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  • 1
    Electronic Resource
    Electronic Resource
    A new side effect of inhaled nitric oxide in neonates and infants with pulmonary hypertension: functional impairment of the neutrophil respiratory burst (1996)
    Springer
    Intensive care medicine 22 (1996), S. 252-258 
    Details
    ISSN: 1432-1238
    Keywords: Key words Inhaled nitric oxide ; Pulmonary hypertension ; Respiratory burst of neutrophils
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract   Introduction: Inhaled nitric oxide (NO) may be beneficial in the treatment of pulmonary hypertension, both of the newborn and in the adult respiratory distress syndrome. Up to now, serious systemic side effects have not been reported. Objective: The effect of inhaled NO on superoxide anion production by neutrophils. Design: Prospective study of a consecutive series of 15 neonates and infants. Setting: Neonatal and paediatric ICUs with a total of 17 beds (university hospital). Measurements and results: Superoxide anion production was determined by a flow cytometric method using dihydrorhodamine 123 (DHR) as an oxidative probe after the priming of neutrophils with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or with Escherichia coli. The generated fluorescence was expressed as relative fluorescence intensity (RFI). Inhalation of NO for more than 24 h reduced the superoxide anion production by neutrophils stimulated with E. coli to below baseline values before NO inhalation (mRFI=158±25 vs 222±24; P=0.03). This decrease was more pronounced after more than 72 h (mRFI=133±17). At this time, superoxide anion production by fMLP-stimulated neutrophils was also decreased (mRFI=40±3, vs 57±5; P=0.03). The reduced capacity of superoxide production persisted throughout therapy with NO and lasted up to more than 4 days after the end of NO inhalation. Conclusion: The results suggest that inhalation of NO in patients with pulmonary hypertension causes reduced superoxide anion production by neutrophils stimulated with E. coli or with fMLP. To determine the clinical importance of this systemic side effect with respect to bacterial infections, a randomized controlled study is necessary.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01712246
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  • 2
    Electronic Resource
    Electronic Resource
    A new side effect of inhaled nitric oxide in neonates and infants with pulmonary hypertension: Functional impairment of the neutrophil respiratory burst (1996)
    Springer
    Intensive care medicine 22 (1996), S. 252-258 
    Details
    ISSN: 1432-1238
    Keywords: Inhaled nitric oxide ; Pulmonary hypertension ; Respiratory burst of neutrophils
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Introduction Inhaled nitric oxide (NO) may be beneficial in the treatment of pulmonary hypertension, both of the newborn and in the adult respiratory distress syndrome. Up to now, serious systemic side effects have not been reported. Objective The effect of inhaled NO on superoxide anion production by neutrophils. Design Prospective study of a consecutive series of 15 neonates and infants. Setting Neonatal and paediatric ICUs with a total of 17 beds (university hospital). Measurements and results Superoxide anion production was determined by a flow cytometric method using dihydrorhodamine 123 (DHR) as an oxidative probe after the priming of neutrophils withN-formyl-methionyl-leucylphenylalanine (fMLP) or withEscherichia coli. The generated fluorescence was expressed as relative fluorescence intensity (RFI). Inhalation of NO for more than 24 h reduced the superoxide anion production by neutrophils stimulated withE. coli to below baseline values before NO inhalation (mRFI=158±25 vs 222±24;P=0.03). This decrease was more pronounced after more than 72 h (mRFI=133±17). At this time, superoxide anion production by fMLP-stimulated neutrophils was also decreased (mRFI=40±3, vs 57±5;P=0.03). The reduced capacity of superoxide production persisted throughout therapy with NO and lasted up to more than 4 days after the end of NO inhalation. Conclusion The results suggest that inhalation of NO in patients with pulmonary hypertension causes reduced superoxide anion production by neutrophils stimulated withE. coli or with fMLP. To determine the clinical importance of this systemic side effect with respect to bacterial infections, a randomized controlled study is necessary.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01712246
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Granulocyte colony-stimulating factor receptor expression on neutrophils of term and preterm neonates with and without signs of infection (1999)
    Springer
    European journal of pediatrics 158 (1999), S. 497-500 
    Details
    ISSN: 1432-1076
    Keywords: Key words Granulocyte colony-stimulating factor receptor ; Flow cytometry ; Neonates
