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PubMed2002

Imaging of abdominal infection using 99m Tc stannous fluoride colloid labelled leukocytes.

Radiolabelling of leukocytes using labelled phagocytosed technetium-99m (99mTc) colloidal radiopharmaceuticals has been reported as a method for imaging infection. This in vivo study compares the use of leukocytes labelled using 99mTc stannous fluoride colloid with leukocytes labelled using indium-111 (111In) oxinate. A total of 26 patients (10 male, 16 female; mean age 52 years, range 23-88 years) referred for the investigation of possible infection were studied using both leukocyte labelling methods simultaneously. Images were acquired 4h and 24h after re-injection of the labelled cells. The images were evaluated qualitatively by two nuclear medicine physicians. The results show a high degree of concordance between the techniques: 11 of the 28 images showed a focus of leukocyte accumulation with both techniques at 24h, and 13 out of 28 showed a normal appearance at 24h with both methods. In four cases the results were discordant; the 99mTc stannous fluoride colloid labelled leukocytes gave a false positive appearance at 24h in three patients and a false negative in one. In conclusion, colloid labelling of leukocytes offers a sensitive method for the detection of infective foci coupled with the high resolution imaging offered by 99mTc. It has the advantage over other in vitro labelling methods of being a simpler, non-labour-intensive procedure employing whole blood, and its use should be considered by departments that have limited facilities for in vitro leukocyte labelling.

Abdominal Abscess↗
PubMed2006

Uncommon findings in Tc-99m macroaggregated albumin venography in distal inferior vena cava obstruction.

In inferior vena cava obstruction, collateral pathways allow the retrograde flow of venous blood from the lower part of the body. Unanticipated findings of Tc-99m macroaggregated albumin (MAA) venography in 3 cases with deep vein thrombosis of the legs and infrarenal inferior vena cava obstruction are presented. Apart from extensive collateral networks in the legs and the abdomen, the visualization of the liver indicates a shunt of the systemic venous blood flow through the paraumbilical vein to the portal vein. The visualization of lumbar and thoracic vertebrae is attributed to venous flow through a dilated vertebral plexus, resulting in trapping of tracer in the neighboring bone marrow.

Aged↗
PubMed2006

Measurement and 3D simulation of self-organized filaments in a barrier discharge.

We report on pattern formation phenomena in the filamentary dielectric barrier discharge between plane glass electrodes. It is for the first time that a three-dimensional (3D) self-organized glow pattern was both observed in an actual experiment and directly calculated in a full 3D discharge simulation in a quantitative manner. Specifically, we investigate the genesis of periodic patterns during the first breakdowns. Despite our simple drift-diffusion discharge model, the correspondence of experimental and numerical findings is surprisingly good.

Electrodes↗
PubMed1992

Structure of bis(2-chloroethyl)ammonium hexachlorostannate.

[(ClCH2CH2)2NH2]2SnCl6, M(r) = 617.48, monoclinic, C2/c, a = 15.67 (2), b = 13.54 (2), c = 13.24 (2) A, beta = 127.9 (2) degrees, V = 2217 A3, Z = 4, D chi = 1.85 g cm-3, lambda(Mo K alpha) = 0.71073 A, mu = 23.70 cm-1, F(000) = 1208, T = 295 K, R = 0.058, wR = 0.071 for 1231 unique reflections. The structure consists of discrete (ClCH2CH2)2NH2+ cations and octahedral SnCl6(2-) anions with the Sn sitting on the twofold axis.

Chemical Phenomena↗
PubMed1991

Antibody-targeted photolysis. Bacteriocidal effects of Sn (IV) chlorin e6-dextran-monoclonal antibody conjugates.

Antibody-targeted photolysis is a technique for damaging or killing cells using light and an antibody-bound photosensitizer. In the present study, immunoconjugates were constructed to selectively kill Pseudomonas aeruginosa bacteria using tin (IV) chlorin e6 which was linked to dextran and then bound to the carbohydrate moiety of a monoclonal antibody specific for Pseudomonas aeruginosa Fisher type I polysaccharide antigen. Killing of Pseudomonas during mid-log phase growth was shown to be dependent upon light dose with complete bacterial cell killing observed at an irradiation dose of 80 J/cm2. Individual components of the immunoconjugates (e.g., antibody or chlorin alone) showed no bacterial cytotoxicity and immunoconjugates constructed with nonbinding antibodies were also ineffective as cytotoxic agents. These studies demonstrate that killing of gram negative bacteria using photoradiation is feasible and suggest that this methodology may be applicable in treatment of infections in man.

