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  • 1
    ISSN: 1432-1440
    Keywords: Lung diseases ; Bone marrow transplantation ; Clinic ; Radiology ; Histology ; Immunology ; Lung function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The case histories of 72 subsequently treated patients — 44 with acute leukemia, 10 with chronic myeloid leukemia, 16 with severe aplastic anemia and 2 with neuroblastoma — were analyzed after bone marrow transplantation (BMT) with respect to pulmonary diseases. Thirty-eight patients suffered from a total of 51 pulmonary complications, which led to death in 20. Of 13 patients, 3 died of bacterial pneumonia, all of them during granulocytopenia; 2 of 6 patients died of fungal pneumonia and 2 out of 3 of a mixed bacterialmycotic infection. Adult respiratory distress syndrome (ARDS) led to death in 2 patients. A granulocyte count under 500/µl correlated significantly (P〈0.002) with the fatal outcome of bacterial, fungal and ARDS pneumonia as well as with bronchitis. Viral pneumonia led to death in 8 of 9 patients; in each there was a significant correlation (P〈0.05) with graft-versus-host disease (GvHD). Patients with repeated episodes of pulmonary illness had significantly more chronic GvHD (P〈0.05); several of these patients displayed a reduction in helper T cells and an increase in suppressor T cells in the peripheral blood. The natural killer (NK) cells were reduced and the percentage of activated NK cell level lay between 6% and 69%. B-cells were absent or deficient. These findings explain in part the absence of specific antibody reactivity. Five of these patients also contracted GvHD-associated obstructive bronchiolitis, which did not respond to therapy. Pulmonary infiltrates of unknown origin (including idiopathic interstitial pneumonia) occurred in 8 of the patients (11.1%), with a fatal outcome in 3 patients. Significant changes (P〈0.05) in lung function after BMT appeared in the form of reduced vital capacity (VC) increased residual volume (RV) and an increase in RV expressed as the percentage of total lung capacity. Pulmonary diseases were the most common complication and cause of death in our patients after BMT.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Acquired immunodeficiency syndrome (AIDS) ; Lymphadenopathy-associated virus (LAV)/human T-lymphotropic virus type III (HTLV-III) ; Seroepidemiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 1984 10,281 sera were collected in the FRG and examined for antibodies to HTLV-III (LAV) with an enzyme-linked immunosorbent assay and confirmative tests. Of the German AIDS patients 81% have antibodies. Individuals belonging to AIDS risk groups, homosexuals, haemophiliacs and i.v. drug abusers, have antibody frequencies between 25%–72%. The detection of HTLV-III antibodies in blood donours indicates that the virus is being transmitted by blood transfusions.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusions Low dose filgrastim in postoperative/posttraumatic patients at risk of and with sepsis may boost host defense by stimulating neutrophil function and simultaneously counteract progression of sepsis by improving an antiinflammatory cytokine response with protective effects on the endothelium.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract DNA of unrelated persons as well as members of families that were totally or partially homozygous or completely heterozygous on the loci of the major histocompatibility class I genes has been isolated from peripheral blood lymphocytes and blot hybridized with the class I pseudogene pHLA 12.4 probe. The autoradiographic DNA patterns were discussed and compared with well-defined serological features. Positive associations with serologically typed alleles had been demonstrated for HLA-A1,11 ; -A2; -A3; -B7; -B14; -B35;-Bw41; and -Cw5.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1076
    Keywords: Key words Kaposi sarcoma  ;  Immunodeficiency  ;   KSHV  ;  Bone marrow transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 3-year-old boy of German descent suffered from two episodes of Streptococcus pneumoniae meningitis within 2 months. One month previously, the first skin lesion of Kaposi sarcoma (KS) had been observed behind his right ear. During the following 2 years KS disseminated not only mucocutaneously but also to visceral organs. Immunological evaluation revealed severe lymphocytopenia with reduced helper/suppressor T-cell ratio and impaired humoral immune response to pneumococci. Extensive laboratory tests gave no evidence for known immunocompromising infections. However, recently described DNA sequences from a Kaposi sarcoma-associated herpesvirus (KSHV) could be identified within skin tissue. As chemotherapy failed to stop tumour progression the patient was referred for bone marrow transplantation. Eighteen months later the KS is in remission and the patient in a good general condition. Conclusion The case supports the hypothesis that KSHV is involved in the aetiology of KS. Bone marrow transplantation is possibly a therapeutic option for KS in patients with immunodeficiency not related to human immunodeficiency virus infection.