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Biomedical subjects

C A Jones

Publications and source records attributed to C A Jones.

At least 181 records · Page 10Linked to original sources
PubMed1987

The National Burn Information Exchange. The use of a national burn registry to evaluate and address the burn problem.

The NBIE, a voluntary registry of specialized burn-care facilities that was founded in 1964, currently has 50 active participants representing 35 per cent of the nation's hospital beds for burned patients. Participating physicians submit information on the initial hospitalization of emergent and acute burn patients and, separately, on the reconstruction process for these patients. As of January 1986, a total of 94,594 patient's data are on file from 130 hospitals; 13,671 of these are reconstructive and 80,923 emergent and acute admissions. Information concerning new patients is submitted at a rate of about 6000 patients annually. The data are analyzed using INQUIRE, an original data retrieval system. Data on treatment methods and outcome have been used to establish baseline standards for the burned patient's care and survival. In addition, these data have been used to document institutional differences in mortality rates and indicate methods used by the more successful hospitals. The data also are being used to describe the long process of recovery from severe burns and to monitor changes in outcomes of burn accidents continually. The result of these analyses has been documentation of an overall improvement in survival and decline in hospitalization times at all levels of burn severity. Data also can be used with institution-specific data to look at organizational variables affecting survival. Use of this epidemiologic data allows prevention projects to be targeted at the groups at greatest risk. A newer application looks at the equity of the HCFA prospective payment system based on the DRGs assigned to burn severity. The NBIE is an example of how a voluntary, national registry, properly computerized and effectively managed, can contribute to resolving the problem it was established to study. The NBIE has been useful in increasing the understanding of health professionals and government decision makers of a complicated disease process. It has had a direct effect on the quality of patient care and on the process of controlling the incidence of burn injuries.

Adolescent↗
PubMed1987

Role of high-avidity binding of human neutrophil myeloperoxidase in the killing of Actinobacillus actinomycetemcomitans.

The binding of the neutrophil enzyme myeloperoxidase (MPO) to microbial surfaces is believed to be the first step in its microbicidal activity. The MPO-H2O2-Cl- system is responsible for most oxidative killing of Actinobacillus actinomycetemcomitans by human neutrophils. There appear to be three forms of MPO (MPO I, II, and III), all of which can kill this organism in the presence of H2O2 and chloride. In this study, we characterized the binding of native human neutrophil MPO to A. actinomycetemcomitans by an elution procedure dependent on the cationic detergent cetyltrimethylammonium bromide. Binding of native MPO was rapid and reached apparent equilibrium within 1 min. A proportion of binding under equilibrium conditions was saturable and highly avid, with a capacity of 4,500 sites per cell and a dissociation constant of 7.9 X 10(-10) M. At equal protein concentrations, more MPO III bound than MPO II, and more MPO II bound than MPO I. The high-avidity interaction was inhibitable with yeast mannan and with the serotype-defining mannan of A. actinomycetemcomitans. Binding was also partially reversible with yeast mannan. MPO bound to the high-avidity sites did not oxidize guaiacol but oxidized chloride, as detected by the chlorination of taurine. MPO bound to the high-avidity sites was incapable of killing A. actinomycetemcomitans alone in the presence of H2O2 and Cl-, but potentiated killing when sufficient additional MPO was provided. The killing of A. actinomycetemcomitans by the MPO-H2O2-Cl- system was inhibited by yeast mannan and a serotype-defining mannan of A. actinomycetemcomitans. We conclude that high-avidity binding of MPO to the surface of A. actinomycetemcomitans is a mannan-specific interaction and that MPO bound to the high-avidity sites is essential but not alone sufficient to kill A. actinomycetemcomitans.

Actinobacillus↗
PubMed1987

Muscarinic cholinergic inhibition of adenylate cyclase in airway smooth muscle.

The goal of our study was to test for an inhibitory effect of acetylcholine on adenylate cyclase activity in canine trachealis muscle. Therefore, cells were dispersed from the muscle enzymatically and lysed, and adenylate cyclase activity was assayed in a membrane suspension isolated from the lysates. Maximal beta-adrenergic stimulation, in the presence of GTP (10(-4) M), increased the activity of adenylate cyclase twofold above the activity induced by GTP alone. In the presence of GTP, acetylcholine (10(-4) M) decreased activity from 97 +/- 21 to 55 +/- 13 pmol cyclic AMP X min-1 X mg protein-1 (means +/- SE; n = 5; P less than 0.05); in the presence of GTP plus isoproterenol (10(-4) M), the acetylcholine-induced decreases were from 163 +/- 29 to 101 +/- 15 pmol cyclic AMP X min-1 X mg protein-1 (P less than 0.05). These decreases were dose dependent and they were altered by a series of cholinergic agents in a pattern consistent with a muscarinic effect. Our results suggest that one biochemical effect of vagal stimulation in the central airways of dogs may be attenuated adenylate cyclase activity in the smooth muscle.