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neutrophils are an essential component of the human host defence system against infection. Recombinant human granulocyte colony-stimulating factor induces neutrophilia and enhances effector functions of mature neutrophils. Since the biological effects of granulocyte colony-stimulating factor (G-CSF) are mediated by its receptor, we investigated the expression of G-CSF receptor on the surface of neutrophils of term and preterm neonates (n = 22) with and without signs of infection and of healthy adults (n = 13) by flow cytometry. In healthy adults, the percentage of neutrophils expressing G-CSF receptor was higher compared to cord blood of term and preterm neonates (87% vs 53%, P 〈 0.05). Between 2 and 32 h of life, neonates with signs of infection showed lower values of G-CSF receptor expression compared to neonates without signs of infection (32% vs 54%, P 〈 0.05). No correlation was detectable between expression of G-CSF receptor and gestational age. Conclusion Expression of granulocyte colony-stimulating factor receptor on neutrophils is lower than in adults. This may adversely affect granulopoiesis and neutrophil function during the neonatal period. Moreover, granulocyte colony-stimulating factor receptor expression seems to be down-regulated during neonatal infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004310051129
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Chédiak-Higashi-Steinbrinck syndrome (CHS) in a 27-year-old woman – effects of G-CSF treatment (1999)
    Springer
    Annals of hematology 78 (1999), S. 321-327 
    Details
    ISSN: 1432-0584
    Keywords: Key words Chédiak-Higashi-Steinbrinck syndrome ; (CHS) ; G-CSF treatment ; Defective leukocyte function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Chédiak-Higashi-Steinbrinck syndrome (CHS) is a rare autosomal recessive disorder which is usually lethal in early childhood. Diagnostic hallmark is the occurrence of giant inclusion bodies in peripheral leukocytes and their bone marrow precursors. We report on a 27-year-old female patient who was admitted for treatment of a skin abscess. She recovered after intravenous antibiotic treatment and surgical incision. Hematological investigation was initiated because of a persisting neutropenia of 15%, with a leukocyte count initially in the normal range but subsequent leukopenia. Case history revealed recurrent skin infections from childhood on, regularly requiring surgical intervention. One year prior to admission a neuropathy had been diagnosed, while a partial albinism had been known for years. Microscopic examinations of peripheral blood and bone marrow aspirate smears were diagnostic for CHS. Additionally, a secondary antibody deficiency was found. Normalization of the white blood cell count, including the differential count, was observed following initiation of G-CSF treatment. Functional assessment of phagocytosis and oxidative burst activity of granulocytes revealed normal results before and after stimulation with G-CSF, however, natural killer cell activity was only weak, with slight improvement after G-CSF treatment in vivo. Cytogenetic analysis showed a normal female karyotype. Although the haploidentical brother of the patient may serve as an allogeneic stem cell donor, transplantation has been postponed because of further deterioration of her already existing CHS-specific neurological impairment. Nevertheless, while receiving G-CSF maintenance treatment our patient experienced no further infectious episodes within 6 months after diagnosis of CHS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002770050522
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Multidrug resistance in androgen-independent growing rat prostate carcinoma cells is mediated by P-glycoprotein (1997)
    Springer
    Urological research 25 (1997), S. 35-42 
    Details
    ISSN: 1434-0879
    Keywords: Prostate cancer ; Dunning tumor Androgen-independent ; Multidrug resistancemdr1b gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostate carcinomas are in general resistant against virtually all cytotoxic drugs. Up to now it has not been thoroughly evaluated whether specific resistance factors, such as the expression of theMDR1 gene, play a role in this multi-agent resistance and whether there is a link between drug resistance and hormone-independent growth. We investigated the resistance patterns of a hormone-sensitive and four hormone-independent Dunning rat carcinoma sublines against four drugs which are substrates of P-glycoprotein (vinblastine, taxol, doxorubicin, and etoposide) and two agents (methotrexate and cis-platinum) which are not transported by this efflux pump. All hormone-insensitive sublines, AT.1, AT. 3.1., MatLu and Mat LyLu, continuously showed a clearly enhanced resistance (3- to 26-fold) against the P-glycoprotein substrates, compared to the hormone-sensitive subline G. Only two of the androgen-independent sublines displayed enhanced resistance against methotrexate, whereas all of them were more sensitive against cisplatin than the androgen-sensitive G cells. By addition of verapamil the resistance against vinblastine (9- to 10-fold) and taxol (6.7- to 26.7-fold) in the hormone-insensitive cells could be almost totally reversed. Furthermore, the fluorescent P-glycoprotein substrate rhodamine-123 was effectively pumped out of the four tested hormone-independent cell lines, whereas the hormone-sensitive G cells were unable to extrude the dye. By reverse transcriptase polymerase chain reaction (RT-PCR) with primers specific for the ratmdr1b gene, the homologue to the humanMDR1 gene, we could easily detectmdr1b expression in the androgen independent cell lines, but not in the G cells. Our results suggest that the product of the ratmdr1b gene is involved in the multidrug resistance of androgen-independent Dunning prostate carcinoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00941904
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    Paper (German National Licenses)
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