Search PubMed⌕ Search

Biomedical subjects

C A Jones

Publications and source records attributed to C A Jones.

At least 199 records · Page 11Linked to original sources
PubMed1985

Evaluation of acute cardiorespiratory responses to hydraulic resistance exercise.

Accurate evaluation of the acute responses to resistance exercise training depends on the stability of the criterion measures. This is particularly true for maximal effort exercise where continuous "all-out" effort for each repetition is encouraged. The present study evaluated reliability of repetition number (repN), respiratory gas parameters (VO2, VCO2, VE), and heart rate (HR) for shoulder (SE), chest (CE), and leg (LE) exercise performed maximally on a single-unit, 3-station hydraulic resistance exercise machine (Hydra-Fitness, Belton, TX). On 2 separate days, 20 college men completed three 20-s bouts of SE, CE, and LE with a 20-s rest between bouts and 5 min between exercise modes. There were no significant differences between bouts or test days for repN, gas measures, or HR. Subjects performed 17, 19, and 21 reps during SE, LE, and CE. VO2 was 1.7 l . min-1 (24.3 ml . kg-1 . min-1) for SE, 1.87 l . min-1 (25.5 ml . kg-1 . min-1) for CE, and 2.1 l . min-1 (28.6 ml . kg-1 . min-1) for LE. These values, averaged, represented 52.8% of the max VO2 determined on a continuous cycle ergometer test. The corresponding HR's during hydraulic exercise averaged 84.6% of HR max. Test-retest reliability coefficients ranged from r = .67 to .87 for repN, r = .41 to .83 for gas measures, and r = .72 to .89 for HR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Inactivation of essential division genes, ftsA, ftsZ, suppresses mutations at sfiB, a locus mediating division inhibition during the SOS response in E. coli.

A dominant sfiB allele has been cloned which renders partial diploids of an sfiB + Escherichia coli host resistant to division inhibition mediated by the SOS response. Transpositional mutagenesis was used to map the position of this sfiB114 allele, carried by a plasmid pLG552 , to an approximately 0.6-kb region overlapping the coding regions for ftsA and ftsZ , two genes essential for normal division. Most Tn 1000 insertions which inactivated sfiB114 also inactivated the ftsA function and caused the disappearance of both a 47-K polypeptide and reduced levels of a 42-K polypeptide in maxi-cells carrying pLG552 . An additional insertion inactivating sfiB114 was mapped to the right of ftsA and resulted in loss of the 42-K but not the 47-K polypeptide in maxi-cells. Moreover, a 2.1-kb BamHI-EcoRI DNA fragment was subcloned which carried ftsA and coded for a 47-K polypeptide but did not carry sfiB114 and did not complement ftsZ . We conclude that sfiB114 is located within ftsZ coding for a 42-K polypeptide. Nevertheless, insertions into ftsZ coding the 47-K polypeptide suppress the sfiB114 allele by substantially reducing the synthesis of the FtsZ ( SfiB114 ) polypeptide. The level of residual FtsZ synthesis was minimal when Tn 1000 was inserted closest to the distal end of ftsA , indicating the presence of a regulatory region essential for maximal expression of ftsZ .

Base Sequence↗
PubMed1984

Use of a soft-agar colony-forming assay to determine the photosensitizing effects of several components of hematoporphyrin derivative.

The photosensitizing/cytotoxic effects of four porphyrin compounds derived from hematoporphyrin were compared using two human tumor cell lines with a soft-agar colony-forming assay. Reproducible dose- and time-dependent increases in reproductive cell death were observed for each porphyrin tested. Two fractions derived from hematoporphyrin derivative (HPD) were found to be better photosensitizers than HPD itself, indicating the potential value of this in vitro assay for detecting the most active component from a heterogeneous mixture.

Agar↗
PubMed1984

Induction of mutations by chemical agents at the hypoxanthine-guanine phosphoribosyl transferase locus in human epithelial teratoma cells.

