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Biomedical subjects

J Richards

Publications and source records attributed to J Richards.

At least 163 records · Page 9Linked to original sources
PubMed1984

A comparison of midazolam and diazepam for intravenous sedation in dentistry.

In a randomised cross-over trial, midazolam, a new water soluble benzodiazepine was compared with the conventional diazepam preparation (Valium) in 34 patients aged 16-45 years who were undergoing outpatient conservation dentistry. Midazolam hydrochloride (0.17 mg/kg) was virtually free of venous complications and showed advantages over diazepam (0.32 mg/kg) in providing a faster onset of action, higher incidence of amnesia and more rapid recovery. Midazolam produced a higher incidence of respiratory side effects hiccough (17.6% compared with 2.9%), brief apnoea following induction (11.8% compared with 5.8%), and airway obstruction during maintenance (8.8% compared with 0%). These may be related to the greater potency of midazolam as suggested by the smaller total dose required. Cardiovascular changes and operating conditions were similar.

Adolescent↗
PubMed1984

Interaction of phorbol derivatives with replicating cells.

The significance of the interaction of phorbol derivatives with replicating cells has been studied in HeLa cells and in tumour promotion experiments. Dose-response relationships for the radiomimetic activity of phorbol derivatives in HeLa cells (Kinzel et al., 1980) were obtained by analysis of the degree of transient blockage in G2 phase of the cell cycle. HeLa cells are shown to be one order of magnitude more sensitive to 12-O-tetradecanoylphorbol-13-acetate (TPA) than to equally mitogenic and irritant but much less promoting derivatives. The susceptibility of HeLa cells reflects the promoting capacity of these compounds. Studies on effects of modifiers on TPA-induced G2 blockage indicate that the influence of TPA, even in a single cell cycle phase, may be the result of a 'multiple site' attack. The significance of the interaction of TPA with replicating mouse epidermal cells in tumour promotion has been demonstrated in animal experiments after initiation with 7-12-dimethylbenz[a]anthracene by using a two-stage protocol which effects promotion with a single dose of TPA followed by repeated treatment with 12-O-retinoylphorbol-13-acetate (Fürstenberger et al., 1981). A single dose of the inhibitor of DNA synthesis, hydroxyurea, given to groups of mice at different times before and after treatment with TPA interferes with tumour formation; almost complete inhibition is observed after 18 h. The interaction of TPA and DNA-synthesizing cells seems to be of crucial importance to the first stage of tumour promotion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Radiomimetic activity of phorbol esters exerted in HeLa cells in comparison with their tumor-promoting capacity.

The biological activities exerted in mouse skin by three closely related phorbol esters were compared with the effects of these compounds on HeLa cells. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate has been shown previously to influence various cell cycle parameters of these cells, thereby mimicking X-irradiation [Kinzel, V., Richards, J., and Stöhr, M. Science (Wash. D. C.), 210: 429-431, 1980]. Qualitatively similar effects were exerted by the mitogenic and irritant but almost nonpromoting "incomplete" phorbol esters 12-O-tetradeca-2-cis-4-trans-6,8-tetraenoylphorbol-13-acetate and 12-O-retinoylphorbol-13-acetate. Cell cycle parameters were analyzed by measuring thymidine incorporation rates, labeling indices, DNA histograms gained through flow cytometry, and mitotic activity. In every case, 12-O-tetradecanoylphorbol-13-acetate was more effective than 12-O-tetradeca-2-cis-4-trans-6,8-tetraenoylphorbol-13-acetate or 12-O-retinoylphorbol-13-acetate. The analysis of the influence of phorbol esters in G2 phase showed that, in order to reach the effectiveness of 10(-8) M 12-O-tetradecanoylphorbol-13-acetate, approximately 10 times the concentration of either 12-O-tetradeca-2-cis-4-trans-6,8-tetraenoylphorbol-13-acetate or 12-O-retinoylphorbol-13-acetate has to be applied. Therefore, the susceptibility of replicating HeLa cells to these phorbol derivatives reflects the promoting rather than the mitogenic and irritant capacity of these compounds.

Cell Cycle↗
PubMed1983

The use of thioesterase II as a rat mammary epithelial cell-specific marker.

The avidin-biotin-peroxidase complex immunoperoxidase technique was employed to determine the intercellular distribution of thioesterase II in rat mammary glands. This enzyme is responsible for shifting the product specificity of the fatty-acid synthetase enzyme complex from long to medium chain fatty acids. Thioesterase II was found exclusively in the cells lining the lumen of the ductal and alveolar structures in glands from mature virgin (150 days old) and pregnant rats. The ductal cell staining intensity was considerably less than that of the alveolar cells in the mature virgin rat glands. No immunoreactive thioesterase II was found in the stromal, adipose, vascular, or myoepithelial components of the gland in the developmental stages examined. In the glands from immature virgin rats (40-45 days old) thioesterase II was again found only in the epithelial cells lining the lumen of the ductal and end-bud structures although this layer was usually more than one cell thick. Quantitative determination of thioesterase II activity in cytosol preparations revealed similar levels in mammary fragments from enzymatically-dissociated glands obtained from mature virgins and in end buds derived from immature virgins, but somewhat higher levels in mammary structures derived from late-pregnant animals. These immunohistological and biochemical results demonstrate thioesterase II's usefulness as a mammary epithelial cell-specific marker.

Animals↗
PubMed1983

Response of end bud cells from immature rat mammary gland to hormones when cultured in collagen gel.

