The acridine orange (AO) binding to the deoxyribonucleoprotein (DNP) complex of individual normal lymphocytes, infectious mononucleosis (IM) lymphoid cells and leukaemic blast cells was determined by microfluorometry. Increased AO binding to DNP was found with increasing cell density on the slide and was similar in the different cell populations. staining Only in exceptional cases of IM, the AO binding was high irrespective of cell density. The increased AO binding was due to changes in the DNP complex, which might be induced by the release of macromolecular substances from the cells. The results show that in clinical cytological studies, the fluorescence intensities cannot be used for the discrimination between normal and malignant cells.

Annals of the New York Academy of SciencesVolume 76, Issue 3 p. 413-441 A COMPARATIVE STUDY OF THE USE OF MICROORGANISMS IN THE SCREENING OF POTENTIAL ANTITUMOR AGENTS* G. E. Foley, G. E. Foley Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorR. E. McCarthy, R. E. McCarthy Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass.Search for more papers by this authorV. M. Binns, V. M. Binns Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass.Search for more papers by this authorE. E. Snell, E. E. Snell Department of Biochemistry, University of California, Berkeley, Calif. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorB. M. Guirard, B. M. Guirard Department of Biochemistry, University of California, Berkeley, Calif.Search for more papers by this authorG. W. Kidder, G. W. Kidder Biological Laboratory, Amherst College, Amherst, Mass. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorV. C. Dewey, V. C. Dewey Biological Laboratory, Amherst College, Amherst, Mass.Search for more papers by this authorP. S. Thayer, P. S. Thayer Biological Laboratory, Arthur D. Little, Inc., Cambridge, Mass.Search for more papers by this author G. E. Foley, G. E. Foley Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorR. E. McCarthy, R. E. McCarthy Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass.Search for more papers by this authorV. M. Binns, V. M. Binns Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass.Search for more papers by this authorE. E. Snell, E. E. Snell Department of Biochemistry, University of California, Berkeley, Calif. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorB. M. Guirard, B. M. Guirard Department of Biochemistry, University of California, Berkeley, Calif.Search for more papers by this authorG. W. Kidder, G. W. Kidder Biological Laboratory, Amherst College, Amherst, Mass. Member, Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, National Cancer Institute, Public Health Service, Bethesda, Md.Search for more papers by this authorV. C. Dewey, V. C. Dewey Biological Laboratory, Amherst College, Amherst, Mass.Search for more papers by this authorP. S. Thayer, P. S. Thayer Biological Laboratory, Arthur D. Little, Inc., Cambridge, Mass.Search for more papers by this author First published: December 1958 https://doi.org/10.1111/j.1749-6632.1958.tb54862.xCitations: 54 † The work reported in this paper was supported in part by Research Grant CY-333S and by Contract SA-43-ph-10S3 between The Children's Cancer Research Foundation, Boston, Mass., and the National Cancer Institute, Public Health Service, Bethesda, Md.; by Contract SA-43-ph-1504 between the Regents of the University of California, Berkeley, Calif., and the National Cancer Institute; by Contract SA-43-ph-1042 between the Board of Trustees of Amherst College, Amherst, Mass., and the National Cancer Institute; and by Contract SA-43-ph-1087 between Arthur D. Little, Inc., Cambridge, Mass., and the National Cancer Institute. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Reference 1 Investigation of Diverse Systems for Cancer Chemotherapy Screening . 