bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detection of bovine leukemia virus antigen in urine from naturally infected cattle
Authors: Gupta Phalguni , Ferrer Jorge F. 
Published: February 2007

AbstractA competitive radioimmunoassay was used to detect the major internal protein (p25) of bovine leukemia virus (BLV) in urine from infected cattle. Whole urine samples from six out of seven infected cattle were found to contain the BLV p25 antigen. Analysis of different fractions of urine indicated that p25 was present in a soluble form as well as in the high‐speed pellet, but not in the low‐speed pellet. Similar results were obtained with urine samples collected from a BLV‐infected cow by catheterization of the bladder.
Incidence of childhood leukemia in shanghai
Authors: Li Frederick P. , Jin Fan , Tu Chi‐Tao , Gao Yu‐Tang 
Published: February 2007

AbstractData of the Shanghai Tumor Registry were examined for incidence rates of leukemia among children, ages 0–14 years. Between 1972 and 1978, leukemia developed in 344 children; 175 (52%) had acute lymphocytic leukemia. The incidence rates were 4.5 per 100,000 boys and 3.3 per 100,000 girls. The incidence of leukemia peaked between 2 and 7 years of age.
Establishment and characterization of a new leukaemic T‐cell line (Peer) with an unusual phenotype
Authors: Ravid Zohar , Goldblum Natan , Zaizov Rina , Schlesinger Michael , Kertes Tamar , Minowada Jun , Verbi Winston , Greaves Melvyn 
Published: February 2007

AbstractWe report the isolation and establishment in continuous culture of a human lymphoid cell line (Peer) from a case of T‐leukemia. The Peer cell line lacks some typical cell‐surface properties of T cells, namely sheep erythrocyte rosette formation and reactivity with two anti‐T‐cell sera, but has focal acid phosphatase and does express two other T‐cell antigens, one defined by a monoclonal antibody, the other related to a T‐cell subset (TH2). The cells are negative for B‐cell markers (Smlg or cytoplasmic μ Fcγ and C3 receptors, mouse erythrocyte rosettes) and EBV (EBNA). In addition, the Peer cell does not possess the typical phenotypic markers of “non‐B, non‐T” leukemia: cALL and la‐like antigens, and the cytoplasmic hexosaminidase isoenzyme I, but is positive for terminal deoxynucleotidyl transferase by enzymatic and immunofluorescent criteria. The cell line requires exogenous L‐asparagine for adequate growth in culture, a property known to be characteristic of certain T cells but not of B cells. The Peer cell line appears to have a maturation arrest at a developmental stage intermediate between the cortical thymocyte and a mature T‐cell subset and to have lost some T‐cell differentiation features.
Surface immunoglobulins on Burkitt's lymphoma biopsy cells from 91 patients
Authors: Gunvén Peter , Klein George , Klein Eva , Norin Torsten , Singh Surjit 
Published: February 2007

AbstractOne hundred and fourteen biopsies from 91 cases of African Burkitt's lymphoma were examined by immunofluorescence methods for the presence of surface‐associated mu, gamma, delta, kappa and lambda chains, as well as for the Fc region of gamma chains and for βic. Only 5% of the biopsies were surface‐Ig‐negative; 18% were negative for mu chains and 61% for gamma chains. Delta chain staining was absent, or borderline in a few tumors. Mu chains, gamma chains in a few highly reactive tumors and, in many cases, the predominant light chain seemed to be clonal markers. They gave no convincing evidence of more than one cell clone, either within single tumors or within syn‐ or metachronous tumors in one individual. Gamma chains in moderately stained tumors, Fc and βic correlated with each other and the first two reactivities decreased after incubation at low pH, indicating that their presence resulted from outside coating of the cells. The results indicated that one clone of B cells is involved in Burkitt's lymphoma in the large majority of cases. This clone is in a state of differentiation at which surface delta chains are not expressed. No prognostic information resulted from the analysis of the markers studied.
A prospective study on the development of hepatocellular carcinoma from liver cirrhosis with persistent hepatitis B virus infection
Authors: Obata Hiroshi , Hayashi Naoaki , Motoike Yoji , Hisamitsu Toju , Okuda Hiroaki , Kobayashi Seiichiro , Nishioka Kusuya 
Published: February 2007

