Faculty Opinions recommendation of Identifying the source of a humoral factor of remote (pre)conditioning cardioprotection.

Author(s):  
Zeljko Bosnjak
Keyword(s):  
Diabetes ◽  
1961 ◽  
Vol 10 (4) ◽  
pp. 289-297 ◽  
Author(s):  
W. E. Dulin ◽  
J. J. Clark ◽  
G. H. Lund ◽  
H. Albert

1963 ◽  
Vol 12 (3) ◽  
pp. 291-297 ◽  
Author(s):  
PAUL R. PATEK ◽  
SOL BERNICK ◽  
DONALD K. MACCALLUM

1974 ◽  
Vol 139 (1) ◽  
pp. 193-207 ◽  
Author(s):  
Abraham I. Kook ◽  
Nathan Trainin

Experiments reported here were performed to understand the mechanism by which THF increases the immunocompetence of spleen cells from NTx mice. Dibutyryl cAMP or substances which increase intracellular levels of cAMP in lymphocytes such as Poly(A:U), theophylline, or PGE2 were shown to mimic the effect of THF and confer reactivity in an in vitro GvH response to spleen cells from NTx mice. Flufenamic acid, an antagonist to PGE2, was shown to inhibit the induction of competence by this substance. It was found that THF induces competence by activating membranal adenyl cyclase which leads to a rise in intracellular cAMP in thymus-derived cells only. These biochemical changes occur before antigenic stimulation and are unrelated to antigenic challenge. These findings indicate that THF exerts its effect via cAMP and are in agreement with the concepts which permit to classify THF as a thymus hormone.


Author(s):  
Z.T. HANDZEL ◽  
R. ZAIZOV ◽  
I. VARSANO ◽  
S. LEVIN ◽  
M. PECHT ◽  
...  

Blood ◽  
1960 ◽  
Vol 16 (2) ◽  
pp. 1145-1154 ◽  
Author(s):  
RUY PÉREZ-TAMAYO ◽  
JAIME MORA ◽  
IRMGARD MONTFORT

Abstract A type of experimental hypersplenism characterized by splenomegaly and thrombocytopenia has been produced in the rat by the repeated intraperitoneal injection of methylcellulose. The urine of these animals was collected and given through a gastric tube to another group of normal rats for a period of 4 weeks. The results were a marked and rapidly developing thrombocytopenia, a delayed but definite anemia with mild reticulocytosis and leukocytosis. When the administration of urine was discontinued, the anemia regressed, but the thrombocytopenia persisted unmodified for 2 weeks. When the urine of hypersplenic rats was again given to this group for 6 additional weeks, it failed to induce anemia or to change the persistent thrombocytopenia. Intragastric administration of urine from normal rats, from rats made anemic by total body radiation and from the hypersplenic group after splenectomy to other groups of normal rats, failed to produce the same changes and only induced moderate leukocytosis. On the basis of these results, it is postulated that in experimental methylcellulose-hypersplenism in the rat there is a humoral factor(s) responsible for the thrombocytopenia, that this humoral factor(s) is eliminated in the urine and that when such urine is given to normal rats, it is responsible for the thrombocytopenia and partially for the anemia that are observed. Such factor(s) are in some important way related to the presence of the spleen.


Blood ◽  
1966 ◽  
Vol 27 (5) ◽  
pp. 654-661 ◽  
Author(s):  
WENDELL F. ROSSE ◽  
THOMAS A. WALDMANN

Abstract 1. Erythropoiesis in birds is stimulated by bleeding and environmental hypoxia and is suppressed by induced polycythemia, indicating that the physiologic response is similar to that in mammals. 2. This response is mediated through a humoral factor which stimulates erythropoiesis of birds but not of mammals. Similarly, the erythropoietin of mammals does not stimulate the erythropoiesis of birds. 3. Although both the erythropoiesis stimulating factor of birds and of mammals appear to require an intact protein structure for biological activity, the erythropoietin of birds differs from that of mammals in that it is not destroyed by sialidase and does not lose its activity when reacted with antibody to human urinary erythropoietin.


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