bluuebunny/crossref_metadata_2025_split huggingface dataset:
High terminal deoxynucleotidyl transferase activity in pediatric patients with acute lymphocytic and acute myelocytic leukemias
Authors: Srivastava B. I. Sahai , Khan Sohaib A. , Minowada Jun , Freeman Arnold 
Published: February 2007

AbstractSpecificity of TdT5 as a marker for ALL was evaluated by determining its activity in cells from normal control subjects and from 35 pediatric patients with ALL, AML, Hodgkin's disease and disseminated Burkitt's lymphoma. We evaluated the DNA polymerase activity, cell surface pheno‐types (E rosettes, EAC rosettes, SmIg and Ia‐like, HTLA and cALL antigens), and hematological and cytochemical characteristics in both the normal and patient groups. DNA polymerase α+β and DNA polymerase γ activity were indiscriminately high in all immature cells as found in ALL, AML, Burkitt's lymphoma and phytohemagglutinin‐stimulated normal lymphocytes, when compared to mature leukocytes found in normal individuals or in patients whose cancer was in remission. High TdT activity was found in 24 of 26 T and non‐T/non‐B ALL patients in active phase as well as in two of three AML patients one of whom had Auer rods. Thus, TdT, although valuable for monitoring ALL patients, may have limitations in separating AML from ALL.
Conditions required for induction of murine p30 by herpes simplex virus
Authors: Isom H. , Colberg A. , Reed C. , Rapp F. 
Published: February 2007

AbstractMouse cells (line N clA cl10) contain 1.2–2.5 ng murine leukaemia virus (MuLV) p30 antigen/mg of protein; this amount of antigen is measurable by competition radioimmunoassay (RIA) but is not detectable by indirect immunofluorescence (IF). Infection of N clA cl10 cells with herpes simplex virus type 2 (HSV‐2) induces expression of MuLV p30. Induction by HSV‐2 does not require either cell or virus DNA synthesis and is optimal 8 h post infection when cells at 50–70% confluence are infected at a multiplicity of infection (MOI) of 5–8 PFU/cell. At an MOI of 2.5, 70–80% of the cells express HSV antigens while none of the cells express p30; at an MOI of 5.0, 70–80% of the cells express HSV antigens but 55% of the cells express p30. Using the conditions reported in this paper for preparation of competing antigen, induction of p30 by HSV‐2 (strain 333) infection is not measurable by competition RIA.
Stimulatory effect of cigarette smoke on the metabolism and covalent binding of benzo(a)pyrene in the trachea of the rat
Authors: Simberg Niklas , Uotila Pekka 
Published: February 2007

AbstractThe activity of aryl hydrocarbon hydroxylase (substrate: benzo(a)pyrene) was increased in the tracheas of rats exposed to cigarette smoke for 1 h daily for either 1 or 10 days. However the degree of increase in activity was lower in the trachea than in the lung. After a single exposure, activity in the trachea was at its highest level 12 h following exposure (3.2‐fold compared to the control), but had returned to the control level within 24 h. Also, the amounts of covalently bound metabolites of benzo(a)pyrene were increased (2‐fold) in nucleic acid and protein fractions of the trachea, when the rats were killed 12 h after a single cigarette smoke exposure. No significant changes in the activity of epoxide hydratase (substrate: styrene oxide) could be detected in the trachea. After repeated exposures the activity of UDP‐glucuronosyltransferase (substrate: methylumbelliferone) was increased (1.7‐fold) in the trachea.
Non‐phorbol mouse skin tumor promoters do not mimic phorbol myristate acetate in its effects on chick embryo fibroblasts
Authors: Driedger Paul E. , Blumberg Peter M. 
Published: February 2007

AbstractPhorbol esters, the most potent class of tumor promoter for mouse skin, have been shown to cause loss of the large external transformation‐sensitive glycoprotein LETS1 from the surface of chicken embryo fibroblasts (CEF) and to cause an increase in the rate of deoxyglucose (DG) transport by these cells. Several compounds which promote mouse skin tumors but which are structurally unrelated to the phorbol esters were tested for their abilities to cause loss of LETS from CEF and to stimulate DG transport. Of the seven compounds tested, only oleic acid (at 140 μM) caused a decrease of more than 20% in LETS, as measured by lactoperoxidase‐catalyzed surface radioiodination. Phenol at 1 mM caused a 70% increase in LETS levels. Only three agents, anthralin, lauric acid and limonene, caused increases in DG transport. Iodo‐acetic acid and canthridin were inactive in both assays. None of the compounds affected CEF LETS levels or DG transport to the extent that the phorbol esters do. Palmitic and stearic acids, which are structurally similar to oleic acid but which do not promote mouse skin tumors, were inactive in both assays. The lack of correspondence between the effects on CEF of the phorbol esters and the non‐phorbol promoters suggests that these two groups may have different mechanisms of action.
Immunological characteristics of leukemia and lymphoma in allogeneic cell immunity: Growth of syngeneic tumors in rats immunized with allogeneic cells
Authors: Hosokawa Masuo , Yamashita Tetsuro , Gotohda Eiki , Takeichi Noritoshi , Kodama Takao , Kobayashi Hiroshi 
Published: February 2007

