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Biomedical subjects

F Herrmann

Publications and source records attributed to F Herrmann.

At least 217 records · Page 12Linked to original sources
PubMed1987

In vitro regulation of human hematopoiesis by natural killer cells: analysis at a clonal level.

We studied the effects of a series of well-characterized clones of human natural killer (NK) cells on the proliferation of highly purified normal marrow hematopoietic progenitor cells. Individual NK clones suppressed granulocyte, monocyte, erythroid, or mixed colony formation in a heterogeneous but clonally stable manner. Inhibition of colony growth required a period of close cell contact between NK cell and progenitor cell with maximum inhibition occurring after 8 to 18 hours of preincubation time. The mechanism of killing was at least partially humoral, however, as cell-free supernatants generated by NK clones "activated" by contact with a target cell also inhibited progenitor cell growth. One of the possible humoral mediators was identified as gamma-interferon by studies with specific neutralizing monoclonal antibodies. These results show that clonal NK lines can be further activated by coming in contact with hematopoietic progenitor cells, resulting in substantial inhibition of colony formation in vitro.

Antigens, Surface↗
PubMed1987

[Is hip sonography in premature infants necessary as a screening procedure?].

Screening sonography of the hip in 132 premature infants indicates that prematurity is not a risk for congenital dysplasia/dislocation of the hip. However, for reasons explained in the text, screening should be carried out before discharge from hospital. Follow-up examinations are necessary only for infants with known risk factors for dysplasia/dislocation of the hip.

Female↗
PubMed1987

Tumor necrosis factor (TNF)-alpha but not TNF-beta induces secretion of colony stimulating factor for macrophages (CSF-1) by human monocytes.

Tumor necrosis factor (TNF)-alpha has been identified as a major inducer of colony stimulating factor (CSF)-secretion by human vascular endothelial cells and fibroblasts. In the present study we assessed the capacity of TNFs to induce release of CSF-1 from highly purified peripheral blood monocyte preparations. Whereas monocytes do not accumulate CSF-1 messenger (m)RNA constitutively and consequently do not produce CSF-1 protein, CSF-1 mRNA and protein secretion became detectable, when monocytes were cultured in the presence of TNF-alpha, that was synergistically enhanced by interferon-gamma (IFN-gamma). However, under identical experimental conditions TNF-beta failed to induce monocyte CSF-1 synthesis. Cultures of monocytes in the presence of TNF-beta before addition of TNF-alpha abolished the CSF-1 inducing capacity of TNF-alpha, suggesting that TNF-beta may act as antagonist to TNF-alpha for CSF-1 production. These data point out a previously unrecognized function of TNF-alpha to modulate CSF-1 release by monocytes and demonstrate disparate biological properties of different TNF species in hematopoiesis.

Colony-Forming Units Assay↗
PubMed1986

T cell-monocyte interactions in the production of humoral factors regulating human granulopoiesis in vitro.

A variety of monocyte functions are modulated by the T cell lymphokine interferon-gamma (IFN-gamma). We assessed the capacity of IFN-gamma to induce release of granulocyte-monocyte stimulating factors (CSF-GM) from highly purified monocyte preparations. Whereas secretion of CSF-GM by monocytes is negligible in the absence of T cells, CSF-GM secretion is inducible when concentrations of IFN-gamma as low as 10 U/ml are present. This effect could be abrogated by specific neutralizing monoclonal antibody to IFN-gamma and was restricted to monocytes, as resting T cells failed to secrete detectable CSF-GM in response to IFN-gamma. The response of monocyte preparations to IFN-gamma was biphasic in that concentrations greater than 250 U/ml did not induce detectable CSF-GM activity. However, this was shown to be due to the release of a humoral inhibitor of G/M-progenitor cells, and not necessarily due to a lack of CSF-GM secretion.

Cell Communication↗
PubMed1986

[Modification of the diagnosis of thyroid gland function by iodine-containing roentgen contrast media].

The influence on the parameters of the thyroid gland BEI, T3-, T4- and TSH-serum level by the iodine-containing oral bile X-ray contrast remedy Falignost is demonstrated. Following a peripheral conversions inhibition from T4 to T3 by the contrast remedy the thyroid hormones in the serum are changed in different kind and duration. This influence is more expressed in patients with liver cirrhosis and continues. The risk of an iodine-induced hyperthyroidism is discussed. In the judgment of a possible disturbance of the function of the thyroid gland anamnestically is always to be asked the question about previous applications of iodine-containing drugs and it must be accordingly be taken into consideration.

Contrast Media↗
PubMed1986

[Unwanted modification of the thyroid gland by drugs with special reference to nonsteroidal antirheumatic agents].