Acetylcholine↗
PubMed1987

Affinities of pirenzepine for muscarinic cholinergic receptors in membranes isolated from bovine tracheal mucosa and smooth muscle.

Muscarinic cholinergic receptors have been classified into subtypes based on their high (M-1 subtype) or low (M-2 subtype) affinities for the nonclassic antagonist pirenzepine, and this classification has important experimental and therapeutic implications. Because muscarinic receptors are abundant in the airways where they mediate several different cellular responses, the goal of this study was to characterize the affinities of pirenzepine for the muscarinic receptors in bovine tracheal mucosa and smooth muscle. After isolating membrane particulates from mucosa and smooth muscle, as well as from bovine cerebral cortex (a known source of M-1 receptors), we used 3H-quinuclidinyl benzilate to label muscarinic receptors in the particulates and performed competition radioligand binding assays in the presence of either atropine or pirenzepine. Receptors from all 3 tissues (mucosa, smooth muscle, and cerebral cortex) were of a relatively uniform affinity for atropine (range of KI values: 0.8 +/- 0.4 X 10(-9) to 2.4 +/- 1.7 X 10(-9) M), as would be predicted for this classic muscarinic antagonist. By contrast, affinities for pirenzepine differed depending on the tissue. In cerebral cortex, the majority of receptors were of high affinity for pirenzepine (KI = 1.8 +/- 1.4 X 10(-8) M). In both mucosa and smooth muscle, receptors were of low affinity for pirenzepine (Kl = 4.8 +/- 0.4 to 6.9 +/- 3.8 X 10(-7) M). We conclude that muscarinic cholinergic receptors in bovine tracheal mucosa and smooth muscle are predominantly of the M-2 subtype.

Animals↗
PubMed1987

Mutagenesis and cytotoxicity in human epithelial cells by far- and near-ultraviolet radiations: action spectra.

Action spectra were determined for cell killing and mutation by monochromatic ultraviolet and visible radiations (254-434 nm) in cultured human epithelial P3 cells. Cell killing was more efficient following radiation at the shorter wavelengths (254-434 nm) than at longer wavelengths (365-434 nm). At 254 nm, for example, a fluence of 11 Jm-2 gave 37% cell survival, while at 365 nm, 17 X 10(5) Jm-2 gave equivalent survival. At 434 nm little killing was observed with fluences up to 3 X 10(6) Jm-2. Mutant induction, determined at the hypoxanthine-guanine phosphoribosyltransferase locus, was caused by radiation at 254, 313, and 365 nm. There was no mutant induction at 334 nm although this wavelength was highly cytotoxic. Mutagenesis was not induced by 434 nm radiation, either. There was a weak response at 405 nm; the mutant frequencies were only slightly increased above background levels. For the mutagenic wavelengths, log-log plots of the mutation frequency against fluence showed linear regressions with positive slopes of 2.5, consistent with data from a previous study using Escherichia coli. The data points of the action spectra for lethality and mutagenesis were similar to the spectrum for DNA damage at wavelengths shorter than 313 nm, whereas at longer wavelengths the lethality spectrum had a shoulder, and the mutagenesis spectrum had a secondary peak at 365 nm. No correlation was observed for the P3 cells between the spectra for cell killing and mutagenesis caused by wavelengths longer than 313 nm and the induction of DNA breakage or the formation of DNA-to-protein covalent bonds in these cells.

Cell Line↗
PubMed1986

Inhibition of metabolic cooperation in Chinese hamster V79 cells by 1 alpha, 25-dihydroxycholecalciferol, the active metabolite of vitamin D3.

The biologically active metabolite of vitamin D3, 1 alpha, 25-dihydroxycholecalciferol (1,25-(OH)2D3), inhibited the metabolic cooperation between cocultivated Chinese hamster V79 cells that are either susceptible or resistant to the cytotoxic effect of 6-thioguanine (TG). This inhibition was characterized by an increased survival of TG-resistant cells when they are cocultured with susceptible cells in the presence of TG. TG-resistant cells in the absence of susceptible cells and after treatment with TG yielded a cloning efficiency of about 90%. Cocultivation of these cells with the susceptible cells reduced this cloning efficiency to about 30%. At 0.5 microgram/ml, 1,25-(OH)2D3 restored the cloning efficiency of the TG-resistant cells in the cocultures to 62%. Phorbol 12-myristate 13-acetate (PMA), a known inhibitor of metabolic cooperation, at 0.5 microgram/ml restored the cloning efficiency to a similar extent. Vitamin D3, 24,25-dihydroxycholecalciferol (24,25-(OH)2D3, and phorbol were ineffective in inhibiting this metabolic cooperation. 1,25-(OH)2D3, unlike PMA, did not inhibit the binding of [3H]phorbol 12,13-dibutyrate (PDBu) to its cellular receptors in either the TG-susceptible or resistant cells. These results indicate that 1,25-(OH)2D3 resembles tumor-promoting agents such as PMA in its capacity to inhibit metabolic cooperation, but this capacity is not mediated through phorbol diester receptors.

