Oncogenicity of the simian adenoviruses

Five of 17 adenoviruses of rhesus or cynomolgus monkey origin induced tumors in newborn hamsters. The tumors appeared between 42 and 280 days after subcutaneous inoculation and had the general characteristics of lymphomas. The tumors were specific by cross-complement fixation tests. An adenovirus recovered from Cercopithecus monkeys appeared to be highly oncogenic; all 23 inoculated hamsters developed tumors within 30 to 40 days.     

Hydrocephalus in mice inoculated neonatally by the oronasal route with reovirus type 1

Mice inoculated neonatally by the oronasal route with reovirus type 1 or 2 developed typical acute disease. Fifteen percent of the mice recovered from the acute infection. No further disease was noted in mice infected with reovirus 2, but 9 percent of the survivors of reovirus I infections developed hydrocephalus at a mean time of 109 days after inoculation. Infectious virus could not be isolated from hydrocephalic mice.     

大熊猫源枝孢样枝孢霉侵染小鼠皮肤的病理学过程

将180只ICR小鼠随机分为试验组和对照组,每组90只。在试验组小鼠两腹侧壁对称取2个点皮下注射大熊猫源枝孢样枝孢霉菌悬液(1×10~6 cfu/mL),接种12 h后(第1天),观察小鼠体况、接种部位表现,最后处死小鼠并取其接种部位的皮肤组织进行组织病理学检查和逆培养,用Image–Pro Plus 6.0统计病理切片中单位面积内免疫细胞数、孢子数和菌丝数,之后每隔24 h按上述步骤同样处理和观察。结果表明:接种后第1～8天小鼠体表特征变化不明显,小鼠机体免疫细胞由大量聚集到逐步减少,孢子与菌丝数由多到少又逐渐增加,处于萌发生长阶段;接种后第9～10天,接种部位出现小红斑,皮肤出现结节状损伤,各器官之间未粘连,其余症状不明显,免疫细胞持续增多;接种后第11～25天,接种部位红斑面积增大,损伤加大,颜色变深,有增生物,小鼠出现瘙痒症状,饮食明显减少,免疫细胞持续增多后逐步减少,孢子与菌丝数减少后急剧增加,再减少后又急剧增加,在第17、25天出现2次高峰;接种后第26天后小鼠饮食持续减少,接种部位出现局部坏死、黏膜粘连等症状,孢子和菌丝数逐渐减少至无。可见,枝孢样枝孢霉感染小鼠后第1～8天为潜伏期;第9～10天为前驱期,第11～25天为发病期,第26天后为转归期。     

Oncogenicity by methyl methanesulfonate in male RF mice

The incidences of lung tumors and thymic lymphomas were increased in young adult male RF mice receiving 30 milligrams of methyl meth anesulfonate per kilogram of body weight daily in the drinking water throughout life. Differences in oncogenicity between treatment with methyl methanesulfonate and with dimethylnitrosamine or diethylnitrosamine suggest a qualitative difference between the site (or sites) of alkylation by methyl methanesulfonate and by dimethylnitrosamine or diethylnitrosamine within the nucleic acids.     

Sarcocystis in mice inoculated with toxoplasma-like oocysts from cat feces

Sarcocysts morphologically similar to Sarcocystis muris were observed in mice after inoculation with Toxoplasma-like oocysts found in feces of a stray cat. Cats that were fed mice infected with the oocysts shed similar oocysts in their feces. Sarcocysts were found histologically in about 50 percent of mice inoculated with 40,000 or more oocysts and examined 42 days or longer after exposure. Most inoculated mice developed low Toxoplasma dye-test antibody titers 3 to 4 weeks after exposure, but Toxoplasma antibody was usually not detectable in infected cats.     

Adenovirus endocarditis in mice

Viral endocarditis developed in 24 percent of 50 newborn mice 6 to 8 days after intraperitoneal inoculation with murine adenovirus. Typical adenovirus intranuclear inclusions were seen in heart-valve lesions, and high titers of virus were recovered from heart tissue. Furthermore, adenovirions were directly visualized by electron microscopy within endothelial cells and fibroblasts of the heart valves.     

Mouse leukemia virus activation by chemical carcinogens

The induction of lymphomas in C57BL mice by methylcholanthrene, urethan, or diethylnitrosamine was accompanied by the development of murine leukemia viral antigen in most of the lymphoid tumors. The cell-free transmission of lymphomas induced by methylcholanthrene and the development of antibody to murine leukemia virus prior to the detection of overt lymphoma in these mice suggest that unmasking of a latent leukemia virus is an indigenous actuating cause of the lymphomas.     