AbstractWe made a prospective study on the development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis with hepatitis B virus infection from April, 1973 to December, 1977. Seven out of 30 patients (23%) with hepatitis B surface antigen (HBsAg)‐positive cirrhosis developed HCC. On the other hand, only 5.9% of the patients with HBsAg‐negative liver cirrhosis developed HCC. These patients were classified into three groups according to their anti‐HB core (anti‐HBc) titers. When the anti‐HBc titer, expressed as a dilution of serum, was 210 or more (Group I),20‐24 % of the liver cirrhosis patients developed HCC either with or without a detectable amount of HBs Ag present in the sera. When the anti‐HBc titer was 29 or less (Group II), only 0–5.7% developed HCC. There was no significant difference between this and the anti‐HBc and HBsAg‐negative group (Group III), which was 4.4%. In five individual cases from group I, HBsAg was detected in serum, and in biopsies of liver cells, before HCC could be detected by angiography and/or rising levels of alphafetoprotein (AFP).In all of these cases, the anti‐HBc titer was higher than 210 throughout the observation period, even before the development of HCC. These findings indicate that active virus proliferation in chronic hepatitis B virus infection precedes the development of HCC as indicated by a higher anti‐HBc titer. Therefore we have prepared these studies to show the pathogenic role of hepatitis B virus in the development of hepatocellular carcinoma.
Restricted expression of endogenous N‐Tropic XC‐positive leukemia virus in hybrids between G and AKR mice: An effect of the Fv‐4r gene
Authors: Odaka Takeshi , Ikeda Hidetoshi , Akatsuka Toshitaka 
Published: February 2007

AbstractG mice carrying the Fv‐4r gene are resistant to exogenous infections of various strains of ecotropic MuLVs (Suzuki, 1975). The expression of endogenous N‐tropic XC‐positive virus was studied in the progency of a cross between G and AKR mice. In the F1, mice, the virus expression was almost completely supressed, and no leukemia developed during I year of observation. Results of successive backcrossings with AKR mice indicated that a single dominant gene, the Fv‐4r, suffices for supression. It can be concluded that the extensive growth of N‐tropic XC‐positive virus is a prerequisite for leukemia development in AKR mice.
Separation of different molecular forms of macrophage‐ and granulocyte‐inducing proteins for normal and leukemic myeloid cells
Authors: Lotem Joseph , Lipton Jeffrey H. , Sachs Leo 
Published: February 2007

AbstractIt is shown that serum of mice treated with endotoxin (ES) contains three separable and functionally distinct forms of macrophage‐ and granulocyte‐inducing (MGI) proteins. One form (MGI‐IM) induced the formation of macrophage colonies from normal bone‐marrow cells and showed on gel filtration an apparent molecular weight of 300,000; a second form (MGI‐IG) induced the formation of granulocyte colonies from normal bonemarrow cells and had an apparent molecular weight of 45–100.000; and the third form (MGI‐2) induced the normal differentiation of MGI+D+ myeloid leukemic cells to macrophages and granulocytes and had an apparent molecular weight of 28,000. Studies on the time course of the decrease of these three activities in ES have indicated that MGI‐2 was more readily inactivated in vivo than MGI‐IM and MGI‐IG. The MGI‐IM in ES isolated after gel filtration was completely neutralized by an antiserum to MGI‐I from mouse L‐cells, whereas the isolated MGI‐IG and MGI‐2 were not affected by this antiserum. Gel filtration under dissociating conditions (6 M guanidinium chloride) resulted in a reduction of the apparent molecular weights of MGI‐IM from 300,000 to 42,000, and of MGI‐IG from 45–100,000 to 28,000, while it produced no change in the 28,000 apparent molecular weight of MGI‐2. Similar studies with conditioned medium produced in vitro from mouse lung and peritoneal macrophages showed that in these conditioned media, MGI‐I (both G and M) in the native form had an apparent molecular weight of 41,000 and MGI‐2 of 24,000, and that both MGI‐I and 2 had an apparent molecular weight of 24,000 under dissociating conditions. The results indicate that MGI‐I exists in serum in vivo and in these conditioned media as aggregated proteins, whereas MGI‐2 does not, and that macrophages and lung tissue are not the only source of the MGI proteins found in ES. It is suggested that all three forms of MGI activity are derived from one precursor protein; that only the MGI‐2 form assayed on leukemic cells should be used for treatment based on the induction of normal cell differentiation in myeloid leukemia; and that MGI‐2 may serve as a survey mechanism for inducing differentiation in myeloid leukemic cells that have lost their responsiveness to the MGI‐I molecules that control the viability, proliferation and differentiation of normal myeloblasts.
Quantitation of extracts containing tumour angiogenesis factor (TAF) by radioimmunometric and radioimmunoassays
Authors: Schor Ana M. , Kumar S. , Phillips P. J. 
Published: February 2007

