bluuebunny/crossref_metadata_2025_split huggingface dataset:
Resistance of teratocarcinoma stem cells to infection with simian virus 40: Early events
Authors: Swartzendruber Douglas E. , Friedrich Thomas D. , Lehman John M. 
Published: February 2005

AbstractMultipotential stem cells of a murine teratocarcinoma are resistant to typical infection with either polyoma virus (PV) or Simian virus 40 (SV40). Differentiated progeny of the stem cells are susceptible to infection in a manner identical to other mouse somatic cells, i.e., they are permissive for PV and nonpermissive for SV40. The early interactions between the stem cells (embryonal carcinoma or EC cells) and SV40 and PV were studied. Virions adsorbed to and penetrated into the cytoplasm and nucleus of EC cells, but did not induce expression of T antigen in the EC nuclei. Purified SV40 DNA was capable of inducing T antigen in differentiated teratocarcinoma cells but not in EC cells. Virus could not be rescued from EC cells previously exposed to SV40. The resistance of the stem cells to infection apparently involves a block in the infectious cycle after adsorption and penetration but before T antigen induction.
The stimulation of DNA synthesis by cytochalasin B in proliferative epidermal and dermal cells
Authors: Rothberg Simon , Nancarrow Grace E. , Church Virgene L. 
Published: February 2005

AbstractCytochalasin B influences a variety of cellular events that are associated with the contractile microfilament system and the formation of binucleate cells. Along with the formation of binucleate cells, cytochalasin B also causes an acceleration of cells from G1 to S in the cell cycleBy pulsing with cytochalasin B for 30 minutes and allowing for a previously established lag time (17.5 hours) a stimulation of thymidine incorporation into DNA of proliferative epidermal and dermal cells was found in both control and stripped epidermisAutoradiographic analysis confirmed that the stimulation was due to an increased number of basal cells accelerated from G1 to S phase. A minimal number of binucleate basal cells, 1 in 300, was observed, which suggests that the stimulated synthesis is independent of binucleate cell formation. The amount of stimulation is maximum with cytochalasin B concentration pulse between 5γ and 30γ/mlThe results suggest a possible link in coupling cell membrane and surface events with subsequent increased cell nuclei synthetic activity.
Diamide effect on the hypertonic calcium uptake by rat red blood cells
Authors: Branca D. , Scutari G. , Siliprandi N. 
Published: February 2005

AbstractRed blood cells of rat exhibit an enhanced hypertonic calcium uptake after incubation with diazenedicarboxylic acids bis (N,N‐dimethylamide) (diamide). Over the ranges reported in this paper the amount of membrane alteration is strongly and linearly dependent on the diamide concentration and on the osmolarity of the incubation medium. Treatment with 2,3‐dihydroxy‐1,4‐dithiolbutane (dithioerythritol or DTE), after diamide removal, restores red blood cells calcium intake to values similar to those of the control. The results indicate that the sinergic action of diamide and hypertonicity can oxidize some thiol groups essential for the cation barrier maintenance.
Mapping G1 phase by the structural morphology of the prematurely condensed chromosomes
Authors: Hittelman Walter N. , Rao Potu N. 
Published: February 2005

AbstractThe object of this study was to develop a map of G1 phase on the basis of the progressive changes taking place in the morphology of the prematurely condensed chromosomes as the cells traverse through G1 and then use this technique to determine the cell cycle location of normal and transformed cell populations in plateau phase. The morphology of the prematurely condensed chromosomes (PCC) of G1 cells in random populations was found to be highly variable. For a better understanding of the relationship between the morphology of the G1‐PCC and their position within G1 phase, synchronized populations of Chinese hamster ovary (CHO) cells in early, mid‐, and late G1 phase were fused with mitotic cells. Early G1 cells resulted in highly condensed G1‐PCC, while late G1 cells gave very extended G1‐PCC. Mid‐G1 cells resulted in PCC of intermediate condensation. To test the validity of these criteria for mapping the position of a cell in the cell cycle, synchronous G1 cell populations were treated with a variety of metabolic inhibitors. Cycloheximide and actinomycin D were shown to block cell in early G1 phase, while excess thymidine and hydroxyurea blocked cells in early S phase. The results presented here indicate that, upon reaching plateau phase, normal cell populations (BALB‐C mouse 3T3, human PA‐2, and WI 38) stop in early G1, while most cells in transformed cell lines (CHO, HeLa, and mouse SV‐3T3) accumulate in late G1.
Inhibition of glucose transport in human erythrocytes by benzylalcohol
Authors: Lacko L. , Wittke B. , Lacko I. 
Published: February 2005