Induction of 6-thioguanine (TG) resistance by chemical mutagens was examined in a line of cells derived from a human epithelial teratocarcinoma cell clone. The cells, designated as P3 cells, have a stable diploid karyotype with 46(XX) chromosomes, including a translocation between chromosomes 15 and 20. Efficient recovery of TG-resistant mutants induced by the direct-acting mutagens: N-methyl-N'-nitro-N-nitrosoguanidine (MNNG); 7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10 -tetrahydrobenzo[a]pyrene (BPDE); and benzo[a]pyrene (B[a]P); activated in a cell-mediated assay, required an expression time of 7 days and a saturation density of 2 X 10(4) cells/60-mm petri dish. The TG-resistant mutant cells induced by MNNG and BPDE maintained their resistant phenotype 4-6 weeks after isolation. This mutant phenotype was associated with a more than 10-fold reduction in hypoxanthine-guanine phosphoribosyl transferase (HGPRT) activity relative to that of the parental P3 cell line, which was shown to catalyze the formation of 4.6 pmoles inosine-5'-monophosphate (IMP)/min/microgram protein. Induction of TG resistance was also observed in P3 cells cocultivated in a cell-mediated assay with human breast carcinoma cells, which are capable of polycyclic aromatic hydrocarbon (PAH) metabolism, after treatment with the carcinogenic PAHs: B[a]P, chrysene, 7,12-dimethylbenz[a]anthracene (DMBA), and 3-methylcholanthrene (MCA). The degree of mutant induction in this assay was related to the carcinogenic potency of these PAHs in experimental animals. The most potent mutagen was DMBA, followed in decreasing order by MCA, B[a]P, and chrysene. DMBA, at 0.4 microM, increased the frequency of mutants for TG resistance from 2 for the control to about 200 TG-resistant mutants/10(6) colony-forming cells (CFC). Benzo[e]pyrene (B[e]P) and pyrene, which are not carcinogenic, were not effective in the assay. None of the PAHs was mutagenic in the P3 cells cultivated in the absence of the PAH-metabolizing cells. These results indicate that the P3 cells can be useful for the study of mutagenesis at the HGPRT locus by direct-acting chemical mutagens, as well as by chemicals activated in a cell-mediated assay.

Biotransformation↗
PubMed1984

Enhancement of chemical-carcinogen-induced cell transformation in hamster embryo cells by 1 alpha,25-dihydroxycholecalciferol, the biologically active metabolite of vitamin D3.

The biologically active metabolite of vitamin D3, 1 alpha,25-dihydroxycholecalciferol [1,25-(OH)2D3], which by itself was not effective in inducing morphological cell transformation in vitro in the Syrian hamster embryo colony assay, enhanced such a transformation in a dose-dependent manner in cells pretreated with a series of known chemical carcinogens. Treatment of the hamster embryo cells with either benzo[a]-pyrene (B[a]P), (+/-)7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene, or N-methyl-N'-nitro-N-nitroso-guanidine for 3 days (stage 1) followed by treatment with 1,25-(OH)2D3 for 4 days (stage 2) increased the transformation frequency compared to the transformation frequency for cells treated with the carcinogen only. Reversing the order of the treatment (i.e., incubating the cells with 1,25-(OH)2D3 prior to B[a]P treatment) did not result in an effective enhancement. Vitamin D3 and 24,25-dihydroxycholecalciferol, another metabolite of this vitamin, also enhanced the frequency of cell transformation but to a lesser degree than did 1,25-(OH)2D3. Pyrene, which is not a carcinogen, did not induce transformed colonies either by itself or when combined with 1,25-(OH)2D3. Benzo[e]pyrene (B[e]P), which is not considered to be a complete carcinogen but can act as a tumor initiator, also was not effective by itself. However, in the two-stage protocol with 1,25-(OH)2D3, B[e]P did induce transformed colonies. Comparison of the enhancing effect of 1,25-(OH)2D3 to that of phorbol-12-myristate-13-acetate (PMA), a known tumor promoter, revealed a heterogeneity in the response to these agents. A high or low responsiveness of the cells to 1,25-(OH)2D3 was not necessarily indicative of a similar responsiveness to PMA. These results indicate that 1,25-(OH)2D3 can act as a promoter of cell transformation in fibroblasts and perhaps other cell types but through a mechanism not necessarily identical to that involving PMA.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

Parameters of hematoporphyrin derivative tumor cell killing efficiency: decomposition of hematoporphyrin derivative at high power densities.

