Plasma and Red Cell Lithium in Affective Disorders

1983 ◽  
Vol 143 (3) ◽  
pp. 311-312 ◽  
Author(s):  
Enrique Alvarez Martinez ◽  
Claudio Udina Ubello ◽  
José Ma Queralto Compano ◽  
Miguel Casas Brugue
Keyword(s):  
1978 ◽  
Vol 41 (3) ◽  
pp. 355-357 ◽  
Author(s):  
G. Beckman ◽  
L. Beckman ◽  
C. Perris ◽  
E. Strandman

1986 ◽  
Vol 10 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Robert J. Hitzemann ◽  
Jack Hirschowitz ◽  
David L. Garver

1977 ◽  
Vol 36 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Alan Rundle ◽  
Barbara Sudell ◽  
Keith Wood ◽  
Alec Coppen

1985 ◽  
Vol 20 (4) ◽  
pp. 451-454 ◽  
Author(s):  
Rita Shaughnessy ◽  
Stuart C. Greene ◽  
Ghanshyam N. Pandey ◽  
Elizabeth Dorus

1978 ◽  
Vol 28 (1) ◽  
pp. 41-47 ◽  
Author(s):  
G. Beckman ◽  
L. Beckman ◽  
B. Cedergren ◽  
C. Perris ◽  
E. Strandman

Author(s):  
Christopher A. Miller ◽  
Bridget Carragher ◽  
William A. McDade ◽  
Robert Josephs

Highly ordered bundles of deoxyhemoglobin S (HbS) fibers, termed fascicles, are intermediates in the high pH crystallization pathway of HbS. These fibers consist of 7 Wishner-Love double strands in a helical configuration. Since each double strand has a polarity, the odd number of double strands in the fiber imparts a net polarity to the structure. HbS crystals have a unit cell containing two double strands, one of each polarity, resulting in a net polarity of zero. Therefore a rearrangement of the double strands must occur to form a non-polar crystal from the polar fibers. To determine the role of fascicles as an intermediate in the crystallization pathway it is important to understand the relative orientation of fibers within fascicles. Furthermore, an understanding of fascicle structure may have implications for the design of potential sickling inhibitors, since it is bundles of fibers which cause the red cell distortion responsible for the vaso-occlusive complications characteristic of sickle cell anemia.


Author(s):  
O. T. Minick ◽  
E. Orfei ◽  
F. Volini ◽  
G. Kent

Hemolytic anemias were produced in rats by administering phenylhydrazine or anti-erythrocytic (rooster) serum, the latter having agglutinin and hemolysin titers exceeding 1:1000.Following administration of phenylhydrazine, the erythrocytes undergo oxidative damage and are removed from the circulation by the cells of the reticulo-endothelial system, predominantly by the spleen. With increasing dosage or if animals are splenectomized, the Kupffer cells become an important site of sequestration and are greatly hypertrophied. Whole red cells are the most common type engulfed; they are broken down in digestive vacuoles, as shown by the presence of acid phosphatase activity (Fig. 1). Heinz body material and membranes persist longer than native hemoglobin. With larger doses of phenylhydrazine, erythrocytes undergo intravascular fragmentation, and the particles phagocytized are now mainly red cell fragments of varying sizes (Fig. 2).


2000 ◽  
Vol 111 (4) ◽  
pp. 1010-1022 ◽  
Author(s):  
Paul Fisch ◽  
Rupert Handgretinger ◽  
Hans-Eckart Schaefer

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