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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Annals of hematology 19 (1969), S. 321-331 
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 1. During the incubation of mixed serum so much lysolecithin is released that the inhibition of an accelerated red blood cell sedimentation rate may be exclusively explained by this substance. On the other hand the simultaneously forming unesterified fatty acids only reach a concentration which hardly affects sedimentation. Whereas after incubation of 30 to 40 hours the breakdown of lecithin and with it the release of lecithin are largely completed, the concentration of the unesterified fatty acids is still increasing. 2. Lysolecithin and oleic acid change the aggregation state and the form of the erythrocytes and they qualitatively affect the red cell sedimentation in an identical manner. The difference is quantitative: the effect of lysolecithin is approximately 17 times stronger than that of oleic acid (μMol/μMol). 3. Lysolecithin, unesterified fatty acids and butazolidine inhibit the accelerated red cell sedimentation by reacting with the surface of the erythrocytes and by causing a change of the form of the erythrocytes.
    Notes: Zusammenfassung 1. Während der Inkubation von Mischserum wird soviel Lysolezithin freigesetzt, daß die Hemmung einer beschleunigten Blutkörperchensenkung allein auf diese Substanz zurückgeführt werden kann. Die gleichzeitig entstehenden unveresterten Fettsäuren erreichen dagegen nur eine Konzentration, die die Senkung kaum beeinflußt. Während der Lezithinabbau und mit ihm die Lysolezithinfreisetzung nach einer 30–40stündigen Inkubation weitgehend abgeschlossen sind, nimmt die Konzentration der unveresterten Fettsäuren noch weiter zu. 2. Lysolezithin und Ölsäure verändern den Aggregationszustand und die Form der Erythrozyten und beeinflussen die Blutkörperchensenkung qualitativ in gleicher Weise. Der Unterschied ist ein quantitativer: Lysolezithin wirkt etwa 17mal stärker als Ölsäure (μMol/μMol). 3. Lysolezithin, unveresterte Fettsäuren und Butazolidin hemmen die beschleunigte Blutkörperchensenkung dadurch, daß sie mit der Erythrozyten-oberfläche reagieren und eine Formveränderung der Erythrozyten verursachen.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Annals of hematology 18 (1969), S. 363-366 
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Thyrotropin-Releasing Hormone ; TRH-test ; TSH ; Triiodothyronine ; Thyrotropin Releasing Hormon ; TRH-Test ; TSH ; Trijodthyronin ; Normalwerte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Nach intravenöser Gabe von TRH (Thyrotropin-Releasing Hormone) wurde bei 78 Normalpersonen zwischen 20 und 85 Jahren die radioimmunologisch meßbare TSH-Ausschüttung von 0–120 min bestimmt. Der maximale TSH-Anstieg (ΔTSHmax) wurde in geschlechtsspezifischen Altersgruppen verglichen. Ergebnisse: 1. Der TSH-Anstieg ist bei Männern zwischen 20 und 59 Jahren signifikant niedriger als bei Frauen gleichen Alters. 2. Die TRH -Antwort vermindert sich bei Männern mit steigendem Lebensalter von 9,73 µU/ml±4,49 SD bei 20–39jährigen über 7,93 µU/ml±4,94 SD bei 40–59jährigen auf 7,37 µU/ml ±3,37 SD bei 60–81jährigen (nicht signifikant). 3. Bei Frauen zeigen die 2 Gruppen der 20–39jährigen und der 40–59jährigen einen gleich hohen TSH-Anstieg, ΔTSHmax 15,6µU/ml±7,6 SD und 15,6µU/ml±8,8 SD, während die Werte der 60–85jährigen Frauen mit 7,7 µU/ml±3,7 SD signifikant tiefer liegen. 4. Frauen unter Einnahme von oralen Kontrazeptiva unterscheiden sich in ihrer TRH-Antwort nicht signifikant von gleichaltrigen Frauen. 5. In dem hier untersuchten weiblichen Kollektiv setzte die Abnahme der TRH-Antwort bei Eintritt der Menopause ein. 6. Die basalen TSH-Werte liegen bei 20–59jährigen Frauen höher als bei Männern und bei älteren Personen. 7. Es findet sich kein Zusammenhang zwischen Thyroxin- oder Trijodthyroninkonzentration im Serum und der TRH-Antwort. 8. Der Anstieg des Serum-Trijodthyronins 120 min nach TRH-Injektion schwankt erheblich und ist bei Personen über 60 Jahren nicht signifikant niedriger. Schlußfolgerungen: Bei klinischer Verwendung des TRH-Testes sind die unterschiedlichen alters- und geschlechts-spezifischen Normalgrenzen unbedingt zu beachten. Es wird vorgeschlagen zur Eingrenzung der Normalbereiche den 2fachen Wert der Standardabweichung (SD) und nicht den 3fachen Wert der mittleren Streuung des Mittelwertes (s ...) zu verwenden Bei quantitativer Beurteilung der maximalen TSH-Ausschüttung muß die TSH-Spitze durch Mehrfachbestimmung 20, 30 und 40 min nach TRH-Injektion gesucht werden