AbstractAn antiserum which is able to inhibit TAF‐induced neovascularization in vivo(TAF antiserum) was used to develop two quantitative assays for TAF‐containing tumour extracts (tumor TAF).I) Radioimmunometric assay (RIMA): the IgG of the TAF antiserum was labelled with 125I. An excess of 125I‐IgG was incubated with increasing concentrations of tumour TAF and the antigen‐bound fraction was precipitated by addition of Clq. 2) Radioimmunoassay (RIA): an excess of iodinated antigen (tumour TAF) was incubated with TAF antiserum diluted so that binding in the absence of unlabelled antigen represented 70–40% of the maximum binding. When tumour TAF was added, competition between labelled and unlabelled antigen for the TAF antibody binding sites resulted in displacement of the former by increasing concentrations of the latter. A second antibody was used to precipitate the bound labelled antigen. Of the two assays, the RIMA was the more sensitive and, due to the lack of a purified antigen, allowed standardization of the results in a more accurate manner. Our data show that there was a good correlation between the ability of tumour TAF to induce angiogenesis in vivo and the degree of antiserum binding detected in vitro by both assays. Preparations containing TAF, whatever the source (i.e. human or animal tumours or tissue culture) shared common antigenic determinants. It is suggested that the quantitative assays should prove valuable in determining the clinical relevance of TAF as a tumour marker.
Tumor metastases and cell‐mediated immunity in a model system in DBA/2 mice X. Immunoselection of tumor variants differing in tumor antigen expression and metastatic capacity
Authors: Schirrmacher V. , Bosslet K. 
Published: February 2007

AbstractWe previously described morphological, functional and antigenic differences between a chemically‐induced DBA/2 lymphoma, Eb, and a spontaneous variant, ESb, which arose in 1968 and had highly increased metastatic capacity. Now we present evidence that the two cell lines, in spite of the differences observed, are still related. (I) Shifts from Eb to ESb can be reproduced after II years. They occur during routine i.p. transplantation, especially when high cell numbers are passaged. (2) ESb variant cells can be recovered from Eb tumor populations after immunoselection in vivowith specific anti‐Eb cytolytic T lymphocytes (CTL).(3) Parental‐type Eb cells can be isolated from ESb tumor populations after immunoselection in vitro with specific anti‐ESb CTL Ten ESb cells mixed with 106Eb cells and inoculated s.c. caused a shift in the mortality curve suggesting that a possible contamination of the Eb population with preexisting ESb variant cells was less than I in 100,000.
Cytogenetic studies on abelson‐virus‐induced mouse leukemias
Authors: Klein George , Ohno Shinsuke , Rosenberg Naomi , Wiener Francis , Spira Jack , Baltimore David 
Published: February 2007

AbstractThe karyotype of Abelson‐virus‐induced murine leukemias was studied by G‐banding. In contrast to the regular trisomy of chromosome 15 in most murine T‐cell leukemias, Abelson leukemias were purely diploid, and remained diploid for up to seven consecutive passages in vivo. The hypothesis is advanced that integration into the recipient cell of the DNA copy of the large cellular insert, carried by the Abelson virus, may perform a function similar to the effects of gene duplication by trisomy in the more slowly developing murine leukemias.
In vivo splenic irradiation eradicates suppressor T‐cells causing the regression and inhibition of established tumor
Authors: Enker Warren E. , Jacobitz Janet L. 
Published: February 2007