AbstractThe growth of transplanted tumors was strongly inhibited in syngeneic Wistar King Aptekman (WKA) rats immunized with allogeneic tumor cells from Donryu rats. This phenomenon of non‐specific immunity against tumors is referred to as “allogeneic cell immunity”. However, an exception to the “allogeneic cell immunity” was observed in leukemias and lymphomas. Four transplanted leukemia or lymphoma lines were not inhibited in syngeneic rats immunized with allogeneic tumor cells. Furthermore, immunization with allogeneic leukemic cells had only a relatively weak inhibitory effect upon a syngeneic fibrosarcoma and no inhibitory effect upon leukemias. In WKA rats immunized with allogeneic lymphoid cells from Donryu rats, the growth of fibrosarcoma, but not of lymphoma, was inhibited. Using transplantation experiments, both fibrosarcoma and lymphoma were defined as antigenic tumors in WKA rats. Transplantation of mixtures of syngeneic tumor cells and allogeneic tumor cells in WKA rats confirmed the above findings. These results revealed that leukemia and lymphoma differ from non‐leukemic tumors in regard to “allogeneic cell immunity”.
Identification and behavior of the precipitating BLV antibodies in sera of leukotic cattle
Authors: Matthaeus W. , Kaaden O. R. , Frenzel B. , Schlotterer E. 
Published: February 2007

AbstractPrecipitating bovine leukemia virus antibodies isolated from bovine leukemic sera by ion‐exchange chromatography, gel filtration and affinity chromatography were identified as immunoglobulins of the IgG1 subclass and IgA class. They proved to be different with regard to molecular size and electrical charge. Immunoglobulins IgG2 and IgM as well as low‐molecular components ranging in the micro‐globulin regions (<4S) failed to precipitate BLV antigens. Individual bovine leukemic sera showed differing precipitating activities against p24 and gp69 antigens. Precipitating monospecific gp69 antibodies represented exclusively the IgG1 subclass. Some unidentified antigens in disrupted BLV preparations showed serological relationship to p24 and gp69, respectively.
DNA damage in liver, colon, stomach, lung and kidney of BALB/c mice treated with 1,2‐dimethylhydrazine
Authors: Brambilla G. , Cavanna M. , Parodi S. , Sciabà L. , Pino A. , Robbiano L. 
Published: February 2007

AbstractDNA single‐strand breaks induced in various organs of BALB/c mice by treatment with a single dose of 1,2‐dimethylhydrazine (DMH) were studied by means of the alkaline elution method modified in order to allow the evaluation of DNA damage in vivo with no need of radioactive prelabelling. DNA damage was detected in liver, lung, kidney, stomach and colon mucosa, with the liver showing the greatest amount of damage. Its degree was dependent on the dose and route of administration. A differential effect was evident in colon mucosa from Swiss and C57BL/6 mice which are respectively susceptible and resistant to the induction of bowel tumors by DMH. The higher degree of DNA damage found in liver in comparison with colon mucosa is consistent with the previously reported higher degree of DNA methylation, but does not correlate with the specificity of this carcinogen in inducing tumors of the large intestine in mice given repeated subcutaneous injections.
Cellular basis of induced α‐fetoprotein synthesis by hepatocytes of adult mouse after hepatotoxic injury and partial hepatectomy
Authors: Mohanty Mira , Das P. K. , Mittal Asha , Nayak N. C. 
Published: February 2007

