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Biomedical subjects

G Klein

Publications and source records attributed to G Klein.

At least 865 records · Page 48Linked to original sources
PubMed1981

Membrane-bound and cellular immunoglobulins in human B-lymphoma lines and derived hybrids.

Hybrids derived from the fusion of cell lines representing different maturation stages were studied for their membrane and cellular immunoglobulin expression. The hybrids can be subdivided into 3 groups, with one common parental line in each group. In the first group, Raji cells represent the common parent: it contains small amounts of membrane and cytoplasmic mu (mu) and kappa (kappa) chains. In the second group, PUT is the common parent, an ouabain and TG-resistant subline of the BL-derived P3HR-1 line. PUT contains a truncated intracellular mu chain. The third group consists of hybrids between K562, an EBV-negative human erythroleukemia line and 2 different BL lines. Membrane-immunoglobulin expression was intermediate between the parental lines in the first two groups derived from the fusion of 2 BL lines. In the third group, hybridization with the K562 cell suppressed the membrane-Ig expression of the B-cell partner. Total cellular immunoglobulin determinations showed that some cells synthesized light chains in excess of heavy chains, others contained an excess of heavy chains, while still others had equal amounts of heavy and light chains. The hybrids showed a variety of patterns, including amplification of the parental phenotypes, appearance of new phenotypic combinations, and eclipse of one or both parental phenotypes. A comparison of the total and the membrane-associated immunoglobulin patterns suggests independent handling of intracellular and membrane immunoglobulin synthesis.

B-Lymphocytes↗
PubMed1981

Relationship between Herpesvirus ateles-associated nuclear antigen (HATNA) and the number of virus genome equivalents in HVA-carrying lymphoid lines.

A DNA-binding antigen (HATNA) was demonstrated in 7 out of 14 cell lines carrying Herpesvirus ateles (HVA) by the acid-fixed nuclear-binding technique. The seven HATNA-positive lines had means of 95, 96, 103, 177, 240, 343 and 326 virus genome equivalents/cell. For the seven HATNA-negative lines, the figures were 4, 8, 10, 33, 39, 72 and 110. This indicates a relationship between the number of HVA genome equivalents/cell and the detectability of HATNA. This association was independent of the virus producer status of the lines.

Animals↗
PubMed1981

The detection of Epstein-Barr virus receptors utilizing radiolabelled virus.

Epstein-Barr virus (EBV) was labelled with 3H-thymidine and purified about 1000-fold from the culture medium by ultracentrifugation on 5 to 30% dextran gradients. The presence of the virus was monitored by radioactivity and Epstein-Barr virus-determined nuclear antigen (EBNA) induction in sensitive indicator cells (Ramos). Peaks for both activities occurred in the 17 to 18% dextran fractions. Unlabelled virus recovered in the peak fraction was labelled with 125I. Both thymidine and 125I-labelled purified virus bound quantitatively to receptor-positive Burkitt lymphoma-derived cell lines but not to EBV-receptor-negative T-lymphocyte-derived cell lines. Thymidine-labelled virus that was allowed to bind to Raji cells was present in the interior of briefly trypsinized cells after 3 h incubation at 37 degrees C. The results provide a convenient method for detecting the EBV receptor by radioactively labelled virus.

Burkitt Lymphoma↗
PubMed1981

Deficiency of malic enzyme: a possible marker for malignancy in lymphoid cells.

Soluble malic enzyme (MEs) has been examined in long-term human lymphoid cell lines cultured from 101 individuals. In 65 out of 66 lines derived from people without lymphoreticular malignancy the enzyme was very active. Lines established from 35 individuals with various forms of lymphoreticular malignancy were also examined, including in some cases more than 1 line derived from the same patient. In all cases where the cell line was thought to be derived from normal cells MEs was active, but in 27 out of 29 lines thought to be derived from malignant cells (from 25 patients) MEs was not detected. In the case of two patients with chronic lymphatic leukaemia 'normal' lines active for malic enzyme, and 'leukaemic' lines lacking malic enzyme, had been cultured from the same individual. Preliminary investigations of the lack of malic enzyme in somatic cell hybrids derived from lymphoma and leukaemia cell lines are compatible with an alteration at the level of the structural locus MEs on chromosome 6. However, the restoration of MEs activity in one line by fusion with mouse teratocarcinoma cells suggests that the alteration may be of a regulatory nature.

Animals↗
PubMed1981

Synthesis of thymidine kinase (TK) in Epstein-Barr virus-superinfected Raji TK-negative cells.