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In vivo activated T cells could be isolated from cerebrospinal fluid (CSF) of a patient suffering from chronic meningitis of unclear origin. Although the patient's skin reactivity to purified protein derivative (PPD) was negative, and peripheral T cells did not proliferate to this antigen in vitro, the majority of T cell clones from CSF specifically recognized PPD on either autologous or allogeneic HLA class II compatible macrophages. Remarkably, peripheral blood mononuclear cells potently suppressed the PPD-specific proliferate responses of healthy donors. The selective enrichment of oligoclonal IgG in the CSF but not in the patient's serum further indicated T and B cell responses lacking systemic feedback control. Analyses of a persisting immune stimulation in the CSF provide a potent diagnostic tool and may explain neurological complications as observed in a number of autoimmune diseases and chronic infections.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 17 (1983), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Human lymphocytes alloactivated in vitro were cloned by limiting dilution in the presence of filler cells and interleukin 2 (IL 2)-containing supernatants of phytohaemagglutinin-stimulated lymphocytes. Clones with allospecific proliferative reactivity (PLT clones), measured by tritiated thymidine (3H-TdR) incorporation, were selected for extensive IL 2-dependent expansion. The cloned lines had finite lifespans, ranging from an estimated minimum of 28 to 〉 65 doublings. Function as PLT reagents, however, was retained in all cases for only an estimated 30 cell doublings. This apparent cessation of function was not caused by loss of the ability to metabolize thymidine, since lines continuing to grow for 〉 30 doublings still incorporated 3H-TdR in the presence of IL 2. An altered requirement for stimulating antigen (number of stimulating cells), or altered response kinetics, did not contribute to loss of PLT function. Exogenous IL 2 added during restimulation to responders previously ‘rested’ overnight without IL 2 did not restore the response. Thus, under present experimental conditions, functional lifespans of cloned PLT reagents appear fixed at ˜ 30 cell doublings.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Intensivmedizin und Notfallmedizin 34 (1997), S. 664-674 
    ISSN: 1435-1420
    Keywords: Key words Neutrophil granulo-cytes ; infection ; sepsis ; granulocyte colony-stimulating factor (G-CSF) ; Schlüsselwörter Neutrophile Granulozyten ; Infektion ; Sepsis ; Granulozyten Kolonien-stimulierender Faktor (G-CSF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bakterielle Infektionen und Infektionskomplikationen stellen für den Intensivpatienten nach wie vor eine Bedrohung dar. Trotz verbesserter Einsicht in die pathophysiologischen Abläufe konnte gerade die unkontrollierte und überschießende Entzündungsreaktion bisher therapeutisch nicht eingedämmt werden. Einen erfolgversprechenden Ansatz verfolgt der Granulozyten Kolonien-stimulierende Faktor (G-CSF), ein hämatopoetischer Wachstumsfaktor, der die Mobilisierung, Teilung und Differenzierung von myeloischen Vorläuferzellen zu neutrophilen Granulozyten positiv reguliert. Seit 1987 wird die rekombinante Form des humanen G-CSF klinisch mit Erfolg für die Behandlung der Chemotherapie-assoziierten Neutropenie, allen angeborenen Formen der Neutropenie sowie auch zur Mobilisierung von Vorläuferzellen für die periphere Progenitorzelltransplantation, eingesetzt. Da G-CSF auch Funktionsstörungen des neutrophilen Granulozyten behebt und darüber hinaus endogen bei bakteriellen Infektionen produziert wird, wird diesem Wachstumsfaktor eine wichtige Funktion bei bakteriellen Infektionen zugesprochen. In tierexperimentellen Infektions-Modellen konnte rhG-CSF das Überleben der Tiere signifikant steigern und reduzierte dabei die Produktion des Tumornekrose-Faktor-α. Bei gesunden Normalspendern zeigt rhG-CSF neben einer Steigerung der Granulozytenaktivität eine Hemmung proinflammatorischer Zytokine. Erste Studien bei Patienten mit Infektionen (Pneumonie) und bei chirurgischen Intensivpatienten haben gezeigt, daß die Therapie mit rhG-CSF keine zusätzlichen Komplikationen auslöst und möglicherweise den klinischen Verlauf positiv beeinflussen kann.