    Notes: Summary 500 µg TRH (Thyrotropin-Releasing Hormone) were injected intravenously in 78 normal subjects aged between 20–85 years, TSH being estimated by radioimmunoassay from 0–120 min. The maximum increase of TSH (ΔTSHmax) was compared in age- and sex-specific groups. Results: 1) The rise of TSH is significantly lower in men than in women of 20–59 years. 2) In men, the TRH response is diminishing clearly but not significantly with increasing age, i.e. 9.73 µU/ml ± 4.49 SD for 20–39 years, 7.93 µU/ml ±4.94 SD for 40–59 years, 7.37 µU/ml ± 3.37 SD for 60–81 years (not significant). 3) In women, the two groups aged 20–39 and 40–59 years show both a high increase of TSH, ΔTSHmax 15.6 µU/ml±7.6 SD and 15.6 µU/ml±8.8 SD, whereas 60–85 year-old women have a significantly lower TSH elevation of 7.7 µU/ml±3.7 SD. 4) The TRH responses of women taking oral contraceptives and those of untreated women of the same age are similar. 5) In the women decreasing TSH responsiveness was observed after the onset of the menopause. 6) Basal TSH of 20–59 year-old women shows higher values than in males and older subjects. 7) There exists no correlation between serum thyroxine or triiodothyronine and the TRH response. 8) The increase of serum triiodothyronine 120 min after TRH injection is considerably inconstant and not significantly lower in subjects over 60 years. Conclusions: The different age- and sex-specific ranges for the normal values of the TRH test have to be taken into account in clinical use. It is proposed that the ranges of the normal values should be fixed rather by the double standard deviation than by the 3-fold standard error (SEM). For quantitative evaluation of the maximum TSH release, values at 20, 30 and 40 min after injection are necessary in order to find the TSH peak.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: Erythrocyte Sedimentation ; Lecithin-Cholesterol-Acyltransferase (LCAT) ; Lysophosphatidyl choline ; Blutkörperchensenkung ; Lecithin-Cholesterin-Acyltransferase (LCAT) ; Lysophosphatidylcholin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Wärmestabilisierung der Blutkörperchensenkung wurde in 158 Fällen untersucht. Sie ist bei Patienten mit einem Leberzellschaden, sei es isoliert oder als Folge von Tumormetastasen, im Vergleich zu der bei Patienten mit einer Entzündung oder einem malignen Prozeß ohne Leberbeteiligung signifikant herabgesetzt. Die Wärmestabilisierung ist im wesentlichen abhängig von der Konzentration des Lysophosphatidylcholin (Lysolecithin), das während der Inkubation im Plasma durch die Lecithin-Cholesterin-Acyltransferase (LCAT) gebildet wird. Die Aktivität der LCAT ist bei Patienten mit einem Leberzellschaden vermindert. Die Wärmestabilisierung wird durch mehrere Faktoren beeinflußt: Albumin bindet Lysophosphatidylcholin und entzieht es der Reaktion mit der Erythrocytenoberfläche. Eine Lysophospholipase senkt die Konzentration des Lysophosphatidylcholin im Plasma durch Abspaltung einer Fettsäure an der α-Position. Agglomerine wirken als Ursache der Senkungsbeschleunigung der Wärmestabilisierung entgegen. Die Konzentration des Albumin und der Agglomerine im Plasma und die Aktivität der Lysophospholipase sind physiologischen und krankheitsbedingten Schwankungen unterworfen. Dadurch wird die Wärmestabilisierung individuell unterschiedlich beeinflußt. Diese erschwert den Rückschluß auf die Aktivität der LCAT, der wesentlichen Ursache der Wärmestabilisierung, so daß diese für die klinische Diagnostik nicht geeignet erscheint.
