvent used widely in the industry, is highly lipophilic and accumulates in the cell membrane impeding transport through it. Its metabolites cause oxygen radical formation that react with unsaturated fatty acids and proteins in erythrocytes leading to lipid peroxidation and protein breakdown. In this study, we aimed to investigate the membrane stabilizing and the oxidative stress—inducing effects of toluene in human erythrocytes. Measurements of osmotic fragility, mean corpuscular volume (MCV), oxidative stress parameters and antioxidant enzyme activities were performed simultaneously both in individuals exposed to toluene professionally (in vivo) and human erythrocytes treated with toluene (in vitro). To measure osmotic fragility, erythrocytes were placed in NaCl solutions at various concentrations (0.1% [blank], 0.38%, 0.40%, 0.42%, 0.44%, 0.46%, 0.48% and 1% [stock]). Percentage of haemolysis in each solution was calculated with respect to the 100% haemolysis in the blank solution. The erythrocyte packs prepared at the day of the above-mentioned measurements were kept at —80°C until the time for determination of malonyldialdehyde and protein carbonyl levels, and catalase (CAT) and glutathione peroxidase activities as indicators of oxidative stress. Toluene increased oxidative stress parameters significantly both in vivo and in vitro; it also caused a significant decrease in the activities of antioxidant enzymes. Osmotic fragility was altered only in the case of in vitro exposure. In conclusion, toluene exposure resulted in increased lipid peroxidation and protein damage both in vivo and in vitro. Although, it is natural to expect increased osmotic fragility due to oxidative properties of toluene, its membrane-stabilizing effect overcame the oxidative properties leading to decreased osmotic fragility or preventing its deterioration in vitro and in vivo toluene exposures, respectively, in the present study.
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20

Try, K. "Lineation of the Osmotic Fragility Curve of Erythrocytes." Scandinavian Journal of Haematology 24, no. 2 (April 24, 2009): 157–61. http://dx.doi.org/10.1111/j.1600-0609.1980.tb02361.x.

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21

Mushtaq, Mazhar. "Perpetual Smoking Compromise the Osmotic Fragility of RBC." Biomedical Sciences 3, no. 3 (2017): 58. http://dx.doi.org/10.11648/j.bs.20170303.11.

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22

Arora, B., R. S. Punia, P. Lal, and D. R. Arora. "The effect of Pregnancy on Erythrocyte Osmotic Fragility." Journal of Nepal Medical Association 32, no. 112 (January 1, 2003): 227–30. http://dx.doi.org/10.31729/jnma.1264.

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23

Epps, Dennis E., Thomas J. Knechtel, Oksana Baczynskyj, Douglas Decker, David M. Guido, Stephen E. Buxser, W. Rodney Mathews, et al. "Tirilazad mesylate protects stored erythrocytes against osmotic fragility." Chemistry and Physics of Lipids 74, no. 2 (December 1994): 163–74. http://dx.doi.org/10.1016/0009-3084(94)90057-4.

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24

Emembolu, J. O., and E. C. Mba. "Red cell osmotic fragility in pregnant Nigerian women." International Journal of Gynecology & Obstetrics 44, no. 1 (January 1994): 73–74. http://dx.doi.org/10.1016/0020-7292(94)90028-0.

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25

Bhalla, Pankaj, and Deepa Agrawal. "Alterations in rat erythrocyte membrane due to hexachlorocyclohexane (technical) exposure." Human & Experimental Toxicology 17, no. 11 (November 1998): 638–42. http://dx.doi.org/10.1177/096032719801701109.