End buds from 4- to 5-week-old rat mammary glands were isolated and cultured within a rat tail tendon collagen gel matrix. Media containing equine serum or porcine serum and cholera toxin promoted growth, but not the production of casein or thioesterase II, nor did they induce a state of differentiation as assessed by cell ultrastructure. Medium supplemented with only 5% porcine serum, insulin and cholera toxin did not support growth or differentiation. However, when prolactin, estradiol, progesterone and hydrocortisone were added to this medium, growth was stimulated greatly and a differentiated state was induced as assessed by the production of casein and thioesterase and by the appearance of a highly secretory ultrastructure.

Animals↗
PubMed1983

Comparison of the growth of normal and neoplastic mouse mammary cells on plastic, on collagen gels and in collagen gels.

The growth of normal and neoplastic mouse mammary cells was compared in primary cultures on plastic, on rat tail collagen gels and in rat tail collagen gels. Cells on plastic grew for the first few days, then stopped with only a 1- to 3-fold increase in cell number after 2 weeks in culture. Cells grown on or in collagen gels grew continuously over the 2-week culture period with up to 10-fold increase in cell number for cultures on collagen gels and a 20-fold increase for cells embedded in collagen gels. The difference in growth rates between cells grown in collagen gel and those grown on collagen gels was due, in part, to the three-dimensional growth of the colonies in collagen gel their two-dimensional growth on collagen gel. Cells grown on and in collagen gel can produce an electron-dense basal lamina-like structure which is associated with collagen IV and laminin as judged by immunofluorescence. Cells grown on plastic do not form this structure. Cis-OH-proline blocks the production of collagen and inhibits the growth of the cultured cells indicating collagen production to be involved in growth. Rat tail collagen gels are a superior substratum for the growth of mouse mammary cells and this may be related to the cells' ability to form a collagen IV-containing basal lamina-like structure.

Animals↗
PubMed1982

Effects of retinoic acid and tumor promoter 12-o-tetradecanoylphorbol-13-acetate (TPA) on the cell cycle of HeLa cells.

The influence of retinoic acid (RA) - a modifier of tumor promotion - on the cell cycle of HeLa cells, and its ability to interfere with the early irradiation-like effects induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) has been investigated by a variety of different techniques. These include measurement of thymidine incorporation and uptake, of labelling and mitotic indices, and of DNA histograms by flow cytometry. Within 24 h RA (2 X 10-5 M) alone caused a short-lasting inhibition of DNA synthesis; later a decrease of cells in S phase and a steady descending mitotic activity were observed. On combined treatment with RA and TPA (10-8 M), the latter seems to dominate RA in two instances: (1) the transient G2 blockage due to TPA is seen as the earliest effect; however, the cultures do not seem to recover as well if RA is also present; (2) the TPA-induced GI blockage appears to be effective but less pronounced in the presence of both chemicals. Where the third typical TPA-induced effect is concerned, however, both compounds seem to act to a comparable degree in the same time frame; namely by an initial inhibition of DNA synthesis which thus might be a point of critical interference if promoter and modifier age given together.

Cell Cycle↗
PubMed1982

Measurement of the response of HELA cells towards the radiomimetic activity of 12-O-tetradecanoylphorbol-13-acetate.

The sensitivity of HeLa cells in the G2 phase of the cell cycle towards the radiomimetic activity of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) (Kinzel et al. (1980) Science, 210, 429-431) has been utilized to establish dose response relationships. This was accomplished by analysis of mitotic curves and determination of cells not affected, a measurement known to be dose dependent in the case of very low X-ray doses. Half maximal activity was exerted by TPA at approximately 5 X 10(-9) M concentration. Mechanistically, however, TPA seems to exert its activity through a route different from that of X-rays or other radiomimetic drugs for 2 reasons: (1) the cellular response does not increase proportionally with dose; (2) cells recover from G2 blockage even in the presence of TPA. Therefore it appears as if the tumor promoter acts indirectly by triggering an exhaustable cellular activity which leads to the radiomimetic response.

Acetone↗
PubMed1981

Complete remission of idiopathic pure red cell aplasia. Case reports.

Two patients with pure red cell aplasia of undetermined aetiology are in sustained, complete remission after immunosuppressive therapy. In the first, short-term supplementary plasmapheresis was used during initial chemotherapy, and in the second, anabolic androgens were administered. In both patients haematopoietic recovery was temporally related to the withdrawal of the cyclophosphamide used to cause immunosuppression in the patients over a 4- and 6-month period respectively.

Adolescent↗
PubMed1981

Early effects of the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate on the cell cycle traverse of asynchronous HeLa cells.

Within 24 hr after incubation of synchronous HeLa cell cultures with small nontoxic doses of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA; 10(-7) or 10(-8) M), a variety of transient alterations in the cell cycle traverse was detected by different techniques. The measurement of thymidine incorporation rates into DNA, of labeling and mitotic indices, and of flow cytometry revealed (a) an inhibition of cells in G1 shortly prior to their entering S phase, (b) a reduced rate of DNA synthesis and a delayed passage of cells through S phase which were in this phase on addition of TPA, (c) a delayed passage through G2 of a portion of cells which were somewhere in the first half of the S phase on addition of TPA, and (d) an instant but short-lasting blockage in G2 immediately before mitosis. The effects of TPA are reminiscent of published results on X-irradiated cell cultures. None of these effects was noticed with the hyperplasiogenic but nonpromoting phorbol ester 4-O-methyl-12-O-tetradecanoylphorbol-13-acetate (10(-6) M). The data were confirmed by experiments with synchronized HeLa cells as described in an accompanying paper.

Cell Cycle↗