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Biomedical subjects

T Hahn

Publications and source records attributed to T Hahn.

At least 91 records · Page 5Linked to original sources
PubMed1992

Superoxide production during refeeding in patients with anorexia nervosa.

The effect of undernutrition and refeeding on superoxide production by polymorphonuclear cells (PMN) was studied in 11 girls suffering from anorexia nervosa (AN) and 17 age-matched, normal, healthy, control subjects. Superoxide anion production by PMNs from undernourished AN patients was comparable to normal, while a significant decrease in this function was observed during the initial period of refeeding. After a more extended period of refeeding, superoxide production by PMNs from AN patients increased and gradually returned toward normal values. Superoxide production correlated with length of the refeeding period (RF), weight as a percentage of ideal weight for height (W/H%), and rate of weight gain (WG). These results imply that a variety of physiological parameters, including susceptibility to infection, may be altered by refeeding undernourished patients.

Adolescent↗
PubMed1992

The interferon system in patients with malignant disease.

Since the interferon (IFN) system involves both IFN producing and IFN responding cells, it is possible to study separately these phenomena, relating them to disease entities as well as to response to therapy. Numerous studies in animals and man suggest effectiveness of IFN and IFN inducer therapy in cancer. However, the competency of the various components of the endogenous IFN system in malignancy has received little attention. These studies show that in malignancy there may be (1) a high incidence of elevated blood levels of IFN; (2) a deficient response of peripheral blood mononuclear cells to endogenous and exogenous IFN; and (3) increased uninduced in vitro IFN production by these cells. These findings indicate that cancer patients are equipped with the ability to produce IFN and suggest that it may be the deficient response of their cells to IFN that plays a role in the development and progression of the disease. Furthermore, the finding of increased spontaneous "uninduced" production of IFN by cells from cancer patients suggests the possibility of an intracellular inducer such as found in persistently virus-infected cells.

Humans↗
PubMed1992

Enhanced response of human circulating erythroid progenitor cells to hGH and to IGF-I in children with insufficient growth hormone secretion.

The response of hematopoietic progenitors to the growth promoting effects of hGH and IGF-I has been documented. In this study, the effects of recombinant hGH and IGF-I on the growth of circulating erythroid burst forming cells (BFU-E) from growth-IGF-I retarded children with insufficient growth hormone secretion (IGHS) were evaluated and compared with values obtained from either children with short stature and normal growth hormone levels (SNGH) or normal donors. Both recombinant hGH and IGF-I had significantly greater stimulatory effects on the growth of BFU-E from the IGHS compared with the SNGH and with the normally growing children. At its optimal concentration of 200 micrograms/L, recombinant hGH had a stimulatory effect on the growth of BFU-E from 11 IGHS children yielding a mean +/- SD value of 2.0 +/- 0.3-fold above the unstimulated controls compared with 1.45 +/- 0.16-fold and 1.36 +/- 0.04-fold stimulation of BFU-E from six SNGH and five normal donors, respectively. Similarly, IGF-I, at its optimal concentration of 0.065 nmol/L (0.5 ng/mL), stimulated IGHS-derived BFU-E growth 1.67 +/- 0.25-fold above unstimulated controls, compared with 1.28 +/- 0.17-fold and 1.3 +/- 0.1-fold stimulation of BFU-E from SNGH and from normal donors, respectively. The hGH- and IGF-I-induced stimulatory effects could be neutralized by their respective specific MAb.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Drinking water fluoridation and caries prophylaxis: with special consideration of the experience in the former East Germany.

Drinking water fluoridation for caries prophylaxis is not a means of primary prevention: i.e., avoidance of sugar and microorganisms in the oral cavity; but rather a means of secondary prevention: e.g., prevention of bacterial production of carboxylic acid from sugar, and therapy: e.g., enhancement of enamel resistance to demineralization by incorporation of fluoride in remineralization of the enamel surface. Currently available epidemiologic studies on the effects of drinking water fluoridation reveal: reduction of the incidence of caries, particularly in children no detrimental health effects; cosmetically undesirable dental fluorosis may occur, however. Nevertheless, introduction of drinking water fluoridation in Germany is not recommendable because of: the greater effectiveness of primary caries prevention, the acceptance of which is reduced, however, by drinking water fluoridation the at least equal prophylactic effect of fluoride via other routes, e.g. via toothpaste the narrow range between beneficial and detrimental dosage the avoidance of fluoride-enriched waste water the prerogative of minimal manipulation of drinking water content.

Dental Caries↗
PubMed1992

[Cytokines in anorexia nervosa--nutritional or neuroimmunal changes?].