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1 Hexachlorocyclohexane (HCH), an organochlorine pesticide having hydrophobic molecule is known to act on membranes. HCH mediated alterations in erythrocyte membrane occur through disorganization of the lipid bilayer. Therefore the changes in erythrocyte membrane fluidity, osmotic fragility and certain membrane bound enzymes were studied. Administration of HCH (technical) to rats at 5 mg/kg, orally, 5 days a week for 1, 2 and 3 months caused marked increase in erythrocyte membrane fluidity, osmotic fragility anddecreaseinlevelsofNa+, K+-ATPase, acetylcholinesterase in erythrocytes and glutathione in blood. 2 These changes indicate that HCH adversely affects membrane structure and function.
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26

Schluter, K. D., G. Jakob, M. Ruiz-Meana, D. Garcia-Dorado, and H. M. Piper. "Protection of reoxygenated cardiomyocytes against osmotic fragility by nitric oxide donors." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 2 (August 1, 1996): H428—H434. http://dx.doi.org/10.1152/ajpheart.1996.271.2.h428.

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In ischemic-reperfused myocardium, myocardial cells are jeopardized not only by reoxygenation-induced hypercontracture but also by the development of a transsarcolemmal osmotic gradient. Here the question of whether osmotic fragility of cardiomyocytes can be reduced by interventions during reoxygenation was addressed. Isolated ventricular cardiomyocytes (from adult rats), exposed to 120 min of hypoxia and subsequent reoxygenation, were used as model. With reoxygenation, medium osmolarity was reduced from 270 to 80 mosM. Loss of sarcolemmal integrity was characterized by enzyme loss from cells (creatine kinase and lactate dehydrogenase). Cardiomyocytes reoxygenated after 120 min of hypoxia hypercontracted, but enhanced enzyme loss was observed only at 80 mosM. The nitric oxide (NO) donors 3-morpholinosydnonimine (10 mM), sodium nitroprusside (10 mM), S-nitroso-N-acetyl-DL-penicillamine (100 microM), and the antilipid peroxidant diphenylphenylenediamine (DPPD, 2.5 microM) reduced enzyme loss with hyposmolar reoxygenation. Agents activating guanosine 3',5'-cyclic monophosphate (cGMP)-dependent pathways [atrial natriuretic peptide (1 microM), urodilatin (1 microM), and 8-bromo-cGMP (10 mM)], the contractile inhibitor 2,3-butanedione monoxime (10 mM), and the SIN-1 metabolite SIN-1C (10 mM) did not protect cardiomyocytes against osmotic fragility. The results show that increased osmotic fragility of isolated adult rat cardiomyocytes can be prevented at the time of reoxygenation by NO donors and DPPD in a cGMP-independent way.
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Igbokwe, N. A., U. K. Sanadabe, B. P. Bokko, and I. O. Igbokwe. "Inhibition of osmotic permeabilty of caprine erythrocytes by mercuric chloride in osmotic fragility models." Sokoto Journal of Veterinary Sciences 16, no. 3 (September 28, 2018): 24. http://dx.doi.org/10.4314/sokjvs.v16i3.4.

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TAKAHASHI, Keiko, Hiroshi YAMAUCHI, Yukio YAMAMURA, and Yoshiro KUDOU. "Effect of trimethylarsine on osmotic fragility of erythrocyte membrane." Sangyo Igaku 31, no. 6 (1989): 440–41. http://dx.doi.org/10.1539/joh1959.31.440.

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Woodard, John C., and Hans G. L. Coster. "An Automated Laser Turbidimeter for Measuring Erythrocyte Osmotic Fragility." Laboratory Medicine 19, no. 12 (December 1, 1988): 806–10. http://dx.doi.org/10.1093/labmed/19.12.806.

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30

Mortensen, Esper. "Studies on the Osmotic Fragility of Normal Human Erythrocytes." Acta Medica Scandinavica 174, no. 3 (April 24, 2009): 289–97. http://dx.doi.org/10.1111/j.0954-6820.1963.tb07925.x.

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Mortensen, Esper. "Studies on the Osmotic Fragility of Normal Human Erythrocytes." Acta Medica Scandinavica 174, no. 3 (April 24, 2009): 299–306. http://dx.doi.org/10.1111/j.0954-6820.1963.tb07926.x.

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Mortensen, Esper. "Studies on the Osmotic Fragility of Normal Human Erythrocytes." Acta Medica Scandinavica 173, no. 6 (April 24, 2009): 693–97. http://dx.doi.org/10.1111/j.0954-6820.1963.tb17454.x.