1955 . A. Gellhorn & E. Hirschberg , Eds . Cancer Research. Suppl. No. 3 : 1 – 112 . 2 Foley , G. E. . 1956 . Current Research in Cancer Chemotherapy. 6 : 3 – 22 . 3 Kidder , G. W. , V. C. Dewey , R. E. Parks , Jr. & G. L. Woodside . 1949 . Science. 109 : 511 – 514 . 4 Eagle , H. & G. E. Foley . 1958 . Cancer Research . In press . 5 Felton , E. A. & C. F. Niven , Jr. . 1953 . J. Bacteriol. 65 : 482 – 483 . 6 Winter , W. D. , Jr. & G. E. Foley . 1956 . J. Infectious Diseases. 98 : 150 – 156 . 7 Kidder , G. W. & V. C. Dewey . 1951 . The biochemistry of ciliates in pure culture . In Protozoa . : 323 – 400 . A. Lwoff , Ed . Academic Press . New York , N. Y . 8 Chang , R. S. . 1954 . Proc. Soc. Exptl. Biol. Med. 87 : 440 – 443 . 9 Eagle , H. . 1955 . Proc. Soc. Exptl. Biol. Med. 89 : 362 – 364 . 10 Difco Manual . 1953 . 9th ed. : 225-226. Difco Laboratories. Detroit, Mich . 11 Difco Manual . 1953 . 9th ed. : 214-215. Difco Laboratories. Detroit, Mich . 12 Kohn , H. I. & J. S. Harris . 1941 . J. Pharmacol. Exptl. Therapy. 73 : 343 – 361 . 13 Difco Manual . 1953 . 9th ed.: 216-217. Difco Laboratories. Detroit, Mich . 14 Difco Manual . 1953 . 9th ed.: 219-220. Difco Laboratories. Detroit, Mich . 15 Difco Manual . 1953 . 9th ed.: 229-230. Difco Laboratories. Detroit, Mich . 16 Difco Manual . 1953 . 9th ed. : 217-218. Difco Laboratories. Detroit, Mich . 17 Mager , J. & M. Aschner . 1947 . J. Bacteriol. 53 : 283 – 295 . 18 Atkin , L. , L. W. Williams , A. S. Schultz & C. N. Frey . 1944 . Ind . Eng. Chem. Anal. Ed. 16 : 67 – 71 . 19 Rabinowitz , J. C. & E. E. Snell . 1947 . J. Biol. Chem. 169 : 631 – 642 . 20 Rabinowitz , J. C. , N. S. Mondy & E. E. Snell . 1948 . J. Biol. Chem. 175 : 147 – 153 . 21 Davis , B. D. & E. S. Mingioli . 1950 . J. Bacteriol. 60 : 17 – 28 . 22 Kidder , G. W. , V. C. Dewey & M. R. Heinrich . 1954 . Exptl. Cell Research. 7 : 256 – 264 . 23 Kidder , G. W. , V. C. Dewey & R. C. Fuller . 1954 . Proc. Soc. Exptl. Biol. Med. 86 : 685 – 689 . 24 Beadle , G. W. & E. L. Tatum . 1945 . Am. J. Botany. 32 : 678 – 686 . 25 Eagle , H. & G. E. Foley . 1956 . Am. J. Med. 21 : 739 – 749 . 26 Association of Vitamin Chemists, Inc . 1951 . Methods of Vitamin Assay . Interscience . New York , N. Y . 27 Foley , G. E. . 1957 . Study of 200 compounds in eight microbiological assay systems . Summary report on Contract SA-43-ph-1053. Cancer Chemotherapy Natl . Service Center. Public Health Service . Bethesda , Md . 28 Snell , E. E. & B. M. Guirard . 1957 . Report on the screening of 200 compounds for inhibitory activity against microorganisms . Summary report on Contract SA-43-ph-1504. Cancer Chemotherapy Natl. Service Center. Public Health Service. Bethesda, Md . 29 Kidder , G. W. & V. C. Dewey . 1957 . Summary of ciliate screening . Summary report on Contract SA-43-ph-1042. Cancer Chemotherapy Natl . Service Center. Public Health Service . Bethesda , Md . 30 Thayer , P. S. . 1957 . Inhibition of the growth of Neurospora by selected chemical compounds . Summary report on Contract SA-43-ph-1087. Cancer Chemotherapy Natl . Service Center. Public Health Service . Bethesda , Md . 31 Hutchings , B. L. , J. H. Mowat , J. J. Oleson , E. L. R. Stokstad , J. H. Boothe , C.W. Waller , R. B. Angier , J. Semb & Y. Subbarow . 1947 . J. Biol. Chem. 170 : 323 – 328 . 32 Survey by Staff of Cancer Chemotherapy National Service Center (Public Health Service) . 1958 . I. Compilation of anti-tumor data from the literature. II. Results of antitumor screening tests under the auspices of the Center . (Compare with appendix to this monograph.) . 33 Foley , G. E. , H. Eagle , E. E. Snell , G. W. Kidder & P. S. THAYER . 1958 . Ann. N. Y. Acad. Sci. 76 ( 3 ): 952 – 960 . 34 Skipper , H. E. . 1953 . Cancer Research. 13 : 545 – 551 . Citing Literature Volume76, Issue3Screening Procedures for Experimental Cancer ChemotherapyDecember 1958Pages 413-441 ReferencesRelatedInformation