Antibodies, Monoclonal↗
PubMed2003

Pits and fissures: relative space contribution in fissures from sealants, prophylaxis pastes and organic remnants.

BACKGROUND: Previous studies by the authors have looked at the nature of the fissure system of human permanent molars and premolars, and has provided evidence for the presence of a prismless layer of enamel. It was noted during these studies that the fissure spaces were often occupied by material other than the fissure sealant. The aim of this study was to define these materials and to look at the percentage contribution of each to the sealed fissure space. METHODS: A sample of teeth, both molars and premolars, were sealed with an unfilled fissure sealant after prophylaxis with a coloured prophylaxis paste. In one group, the crown of the tooth was removed by dissolution in hydrochloric acid following placement of the sealant. This revealed a negative image of the fissure system and its contents. The second group of teeth was sectioned following sealing, and the contents of the fissure space were analyzed. RESULTS: The negative image of the fissure system displayed the fissure contents by colour and the sectioned teeth were able to be computer analyzed to establish the relative contribution of sealant, prophylaxis paste and organic material to the fissure space. CONCLUSIONS: Sealant contribution was in the range of 14-96 per cent, prophylaxis paste from 0-50 per cent and organic remnants 0-55 per cent. The presence of these last two components could contribute to sealant loss.

Bicuspid↗
PubMed2006

Assessment of differential branch pulmonary blood flow: a comparative study of phase contrast magnetic resonance imaging and radionuclide lung perfusion imaging.

OBJECTIVES: To test whether magnetic resonance (MR) imaging can be used to assess differential lung blood flow as accurately as isotope lung perfusion studies in patients investigated for congenital heart disease. METHODS AND RESULTS: Radionuclide lung perfusion and MR imaging were performed in 12 children with suspected unilateral branch pulmonary artery stenosis (mean age 12.1 (5.9) years, range 3.1-17.2 years). A non-breath hold, fast gradient echo phase contrast MR sequence was used to measure flow in the pulmonary trunk and one pulmonary artery to calculate differential flow. Good agreement was shown between the two imaging methods by Bland-Altman analysis. There was excellent correlation between the radionuclide and MR phase contrast calculated total lung blood flow (r = 0.98, p < 0.0001). CONCLUSION: MR phase contrast is an accurate method for measuring differential total right and left lung blood flow. If MR imaging is performed to assess the branch pulmonary arteries, differential lung blood flow can be also measured, avoiding the need for an additional radionuclide lung perfusion scan and reducing the overall radiation burden to this group of patients.

Adolescent↗
PubMed1992

Inhibition of erythrocyte 5-aminolaevulinate hydrolase activity by tin and its prevention by selenite.

Mice were injected with either SnCl2 (intraperitoneal) or Na2SeO3 (subcutaneous) alone or together at doses of 50 mumol/kg body weight. After 20 hours blood was collected and the concentrations of tin (Sn) and Selenium (Se) and the activity of 5-aminolaevulinate hydrolyase (ALA dehydratase, EC 4.2.1.24) in blood were determined. The concentrations of Sn in whole blood were 4.9 (SD 1.5) nmol/ml (n = 4) and ALA dehydratase activity was 10% of the control in Sn treated animals. Concentrations of Sn were 2.6 (SD 0.6) nmol/ml and ALA dehydratase activity was 92% of that in control animals when Sn and Se were simultaneously injected. The supernatant from lysed erythrocytes from Sn treated mice were applied to a Sephacryl S-300 column. The predominant peak containing Sn was eluted at the position of haemoglobin; a second peak was eluted at the position of ALA dehydratase. When the supernatant of lysed erythrocytes from mice injected with Sn and Se was chromatographed, a negligible amount of Sn was detected in the ALA dehydratase fraction. It thus appears that Sn binds to ALA dehydratase molecules and inhibits enzyme activity, and that simultaneous injection of Se prevents Sn binding to ALA dehydratase, thereby preventing the inhibition of ALA dehydratase activity by Sn.