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Mortensen, Esper. "Studies on the Osmotic Fragility of Normal Human Erythrocytes." Acta Medica Scandinavica 175, no. 4 (April 24, 2009): 515–22. http://dx.doi.org/10.1111/j.0954-6820.1964.tb00601.x.

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MORTENSEN, ESPER. "Studies on the Osmotic Fragility of Normal Human Erythrocytes." Acta Medica Scandinavica 175, no. 5 (April 24, 2009): 529–32. http://dx.doi.org/10.1111/j.0954-6820.1964.tb00604.x.

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35

Wu, San-Giang, Fu-Rong Jeng, Shu-Yi Wei, Chin-Zung Su, Tieh-Chi Chung, Wen-Jou Chang, and Hsueh-Wen Chang. "Red Blood Cell Osmotic Fragility in Chronically Hemodialyzed Patients." Nephron 78, no. 1 (December 19, 1997): 28–32. http://dx.doi.org/10.1159/000044878.

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36

Slappendel, R. J. "Abnormal Osmotic Fragility of Erythrocytes in Dogs and Cats." Veterinary Quarterly 20, sup1 (January 1998): S38—S39. http://dx.doi.org/10.1080/01652176.1998.10807399.

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Dariyerli, Nuran, Selmin Toplan, Mehmet Can Akyolcu, Husrev Hatemi, and Gunnur Yigit. "Erythrocyte Osmotic Fragility and Oxidative Stress in Experimental Hypothyroidism." Endocrine 25, no. 1 (2004): 01–06. http://dx.doi.org/10.1385/endo:25:1:01.

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Yamamoto, Ayako, Norihiro Saito, Yumiko Yamauchi, Masahide Takeda, Shigeharu Ueki, Masamichi Itoga, Keiya Kojima, and Hiroyuki Kayaba. "Flow Cytometric Analysis of Red Blood Cell Osmotic Fragility." Journal of Laboratory Automation 19, no. 5 (October 2014): 483–87. http://dx.doi.org/10.1177/2211068214532254.

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39

O'Dell, Boyd L., Jimmy D. Browning, and Philip G. Reeves. "Zinc Deficiency Increases the Osmotic Fragility of Rat Erythrocytes." Journal of Nutrition 117, no. 11 (November 1, 1987): 1883–89. http://dx.doi.org/10.1093/jn/117.11.1883.

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40

Yücel, Rıfat, Semra Özdemir, Nuran Darıyerli, Selmin Toplan, M. Can Akyolcu, and Günnur Yiğit. "Erythrocyte osmotic fragility and lipid peroxidation in experimental hyperthyroidism." Endocrine 36, no. 3 (October 23, 2009): 498–502. http://dx.doi.org/10.1007/s12020-009-9251-6.

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41

Richieri, Gary V., and Howard C. Mel. "Temperature effects on osmotic fragility, and the erythrocyte membrane." Biochimica et Biophysica Acta (BBA) - Biomembranes 813, no. 1 (February 1985): 41–50. http://dx.doi.org/10.1016/0005-2736(85)90343-8.

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42

Mustafa, Ibrahim, Asma Al Marwani, Khuloud Mamdouh Nasr, Noora Abdulla Kano, and Tameem Hadwan. "Time Dependent Assessment of Morphological Changes: Leukodepleted Packed Red Blood Cells Stored in SAGM." BioMed Research International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/4529434.

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Usually packed red blood cells (pRBCs) require specific conditions in storage procedures to ensure the maximum shelf life of up to 42 days in 2–6°C. However, molecular and biochemical consequences can affect the stored blood cells; these changes are collectively labeled as storage lesions. In this study, the effect of prolonged storage was assessed through investigating morphological changes and evaluating oxidative stress. Samples from leukodepleted pRBC in SAGM stored at 4°C for 42 days were withdrawn aseptically on day 0, day 14, day 28, and day 42. Morphological changes were observed using scanning electron microscopy and correlated with osmotic fragility and hematocrit. Oxidative injury was studied through assessing MDA level as a marker for lipid peroxidation. Osmotic fragility test showed that extended storage time caused increase in the osmotic fragility. The hematocrit increased by 6.6% from day 0 to day 42. The last 2 weeks show alteration in the morphology with the appearance of echinocytes and spherocytes. Storage lesions and morphological alterations appeared to affect RBCs during the storage period. Further studies should be performed to develop strategies that will aid in the improvement of stored pRBC quality and efficacy.
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43

