Disease relevance of Luminescence

• Using bioluminescence detection of glutamate release from freshly prepared brain slices, we show that implanted glioma cells continue to secrete glutamate [1].
• Extent of O-2-release and chemiluminescence, attributed to singlet oxygen, has been compared in human monocytes and neutrophils during phagocytosis, stimulation by the surface-active agent phorbol myristate acetate, or contact with aggregated IgG in a model of immune complex disease [2].
• In ulcerative colitis, luminol chemiluminescence correlated with microscopic inflammation (Spearman's p = 0.74, P = 0.0001) and was decreased by sodium azide (-89%, P less than 0.05), taurine (-31%, P less than 0.05), catalase (-23%, P less than 0.05), and dimethyl sulfoxide (-29%, P less than 0.05) [3].
• The lactose permease of Escherichia coli was labeled with eosinyl-maleimide, reconstituted into vesicles of dimyristoylphosphatidylcholine and subjected to time-dependent phosphorescence anisotropy measurements in order to determine the rotational diffusion coefficient [4].
• LuxR, the Vibrio fischeri luminescence gene (lux) activator, is the best-studied member of a family of bacterial transcription factors required for cell density-dependent expression of specific genes involved in associations with eukaryotic hosts [5].

Psychiatry related information on Luminescence

• DESIGN: The determinations made include the plasma total antioxidant capacity (TRAP) and tert-butyl hydroperoxide-initiated chemiluminescence and catalase activity in erythrocytes from 18 patients with probable Alzheimer's disease and 18 matched control subjects with normal cognitive function [6].
• These measurements were used to characterize and optimize the sensitivity of the construct by determining the conditions at which the culture exhibited maximum specific bioluminescence and minimum response time to ethanol induction in batch cultivation [7].
• Effect of in vivo corticosterone and acute food deprivation on rat resident peritoneal cell chemiluminescence after activation ex vivo [8].
• Effect of cysteine ethylester hydrochloride (Cystanin) on host defense mechanisms (V): Potentiation of nitroblue tetrazolium reduction and chemiluminescence in macrophages or leukocytes of mice or rats [9].

High impact information on Luminescence

• Cation binding to beta 3 (118-131) was demonstrated by terbium luminescence and mass spectroscopy [10].
• Nitric oxide release from cultured bovine aortic endothelial cells was detected by chemiluminescence and bioassay experiments compared the vasodilator potencies of nitric oxide, S-nitrosocysteine, and EDRF [11].
• The spectral sensitivity of rhodopsin is well matched to typical spectra of bioluminescence of organisms found at lesser depths, but other animals detect such emissions without the unusual features of the R. exoculata eye [12].
• Agents which can prevent chemiluminescence and cytochrome c reduction, such as superoxide dismutase (SOD), reduced NK-mediated cytolysis and agents which increased chemiluminescence, such as interferon, also increased NK-mediated cytolysis [13].
• Histamine-coated particles generate superoxide (O-2) and chemiluminescence in alveolar macrophages [14].

Chemical compound and disease context of Luminescence

• Exploiting luminescence spectroscopy to elucidate the interaction between sugar and a tryptophan residue in the lactose permease of Escherichia coli [15].
• Dihydropyridine effects indicated that slow Ca channels play a predominant role: The agonist Bay K 8644 (0.3-1 microM) increased force and aequorin luminescence, whereas the antagonist nitrendipine (1-30 microM) abolished the tetanus [16].
• Nitric oxide metabolites (nitrites + nitrates [NOx]) were measured by chemiluminescence in 105 ascites samples obtained from 87 cirrhotic patients and in 87 simultaneously obtained serum samples [17].
• Chemosensitivity testing of human tumors using a microplate adenosine triphosphate luminescence assay: clinical correlation for cisplatin resistance of ovarian carcinoma [18].
• Vibrio harveyi aldehyde dehydrogenase. Partial reversal of aldehyde oxidation and its possible role in the reduction of fatty acids for the bioluminescence reaction [19].

