bluuebunny/crossref_metadata_2025_split huggingface dataset:
Production et Analyse D'un Complexe Viral Dérivé D'un Virus des Radioleucoses de la Souris C57BL
Authors: Mamoun R. , Guillemain B. , Astier T. , Portail J. P. , Legrand E. , Duplan J. F. 
Published: February 2007

Production and analysis of a viral complex derived from a radiation‐induced leukemia virus of the C57BL mouseThe MuLV isolate RadLV‐Rs derived from a radiation‐induced leukemia of a C57BL mouse was shown to induce preferentially lymphoreticulum cell neoplasms of spleen and lymph nodes rather than thymomas. Several cell lines were established in culture from spleen or lymph node tumors induced by RaLV‐Rs. These lines were originally composed of round shaped virus‐producing cells but their ability to produce virus disappeared progressively with serial passages and simultaneously they were growing as a monolayer of polygonal epithelial‐like cells. Several clones were derived from one of the tumor cell lines and the presence of round cells correlated positively with the viral release. Besides these morphological differences the karyotype of the clones chronically producing virus was strongly modified. Thus, cells of clone 13‐3C (producing a virus called 13C) contained 43 chromosomes, a large number of which were metacentrics or minutes. On the opposite, clone 13‐2D which had the same origin as 13–3C but did not produce virus had 70 acrocentric chromosomes. The in vitro produced virus 13C had the same pathogenic effects as the original RaLV‐Rs; on the basis of its biochemical and morphological properties it could be classified as a type‐C retrovirus and it also induced Gross type cell surface antigens. In contrast to most of the MuLV, 13C virus did not show any helper activity on the MSV integrated in S+L‐ mouse cells, however syncytia formation was readily observed after cocultivation of 13–3C and XC cells. The 13C virus was shown to be a complex composed of an ecotropic MuLV which preferentially infects B type mouse cells (MuLV‐B) and a xenotropic virus (MuLV‐X). The MuLV‐B had no helper activity for integrated MSV and did not induce XC syncytia formation. The MuLV‐X was a potent helper for MSV in S+L‐ mink cells but did not induce XC syncytia formation.
Epstein‐barr virus infection following bone‐marrow transplantation
Authors: Sullivan John L. , Wallen William C. , Johnson F. Leonard 
Published: February 2007

AbstractA 12‐year‐old patient with acute lymphoblastic leukemia received a bone‐marrow transplant (BMT) from a matched sibling donor. Nine weeks prior to transplant the donor experienced Epstein‐Barr virus (EBV)‐induced infectious mononucleosis. The bone‐marrow recipient was EBV‐negative at the time of transplant; however, 4 weeks post transplant the recipient developed clinical symptoms of graft‐versus‐host disease (GVHD) coincident with serological evidence of acute EBV infection. In addition, a lymphoblastoid cell line positive for Epstein‐Barr nuclear antigen was established from a bone‐marrow sample obtained at the onset of symptoms compatible with GVHD. Sera obtained from the recipient over the ensuing 2 months showed the appearance of antibodies to specific EBV antigens consistent with a primary immune response to EBV infection. This association of acute EBV infection with symptoms of GVHD in a BMT recipient suggests a need for further investigation of the epidemiology of EBV infections in human bone‐marrow transplantation and the relationship between EBV infection and GVHD.
Cytocidal activity and proliferative ability of macrophages infiltrating the EMT6 tumor
Authors: Stewart Carleton C. , Beetham Karen L. 
Published: February 2007

AbstractThe EMT6 mouse tumor was selected for use in the study of cytocidal activity and proliferative ability of infiltrating macrophages because of its high plating efficiency when explanted to culture. The plating efficiency for cells directly plated in culture from the tumor was 28±9.3%, irrespective of the size of the tumor. Of the adherent cells derived from the tumor, the fraction that was macrophages increased from 27% at 7 days to 47% at 28 days after initial injection. Time‐lapse cinemicrography was used to directly observe adherent cells derived from the tumor, and macrophages were found to be cytocidal. When grown in the presence of L‐cell conditioned medium no macrophage colonies were found when cultures were established from untreated mice even though most tumor cell colonies contained macrophages. When mice were first treated with 0.8 mg BCNU prior to establishment of the cultures, in order to reduce the frequency of colony‐forming tumor cells, approximately half the colonies found contained only macrophages. These results show that macrophages in this tumor are cytocidal and capable of proliferation.
Surface expression of murine leukemia virus structural polypeptides on host cell and the virion
Authors: Schneider Josef , Hunsmann Gerhard 
Published: February 2007

