bluuebunny/crossref_metadata_2025_split huggingface dataset:
Estimation of Circadian Variations In Cell Cycle Phase Durations In Murine Epidermal Basal Cells
Authors: Thorud Erik , Aarnæs Erik , Clausen Ole Petter F. , Bjerknes Rolf , Anker Peder 
Published: May 2008

AbstractCircadian variations in the proliferative activity of squamous epithelia are well known. However, circadian variations in the duration of the various cell cycle phases (S, G2 and mitosis) have been disputed. the percent labelled mitoses method, which is traditionally used to obtain duration of cell cycle phases, is poorly suited for identification of circadian variations. Therefore methods combining changes in compartment size (cell cycle phase) and cellular flux through the compartments have been used. Three different methods using such data are presented. These incorporate various simplifying assumptions that cause methodological errors. Limits for use of the different methods are indicated. the use of all three methods gives comparable and pronounced circadian variations in the duration of S and G2 phase. These results are also compatible with circadian variations in the mitotic duration, but they may also represent artefacts due to sensitivity to model errors.
Mathematical Model of Acute Myeloblastic Leukaemia: an Investigation of the Relevant Kinetic Parameters
Authors: Djulbegović Benjamin , Svetina Saša 
Published: May 2008

AbstractA simple model of acute myeloblastic leukaemia (AML) development is introduced, explicitly including cell growth, cell differentiation and cell‐cell interaction. Each of these processes is described by a single model parameter. It is hypothesized that the leukaemic cell is characterized by an alteration of only one of these processes. the kinetic behaviour of the AML system is examined separately for possible alterations of each of the three parameters describing the three processes involved. It is shown that, on the basis of the existing data on AML kinetics, the alteration of the growth and cell‐cell interaction parameters can be eliminated as a possible source of AML. Thus kinetic data support the modification of the differentiation process as the origin of the AML state. Further, the growth characteristics of normal and leukaemic cells in the presence of each other are analysed. It is shown how the initial growth of leukaemic cells depends on the difference in the differentiation of normal and leukaemic cells and how the same difference determines the decay of normal cells in the presence of the predominantly leukaemic population. Correlations between the kinetic parameters of the normal and leukaemic populations are suggested to characterize the leukaemic state.
Effect of Vinblastine On the Cell Cycle and Migration of Ameloblasts of Mouse Incisors As Shown By Autoradiography Using 3H‐Thymidine
Authors: Mercedes Maria , Samperiz Fernandez , Blumen Guilherme , Merzel Jose 
Published: May 2008

Abstract. The effects of vinblastine on the cell cycle and the migration of ameloblasts were studied in the lower incisors of mice by labelling the cells with 3H‐thymidine ([3H]TdR) and radioautography. A group of mice received 2 μg/g of body weight vinblastine intraperitoneally and 6 hr after these animals and those of a control group were injected with 1μCi/g body weight of [3H]TdR, and sacrificed at time intervals from 0.75 hr to 15 days.The generation time of ameloblasts in the progenitor compartment was 14.8 hr in animals treated with vinblastine and 17 hr in the controls, using the FLM curve method; with the grain dilution method the duration was respectively 29.25 hr and 25.96 hr. the thymidine labelling index of the treated animals was 50% higher than the controls. the velocity of ameloblast migration, determined either by the displacement of the most incisally labelled cell or by the grain dilution method, was lower in the experimental group (2.48 cell positions/hr and 9.18 μ/hr respectively) as compared with the control (3.21 cell positions/hr and 18.88 μm/hr respectively).The results on the ameloblast production rate are contradictory but the slowing down in the velocity of cell migration is compatible with a decrease of the rate of cell production in the progenitor compartment as a vinblastine effect.
Epidermal Tissue Homeostasis
Authors: Budtz Povl E. 
Published: May 2008

