Leg Ulcer in a Patient with Beta-Thalassemia and Glucose-6-Phosphate-Dehydrogenase Deficiency

1990 ◽  
Vol 29 (6) ◽  
pp. 426-427 ◽  
Author(s):  
T. Lotti ◽  
M. Benci ◽  
G. M. Palleschi ◽  
F. Cantini ◽  
R. Palchetti ◽  
...  
2018 ◽  
Vol 11 (1) ◽  
pp. 165-167
Author(s):  
Usman Ahmad

This paper was aimed at expatiating the relevance to which falciparum malaria are protected due to various genetically modified factors which include Hemoglobin S, Hemoglobin E, Hemoglobin C, Hemoglobin F, Alpha and beta thalassemia, ovalocytosis, Glucose – 6- Phosphate dehydrogenase deficiency, Human leucocyte antigen (HLA) – BW53, DRBI 1302, DQBI 0501, Pyruvate kinase or PKLR gene. However, human genetics is one of the elements can be used in planning of co- ordinated attack on disease, since it sometime give an avenue to differentiate those groups or individual who are susceptible from those who are not.Keywords: malaria, hemoglobin, genetically modified factors


Author(s):  
Briantais Antoine ◽  
Froidefond Margaux ◽  
Seguier Julie ◽  
Swiader Laure ◽  
Durand Jean Marc

1999 ◽  
Vol 55 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Yousef M Abdulrazzaq ◽  
Rosette Micallef ◽  
M Mansoor Qureshi ◽  
Adekunle Dawodu ◽  
Ibrahim Ahmed ◽  
...  

2007 ◽  
Vol 49 (4) ◽  
pp. 463-467
Author(s):  
CHUN DENG ◽  
CHUN-BAO GUO ◽  
YOU-HUA XU ◽  
BING DENG ◽  
JIA-LIN YU

1977 ◽  
Vol 145 (4) ◽  
pp. 983-998 ◽  
Author(s):  
S J Klebanoff

Estradiol binds covalently to normal leukocytes during phagocytosis. The binding involves three cell types, neutrophils, eosinophils, and monocytes and at least two reaction mechanisms, one involving the peroxidase of neutrophils and monocytes (myeloperoxidase [MPO]) and possibly the eosinophil peroxidase, and the second involving catalase. Binding is markedly reduced when leukocytes from patients with chronic granulomatous disease (CGD), severe leukocytic glucose 6-phosphate dehydrogenase deficiency, and familial lipochrome histiocytosis are employed and two populations of neutrophils, one which binds estradiol and one which does not, can be demonstrated in the blood of a CGD carrier. Leukocytes from patients with hereditary MPO deficiency also bind estradiol poorly although the defect is not as severe as in CGD. These findings are discussed in relation to the inactivation of estrogens during infection and the possible role of estrogens in neutrophil function.


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