AbstractThe dynamics of α‐fetoprotein (AFP) production by hepatocytes following different experimental manoeuvres that are known to induce regeneration of the liver was studied in young adult mice by simultaneous identification of dividing cells arrested during mitosis and of cells containing immuno‐histochemically detectable AFP. After 70% hepatectomy AFP was produced by a few, largely periportally located hepatocytes, following waves of brisk and active cell division. Carbon tetrachloride (CCl4)‐induced hepatic injury, on the other hand, led to participation of a relatively larger number of cells in early AFP synthesis preceding a less extensive cell proliferation. Initially, AFP‐producing cells were located in the peripheral part of the lobule but later they were more centrally placed, most often surrounding the zone of necrosis. Cells in mitosis often contained large amounts of AFP. CCl4 administration 48 h after 70% hepatectomy resulted in extensive AFP production by approximately a quarter of all surviving liver cells, although the concurrent rate of cell division was low. Intoxication with dimethylnitrosamine showed a pattern identical to that of hepatectomy but both cell division and AFP production were of comparatively lower magnitude. It is concluded that at least two distinct modes exist for augmented synthesis of AFP by hepatocytes of adult animals. In one, pre‐existent cells are stimulated to produce the protein before and irrespective of cell division while in the other, small amounts are synthesized by newly generated cells. Combination of the two mechanisms results in high levels of AFP production by stimulation of a large number of young hepatocytes.
Metabolism and DNA binding of polycyclic aromatic hydrocarbons by human diploid fibroblasts
Authors: Baird William M. , Diamond Leila 
Published: February 2007

AbstractThe metabolism of three carcinogenic polycyclic aromatic hydrocarbons was measured in mid‐(population doubling levels of 20–39) and late‐(population doubling levels > 55) passage cultures of WI‐38 human diploid fibroblasts. Cultures of mid‐and late‐passage cells metabolized these hydrocarbons to both water‐ and organic solvent‐soluble derivatives. In stationary cultures, the same amounts of benzo(a)pyrene (BP) and 3‐methyl‐cholanthrene were metabolized per cell, but late‐passage cells metabolized only one‐third as much 7,12‐dimethylbenz(a)anthracene per cell as mid‐passage cells. The DNA adducts formed from BP in WI‐38 cells were examined by chromatography of enzyme‐degraded DNA samples on Sephadex LH20 columns. On columns eluted with methanol‐water gradients, the [3H]BP‐deoxyribonucleoside adducts eluted in the same volume as the product peak isolated from DNA that had been reacted with 7,8‐dihydroxy‐9,10‐epoxy‐7,8,9,10‐tetrahydroBP. On columns eluted with borate‐containing methanol‐water gradients, 62% of the cellular products eluted in the same volume as the product peak isolated from DNA that had been reacted with (±) 7α,8β‐dihydroxy‐9β,10β‐epoxy‐7,8,9,10‐tetrahydroBP (the anti‐isomer) and 35% eluted in the same volume as a product peak isolated from DNA that had been reacted with (±) 7α,8β‐dihydroxy‐9α,10α‐epoxy‐7,8,9,10‐tetrahydroBP (the syn‐isomer). Thus, more than one type of DNA adduct is formed in these cells, possibly through the reacticn of different isomers of this BP‐diol‐epoxide with DNA.
Some mechanisms involved in cancer cell detachment by necrotic material
Authors: Weiss Leonard 
Published: February 2007

AbstractFactors influencing cell detachment are thought to play a role in metastasis and invasion. Previous studies on cylinders punched from Walker 256 (W‐256) tumors growing in rats showed that detachment of viable cancer cells was facilitated by their proximity to necrotic regions and exposure to a necrotic extract. By the use of pure cultures of W‐256 cells, it is shown that necrotic extracts which are rich in lysosomal hydrolases act directly on W‐256 cells, facilitating their in vitro detachment. Lysosomal enzymes have previously been shown to facilitate cell detachment. The partial inhibition of this process by hydrocortisone suggests that the extracts also act by labilizing the W‐256 cell lysosomes; this enzyme release is also demonstrable by direct assay. Although secondary lysosomes could not be visualized in the W‐256 cells, both they and macrophages release lysosomal hydrolases on freeze‐thawing, and could both account for the high enzyme content of the necrotic regions, by a process of continuous secretion and/or cell input. Histologic examination of perinecrotic and peripheral regions of tumors showed a higher proportion of macrophages in the former, which is thought to be mainly due to differential trapping of the macrophages. The results emphasize the functional properties of necrotic regions of tumors and the necessity of referring to specific regions of the same tumor when referring to its metastatic and other properties.
Relevance of circulating immune complexes in childhood acute lymphoblastic leukaemia
Authors: Clague Roy B. , Kumar Shant , Hann Ian M. , Jones Patricia H. Morris , Holt P. J. Lennox 
Published: February 2007

