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Biomedical subjects

E Klein

Publications and source records attributed to E Klein.

At least 289 records · Page 16Linked to original sources
PubMed1988

The role of endoscopic retrograde cholangiopancreatography in the diagnosis and treatment of adult choledochal cyst.

Five patients with adult choledochal cyst were diagnosed by endoscopic retrograde cholangiopancreatography (ERCP). Four patients had type I and one patient had type III choledochal cyst with abnormal pancreaticobiliary duct anatomy. One patient had a tubular adenoma of the distal common bile duct. All patients were treated surgically (excision of cyst with biliary and enteric reconstruction in two patients; cystojejunostomy, two, and transduodenal sphincterotomy, one patient). The follow-up period ranged from two to nine years, with a mean of four years. One patient had recurrent cholangitis develop and was treated successfully by nasobiliary tube flushing. ERCP should be used when choledochal cyst is suspected by ultrasonography, aiming at demonstrating both biliary and pancreatic duct anatomy and enabling the planning of the surgical procedure. Nasobiliary tube flushing provides an alternative therapeutic modality in patients in whom surgical treatment is contraindicated.

Adolescent↗
PubMed1988

Adenosine uptake sites in brain: regional distribution of putative subtypes in relationship to adenosine A1-receptors.

Adenosine uptake sites have been characterized and localized in guinea pig and pointer dog brain by in vitro autoradiography, using as probes 3H-nitrobenzylthioinosine (3H-NBI) and the recently available 3H-dipyridamole (3H-DPR). In guinea pig brain and, to a lesser extent, in pointer dog brain, 3H-DPR was found to label more high-affinity binding sites than 3H-NBI and NBI inhibited 3H-DPR binding having pseudo-Hill coefficients smaller than 0.5. 3H-DPR and 3H-NBI labeled brain structures with different intensities in guinea pig brain, as was revealed by quantitative analysis. While the intensity of 3H-DPR binding varied about 4-fold in neuron-containing structures, 8-fold differences were observed for 3H-NBI binding with phylo- and ontogenetically older brain areas such as hypothalamus and various brain stem structures showing relatively higher densities. These findings raise the interesting possibility of adenosine uptake site heterogeneity (NBI-sensitive and insensitive) in guinea pig brain, complementing the well-established adenosine receptor heterogeneity (A1 and A2). As adenosine's neurodepressant effects are believed to be mainly mediated by adenosine A1-receptors, these were localized using 3H-cyclohexyl-adenosine (3H-CHA) as a ligand probe. In guinea pig brain, the highest receptor densities were seen in hippocampus and claustrum, while only relatively low levels were found in hypothalamus and various brain stem structures. As was previously described for rat brain, major discrepancies in the regional distribution of adenosine A1-receptors and adenosine uptake sites, as labeled by 3H-NBI, were seen in guinea pig brain. These discrepancies were only partly abolished (e.g., in cerebellum) by the use of 3H-DPR as an additional ligand probe for adenosine uptake sites. Adenosine uptake site heterogeneity, therefore, probably does not explain the previously described discrepancies in rodent brain between the distribution of adenosine A1-receptors and uptake sites. Because of the low affinity of 3H-DPR for adenosine uptake sites in rat and mouse brain, these species could not be investigated with this new radioligand probe. In pointer dog brain, as compared to guinea pig brain, a more similar distribution pattern of adenosine A1-receptors and adenosine uptake sites in the brain structures investigated (e.g., hippocampus) could be observed. The situation in guinea pig brain can, therefore, not be universalized to other species.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1987

Paired Epstein-Barr virus (EBV)-negative and EBV-converted Burkitt lymphoma lines: stimulatory capacity in allogeneic mixed lymphocyte cultures.

Epstein-Barr virus (EBV)-negative Burkitt lymphoma lines (BLE-) and their in vitro EBV-converted sublines (BLEc), obtained by infection with the P3HRI and B95-8 strains of EBV, were compared for their capacity to induce T-lymphocyte proliferation in allogeneic mixed lymphocyte cultures (MLC). Regardless of the virus strain used for conversion, the BLEc lines induced a considerably stronger primary MLC response than their EBV-negative parentals. Only the BLEc lines were able to maintain T-lymphocyte proliferation in repeated stimulations. The low proliferative response observed in cultures stimulated with BLE- cells was not due to the generation of suppressor cells or to the release of inhibitory factors. The increased stimulatory capacity of BLEc lines was unrelated to changes in expression of MHC class-I and class-II antigen, or of B-cell activation markers, and was not due to the reactivation of EBV-specific memory T cells, since lymphocytes from EBV-seropositive and seronegative donors responded similarly. The results indicate that the capacity of BL cells to elicit cellular immune responses may be influenced by their EBV-carrying status.

