(1) MAF-G activity was inhibited by mitomycin C and colchicine, which inhibit DNA synthesis and mitosis, respectively, but not by 2-deoxy-D-glucose, an inhibitor of glucose metabolism.
(2) With the stimulated liver being irradiated, the number of cells synthetizing DNA and entering into mitosis was seen reduced almost twice, whereas DNA synthesis and entering into mitosis were delayed, resp., by 4 and 6 hours.
(3) The distribution of cells at the stage of DNA synthesis and mitosis in all the parietal peritoneum speaks of the absence of special proliferation zones.
(4) Isoproterenol [IC 50 approximately 1 X 10(-9) M], prostaglandins, dibutyryl cyclic AMP [IC 50 approximately 2 X 10(-5) M], papaverine, theophylline and 5' AMP were inhibitory in the assay, whereas dibutyryl cyclic GMP and the cholinergic stimulator carbamylcholine either stimulated or had no effect on mitosis.
(5) Despite severe defects in the 1st or 2nd meiotic spindles in all mutants, no effect on mitosis was observed.
(6) Since transcription does not take place during mitosis, the amount of protooncogene products is rapidly decreased (they are extremely unstable).
(7) The role played by macrophages in two effects of lipopolysaccharide (LPS) on the immune system of the mouse-substitution for helper T cells and induction of B-cell mitosis-has been investigated.
(8) The results obtained allow to conclude that heterophasic condition of the fused cells is one of the causes of pathological mitosis of polykaryons and of their death.
(9) The effect of intracerebroventricular injection of the mitosis inhibitor colchicine on expression of mRNA for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin 3 was studied in the rat brain with in situ hybridization.
(10) The major events of mitosis have traditionally been considered to represent two distinct pathways and have been studied by two separate groups of workers.
(11) The V79 cells were treated for 30 min and in general, loss of a stainable spindle could be demonstrated at slightly higher concentrations than c-mitosis.
(12) However, unlike animal cell calmodulin, endosperm calmodulin appears to associate with kinetochore microtubules throughout mitosis, which suggests a specialized role for higher plant calmodulin in the regulation of kinetochore microtubule dynamics.
(13) This finding is directly opposed to that in rat skin where mitosis is stimulated.
(14) The restriction enzymes were introduced by electroporation into exponentially growing cells during the second replication cycle in bromodeoxyuridine, and SCEs were analyzed at mitosis.
(15) The absence of these mRNAs in mitosis and their disappearance at 4 hr and later in meiosis suggest that the rec7 and rec8 gene products may be involved primarily in the early steps of meiotic recombination in S. pombe.
(16) The distribution of bone marrow cells within the cell cycle was determined by flow microfluorometry and 7 hours after treatment with vincristine consisted of 69% in G1, 21% in S, and 9% in mitosis.
(17) In contrast, in HeLa, a human epithelial cell, keratin-containing IFB appear to dissemble as cells enter mitosis (Franke, W. W., E. Schmid, C. Grund, and B. Geiger, 1982, Cell, 30:103-113).
(18) After administration of vinblastine, a drug blocking mitosis in metaphasis, the percentage of lymphoblasts decreases whereas the percentage of X cells increases.
(19) The ultrastructure study, done before the 19th week ("pretumor" phase) confirms some previous observations (increase in the zone of mitosis, secretory changes, mutation producing effects).
(20) Still, they gave valuable information in relation to environmental screening; thus, the finding of c-mitosis may indicate risks of aneuploidy.
Senescence
Definition:
(n.) The state of growing old; decay by time.
Example Sentences:
(1) The proliferation of this cell type may represent an escape from the senescence pathway and progression to immortal tumor cells.
(2) In senescent rats, however, the proportions of salt-soluble and detergent-soluble AChE may differ from those in young rats.
(3) In addition, we have shown that long-lived, presumably non-senescent, strains do not arise by suppressor mutation, but lose senescence plasmid DNA by another mechanism.
(4) Senescent (26-28 months) Fischer 344 rats were shown to have a lower density of D2 sites (-36%) without any change in affinity in membranes prepared from homogenized caudate-putamen (CPU), as compared to young adult (5-6 months) rats.
(5) The cell cycle-dependent changes in the transglutaminase mRNA levels strongly support the implicated involvement of the enzyme in cell growth, differentiation, and senescence.
(6) The increased levels of HK1 could affect other erythrocyte metabolic pathways slowing down the physiological rate of cellular senescence and result in increased activity levels of other cell-age-dependent enzymes.
(7) Advancing age was associated with a reduction in cell proliferative responses to PHA in both substrains, although the rate of decline was significantly more rapid in the senescence-prone animals.
(8) Instead of degenerative changes, these results show an activation of the vasopressinergic system in senescence and in SDAT patients, similar to earlier observations in the aged rat and in accordance with a rise in human neurophysin and VP levels reported recently.
(9) Thus, constitutive expression of specific cytochrome P450 genes is repressed or activated in senescent rats.
(10) Mild daily exercise, maintained throughout adult life into early senescence, attenuates muscle atrophy and promotes adaptive enzymatic changes in atrophying muscles.
(11) A second set of experiments which involved the injection of E2 into senescent male as well as female rats indicated that there were no sex differences in improvements in inclined screen performance, and that once the E2 injections were discontinued, performance returned to preadministration levels.
(12) Additionally, analysis of the multiple steps occurring in the El cultures, as well as in the emergence of the continuous cell lines, could potentially elucidate the processes occurring during human epithelial cell carcinogenesis and escape from senescence.
(13) Significant anamnestic SIgA responses were shown after oral immunization with DNP-BGG in adult rats, but was not observed in the senescent and midlife (10-12 months) rats.
(14) Modulation of cellular senescence by growth factors, hormones, and genetic manipulation is contrasted, but newer studies in oncogene involvement are omitted.
(15) Under the same conditions, PM from senescent mice generated 62% of the initial O2- produced in response to zymosan, and 45% in response to OZ.
(16) Untreated cells, or cells treated with MCA or TPA only, usually became senescent around 6-8 weeks after plating and died, but those treated with both MCA and TPA became immortalised and underwent transformation to a phenotype capable of growth in soft agar.
(17) Because immune senescence most profoundly affects T lymphocyte functions, we suspected that LIA production would decline with age.
(18) Abnormal granular structures, which stained positively with periodic acid-Schiff (PAS-positive granular structures; PGS), were observed in the brain of senescence accelerated mouse (SAM).
(19) In senescent females the number of small IMPs was decreased in the perikarya and dendritic shafts compared to young females while the number of large particles was increased in the outer leaflet of the membrane of dendritic shafts, reaching values similar to those observed in males.
(20) Our data suggest that the release of u-PA antigen by human macrovascular endothelial cells can be used as an indicator of cell senescence.