In two retrospective clinical studies was investigated the influence of the modern non-steroidal antirheumatic drugs indometacin and diclofenac (Rewodina) on the thyroid gland and corresponding peripheral hormone parameters. Under longterm treatment with indometacin a moderate strumigenic effect could be observed, which could not clearly be proved under the diclofenac therapy. In all patients with rheumatoid arthritis, independent of the kind of pharmacotherapy, decreased T3-hormone levels were found in normal serum T4-values. The findings are discussed as "low-T3-syndrome" in rheumatoid arthritis, induced by the disease lasting for many years possibly in combination with the long-term therapy with antirheumatic drugs. In a second series of investigations in 75 out of 3,104 patients (2.4%) with a bland struma distinct references to a medicamentous evocation of the enlargement of the thyroid gland were found. Anticonvulsive drugs and the antidepressive drug lithium stood in the first place as inductors of such medicamentous struma. Of the non-steroidal antirheumatic drugs only some cases could be ascribed to phenylbutazone, whereas the more modern preparations indometacin and diclofenac in none of our patients could with certainty be made responsible for a development of struma.

Anti-Inflammatory Agents↗
PubMed1986

[Leukocyte function in patients with hyperthyroidism].

In 20 patients with hyperthyroidism the behaviour of the agglomeration of leucocytes as well as of the adhesivity before and after the methimazol therapy was investigated. The agglomeration of leucocytes was directly inhibited neither by the overfunction of the thyroid gland nor by methimazol. By means of a stimulation test an undisturbed ability of leucocytic activation in hyperthyroidism could be proved. The adhesivity at the glass slide, however, was slightly restricted in untreated hyperthyroidism. It normalized under thyrostatic therapy.

Adolescent↗
PubMed1986

Establishment of an interleukin 2-dependent T cell line derived from a patient with severe aplastic anemia, which inhibits in vitro hematopoiesis.

Circulating mononuclear cells from a patient developing severe aplastic anemia during the course of non-A, non-B hepatitis were found to be virtually entirely composed of in vivo activated suppressor T cells (Ia+T8+). These cells were used to establish a new permanent cell line, termed SMAA, by using phytohemagglutinin, Ebstein-Barr virus-transformed irradiated B cells, allogeneic irradiated peripheral blood mononuclear cells, and recombinant interleukin 2 to investigate the relationship of aplastic anemia-derived circulating T cells to bone marrow failure. SMAA cells, now in continuous culture for more than 9 mo, were shown to inhibit proliferation of purified myeloid progenitors and their differentiation into early and late appearing neutrophil and eosinophil colonies by 90%, whereas monocyte colonies were much less affected. Similarly, growth of erythroid colonies and bursts was almost completely inhibited, as was anti-mu-induced B cell proliferation and lectin-induced T cell proliferation. This inhibition of hematopoiesis was mediated by the release of a soluble factor that was sensitive to acid (pH 2), heat (56 degrees C), and trypsin. Monoclonal and polyclonal antibodies to interferon-gamma could abrogate the inhibitory effects of SMAA supernatant, but more than 10(4) neutralizing U/ml had to be added. The effects of SMAA could be duplicated by adding 10(4) U/ml of purified recombinant interferon-gamma to colony and proliferation assays. The concentration of interferon-gamma in SMAA supernatant was estimated to be greater than 3 X 10(3) National Institutes of Health reference U/ml by immunoradiometric assay. These results demonstrate that some patients with aplastic anemia have circulating T cells that are capable of prolonged in vitro secretion of interferon-gamma causing severe inhibition of in vitro hematopoiesis, and these cells can be expanded into permanent lines for studies on their regulatory properties.

Adult↗
PubMed1986

[Statistical principles for the validation of diagnostic procedures. A contribution to quality assurance exemplified by Doppler sonography].

This article presents an introduction to some basic considerations for the evaluation of diagnostic tests and procedures. In order to determine the characteristics of a diagnostic procedure sensitivity and specificity are estimated from results of an evaluation study. The statement of confidence limits gives an idea of the safety of the estimates. Different scales of measurement and their respective distributions must be taken into consideration. Quite often sensitivity and specificity are dependent on various threshold values. ROC-curves can be used to study this dependence. In practice the interpretation of test results relies on the predictive value. The Bayes formula permits calculation of the predictive value depending on sensitivity, specificity and prevalence. This paper illustrates the application of statistical methods by analysing data of Doppler ultrasound studies.

Diagnosis, Differential↗
PubMed1986

Relationship between HLA-DR expression by normal myeloid progenitor cells and inhibition of colony growth by prostaglandin E. Implications for prostaglandin E resistance in chronic myeloid leukemia.

The expression of HLA-DR antigens by normal myeloid progenitor cells (CFU-GM) has been linked to inhibition of colony growth by prostaglandin E (PGE), while resistance to the inhibitory effects of PGE in chronic myeloid leukemia (CML) has been attributed to a lower fraction of HLA-DR+ CFU-GM in this disease. However, we have previously shown that virtually all CFU-GM in normal bone marrow (NBM) as well as CML peripheral blood express HLA-DR antigens, which raises the possibility that these surface molecules may not be the sole determinants of a progenitor cell's sensitivity to PGE. In order to evaluate the relationship between HLA-DR expression and prostaglandin inhibition, we partially purified NBM progenitor cells using fluorescence-activated cell sorting to prepare cell fractions with high and low HLA-DR antigen density. Normal progenitor cells with high DR density tended to form monocyte colonies in agar culture, whereas the low DR density fraction was enriched for granulocyte colony-forming cells. Inhibition by PGE was greatest in the high DR+ fraction and was largely restricted to monocyte progenitor cells. Inhibition of CFU-GM by PGE was less in CML than in NBM, but this decreased inhibition correlated with a significantly lower number of monocyte-CFU in CML. These data suggest that high HLA-DR antigen density may select for normal progenitor cells that are committed to monocyte differentiation and are, therefore, more likely to be inhibited by PGE. The relative deficit of monocyte progenitor cells in CML may partially explain the phenomenon of PGE resistance in this disease.

