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Female mice bearing the Ehrlich carcinoma or P388 lymphocytic leukemia tumors in ascites form were given sublethal doses of whole-body x-irradiation and the thiol binding agents N-ethylmaleimide, hydroxy-mercuribenzoate, or iodoacetamide, injected intraperitoneally prior to irradiation, as a single treatment. These compounds were found previously to sensitize mice to radiation lethality. Enhanced tumor cell killing was observed as measured by tumor cell count, along with slightly longer survival times of the host animal. Increasing the dose of either radiation or drug alone also caused an increase in tumor cell killing, but at the expense of earlier mortality of the host animal. At the doses employed the sensitizers examined appeared more effective on these two ascites tumors han on the host. The mechanism of enhancement of radiation killing of tumor cells by these drugs is not clear, although it appears not to be due to additive toxicity effects. Similar experiments with several cancer chemotherapy agents showed that those compounds did not act as radiosensitizers.

Dose-survival curves of four strains of E. coli-B/r her- try-, Bs-1, B/r CSH, and 15T-were obtained in the presence and in the absence of non-toxic levels of several thiol-binding agents-N-ethylmaleimide (NEM), iodoacetamide (IA), and hydroxymercuribenzoate (HMB). The degree of radiosensitization by these agents was estimated from the increase in slope of the dose-survival curve, under anoxic and aerobic conditions. Chemical sensitization of both radioresistant and radiosensitive strains of bacteria with the thiol-binding enzyme poisons NEM, IA, and HMB has been observed. NEM sensitized only under anoxic conditions, IA sensitized under both anoxic and aerobic conditions, although to a much greater extent aerobically, and HMB sensitized only under aerobic conditions. The formation of long-lived radiolytic products toxic to bacteria is observed in sensitization by IA. When sensitization occurs, the magnitude of the dose-modifying factor is equal to or greater than the oxygen enhancement ratio. Inhibition of an energy-requiring enzymic repair process does not seem to be involved as a primary mechanism of sensitization. Interference by thiol-binding agents with a "rapid repair" process which is different from the usual "enzymic repair," and which operates in radio-sensitive as well as in radioresistant bacteria, is suggested.

Immune reactivity of mice with various incidences of spontaneous tumors was measured at different points in their lifespan. Cytotoxic activity of immune sera from 3- and 12-month-old mice was high or moderately high in AKR/J, SJL/J, and A/HeJ mice in which high incidences of spontaneous tumors occur by the 12th month, and in SWR/J and C3HeB/-FeJ mice in which high incidences of spontaneous tumors reportedly occur after 18 months of age. A decrease in primary antibody response accompanied old age in 4 of the 6 strains tested (including randombred Swiss ICR/Ha), but not in AKR/J or A/HeJ mice. These facts, together with previous tests of cellular response in these mice, imply that under these experimental conditions little correspondence exists between humoral and cellular response. Further, host immunity may be only secondarily implicated in neoplastic formation.

The structure of the specific granules of eosinophil leukocytes has been studied by electron microscopy in sections of tissues, buffy coats, and sediments of peritoneal washings of rats, mice, guinea pigs, and men. The core of eosinophil granules is a crystal which has a cubic lattice with a repeat of approximately 30 A in rodents and approximately 40 A in man. The chemical composition of the core is discussed in connection with recent cell fractionation studies, and the hypothesis that the core is a crystal of peroxidase is considered.

Mycoplasmas recovered from the respiratory tract and genitourinary system of dogs, with and without respiratory infection, have been characterized by biological and immunological methods. Some of the isolates were indentified as being similar to the three species of canine mycoplasmas described earlier under the designation Mycoplasma spumans, M. canis, and M. maculosum. Other mycoplasmas placed in three groups (A, C, and D) were found to be clearly distinct from the three classified species. Group A strains fermented glucose but not mannose and were serologically distinct from other canine mycoplasmas recovered in this study. These strains were subsequently found to be biologically and serologically related to a previously reported, but unclassified, canine mycoplasma. Group D strains differed in some biological properties but were serologically related. These were found to be nonfermenting mycoplasmas representing isolations from the throat and bladder of dogs. They were serologically distinct from other canine mycoplasmas and were apparently unrelated to other known mycoplasma serotypes. Group C mycoplasmas were recovered only from the lungs of dogs. Within the group, they differ in some immunological properties but appear to be serologically distinct from other canine strains. They can also be separated from other dog strains in their ability to ferment glucose and mannose. Group B strains were found to have biological properties similar to M. canis strains but seemed to be only partially related to this serotype when examined in several serological techniques. It is suggested that these strains might represent antigenic variants of M. canis.