AbstractThe inhibition of glucose transport by the non‐ionizable local‐anesthetic benzylalcohol is of the mixed type and independent of pH. The affinity of benzylalcohol to the free carrier is about three times larger than that to the carrier‐glucose complex.
The role of myonuclei in muscle regeneration: An in vitro study
Authors: Pullman William E. , Yeoh George C. T. 
Published: February 2005

AbstractIt is well established that during muscle regeneration, the satellite cells which are in a state of mitotic arrest, can initiate cell division to produce myoblasts which subsequently fuse to form myotubes. However, whether myonuclei, contained within damaged myotubes, or “freed” as a result of the trauma, play any role in muscle regeneration remains unresolved.In myogenic cultures, it is possible to obtain renewed myogenesis when initial cultures are sub‐cultured. The aim of this study, was to obtain evidence of the participation by myonuclei of primary cultures in myogenesis which occurs subsequently in secondary cultures. In culture, myonuclei can be labelled with H3‐thymidine and their ultimate fate, either as “free” myonuclei or myonuclei associated with disrupted myotubes can be followed unequivocally. Three types of experiments are performed: (i) Primary myogenic cultures containing only myotubes are subcultured. (ii) Primary myogenic cultures containing myotubes with labelled myonuclei are disrupted and subcultured. (iii) Primary myogenic cultures containing myotubes with unlabelled myonuclei are mixed with labelled mononucleated myogenic cells and sub‐cultured.In all instances no evidence of myogenesis from myonuclei is obtained. It is concluded that myonuclei, which were rendered postmitotic during myogenesis, remain so when muscle is disrupted and cannot re‐enter the mitotic cycle.
Uridine transport and phosphorylation in mouse cells in culture: Effect of growth‐promoting factors, cell cycle transit and oncogenic transformation
Authors: Rozengurt Enrique , Mierzejewski Karl , Wigglesworth Noel 
Published: February 2005

AbstractThe rapid increase in uridine uptake produced by the addition of serum to quiescent cultures of fibroblasts is primarily caused by an enhanced rate of nucleoside phosphorylation. While quiescent and serum‐stimulated cells display identical initial rates of transport, they show a considerable change in the composition of the acid‐soluble pools labelled with [3H] uridine for five seconds. The radioactivity recovered in the phosphorylated pools increases 2‐, 3‐, 4‐ and 6‐fold after addition of serum to cultures of Swiss 3T3 cells, tertiary mouse embryo fibroblasts, Swiss 3T6 and Balb 3T3, cells respectively. Furthermore, insulin, a growth factor isolated from medium conditioned by SV40 BHK cells (FDGF) and epidermal growth factor (EGF) also stimulate uridine phosphorylation within minutes.The initial rate of uridine uptake is 2‐ to 3‐fold faster in rapidly growing normal and Simian virus 40 or polyoma virus transformed 3T3 cells as compared to untransformed 3T3 cells in the quiescent state. When quiescent cultures of 3T3 or mouse embryo cells are stimulated to leave G1 and enter into DNA synthesis, transport increases several hours after addition of serum and apparently coincides with the S phase of the cell cycle. The results demonstrate that an increase in uridine phosphorylation is a rapid metabolic response elicited by growth‐promoting agents in a variety of cell types and that uridine transport and phosphorylation are independently regulated.
Karyology and tumorigenicity of a Simian virus 40‐transformed chinese hamster cell clone
Authors: Lehman John M. , Trevor Katrina 
Published: February 2005

AbstractA pseudodiploid clone of Chinese hamster cells transformed in vitro with Simian virus 40 (SV40) was isolated from soft agar and injected into nude mice through three successive passages with a short in vitro cultivation between each animal inoculation. The original clone and the three subsequent tumor populations were characterized in regard to SV40 T antigen staining, modal chromosome number, and Giemsa‐banded karyotype. All tumor cell lines maintained the pseudodiploid mode, as well as the positive SV40 T antigen staining. Nonrandom chromosomal changes included loss of one of the X chromosomes, additions of abnormal variants of chromosomes No. 1 and No. 2, the appearance of unidentified marker chromosomes, and the loss of autosomes No. 5, No. 6, and No. 11. The deletion of one of the X chromosomes occurred with about the same frequency in all cell lines. Additions of abnormal chromosomes No. 1 and No. 2 tended to recur more often in the tumor cell lines than in the original clone. The appearance of marker chromosomes, as well as the loss of autosomes No. 5, No. 6, and No. 11 demonstrated a correlation with tumorigenicity. Yet, the three successive passages of the cells through the animal did not select for a tumor population with a single, homogeneous karyotype.
Cholera toxin stimulates division of 3T3 cells
Authors: Pruss Rebecca M. , Herschman Harvey R. 
Published: February 2005

