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Biomedical subjects

G Klein

Publications and source records attributed to G Klein.

At least 667 records · Page 37Linked to original sources
PubMed1985

Prenalterol: a partial beta 1-adrenoceptor agonist or a beta-blocker with intrinsic activity?

Hemodynamic studies have demonstrated a significantly reduced beta 1-adrenoceptor stimulating effect of prenalterol compared to dobutamine suggesting a partial agonism on the receptor. In order to prove this hypothesis we administered 80 micrograms/kg of prenalterol within 5 minutes in 8 healthy volunteers during a continuous infusion of dobutamine (15 micrograms/kg/min). In addition to heart rate, blood pressure and the double product, the systolic time intervals QS2I, PEP and LVET and the echocardiographically determined parameters FS and Vcf were measured for evaluation of ventrical function. The injection of prenalterol caused a distinct attenuation of the cardiostimulating effects of dobutamine: there was a prompt fall in heart rate and systolic blood pressure and a typical negative inotropic effect on the parameters of left ventricular function. In the experimental conditions selected, the effects of prenalterol were those of a beta-sympatholoytic agent. Prenalterol should therefore be classified as a partial beta 1-adrenoceptor agonist or as a beta-blocking agent with pronounced intrinsic sympathomimetic activity. The beta 1-stimulating potency of prenalterol amounts to about 60% of a full agonist.

Adrenergic beta-Agonists↗
PubMed1985

Surface marker characterization of EBV target cells in normal blood and tonsil B lymphocyte populations.

Human FACS-sorted B lymphocyte subpopulations were investigated for their susceptibility to immortalization by Epstein Barr virus (EBV). Only B cells reacting with the monoclonal antibody B2 were immortalized, whereas cells reacting with anti-human IgG or the monoclonal antibody BB2 were not responding. Cells positive or negative for IgM, IgD, Burkitt's lymphoma antigen (BLA), BB1, and HB2 were all transformed by EBV.

Antigens, Surface↗
PubMed1985

Immune response to Epstein-Barr virus (EBV) in ataxia-telangiectasia: EBV-specific antibody patterns and their relation to cell-mediated immunity.

Epstein-Barr virus (EBV)-specific antibody titers were investigated in 60 patients with ataxia-telangiectasia (AT) and 22 healthy members of their families. In addition, we studied 36 patients with primary immunodeficiencies, Behçet disease, and other conditions and 61 unrelated healthy controls. Twenty-seven AT patients were examined sequentially at intervals varying from 2 months to 8 years. The AT patients showed an increased incidence (66.6%) of high antibody titers (greater than or equal to 1:320) to viral capsid antigen (VCA) and also a high incidence (35%) of antibody titers to early antigens (EA), but low titers (less than 1:10) of antibodies to the EBV-associated nuclear antigen (EBNA) in 35% of the patients. The geometric mean titers (GMT) of antibodies to VCA were five to six times higher; those of anti-EBNA were five times lower in AT patients as compared with control groups. In serial determinations, anti-VCA and anti-EBNA titers remained constant with the exceptions of two patients who developed ALL and Hodgkin lymphoma. The patients with other diseases did not differ significantly from the controls, with the exception of lower titers (less than 1:10) of anti-EBNA (52.8%). AT patients with low anti-EBNA titers tended to have more advanced T-cell deficiencies than those with moderate anti-EBNA titers, as detected by total lymphocyte and E-rosetting cell counts and skin test responses. The percentage of patients with low serum IgA levels was found to be higher in the low anti-EBNA group than in the moderate anti-EBNA group (44.5 vs 20%).

Adolescent↗
PubMed1985

YAC-1 MHC class I variants reveal an association between decreased NK sensitivity and increased H-2 expression after interferon treatment or in vivo passage.

