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G Klein

Publications and source records attributed to G Klein.

At least 775 records · Page 43Linked to original sources
PubMed1982

Thymus independence of hybrid resistance against a panel of T-cell lymphomas of H-2b origin.

Adult thymectomy, followed by whole-body irradiation and reconstitution with fetal liver, was performed to study the T-cell dependence of F1 hybrid resistance to a panel of lymphomas of H-2b origin. Previously, the pattern of hybrid resistance against the same lymphomas was found to correlate with the pattern of NK-activity in a spectrum of F1 hybrids (Kiessling et al., 1975). We now show that hybrid resistance against three lymphomas of C57BL/6 origin, P-52-127-166, RBL-5 and EL-4 and against YLD, of C57L origin, is expressed in the absence of thymus. In another series of experiments, the effectors responsible for hybrid resistance to the transplanted lymphoma EL-4 were studied by reconstituting thymectomized and non-thymectomized C57BL mice with syngeneic bone marrow from NK-deficient beige mutant or wild-type C57BL donors. While the recipients of beige bone marrow had a clearly reduced tumor resistance, thymectomy did not decrease resistance further. This study supports the hypothesis that resistance to these lymphomas in F1 hybrids as well as in syngeneic mice is mainly mediated by natural killer cells.

Animals↗
PubMed1982

Non-random duplication of chromosome 15 in T-cell leukemias induced in mice heterozygous for reciprocal and Robertsonian translocations.

Two translocation--carrying stocks of mice, T(7;15)9H and Rb(4;15) were resistant to chemical leukemogenesis by 7,12-dimethylbenz(a)-anthracene (DMBA) or methylnitroso-N-urea (MNU). Lymphomas were induced in F1 hybrids derived from crossing these two stocks with various susceptible strains. In T-cell leukemias originating from F1 hybrids with Rb(4;15) as one parent and strain CBA or ASW as the other, the translocation chromosome was present in two copies. In trisomic tumors derived from Rb(4;15) X AKR F1 cross, the AKR-derived chromosome 15 was duplicated regularly. In contrast, all trisomic lymphomas of the T(7;15)9H F1 outcrosses showed duplication of the non-translocated chromosome 15 and not of the (7;15) translocation chromosome. It is suggested that the resistance of the T(7;15)9H stock to chemical induction of T-cell leukemia may be related to the position of the translocation on chromosome 15 (band D2). Our previous studies (reviewed by Klein, 1981) have indicated that this area may contain an oncogene that needs to be activated and subsequently undergo duplication in the course of leukemia development. In our previous studies on trisomic leukemias induced in heterozygotes (Wiener et al., 1979, 1980 b), we have found that duplication was non-random in all investigated crosses, unless the normal and the translocation marker carrying chromosomes were derived from the same inbred strain. A "duplication preference" scale could be established between chromosomes No. 15 derived from different strains. This suggested that the likelihood of leukemia development was different, depending on the genetic origin of chromosome 15. In the present study, we have found that the duplication of chromosome 15 occurred at random in the CBAT6T6 X C3H F1 cross. This is attributed to the close genetic relationship between the two strains, as indicated by their shared isoenzyme and other markers.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Spontaneous aggregation of the mitochondrial natural ATPase inhibitor in salt solutions as demonstrated by gel filtration and neutron scattering. Application to the concomitant purification of the ATPase inhibitor and F1-ATPase.

(1) The natural ATPase inhibitor (IF1) from beef heart mitochondria has a tendency to form aggregates in aqueous solutions. The extent of aggregation and the structure of the aggregates were assessed by gel filtration and small-angle neutron scattering. IF1 polymerization was found to depend on the salt concentrations, pH of the medium and concentration of IF1. The higher the salt concentration, the lower the aggregation state. Aggregation of IF1 was decreased at slightly acidic pH. It increased with the concentration of IF1 as expected from the law of mass action. (2) Neutron scattering showed the aggregation of IF1 in 2 M ammonium sulfate solutions. The predominant species is the dimer which has a somewhat elongated shape. (3) The Sephadex G-50 chromatography that is supposed to deprive beef heart submitochondrial particles of loosely bound IF1 (Racker, E. and Horstman, L.L. (1967) J. Biol. Chem. 242, 2547-2551) was shown to have a limited effectiveness as a trap for IF1. The reason was that IF1 released from the particles formed high molecular weight aggregates that were not separated from the membrane vesicles by Sephadex G-50 chromatography. (4) The above observations provide the basis for a simple method of purification of beef heart IF1 which combines the recovery of the supernatant from submitochondrial particles with the last three steps of the IF1 preparation described by Horstman and Racker (J. Biol. Chem. (1970) 265, 1336-1344). The particles recovered in the sediment were deprived of IF1 and could therefore be used for preparation of F1-ATPase. The advantage of this method is that both IF1 and F1-ATPase can be prepared from the same batch of mitochondria.