Antigens, Viral↗
PubMed1987

Defective cell-mediated response to EBV-transformed B cells in a healthy individual with regular EBV antibody titers.

We have analyzed the EBV-related immune parameters of a healthy EBV-seropositive individual (ST) who has regular antibody titers but defective inhibitory capacity toward the growth of autologous EBV-infected B cells. This in vitro function reflects the EBV-specific memory because it does not occur in experiments performed with cells of seronegative individuals. An analysis of events following in vitro EBV infection showed that lymphocytes of ST behaved in some tests in the same way as those collected from seronegative individuals. These parameters were: lack of gamma-IFN production 24 hr after EBV infection; low production of soluble factors that inhibit EBV-induced B-cell proliferation; lack of generation of LCL selective cytotoxicity after repeated stimulation with autologous LCL; and high proportion of EBNA-positive cells in 7-day-old EBV-infected cultures. On the other hand, cellular memory to the virus detected by the production of IL-2 24 hr after infection, and by the production of LIF upon exposure to EBV-encoded antigens, conformed with the results obtained with seropositive individuals. T-cell-mediated inhibition of EBV-induced B-cell growth in vitro has been regarded as a corollary of in vivo control of EBV-infected B cells. However, it is absent or has a low efficiency in certain disease categories which are not accompanied by risk of B-EBV growth. Our results with a healthy individual also indicate that several mechanisms contribute to a harmless life-long virus carrier state.

Adult↗
PubMed1987

Autologous mixed lymphocyte-tumor reaction and autologous mixed lymphocyte reaction. I. Proliferation of two distinct T-cell subsets.

In patients with carcinomatous pleural effusions blood T lymphocytes proliferated in vitro in response to autologous, freshly isolated effusion tumor cells in the autologous mixed lymphocyte-tumor culture (AMLTC) and to autologous blood non-T cells in the autologous mixed lymphocyte culture (AMLC). Treatment of the stimulator cells with the anti-HLA-DR monoclonal antibody (MAb) abrogated the stimulatory capacity in AMLC, but not in AMLTC. A subset of T cells that formed rosettes with autologous erythrocytes showed proliferative response to autologous non-malignant cells, whereas this subset did not respond to autologous tumor cells. Non-adherent lymphocytes were fractionated by centrifugation on discontinuous Percoll density gradients. Medium-sized T lymphocytes were excellent responders in AMLC, but were weak responders in AMLTC. Small T lymphocytes proliferated preferentially in AMLTC, but responded poorly in AMLC. Large granular lymphocytes (LGL) did not proliferate in mixed cultures of either type. Instead, LGL suppressed the T-cell proliferation in AMLTC. The same suppressor LGL, however, had no inhibitory effect on AMLC. Elimination of the CD4 subset reduced or abolished proliferative response in AMLC in all cases, whereas it was ineffective in diminishing the reaction in 6 of 8 AMLTC. In contrast, removal of the CD8 subset decreased or eliminated T-cell proliferation in 4 of 8 AMLTC, but in none of the AMLC. These results indicate that the autoreactive T lymphocytes detectable in response to tumor cells and non-malignant non-T cells differ in several characteristics. Thus, the reaction in the AMLTC is not due to contaminating non-malignant cells in the stimulator population and may be a tumor-induced proliferative response.

Adult↗
PubMed1987

[Clinical aspects of reperfusion arrhythmia following intravenous thrombolysis in acute myocardial infarct].