    Notes: Summary Heat-induced inhibition of erythrocyte sedimentation (HIES) was examined in 158 cases. HIES is significantly lower in patients with a liver cell damage isolated or due to metastases of a neoplastic process in comparison to that in patients suffering from inflammation or malign tumor not involving the liver. Generally, HIES depends upon the concentration of lysophosphatidyl choline (lysolecithin) which is set free in plasma by lecithin-cholesterol-acyltransferase (LCAT) during incubation. In patients with liver cell damage, LCAT is diminished. HIES is being influenced by several factors: Lysophosphatidyl choline is bound to albumin, and this prevents its reaction on the erythrocyte surface. Lysophospholipase reduces the concentration of lysophosphatidyl choline in the plasma by splitting off its fatty acid in the α-position. Specific serum proteins, the so-called agglomerines, which are responsible for the acceleration of erythrocyte sedimentation, are counteracting the HIES. The concentration of albumin and agglomerines in plasma and the activity of lysophospholipase are subject to physiologically and pathologically caused deviations. Thereby, HIES is being influenced individually at varying degrees. This makes it difficult to estimate the LCAT activity which represents the principal cause of HIES. As a consequence, HIES seems not to be suitable for clinical diagnostics.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. 352-367 
    ISSN: 1432-1440
    Keywords: Environmental tobacco smoke (ETS) ; Passive smoking ; Smoking ; Biomonitoring ; Gas phase ; Particle phase ; Genotoxic substances
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary For the purpose of risk evaluation, passive smoking is frequently regarded as low-dose cigarette smoking. However, since the physical, chemical and biological properties of mainstream smoke (MS), which is inhaled by the smoker and environmental tobacco smoke (ETS), which is breathed by the passive smoker are quite different, risk extrapolation from active smoking to passive smoking is of doubtful value. In a series of experimental exposure studies we compared the uptake of tobacco smoke constituents by active and passive smoking. The results show that biomarkers which were found to be elevated after experimental ETS exposure, such as nicotine and cotinine in plasma and urine as well as thioethers in urine, indicate gas-phase exposure in passive smokers, but particle-phase exposure in active smokers. Biomarkers which should indicate the uptake of particle-bound, genotoxic substances with ETS, such as urinary mutagenicity, metabolites of polycyclic aromatic hydrocarbons (PAH) and DNA adducts, were not found to be elevated even after extremely high ETS exposure. From these results we conclude that a risk evaluation for passive smoking on the basis of dosimetric data is currently not possible.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    International archives of occupational and environmental health 65 (1993), S. 83-88 
    ISSN: 1432-1246
    Keywords: DNA single strand breaks ; Nick translation ; Unscheduled DNA synthesis ; Smoking ; DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a controlled study, ten male volunteers (five smokers and five nonsmokers) were subjected to different smoking conditions and compared to five non-smokers, not exposed to cigarette smoke. During the 4 days of the study, nonsmoking periods were strictly controlled. On the first day the ten subjects were sham exposed. On the second day the five smokers smoked 24 cigarettes in 8 h, while the five nonsmokers were exposed to the environmental tobacco smoke. After another day of sham exposure the smoke exposure was repeated under the same conditions. Blood was drawn before and after exposure and DNA single-strand breaks (SSBs) were analyzed in lymphocytes immediately (1 h) after isolation of cells and after 4 h incubation at 37°C, using a modified assay based on the nick translation reaction. Base levels of unscheduled DNA synthesis (UDS) and UDS levels were determined after 1 h incubation