AbstractCholera toxin was used in an attempt to inhibit epidermal growth factor stimulated 3T3 cell division. Instead, cholera toxin alone at low concentrations (10−10 M), was able to stimulate cell division and could augment EGF stimulated cell division. The mitogenic effect of cholera toxin can occur despite a dramatic increase in the intracellular levels of cAMP in 3T3 cells. Cholera toxin stimulated mitogenesis could not be mimicked by choleragenoid, the binding but inactive subunit of cholera toxin, or by other agents which elevate cAMP levels in 3T3 cells.
T98G: An anchorage‐independent human tumor cell line that exhibits stationary phase G1 arrest in vitro
Authors: Stein Gretchen H. 
Published: February 2005

AbstractT98 and T98G are two related cell lines that were derived from a human glioblastoma multiforma tumor. T98G has almost twice as many chromosomes as T98, suggesting that it is a polyploid variant of T98. Three aspects of control of cellular proliferation were studied in T98 and T98G cells in comparison to WI‐38 normal human diploid cells. WI‐38 cells have the following properties: (1) they can undergo only a limited number of population doublings in vitro; (2) they cannot proliferate without anchorage; and (3) they become arrested in G1 phase under stationary phase conditions. T98 cells differ from normal cells in all three of these properties, as do many other transformed cell lines. However, the derivative of T98, namely T98G, expresses an unique combination of normal and transformed aspects of the control of cellular proliferation. T98G cells are like normal cells in that they become arrested in G1 phase under stationary phase conditions, yet they also exhibit the transformed characteristics of anchorage independence and immortality. Thus, T98G cells demonstrate that transformation to immortality and anchorage independence can exist without concomitant loss of the normal mechanism for G1 arrest in response to stationary phase conditions. This result supports the hypothesis that each of these three aspects of control of cellular proliferation can be altered independently. Partially transformed cell lines, such as T98G, should be useful for sorting out the biochemical changes associated with transformation in each of these aspects.
Repair and survival after UV in quiescent and proliferating Microtus agrestis cells: Different rates of incision and different dependence on DNA precursor supply
Authors: Collins Andrew R. S. , Johnson Robert T. 
Published: February 2005

AbstractCultured cells of Microtus agrestis, the common field vole, perform unscheduled DNA synthesis after UV irradiation. They respond to incubation with a DNA synthesis inhibitor (1‐β‐D‐arabinofuranosylcytosine) following UV in ways typical of cells capable of excision repair, with reduced survival and an accumulation of breaks in pre‐existing DNA.Microtus cells irradiated with UV in a quiescent pre‐S‐phase state are more sensitive to UV than are proliferating cells, in terms of survival. Adding DNA precursors (deoxyribonucleosides), and—in the case of proliferating cells—growing in complete rather than dialysed serum, enhance UV survival.Quiescent cells show a higher rate of endonucleolytic incision of DNA after UV than do proliferating cells.The balance between incision (producing single‐strand DNA breaks) and repair DNA synthesis (leading to rejoining of breaks) is shifted by the addition of deoxyribonucleosides, which suggests that DNA precursor supply is a rate‐limiting factor in repair. The lower survival of quiescent cells (in the absence of added deoxyribonucleosides) may be due to insufficient precursor supply to meet the demands of the high incision rate.
Steroid hormone toxicity in human fibroblasts does not correlate with high affinity receptor content
Authors: Breslow J. L. , Epstein J. , Forbes G. B. , Fontaine J. H. 
Published: February 2005

AbstractHuman diploid skin fibroblasts derived from normal individuals and those with the testicular feminization syndrome (TFM) have been shown to be killed to the same degree by dihydrotestosterone in spite of the absence of high affinity cellular androgen receptors in the TFM fibroblasts. Furthermore, several different normal fibroblast strains from various anatomical sites all showed similar amounts of androgen‐induced cytotoxicity even though their respective receptor contents differed by as much as ten‐fold. These results suggest that steroid‐induced cytotoxicity in human fibroblasts in not correlated with receptor content, unlike murine lymphoid cells in which the receptor content has been shown to be closely related to their ability to survive hormone exposure.
Characteristics of concanavalin A‐resistant Chinese hamster ovary cells and certain revertants
Authors: Cifone M. A. , Hynes R. O. , Baker R. M. 
Published: February 2005