Two H-2 negative variants of the YAC-1 lymphoma were selected by mutagenization and sequential in vitro selections and compared with wild-type cells for changes in NK sensitivity and H-2 expression after interferon treatment or in vivo passage. The H-2 negative variants and the low H-2 expressor YAC-1 wild-type cells had similar NK sensitivity. However, IFN-beta or recombinant IFN-gamma pretreatments increased the H-2 expression of YAC-1 and protected them from NK lysis, whereas the H-2 variants, which remained H-2 negative, were not protected and often more sensitive to NK lysis. The H-2 variants were similarly susceptible as wild-type cells to three other cellular effects of interferon: protection from virus infection, modulation of Con A capping, and inhibition of cell proliferation. Thus, the only interferon-mediated effect that distinguished the H-2 negative variants from wild-type cells was the inability of the former to increase their H-2 expression and decrease their NK sensitivity. The wild-type YAC-1 line showed increased H-2 expression and decreased NK sensitivity after in vivo passage. In contrast, in vivo passaged H-2 variants showed no reexpression of H-2, and remained NK sensitive. The altered responses to interferon and in vivo passage were specific for loss or down-regulation of H-2, because Thy-1 loss (H-2 positive) YAC-1 variants behaved as the wild-type cells in all respects. This study supports the hypothesis that NK cells may function in vivo to eliminate host cells that fail to express H-2 after interferon stimulation during an immune response; such cells are a potential threat because they may escape recognition by T lymphocytes despite the expression of viral or tumor-associated antigens.

Animals↗
PubMed1985

[Physiologic effect of short AV intervals on LV filling time in VDD pacemakers--mitral valve closure in relation to atrial and ventricular contraction].

The effect of mitral valve closure on LV filling time and the onset of LV systole were assessed in 21 normals, 11 patients with left bundle branch block and in 19 patients with VDD pacemakers, which were programmed for the AV intervals 50, 150 and 250 ms, by means of echo-apexcardiography. Mitral valve closure was significantly delayed with increasing delay of intraventricular conduction: 52 +/- 11 ms in normals, 65 +/- 20 ms in LBBB patients and 127 +/- 14 ms in VDD patients. There was a similar distribution of the apexcardiographic upstroke and aortic valve opening in the 3 groups. With increasing AV intervals mitral valve closure was earlier: 127 +/- 14 ms at AV = 50 ms, 83 +/- 38 ms at AV = 150 ms and 20 +/- 75 ms at AV = 250 ms whereas the onset of LV systole and mitral valve opening remained unaltered. Thus filling time expressed in percent of cycle length was reduced from 50 +/- 6% at AV = 50 ms to 45 +/- 9% and to 38 +/- 10% at AV = 250 ms (p less than 0.001). The late onset of LV systole in VDD pacemaker patients therefore reduces LV filling time unless this is compensated by programming a short AV interval in order to maintain the physiological interval between atrial and ventricular contraction.

Adult↗
PubMed1985

[Autoimmune hemolysis caused by anti-Pr].

Following an infection with mycoplasma pneumoniae, an anti-Pr-antibody developed in a hitherto healthy man, aged 41. Within a period of 5 days the antibody caused a severe autoimmune hemolytic reaction. The patient died on the fifth day after admission due to hemolysis and uremia. The autoantibody showed a reactivity with a broad thermal range from 4 degrees C to 37 degrees C. As an initial warning sign, the patient presented an expressed livedo reticularis. Massive wholeblood exchanges could not stop the fatal process.

Adult↗
PubMed1985

[Blood levels and therapeutic effectiveness of piroxicam as affected by the time of administration].

The nonsteroidal antirheumatic preparation hydroxy-2-methyl-N-(2-pyridyl)-2H-1.2-benzothiazine-3-carboxamide 1,1-dioxide (piroxicam, Feldene) from the oxicam group is administered as a single dose of 20 mg/d. The question hence arose as to whether the therapeutic efficacy and the blood level curve (steady state) depend on the time of application. The investigation was carried out in 30 patients with arthroses of peripheral joints receiving the daily dose of piroxicam in the morning, at noon or in the evening. The results showed that irrespective of the time of administration the single dose of 20 mg/d led to a steady-state plasma level with the concentration required for efficacy. The result of therapy attained clinically also proved to be independent of the time of administration.

Anti-Inflammatory Agents↗
PubMed1984

Subgroup analysis of BL-cell lines with polyclonal BL-specific antibodies.