Hematoporphyrin derivative (HpD) tumor cell killing efficiency has been evaluated as a function of power density, optical spectrum, HpD concentration, and HpD preparation using trypan blue exclusion assay. Cell survival curves for Mayo Clinic HpD and for Photofrin were equivalent at all concentrations and power densities for both violet and red light. Survival curves for red light demonstrated a two-fold increased cellular killing efficiency at higher densities (160 mW/cm2). However, for violet light an irreversible and marked decrease in cellular killing efficiency was found as the power density was increased. This phenomena of decreased cellular killing efficiency of violet light at high power densities is consistent with a process of photo-decomposition of HpD and is most pronounced at low concentrations (less than 25 micrograms/ml).

Cell Survival↗
PubMed1984

Phenol-soluble nonhistone chromatin proteins in chronic lymphocytic leukemia.

The altered gene expression seen in cancer could relate to differences in nonhistone chromatin proteins between normal and malignant tumor cells. Phenol-soluble nonhistone chromatin proteins were isolated from human normal and leukemic (chronic lymphocytic leukemia) B-cells, as well as long-term cultured human B-lymphocyte cell lines. High-resolution two-dimensional electrophoretic maps identified a group of three nuclear proteins with a molecular weight of 45,000 to 50,000 and an isoelectric range of 4.5 to 4.7, which were associated only with the human leukemic B-cells. Leukemic B-cells and cultured B-cell lines also expressed a variant form of nuclear actin and tubulin.

B-Lymphocytes↗
PubMed1983

Monoclonal antibodies to leucine enkephalin.

Monoclonal antibodies to leucine enkephalin have been produced after fusion of mouse myeloma cells with spleen cells from hyper-immune mice. Hybrid clones 2D1 and SL1 were characterised using radioimmunoassay and an enzyme-linked immunosorbent assay. The antibody 2D1 was of low affinity and showed a maximum sensitivity of 0.1ng. The antibody binds equally well to the sulphated leucine enkephalin and to methionine enkephalin. It does not cross-react with dynorphin, methionine enkephalin-arg-phe or oxidised methionine enkephalin. The hybrid clone SL1 appears to be specific for leucine enkephalin. Preliminary immunocytochemical studies have shown that both antibodies bind specifically to leucine enkephalin in defined areas of the central nervous system.

Animals↗
PubMed1983

Enzyme-linked immunosorbent assay for leucine and methionine enkephalins.

An enzyme-linked immunosorbent assay for enkephalins was developed by coupling the peptides to a carrier molecule (bovine serum albumin) in order to allow the antibody-antigen reaction to take place in the solid phase. The assay was shown to be highly reproducible. Its sensitivity was 14 nmol/liter for leucine enkephalin and 27 nmol/liter for methionine enkephalin, which is similar to that obtained when the same antibodies were used in radioimmunoassay.

Antibodies↗
PubMed1983

Cell specific activation of benzo[a]pyrene by fibroblasts and hepatocytes.

The cell specific activation of benzo[a]pyrene (BP) by embryonic fibroblasts and by mature hepatocytes to intermediates that can interact with DNA, or cause mutations in Chinese hamster V79 cells has been investigated. At BP concentrations of up to 15 muM, BP was activated to mutagenic intermediates for the V79 cells by embryonic fibroblasts but not by hepatocytes. However, hepatocytes from rats that had been pretreated with an inducer of the mixed function oxidases, 3-methylcholanthrene, did metabolize higher doses of BP (greater than 15 muM) to mutagenic intermediates. BP was extensively metabolized by both cell types, but the hepatocytes and fibroblasts showed differences both in the profiles of BP metabolites and the nature of the BP-DNA adducts formed. Hepatocytes metabolized BP principally to 4,5-dihydro-4,5-dihydroxybenzo[a]pyrene, phenols, and quinones, which underwent further metabolism to water-soluble metabolites. Metabolism of BP to 7,8-dihydro-7,8-dihydroxybenzo[a]-pyrene (BP-7,8-diol) occurred but proceeded rapidly to the formation of triols and tetraols. Fibroblasts metabolized BP predominantly toward the formation of BP-7,8-diol. The proportion of primary metabolites undergoing further metabolism to conjugates was less extensive than in the hepatocytes. Hepatocytes bound more BP to their DNA than the fibroblasts. In the hepatocytes the major DNA adducts formed were hydrophilic derivatives, and no [+/-]7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) adducts were detected even after treatment with BP-7,8-diol. In the fibroblasts, the major BP--DNA adduct was derived from the reaction of BPDE with deoxyguanosine. These results suggest that the differences in the response of embryonic fibroblasts and mature hepatocytes in the activation of BP to a mutagen for mammalian cells is determined at least in part by the overall balance of oxidation and detoxification processes in the cells and, hence, by the levels of critical oxidative intermediates that interact with DNA.