    Notes: Summary Bacterial infections still pose a threat to intensive care patients. The progression of an infection once contracted often leads to severe sepsis with subsequent organ failure and death. Despite better understanding of the pathophysiological course, the hyperinflammatory reaction cannot be retained. Granulocyte colony-stimulating factor (G-CSF) regulates the multiplication and differentiation of neutrophil precursors and modulates neutrophil function. Since 1987, recombinant human G-CSF (r-metHuG-CSF) has been approved for the treatment of chemotherapy-induced neutropenia, all forms of congenital neutropenia, as well as for the mobilization of progenitor cells for peripheral progenitor cell transplantation. Since G-CSF modulates the function of neutrophil granulocytes and since its endogenous production is induced by bacterial infection, it has been assumed to have an important role in bacterial infections. In animal models of infections it has been shown that rhG-CSF could significantly increase the survival rates and reduced the endogenous production of TNF-α. In healthy volunteers G-CSF improves the granulocyte function and has an anti-inflammatory effect on the cytokine network. First clinical studies in patients with infections (pneumonia) as well as surgical intensive care patients have shown that the administration of G-CSF is safe and that it might have a beneficial effect on the clinical course.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-1420
    Keywords: Key words Granulocyte colony-stimulating factor ; systemic inflammatory response syndrome ; sepsis ; immunodeficiency ; immunocompromised host ; Schlüsselwörter Granulozyten Kolonie-stimulierender Faktor ; Systemic Inflammatory Response Syndrome ; Sepsis ; Immun-defizienz ; immunsupprimierter Patient
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Intensivtherapiepflichtige Patienten sind hochgradig gefährdet, ein „Systemic Inflammatory Response Syndrom (SIRS)“, eine Sepsis, einen septischen Schock sowie eine Multiorgandysfunktion zu entwickeln, die mit einer hohen Letalität verknüpft sind. Auf eine Infektion bzw. auf ein Trauma größeren Ausmaßes reagiert das Immun-system mit einer pro-inflammato-rischen Reaktion, der eine, ebenfalls oft überschießende, anti-inflammatorische Reaktion folgt. Diese kompensatorische, anti-inflammatorische Reaktion wurde als „Compensatory Anti-inflammatory Response Syndrome (CARS)“ bezeichnet. Letzteres manifestiert sich als systemische Immundefizienz, Anergie und resultiert in einer erhöhten Infektanfälligkeit. Klinische und experimentelle Studien weisen darauf hin, daß ein hämatopoetischer Wachstumsfaktor, der Granulozyten Kolonie-stimulierende Faktor (G-CSF), dieser Immun-defizienz entgegenwirken könnte. Die Gabe von G-CSF erhöht bei nicht-neutropenischen, postoperativen und posttraumatischen Patienten mit hohem Sepsisrisiko die Granulozytenzahl, steigert deren Funktionsleistung und senkt die Inzidenz einer Sepsis. Darüberhinaus gibt es Hinweise, daß G-CSF in hyperinflammatorischen Situationen zu einem anti-inflammatorischen Zytokinreaktionsmuster beiträgt und damit als prophylaktisches Therapeutikum geeignet ist. Somit könnte G-CSF einerseits neutrophile Granulozyten aktivieren und andererseits aufgrund der anti-inflammatorischen Effekte gleichzeitig einer überschießenden Entzündungsreaktion entgegenwirken. Unter diesen Gesichtspunkten ist die G-CSF-Gabe als eine vielversprechende Therapieoption bei intensivtherapie-pflichtigen Patienten mit erhöhtem Sepsisrisiko, mit manifester Sepsis, SIRS, CARS und dem sogenannten „Mixed Antagonistic Response Syndrome (MARS)“ anzusehen. Um eine effektive Therapie sowohl der hyperinflammatorischen Phasen bei Sepsis, SIRS und MARS als auch der sekundären, transienten Immundefizienz bei MARS und CARS mit G-CSF zu erzielen, wird G-CSF einer geeigneten Subgruppe von Patienten und gemäß eines optimalen Zeit- und Dosierungs-Schema appliziert werden müssen.