Abstract. Toad epidermis is a suitable model for studies on tissue homeostasis because cell pool size, influx into and efflux from the cell pool can be easily determined. the cell pool size was obtained by cell counting on photomicrographs, the influx (cell birth rate) was assessed by the metaphase‐arrest technique, and the efflux (cell loss by moulting) assessed by counting the number of cells in the corneal layer and recording of intermoult periods. the importance of the methods for assessing these parameters per square unit of skin surface is emphasized.These parameters were studied in eight groups of ten adult male toads sacrificed at various hours of the day. There were minor variations in the cell birth rate, fluctuating around a mean of 26 cells/mm2/hr (obtained at the metaphase collection period from 11.00‐14.00 hours). By summation of the cell productions during the eight metaphase collection periods of 3 hr, and extrapolation to an intermoult period (time between two moults), a calculated cell production of about 6340 cells/mm2 in 10.3 days was obtained, whereas the cell loss at each moult was only 2370 cells/mm2. Thus the cell production rate exceeds the rate of cell loss through moults by a factor of 2.7. Arguments are presented that the ‘surplus’ of cells produced cannot be permanently accommodated within the living epidermis. Consequently a cell deletion rate beyond that by moulting of about 4000 cells/mm2 in 10.3 days or 16 cells/mm2/hr can be calculated.These results are discussed in relation to current concepts of tissue homeostatic mechanism(s). the results are consistent with the hypothesis that controlled cell deletion may be a tissue homeostatic mechanism complementary to controlled cell divisions.
Establishment and Growth Kinetics of the Mutant Ehrlich‐Lettré Ascites Cell Strain Hd33 In Permanent Suspension Culture1,2
Authors: Granzow Christof , Granzow Viola , Edler Lutz , Sauer Wolfgang 
Published: May 2008

AbstractCells of a mutant in vivo subline of the Ehrlich‐Lettré mouse ascites tumour (ELAT) were converted to growth in suspension culture. Kinetic analysis revealed the selective character of the conversion process; without a detectable adaptation period, a fraction of about 2 × 10‐5 of the explanted cells continued to grow in vitro. the resulting, mutant Ehrlich‐Lettré ascites cell strain was designated HD33 and propagated uninterruptedly from 1974 on. the corresponding in vivo ELAT subline HD33 was derived from the HD33 ascites cell strain by intraperitoneal retransplantation.In HD33 cell suspension cultures, the population doubling time, the average intermitotic interval, as determined by videomonitoring, and the average duration of the cell cycle, as determined from percentage of labelled mitoses (PLM) data, were all measured at 15 hr. Cell loss and quiescent compartments were insignificant. the duration of the G1 phase was effectively zero. Both PLM data and [3H]/[14C] thymidine double‐labetling measurements revealed an S‐phase duration of between 11 and 12 hr. the G2 phase lasted 3–5 hr.The HD33 strain differs from comparable suspension strains of wild‐type Ehrlich ascites cells in the insignificant role of density‐dependent inhibition in growth, and the striking prolongation of the S phase which is associated with an excessive, cytoplasmic storage of glycogen by the mutant cells.
Influence of Growth Hormone and Thyroxine On Cell Kinetics In the Proximal Tibial Growth Plate of Snell Dwarf Mice
Authors: Smeets Ton , van Buul‐Offers Sylvia 
Published: May 2008

Abstract. In Snell dwarf mice, the influence of short‐term treatment with human growth hormone (hGH) or thyroxine on the proliferative and sulphation activity of the proximal tibial growth plate was studied. By autoradiographic methods, the [3H]methylthymidine incorporation after a single injection was measured, after 2 hr incorporation time. the labelling index was calculated and the number of labelled mitoses was counted. In addition, the distribution of the labelled nuclei over the proliferating and degenerating zones was determined by continuous labelling for 25 and 73 hr.In untreated dwarf mice after [3H]‐methylthymidine administration, the number of labelled nuclei in the growth plate is low. Labelling occurs, as expected, mainly in the cells of the proliferative zones. the number of labelled nuclei in control dwarf mice was similar after 25 and 73 hr continuous labelling. This suggests that many cells are in a resting Go or prolonged G1 phase. Both hGH and T4 treatment induce a significant increase of the number of labelled nuclei per growth plate and of the number of mitoses. Since hormonal treatment induces a small number of mitoses after 2 hr incorporation of the label, the minimal G2 phase of the cell cycle is less than 2 hr. In addition, treatment with hGH and T4 stimulates chondrocytes in the zone of proliferative and hypertrophic cells to actively incorporate [35S]‐sulphate.
Complement Split Product C5a Mediates the Lipopolysaccharide‐Induced Mobilization of Cfu‐S and Haemopoietic Progenitor Cells, But Not the Mobilization Induced By Proteolytic Enzymes
Authors: Molendijk W. J. , van Oudenaren A. , van Dijk H. , Daha M. R. , Benner R. 
Published: May 2008

