Let's call it “color‐gamut rendering”

The term “color gamut” historically has been associated with color output such as optimal color stimuli and additive and subtractive imaging systems. Recently, this term has been used with input devices such as scanners and digital cameras. It is proposed that the term “color‐gamut rendering” should be used instead of input devices. This clarifies the distinction between input (analysis) and output (synthesis) color systems in terms of the effect of an input system on defining the colorimetric properties of an output system. © 2007 Wiley Periodicals, Inc. Col Res Appl, 32, 334–335, 2007     

Efficacy of gadolinium in MR brain imaging of HIV-infected patients

PURPOSE: To determine the value of gadolinium in routine head MR imaging of HIV-infected patients. METHODS: One hundred and three consecutive human immunodeficiency virus-infected patients referred for head MR imaging were scanned without and with intravenous gadopentetate dimeglumine (Gd-DTPA) contrast. RESULTS: The precontrast scans of 82 patients were either normal, or had atrophy or diffuse white matter changes only. Sixteen of these 82 demonstrated enhancing abnormalities: eight meningeal/ependymal enhancement and eight focal enhancing lesions. Twenty-one of the 103 scans had focal or mass lesions on the precontrast images; in eight of these scans, new information was obtained with Gd-DTPA. Of the 24 patients in both groups where new information was obtained with Gd-DTPA, the information contributed to a change in the clinical care of nine patients. CONCLUSION: Gadolinium-enhanced MR is useful in the management of selected patients with human immunodeficiency virus infection, for example those with symptoms suggesting meningeal involvement, focal brain lesions, or if the unenhanced MR does not explain all the patient's symptoms.     

Two residues that may ligate Ca2+ in transmembrane domain six of the plasma membrane Ca(2+)-ATPase

In order to identify Ca2+ ligands in the putative transmembrane domain 6 of the plasma membrane Ca2+ pump, amino acids Asn879, Met882, Asp883, and Ser887 were singly altered. Asn879, Met882, and Asp883 were chosen because the corresponding amino acids have been proposed as Ca2+ ligands in the sarcoplasmic reticulum Ca2+ pump (Clarke, D. M., Loo, T. W., and MacLennan, D. H. (1990) J. Biol. Chem. 265, 6262-6267). For the alterations, a fully active truncated version of the pump was used, because the interaction of Ca2+ with the pump could be studied without interference from calmodulin binding. The mutants at Asn and Asp did not carry out ATP-supported Ca2+ uptake and formed no acylphosphate from [gamma-32P]ATP, suggesting that, like the corresponding amino acids in the sarcoplasmic reticulum Ca2+ pump, these two are Ca2+ ligands. However, all the mutants at the position of Met882 showed some activity. Indeed, the Met882--> Ile mutant was fully active at a saturating Ca2+ concentration and only the K1/2 for Ca2+ activation was shifted slightly upward. Converting the Met to Thr (which is the corresponding residue in the sarcoplasmic reticulum Ca2+ pump) reduced the activity to 20% of the wild type, further emphasizing the differences between the two Ca2+ pumps. The mutant Ser887--> Ala was expressed in greater amounts than, and had a specific activity about 50% higher than, the wild type, indicating that this serine also could not be a Ca2+ ligand and could not replace the missing Thr at position Met882.     

The kappa opioid receptor expressed on the mouse R1.1 thymoma cell line down-regulates without desensitizing during chronic opioid exposure

The R1.1 mouse thymoma cell line expresses a single class of kappa opioid receptors that is negatively coupled to adenylyl cyclase through a Bordetella pertussis toxin-sensitive inhibitory guanine nucleotide-binding protein. The aim of the present study was to determine whether chronic opioid treatment of R1.1 cells altered either the binding properties or the functional response associated with the kappa opioid receptor. Culturing of R1.1 cells with the kappa-selective agonist (trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzeneacetamide methane-sulfonate hydrate (U50,488) for 3 hr and longer, followed by extensive washing of R1.1 cell membranes, produced a concentration- and time-dependent reduction in the binding of the kappa-selective ligand (5 alpha,7 alpha,8 beta)-(-)-N-methyl-N-(7-(1-pyrrolidinyl)-1- oxaspiro(4,5)dec-8-yl) benzeneacetamide ([3H]U69,593). Culturing of R1.1 cells with 100 nM U50,488 for 24 hr produced approximately a 50% reduction in the Bmax value for [3H]U69,593 and [3H]naloxone binding. In contrast to the reduction in binding, there was no change in the inhibition of adenylyl cyclase activity by (-)-U50,488. To determine whether kappa opioid receptor function was maintained by spare receptors after agonist-induced down-regulation, membranes from untreated R1.1 cells were incubated with 400 nM of the irreversible opioid antagonist beta-chlornaltrexamine (beta-CNA) followed by extensive washing. beta-CNA produced a 50% reduction in the [3H]U69,593 binding and a 6-fold increase in the IC50 value for (-)-U50,488 inhibition of adenylyl cyclase activity, with no change in the maximal inhibition of cyclic AMP levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Flavopiridol: a cytotoxic flavone that induces cell death in noncycling A549 human lung carcinoma cells

Flavopiridol (NSC 649890, L86-8275), a potent inhibitor of cyclin-dependent kinase 1/p34cdc2 phosphorylation and kinase activity, is currently undergoing Phase I clinical testing as a potential antineoplastic agent. Previous studies have suggested that flavopiridol is cytostatic but not cytotoxic when applied to exponentially growing cells. In the present study, various human tumor cell lines were assayed for trypan blue exclusion and ability to form colonies after exposure to flavopiridol under a variety of growth conditions. When log phase A549 non-small cell lung cancer cells were examined 72 h after the start of a 24-h flavopiridol exposure, as many as 90% of the cells accumulated trypan blue. A 24-h exposure to 250-300 nM resulted in trypan blue uptake in 50% of A549 cells at 72 h and a 50% reduction in colony formation. Similar results were observed in HCT8 ileocecal adenocarcinoma, T98G glioblastoma, MCF-7 breast adenocarcinoma, and HL-60 leukemia cells. With A549 cells, identical results were obtained in actively growing logarithmic phase cells and growth-arrested confluent cells. Treatment with the DNA synthesis inhibitor aphidicolin only minimally affected the cytotoxicity of flavopiridol. In contrast, the RNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole or the protein synthesis inhibitor cycloheximide reduced the cytotoxicity of flavopiridol. These results suggest that: (a) flavopiridol is not only cytostatic, but also cytotoxic to a variety of human tumor cell lines; (b) flavopiridol is equally active against cycling and noncycling A549 cells; and (c) RNA and protein synthesis appear to play a role in flavopiridol-induced cytotoxicity.     

Accuracy and stability improvements of integral equation modelsusing the partial element equivalent circuit (PEEC) approach

The partial element equivalent circuit (PEEC) technique is a formulation which transforms an electric field integral equation (EFIE) into a full-wave equivalent circuit solution. In this paper, improvements are made to the PEEC model through the development of a refined method of computing both the partial inductances as well as the coefficients of potential. The method does not increase the number of unknowns. In addition, damping is added to the PEEC model in order to further reduce nonphysical resonances which may occur above the useful frequency range, The observations and solutions presented in this paper are especially important for time domain solvers. The effectiveness of the method is illustrated with several examples