Alprostadil↗
PubMed1986

Possibilities and problems in genomic diagnosis of Duchenne muscular dystrophy with molecular probes.

Selected families affected with Duchenne muscular dystrophy from an extensive pedigree analysis with linked restriction fragment length polymorphisms and creatine kinase estimations are compiled to demonstrate the various counselling situations for carrier determination and prenatal diagnosis. The creatine kinase determination suffers from approximately 30% false negative values in carrier determination. The DNA analysis is limited by the uninformativity of the DNA markers and the occurrence of meiotic crossovers between the particular restriction fragment length polymorphism pattern and the Duchenne muscular dystrophy locus. The use of markers bridging the Duchenne muscular dystrophy locus, such as 754 and C7, is presently best suited for this purpose but is applicable to only a relatively small number of cases. The use of the physically closer probe, pERT 87, is much more informative althrough it too recombines with the Duchenne muscular dystrophy locus. DNA analysis allows prenatal diagnosis for unaffected boys from the restriction fragment length polymorphism pattern confined to the healthy grandpaternal X-chromosome in cases where the carrier status of the mother is established or in doubt. As in the case of carrier determination, crossover events and uninformativity of restriction fragment length polymorphisms limit the feasibility of this approach.

Alleles↗
PubMed1986

Effects of recombinant human GM-CSF on proliferation of clonogenic cells in acute myeloblastic leukemia.

Proliferation of acute myeloblastic leukemia (AML) cells in vitro is limited in most cases to a small subset of blasts that have several properties of stem cells. These leukemic colony-forming cells (AML-CFU) generally require addition of exogenous growth factors for proliferation in agar or methylcellulose. These factors can be supplied by media conditioned by phytohemagglutinin-stimulated normal leukocytes or by CSF-secreting tumor cell lines. However, the exact factor or factors required for stimulation of AML-CFU growth have not been defined. We compared the AML-CFU stimulatory activity of a human recombinant GM-CSF with that of GCT-CM, Mo-CM, and the PHA-leukocyte feeder system in 15 cases of AML. In each of the 12 cases that required exogenous growth factors for maximum AML-CFU growth, recombinant GM-CSF could replace either GM-CSF or Mo-CM, and could partially replace the PHA-leukocyte feeder system. These results indicate that this GM-CSF is a growth promoter of AML-CFU in these culture systems.

Adult↗
PubMed1985

Expression of interleukin 2 receptors and binding of interleukin 2 by gamma interferon-induced human leukemic and normal monocytic cells.

Gamma interferon induced surface expression of interleukin 2 (IL-2) receptors on normal human monocytes and the monocytoid cell lines U937 and HL60. These receptors were detected by anti-IL-2 receptor monoclonal antibodies, and U937 IL-2 receptors were indistinguishable from T lymphocyte IL-2 receptors by immunoprecipitation. Also, U937 IL-2 receptors bound biologically active IL-2. These results suggest a role for monocyte IL-2 receptors in T cell/monocyte interaction during an immune response.

Antibodies, Monoclonal↗
PubMed1985

Human X chromosome markers and Duchenne muscular dystrophy.

Two DNA markers, a random DNA fragment 754 and the cDNA sequence encoding the gene for ornithine transcarbamylase (OTC) have been studied in kindreds segregating for Duchenne muscular dystrophy. 754 and OTC are located close physically to the mutation in the region Xp21 below the breakpoints in two Duchenne females. The genetic distance was found to be approximately 10cM between 754 and DMD (two crossovers in 26 meioses) and to be approximately 10cM between OTC and DMD (two crossovers in 26 meioses). Physical data suggest the order DMD-754-OTC. The frequency of recombination compared to physical distance between these markers and DMD suggests that there may be a hot spot of recombination. The relevance of these observations for the isolation of the DMD mutation and clinical use of these probes is discussed.

Chromosome Mapping↗
PubMed1985

A comparison of membrane marker phenotypes in hairy-cell leukemia and phorbol-ester induced B-cll cells using monoclonal antibodies.

The neoplastic cells from 14 cases of hairy-cell leukemia were investigated in order to determine their membrane phenotype on the basis of their reactivity with a large panel of B-, T-, myeloid/monocytic- and non-lineage restricted monoclonal antibodies. The data were compared to those from monoclonal antibody studies on phorbol-ester (TPA) induced cells from 10 patients with B-type chronic lymphocytic leukemia. The study has so far revealed further evidence for the B-cell nature of hairy-cells leukemia and demonstrates a developmental link between the two cell types, suggesting that hairy-cells represent a more advanced differentiation stage along the B-cell lineage.

Antibodies, Monoclonal↗