Abou-Seif, M. A. M. "Oxidative Stress of Vanadium-Mediated Oxygen Free Radical Generation Stimulated by Aluminium on Human Erythrocytes." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 35, no. 2 (March 1998): 254–60. http://dx.doi.org/10.1177/000456329803500209.

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It has been suggested that aluminium stimulates vanadium-mediated superoxide radical generation. The oxidative stress of generated superoxide radicals on antioxidant enzyme activity, oxidation of NADH and NADPH, membrane lipid peroxidation and osmotic fragility in human red blood cells (RBC) was investigated. RBC were incubated with varying concentrations of vanadium and aluminium ions at 37°C for 2 h. RBC incubated with vanadium ions showed significantly increased superoxide dismutase and catalase activities, and oxidized NADH and NADPH concentrations compared with control RBC preparations. Erythrocyte lipid peroxidation was assessed by measuring thiobarbituric acid reactivity. RBC incubated with elevated levels of vanadium showed significantly increased membrane lipid peroxidation when compared with control RBC; it increased further on addition of aluminium. A significant positive correlation was observed between the extent of vanadium induced membrane lipid peroxidation and the osmotic fragility of treated RBC. In the presence of vanadium, aluminium stimulates superoxide dismutase and catalase activities, NADH and NADPH oxidation and membrane lipid peroxidation, as well as increasing osmotic fragility of human erythrocytes. The stimulatory effect of aluminium was dependent on concentration. These results may have implications for the mechanism of toxicity of aluminium and vanadium in haemodialysis patients.
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44

Igbokwe, NA, NA Ojo, and IO Igbokwe. "Phenotypic drift in osmotic fragility of Sahel goat erythrocytes associated with variability of median fragility." Sokoto Journal of Veterinary Sciences 13, no. 2 (September 8, 2015): 6. http://dx.doi.org/10.4314/sokjvs.v13i2.2.

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45

Akuzawa, M., M. Matumoto, K. Okamoto, F. Nakashima, M. Shinozaki, and M. Morizono. "Hematological, Osmotic, and Scanning Electron Microscopic Study of Erythrocytes of Dogs Given β-acetylphenylhydrazine." Veterinary Pathology 26, no. 1 (January 1989): 70–74. http://dx.doi.org/10.1177/030098588902600111.

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Hematologic examinations, osmotic fragility tests, and scanning electron microscopy of erythrocytes were done on blood of dogs given 5 mg/kg of β-acetylphenylhydrazine for 5 weeks. Reticulocytes, Heinz bodies, and serum total bilirubin values increased in the 1st week. Reticulocyte numbers peaked in the 2nd week, and reticulocytosis persisted through the 5th week. Erythrocyte, packed cell volume, and hemoglobin values decreased markedly and became lowest in the 2nd week. Mean corpuscular volume increased in the 1st week and remained increased for the duration of treatment. Erythrocyte osmotic fragility was increased after 1 week of treatment. Echinocytes were increased with a peak level of 47.6% at week 1 of treatment. Increased numbers of acanthocytes and schizocytes also were detected.
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46

Sultana, Nayma, Noorzahan Begum, Shelina Begum, Sultana Ferdousi, and Taskina Ali. "Effects of Oral Supplementation of Vitamin E on Fragility of RBC in Hemolytic Anemic Patients with G6PD Deficiency." Bangabandhu Sheikh Mujib Medical University Journal 1, no. 1 (November 11, 2009): 6. http://dx.doi.org/10.3329/bsmmuj.v1i1.3688.