Natural cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor (TNF-alpha) by mononuclear cells in vitro, and PHA-induced interferon (IFN-gamma) production were examined by standard methods in 14 females with anorexia nervosa (AN) and marked weight loss and in 16 normal matched controls. The results were confirmed by neutralization with monoclonal antibodies. In the anorectic patients there was a significant increase in TNF production (16 +/- 5 vs 4 +/- 3 mu/ml), and depressed CMC (4 +/- 2 vs 10 +/- 3 lytic units per 50/10(6) cells) and IFN-gamma production (172.5 +/- 25 vs 367 +/- 34 mu/ml). Following successful refeeding and nutritional rehabilitation, all values returned to normal. Thus there are changes in cytokines and defective natural cytotoxicity in AN, apparently related to undernutrition and not to neuroimmunomodulation. The increased TNF-release may further suppress food intake and enhance tissue catabolism, suggesting that nutritional rehabilitation should be the earliest therapeutic goal in anorexia nervosa.

Anorexia Nervosa↗
PubMed1992

Thymic humoral factor-gamma 2, an immunoregulatory peptide, enhances human hematopoietic progenitor cell growth.

Thymus humoral factor-gamma 2 (THF gamma 2), an octapeptide important for T-lymphocyte regulation, was assessed for its effect on the in vitro growth of human hematopoietic progenitor cells. This was achieved using a recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF)-stimulated myeloid cell colony formation (granulocyte-macrophage colony-forming cells, GM-CFC) assay as well as a recombinant erythropoietin (rEpo)-stimulated erythroid burst formation (erythroid burst-forming units, BFU-E) assay. Cells were obtained from bone marrow (BM) and peripheral blood (PB) of normal healthy donors and from patients with suppressed bone marrows. The latter group included aplastic anemia, leukemia, and lymphoma patients and patients with solid tumors who responded to intensive chemotherapy with significant pancytopenia. THF gamma 2 significantly enhanced normal BM and PB GM-CFC and PB BFU-E by 2- to 2.5-fold. This effect was totally dependent on the presence of the respective growth factors, that is, rGM-CSF or rEpo, and was specifically reversed by an anti-THF gamma 2 antiserum. Furthermore, although THF gamma 2-induced enhancement of GM-CFC colony formation was not affected by lymphocyte or monocyte depletion, the augmenting effect of the peptide on BFU-E was completely abrogated in the absence of lymphocytes. THF gamma 2-induced augmented growth of progenitor cells derived from severely suppressed marrows was minimal. However, cells from moderately neutropenic patients with leukemia in remission or with lymphoma under chemotherapy responded to the peptide similarly to cells from normal donors. These results suggest a stimulatory role for THF gamma 2 on human myeloid and erythroid hematopoietic progenitor cells. They also suggest the lymphocyte dependence of BFU-E enhancement and lymphocyte independence of GM-CFC stimulation by THF gamma 2. In the former case the thymus-derived peptide may act through the induction of certain erythroid-enhancing lymphokines.

Adjuvants, Immunologic↗
PubMed1991

Tumor necrosis factor-alpha and anorexia--cause or effect?

Tumor necrosis factor-alpha (TNF-alpha) is a principal cytokine that may induce weight loss in malignancies and certain chronic infections. Short-term caloric deprivation has been found to facilitate in vitro TNF-alpha production, while increased spontaneous production of TNF-alpha has been found in patients with anorexia nervosa (AN). In the present work, we studied in vitro TNF-alpha production in other types of chronic undernutrition and the changes in TNF-alpha production during the refeeding of patients with AN. Undernutrition was evaluated by calculating fat body mass (FBM) from skinfold measurements and lean body mass (LBM) by total body potassium (TBK) counting. Spontaneous and induced TNF-alpha production by peripheral blood mononuclear cells (PBMC) was studied in six chronically malnourished patients with no intercurrent infections, seven patients with AN, and 16 age-matched normal healthy subjects. Spontaneous TNF-alpha production was in the normal range in the chronically undernourished subjects (4.3 +/- 1.5 v 5.0 +/- 1.9 U/mL), but significantly increased in the seven patients with AN (221 +/- 327 v 5.0 +/- 1.9 U/mL, P less than .0006). During refeeding of patients with AN, TNF-alpha production decreased to the normal range concomitantly with weight gain. We concluded that chronic undernutrition, in general, is not always associated with increased TNF-alpha production and that it still remains to be determined whether TNF-alpha plays a primary role in the pathogenesis of AN.

Adolescent↗
PubMed1991

Inhibition of acetylcholinesterase and butyrylcholinesterase by the organophosphorus insecticide methylparathion in the central nervous system of the golden hamster (Mesocricetus auratus).

