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  • 1
    ISSN: 0942-0940
    Keywords: Astrocytoma ; progressive ; low-grade ; prognostic ; factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to study survival and identify prognostic factors in progressive supratentorial low grade astrocytoma, 46 cases of diffusely growing glioma (1982–1989), in which stereotactic biopsy revealed a diagnosis of astrocytoma grade II according to Kernohan, were evaluated. Only patients with definite tumour growth on consecutive CT scans were included. All patients received a full course of fractionated radiotherapy. All tumour biopsy specimens were re-evaluated according to both the Kernohan and Daumas-Duport grading systems. Follow-up for at least 5 years showed a median survival of 47.5 months (1 year 71%, 5 year 41%). In Cox' multivariate analysis 4 factors turned out to give the best fitting prognostic model for survival: age, duration of symptoms, preoperative neurological examination and CT-contrast enhancement. Numerical scoring was performed by giving either 1 or 0 for: age 〉 or 〈 40 years, symptom duration 〈 or 〉 1 year, presence or absence of focal deficit, and presence or absence of CT-contrast enhancement. Combining these factors in a score ranging from 0–4 resulted in 3 distinct groups with respect to median survival (〈 2 ∶ 66.5 months, 2 ∶ 40 months, 〉 2 ∶ 10 months, P=0.0015). Although 17 cases with Kernohan grade II were upgraded using Daumas-Duport criteria (13 grade III, 4 grade IV), these cases did not form a separate survival-group. Additional parameters are needed to assess prognosis by neuropathological means, as some “low-grade” tumours are less benign than others, giving rise to a variable natural history.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Methylnitrosourea ; Ethylnitrosourea ; Developing nervous system ; Malignant cell transformation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since both short-term and long-term effects of MNU and ENU are caused by the alkylations of cellular macromolecules, short-term effects might be relevant to the problem of carcinogenesis. Our experiments show mitotic inhibition in proliferating cells in both neural and extraneural tissues. This inhibition is much longer in the neural tissues, and is confined to the two proliferating cell matrices (SEL and EGL) which exist in the period of sensitivity to the carcinogens. Further experiments revealed that this inhibition was caused by a temporary cell cycle arrest in or before entrance into the S-phase. Re-entrance into the cell cycle occurs, however, long before the chemically induced alterations in the cellular macromolecules have been repaired. This observation might be relevant to a better understanding of the process of malignant cell transformation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 54 (1980), S. 167-179 
    ISSN: 0942-0940
    Keywords: Brain tumour ; stereotactic biopsy technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The techniques of stereotactic biopsy of mass lesions of the brain are described, and the indications discussed. Since computerized axial tomography has become available the decision to perform a stereotactic biopsy is made more frequently than previously. Stereotactic techniques in neuro-oncology are a continuously expanding field of largely diagnostic and sometimes therapeutic procedures. It now seems likely that most centres concerned with brain tumour patients will make use of stereotactic biopsies in the future. A series of 60 stereotactic biopsies performed in the management of otherwise inaccessible tumours of the brain is presented.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 72 (1984), S. 1-14 
    ISSN: 0942-0940
    Keywords: Intractable pain ; percutaneous cordotomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Factors that might have contributed to failure of high cervical percutaneous cordotomy in 23 patients with intractable pain were investigated. Cordotomy failed in 3 patients, 20 had initially good pain relief (87%). True recurrence occurred in 5 patients, 3 of them developed pain elsewhere. Analysis of these three types of failure showed a purely technical cause in 2 cases; other failures or recurrences were due to the underlying disease being not strictly unilateral, or possibly to the existence of other ascending pathways carrying nociceptive impulses apart from the spinothalamic tract. There was no influence of age, sex, type of cancer or previous medication on the result of percutaneous cordotomy. Patients with plexus involvement did better than those with bone metastasis.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 86 (1976), S. 23-31 
    ISSN: 1432-1335
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 8 Tage alte Ratten wurde 20 oder 100 mg/kg Körpergewicht von MNU oder ÄNU gegeben und danach 10 μCi/g Körpergewicht (3H-Methyl)-Thymidine. In den Experimenten mit 100 mg MNU oder ÄNU wird im zentralen Nervensystem und im nicht-nervösen Gewebe eine totale Inhibition der S-Phase-Radioaktivität festgestellt, die bei MNU wesentlich länger dauerte. Außerdem fand die Wiederkehr von S-Phase Zellen im zentralen Nervensystem später statt (36–48 Std) als im nicht-nervösen Gewebe (24–36 Std). In allen untersuchten Geweben geschieht diese Wiederkehr von S-Phase Zellen immer 12 Std früher als die Rückkehr von M-Phase Zellen. In den Experimenten mit 20 mg MNU oder ÄNU wird im zentralen Nervensystem und im nicht-nervösen Gewebe eine eindeutige Verminderung der S-Phase-Radioaktivität nur im ersten Interval (6 Std) beobachtet. Es ergeben sich nur kleine Unterschiede zwischen den verschiedenen Geweben und Substanzen. In den sich entwickelnden Geweben der Ratte besteht offenbar eine Tendenz zur Abnahme der Mitose-Aktivität und der S-Phase-Radioaktivität bei steigenden Einzeldosen von MNU oder ÄNU. Unsere Befunde weisen auf eine Blockierung in der S-Phase oder vor dem Eintreten der S-Phase hin bei den betreffenden Zellen die der Wirkung dieser Substanzen exponiert wurden. Die stärkere cytotoxische Wirkung von MNU im Vergleich mit ÄNU wird besprochen. Die Rückkehr der DNA-Synthese und das Wiedereintreten in den Cyclus der geschädigten Zellen findet früher statt als die Eliminierung aus DNA von chemisch geänderten Basen und könnte Bedeutung haben für das Problem der Onkogenese.