Mild Tween 80-ether treatment of mouse mammary tumor virus (MTV) results in disruption of the viral membrane and release of subviral components. Prolonged lipid extraction, however, results in virtually complete solubilization of the virion. Soluble proteins have been separated by Sephadex G-200 chromatography and used for immunization of rats These antisera identify five viral antigens (designated MTV-s1, s2, s3, s4, and s5). The s1 and s2 antigens are group-specific, and are the antigens of the viral nucleoid. MTV-s3 antigen is a structural protein of the viral membrane. Poly-acrylamide gel electrophoresis of MTV shows five major polypeptides in the virion; the molecular weights of these are p1 (90,000), p2 (70,000), p3 (52,000), p4 (33,000), and p5 (23,000). The major protein of the virus is p3; it is found in the nucleoid and carries the s1 antigen. Protein p5 is the structural protein of the membrane, and it carries the s3 antigen. Antisera prepared against isolated MTV proteins were used also in immunofluorescence tests to determine the intracellular deposition of MTV antigens. These studies show that all MTV structural proteins are synthesized cytoplasmically. Screening of a variety of neoplasms by immunofluorescence and immunodiffusion tests demonstrates MTV infection in only three types of neoplastic diseases, mammary tumors, ML+ leukemias, and Leydig cell tumors of MTV-infected mice. Mammary tumors synthesize all viral structural proteins, while the synthesis of MTV proteins in the ML+ leukemias and Leydig cell tumor is limited to the s1 and s2 antigens. Electron microscopic examination of these tissues confirms the synthesis and accumulation of viral nucleocapsids (A particles) without the production of budding virions.

Following fertilization of the egg of the sand dollar Echinarachnius parma, tritiated thymidine (H(3)TDR) was taken up independently by the male and female pronuclei beginning within about 15 to 20 minutes, and the labeled pronuclei fused at about 30 to 40 minutes. At cleavage 90 minutes later the labeled nuclear material was distributed to both daughter cells. Unfertilized eggs and sperm exposed to H(3)TDR did not show nuclear localization of thymidine. DNA replication, thus, is initiated in the haploid pronuclei shortly after fertilization and prior to fusion. The major portion of DNA synthesis, as evidenced by thymidine uptake, appears to be during a 20 to 30 minute period after fertilization. Fertilization is associated with the activation of a mechanism which initiates early and independent replication of DNA in both the male and female pronuclei.

Cytomegaloviremia was documented in seven patients. Three patients were renal transplant recipients and two were liver transplant recipients. One was a postcardiac surgery patient, and one had acute myelogenous leukemia. The transplant patients had received only banked blood or fresh frozen plasma and developed evidence of infection about 1 month after surgery. Illness varied from no apparent signs to fever alone, fever and a morbilliform rash, hepatitis and an infectious mononucleosis syndrome. The virus was isolated from the blood erythrocyte layer, the leukocyte layer, and the plasma and serum, in that order of frequency. In vitro studies demonstrated persistence of inoculated cytomegalovirus in the presence of erythrocytes (and tissue culture media) for up to 21 days. In whole blood under banking conditions, inoculated virus was recovered after 28 days and, in fresh frozen plasma, after 97 days.

Tritium-labeled deoxyribonucleic acid (DNA) from pneumococci and from human leukocytes was added to growing cultures of HeLa cells at 37 degrees C. Autoradiography revealed an extensive localization of tritium in the nuclear regions. The label could not be removed by treatment with ribonuclease or dilute perchloric acid, but quantitative removal from the cells could be effected with deoxyribonuclease. Chemical and radioactivity determinations on nucleic acids isolated from the exposed HeLa cells revealed the presence of tritium in all 4 DNA bases. About 12 microg. of tritiated DNA was recovered from 6 x 10(6) HeLa cells which had been exposed for 24 hours to 240 microg. of the human DNA. From this, it is concluded that the amount of DNA, or its degradation products, taken up by the cells was equivalent to at least 10 per cent of the normal HeLa cell complement.