Biological context of Luminescence

• The bioluminescence phenotype requires genes for regulatory and biochemical functions, the latter encoded by five lux genes contained in a single operon [20].
• Incubation of human monocytes with anti-CD36 MAbs or IRBC resulted in stimulation of the respiratory burst as measured by reduction of nitroblue tetrazolium and generation of chemiluminescence [21].
• Membrane potential, tension and aequorin luminescence were measured during exposure to elevated [Ca2+]0, strophanthidin and/or isoproterenol (to induce DADs), or cesium chloride (to induce EADs) [22].
• In this report, dimers of glycoprotein hormone receptors were demonstrated in living cells, with a combination of biophysical (bioluminescence resonance energy transfer and homogenous time resolved fluorescence/fluorescence resonance energy transfer), functional and biochemical approaches [23].
• We have used in vivo cab2::luciferase gene bioluminescence markers containing site-directed mutations in the CUF-1 and CGF-1 binding sites to define the role of these proteins in CAB2 regulation and to further delineate the terminal genomic targets of the phytochrome and circadian clock signal transduction pathways [24].

Anatomical context of Luminescence

• Monocytes generated O-2-and chemiluminescence with each of the three stimuli, although values were significantly less than those of neutrophils from the same individuals [2].
• Mild glutaraldehyde treatment of effector cells abrogated their ability to generate chemiluminescence, whereas K562 target cells treated in the same way were almost fully able to induce a chemiluminescence response to NK-enriched lymphocytes [25].
• Deoxycholate (0.5-5 mM) increased superoxide dismutase sensitive chemiluminescence 2-10-fold and stimulated superoxide production as measured by cytochrome c reduction in colonic mucosal scrapings or crypt epithelium [26].
• The rotational diffusion of concanavalin A receptors of viable Friend erythroleukemia cells and the band 3 anion transport system of human erythrocytes has been measured via the time-dependent phosphorescence emission intensity and anisotropy of triplet probes excited by a 5-ns laser pulse [27].
• The contribution of NO to acetylcholine-induced endothelium-dependent hyperpolarization and relaxation of the rabbit carotid artery was determined by measuring NO with electrochemical and chemiluminescence techniques [28].

Associations of Luminescence with chemical compounds

• Although the ruthenium-modified oligonucleotide hybridized to an unmodified complement luminesces intensely, the ruthenium-modified oligomer hybridized to the rhodium-modified oligomer shows no detectable luminescence [29].
• These include electron spin resonance, thermoluminescence, optically stimulated luminescence, uranium series, and amino acid racemization [30].
• We report that light production by fireflies can be stimulated by nitric oxide (NO) gas in the presence of oxygen and that NO scavengers block bioluminescence induced by the neurotransmitter octopamine [31].
• Single-molecule luminescence spectroscopy measurements on CdSe quantum rods with an aspect ratio between 1 and 30 confirm a sharp transition from nonpolarized to purely linearly polarized emission at an aspect ratio of 2 [32].
• Singlet-oxygen chemiluminescence in peroxide reactions [33].

Gene context of Luminescence

• RANTES, but not MIP-1 alpha, induced a biphasic chemiluminescence response, however, of lower magnitude than C5a [34].
• Herein, we report that living cells stably transfected with a codon-humanized Rluc show coelenterazine-mediated bioluminescence in a highly MDR1 Pgp-modulated manner [35].
• Here, we imaged p53 transcriptional activity in Bax-/- carcinomas by using bioluminescence, in vivo, and find that p53 is required for sensitization to TRAIL by CPT-11 [36].
• To analyze effects of CXCR4 on metastases to the lung, an organ commonly affected by metastatic breast cancer, we injected tumor cells intravenously and monitored cell growth with bioluminescence imaging [37].
• The two monokines identified to be secreted in response to LPS and to be inhibited by dexamethasone, IL-1 and TNF, had, however, no comparable effect on chemiluminescence [38].

Analytical, diagnostic and therapeutic context of Luminescence

• Three, 12, or 24 hours later, tumor blood flow and adenosine triphosphate (ATP) concentrations were measured by [4-N-methyl-14C]iodoantipyrine autoradiography and quantitative ATP imaging bioluminescence, respectively [39].
• Tissues were analysed by sodium phosphotungstic acid precipitation of PrP(Sc) and western blotting using high sensitivity enhanced chemiluminescence [40].
• Superoxide production by human aortic endothelial cells was monitored by lucigenin chemiluminescence, and expression of the adhesion molecules vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 were quantified by flow cytometry [41].
• Results of carbon monoxide titration experiments and data from absorption and excitation-emission spectra provide convincing evidence that the observed emission originates from a fluorescent copper(I)-carbon monoxide complex, and this emission is interpreted as charge-transfer luminescence [42].
• Electrical stimulation of the sympathetic nerves or adrenaline injection caused an elevation of bioluminescence in the liver area of transgenic mice carrying mPer1 promoter-luciferase [43].

References