    Notes: Summary 8 days old rats were exposed to 20 or 100 mg/kg b.w. of either Methylnitrosourea (MNU) or Ethylnitrosourea (ENU), followed by injection of 10 μCi/g b.w. of (3H-methyl)-Thymidine. After a 100 mg dose of MNU or ENU in both neural and extraneural tissues a total inhibition of S-phase radioactivity is observed that lasts longer for MNU than for ENU. Moreover reappearance of S-phase cells in the neural tissues is later (36–48 h) than in the extraneural tissues (24–36 h) for both drugs. In both neural and extraneural tissues reappearance of S-phase cells is consistently found to occur about 12 h earlier than recurrence of M-phase cells. After a 20 mg dose of MNU or ENU in both neural and extraneural tissues a clear decrease in S-phase radioactivity is found after a 6 h' interval only. There are only slight differences between the various tissues and drugs. In developing rat tissues there is obviously a trend for both mitotic activity and S-phase radioactivity to decrease with increasing single doses of MNU or ENU. Our results point to an arrest in or before entering the S-phase of the cells involved. The more pronounced cytotoxic activity of MNU as compared to ENU is discussed. Recurrence of DNA synthesis and re-entrance of damaged cells into their cycle prior to the elimination of altered bases from DNA might be of importance for the problem of oncogenesis.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 77 (1972), S. 308-317 
    ISSN: 1432-1335
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Verschiedene Einzeldosen von ÄNU und MNU führten zu letalen Schäden nur an proliferierenden Zellen, wenn sie Ratten in perinatalem Alter gegeben wurden. Dieser akute Effekt wurde sowohl im Nervensystem wie im nicht-nervösen Gewebe beobachtet. Im zentralen Nervensystem sind die proliferierenden Zellen beschränkt auf die subependymalen und äußeren granulären Matrixzonen sowie die von ihnen auswandernden Zellen. Semiquantitative Messungen des Prozentsatzes der letal geschädigten Zellen und die Dosisschwelle beider Substanzen wurden an diesen Matrixzellen durchgeführt. Die Daten zeigten eine lineare Beziehung, was anzeigt, daß die Menge von alkylierenden Gruppen den für die beobachtete Zellschädigung ausschlaggebenden Faktor darstellt. Außerdem war der Prozentsatz der letal geschädigten Zellen in dem proliferierenden System in jedem, während der Hirnreifung untersuchten Alter derselbe für eine äquimolare Dosis beider Substanzen. Auch der durch sie ausgelöste Umfang der Mitosehemmung wurde berechnet und erwies sich als identisch für äquimolekulare Dosen beider Substanzen. Diese Hemmung wurde vollständig bei Dosen, die höher waren als 120 mg/kg Körpergewicht. Nicht sich teilende Zellen in neuralem und nicht neuralem Gewebe schienen Resistenz gegenüber der letalen Schädigung innerhalb der in den vorliegenden Untersuchungen benützten Dosisbereichen zu zeigen. Allerdings konnte eine subletale Schädigung und Wiederherstellung nicht ausgeschlossen werden. Die mögliche Rolle dieses Wiederherstellungsmechanismus bei der Cancerogenese durch ÄNU und MNU wird kurz besprochen.