    Notes: Summary Intensive care patients bear a high risk to manifest “systemic inflammatory response syndrome (SIRS)”, sepsis, septic shock and multiple organ dysfunction which are associated with a high mortality rate. As a consequence of an initial infection or trauma, a hyperinflammatory activation of the immune system follows and an anti-inflammatory response (named “compensatory anti-inflammatory response syndrome (CARS)” occurs consecutively. This latter state manifests as systemic immune dysfunction, anergy and causes increased susceptibility to infections. Results of clinical and experimental studies are discussed providing evidence for the use of a hematopoietic growth factor named granulocyte colony-stimulating factor (G-CSF) to counteract this immunodeficiency. In non-neutropenic, posttraumatic/postoperative patients with an increased risk of sepsis, G-CSF increases neutrophil count and function and decreases the incidence of sepsis. Moreover, recent studies suggest that G-CSF contributes to an anti-inflammatory cytokine response in hyper-inflammatory states and is considered as a promising therapeutic agent given prophylactically. Thus, G-CSF may activate neutrophils on the one hand and at the same time may counteract progression of an excessive inflammatory reaction due to anti-inflammatory effects on the other hand. In this context, G-CSF treatment appears to be a promising therapeutic option in intensive care patients at risk of sepsis, SIRS, CARS and the “mixed antagonistic response syndrome (MARS)”. Regarding effective therapy of hyperinflammatory states of sepsis, SIRS and MARS as well as the secondary, transient immunodeficiency of CARS and MARS by G-CSF, the drug will have to be administered to accurately defined patient groups and due to optimal timing and dosage schedules.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Human genetics 〈Berlin〉 65 (1984), S. 242-247 
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The Dwl specificity was highly correlated with the serologically determined HLA-DR1 antigen in the Eighth International Histocompatibility Workshop 1980. By testing a large number of HLA-Dwl, DR1 defined homozygous typing cells (HTC) in a checkerboard primary mixed lymphocyte reaction, on a panel of about 30 HLA-DR1 heterozygous individuals, and in family segregation, three Dwl “subtypes” could be defined in association with certain HLA-A, -B, and -C-antigens. HTC TA, FRI, and FRA carrying the HLA haplotypes A11, B35, Cw4 or A3, B35, Cw4 in the homozygous state gave positive typing results with most HLA-DR1 positive panel members and stimulated only four other Dw1 HTCs (SRR≦35%). In contrast to this operationally “broad” specificity, Dw1-HTC-HEN (HLA-A2, B44, C-, homozygous) was non-stimulatory to all HTCs except one, but gave high responses against these, leading to the definition of a “narrow” specificity included in the “broad” one. Another such “narrow” specificity was represented by HTC FEE (HLA-A2, B27, Cw2 homozygous). Typing patterns with FEE were mostly different from those defined with other HTC. In family studies a specific typing pattern for this HTC could be shown to segregate with HLA. However, within some of these responses a contribution of the HLA haplotype in the trans position must be assumed.
    Type of Medium: Electronic Resource
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