AbstractClones of Chinese hamster ovary (CHO) cells were isolated by single‐step selection for resistance to killing by Concanavalin A (ConA) and certain cellular and membrane properties were examined. The ConA‐resistant isolates were only about 2‐fold more resistant than wild type cells to the selecting lectin, but exhibited pleiotropic temperature‐sensitivity for growth, markedly altered morphology and adherence, and significant differences in susceptibility to other agents such as colchicine. Two revertants to full temperature‐resistance were isolated from different ConA‐resistant mutants. One revertant clone had reacquired wild type sensitivity to ConA while the other revertant remained ConA‐resistant. The two series of wild type, ConA‐resistant, and temperature revertant clones were analyzed for altered mobility of cell surface glycoproteins using lactoperoxidase/125I and galactose oxidase/[3H]borohydride labelling procedures. The ConA‐resistant clones showed increased mobility on polyacrylamide gels of three classes of labelled proteins, in the molecular weight ranges 225,000, 200,000, and 130,000 daltons. These changes persisted in the temperature‐revertant that remained ConA‐resistant, while two of the altered protein classes were restored to wild type mobility in the revertant that regained ConA‐sensitivity. Cell hybridization experiments indicated that the temperature‐sensitive phenotypes of different ConA‐resistant isolates are recessive and noncomplementing, implying that the same gene is affected in each case. The reversions to temperature resistance appear to be recessive suppressor mutations in different genes.
Tuftsin‐macrophage interaction: Specific binding and augmentation of phagocytosis
Authors: Bar‐Shavit Zvi , Stabinsky Yitzhak , Fridkin Mati , Goldman Rachel 
Published: February 2005

AbstractThe binding of [3H]tuftsin to normal and in vivo stimulated mouse peritoneal macrophage populations was studied at 22°C. The [3H]tuftsin binding to thioglycollate‐stimulated macrophages was shown to be rapid and saturable, with an equilibrium dissociation constant (KD) (calculated from a Scatchard plot) of 5.3 × 10−8 M. The calculated number of binding sites per macrophage amounts to approximately 72,000. Binding competition studies with unlabelled tuftsin yielded a KD of 5.0 × 10−8 M. [3H] [N‐Acetyl‐Thr1]tuftsin, an inactive analog of tuftsin, failed to bind specifically to thioglycollatestimulated macrophages. [N‐Acetyl‐Thr1]tuftsin and the tripeptide [Des‐Arg4]tuftsin failed to compete for tuftsin binding sites, while [D‐Arg4]tuftsin, an analog with small tuftsin‐like activity, exhibited a low degree of inhibition of [3H]tuftsin binding. Thus a rather high degree of specificity is involved in the binding of the tetrapeptide.Normal as well as six different macrophage populations induced by stimulation with thioglycollate, concanavalin‐A, starch, mineral oil, glucan and Bacillus Calmette Guerrin (BCG), exhibited a similar degree of binding of [3H]tuftsin. Corynebacterium parvum (CP)‐stimulated macrophages, on the other hand, showed a 6‐ to 10‐fold‐lower capacity for tuftsin binding.See Note added in proof on p. 62.
Under similar experimental conditions, mouse fibroblast and lymphocyte preparations revealed no detectable specific binding.Tuftsin augmented the phagocytic response of normal and stimulated macrophages assessed both for phagocytosis mediated via the Fc‐receptor and via non‐specific receptors. CP‐stimulated macrophages did not exhibit an increased phagocytic response upon treatment with tuftsin.
Long acting cAMP analogues enhance sulfate incorporation into matrix proteoglycans and suppress cell division of fetal rat chondrocytes in monolayer culture
Authors: Miller R. P. , Husain M. , Lohin S. 
Published: February 2005