The toxic effects of the organophosphorus pesticide methylparathion are primarily caused by the inhibition of acetylcholinesterase activity in the central nervous system, whereas the relationship between butyrylcholinesterase and poisoning symptoms is unclear. The presumed different effects of methylparathion on acetylcholinesterase in various regions of brain and spinal cord suggest differences in the distribution of molecular enzyme forms. In the present work, the in vitro and in vivo effects of methylparathion on acetylcholinesterase and butyrylcholinesterase were studied in whole brain homogenates of golden hamsters with biochemical methods. Furthermore, acetylcholinesterase activity was determined in regions of the nervous system by quantitative histochemistry (microdensitometry). Biochemically, very low IC50 values of the hydrophilic and lipophilic fractions of both enzymes were measured. Analysis of the time course of enzyme inhibition revealed maximum inhibition 45 min after methylparathion application. Using microdensitometry different degrees of acetylcholinesterase inhibition were found in various areas of the brain. The highest inactivation was observed in the Substantia nigra and in thalamic nuclei; in several regions of the cerebellum, the inhibition rate was comparatively lower. In conclusion, methylparathion acts as an potent inhibitor of acetylcholinesterase and butyrylcholinesterase in the hamster nervous system. The region-specific different inactivation of acetylcholinesterase might be caused by the existence of multiple forms of the enzyme in various brain regions.

Acetylcholinesterase↗
PubMed1991

Ciprofloxacin inhibits human hematopoietic cell growth: synergism with tumor necrosis factor and interferon.

The cytokines tumor necrosis factor (TNF) and interferon (IFN) induce antiproliferative and cytotoxic activity in a variety of cell types. Ciprofloxacin (CFN)--a new fluoroquinolone antibiotic--has also been described, at high concentrations, to suppress hematopoietic cell growth and to affect cytokine production. This study examines the possible relationship between TNF alpha and IFN gamma, as components of host defense mechanisms, and CFN. To investigate the effect of CFN, either alone or combined with TNF or IFN, on normal human hematopoiesis, we examined in vitro changes in hematopoietic progenitor cell growth. We also studied the effect of CFN on human cytokine production by determining TNF, IFN, and colony-stimulating factor (CSF) production by human mononuclear leukocytes (MNC). Granulocyte and monocyte colony formation (granulocyte-macrophage colony-forming cells, GM-CFC) as well as erythroid burst formation (erythroid burst-forming units, BFU-E) were inhibited only by high nontherapeutic levels of CFN. Lower CFN concentrations, however, were inhibitory in the presence of low, noninhibitory concentrations of human recombinant (r)IFN gamma or rTNF alpha. CFN induced a striking dose-dependent increase in IFN gamma production and a decrease in CSF production by mitogen-stimulated MNC. No effect was observed, however, on TNF production by stimulated MNC. The synergistic inhibition of hematopoietic progenitor cell proliferation, achieved by combining low doses of CFN and of antiproliferative cytokines, may explain the occasional case of leukopenia or anemia observed in infected patients receiving CFN. This effect may also indicate the applicability of such a combination against malignant cell growth.

Cell Division↗
PubMed1991

Tumor necrosis factor in familial Mediterranean fever.

PURPOSE: The pleiotropic inflammatory effects of tumor necrosis factor (TNF) prompted a study of this cytokine in familial Mediterranean fever (FMF), a recurrent polyserositis of unknown etiology. PATIENTS AND METHODS: Thirty-six asymptomatic and 24 patients with acute FMF were studied and compared with 20 matched healthy subjects. TNF levels were measured by bioassay in the plasma and in supernatants of peripheral blood mononuclear cells (PBMC) incubated alone or with an inducer (lipopolysaccharide, phytohemagglutinin [PHA], or Sendai virus). Cytotoxicity could be abolished in all cases by preincubation with monoclonal anti-TNF-alpha antibodies. RESULTS: No TNF was found in plasma and non-induced PBMC supernatants. Induced TNF production was markedly decreased in patients with acute FMF and increased in asymptomatic FMF patients to levels over those of control subjects (p less than 0.05). Thus, PHA-induced TNF levels were 4 U/mL in patients with acute FMF, 25 U/mL in asymptomatic patients, and 14 U/mL in healthy control subjects (median values), and the other inducers gave similar results. Retesting of patients first studied during an acute episode when their disease was quiescent also revealed a fivefold increase in TNF production. These results were independent of the use of colchicine, which also had no effect on TNF levels when taken by volunteers (1 mg/day) or when added to the PBMC cultures (10(-7) M). CONCLUSIONS: Since TNF has a very short half-life in plasma, the capacity of PBMC to respond to TNF inducers may more accurately reflect its synthesis. A marked decrease in this response in acute FMF suggests "exhaustion" of cells that are already highly activated to produce TNF and the possible participation of TNF in the pathogenesis of FMF.

Adult↗
PubMed1990

Tumour necrosis factor production and cell-mediated immunity in anorexia nervosa.