Abstract. Intravenous (i.v.) injection of mice with lipopolysaccharide (LPS), and the proteolytic enzymes trypsin and proteinase, mobilizes pluripotent haemopoietic stem cells (CFU‐s) as well as granulocyte‐macrophage progenitor cells (GM‐CFU) and the early progenitors of the erythroid lineage (E‐BFU) from the haemopoietic tissues into the peripheral blood. We investigated the involvement of the complement (C) system in this process. It appeared that the early mobilization induced by LPS and other activators of the alternative complement pathway, such as Listeria monocytogenes (Lm) and zymosan, but not that induced by the proteolytic enzymes, was absent in C5‐deficient mice. the mobilization by C activators in these mice could be restored by injection of C5‐sufficient serum, suggesting a critical role for C5.The manner in which C5 was involved in the C activation‐mediated stem cell mobilization was studied using a serum transfer system. C5‐sufficient serum, activated in vitro by incubation with Lm and subsequently liberated from the bacteria, caused mobilization in both C5‐sufficient and C5‐deficient mice. C5‐deficient serum was not able to do so. the resistance of the mobilizing principle to heat treatment (56°C, 30 min) strongly suggests that it is identical with the C5 split product C5a, or an in vivo derivative of C5a. This conclusion was reinforced by the observation that a single injection of purified rat C5a into C5‐deficient mice also induced mobilization of CFU‐s.
Effect of Cyclophosphamide On the Proliferation of L 1210 Ascites Tumour Cells and of Jejunal Crypt Cells In the Mouse
Authors: Schäfer E. , Maurer‐Schultze B. 
Published: May 2008

Abstract. Cyclophosphamide (CY) does not act in a cell‐cycle specific manner. i.e. exclusively on proliferating cells. It also kills non‐proliferating cells, as shown by application of CY to L 1210 ascites tumour‐bearing mice during plateau phase growth of the tumour. Moreover, treatment with CY of L 1210 ascites tumour cells, double‐labelled with [3Hl and [14C]‐thymidine, suggests that CY is not cell cycle phase dependent, but kills cells out of all cycle phases.There is also an extensive cytocidal effect of CY (300 mg/kg) on the jejunal crypt cells of the mouse, which is even more pronounced than that of cisplatinum (DDP, 13 mg/kg). However, rapid regeneration of crypt cells occurs after treatment with the drugs.
Pluripotent Haemopoietic Stem Cell Entry Into Dna Synthesis In Vitro After Stimulation By Ara‐C Treatment In Vivo
Authors: Izumi H. , Guigon M. , Frindel E. 
Published: May 2008

Abstract. Non‐cycling pluripotent bone marrow stem cells (CFU‐S), taken 3 hrs after injection of 20 mg of Ara‐C, have been shown to enter DNA synthesis at 1 to 3 hr after being cultured in α‐medium. This phenomenon was observed when bone marrow was incubated as a plug, but not when incubated as a cell suspension in the present experimental conditions.These results suggest that a medullary structure is necessary in order to observe this effect and/or that accessory cells are destroyed during the process of single cell preparation.
Circadian Variation In Migration Velocity In Small Intestinal Epithelium
Authors: Kaur P. , Potten C. S. 
Published: May 2008

Abstract. The variation in migration rates of cells within the small intestinal epithelium was studied over a 24‐hr period at 3‐hr intervals (migration of cells was studied independently for the crypts and the villi using the changing distributions of [3H]TdR labelled cells as an indicator of cell migration).Clear changes in the rates of cell movement were observed during a 24‐hr period for both crypt and villus epithelium. the rates of cell migration in these two compartments did not correlate well with the exception of samples taken at 18.00 hours. At this time of day there appeared to be no cell movement at all in either crypts or villi. There was not a good correlation between the migration velocity throughout the day and the changes in the number of mitoses.It is proposed that mitotic rates do not directly govern migration rates but that the converse may be true. Further, the lack of correlation between crypt and villus migration rates at any time of day suggest that the mechanisms controlling all movement in these two regions of small intestinal epithelium may be different.
Cell Migration Velocities In the Crypts of the Small Intestine After Cytotoxic Insult Are Not Dependent On Mitotic Activity
Authors: Kaur P. , Potten C. S. 
Published: May 2008