    Notes: Summary Various single doses of ENU and MNU given to rats at the perinatal age caused lethal damage in proliferating cells only; this acute effect was observed in both neural and extraneural tissues. In the central nervous system, proliferating cells are confined to the subependymal and the external granular matrices including waves of cells migrating out from them. Semi-quantitative measurements on the percentages of lethally damaged cells and the dose-levels of both drugs were performed for these matrices. Plotting these data showed a linear relationship, which indicates that the amount of alkylating groups administered is the factor responsible for the cellular injury observed. Moreover, at all ages investigated during the period of cerebral maturation the percentage of lethally damaged cells within a proliferating system for a given equimolar dose of either ENU or MNU was the same. The extent of mitotic inhibition caused by these drugs was calculated also and was found to be the same for both ENU and MNU in equimolar doses; this inhibition became complete at higher doses than 120 mg/kg body weight. Non-dividing cells in both neural and extraneural tissues appeared to be resistant to lethal damage within the dose-range used in this study. Sublethal damage and subsequent repair synthesis cannot be ruled out, however. The possible role of this repair mechanism in the process of carcinogenesis by ENU and MNU is briefly discussed.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 79 (1973), S. 255-266 
    ISSN: 1432-1335
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung An 8 Tage alten Batten wurde 100 mg/kg Körpergewicht von Methyl-Nitroso-Harnstoff (MNU) oder Äthyl-Nitroso-Harnstoff (ÄNU) gegeben. Im nichtnervösen Gewebe dauert die Mitosehemmung nach MNU länger als nach ÄNU. Im Falle von ÄNU nimmt die Menge von teilenden Zellen rasch zu, wenn sie wieder erscheinen; dagegen werden in den MNU-behandelten Tieren wieder erscheinende Teilungsfiguren in jedem untersuchten Interval nur in kleiner Zahl beobachtet. Die letal geschädigten Zellen verschwinden langsam, doch für beide Substanzen gleich schnell. Im zentralen Nervensystem stellt sich die Dauer der Mitosehemmung als wesentlich länger heraus. Die Teilungsfiguren nehmen aber, wenn sie wieder erscheinen, wie im nicht-nervösen Gewebe, in den ÄNU-behandelten Tieren rasch zu, während nach MNU in jedem Interval nur eine kleine Zahl von teilenden Zellen gefunden wird. Die letal geschädigten Zellen verschwinden viel später im Nervensystem als im nicht-nervösen Gewebe, doch wieder gleich schnell für beide Substanzen. Oft wurden in allen untersuchten Geweben abnormale Mitosen beobachtet. Ein Aufschub des Zelltodes wurde in allen untersuchten Geweben gefunden, wenn—nach der Applikation von MNU oder ÄNU — die Protein-Synthese durch Cycloheximid blockiert wurde; dieser Befund weist daraufhin, daß der Zelltod ein aktiver Prozeß ist, der auf de novo Synthese der Proteine beruht. Im Vergleich mit ähnlichen Ergebnissen für bekannte Alkylantien in der Literatur, sind unsere Befunde eine weitere Unterstützung für die Annahme, daß die eytotoxische Wirkung von MNU und ÄNU auf Alkylierung von cellulären Makromolekülen zurückzuführen ist. Die auffallenden Unterschiede für die Mitosehemmung zwischen MNU und ÄNU können hinsichtlich der bekannten Differenz in LD 50-Dosen beider Substanzen von Bedeutung sein.
    Notes: Summary 8 days old rats were exposed to 100 mg/kg b. w. of either Methylnitrosourea (MNU) or Ethylnitrosourea (ENU). In the extraneural tissues mitotic inhibition lasts longer after MNU than after ENU. In the case of ENU, the number of mitotic cells rapidly increases once they reappear, whereas in the MNU-treated material reappearing mitotic figures are present in small numbers only at all intervals studied. Lethally damaged cells disappear slowly, but at the same rate for both MNU and ENU. The neural tissues show a much longer duration of mitotic inhibition. But as in the extraneural tissues after their reappearance in ENU-treated animals mitotic figures rapidly increase in number, whereas after MNU only a very limited number of cells in mitosis is found at all intervals. Lethally damaged cells in the neural tissues disappear much later than in the extraneural ones, but again at the same rate for both MNU and ENU. Among the mitotic figures in all tissues examined abnormal ones are frequently noticed. Delay of cellular death was observed in all tissues examined when — after exposure to MNU or ENU — protein synthesis was blocked by cycloheximide, indicating that cell death is an active process depending on de novo synthesis of protein(s). In comparison with similar results for well-known alkylantia in the literature, our findings add further evidence that the cytotoxic action of both MNU and ENU is caused by alkylation of cellular macromolecules. The marked differences for mitotic inhibition between MNU and ENU may be significant with respect to the well-known difference in LD-50 of these compounds.
    Type of Medium: Electronic Resource
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