Fourteen patients with anorexia nervosa (AN) were studied for the production of tumour necrosis factor (TNF), the activation of the interferon (IFN) system and cell-mediated cytotoxicity (CMC) and the results were compared with 16 age-matched healthy women. AN patients had significantly increased spontaneous TNF production by peripheral blood mononuclear cells (PBMC) in vitro (16 +/- 5 U/ml versus 4 +/- 3 U/ml in the control group; P less than 0.05), although no TNF was detectable in the plasma from either group. TNF production in vitro, following stimulation of PBMC by phytohaemagglutinin (PHA) or tumour cells, was similar in AN patients and controls; however, lipopolysaccharide (LPS) induced TNF production was found to be lower in AN (P less than 0.1). CMC was significantly lower in AN patients (4 +/- 2 versus 10 +/- 3 in controls, expressed as lytic units/10(6) cells; P less than 0.05), but no difference could be found between AN and controls in IFN activity as reflected by the level of the IFN-induced enzyme 2'-5' oligoadenylate synthetase (2-5A) in PBMC. Beta-endorphins in the plasma were higher in the AN group (P less than 0.05) but these levels could not be correlated to those of IFN, CMC or TNF. Defective CMC and increased TNF production by PBMC in patients with anorexia nervosa may possibly result from the nutritional deficiencies and neuroendocrine abnormalities associated with the disease, and may contribute to the pathophysiology of AN.

Adolescent↗
PubMed1990

Interferon system and natural killer cell activity in myasthenia gravis.

The autoimmune response in myasthenia gravis is well characterized, but little is known about the mechanisms initiating it. We have studied the interferon system and natural killer cell activity in 25 patients with myasthenia gravis and compared them to 68 healthy subjects and 96 patients with acute viral infections. Forty-four per cent of patients had circulating interferon (greater than 16 mu/ml), and in a similar proportion their peripheral blood mononuclear cells were in an antiviral state, i.e., showed low levels of viral replication when infected by vesicular stomatitis virus. Spontaneous in vitro interferon production by patients' peripheral blood mononuclear cells was also common (greater than 10 mu/ml, 32 per cent), while the response to the alpha-interferon inducer poly I:C was lower than expected, possibly reflecting the already high state of activation of the interferon system. These results were essentially similar to those obtained in patients with viral illnesses and differed significantly from healthy controls. In many myasthenia gravis patients (16 of 22, 73 per cent), a markedly deficient natural killer cell activity was found, with a median cytotoxicity of 6.5 per cent compared to 29 per cent in healthy subjects (p less than 0.005). Thus, many patients with myasthenia gravis have evidence of an activated interferon system and defective natural killer cell activity, suggesting an occult viral infection or reflecting nonspecific stimulation which may nevertheless contribute to the pathogenesis of the autoimmune response.

Acute Disease↗
PubMed1990

TNF, interferon-gamma and cell-mediated cytotoxicity in anorexia nervosa; effect of refeeding.

"Natural" cell-mediated cytotoxicity (CMC), spontaneous release of tumor necrosis factor-alpha (TNF-alpha) by mononuclear cells in vitro and PHA-induced interferon-gamma (IFN-gamma) production were examined by standard methods (confirmed by neutralization with monoclonal antibodies) in 14 female patients with marked weight loss due to anorexia nervosa (AN) and 16 matched healthy controls. We found a significant increase in TNF production in AN, as well as a depressed CMC and IFN-gamma production. Following successful refeeding and nutritional rehabilitation of the AN patients, all results normalized to levels similar to those of controls. Thus, undernutrition in AN is accompanied by changes in cytokines and defective "natural" cytotoxicity. The implications in vivo are unclear but our findings may reflect nutritional-related immunodeficiency in AN and moreover, the increased TNF-release may further suppress food intake and enhance tissue catabolism in anorexia nervosa.

Anorexia Nervosa↗
PubMed1990

[The detection of legionellae in a water pipe system using gene probe technics and culture methods].

In a new hospital building, cold and warm water systems were examined for microbiological parameters before opening. All of the 35 sampling sites showed elevated colony counts, i.e. greater than 100 cfu/ml. 11 of these contained Legionella species at various times. While Escherichia coli, coliform bacteria and Pseudomonas aeruginosa could not be found, Legionella longbeachae serogroup 1 + 2 was identified in 13 samples. Only one sample contained Legionella pneumophila serogroup 3. Legionella species were detected using a commercial gene probe assay and culture techniques. The gene probe method proved to be superior to the culture techniques insofar as significantly positive results were obtained more frequently, and evidence for the presence of Legionella of different species and serogroups could be obtained with a single procedure. The gene probe method appears to be a suitable screening method for the detection of Legionella species.

Colony Count, Microbial↗