AbstractSplenic irradiation has been employed in tumor‐bearing animals to eradicate non‐specific, spleen‐seeking suppressor T cells, and to inhibit established tumor growth. MC1315 tumor‐bearing BALB/c mice were treated with 400 R splenic irradiation. Untreated mice or mice receiving 400 R splenic irradiation plus reconstitution with syngeneic spleen cells served as controls. Statistically significant inhibition of tumor growth, regression of established lethal tumor, and the disappearance of suppressor cell activity from the spleens of tumor‐regressed mice were observed. Tumor growth inhibition was statistically significant at the p < 0.001 level. We postulate that non‐specific, spleen‐seeking, radiation‐sensitive suppressor T cells are in a large measure responsible for mediating progressive tumor growth. By taking advantage of their radiosensitivity and by exploiting their spleen‐seeking nature, we have achieved significant regression of established tumor in up to 50% of the animals treated. These findings lend further support to the role of suppressor cells in abrogating anti‐tumor immunity, and suggest that their manipulation may have potential implications for the design of human adjuvant therapy.
Changes in the expression of two Epstein‐Barr virus‐associated antigens, EBNA and RANA, during the cell cycle of transformed human B lymphoblasts
Authors: Slovin Susan F. , Vaughan John H. , Carson Dennis A. 
Published: February 2007

AbstractTwo methods of cell synchronization, density‐dependent arrest and double thymidine block, were used to assign two Epstein‐Barr virus‐associated antigens to different parts of the growth cycle of the human B lymphoblastoid cell lines, WI‐L2 and Raji. The Epstein‐Barr nuclear antigen (EBNA), as detected by anti‐complement immunofluorescence, was maximally expressed during early S phase, decreased during the G2 and M phases, and was absent in early G1. In contrast, the rheumatoid arthritis nuclear antigen (RANA), as detected by anti‐immunoglobulin immunofluorescence with a prototype serum from a patient with rheumatoid arthritis, was maximally expressed during early G1 phase, progressively decreased during S and early G2, and reappeared during late G2/M.
Lymphocytes that mediate systemic resistance to in vivo growth of a carcinogen‐induced syngeneic tumor
Authors: Crum E. D. 
Published: February 2007

AbstractWistar rats immunized with irradiated syngeneic methylcholanthrene‐induced sarcoma, Mc7, are able to suppress a subsequent challenge of this tumor. Cells obtained from thoracic‐duct lymph of these tumor‐immunized animals and infused intravenously into normal syngeneic rats transfer specific tumor resistance to the recipients. These mediators of tumor resistance have the characteristics of T lymphocytes that are in a non‐proliferating state and have an effective life span of at least 2 weeks in normal recipient rats.
Induction of transplantation immunity to rat colon carcinoma isografts by implantation of intact fetal colon tissue
Authors: Hedlund G. , Sjögren H. O. 
Published: February 2007

AbstractThe objective of this study was to demonstrate whether intact fetal colon tissue can induce immunity to large‐bowel cancer isografts. Adult rats were immunized against fetal antigens by implantation of mitomycin‐C‐treated intact fetal colon tissue beneath the renal capsule. Control animals received implants of pieces of intact adult colon tissue. Kidneys containing the implants were removed after 3 or 5 weeks and the rats were challenged with isografts of a 1,2‐dimethylhydrazin (DMH)‐induced colon carcinoma. Significant inhibition of tumor growth was observed in immunized groups compared to controls. The present results indicate that some embryo‐fetal antigens expressed in intact colon tissue of 13 to 15‐day‐old fetuses are also expressed in colon carcinoma cells and can act as transplantation antigens.
Development of carcinogen‐induced skin tumors in mice with varied states of immune capacity
Authors: Outzen Henry C. 
Published: February 2007

AbstractThe incidence of tumor formation in MCA‐treated skin grafted onto maximally immunosuppressed mice that had been restored to varying extents with normal spleen cells was significantly greater in the mice with intermediate immune capacities than in those that had either minimal or maximal capacities. A similar biphasic tumor incidence curve was observed when MCA‐treated skin was grafted onto mice of varying immune capacities, produced by thymectomy and varying doses of whole‐body irradiation. Significantly more tumors occurred in the mice given moderate doses of irradiation than in those given higher or lower doses. That both of these procedures were actually able to induce discrete levels of immunocompetence was demonstrated by measuring skin allograft rejection times. The immunomodulated mice were observed to have skin graft rejection times which strongly correlated with the number of immunologically competent spleen cells transferred into them. The outgrowth potential of syngeneic normal mammary epithelial cells grafted into cleared mammary fat pads was similar in both immunologically altered and normal control mice, showing that immunoaltered and normal control mice were equally able to support the growth of transplanted normal tissues. These results, which conform with the predictions of the immunostimulation hypothesis, suggest that the immune response is able to stimulate as well as inhibit oncogenesis.
Human lymphocyte/human erythrocyte rosettes. I. Blood “H” rosettes are high‐affinity E‐rosette‐forming T lymphocytes occurring in high frequency
Authors: Gallinger Lucy A. , Pross H. F. , Baines M. G. 
Published: February 2007