Annals of the New York Academy of SciencesVolume 76, Issue 3 p. 952-960 STUDIES ON THE USE OF IN VITRO PROCEDURES FOR THE SCREENING OF POTENTIAL ANTITUMOR AGENTS: COMPARISON OF ACTIVITY IN MAMMALIAN CELL CULTURES AND MICROBIOLOGICAL ASSAYS ALONE AND IN COMBINATION WITH EXPERIMENTAL ANTITUMOR ACTIVITY* G. E. Foley, G. E. Foley Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass. These studies were supported in part by Contract Sa-43-ph-1053 between the National Institutes or Health and The Children's Cancer Research Foundation, and Research Grants C-2782 and CY-3335 to The Children's Cancer Research Foundation from the National Cancer Institute.Search for more papers by this authorH. Eagle, H. Eagle Section on Experimental Therapeutics, Laboratory of Infectious Diseases, National Institute of A Allergy and Infectious Diseases, Public Health Service, Bethesda, Md.Search for more papers by this authorE. E. Snell, E. E. Snell Department of Biochemistry, University of California, Berkeley, Calif. These studies were supported in part by Contract Sa-43-ph-1504 between the National Institutes of Health and the Regents of the University of California.Search for more papers by this authorG. W. Kidder, G. W. Kidder Biological Laboratory, Amherst College, Amherst, Mass. These studies were supported in part by Contract Sa-43-ph-1042 between the National Institutes of Health and the Board of Trustees of Amherst College.Search for more papers by this authorP. S. Thayer, P. S. Thayer Biological Laboratory, Arthur D. Little, Inc., Cambridge, Mass. These studies were supported in part by Contract Sa-43-ph-1087 between the National Institutes of Health and Arthur D. Little, Inc.Search for more papers by this author G. E. Foley, G. E. Foley Laboratories of Microbiology, The Children's Cancer Research Foundation, and the Department of Pathology, Harvard Medical School, at The Children's Medical Center, Boston, Mass. These studies were supported in part by Contract Sa-43-ph-1053 between the National Institutes or Health and The Children's Cancer Research Foundation, and Research Grants C-2782 and CY-3335 to The Children's Cancer Research Foundation from the National Cancer Institute.Search for more papers by this authorH. Eagle, H. Eagle Section on Experimental Therapeutics, Laboratory of Infectious Diseases, National Institute of A Allergy and Infectious Diseases, Public Health Service, Bethesda, Md.Search for more papers by this authorE. E. Snell, E. E. Snell Department of Biochemistry, University of California, Berkeley, Calif. These studies were supported in part by Contract Sa-43-ph-1504 between the National Institutes of Health and the Regents of the University of California.Search for more papers by this authorG. W. Kidder, G. W. Kidder Biological Laboratory, Amherst College, Amherst, Mass. These studies were supported in part by Contract Sa-43-ph-1042 between the National Institutes of Health and the Board of Trustees of Amherst College.Search for more papers by this authorP. S. Thayer, P. S. Thayer Biological Laboratory, Arthur D. Little, Inc., Cambridge, Mass. These studies were supported in part by Contract Sa-43-ph-1087 between the National Institutes of Health and Arthur D. Little, Inc.Search for more papers by this author First published: December 1958 https://doi.org/10.1111/j.1749-6632.1958.tb54913.xCitations: 12 † This paper was not presented at the conference on which this monograph is based; it is the final report of the Subcommittee on Tissue Culture and the Subcommittee on Microbiology, Screening Panel, Cancer Chemotherapy National Service Center, Bethesda, Md., and is included here as a valuable adjunct to the work already presented. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Reference 1 Eagle , H. & G. E. Foley . 1956 . The cytotoxic action of carcinolytic agents in tissue culture . Am. J. Med. 21 : 739 – 749 . 2 Eagle , H. & G. E. Foley . 1958 . Cytotoxicity in human cell cultures as a primary screen for the detection of anti-tumor agents . Cancer Research . In press . 3 Foley , G. E. & H. Eagle . 1958 . The cytotoxicity of anti-tumor agents for normal human and animal cells in first tissue culture passage . Cancer Research . In press . 4 Foley , G. E. , R. E. McCarthy , V. M. Binns , E. E. Snell , B. M. Guirard , G. W. Kidder , V. C. Dewey & P. S. Thayer . 1958 . A comparative study of the use of microorganisms in the screening of potential antitumor agents . Ann. N. Y. Acad. Sci. 76 ( 3 ): 413 – 438 . 5 Survey by Staff of Cancer Chemotherapy National Service Center . 1958 . I. Compilation of anti-tumor data from literature. II. Results of antitumor screening tests under the auspices of the Center . (See APPENDIX to this monograph.) . 6 Farber , S. . Personal communications . 7 Schneiderman , M. & P. Armitage . 1958 . Statistical problems in a mass screening program . Ann.N. Y.Acad. Sci. 76 ( 3 ): 896 – 900 . 8 Handler , A. H. . 1951 . Transplantation of heterospecific tumor tissue into the cheek pouch of the golden hamster (Mesocricetus auratus). Doctoral dissertation . Boston Univ . Boston , Mass . Citing Literature Volume76, Issue3Screening Procedures for Experimental Cancer ChemotherapyDecember 1958Pages 952-960 ReferencesRelatedInformation