with methyl methanesulfonate. Duplicate analysis using the same method was performed in a second laboratory after transportation of blood samples at 0°C on a train from Munich to Hamburg. Tobacco smoke exposure of the subjects increased COHb and plasma cotinine levels. SSBs could be detected in all probands with some inter-individual day-to-day and morning-to-evening variations. In four of five active smokers, SSB increases were found after smoking. In nonsmokers exposed to tobacco smoke no exposure-related variation in SSB levels could be detected. In lymphocytes which were incubated in culture medium (DME/H) for 4 h at 37°C, SSBs correlated significantly with the SSBs of fresh (NT1) samples but the SSB level was lower in almost all cases and the effect of smoking was not as pronounced as in the NT1 samples. Larger interindividual variations and higher values in general were detected after 8–9h of transportation. Therefore, we recommend immediate determination of SSBs as soon as possible after blood sampling. We conclude that the modified nick translation assay is sensitive enough to detect SSBs caused by an in vivo genotoxic exposure when possible interindividual differences are considered in the study design and could therefore be used in biological monitoring of exposures at the workplace.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Keywords: DNA single-strand breaks ; DNA repair ; Nick translation ; Smoking ; Environmental tobacco smoke ; Biological monitoring
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The detection of DNA single-strand breaks (SSB) in human mononucleated white blood cells (MWBC) using a modified version of the nick translation assay is presented. This assay allows rapid and sensitive examination of SSB using only 5 ml heparinized blood for an eightfold determination. The assay was standardized by incubation of MBWC in vitro with N-methyl-N′-nitro-N-nitro-soguanidine (MNNG), a known genotoxic agent. In vitro incubation of MWBC with MNNG induced a dose-dependent increase in DNA-SSB at doses between 5 and 500 μM MNNG. The detection limit for the assay was 5 μM MNNG. To assess the suitability of this assay to detect SSB in vivo a controlled study was performed in which volunteer smokers (n = 5), nonsmokers (n = 5) exposed to environmental tobacco smoke (ETS), and nonsmoker controls (n = 5) were compared. The study lasted 4 experimental days, 2 control and 2 exposure days. On control days (days 1 and 3) smokers and nonsmokers sat in an unventilated 45 m3 room for 8 h. On the exposure days (days 2 and 4) each of the five smokers smoked 24 cigarettes in 8 h, while the five nonsmokers were exposed to the ETS generated by the smoking volunteers. High exposure to tobacco smoke was confirmed by dosimetry of carboxyhemoglobin (COHb), plasma nicotine and cotinine levels. Blood was drawn before and after each exposure on all 4 experimental days for determination of DNA-SSB in lymphocytes immediately after isolation of blood cells. COHb, plasma nicotine, and cotinine levels were considerably increased in both smokers and nonsmokers exposed to ETS on days 2 and 4. DNA-SSB were detected in all volunteers with intra-and interindividual day to day and morning to evening variations. After smoking, SSB increased on day 2 and on day 4 in smokers. In nonsmokers exposed to ETS no exposure-related variation in SSB levels was found. We conclude that the modified nick translation assay is sensitive enough to detect SSB induced in vivo by exposure to a genotoxic agent and could therefore be used in biological monitoring at the workplace.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 116 (1990), S. 591-598 
    ISSN: 1432-1335
