Die 24 Std-Mitoserhythmik beim Ehrlichschen M�use-Ascites-Carcinom nach Ovarektomie und Adrenalektomie

Meng, Kun; Pohle, K.

doi:10.1007/bf00525134

Cited by 7 publications

(2 citation statements)

References 9 publications

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“…Bone marrow damage by S-stage-specific chemotherapeutic agents would be expected to be minimized by treatment during the middle of the dark span. (Rosene and Halberg, 1970), rat sarcomas Woutilainen, 1953), an immunocytoma in rats , L1210 acute lymphocytic leukemia (Haus and Halberg, 1978), or some forms of Ehrlich ascites tumor (Meng and Pohle, 1961).…”

Section: Rhythmic Changes In Responsiveness Susceptibility and Resimentioning

confidence: 99%

Chronobiology in hematology and immunology

et al. 1983

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The hematopoietic and the immune systems in all their components are characterized by a multifrequency time structure with prominent rhythms in cell proliferation and cell function in the circadian, infradian, and rhythms in cell proliferation and cell function in the circadian, infradian, and circannual frequency ranges. The circulating formed elements in the peripheral blood show highly reproducible circadian rhythms. The timing and the extent of these rhythms were established in a clinically healthy human population and are shown as chronograms, cosinor summaries and, for some high-amplitude rhythms, as time-qualified reference ranges (chronodesms). Not only the number but also the reactivity of circulating blood cells varies predictably as a function of time as shown for the circadian rhythm in responsiveness of human and murine lymphocytes in vitro to lectin mitogens (phytohemagglutinin and pokeweed mitogen). Some circadian rhythms of hematologic functions appear to be innate and are presumably genetically determined but are modulated and adjusted in their timing by environmental factors, so-called synchronizers. Phase alterations in the circadian rhythms of hematologic parameters of human subjects and of mice by manipulation of the activity-rest or light-dark schedule and/or of the time of food uptake are presented. Characteristically these functions do not change their timing immediately after a shift in synchronizer phase but adapt over several and in some instances over many transient cycles. The circadian rhythm of cell proliferation in the mammalian bone marrow and lymphoid system as shown in mice in vivo and in vitro may lend itself to timed treatment with cell-cycle-specific and nonspecific agents in an attempt to maximize the desired and to minimize the undesired treatment effects upon the marrow. Differences in response, and susceptibility of cells and tissues at different stages of their circadian and circaseptan (about 7-day) rhythms and presumably of cyclic variations in other frequencies are expected to lead to the development of a chronopharmacology of the hematopoietic and immune system. Infradian rhythms of several frequencies have been described for numerous hematologic and immune functions. Some of these, i.e., in the circaseptan frequency range, seem to be of importance for humoral and for cell mediated immune functions including allograft rejection. Infradian rhythms with periods of 19 to 22 days seem to occur in some hematologic functions and are very prominent in cyclic neutropenia and (with shorter periods) in its animal model, the grey collie syndrome.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Rhythmic Changes In Responsiveness Susceptibility and Resimentioning

confidence: 99%

Chronobiology in hematology and immunology

et al. 1983

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“…By comparison, the circadian mitotic rhythm examined by Meng and Pohle in mice carrying an Ehrlich ascites carcinoma persisted with a time-macroscopically reduced amplitude after a bilateral adrenalectomy but perhaps without removal of ectopic tissue [261]. …”

Section: Puzzle #8: Collaterally Hierarchical Cellulo-neuroendocrine mentioning

confidence: 99%

Transdisciplinary unifying implications of circadian findings in the 1950s

Halberg

Cornélissen

Katinas

et al. 2003

J Circadian Rhythms

101

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A few puzzles relating to a small fraction of my endeavors in the 1950s are summarized herein, with answers to a few questions of the Editor-in-Chief, to suggest that the rules of variability in time complement the rules of genetics as a biological variability in space. I advocate to replace truisms such as a relative constancy or homeostasis, that have served bioscience very well for very long. They were never intended, however, to lower a curtain of ignorance over everyday physiology. In raising these curtains, we unveil a range of dynamics, resolvable in the data collection and as-onegoes analysis by computers built into smaller and smaller devices, for a continued self-surveillance of the normal and for an individualized detection of the abnormal. The current medical art based on spotchecks interpreted by reference to a time-unqualified normal range can become a science of time series with tests relating to the individual in inferential statistical terms. This is already doable for the case of blood pressure, but eventually should become possible for many other variables interpreted today only based on the quicksand of clinical trials on groups. These ignore individual differences and hence the individual's needs. Chronomics (mapping time structures) with the major aim of quantifying normalcy by dynamic reference values for detecting earliest risk elevation, also yields the dividend of allowing molecular biology to focus on the normal as well as on the grossly abnormal.

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Control of Diurnal Fluctuations in Responsiveness to External Factors

Bünning¹

1967

Heidelberg Science Library

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Die 24 Std-Mitoserhythmik beim Ehrlichschen M�use-Ascites-Carcinom nach Ovarektomie und Adrenalektomie

Cited by 7 publications

References 9 publications

Chronobiology in hematology and immunology

Chronobiology in hematology and immunology

Transdisciplinary unifying implications of circadian findings in the 1950s

Control of Diurnal Fluctuations in Responsiveness to External Factors

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