Aging increases susceptibility of mouse skin to DMBA carcinogenesis independent of general immune status

The dependence of chemical carcinogenesis on age of target tissue was studied by repeated DMBA-treatment of mouse skin grafted from old and young syngeneic donors to young recipients. Carcinomas developed on 39 percent (1.6/41) of grafts from old donors and on 12 percent (5/41) of grafts from young donors. The incidence of nonskin lymphoid tumors was highest in male recipients bearing grafts from old donors.     

Warfarin treatment of mice bearing autochthonous tumors: effect on spontaneous metastases

Long-term oral administration of sodium warfarin significantly reduced the incidence of spontaneous metastases in the lungs from 83 percent in controls to 8 percent in treated C57/BL/6N mice. The size and weight of primary tumors in mice treated with warfarin were less than in control mice. Length of survival was unaffected.     

Carcinogenic substances from pituitary glands of cattle

Lipid extracts from the pituitary gland of cattle were prepared which, when injected into a pure strain of white mice, caused development of malignant tumors in 26.8 per cent of the 67 animals injected, which corresponds with the numerical results obtained by investigators working with human liver extracts. Evidently the carcinogenic power of these lipid extracts is low. The tumors developed chiefly in organs at a distance from the site of injection, exhibiting various histological types including carcinoma as well as sarcoma. The tumors developed at an earlier date after injection of extracts from the anterior lobe as compared with those developing after injection of the posterior lobe extracts, the average period of time necessary for their development being 9.3 months for the anterior lobe extracts and 14 months for posterior lobe extracts.     

Rapid viral induction of plasmacytomas in pristane-primed BALB-c mice

Strain BALB/c mice were injected intraperitoneally with 0.5 milliliter of pristane, and 39 to 56 days later they were infected with Abelson murine leukemia virus, which is a lymphosarcomagenic variant of Moloney virus. Fifty-eight percent of the mice developed lymphosarcoma, and 28 percent developed immunoglobulin-producing plasmacytomas within 20 to 93 days (77 to 149 days after the pristane injection). Two of 57 control mice developed plasmacytomas at days 138 and 166 after a single injection of pristane; no plasmacytomas were found in mice treated with virus alone.     

Experimental therapy of human glioma by means of a genetically engineered virus mutant.

Malignant gliomas are the most common malignant brain tumors and are almost always fatal. A thymidine kinase-negative mutant of herpes simplex virus-1 (dlsptk) that is attenuated for neurovirulence was tested as a possible treatment for gliomas. In cell culture, dlsptk killed two long-term human glioma lines and three short-term human glioma cell populations. In nude mice with implanted subcutaneous and subrenal U87 human gliomas, intraneoplastic inoculation of dlsptk caused growth inhibition. In nude mice with intracranial U87 gliomas, intraneoplastic inoculation of dlsptk prolonged survival. Genetically engineered viruses such as dlsptk merit further evaluation as novel antineoplastic agents.     

Lymphocytic Choriomeningitis Infection in Neonataily Thymectomized Mice Bearing Diffusion Chambers Containing Thymus

Normal, nonoperated Swiss mice which had been inoculated intracerebrally with lymphocytic choriomeningitis virus showed a 100-percent mortality within 8 days after virus challenge. Neonatally thymectomized mice, with or without empty intraperitoneal diffusion chambers, were protected from the lethal effects of the virus, with no animals dying within 14 days after inoculation. Cell-tight Millipore diffusion chambers containing newborn thymic tissue, implanted intraperitoneally into neonatally thymectomized mice, restored the susceptibility of 52 percent of these mice to the lethality of the virus infection. The percentage restoration with subcutaneous thymic grafting was similar. A humoral mechanism of action of the tissue in the chamber is proposed.     

Rapid immunological induction of murine lymphomas: evidence for a viral etiology

A graft-versus-host reaction induced in (SJL/J x C57BL/1)F(1) hybrid mice by injection of SJL/J spleen cells resulted in 100 percent incidence of tumors at 40 days. Transplantation studies revealed that the tumors were antigenically C57BL/1. Since both SJL/J and C57BL/1 mice carry tumorigenic virus, the evidence suggests a viral etiology.     

Complement-fixing antigens in hamster tumors induced by the Bryan strain of Rous sarcoma virus

Hamster tumors transplanted subcutaneously from primary intracranial tumors which developed after inoculation of the Bryan strain of Rous sarcoma virus, contained virusspecific tumor antigens indistinguishable from those induced by the Schmidt-Ruppin strain.     