    Keywords: ETS ; benzene ; biomonitoring ; risk evaluation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to assess the uptake of benzene from environmental tobacco smoke (ETS) and to estimate its contribution to the total body burden of benzene observed in non-smokers, two experimental studies have been conducted. Controlled exposure to high levels of ETS equivalent to 10 ppm CO for 9 h and 20 ppm for 8 h resulted in a nonsignificant increase in blood benzene levels and a significant increase in exhaled CO, COHb and cotinine in serum and urine. The slightly rising blood concentration of benzene following experimental ETS exposure was paralleled by an increased exhalation of benzene and aromatic hydrocarbons and in contrast to blood levels, this increase was significant. The blood levels of benzene obtained during exposure were comparable to those observed at the time of admission to the laboratory, when biomarkers of ETS uptake, e. g. cotinine in serum and urine, were at the limit of detection, thus demonstrating that these background levels were not from ETS exposure. No difference in the urinary excretion of phenol, the main metabolite of benzene, was found during the experimental periods. The background levels of urinary phenol in unexposed nonsmokers were rather high, demonstrating that phenol excreted in urine must be formed from several endogenous and exogenous precursors. In the ligth of our findings it is highly questionable whether exposure to benzene from ETS under real life conditions poses a cancerogenic risk to the general population, which is measurable today or in the future by toxicological or epidemiological methods.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1573-6822
    Keywords: cytokines ; environmental tobacco smoke (ETS) ; immune system ; prostaglandin E2 ; smoking
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Controversial results have been published on the immune response to cigarette smoking while the effects of exposure to environmental tobacco smoke (ETS) have not yet been reported. In a controlled study, acute effects of smoking and of a high environmental exposure to ETS on immunological parameters have been investigated. The study consisted of four experimental days, two control and two exposure days. On control days, 1 and 3, smokers (n=5) and nonsmokers (n=5) sat in an unventilated 45 m3 room for 8 h. On the exposure days, 2 and 4, each of the smokers smoked 24 cigarettes in 8 h, while the nonsmokers were exposed to the ETS generated by the smoking volunteers. Blood was drawn before and after each exposure session on all four experimental days for dosimetry of tobacco smoke exposure and determination of the immune response. Flow cytometry using monoclonal antibodies was used to determine CD3+ cells (whole T cells), CD19+ cells (B lymphocytes), CD16+ and CD56+ cells (natural killer cells), CD4+ cells (T-helper cells), CD8+ cells (T-suppressor cells), the CD4+/CD8+ (helper/supressor ratio), and Fc receptors on granulocytes. Serum was analyzed for soluble CD14 receptors (scD14), interleukin 1, interleukin 6 and prostaglandin E2 (PGE2). Functional stimulation assays were performed to determine the basal and induced level of reactive oxygen intermediate (ROI) production by polymorphic neutrophils. Exposure to tobacco smoke in both groups was confirmed by dosimetry of carboxyhemoglobin, plasma nicotine, and cotinine levels. In comparison to nonsmokers, smokers had elevated granulocyte cell counts, increased CD16+ and CD56+ cell levels and decreased CD3+ and CD19+ levels. Acute smoking, but not exposure to ETS, resulted in a slight decrease in the number of CD19+ cells and an increase in the number of granulocytes; the latter was restricted to one subject. Acute smoking and exposure to high experimental concentrations of ETS resulted in a slight increase in CD16+ and CD56+ cells. None of the changes determined in immunological parameters after either acute smoking or exposure to ETS reached statistical significance. Serum sCD14, cytokine and PGE2, functional stimulation of in vitro ROI production, and changes in Fc receptors were not affected by acute smoking or exposure to ETS. Although no clear guidelines exist to assess immunotoxicity in man, our data do not favor immunosuppression and the possibility of increased risk of infection in nonsmokers exposed to ETS under real-life conditions.
    Type of Medium: Electronic Resource
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