A Burkitt's lymphoma (BL)-specific antibody (anti-GP70), previously described, was used to analyse 22 different BL-cell lines. The results indicated specificity of antibodies to lines that contain both surface membrane Ig (SmIg) and cytoplasmic Ig (CyIg). BL-cell lines derived from more immature B cells that do not have SmIg but rather have only CyIg were negative. A comparative study with antibody to common ALL antigen (CALLA) and to another BL-specific antigen (BLA) revealed coexpression of GP70 with those two antigens, but no identity between them.

Animals↗
PubMed1984

[Lipoprotein Lp(a) as a risk factor for heart infarct--a family study].

Lp(a) concentrations, apolipoprotein A-I and B, and various lipid parameters were measured from members of 3 families in which myocardial infarction frequently occurred. No correlation could be found between Lp(a) concentration and other lipoprotein parameters. It has been demonstrated that myocardial infarction and atherosclerotic diseases occur only in patients with Lp(a) concentrations higher than 70 mg/dl. An unfavourable Apo B/Apo A-I relation or LDL/HDL relation, associated with high Lp(a) concentration seems to play a decisive role in the development of atherosclerosis or myocardial infarction. The study suggests that subjects with Lp(a) values higher than 100 mg/dl could suffer from a special form of hyperlipoproteinemia ("Hyper-Lp(a)").

Adolescent↗
PubMed1984

Studies on the polyoma-virus-induced tumor-specific transplantation antigen (TSTA)--does middle or large T-antigen play a role?

Mice and rats could be immunized against the polyoma-virus-induced tumor-specific transplantation antigen (TSTA) by repeated inoculation of frozen or irradiated cells of an MT-cDNA-transformed rat cell line (2.8) that contains only the polyoma middle T-antigen, or by cells that carried a host range mutant and expressed a full-length large T-antigen, but only non-functional N-terminal fragments of small and middle T. This shows that neither large T nor an intact middle T is necessary to elicit a polyoma tumor-specific graft rejection response. Either one of them is sufficient by itself.

Animals↗
PubMed1984

Further studies on the asymmetry of chromosome 15 duplication in trisomic leukemias of heterozygous origin: preferential status of the AKR chromosome.

Four combinations of translocation heterozygotes with cytogenetically distinct chromosomes 15 were used to investigate whether the T-cell leukemia-associated preferential duplication of the AKR-derived chromosome 15 (AKR-15) is determined by factors within this chromosome, or is due to genes within the AKR genotype, but outside chromosome 15. Two of the four combinations were also used to determine whether the AKR-15 duplication preference could be cancelled by MCF-viremia in permissive F1 hybrids. Chemically and virally induced 15-trisomic leukemias showed the same AKR-15 duplication preference, which was due to some autonomous property of AKR-15 itself. It was maintained in (C57BL 6;15 X C57BL) F1 leukemias, where 6;15 is the only AKR-derived chromosome propagated on the C57BL/background. In the (C57BL 6;15 X AKR) F1 hybrid cross where both chromosomes 15 are of AKR origin, duplication occurred at random. To approach the second question, MCF viremia was induced by neonatal virus inoculation into permissive (AKR 6;15 X B6Fv-In) F1 hosts. The preferential duplication status of the AKR-derived 6;15 remained unchanged.

Animals↗
PubMed1984

Chromosomal translocations activating myc sequences and transduction of v-abl are critical events in the rapid induction of plasmacytomas by pristane and abelson virus.