In accordance with the majority of the reports in the literature reperfusion arrhythmias were observed in more than 30% of the patients with acute myocardial infarction (n = 25) under or immediately after a highly dosed short-term infusion with streptokinase. With reference to indirect signs the recanalisation rate was assumed with 75%. Only one third of the reperfusion arrhythmias had haemodynamically significant characteristics and required an influence. Though in literature from animal experimental findings directive conclusions for the therapy are to be derived, the procedure in practice is still vastly empirical. In the ventricular tachycardia lidocaine, procainamide and ajmalin may be recommended. In ineffectiveness or particularly threatening situations the electrotherapy (cardioversion, DC-shock) is to be preferred. The concept inaugurated by Corr and Witkowski apply alpha-adrenoreceptor blockers has not yet entered the clinical practice. Possible problems in the treatment of reperfusion arrhythmias in the prehospital phase should at present still be a reason not to antedate the thrombolytic therapy into this phase.

Arrhythmias, Cardiac↗
PubMed1987

Characterization of EBV-carrying B-cell populations in healthy seropositive individuals with regard to density, release of transforming virus and spontaneous outgrowth.

Peripheral or tonsil lymphocyte populations of EBV-seropositive donors give rise to EBV-carrying LCLs upon in vitro explantation. Such lines can arise either by a 2-step mechanism, namely release of virus from some of the explanted cells followed by infection of previously uninfected B cells, or by direct outgrowth of virus-harboring B cells (Rickinson et al., 1974; Dalens et al., 1975; Hinuma and Katsuki 1978; Katsuki et al., 1979). We observed that cells responsible for both the 2-step mechanism and for direct outgrowth are found in the purified B-cell compartment. Virus release was more frequent than direct outgrowth. The majority of virus-releasing cells were found in the low-density fraction that contains large, activated B blasts. Cells that were capable of spontaneous outgrowth in the presence of the viral inhibitor PFA and of virus-neutralizing antibody gave rise to cell lines that carried the sex chromosome marker of the original donor, rather than that of admixed cord blood lymphocyte of the opposite sex. Such cells were found in both the low- and the high-density fractions. The majority of the EBV-carrying B cells in vivo are thus low-density blasts. Rare small B cells of high density harboring EBV were capable of spontaneous outgrowth. This may be indicative of a host control mechanism that is removed upon cultivation in vitro.

B-Lymphocytes↗
PubMed1987

Chronic lithium treatment increases the phosphorylation of a 64-kDa protein in rat brains.

Despite the wide clinical use of lithium in the treatment of manic depressive illness there is no adequate explanation for its mechanism of action. In the light of lithium's suggestive effects on the second messenger system in the brain, we studied the effects of chronic dietary lithium treatment (achieving blood levels in the therapeutic range) on protein phosphorylation in different areas of rat brain. An increase in the phosphorylation of a 64-kDa membrane-associated protein was evident in the lithium-treated rats compared to controls. This increase was observed only under basal phosphorylating conditions and was abolished when the phosphorylation was performed in the presence of Ca2+ or Ca2+ and calmodulin. The possibility that this 64-kDa protein affected by lithium is the beta-subunit of the calmodulin-dependent protein kinase or a different protein which co-migrates with it is discussed.

Animals↗
PubMed1987

Activation of B lymphocytes by Epstein-Barr virus/CR2 receptor interaction.

Epstein-Barr virus (EBV) infects and transforms human B lymphocytes. The virus receptor was shown to be identical to the complement receptor CR2. The consequences of EBV/CR2 receptor interaction on B lymphocyte activation were analyzed by infection of B cells with the transforming (B95-8) and the nontransforming (P3HR1) virus strains and with UV-inactivated B95-8 virus. Similar to mitogens and antibodies against surface IgM and CR2 receptor, transforming and nontransforming EBV induced the release of leukocyte migration inhibitory factor (LIF). LIF production occurred early after infection and was not affected by irradiation of the B95-8 virus with doses of UV-light which prevented the expression of viral functions. B lymphocytes infected with UV-inactivated virus responded to T cell-derived B cell growth factors. The results demonstrate that binding of EBV to the CR2 receptor activates the B cells. Progression of the infected cells in the activation pathway required helper cell-derived factors or signals provided by the intact viral genome. The nontransforming P3HR1 virus induced a low level of RNA synthesis and increase of cell size and major histocompatibility complex class I antigen expression. Only the transforming virus induced expression of EBV nuclear antigens and cellular DNA synthesis.

Antibodies↗
PubMed1987

Alternative pathway of complement activation by stimulated T lymphocytes. I. Binding of C3 fragments.