Epstein-Barr virus (EBV) from P3HR-1 cells, but not from B95-8 cells, can induce the synthesis of thymidine kinase (TK) in TK-negative Raji cells. The synthesis of TK was slightly reduced, but not inhibited, when cells were cultivated in the presence of cytosine arabinoside (ara-C). On the other hand, the synthesis of TK in ordinary Raji cells was enhanced in the presence of the drug. Thymidine-beta-D-arabinofuranoside (ara-T) was capable of reducing the conversion rate of thymidine to TdR nucleotides by extracts prepared from superinfected Raji TK-cells, but had no influence on TK activity in cell extracts from ordinary Raji cells and EBV-negative Ramos cells. This suggested a broader substrate specificity of the virally induced enzyme.

Arabinonucleosides↗
PubMed1981

Cell surface glycoprotein patterns of two EBV-negative lines and their EBV converted sublines.

Cell surface galactosyl-glycoprotein patterns were compared between Ramos and BJAB, two Epstein-Barr virus (EBV)-negative Burkitt lymphoma lines, and their acutely EBV-superinfected and stably EBV-converted derivatives. A major difference between Ramos and its EBV-infected variants was the appearance of a 69,000 mol. wt. galactosyl-glycoprotein (GP69) in the latter. The same phenomenon was found in BJAB along with the additional appearance of a 71,000 mol. wt. galactosyl-glycoprotein (GP71) in the EBV-infected cells. GP71 was present in Ramos and in its EBV-converted derivatives.

Burkitt Lymphoma↗
PubMed1981

Long-term study of the protective effect of ketotifen in children with allergic bronchial asthma. The value of a provocation test in assessment of treatment.

The effect of ketotifen on allergic symptoms and parameters of respiratory function were studied in 23 allergic children during a period of 6 months therapy. A reduction in nocturnal dyspnea and dyspnea during exercise was observed in 17 patients. Improvement of the FVC, PEF and FEV1 was detected in 14, 15 and 19 patients, respectively. Following a 4-day treatment with ketotifen, a further 15 patients with allergen-induced bronchospasm were challenged by inhalative provocation test, comparing the protective effects of ketotifen and of DSCG in a randomized double-blind crossover study. 7 of 15 patients showed an improved allergen tolerance to the immediate hypersensitivity with ketotifen and 5 patients with DSCG. A protective effect with respect to the delayed hypersensitivity reaction was observe in 2 of 8 patients with ketotifen and in 1 with DSCG.

Adolescent↗
PubMed1981

Epstein-Barr virus receptor expression is correlated to cell cycle phase.

Epstein-Barr virus (EBV) receptor positive cells absorbed FITC-conjugated virions and were subsequently stained for DNA content with propidium iodide. These cells were analyzed by flow cytometry to determine the relationship between cell cycle and EBV receptor (EBVR) expression on single cells. EBVR was present throughout the entire cell cycle. The level of expression, however, varied; increasing in G1 and G2/M while remaining approximately constant in S phase. Analysis of receptor density in terms of cell size demonstrated that smaller cells, in early G1, have a greater density of receptors per unit membrane than larger G2/M and S phase cells.

Animals↗
PubMed1981

[Use of beta-adrenergic blocking agents in acute myocardial infarction (author's transl)].

Beta-adrenergic blocking agents exert a number of pharmacologic effects which may potentially be beneficial and warrant their use in acute myocardial infarction: by decreasing heart rate, myocardial contractility and systolic blood pressure, reducing catecholamine-induced lipolysis and antagonizing the oxygen-wasting effects of catecholamines on the myocardium, myocardial oxygen balance may be improved thus reducing ischemia. Theoretically this may lead to a limitation of infarct size by protecting underperfused myocardium from ultimate necrosis. Definite proof for such a positive effect in man, however, is not yet available. In animals a number of experimental findings either indirectly of directly demonstrate the potential protective effect of beta-blockers on ischemic myocardium. Early treatment is able to significantly prolong myocardial survival time and limit the area of myocardial damage to about 50% as compared with untreated controls. Experience with treatment of myocardial infarction in man has shown that beta-blocking agents are well tolerated in patients presenting in hemodynamically stable condition (Killip groups I and II). By reducing heart rate as well as pressure and volume work of the heart and reducing serum-free-fatty-acid concentration, myocardial oxygen demand is greatly diminished. A reduction of myocardial O2-consumption and improvement in oxygen balance has been demonstrated in man. Total enzyme appearance of creatine-phosphokinase is significantly lower in patients treated with beta-blocking drugs early in the course of of myocardial infarction (within four hours following onset of acute symptoms) as compared with untreated controls. Furthermore the number of ventricular ectopic beats and the severity of chest pain are reduced. In some studies there was a significant reduction in mortality for selected groups of patients with myocardial infarction treated with beta-blocking agents. In conclusion, beta-adrenoceptor blocking agents appear to represent a promising therapeutic principle for protecting ischemic myocardium in acute infarction. Additional investigations are urgently necessary to clarify the question of which patients may profit from such management. Pending the results of such studies, a general recommendation for the treatment of myocardial infarction with beta-blockade can not yet be given.