Animals↗
PubMed1986

Ethics, technology, and the high cost of dying: a public forum.

To increase public awareness of the complexity of the issues surrounding care for the terminally ill, a county medical society and a local hospital council co-sponsored a public forum in October 1985. Panel members discussed the case of a terminally ill cancer patient from the medical, psychologic, economic, legal, and family perspectives. Panel members stressed the importance of helping the dying person to choose the preferred treatment and to achieve an emotionally satisfying death. The audience responded by pointing out the barriers to achieving death with dignity, which include poverty, lack of social support, and difficulty in facing and talking about death. In an evaluation questionnaire, the audience indicated that the emotional aspects and the communication problems involved in care for the terminally ill caused them more concern than the legal and ethical issues.

Aged↗
PubMed1986

Optic disc swelling in sympathetic ophthalmitis and Harada's disease.

In sympathetic ophthalmitis and Harada's disease the fundus appearance is characterised by pale areas of elevated retina associated with a diffuse choroidal abnormality on fluorescein angiography. Optic disc swelling, though constant, is rarely prominent. Four patients, one with sympathetic ophthalmitis and three with Harada's disease, are described, in whom optic disc swelling with visual loss was the predominent sign at one stage of the disease.

Adult↗
PubMed1986

Activation of the colon carcinogen 1,2-dimethylhydrazine in a rat colon cell-mediated mutagenesis assay.

Suspensions of rat colon epithelial cells metabolized the potent colon carcinogen, 1,2-[14C]dimethylhydrazine (DMH), into 14C-labeled, alkali-soluble volatile products, presumably CO2. The colon cell suspensions, however, were less effective than rat hepatocyte suspensions. In addition, we used a cell-mediated mutagenesis assay to test rat colon epithelial cells grown from tissue explants for their ability to metabolize DMH into products mutagenic for human P3 teratoma cells. Mutagenesis in the P3 cells was indicated by an acquired resistance to 6-thioguanine. Cocultivation of the colon cells with the P3 cells in the cell-mediated assay resulted in mutagenesis, whereas in the absence of the colon cells, no mutagenesis by DMH was observed. Similar results were obtained in a hepatocyte-mediated mutagenesis assay. Colon cells were also able to activate another carcinogen, benzo(a)pyrene, into products mutagenic for the P3 cells. Individual epithelial clonal populations isolated from the colon cultures grown from tissue explants, however, expressed different capacities to activate DMH and benzo(a)pyrene into mutagens, and a high degree of DMH activation by cells from a colon clone was not necessarily associated with a similar degree of benzo(a)pyrene activation. Our results indicate that the colon itself contains epithelial cell types capable of effectively converting DMH into mutagenic (and presumably carcinogenic) products without necessarily involving intermediary metabolism by hepatocytes as previously thought.

1,2-Dimethylhydrazine↗
PubMed1986

Horizons in burn care.

The renaissance of burn care began during World War II. From 1960 to the present there has been a rapid advance in burn medicine that has resulted from a better understanding of the emotional, physical, and physiologic problems occurring in the severely burned individual. Now, even the most severely burned have an excellent chance of returning to a functioning, useful place in society. We foresee continued improvements in the organization and delivery of burn care and the results therefrom.

Burn Units↗
PubMed1985

Changes in plasma opioid concentrations after physiotherapeutic exercises for arthritic patients.

Plasma concentrations of [met]enkephalin (ME) and beta-endorphin (beta E) were measured in samples obtained immediately before and after physiotherapeutic exercises for patients with ankylosing spondylitis (AS), osteoarthritis (OA), or knee injuries. Correlations were sought between opioid peptide concentrations or changes therein, and nature, severity and duration of disease, age, severity of pain reported and pain threshold. No correlation was found with any of the pain parameters. However, there was a possible relationship between age or duration of disease and changes in ME concentrations.

Adult↗
PubMed1985

Soft agarose culture human tumour colony forming assay for drug sensitivity testing: [3H]-thymidine incorporation vs colony counting.

In vitro drug sensitivity testing, both by optical colony counting and by a [3H]-TdR incorporation assay, was performed on human tumour cells proliferating in soft agar cultures. Cells from two different human tumour cell lines, 5 different human tumour xenografts, and 94 different primary human tumour specimens of various histologic types were studied. Regression analysis comparing the results of the colony counting assay and the [3H]-TdR assay revealed good to excellent correlations between the two assay endpoints for quantitating the effect of in vitro anticancer drug exposure for a large number of different agents. The presence of pre-existing tumour cell aggregates complicates the performance of the optical colony counting assay. The [3H]-TdR incorporation assay is more sensitive and reproducible than the colony counting assay when performed on samples containing a large number of initially seeded tumour cell aggregates.

Antineoplastic Agents↗