AbstractThe expression of murine leukemia virus structural polypeptides on the surface of cells producing exogenous Friend leukemia virus, endogenous ecotropic AKR and xenotropic BALB/c virus was investigated. Antisera to Friend virus gp71, p30, p15E, p12 and p10 were employed in a complement‐dependent chromium release assay and to immuno‐precipitate lactoperoxidase iodinated surface polypeptides prior to analysis in polyacrylamide gel electrophoresis. With the latter technique gag‐gene encoded proteins and their precursors were not discovered on the viral and cellular surface membranes. Only env‐gene encoded polypeptides gp85, gp71 and p15E were detectable. p15E is embedded into the lipid membrane. gp85 is formed by disulfide linkage of p15E to surface‐exposed gp71. The ratio of gp71 to gp85 is variable and apparently determined by the host cell. Antibodies of strong cytotoxicity are those against type‐ and group‐specific epitopes of gp71 as well as type‐specific epitopes of p12.
Genetic dissociation of different cellular effects of interferon on myeloid leukemic cells
Authors: Lotem Joseph , Sachs Leo 
Published: February 2007

AbstractMutant clones of mouse myeloid leukemic cells have been used to study the effect of mouse interferon on the expression of different cellular genes. The cell mutants, MGI+D+, MGI+D− and MGI−D−, differed in their competence to be induced to undergo cell differentiation by the normal macrophage and granulocyte protein inducer MGI or the steroid hormone dexamethasone. The growth of all the clones tested was inhibited by interferon, but there was a 20‐fold difference in sensitivity to growth inhibition in different clones. This difference was not associated with the same difference in susceptibility to the cytotoxic effect of cytosine arabinoside and actinomycin D, or with cell competence for the induction of differentiation. The variation in cytotoxic effect of interferon on different malignant cell populations should, therefore, be taken into consideration in the possible clinical use of interferon as an anti‐tumor agent. Some MGI+D+ clones, but none of the MGI+D− or MGI−D− clones, showed, in addition to a high sensitivity to growth inhibition by interferon, a 14‐ and 2‐fold enhancement of the induction of lysozyme by dexamethasone and MGI, respectively, and a slight induction of Fc rosettes with dexamethasone. But interferon had no effect on induction of C3 rosettes, immune phagocytosis and differentiation to mature macrophages or granulocytes. The enhancing effect on lysozyme induction by interferon was also obtained with cordycepin, vinblastine, or 2‐deoxy‐D‐glucose, although neither interferon nor any of these other compounds alone induced any of the differentiation‐associated properties. A MGI+D− mutant, derived from an MGI+D+ clone with an enhancement of lysozyme induction by interferon, showed the same high sensitivity to growth inhibition by interferon as its parental MGI+D+ clone, but there was no enhancement of the induction of lysozyme by MGI or dexamethasone. The results indicate that interferon can exert a selective enhancing effect on the expression of some genes involved in differentiation in clones with the appropriate genotype and that, by using appropriate cell mutants, it is possible to genetically dissociate different cellular effects of interferon.
Primary epstein‐barr virus infections in African infants. II. Clinical and serological observations during seroconversion
Authors: Biggar Robert J. , Henle Gertrude , Böcker Jörg , Lennette Evelyne T. , Fleisher Gary , Henle Werner 
Published: February 2007

AbstractOf 27 Ghanaian infants examined monthly for the first 15 months of life and once more at 21 months, 12 acquired primary Epstein‐Barr virus (EBV) infections by the age of 1 year and 9 others seroconverted during the subsequent period of observation. The seroconversions were not accompanied by significant clinical or physical signs of illness and in none of the infants was a diagnosis of infectious mononucleosis (IM) suspected on the basis of hematologic observations. The 12 early seroconverters, providing the most extensive follow‐up data, showed transient IgM antibody responses to EB viral capsid antigen (VCA) which in some cases initially exceeded the corresponding IgG antibodies in titer. Peak VCA‐specific IgG titers were noted 2 months after seroconversion and were comparable to those seen in IM. Most of the infants developed antibodies to the EBV‐induced early antigen complex which were directed, however, against the R (restricted) component, as observed in Burkitt's lymphoma, and not against the D (diffuse) component, as noted in IM. Low titers of VCA‐specific IgA antibodies emerged in five of the cases. Usually, EBV‐neutralizing antibodies were already present in the first anti‐VCA‐positive serum but antibodies to the EBV‐associated nuclear antigen (EBNA) and antibody‐dependent cell‐mediated cytolysis (ADCC) became detectable only months after seroconversion. No heterophil antibody responses, or at most barely significant ones, were recorded. Attempts to demonstrate EBV in throat swab specimens met with limited success, suggesting a low degree of viral excretion during silent seroconversions. Possible explanations for the differences between clinical, hematologic and serologic responses to primary EBV infections in infancy and later in life are discussed.
Interaction of the B95‐8 and P3HR‐1 substrains of epstein‐barr virus (EBV) with peripheral human lymphocytes
Authors: Steinitz Michael , Bakács Tibor , Klein George 
Published: February 2007