Abstract. The role of mitotic activity in the normal process of intestinal epithelial cell migration was investigated. the movement of [3H]TdR‐labelled cells in the crypt‐villus column was used to study migration both in the crypts and on the villi. Radiation alone or in conjunction with other cytotoxic agents (hydroxyurea, cyclophosphamide and isopropyl‐methane sulphonate) was used to eliminate cell division activity and to decrease crypt cellularity. This was done in order to determine the role of ‘mitotic pressure’ in driving cell migration.It has been clearly demonstrated in this study that cell migration, both within the crypts and on the villi, can take place in the complete absence of mitotic activity and after a drastic decrease in crypt cellularity. These results add to the continually mounting evidence against the idea that the ‘pressure’ generated by mitoses within the crypt or indeed in other epithelial regions is responsible for propelling epithelial cells. the data also demonstrate that the migration mechanisms are resistant to cytotoxic exposure.
Circadian synchronization of hepatocyte proliferation in young rats: the role played by adrenal hormones
Authors: Barbason H. , Herens Ch. , Mormont M.‐C. , Bouzahzah B. 
Published: May 2008

Abstract. From the 20th day to the 30th day of life, the mitotic rhythm is progressively induced by a reduction in nocturnal values, while diurnal rhythms remain unchanged. Mitotic peaks emerge at 10.00 hours.A labelling index wave occurs 8 hr before the corresponding mitotic wave, with a peak at 02.00 hours and a minimum in the evening, coincidental with the acrophase of plasma corticosterone level (activity phase).Labelled mitoses curves and metaphase accumulation after colchicin injection show that the duration of the S, G2 and M phases remain approximately constant and that the circadian variation is due to a variation in the rate of cells that enter these successive phases. During the synchronization period (from day 20 to 30), the growth fraction decreases progressively. Adrenalectomy at this time is followed by a higher cell proliferation and all rhythms disappear after 2 days.Corticosterone injected before the triggering of the rhythmic activity in 17‐day‐old rats immediately reduces the labelling index, while the mitotic index is decreased 10 hr later; this delay is equal to the S + G2 duration.The results are discussed. They favour the hypothesis that the circadian variation of corticosterone is responsible for the induction of a circadian variation in developmental cell proliferation by inhibition of the G1‐S transition when it is higher in the evening.The circadian rhythm of hepatic cell proliferation in rats appears on the 20th day of life, when the hypothalamo‐adrenal axis is mature enough for circadian activity to occur.
Long duration of mitosis and consequences for the cell cycle concept, as seen in the isthmal cells of the mouse pyloric antrum. II. Duration of mitotic phases and cycle stages, and their relation to one another
Authors: El‐Alfy M. , Leblond C. P. 
Published: May 2008

Abstract. The kinetics of isthmal cells in mouse antrum were examined in three ways: (a) the duration of cell cycle and DNA‐synthesizing (S) stage was measured by the ‘fraction of labelled mitoses’ method; (b) the duration of interphase and mitotic phases was determined from how frequently they occurred; and (c) mice were killed at various intervals after an intravenous injection of 3H‐thymidine to time the acquisition of label by the various phases of mitosis.The duration of the isthmal cell cycle was found to be 13.8 hr and that of the DNA‐synthesizing (S) stage, 5.8 h. Estimates for the duration of the G1 and G2 stages were 6.8 and 1.0 hr, respectively.From the frequency of mitotic phases, defined as indicated in the preceding article (El‐Alfy & Leblond, 1987) and corrected for the probability of their occurence, it was estimated that prophase lasted 4.8 hr; metaphase, 0.2 hr; anaphase, 0.06 hr and telophase, 3.3 hr, while the interphase lasted 5.4 hr. In accordance with this, the duration of the whole mitotic process was 8.4 hr.Ten minutes after an intravenous injection of 3H‐thymidine, 38% of labelled isthmal cells were in interphase and 62% in early or mid prophase, while cells in late prophase and other mitotic phases were unlabelled. After 60 min, label was in late prophase, after 120 min, in mid telophase and after 180 min, in late telophase.We conclude that there is overlap between some mitotic phases and cycle stages. Thus, while nuclei are at interphase during the early third of S, they are in prophase during the late two‐thirds as well as during G2. Also, nuclei are in telophase during the early half of G1 but at interphase during the late half. Differences in nuclear diameter show that subdivision of both S and G1 into early and late periods is practical.
The effect of prolonged stress‐inducing electrical stimulation on cell proliferation in rat palatal epithelium
Authors: Østergaard E. , Fisker A. V. , Karring T. 
Published: May 2008