AbstractHuman lymphocytes will rosette with human red blood cells under certain conditions (H rosettes). The work presented in this paper documents the following: (1) a reproducible short‐term assay for the detection of H rosettes in proportions similar to those reported recently in the literature (25–30%); (2) technical improvements on the basic assay system demonstrating that, in fact, 40–65% of human lymphocytes form H rosettes; (3) the fact that, in normal donors, auto and allo H rosettes are formed by identical lymphocyte subpopulations; (4) that H rosettes are formed independently of the ABH, Rh and Thomsen‐Freidenreich (TF) red‐cell antigens on the indicator red cells; and (5) that H rosette‐forming cells consist almost entirely of T lymphocytes having high‐affinity receptors for sheep erythrocytes. The large difference in size between sheep and human RBC made it possible to do double rosette assays in which high‐and low‐affinity E‐rosette‐forming T cells could be visualized on the same slide. As with T lymphocytes in general, a large proportion of HRFC was found to have Fc‐IgM receptors while a smaller proportion has Fc‐IgG receptors. Studies done on a small group of leukemic patients supported the T‐cell nature of the H rosette‐forming cell.
Epstein‐Barr virus‐related serology in marrow transplant recipients
Authors: Lange Beverly , Henle Werner , Meyers Joel D. , Yang Lily C. , August Charles , Koch Penelope , Arbeter Allan , Henle Gertrude 
Published: February 2007

AbstractSerial sera from 50 marrow transplant recipients were examined for their spectra and titers of antibodies to EBV‐specific antigens. Immediately before or after transplant, blood products passively transferred antibodies to EB viral capsid antigen (VCA) and EBV nuclear antigen (EBNA). In most recipients, passively‐transferred antibodies were replaced by endogenous antibodies regardless of whether donor or recipient had EBV antibodies before transplantation. Commencement or resumption of endogenous EBV antibody production was not associated with signs of infectious mononucleosis or heterophil antibody responses. Antibodies to VCA rose to abnormally high titers, followed successively by antibody to early antigens (EA), and disproportionately low levels of anti‐EBNA. Unusually high anti‐VCA and anti‐EA levels persisted when tests of immune function returned to normal. Antibodies to other herpes group viruses showed no consistent changes. We conclude that (1) EBV does not cause significant clinical problems in marrow transplant recipients; (2) persistent EBV infection can become established or reestablished in the presence of antibodies to EBV; (3) marrow transplant recipients show the same exaggerated immune response to EBV as other immunodeficient patients; and (4) the pattern of EBV‐specific antibodies may be a more sensitive measure of defective cell‐mediated immunity than most conventional tests of immune function.
Difficulties encountered in the application of clark classification and the Breslow thickness measurement in cutaneous malignant melanoma
Authors: Prade M. , Sancho‐Garnier H. , Cesarini J. P. , Cochran A. 
Published: February 2007

AbstractThe purpose of this study was to analyse the reproducibility of Clark's classification and Breslow's measure of tumor thickness to determine if there is general agreement among pathologists regarding these parameters and whether these pathologists reach consistent conclusions concerning each slide. Three successive workshops including a panel of pathologists were held at Amsterdam, in May 1977; at Villejuif in June 1977, followed by circulation of slides and at Villejuif again, in June 1978, followed by slide projection. This was necessary because of the great divergencies of opinion noted at the first meeting at Amsterdam. These sessions gave a better understanding of the divergencies and finally indicated that general agreement could only be reached by slide presentation followed by discussion. Regarding histogenesis, agreement between pathologists was improved after discussion from 6/11 cases to 11/13 cases. Regarding the level, no initial agreement was reached (Amsterdam). At the second meeting an agreement was obtained in 4/13 cases and finally in 11/13 cases (Villejuif). Clark's classification is more difficult to use than Breslow's because it depends on a discontinuous variable, the choice of the infiltration level. Breslow's classification, on the other hand, is based on a continuous variable. Because of frequent discrepancies, the classification of patients into various therapeutic groups according to Clark's level and Breslow's thickness necessitates that all cases included in therapeutic trials be reviewed by a panel of pathologists.