AbstractTwo substrains of the Epstein‐Barr virus derived from the B95‐8 and P3HR‐1 cell lines were studied for their interaction with human peripheral lymphocytes. It has been previously shown that B95‐8 virus has and P3HR‐1 virus lacks lymphocyte‐transforming (“immortalizing”) properties. DNA stimulation induced by B95‐8 virus showed a good correlation with the number of surface Ig‐positive cells. P3HR‐1 virus added before B95‐8 virus completely abolished the stimulation of DNA synthesis. It also prevented EBNA induction by B95‐8 virus. P3HR‐1 virus added after B95‐8 virus diminished DNA stimulation by the latter in a time‐dependent fashion. P3HR‐1 virus did not inhibit DNA stimulation by phytohaemagglutinin but was inhibitory if added before a B‐cell mitogen (Staphylococcus Aureus). The origin of P3HR‐1 virus and its relationship to the transformation process are discussed.
Presence of EBNA in nasopharyngeal carcinoma and control patient tissues related to ebv serology
Authors: Huang D. P. , Ho H. C. , Henle W. , Henle G. , Saw D. , Lui M. 
Published: February 2007

AbstractA search was made for Epstein‐BARR virus (EBV) associated nuclear antigen (EBNA) in touch preparations of fresh biopsy material from 26 carcinomas of the nasopharynx, 39 other tumours of the head and neck, the nasopharyngeal mucosa of 32 patients in whom nasopharyngeal neoplasm had been excluded, and the mucosa from enlarged but non‐neoplastic tonsils removed from 12 patients. EBNA‐positive cells were uniformly detected in the preparations from the undifferentiated and poorly differentiated squamous‐cell carcinomas of the nasopharynx, provided they contained tumour‐cell aggregates. Such cells were not detected in the preparations from the single case of well‐differentiated papillary adenocarcinoma in the nasopharyngeal carcinoma group. There were no moderately or well‐differentiated squamous‐cell carcinomas among the nasopharyngeal carcinoma group. Among other tumours of the head and neck, only three undifferentiated carcinomas of the nasal fossa were found to contain EBNA‐positive cells. None of the nasopharyngeal or tonsillar mucosal preparations contained such cells. These findings confirm the unique regular association of EBNA with nasopharyngeal carcinoma of undifferentiated and poorly differentiated squamous‐cell types (NPC). The EBV‐related serological findings support the value of tests for IgG and IgA antibodies to VCA and EA(D) in the exclusion of NPC in patients with suspicious symptoms and the differentiation between NPC and other tumours of the head and neck. Examination of biopsy specimens for the presence of EBNA‐positive cells or EBV‐DNA is essential, however, for confirmation of the diagnosis.
Failure of selective screning for breast cancer by combining risk factors
Authors: Soini Irma , Hakama Matti 
Published: February 2007

AbstractThe possibilities of selective screening to reduce the costs of screening programmes for breast cancer were considered. Discriminant function analysis was used in an effort to describe a high‐risk group of breast cancer, which will be subjected to screening. The high‐risk group consisted of females with a combination of reproductive and hormone use characteristics. One‐fifth of the breast cancer cases remained in the low‐risk group, when the high‐risk group was small enough (two‐thirds of the population) to yield a meaningful reduction in costs. Selective screening for breast cancer seems to have only limited applicability and is not effective enough for application in public health work.
Activation of complement by spontaneous leukemic cells of AKR mice
Authors: Okada Noriko , Okada Hidechika 
Published: February 2007