AbstractCirculating immune complexes have been measured using the (125I)C1q binding test in 216 sera from 135 children with acute lymphoblastic leukaemia. Increased circulating immune complexes were detectable in 10.7% of the sera and 10.4% of the children. There was no correlation between the presence of circulating immune complexes and prognosis, but a strong correlation with a history of recent infection.
Genetics of SV40 T‐antigen expression: Studies of twins, heritable syndromes and cancer families
Authors: Blattner W. A. , Lubiniecki A. S. , Mulvihill J. J. , Lalley P. , Fraumeni J. F. 
Published: February 2007

AbstractSusceptibility of human skin fibroblasts to SV40 virus infection has been suggested as a marker of cancer risk. To evaluate the role of heritable factors in the regulation of SV40 T‐antigen, fibroblasts from 9 pairs of identical twins and 129 members of cancer‐prone families, including 16 with cancer, were tested in a 3‐day immunofluorescence assay. In the twin study, the variance of T‐antigen values was significantly less in identical than in fraternal or non‐twin sibs, suggesting a heritable component in the regulation of SV40 infection. In the families, T‐antigen values of parents and children were compared to models of Mendelian inheritance. At least three modes of inheritance—autosomal dominant, recessive, and X‐linked—were observed. The distribution of offspring values compared to those of their parents suggested that interaction of multiple genetic factors influences the T‐antigen value in individual patients. With the exception of Fanconi's anemia, the values for patients with cancer or predisposing syndromes were not uniformly elevated. The utility of this assay as a marker of cancer risk appears limited because of the complexity of factors that influence T‐antigen expression in individual cases.
Primary epstein‐barr virus infections in african infants. I. Decline of maternal antibodies and time of infection
Authors: Biggar Robert J. , Henle Werner , Fleisher Gary , Böcker Jörg , Lennette Evelyne T. , Henle Gertrude 
Published: February 2007

AbstractThirty‐one infants living in Accra, Ghana, an area endemic for Burkitt's lymphoma, were visited at monthly intervals for the first 15 months of life and once again at 21 months. Sera obtained at each visit were tested for antibodies to Epstein‐Barr virus (EBV) capsid antigen (VCA), EBV‐induced early antigens (EA) and EBV‐associated nuclear antigen (EBNA) by immunofluorescence techniques as well as for EBV‐neutralizing antibodies and antibody‐dependent cell‐mediated cytolysis. All infants had maternal antibodies to VCA at 1 month of age and the majority also antibodies detected by the other tests, except anti‐EA. The maternal anti‐VCA titers declined in subsequent months according to a half‐life of nearly 5 weeks. Depending on the initial titers, all infants became seronegative for all antibodies by 2–8 months of age, with anti‐VCA persisting longest. The earliest primary EBV infection occurred in the third month after maternal antibodies to VCA had become non‐detectable. By 12 months of age, 44% of the infants had seroconverted, by 15 months, 62% and by 21 months, 81%. There was no seasonal variation in the incidence of infections. Infants from families of the lowest socio‐economic level tended to become infected somewhat earlier than those from better situated families (p = 0.22) but no other factors, such as household size or crowding, seemed to be associated with enhanced risk of early infection.
Expression of oncofetal antigens on murine sarcomas characterized for expression of endogenous MuLV
Authors: Pollack Sylvia B. 
Published: February 2007

AbstractA rabbit antiserum raised by repeated immunization with BALB/c fetuses obtained at 10–14 days of gestation was used to search for oncofetal antigens (OFA) in murine sarcomas which had previously been characterized for the expression of endogenous murine leukemia virus (MuLV). Iodinated protein A from staphylococcus aureus (IPA) was used to quantitate binding of the antiserum to cultured tumor or fetal cells or to saline extracts of tumors and fetuses. Use of the “antigen” extracts facilitated the assay: the extracts bound to plastic and served as targets for the binding assay, eliminating the need to establish tumors in culture. After absorbtion in vitro and in vivo with adult tissues the rabbit antiserum bound to day 10–14 fetal cells and extract but not to endogenous MuLV (BALB virus 1). The antiserum bound equally well to MuLV‐negative and MuLV‐positive sublines of MCA‐induced sarcomas 1420 and 1414 but not to Moloney sarcoma cells and MCA‐induced sarcoma 1386. Thus, the absorbed antiserum detects a class of common cross‐reacting antigens which are serologically distinct from MuLV‐associated antigens.
Longitudinal study of epstein‐barr virus antibody titers and excretion in pediatric patients with Hodgkin's disease
Authors: Lange Beverly , Arbeter Allan , Hewetson John , Henle Werner 
Published: February 2007