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<p><strong>Background: </strong>Vitamin E has role in maintaining the integrity of red cell membrane by preventing oxidation of polyunsaturated fatty acids and thereby protects cells from oxidative stress- induced lysis in G6PD deficiency, which can be reflected by changes in osmotic fragility of RBC and some absolute values like MCV, MCH &amp; MCHC.</p> <p><strong>Objective: </strong>To observe the effects of vitamin E supplementation on fragility of RBC in order to evaluate role of this antioxidant vitamin in reducing chronic hemolysis in G6PD deficient patients.</p> <p><strong>Methods: </strong>For this, a total number of 102 subjects with age ranged from 5 to 40 years of both sexes were included in the study. Among them 68 were G6PD enzyme deficient patients, of whom 34 were in supplemented group (study group) and 34 were in non-supplemented group (control group). The supplemented group received vitamin E supplementation for 60 consecutive days at a dose of 800 IU/day for adult and 400 IU/day for children &lt; 12 years (in a divided dose i,e. 4 times daily). Age and sex matched 34 apparently healthy subjects with normal blood G6PD level were taken to observe the base line data (healthy control) and also for comparison. All the G6PD deficient patients were selected from Out Patient Department (OPD) of Hematology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh during the period of July 2005 to June 2006 and all the healthy subjects were selected from personal contact. Blood G6PD level, osmotic fragility of RBC were measured by standard techniques and MCV, MCH, and MCHC were obtained by calculation. All the parameters were measured on day 1 (one) of their first visit and also were on day 60 in deficient group. Data were compared among the deficient groups, also in supplemented group just before and after supplementation. Analysis of data was done by appropriate statistical method.</p> <p><strong>Results: </strong>Mean starting and completing points of osmotic fragility of RBC were significantly higher but MCV, MCH, MCHC were significantly lower in patients suffering from hemolytic anemia due to G6PD deficiency in comparison to those of the healthy control. After supplementation with vitamin E starting and completing points of osmotic fragility of RBC were significantly decreased whereas, MCV, MCH, MCHC were significantly increased towards those of healthy control in supplemented group of patients in comparison to those of their pre-supplemented (day-1) and non-supplemented groups both on day 1 and day 60.</p> <p><strong>Conclusion: </strong>From this study it may be concluded that, disturbances of some of the hematological parameter like higher osmotic fragility of RBC and lower MCV, MCH, MCHC occur in G6PD deficient hemolytic anemic patients, which returned towards normal after supplementation of vitamin E, which clearly indicates the role of this anti-oxidant vitamin in maintaining red cell membrane integrity and thereby decreases the rate of hemolysis in this group of patients. So, vitamin E can be supplemented along with other drugs for better management of the patients.</p> <p><strong>Key words: </strong>Osmotic fragility, G6PD, hemolytic anemia, vitamin E.</p><p>DOI: 10.3329/bsmmuj.v1i1.3688</p> <p><em>BSMMU J </em>2008; 1(1): 6-10</p>
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47

Igbokwe, N. A. "A review of the factors that influence erythrocyte osmotic fragility." Sokoto Journal of Veterinary Sciences 16, no. 4 (February 5, 2019): 1. http://dx.doi.org/10.4314/sokjvs.v16i4.1.

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48

Maccioni, L., and A. Cao. "Osmotic fragility test in heterozygotes for alpha and beta thalassaemia." Journal of Medical Genetics 22, no. 5 (October 1, 1985): 374–76. http://dx.doi.org/10.1136/jmg.22.5.374.

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49

Godal, H. C., A. T. Elde, N. Nyborg, and F. Brosstad. "The Normal Range of Osmotic Fragility of Red Blood Cells." Scandinavian Journal of Haematology 25, no. 2 (April 24, 2009): 107–12. http://dx.doi.org/10.1111/j.1600-0609.1981.tb01374.x.

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50

Jóźwiak, Z., and D. PaŁecz. "Influence of Heat Treatment on Osmotic Fragility of Carp Erythrocytes." International Journal of Radiation Biology 54, no. 2 (January 1988): 299–303. http://dx.doi.org/10.1080/09553008814551721.

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