Animals↗
PubMed1985

Inhibition of monoamine oxidase by metaiodobenzylguanidine, a new radiodiagnostic agent.

Metaiodobenzylguanidine, which is used in the diagnosis and treatment of pheochromocytoma, produced 50% inhibition of monoamine oxidase at a concentration of 8 X 10(-6) M in vitro. These results suggest that a careful study of the structure of a new radiodiagnostic agent should be done to anticipate and prepare for possible unwanted biological effects when administering the preparation to patients.

3-Iodobenzylguanidine↗
PubMed2005

Use of translucent indium tin oxide to measure stimulatory effects of a passive conductor during field stimulation of rabbit hearts.

Biomathematical models and experiments have indicated that passive extracellular conductors influence field stimulation. Because metallic conductors prevent optical mapping under the conductor, we have evaluated a passive translucent indium tin oxide (ITO) thin-film conductor to allow mapping of transmembrane potential (V(m)) and stimulatory current under the conductor. A 1-cm ITO disk was patterned photolithographically and positioned between 0.3-cm(2) mesh shock electrodes on the ventricular epicardium of isolated perfused rabbit hearts stained with 4-{2-[6-(dibutylamino)-2-naphthylenal]ethenyl}-1-(3-sulfopropyl)-, hydroxide, inner salt (di-4-ANEPPS). For a 1-A, 10-ms shock during the action potential plateau, optical maps from fluorescence collected using emission ratiometry (excitation at 488 nm and emissions at 510-570 and >590 nm) indicated that the disk altered V(m) by as much as the height of an action potential. DeltaV(m) became more positive near the edge of the disk, where the ITO conductance gradient was parallel to applied current, and more negative near the opposite edge, where the gradient was not parallel to current. For diastolic shocks, the disk expedited membrane excitation at the sites of positive DeltaV(m) in the heart and in a cardiac model with realistic ITO disk surface and interfacial conductances. Optical maps of ITO transmittance and the model indicated that the disk introduced anodal and cathodal stimulatory current at opposite edges of the disk. Thus ITO allows study of the stimulatory effects of a passive conductor in an electric field.

Animals↗
PubMed2002

Heme oxygenase-1 localization in the rat nephron.

BACKGROUND/AIMS: Renal tubules undergo oxidative injury in various nephropathies. It is unknown whether tubular cells possess mechanisms to attenuate this form of injury. Heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, may provide such a mechanism by reducing levels of free heme, a prooxidant molecule, and by limiting activity of heme-containing prooxidant enzymes. Determination of the distribution of HO-1 in the nephron may identify those segments where HO-1 can afford protection against oxidative injury. METHODS: Rats were injected subcutaneously with two different inducers of HO-1: Stannous chloride and cobalt protoporphyrin. At completion of injections, frozen sections of kidneys were stained for HO-1 using a biotin-conjugated monoclonal anti-HO-1 antibody. To identify the origin of tubules staining positive for HO-1, Tetragonolobus purpureas (TP)-derived lectin and Arachnis hypogaea (AH)-derived lectin were applied to sequential sections of the kidney cortex. RESULTS: In rats injected with either HO-1 inducer, HO-1 was immunolocalized in tubules but not in glomeruli. Staining of sequential sections with TP-derived lectin, which binds mainly to proximal tubular cells, was negative in the tubules that stained positive for HO-1. Staining of sequential sections with AH-derived lectin, which binds mainly to distal and collecting tubular cells, was positive in those tubules that were also positive for HO-1. CONCLUSIONS: In kidneys of rats injected with inducers of HO-1, distal and collecting tubular cells were identified as the main segments of the nephron that express HO-1. We suggest that the distal nephron, by expressing HO-1, may be less vulnerable to oxidative injury.

Animals↗
PubMed2001

Epoxyeicosatrienoic acid-mediated renal vasodilation to arachidonic acid is enhanced in SHR.

