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At least 73 records · Page 4Linked to original sources
PubMed1962

An electron microscopic study of the cleavage furrow in mammalian cells.

The process of cytoplasmic cleavage has been studied in thin sections of rat erythroblasts and the cells of mouse leukemia and Walker 256 carcinoma of the rat. The development of the cleavage furrow begins in relation to the mid-body, which, earlier, appears on the equatorial plane in association with the continuous fibers of the spindle. The earliest evidence of a cleavage furrow is the presence of a vesicle or vesicles close to the mid-body. Subsequently, many smaller vesicles are seen in the equatorial plane. The cleavage furrow probably develops by the fusion of these vesicles so that a new plasma membrane is formed between the daughter cells, and extends from the telophase intercellular bridge to the cell margin. During the stage of formation of the vesicles, cisternae, believed to be part of the endoplasmic reticulum, assume an intimate relationship with the cleavage plane, and they may perhaps be involved in the formation of the vesicles.

Animals↗
PubMed1960

Further electron microscope studies of a mouse leukemia induced by cell-free filtrates.

Further electron microscope observations of tissues from Swiss and DBA/2 mice with leukemia transmissible by cell-free filtrates to the adult animals are presented. The cytological characteristics of the leukemic cells, the fine structure of the viruses, and the virus host-cell relationships have been examined. The leukemia virus has an external diameter averaging 870 A, and appears to be formed at the level of cell membranes by a budding process. The viruses are observed most frequently in intercellular spaces, but are also often found within cytoplasmic vacuoles of megakaryocytes. Lead hydroxide staining was applied to the study of the leukemic material. The viruses have been found to have a considerable affinity for this lead salt, only comparable in intensity to the affinity shown by RNP granules for the same chemical.

Animals↗
PubMed1954

Viral hepatitis associated with transplantable mouse leukemia. I. Acute hepatic manifestations following treatment with urethane or methylformamide.

An hepatic disease caused by a filterable agent carried in leukemic mice is described. Ordinarily the virus remains latent and asymptomatic. If, however, the mice are treated with urethane or methylformamide before and after virus inoculation, the disease becomes manifest and is characterized by extremely marked liver necrosis. Infant mice, a large percentage of weanlings, and adult Bagg albino mice are killed when injected with a filtrate from organs of diseased animals. Adult F1 and Swiss mice show signs of the disease but generally recover. They succumb, however, when simultaneously treated with urethane or methylformamide. By continuing the treatment of consecutive transfer generations an acute disease can be induced which finally kills all adult F1 mice without the treatment. At this stage the original leukemia may be lost. Mice which have recovered from the subacute disease are resistant to the acute disease, and mice injected with the latent form of the agent are immune to the subacute disease. However, even immunized animals lose their resistance if they are treated with urethane. The acute or subacute disease can be reduced to the latent stage by passing the agent through several generations of immunized animals. The relationship of this hepatitis virus of mice to viruses causing similar diseases is discussed, as is the possibility that these agents are closely related, if not identical.

Animals↗
PubMed1955

Acute hepatitis associated with mouse leukemia. V. The neurotropic properties of the causal virus.

Observations on the behavior of MHV (Pr) in the cerebral tissue of Princeton and Swiss weanling mice indicated a limited neurotropism. The virus migrated to the brain on intraperitoneal injection and was established there by cranial passage, though with difficulty in Swiss mice. Intracerebral multiplication was rarely followed by outward signs of nervous disorder. A slight pathologic reaction occurred in the brains of intracerebrally injected Princeton mice, but it was negligible compared with that of the ensuing hepatitis. In Swiss mice, injected intracerebrally with a mixture of MHV (Pr) and Eperythrozoon coccoides, a related virus with restricted pathogenicity and host range, possibly a mutant, was isolated from the liver and brain. MHV (C), an actively hepatotropic virus recovered from leukemic Balb C mice, was much more neurotropic than MHV (Pr). Intracerebral injection of Balb C and Swiss weanling mice was attended by marked leptomeningeal and encephalitic lesions. Paralysis of the extremities occurred in some of the animals. The virus was essentially inactive in Princeton mice. During the intracerebral passage of MHV (C) in Swiss mice a pleuropneumonia-like organism was isolated from the brain. In conjunction with the virus this organism produced a vigorous leukocytic reaction.

Animals↗
PubMed1957

Cell-free transmission in adult Swiss mice of a disease having the character of a leukemia.

A disease with the characteristics of a leukemia has been found to be serially transmissible in adult Swiss mice by means of cell-free filtrates. Thus far, the disease has been transmitted through twenty-six serial passages with filtrates as well as cell suspensions. The agent readily passes through Selas 03, Berkefeld N, and gradocol membrane filters-these last having an average pore size of 220 mmicro. Filtrates remain stable when stored for long periods at -70 degrees C. or when lyophilized. Splenic tissue containing the agent, which was subjected to massive doses of x-ray (50,000 r),-far more than sufficient to kill the cells,-show undiminished infectivity. The agent is inactivated by heating to 56 degrees C. for 30 minutes and by exposure to ether or formalin. The disease can be transmitted to adult Swiss mice or DBA/2 mice, but not to adult PRI, C(3)H, A, C(57)B1/6, or F(1)(C(58) x BALB) mice. Intraperitoneal, subcutaneous, intracerebral, and intramuscular injections are all effective.

Animals↗
PubMed1952

Acute hepatitis associated with mouse leukemia. I. Pathological features and transmission of the disease.

On four occasions a naturally occurring mouse leukemia, which was maintained by serial passage in weanlings of the Princeton strain, was superseded by a syndrome typical of acute hepatitis. Once initiated, the disease was regularly transmissible by the injection of liver suspensions of sick mice. It was also passed, though irregularly, by feeding such suspensions, and it also followed cannibalism. The course of the disease after intraperitoneal injection of liver suspensions into normal weanlings was commonly less than 7 days and the mortality rate nearly 100 per cent. Focal or diffuse necrosis of the liver was the only constant lesion at autopsy. On recovery, which occurred only in exceptional cases, cirrhosis was often found. The primary source of the disease was undetermined. Latent carriage by healthy mice was not detectable on direct examination nor by the serial passage of suspensions of normal livers.

Acute Disease↗
PubMed1952

Acute hepatitis associated with mouse leukemia. II. Etiology and host range of the causal agent in mice.

The etiological agent of the acute hepatitis encountered in weanling mice of the Princeton strain is a virus found in the liver, spleen, kidneys, heart's blood, urine, and intestinal contents of experimentally infected animals. Older Princeton mice and weanlings from four other strains (Swiss, Webster's BSVS, C albino) and Bagg) proved to be less susceptible than Princeton weanlings. The virus was demonstrable in Berkefeld V filtrates of liver suspensions and in supernatants after centrifugation at 10,000 G. In whole liver suspensions it was detectable in decreasing amounts through a dilution of 10(-7). Aureomycin and terramycin had no detectable effect on the activity of the virus in weanlings.

Animals↗