Individual tumors of multifocal EB virus-induced malignant lymphomas in tamarins arise from different B-cell clones

Cotton-top tamarins were inoculated with sufficient Epstein-Barr virus to induce multiple tumors in each animal within 14 to 21 days. The tumors consisted of large-cell lymphomas that contained multiple copies of the Epstein-Barr virus genome and generated Epstein-Barr virus-carrying cell lines showing no detectable consistent chromosomal abnormality. Hybridization of tumor DNA with immunoglobulin gene probes revealed that each lymphoma was oligo- or monoclonal in origin and that individual tumors from the same animal arose from different B-cell clones. Thus the virus induced multiple transformation events in tamarins in vivo to cause malignant tumors resembling the Epstein-Barr virus-associated lymphomas of patients with organ transplants.     

Poliovirus host range is determined by a short amino acid sequence in neutralization antigenic site I

The mouse-adapted strain of poliovirus type 2 (Lansing) induces fatal poliomyelitis in mice after intracerebral inoculation, whereas mice inoculated with poliovirus type 1 (Mahoney) show no signs of disease. Previous work indicated that the adaptation to mouse virulence is associated with the viral capsid proteins and that mutations in neutralization antigenic site I of poliovirus reduce neurovirulence of the Lansing strain in mice. The role of antigenic site I in mouse neurovirulence was further explored by constructing an antigenic hybrid virus. Six amino acids in antigenic site I of the Mahoney strain were replaced with a sequence specific for the Lansing strain by using a mutagenesis cartridge. The hybrid virus was neutralized by polyclonal antisera elicited by the type 1 and type 2 strains of poliovirus and by neutralizing monoclonal antibodies directed against antigenic site I of type 2 virus. The hybrid virus induced paralytic disease in mice, an observation demonstrating that a short sequence of amino acids in antigenic site I is an important determinant of poliovirus host range. Antigenic site I may be involved in attachment of poliovirus to cells of the mouse central nervous system.     

THE PROTECTION OF PANCREATIC LIPASE BY ACACIA GUM

In this preliminary note we describe the results obtained by inoculation of the skin of the scrotum of four black rabbits with serous fluid expressed from an initial pinta lesion. The inoculation was made intradermally, as superficially as possible, with serous fluid rich in treponemata and diluted with normal salt solution. A papule appeared at the point of inoculation in one of the four rabbits on the 105th day. One hundred and fifteen days after inoculation the papule presented a circular erosion on an indurated base. The serous fluid expressed from this lesion contained numerous treponemata on dark-field examination, and these were easily impregnated by the Fontana-Tribondeau method. A volunteer inoculated with serous fluid expressed from the rabbit's lesion developed a typical initial pinta lesion at the point of inoculation, thus proving that the scrotal lesion of the rabbit was produced by Treponema carateum or Treponema herrejoni, the causal agent of pinta, mal del pinto or carate. Four rabbits inoculated with serous fluid from the scrotal lesion of the rabbit have not yet developed visible lesions.     

THE EXPERIMENTAL TRANSMISSION OF PINTA,MAL DEL PINTO OR CARATE TO THE RABBIT

In this preliminary note we describe the results obtained by inoculation of the skin of the scrotum of four black rabbits with serous fluid expressed from an initial pinta lesion. The inoculation was made intradermally, as superficially as possible, with serous fluid rich in treponemata and diluted with normal salt solution. A papule appeared at the point of inoculation in one of the four rabbits on the 105th day. One hundred and fifteen days after inoculation the papule presented a circular erosion on an indurated base. The serous fluid expressed from this lesion contained numerous treponemata on dark-field examination, and these were easily impregnated by the Fontana-Tribondeau method. A volunteer inoculated with serous fluid expressed from the rabbit's lesion developed a typical initial pinta lesion at the point of inoculation, thus proving that the scrotal lesion of the rabbit was produced by Treponema carateum or Treponema herrejoni, the causal agent of pinta, mal del pinto or carate. Four rabbits inoculated with serous fluid from the scrotal lesion of the rabbit have not yet developed visible lesions.     

Avian v-myc replaces chromosomal translocation in murine plasmacytomagenesis

Deregulation of c-myc expression in association with chromosomal translocations occurs in over 95% of murine plasmacytomas, rat immunocytomas, and human Burkitt lymphomas. Infection with a murine retrovirus (J-3) containing an avian v-myc rapidly induced plasmacytomas in pristane-primed BALB/cAn mice. Only 17% of the induced plasmacytomas that were karyotyped showed the characteristic chromosomal translocations involving the c-myc locus. Instead, all of the translocation-negative tumors demonstrated characteristic J-3 virus integration sites that were actively transcribed. Thus, the high levels of v-myc expression have replaced the requirement for chromosomal translocation in plasmacytomagenesis and accelerated the process of transformation.