Plasmacytomas with short latent periods can be induced in BALB/c mice by a single intraperitoneal (i.p.) injection of 0.5 ml pristane followed 20-40 d later by an injection of Abelson virus. The karyotypes of 18 such tumors were determined; 10 of these had rcpt 12;15, 5 had rcpt 6;15 and 3 had no translocations, but two of these have been shown to have interstitial deletions of chromosome 15. The specific breakpoints were the same as described in pristane-induced plasmacytomas, i.e., at 15D2 /3, 6C2 , and 12F2 . Near diploid karyotypes and trisomy of chromosome 11 were frequently seen. All of the Abelson-plus-pristane-induced plasmacytomas (ABPC) were studied as transplanted tumors, contained integrated v- abl sequences, and actively transcribed v- abl mRNA. All but one of these tumors contained abundant myc RNA transcripts. The shortness of the latent periods of the ABPC suggests that the rcpt 12;15 and rcpt 6;15 occur soon after pristane administration and are present at the time Abelson virus is introduced. In this form of plasmacytomagenesis , activated v- abl genes appear to bypass other genetic changes that require a much longer period of time in pristane plasmacytomagenesis . Nonetheless, the consistent finding of chromosome-15 alterations and abundant myc expression in these plasmacytomas emphasize the apparent need for multiple events even in the genesis of some tumors induced by rapid transforming viruses.

Abelson murine leukemia virus↗
PubMed1984

[Cardiac arrhythmias and their clinical significance in mitral valve prolapse].

Among 160 patients with mitral-valve prolapse but no other illness there were 118 with cardiac arrhythmias. 30 had frequent or multifocal ventricular premature systoles, 21 had coupled ventricular extrasystoles, and seven had ventricular tachycardia. In six patients the prematurity index was under 1. Supraventricular premature systoles were registered in 56 patients, with seven each having paroxysmal atrial tachycardia and paroxysmal atrial flutter or fibrillation. Ventricular arrhythmias were significantly more frequent in late-systolic prolapse and with positive auscultation findings (systolic click or systolic murmur). Long-term ECG monitoring was more valuable than an exercise ECG. About half the patients with frequent arrhythmias had palpitations and rapid heart action. Coupled ventricular premature systoles and ventricular tachycardias, as well as R-on-T were relatively rare; our findings thus tend to suggest a relatively favourable prognosis for these arrhythmias.

Adolescent↗
PubMed1984

Distinction between Burkitt lymphoma subgroups by monoclonal antibodies: relationships between antigen expression and type of chromosomal translocation.

Twenty-six lines derived from 22 Burkitt lymphoma patients were examined for cytoplasmic vs. surface immunoglobulin and the expression of the monoclonal-antibody-detected BLA, CALLA and LB-I antigens. Six of the lines carried the variant translocations 8;2 or 8;22 (three each), 17 lines had the typical 8;14 translocation, I was translocation-negative (BJAB) and 2 were not examined cytogenetically. Depending on their immunoglobulin and surface marker expression, the BL lines could be subdivided into several subgroups. There was a strong inverse correlation between the expression of the CALLA and the LB-I marker. All BLA-lines were CALLA-, whereas the CALLA+ lines could be either BLA- or BLA+. All six variant translocations belonged to the CALLA-BLA-LBI+ category. Only one set of three lines, derived from the patient with the 8;14 translocation, belonged to the same subgroup. This suggests that the typical vs. the variant translocation freezes the BL cell at a different stage of differentiation. The variant translocation-carrying subtypes represent probably a somewhat more advanced stage of differentiation.

Antibodies, Monoclonal↗
PubMed1984

Triplication of one chromosome No. 15 with an altered c-myc containing EcoRI fragment and elimination of the normal homologue in a T-cell lymphoma line of AKR origin (TIKAUT).

An ouabain- and thioguanine-resistant subline (TIKAUT) of spontaneous AKR lymphoma, TKA, was trisomic for chromosome 15 and contained a single 33 kb EcoRI fragment, containing the oncogene c-myc. The original TKA lymphoma and derived in vitro line contained the same 33 kb fragment, as well as a normal 22 kb fragment. It has been concluded that the original 15-trisomic TKA tumor has duplicated a 15-chromosome that contained the changed fragment, while maintaining the normal fragment as well. Subsequently, in the derived TIKAUT line, the changed chromosome duplicated again, giving rise to three copies, and the normal homologue was eliminated altogether. This confirms our earlier somatic hybrid study showing that the duplicated 15-chromosome of a T-cell leukemia confers an advantage on the cell that favors tumorigenicity, whereas the normal homologue exerts a counteracting influence. Therefore, in the course of tumor progression, the changed chromosome tends to be amplified, whereas its normal homologue tends to be eliminated.

Animals↗