AbstractComplement activation via the alternative pathway by tumor cells was tested by rosette formation of human erythrocytes (HuE). Test cells were treated with C4‐deficient guinea‐pig serum (C4DS) in the presence of Mg++ and absence of Ca++, following which 10–30% of lymphoma cells and 10–17% of thymoma cells of spontaneous leukemia in AKR mice formed rosettes. The incidence of rosette formation did not change significantly after transplantation of these cells to other non‐leukemic AKR mice or after in vitro cultivation. Following treatment with fresh C4DS, however, normal AKR mouse thymocytes as well as lymph‐node cells contained only 3–4% HuE‐positive cells. These findings suggest that the ability of non‐specific activation of complement (NAC) may be increased when normal AKR mouse cells become transformed into leukemic cells and/or that the leukemic cells arise from thymus cells which possess NAC ability. This interpretation was further confirmed by the finding that a higher proportion of leukemic cells than of normal thymocytes were lysed by mouse complement in Mg++‐EGTA. The fact that NAC‐positive AKR thymoma cells were lysed effectively by homologous C3H/He plasma agrees with earlier findings that in leukemic AKR mice supplemented with C5 a temporary regression of leukemia occurs.
Effect of light on the hydrocarbon‐DNA adducts formed in hamster embryo cells
Authors: Baird William M. 
Published: February 2007

AbstractPolycyclic aromatic hydrocarbons are metabolically activated and bind to DNA in hamster embryo cell cultures. The effect of light exposure on the DNA adducts formed from two hydrocarbons of different photosensitivities was investigated by exposing cells to light during hydrocarbon treatment and by exposing DNA to light after isolation from cells treated with hydrocarbon in darkness. The total hydrocarbon‐DNA adducts formed per mg DNA in cells treated with the highly photosensitive hydrocarbon 7,12‐dimethylbenz(a)anthracene (DMBA) in the presence of light was less than in cells treated in darkness. No appreciable amounts of hydrocarbon‐DNA adducts were formed in cells treated with a major photo‐oxidation product of DMBA, the 7,12‐endoperoxide, in either the presence or absence of light. DMBA‐deoxyribonucleoside adducts were analyzed by chromatography on Sephadex LH20 columns. Exposure to light of the DMBA‐deoxyribonucleoside adducts obtained by enzymatic degradation of DNA isolated from cells treated with DMBA in darkness converted more than half to photoproducts. DNA that was exposed to light prior to degradation contained less than half as many photoproducts and had an elution profile similar to that obtained from DNA isolated from cells treated with DMBA in the presence of light. With the less photosensitive hydrocarbon benzo(a)pyrene, benzo(a)pyrene‐DNA adducts were identical for DNA from cells treated with benzo(a)pyrene in darkness, DNA from cells treated in the presence of light, and DNA exposed to light after isolation. These results indicate that exposure to light does not alter the mechanism of binding of hydrocarbons to DNA in hamster embryo cells, but does affect the DNA adducts of the photosensitive hydrocarbon DMBA in a similar manner in cells and in isolated DNA.
Effects of carcinogen dose on the characteristics of the tracheal tumor response induced by N‐nitroso‐N‐methylurea in hamsters
Authors: Yarita Tsutomu , Nettesheim Paul 
Published: February 2007

AbstractTracheal tumors were induced by repeated intratracheal exposures to the carcinogen N‐nitroso‐N‐methylurea (NMU), using a catheter system previously described. Carcinogen concentrations of 0.25, 0.50 and 1.0% were employed in 20 or 30 twice‐weekly exposures. Most of the tumors developed in the mid‐portion of the tracheas. Virtually all tumors developed after the end of the 10‐ to 15‐week exposure period. Tumor incidence ranged from 20–94% with mean tumor induction times of 13–46 weeks, depending on NMU concentration and frequency of exposure (i.e., dose). At lower doses, mostly non‐invasive tumors were induced; at higher doses, mostly invasive carcinomas of various histological types (epidermoid, adeno‐, epidermoid‐adeno, and anaplastic large‐ and small‐cell carcinomas) were induced. Adenocarcinomas were most frequent at low NMU concentrations. The possible mechanisms of the carcinogen dose effects are discussed.
Inhibition of morphological transformation induced with N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in cultures of hamster embryo cells by 5′‐bromo‐2′‐deoxyuridine‐photolysis
Authors: Mironescu Stefan G. D. 
Published: February 2007