Abstract. This study examines whether blocking of cell division by stress‐inducing electrical stimulation can be maintained for a prolonged period of time and whether this results in the accumulation of a large number of cells ready to divide when the block is released.A total of 96 rats was subjected to electrical stimulation at intervals of 30 min for periods of 2,4,6 or 12 hr. Groups of animals were killed every second hour during these stimulation periods. After 2, 4 and 6 hr groups of animals were exempted from further stimulation and killed 2 or 4 hr later. After termination of the 12 hr stimulation period, groups of animals were killed every second hour during the succeeding 24 hr. Forty‐eight animals were left undisturbed and served as controls. Two and a half hours prior to death, each of the experimental and control animals was injected intraperitoneally (i.p.) with colchicine. Histological sections of the palatal mucosa were prepared and the numbers of arrested metaphases were counted.The electrical stimulation for 2, 4, 6 and 12 hr consistently resulted in a reduced number of cells entering mitosis, indicating a blockade at the G2/M transition. However, with an increase in the length of electrical stimulation, an increasing number of cells passed the block, while a decreasing number entered mitosis during the first 4 hr following cessation of the stimulation. The sum of metaphases accumulated during the various stress periods and the following 4 hr was always similar and consistently lower than the number of metaphases accumulated in the control animals within the same time periods. This observation indicates that, during stress‐inducing electrical stimulation and the succeeding 4 hr, only a defined number of cells can enter the mitotic phase. Thus, in addition to the block at the G2/M transition, there appears to be another block of cell division at an earlier stage in the cell cycle.
Haemopoietic stem cell proliferation in the bone marrow of Sl/Sld mice
Authors: Wright E. G. , Lorimore S. A. 
Published: May 2008

Abstract. In marrow from Sl/Sld mice (but not +/+ mice) day 7 and day 8 CFU‐S proliferate whilst day 10 and day 12 CFU‐S exhibit negligible proliferation. Media conditioned by both +/+ and Sl/Sld marrow contains an inhibitor of CFU‐S proliferation but day 8 CFU‐S in +/+ and Sl/Sld marrow show marked dose‐response differences to this factor. To inhibit the proliferation of Sl/Sld CFU‐S required approximately ten times the concentration of inhibitor that inhibited the proliferation of +/+ CFU‐S. Thus abnormally responsive day 8‐CFU‐S were shown to proliferate in an inhibitory environment.Abnormalities in Sl/Sld CFU‐S function were also demonstrated in heterotopic transplantation experiments using +/+ and Sl/Sld donors and hosts to obtain ectopic bone marrow with various stromal (donor) and haemopoietic (host) combinations. Day 8 Sl/Sld CFU‐S were seen to proliferate, irrespective of whether the stromal environment was derived from Sl/Sld or +/+ marrow.Sl/Sld mice are generally regarded as animals in which there is a genetically determined defect in haemopoiesis due to an abnormality in the haemopoietic environment. It is difficult, however, to attribute the abnormal CFU‐S behaviour in these experiments to environmental factors and the results are consistent with mutation at the Sl locus affecting the responses of CFU‐S to regulatory signals, i.e. the genetic defect is not confined to the stromal environment.
Effect of graft versus host reaction on cell cycle time in neonatal mouse jejunum
Authors: Lund E. K. , Smith M. W. 
Published: May 2008

Abstract. The duration of cell cycle parameters in control mouse jejunum has been compared with that found following induction of a graft‐versus‐host reaction (GvHR) during the first 3 weeks of postnatal life.Values for tc, and tG1 were found to decrease progressively during normal development: estimates for the whole crypt column in 21‐day‐old mice were approximately half to one quarter those found 6 days after birth 12.1 ± 0.5 hr and 24.2 ± 0.3 hr for tc; 2.8 ± 0.3 hr and 12.1 ± 0.3 hr for tG1 respectively; (means ± SE).tS and tG2 were found to remain approximately constant during this period of neonatal development.Injecting foreign spleen cells into 3‐day‐old mice produced no effect on crypt cell proliferation or cell cycle parameters measured 3 days later. GvHR mice studied 8 days after spleen cell injection, however, showed both an increase in crypt cell proliferation and decreases in the values for tc and tG1, to levels similar to those normally found in 21‐day‐old control animals (tc 12.4 ± 0.4 hr and tG1 5.4 ± 0.4 hr for 11‐day‐old GvHR mice). The possible mechanism leading to these changes is discussed.The ability of GvHR to stimulate cell proliferation is used in the present work to test the hypothesis that the total number of cell divisions taking place after birth determines the temporal sequence of changes in disaccharidase content produced during neonatal development.