Acute Disease↗
PubMed1981

Cellular immune defects to Epstein-Barr virus-determined antigens in young males.

Three males with the X-linked lymphoproliferative syndrome (XLP) with hypo- or agammaglobulinemia following Epstein-Barr virus (EBV) infection and two males with the chronic mononucleosis syndrome were investigated for immune responses to EBV-determined antigens. Males with XLP showed profound cellular immune defects. Markedly diminished responses of natural killer cell and interferon-activated killer cell activities and impaired leukocyte migration inhibition responses to phytohemagglutinin were determined in patients with XLP. The two patients with chronic mononucleosis showed less severe defects. All patients showed partial or complete impairment of their EBV-specific immune responses as measured by leukocyte migration inhibition. EBV-specific antibodies were markedly diminished against EBV-associated nuclear antigen, early antigen, and viral capsid antigen in males with XLP. In contrast, patients with chronic mononucleosis had elevated antibodies to most EBV-specific antigens. Individuals with life-threatening EBV-induced lymphoproliferative disorders may exhibit multiple defective immune mechanisms against the virus.

Adolescent↗
PubMed1981

Proliferation inhibitory effect of human alpha interferon on primary explants of Burkitt lymphoma: inverse relationship to patient survival.

Eleven biopsies from 9 patients with Burkitt's lymphoma were tested for their sensitivity to the cell multiplication inhibitory activity of interferon. Three were resistant to interferon while 8 were sensitive to various degrees. Different biopsies from the same patient did not differ in interferon sensitivity. These results indicate that Burkitt's lymphoma cells might be resistant to interferon already in vivo as previously shown for some derived cell lines tested in vitro. The results imply an inverse relationship between patient survival and interferon sensitivity of the tumor cells.

Burkitt Lymphoma↗
PubMed1981

Cell-surface immunoglobulin and insulin receptor expression in an EBV-negative lymphoma cell line and its EBV-converted sublines.

Membrane Ig and insulin receptors were assayed in the EBV-negative Ramos lymphoma line and its EBV-converted sublines by surface fluorescence. 125I-protein A-binding assay, immunoprecipitation, and insulin receptor assay. The original Ramos line expressed surface IgM but not IgD and had a low concentration of insulin receptors. Ten of 10 converted lines expressed IgD and a variable but usually high insulin-binding capacity. Molecular weight analysis of immunoprecipitated Ig showed the presence of 2 mu-chains and 2 delta-chains. One of each heavy chain type could be characterized as membrane Ig, whereas the other was cytoplasmic. Antisera against the lambda-chain precipitated mu and delta heavy chains as well, indicating that the delta-chain expressed on the membrane of the EBV-converted Ramos lines is bound to the lambda light chain. The results show that the differentiation of a Burkitt lymphoma line is not completely "frozen" and can be induced to change in a more "activated" direction by EBV conversion.

Binding Sites↗
PubMed1981

Membranes of EBV-carrying virus nonproducer cells inhibit leukocyte migration of EBV-seropositive but not seronegative donors.

We have previously shown that the leukocytes of healthy EBV-seropositive (but not seronegative) donors respond with migration inhibition (LMI) when confronted with extracts of EBV-carrying (but not EBV negative) cells. In the present study, we have examined whether this EBV-specific LMI response is capable of detecting a membrane antigen on the surface of EBV-carrying virus nonproducer cells. Crude membranes from EBV-genome carrying and EBV-negative cell lines were used as antigen. Contamination with the EBV-determined nuclear antigen (EBNA) was ruled out. Membranes from EBV-genome carrying nonproducer cells inhibited the migration of leukocytes from healthy seropositive donors, whereas membranes from EBV-negative lines had no such effect. Seronegative donors did not show any LMI. The clear difference between the EBV-negative Ramos line and its EBV-converted sublines was particularly conclusive in showing that the membrane component is determined or induced by the viral genome.

Antigens↗
PubMed1981

Human B lymphocytes activated by Epstein-Barr virus (EBV) or by mitogens suppress mitogen-induced immunoglobulin production.

Polyclonal activation of human B lymphocytes by LPS or protein A, alone or in combination or by Epstein-Barr virus (EBV), generates suppressive conditions that inhibit the response of human B lymphocytes to pokeweed mitogen (PWM), measured by the induction of immunoglobulin-secreting cells (PFC). Moreover, EBV-transformed B cell lines of normal or neoplastic (Burkitt lymphoma) origin also suppressed the PWM-induced immunoglobulin production of normal B cells. Cell separation experiments have shown that mitogen activated autologous B cells stimulate suppressor T cells in a similar way as B cell-derived lymphoblastoid cell lines. The significance of this phenomenon is considered in relation to the escape of the activating microorganism or virus from immune control and the occurrence of network interactions within the immune system.

Antibody-Producing Cells↗