AbstractThe present study was performed in order to determine whether type III transformed foci induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine originate from the small subpopulation of cells stimulated by the carcinogen to enter DNA synthesis. During the last 30 min of variable treatment periods using different doses of N‐methyl‐N′‐nitro‐N‐nitrosoguanidine, administered alone or in association with the thymidine analogue, 5′‐bromo‐2′‐deoxyuridine (0.98 × 10−5 M), the density‐inhibited monolayers of hamster embryo cells were exposed to fluorescent light and then assayed for abnormal growth patterns by the focus formation method. Mock‐irradiated cultures as well as monolayers whose medium lacked N‐methyl‐N′‐nitro‐N‐nitro‐soguanidine, 5′‐bromo‐2′‐deoxyuridine, or both, served as controls. The cytotoxicity of 5′‐bromo‐2′‐deoxyuridine + N‐methyl‐N′‐nitro‐N‐nitrosoguanidine + photolysis (BMP) protocol on confluent as well as logarithmically growing hamster embryo cells was estimated in single‐cell survival experiments. Plating efficiency determinations have demonstrated that, unlike their actively growing counterparts, confluent hamster embryo cell mono‐layers are extremely resistant to the cytotoxic effects of the BMP protocol. The quantitative transformation assays indicated that: (1) in non‐illuminated cultures addition of 5′‐bromo‐2′‐deoxyuridine to carcinogen‐containing medium does affect transformation frequency of hamster embryo cells in the sense that the incidence of type III foci did not subside at later intervals during the post‐carcinogen administration period as it did in the absence of the analogue; (2) irradiation of N‐methyl‐N′‐nitro‐N‐nitrosoguanidine and halogenated pyrimidine analogue‐treated cultures with fluorescent light practically suppressed transformation; (3) analogueadded and analogue‐removed experiments pointed out that the event(s) on which 5′‐bromo‐2′‐deoxy‐uridine fluorescent light sensitization of morphological transformation largely depends, takes place between 5 and 15 h after N‐methyl‐N′‐nitro‐N‐nitrosoguanidine administration, i.e., during the period of maximal carcinogen‐stimulated DNA synthesis; and (4) neither fluorescent light nor 5′‐bromo‐2′‐deoxyuridine, singly or in combination, were able to transform cultures of hamster embryo cells. These findings are strong indirect arguments for the concept that carcinogen‐induced DNA synthesis and the initiation of transformed clones are causally related.
Differences in the capacity of simian virus 40 (SV40) tumor antigens on cells, membranes and in soluble form to induce transplantation immunity in hamsters and mice
Authors: Law Lloyd W. , Takemoto Kenneth K. , Rogers Michael J. , Henriksen Ole , Ting Robert C. 
Published: February 2007

AbstractThe immunogenicity of the SV40 tumor‐specific transplantation antigen (TSTA) on cells, cell particulates and solubilized membranes was studied in mice and in Syrian hamsters. Immunizations were done with various concentrations of tissue‐culture‐passaged, non‐virus‐releasing transformed cells, purified cell membranes and in some cases purified nuclei and papain‐solubilized membranes obtained from several species, including the mouse, hamster, man, and sheep. All transformed cell lines were T‐antigen‐positive. The immunosensitive mKSA line of BALB/c mice and the immunosensitive SV34 cell line of the hamster were used for tumor challenge. All materials, regardless of source and of type of preparation, were strikingly immunogenic in the mouse but only SV40 virus and SV34 (hamster) cells provided protection against tumor cell challenge in the hamster. Also, in a limited study, BKV‐transformed hamster cells and purified cell membranes and JCV‐transformed hamster cells were found to be immunogenic by the tumor rejection assay in the mouse but not in the hamster. SV40 immunization did not protect the hamster against BKV‐ and JCV‐transformed hamster cells. These results are discussed in terms of possible different specificities resident on the TSTA molecule.
Virus‐induced papillomas of the alimentary tract of cattle
Authors: Jarrett W. F. H. , Murphy J. , O'Neil B. W. , Laird Helen M. 
Published: February 2007

AbstractAn abattoir survey was carried out to determine the incidence and aetiology of squamous papillomas of the alimentary tract of cattle in Scotland and North England as they were suspected of being involved in the genesis of alimentary carcinoma in certain localized geographical areas. A total of 7,746 cattle of a wide age range was examined. Various subsets of this number were subjected to analyses of certain specific factors. The calculated overall incidence was 19% and the detailed site incidence and tumour multiplicity are given. The sites at which papillomas were found were identical with those at which carcinoma had been noted in animals from a high‐cancer area. The number of sites affected by papilloma and the tumour multiplicity were much lower in the general population than in the high‐cancer area. Inclusion bodies, identified by electronmicroscopy as virus, were found in tumour cell nuclei and a typical papilloma virus was purified from the tumours. The structure of the tumours is described and the possible plurality of bovine papilloma‐viruses is discussed in the light of recent findings in the human viruses. The general interest of a naturally occurring and geographically localized oncogenic system, in which an environmental carcinogen and a virus might be involved, is extended.