The data derived from analysis of 1,2-dihydro-s-triazine inhibition in a number of microbiological systems indicates that the primary mechanism of action of these compounds is interference with the reduction of pteroylglutamic acid in the biosynthesis of citrovorum factor, while higher concentrations also may interfere with the utilization of citrovorum factor in certain microbiological systems. There also is some evidence that the phenyldihydrotriazines interfere with the utilization ofp-aminobenzoic acid.

Two cases of septicemia with Streptococcus equinus, a group D streptococcus, are reported, and the literature pertaining to infections with this organism is reviewed. Both of our patients presented with obvious signs of infection, had S equinus isolated from multiple blood cultures, and had a good clinical response to penicillin therapy, alone or in combination with streptomycin. In vitro testing of the isolates confirmed susceptibility to penicillin. S equinus should now be recognized as a human pathogen as are the other group D streptococci, S bovis and the enterococci.

AMONG the many factors which long have been considered in various studies on the reaction of different individuals to infection with the tubercle bacillus, the idea of constitutional differences is even older than our knowledge of the tubercle bacillus itself. Hirsch (11) stated that phthisis (tuberculosis) appears in the successive generations of certain families too regularly to deny hereditary elements. More recent studies have established the validity of these early observations both by the experimental approach [Lurie (13)] and by the epidemiologic method [Puffer (14)]. In addition to these broader host or constitutional differences, variations in tuberculosis of similar import in the two sexes are well known. As pointed out by Dauer (7), during the past 75 years there has been little change in the ratio of female to male mortality between 20 and 29 years of age, although total mortality from tuberculosis has been steadily declining. It appears that the factors responsible for the difference in the ratio of female to male deaths from tuberculosis has remained constant, and is unrelated to the factors to which the general decline in mortality has been attributed.

STUDIES of the epidemiologic features of poliomyelitis, such as geographic prevalence (Aycock, 1939), and age distribution (Aycock, 1928), as well as the extensive occurrence of subclinical infection as evidenced by the development of serologic immunity (Aycock & Kramer, 1930), all indicate a widespread and more or less uniform dissemination of the virus, of the order of that of the virus of measles; for example (Aycock, 1934). The extensive occurrence of subclinical infection and the gradation from frank to mild or abortive forms of the clinical disease in themselves indicate that par.alysis is selective- the exceptional rather than the usual manifestation of infection with the virus-an event which might be compared epidemiologically with the occurrence of the complication of otitis media in measles (Aycock, 1942a).

CONTINUING the study previously reported,1 the hemolytic streptococci isolated from throat swabs of patients admitted to various Massachusetts hospitals with scarlet fever during 1944 were classified as to serologic type. The laboratory studies were again done at the Department of Preventive Medicine and Epidemiology, Harvard Medical School, and arrangements for the provision of throat cultures were made through the co-operation of the Division of Communicable Diseases, Massachusetts Department of Public Health.During the past year a total of 839 additional throat swabs were examined, of which 640 (76.3 per cent) were positive for Group A hemolytic streptococci.ǁ The methods employed . . .

EARLY MEDICAL literature is replete with explanations of the causation of disease derived from long observation of the individual and his response to external environment. Lacking the tools of modern biological science, these early students by necessity devoted considerable attention to the idea of variations of the host in his reaction to a supposedly constant environment. Joseph Gallup, writing in Vermont in 1815, stated: “This state of the human body has been denominated a predisposition to disease; but we are not here to understand it as being actual disease; only a susceptibility or aptitude to particular diseased action in the system, when thrown into any state of commotion by exciting causes, which are very numerous. It may be a very curious question to determine, what actual change takes place in the system, that should render it so liable to the attack of fever from slight causes, which would not be noticed at another time.

Staphylococcus and Streptococcus Carriers. Sources of Food-borne Outbreaks in War Industry Sources of Food-borne Outbreaks in War Industry V. A. Getting, A. D. Rubenstein, and G. E. Foley CopyRight*Presented at a Joint Session of the Epidemiology, Health Officers, Maternal and Child Health, and Laboratory Sections of the American Public Health Association at the Seventy-second Annual Meeting in New York, N. Y., October 14, 1943. https://doi.org/10.2105/AJPH.34.8.833 Published Online: August 29, 2011

Serological Types of Hemolytic Streptococci Isolated from Multiple Cases of Scarlet Fever in the Same Household G. E. Foley, S. M. Wheeler, and W. L. Aycock CopyRight https://doi.org/10.2105/AJPH.34.10.1083 Published Online: August 29, 2011

A Food-Borne Streptococcus Outbreak V. A. Getting, S. M. Wheeler, and George E. Foley CopyRight https://doi.org/10.2105/AJPH.33.10.1217 Published Online: August 29, 2011