AbstractNineteen pediatric patients with Hodgkin's disease (HD) who had experienced primary Epstein‐Barr virus (EBV) before, or in one case after, diagnosis, were studied longitudinally for changes in the titers and spectra of EBV‐related antibodies, excretion of EBV into the oropharynx, the number of EBV‐carrying lymphoid cells in the peripheral blood, and clinical signs and symptoms suggestive of reactivation of the latent virus. The incidence and geometric mean titers of IgG antibodies to viral capsid antigen (VCA) in the HD patients at the time of diagnosis and in the controls were similar. The anti‐VCA titers of the patients rose above control levels during and after therapy and remained elevated for up to 7 years of observation. At no time were heterophil or VCA‐specific IgM antibodies detected. Antibodies to EBV‐induced early antigens were more common in patients (ultimately 80%) than in controls (9%). In contrast, antibody levels to EBV‐associated nuclear antigen were disproportionally low in the patients. Excretion of EBV was noted at increased frequency in the patients but the number of circulating, EBV‐carrying lymphoid cells was the same as in controls. No discrete clinical syndrome was associated with rising antibody titers or viral excretion. While these results are best explained by a presumed reactivation of the persistent EBV infection by immunosuppressive effects of HD or its therapy, they have not provided direct evidence for this suggestion.
Stimulation of human NK‐cell activity by cultured cells. I. Response of normals
Authors: Grohmann P. , Holmes W. , Porzsolt F. , Quirt I. , Miller R. G. , Phillips R. A. 
Published: February 2007

AbstractNatural cell‐mediated cytotoxicity, observed on co‐cultivation of peripheral blood lymphocytes (PBL) with malignant melanoma tumor cells (M4), is described. The activity was inhibited when PBL were cultured in autologous serum. Studies using competitive inhibition with cold targets and stimulation of PBL with other tumor cell lines failed to detect specificity.
Frequent elevation of tissue polypeptide antigen in the sera of workers exposed to bladder carcinogens
Authors: Kumar Shant , Wilson Philip , Brenchley Paul , Taylor Geoffrey , Björklund Bertil , Eklund Gunnar 
Published: February 2007

AbstractA group of 108 male workers previously exposed to bladder carcinogens and a group of 26 patients with carcinoma of the bladder differed significantly from a control group comprising 63 healthy male donors with respect to their levels of tissue polypeptide antigen (TPA). The risk group exhibited 4–6 times more frequent elevations of TPA than did the group of healthy donors.
Carcinogenesis of N‐nitrosodiethylamine (DENA) in chickens and domestic cats
Authors: Schmähl D. , Habs M. , Ivankovic S. 
Published: February 2007

AbstractThe environmental carcinogen N‐nitrosodiethyl‐amine (diethylnitrosamine, DENA) has been found to be carcinogenic in 18 animal species. In this study we demonstrate that, after intramuscular injection in chickens, it induces hepatocellular carcinomas of the liver and adenocarcinomas of the kidney. Oral administration in domestic cats causes malignant hepatomas and tumors of the esophagus and kidney. Since DENA is carcinogenic in all species in which it has been tested adequately it can be expected to be a human carcinogen, too.
Differentiation of mouse myeloid leukemia cells is inhibited by a factor from non‐differentiating leukemia cells
Authors: Okabe Junko , Hayashi Moriaki , Honma Yoshio , Hozumi Motoo 
Published: February 2007

AbstractMouse myeloid leukemia cells (MI) were induced to differentiate by a factor(s) (D‐factor) in ascitic fluid. An inhibitory activity (I‐activity) for the induction of differentiation was present in conditioned medium and lysate of MI cells resistant to the D‐factor. The I‐activity was non‐dialyzable, heat‐labile and protease‐sensitive. Most of the activity was recovered in the fraction precipitated with 30–50% saturated ammonium sulfate. The fraction inhibited induction of phagocytic activity, migrating activity and morphological changes in MI cells, which are typical properties of differentiated MI cells. Low levels of I‐activity were detected in conditioned medium or lysate of MI cells sensitive to the D‐factor. The resistant MI cells were sensitized to the D‐factor by treatment with a low concentration (5–10 ng/ml) of actinomycin D. The I‐activity in conditioned medium of actinomycin D‐treated resistant cells decreased with development of sensitivity to the D‐factor. These results suggest that production of the I‐activity in the resistant cells is closely associated with resistance of the MI cells to the D‐factor.