We tested the hypothesis that cyclooxygenase-independent vasodilation produced by arachidonic acid (AA) is mediated by epoxyeicosatrienoic acids (EETs) and is blunted in the spontaneously hypertensive rat (SHR). At normal perfusion pressure (PP; 70 to 90 mm Hg), AA constricted the renal vasculature in both SHR and normotensive Wistar-Kyoto rats, an effect abolished by cyclooxygenase inhibition, and converted to vasodilation when PP was raised to approximately 200 mm Hg. Unexpectedly, renal vasodilation elicited by AA was greater in the SHR at high PP; for example, 2.5, 5, and 10 microg of AA produced PP declines of 54+/-9, 92+/-10, and 112+/-5 mm Hg, respectively, in SHR compared with 26+/-3, 45+/-5, and 77+/-6 mm Hg in Wistar-Kyoto rats (P:<0.01). However, the renal vasodilator responses to acetylcholine (0.1 microg) and sodium nitroprusside (1 microg) did not differ between strains, indicating that vascular responsiveness to AA was independent of intrinsic changes in vascular smooth muscle. Hyperresponsiveness of the renal vasculature to AA may be unique for the SHR, because it did not occur in Sprague-Dawley rats with angiotensin II-induced hypertension. 5,8,11,14-Eicosatetraynoic acid (ETYA; 4 micromol/L), an inhibitor of all AA pathways, attenuated the vasodilator responses to AA, as did treatment with stannous chloride, which depletes cytochrome P450 enzymes, suggesting that a cytochrome P450 AA metabolite mediated the renal vasodilation. N:-Methylsulfonyl-12,12-dibromododec-11-en-amide (DDMS; 2 micromol/L), a selective omega-hydroxylase inhibitor, did not affect AA-induced vasodilation, whereas selective inhibition of epoxygenases with either miconazole (0.3 micromol/L) or N:-methylsulfonyl-6-(2-propargyloxyphenyl) hexanamide (MS-PPOH; 12 micromol/L) did, indicating that one or more EETs were involved in the renal vasodilator action of AA at high PP. This conclusion was supported by the demonstration that AA greatly enhanced the renal efflux of EETs at high PP but not at basal PP.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1991

Arachidonic acid elicits endothelium-dependent release from the rabbit aorta of a constrictor prostanoid resembling prostaglandin endoperoxides.

This study was designed to investigate the mediator(s) of endothelium-dependent arterial constrictor responses evoked by arachidonic acid in vitro. A segment of descending rabbit thoracic aorta was isolated and perfused (1-2 ml/min) with oxygenated Krebs' bicarbonate buffer. Changes in the vascular smooth muscle-contracting activity of the aortic effluent were detected by superfusion bioassay using either strips of rabbit aorta or rings of dog saphenous vein, both denuded of endothelium and exposed to indomethacin (10 microM). Arachidonic acid (5-50 micrograms) injected into the inflow of the perfused aorta caused a dose-related increase in the vascular smooth muscle-contracting activity of the aortic effluent, whereas arachidonic acid added directly into the aortic effluent did not. The arachidonic acid-induced elevation of vascular smooth muscle-contracting activity in the aortic effluent was not apparent when indomethacin (10 microM) was added to the aortic inflow to inhibit cyclooxygenase, when the endothelium of the perfused aorta was removed by rubbing, or when the thromboxane A2/prostaglandin H2 receptors of the vascular tissues used for bioassay were blocked with an antagonist (1 microM SQ29548), and was unaffected when an inhibitor of thromboxane synthase (10 microM CGS 13080) was added to the aortic inflow. This effect of arachidonic acid was accompanied by release of prostaglandin H2 (measured as prostaglandin F2 alpha after reduction with SnCl2) in amounts sufficient to elicit contraction of the vascular tissues used for bioassay and was attenuated when a reducing agent (2 mM FeCl2) that converts prostaglandin H2 to 12-heptadecatrienoic acid was added to the aortic effluent. Collectively, these observations suggest that arachidonic acid stimulates endothelium-dependent release from the perfused aorta of a prostanoid that contracts vascular smooth muscle via interaction with thromboxane A2/prostaglandin H2 receptors. The study also suggests that the prostanoid responsible for the vascular smooth muscle-contracting activity of the aortic effluent is a prostaglandin endoperoxide(s) rather than thromboxane A2.

Animals↗