Human blood lymphocytes cultured for 3 days with concanavalin A (Con A), phytohemagglutinin or pokeweed mitogen, in mixed lymphocyte culture with added interleukin 2 and stimulated by a lymphoblastoid cell line were found to activate and bind C3 molecules when exposed to human serum. The split products of C3 were detected in the supernatants and on the surface of the activated cells. The surface-attached C3 fragment on the Con A blast was identified as C3b by immune adherence i.e. binding of CR1 carrying human erythrocytes. In the Con A-stimulated population the majority of cells that activated and bound C3 were CD3 and Fc gamma receptor (CD16)-positive but complement receptor-negative blasts. In this cell subset both CD4 and CD8-positive cells were detected but their frequency suggested that a proportion of them carried both markers.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Alternative pathway of complement activation by stimulated T lymphocytes. II. Elevation of cytotoxic potential against complement receptor-carrying cell lines.

Exposure of lectin-stimulated (concanavalin A, phytohemagglutinin and pokeweed mitogen) blood lymphocytes to human serum or to purified C3 increased their cytotoxic capacity towards complement receptor positive targets such as Raji and Daudi cells. The lysis of complement receptor-negative lymphoblastoid cell lines was not influenced. The lytic capacity of lymphocytes exposed to 12-O-tetradecanoylphorbol 13-acetate was not elevated by human serum. Lectin-stimulated lymphocytes were previously shown to activate and bind C3. The results using lymphocytes activated in different ways and targets with or without complement receptor expression suggest that the C3b deposited on lymphocytes binds to the complement receptor on the targets. This contact elevates the avidity between the two cells as indicated also by the increased frequency of the lymphocyte-target conjugates. On the basis of immune adherence the C3 fragment bound on the lymphocytes was identified as C3b. The increase of the conjugate formation and cytotoxicity was abrogated when the target cells, Raji, were pre-exposed to purified C3d which occupy the CR2 receptor. The majority of lymphocytes responsible for the cytotoxicity were CD8+.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1987

Lysis of autologous tumor cells by blood lymphocytes activated in autologous mixed lymphocyte tumor cell culture--no correlation with the postsurgical clinical course.

Mixed lymphocyte tumor cell cultures (MLTC) were initiated with cells collected at the time of surgery from 62 patients with the following diagnoses: 12 squamous cell carcinoma, 14 adenocarcinoma of the lung, 17 osteosarcomas, and 16 soft tissue sarcomas. The lytic effect generated against autologous tumor cells was tested on the 7th day. These patients had been part of previous evaluation, which revealed that the lysis of autologous tumor cells by freshly collected lymphocytes correlated with the postsurgical clinical course. Patients with long survival exhibited autotumor lysis without previous activation. Blood lymphocytes of about half of the primarily nonreactive patients were stimulated for lytic function in MLTC. However, this parameter showed no correlation with the clinical course.

Aged↗
PubMed1987

Auto-tumor immunity in patients with solid tumors: participation of CD3 complex and MHC class I antigens in the lytic interaction.

In a number of experiments performed with blood lymphocytes of patients, the high density subset lysed autologous tumor cells separated from the surgical specimens. The lysis was abrogated by pretreatment of the effector cells with antibodies (OKT3) directed against the T3 molecule associated with the T cell receptor and by pretreatment of the target cells with antibodies (W6/32) directed against the monomorphic part of the MHC class I antigens. This subset lyses only autologous tumor cells. The selectivity and the characteristics shared with antigen specific cytotoxic T lymphocytes (CTL) suggest that the auto-tumor lysis by the effectors reflects an immune response against the tumor cells. The low density lymphocytes, separated from the blood, can lyse both auto- and allogeneic tumor cell. In the autologous system, incubation of the effectors with the mAb OKT3 had no inhibitory effect and incubation of the targets with the anti W6/32 mAb inhibited their lysis only in some experiments. The nature of the reactivity of the LD lymphocytes remains to be defined. Whether it is similar to the indiscriminative natural killing or whether part of these lymphocytes are antigen(s) specific and exhibit a high avidity interaction with the target remains to be seen. It is possible that both types of target recognition occur since the LD lymphocyte population is heterogeneous.

Aged↗