Animals↗
PubMed1983

The synthesis and release of [3H-tyrosine1]methionine5-enkephalin from guinea pig brain slices.

Stores of methionine-enkephalin were labelled on the N-terminal by incubation of whole brain slices with [3H]tyrosine (10 microCi/ml). The 3H radioactivity corresponding to the position of authentic Met-enkephalin after extraction on Amberlite XAD2 and separation by thin-layer chromatography was taken as an index of synthesis. Maximal incorporation of the labelled tyrosine into Met-enkephalin was attained after 4 h of incubation at 37 degrees C and was inhibited in the presence of 10 microM cycloheximide. Isolated nerve terminals failed to incorporate any [3H]tyrosine. The labelled compound had opiate-like activity and consisted of the same five amino acids as an authentic standard. Incubations with leucine aminopeptidase indicated that the labelled tyrosine was on the N-terminus, and removal of this tyrosine resulted in loss of opiate-like activity. The incorporation of [14C]glycine, selected as an alternative precursor, was consistent with de novo synthesis and not N-terminal exchange. A radioimmunoassay was also used to quantify the amount of labelled Met-enkephalin. KCl (50 mM) elicited a Ca2+-dependent release of the synthesized [3H]Met-enkephalin from whole brain slices and also from isolated nerve terminals. The release of Met-enkephalin radioimmunoactivity paralleled that of [3H]met-enkephalin. Preliminary investigations have suggested that carbamyl choline inhibited this release, and its effect was partially reversed by atropine.

Animals↗
PubMed1983

The biological activity of a single dose of tamoxifen in the adult ovariectomized rat.

1 The peripheral and central activities of tamoxifen were studied in the ovariectomized adult rat, up to 16 d after a single dose of 7.0 or 0.7 mg/kg. 2 Food consumption and body weight were decreased; only food consumption returned to control values after 16 d. 3 The weights of the uterus and of the uterine luminal fluid were increased for up to 8 d. 4 Serum follicle-stimulating hormone (FSH) concentrations decreased, but only significantly 1 and 8 d after 7.0 mg tamoxifen/kg. Serum luteinizing hormone (LH) and prolactin concentrations were elevated for up to 4 d. 5 Lordosis behaviour was absent throughout the period studied. 6 Within 3 d of administration, tamoxifen partially antagonized the oestrogen-induced changes in uterine luminal fluid, prolactin and LH secretion and lordosis behaviour. 7 Tamoxifen did not alter oestrogen-induced changes in uterine weight, food consumption and body weight. 8 The experiments demonstrate that tamoxifen is active for up to 16 d after a single intraperitoneal dose; oestrogen agonist, partial agonist and antagonist activities were demonstrated. The duration and type of activity depends upon the dose of tamoxifen and the target tissue response examined.

Animals↗
PubMed1983

Binding of Todd-Hewitt broth antigens by Streptococcus mutans.

Streptococcus mutans 10449, grown in chemically defined culture medium, was tested for its ability to bind 3H-labeled Todd-Hewitt broth components (greater than 12,000 Mr). Maximum adsorption of radioactivity occurred within 5 min at room temperature, and cell-bound material was not completely removed by extended washing with buffer. Heat-killed, arsenate-inhibited, and viable bacteria bound similar quantities. Only 0.09% of the radioactivity in the preparation of high Mr Todd-Hewitt broth components was removed by absorption with excess numbers of S. mutans 10449 cells. Binding followed saturation kinetics and was competitively inhibited by unlabeled medium components, both the dialyzable and nondialyzable fractions. Other oral streptococci were also found to bind these complex medium components. Rabbit antiserum elicited to the high-molecular-weight Todd-Hewitt broth components reacted with monkey cardiac muscle and with S. mutans coated with medium components. Absorption of the anti-Todd-Hewitt broth serum with homogenized heart removed antibodies that reacted with Todd-Hewitt broth-coated S. mutans. Therefore, the tissue-specific antigens of this beef heart infusion medium that adsorb to S. mutans can interfere with the detection and characterization of antigens shared by these bacteria and animal tissues.

Adsorption↗