@article {2189,
	title = {Separation of anticomplementary material and plasminogen from a cytotoxic factor active against Ehrlich ascites cells in Cohn fractions I-3 b fluorocarbon and n-butanol},
	journal = {Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine},
	volume = {126},
	number = {2},
	year = {1967},
	pages = {564-568},
	author = {Isaac Ginsburg and T. Dishon}
}
@article {1692,
	title = {Organ Lesions Produced in Rabbits by Group a Streptococci and Some of their Extracellular Products},
	journal = {The American Journal of Pathology},
	volume = {51},
	number = {3},
	year = {1967},
	pages = {351-371},
	abstract = {Many studies have been made of tissue alterations due to infections
with Group A streptococci in laboratory animals. Cardiac lesions characterized
by muscle necrosis, myocarditis, and giant-cell formation have
been reported in a variety of laboratory animals following injections of
living Group A streptococci and some of their products.1l Some of these
lesions were described as quite similar to the Aschoff bodies of rheumatic
carditis.4 The mechanism of formation of these cardiac lesions has been
attributed to toxic effects of streptococcal products,6 7 to immune response
to streptococcal components (hypersensitivity or autoimmunity)
,10 or to combinations of these processes.
Among these studies, the pharyngeal cavity of animals was used as the
portal of entry of streptococci only in that of Glaser et al.,11 who found
cardiac lesions within 72 hr. of a single intratonsillar injection of virulent
Group A streptococci. These lesions were focal, and showed muscle
necrosis, infiltrations of mononuclear cells, and occasional giant cells.
No streptococci could be isolated from such lesions, and it was concluded
that the lesions were probably not caused by an immunologic
process."{\textquoteright}
The present report describes the induction of lesions in cardiac and
other tissues of rabbits following injection, by intratonsillar and other
routes, of streptococcal extracellular products (SEP) obtained from
Group A streptococci grown in steady-state culture. These lesions occured
soon after single injections of these materials and probably reflect
direct toxic effect on the cells of these tissues.},
	author = {N. Zeiri and Z. Bentwich and J. H. Boss and Isaac Ginsburg and T. N. Harris}
}
@article {1645,
	title = {Cell sensitizing products of streptococci},
	journal = {Immunology},
	volume = {13},
	number = {3},
	year = {1967},
	pages = {555-564},
	abstract = {Various streptococcal species produce an haemosensitizing factor during the logarithmic phase of growth. A variety of mammalian cells sensitized with this factor become agglutinated following the addition of antistreptoccocal serum and also undergo cytopathic changes in the presence of complement. The haemosensitizing factor is thermostable and is unaltered by trypsin, papain, chymotrypsin, lipases or ribonucleases. Attempts to destroy the binding sites on the cell membrane by treatment with phospholipase C from Clostridium welchii or by neuraminidase failed. Treatment with trypsin or papain on the other hand markedly increased the binding capacity of red blood cell for the haemosensitizing factor.

Studies on the nature of the binding sites on the erythrocyte membrane of the haemosensitizing factor suggest that cholesterol and phospholipids constitute some of the binding sites for this factor.},
	author = {T. Dishon and Ruth Finkel and Z. Marcus and Isaac Ginsburg}
}