Adenosine Triphosphatases↗
PubMed1982

[Lung functions in children with marked alpha 1-antitrypsin deficiency (Pi-Z type) (author's transl)].

Various lung volumes and flows were measured in five children (aged 9-11 years), a male adolescent and one adult, all carriers of the homozygotic form of alpha 1-antitrypsin deficiency (Pi-Z type). In five patients lung function tests demonstrated overdistention, in three decreased CO diffusion capacity, as an expression of pulmonary emphysema at an early stage. Airway obstruction was not demonstrable in any of the patients (normal values for FEV 1, Tiffeneau test, peak flow and V25, V50 and V75). There was a correlation between the level of alpha 2-macroglobulin and the CO diffusion capacity, as well as between alpha 1-antitrypsin level and residual volumes. In one child there was evidence of minor liver involvement; in the other six patients, all liver-dependent serum enzymes were within normal limits. The findings suggest that the lung changes typical of adult homozygotic carriers of alpha 1-antitrypsin deficiency have their beginning in childhood.

Adult↗
PubMed1982

Reactivity with patient antibodies of partially purified gp40 antigen from immune complexes in Burkitt's lymphoma and nasopharyngeal carcinoma.

A glycoprotein antigen (gp40) was previously identified as a major component of immune complexes isolated from sera of patients with Burkitt's lymphoma (BL) and nasopharyngeal carcinoma (NPC). In the present work gp40 was partially purified from a pool of BL/NPC sera. Sera of patients with BL and NPC as well as sera of patients with other malignant and non-malignant diseases were tested for antibodies against gp40, using a double antibody radioimmunoassay. Practically all normal sera and sera of patients with non-malignant diseases had antibodies capable of binding radioiodinated gp40. In contrast, sera of patients with BL or NPC had very low binding, while sera of patients with other malignant diseases had intermediate binding values. The low binding activity of BL/NPC sera was shown to be due to inhibition by excess gp40 present in such sera. Effusions of patients with breast or ovarian cancer also contained demonstrable amounts of gp40. The origin of gp40 is still unknown.

Antibodies↗
PubMed1982

Migration inhibition caused by EBV-specific 48K subcomponent of EBNA and the associated 53K cellular protein.

Leukocytes from EBV-seropositive but not seronegative healthy donors responded with significant migration inhibition to the 48K subcomponent of the Epstein-Barr virus determined nuclear antigen (EBNA), known to carry the virally determined antigenic specificity. A concentration of 10 micrograms/ml was still effective while 5 micrograms/ml had no detectable effect. EBNA-associated cellular 53K protein had no effect by itself, but it potentiated the effect of 48K, even if the latter was added at the subliminal concentration of 5 micrograms/ml. The related 53K protein, isolated from EBV-negative human lymphoma cells, was also effective, whereas the corresponding murine-tumor-associated 53K had no potentiating effect. Immunization of mice with an extract of DNA-binding proteins from EBV-carrying Raji cells, known to contain both 48K and 53K, induced a significant macrophage migration inhibition response, to both human 48K and 53K. Murine 53K was ineffective, however. Human but not murine 53K increased the migration inhibitory activity of subliminal concentrations of 48K in the murine macrophage system as well. These findings suggest that human but not murine 53K may reconstitute with 48K (EBNA) to form a highly immunogenic complex.

Animals↗
PubMed1982

Non-random chromosomal changes involving chromosomes 6 and 7 in spontaneous rat immunocytomas.

G-banding analysis of seven Ig-secreting spontaneous rat immunocytomas showed a consistent translocation of the distal part of the q-arm of chromosome 7 to the telomeric end of chromosome 6. The breakpoints were assigned to q3.3 on chromosome 7 and q3.2 on chromosome 6. Previously, we found a similar translocation pattern in mouse plasmacytomas induced by different agents. The distal part of the q-arm of chromosome 15 was translocated to the telomeric end of chromosome 12, known to carry Igh, the immunoglobulin heavy chain cluster. The banding homologies between the chromosomes involved in the translocation in the two species suggest that a similar mechanism is responsible for plasmacytomagenesis in both. We also predict that the rat Ig heavy chain gene cluster will be located to the terminal segment of chromosome 6.

Animals↗