AbstractThe relationship between replication and the synthesis of matrix sulfated proteoglycans was investigated with fetal rat chondrocytes grown in monolayer culture. The effect of N6 O2′ dibutyryl adenosine 3′, 5′ cyclic monophosphate (DBcAMP), adenosine 3′, 5′ cyclic monophosphate (cAMP), 8 Bromo adenosine 3′, 5′ cyclic monophosphate (8 Br‐cAMP), sodium butyrate and hydroxyurea was examined. Between 0.05 and 0.5 mM DBcAMP, a dose related inhibition of cell division and stimulation of [35SO] incorporation into matrix proteoglycans was demonstrated. At the higher concentrations of DBcAMP, cell division was completely inhibited and the enhancement of [35SO] incorporation into matrix proteoglycans ranged between 40 and 120% (P < 0.01). Utilizing 14C‐glucosamine and photometric determination of proteoglycans with Alcian Blue, it was demonstrated that the increase in sulfate incorporation reflected enhanced accumulation of extracellular matrix. The effects of DBcAMP were mimickled by 8 Br‐cAMP, suggesting they were mediated by the adenylyl cyclase system. cAMP (0.05‐0.5 mM), sodium butyrate (0.1‐0.5 mM) and hydroxyurea (0.5‐5 mM) partially or fully inhibited cell division, but either failed or only slightly enhanced sulfate incorporation. The enhanced sulfated proteoglycan deposition promoted by DBcAMP began 8 to 12 hours after serum stimulation, its onset occurred prior to thymidine incorporation and the effect persisted for 28 hours. Determination of cell volume demonstrated an increase in size of DBcAMP treated chondrocytes between 8 and 12 hours, coincident with the onset of increased sulfate incorporation. These results are consistent with a model where matrix sulfated proteoglycan deposition by chondrocytes is mediated by intracellular cAMP levels and occurs in the G1 phase of the cell cycle.
Postnatal development of peroxisomal and mitochondrial enzymes in rat liver
Authors: Krahling Jeffrey B. , Gee Robert , Gauger John A. , Tolbert N. E. 
Published: February 2005

AbstractSubcellular organelles from livers of rats three days prenatal to 50 weeks postnatal were separated on sucrose gradients. The peroxisomes had a constant density of 1.243 g/ml throughout the life of the animal. The density of the mitochondria changed from about 1.236 g/ml at birth to a constant value of 1.200 g/ml after two weeks.The peroxisomal and mitochondrial fatty acid β‐oxidation and the peroxisomal and supernatant activities of catalase and glycerol‐3‐phosphate dehydrogenase were measured at each age, as well as the peroxisomal core enzyme, urate oxidase, and the mitochondrial matrix enzyme, glutamate dehydrogenase. All of these activities were very low or undetectable before birth. Mitochondrial glutamate dehydrogenase and peroxisomal urate oxidase reached maximal activities per g of liver at two and five weeks of age, respectively.Fatty acid β‐oxidation in both peroxisomes and mitochondria and peroxisomal glycerol‐3‐phosphate dehydrogenase exhibited maximum activities per g of liver between one and two weeks of age before weaning and then decreased to steady state levels in the adult. Peroxisomal β‐oxidation accounted for at least 10% of the total β‐oxidation activity in the young rat liver, but became 30% of the total in the liver of the adult female and 20% in the adult male due to a decrease in mitochondrial β‐oxidation after two weeks of age. The greatest change in β‐oxidation was in the mitochondrial fraction rather than in the peroxisomes. At two weeks of age, four times as much β‐oxidation activity was in the mitochondria as in the peroxisomal fraction. Peroxisomal glycerol‐3‐phosphate dehydrogenase activity accounted for 5% to 7% of the total activity in animals younger than one week, but only 1% to 2% in animals older than one week.Up to three weeks of age, 85% to 90% of the liver catalase was recovered in the peroxisomes. The activity of peroxisomal catalase per g of rat liver remained constant after three weeks of age, but the total activity of catalase further increased 2.5‐ to 3‐fold, and all of the increased activity was in the supernatant fraction.
Membrane potential measurements during rat liver regeneration
Authors: Wondergem Robert , Harder David R. 
Published: February 2005

AbstractMembrane potential was measured in perfused rat liver and was shown to increase from −33 ± 1.0 mV in livers from normal rats to −50 ± 1.1 mV in livers from rats 12 hr after partial hepatectomy. The hyperpolarization of the membrane in regenerating liver was no longer evident after perfusion with 1 mM ouabain for 5 min. Ouabain had a small (4 mV) depolarizing effect on membrane potential in normal liver. The potential measured in normal and regenerating liver decreased as a function of the external potassium concentration above 5 mM; however, the potential was more electronegative in regenerating liver compared to normal liver at all values of external potassium concentration, and the differences in potential between the two kinds of cells did not decrease at higher concentrations of external potassium. Thus, a plot of membrane potential vs external potassium concentration resulted in approximately parallel curves for the two different cell types. We conclude that hyperpolarization of the liver cell membrane is an early event during rat liver regeneration and results from an electrogenic Na‐K pump.